STG-2
STG-2
Guidelines
ln Homoeopathy
Volume 3
DISCLAIMER
ISBN: 978-93-81458-63-1
The AYUSH (Ayurveda, Yoga and Naturopathy, Unani, Siddha Sowa-Rigpa and Homoeopathy)
systems in India, getting involved in several programmes in the last few years have shown to be
successful in improving service delivery. Standard Treatment Guidelines (STG) are ‘‘systematically
developed statements to assist practitioners and patient decisions about appropriate health care for
specific clinical circumstances.’’ They are intended to offer concise instructions on how to provide
healthcare services. The most important benefit of clinical practice guidelines is their potential to
improve both quality and process of care and clinical outcomes. The comments on earlier STGs
published by the council reviewed by international reviewer, are encouraging and overwhelming.
Realizing the importance of traditional systems of medicines in addressing public health issues, the
National Health Policy (NHP) was launched in 2017, mainstreaming the potential of AYUSH systems
within a pluralistic system of integrative healthcare. The foremost aim of medical research is to
translate research into public benefit. To strengthen the integrative care, more documentation is
essential. More the scientific rigour, more tangible are the results and better these would be adopted
for users and beneficiaries. The research findings published in different journals are placed logically
and up-to-date under different disease conditions will help to reach to every homoeopath and
improve the health care delivery.
The guidelines list the preferred treatments for common health problems experienced by people
to be used at all levels within the health delivery system, both public and private. These standard
treatment guidelines will help to rationalize medical practice. There is an urgent need to protect the
population from irrational and unethical practice. Also, educating people and health professionals
about the hazards of irrational curative care is another necessity of our times. Rationalizing clinical
health care also reduces costs for the public health deliveries and makes the system more effective
and reliable.
Subsequent to earlier two volumes of standard treatment guidelines covering 35 clinical conditions,
this third volume covers 20 more clinical conditions. This will further enhance the knowledge and
improve in documentation skills of homoeopathic practitioners, academicians and students at large.
These are: Adhesive capsulitis, Acne, Anxiety disorders, Aphthous stomatitis, Atopic dermatitis,
Breast fibroadenoma, Chikungunya, Chronic suppurative otitis media, Diabetic foot ulcer, Diabetic
neuropathy, Gout, Migraine, Post-operative pain, Rheumatoid arthritis, Scabies, Sciatica syndrome,
Schizophrenia, Sub-clinical hypothyroidism, Tinea and Warts. Similar to earlier ones the STGs in this
volume are prepared, based on data from national and international research studies, authoritative
texts, expert consensus, scientific evidence of acceptable approaches to diagnosis, management
and/or prevention of specific diseases.
The STGs developed are structured and systematically arranged throughout touching upon clinical
definition, incidence, aetiology, pathophysiology, diagnosis (clinical presentation, investigations),
complications, caution lines, evaluation and assessment with validated scales, general management,
homoeopathic management, names of commonly used medicines based on research and experience
of experts, indications of medicines (generalities and characteristic particulars).
We hope that the document will truly help in ‘Linking Education and Clinical Practice with Research’,
motivating the homeopathic professionals including academicians, clinicians, researchers and
teachers to contribute their success stories through case reports, case series and clinical research
studies.
Gout Dr. Pooja Gautam, RO(H)/S -1, Dr. (Mrs.) Jaya Gupta, RO(H)/S-4, CCRH Hqrs., New Delhi
RRI(H), Guwahati, Assam Dr. Mohit Mathur, Reader (NFSG), Nehru Homoeopathic
Medical College & Hospital, Delhi
Dr. Nikunj Jani, Additional Reader, Dept. of Repertory,
MLDMHI, Palghar
Migraine Dr. Renu Bala, RO(H)/ S -1, RRI(H), Prof.(Dr.) L.K.Nanda , Chairman, SCCR, CCRH
Imphal, Manipur Prof.(Dr.) Shama Rao, Dept. of Practice of Medicine,
MLDMHI, Palghar
Post-operative pain Dr. Harleen Kaur, RO(H)/ S -1, Dr. Prof.(Dr.) L.K.Nanda , Chairman, SCCR, CCRH
Jyoti Sachdeva, RA, Dr. Surbhi Jain, Dr Bipin Jain, HOD, Dept. of Homoeopathic Materia
RA, Dr. Daisy Katarmal, SRF(H), Medica at MLDMHI, Palghar
CCRH Hqrs. New Delhi
Rheumatoid Dr. Ritika Hassija Narula, RO(H)/ Dr. Mohit Mathur, Reader (NFSG), Nehru Homoeopathic
arthritis S-1, Dr. Jagyesini Sharma, JRF(H), Medical College & Hospital, New Delhi
CCRH Hqrs. New Delhi Dr. Nikunj Jani, Additional Reader, Department of
Repertory, MLDMHI, Palghar
Scabies Dr. Lipipushpa Debata, RO(H)/ S-3, Dr. Raj K. Manchanda, Director, Dte. of AYUSH, Govt. of
HDRI, Lucknow NCT of Delhi
Dr. P.S. Chakraborty, RO(H)/S-4, DACRRI(H), Kolkata
Dr. Sachin Junagade, Lecturer, Dept. of Organon of
Medicine, MLDMHI, Palghar
Sciatica syndrome Dr. Pritha Mehra, RO(H)/ S-3, Dr. Dr. J.D. Daryani, Chairman, SCDPR, CCRH
Pooja Pandey, JRF(H), DDPRCRI(H), Dr. K. C. Muraleedharan, RO(H)/ S-4, NHRIMH, Kottayam
Noida
Schizophrenia Dr. Vinitha E.R, RO(H)/ S -1, Dr. Dr. Ashok Sharma, CMO (SAG). Dte. Of AYUSH, Govt. of
Jayashree Janagam, Asst. Professor, NCT of Delhi
Dept. of Psychiatry, NHRIMH, Dr. K. C. Muraleedharan, RO(H)/ S-4, NHRIMH, Kottayam
Kottayam Dr. Rajesh Yadav, Lecturer, Dept. of Psychiatry, MLDMHI,
Palghar
Subclinical Dr. Debadatta Nayak, RO(H)/ S -3, Dr. Raj K. Manchanda, Director, Dte. of AYUSH, Govt. of
hypothyroidism Dr. Tabasum Parveen, JRF(H), NCT of Delhi
Dr. Nisha Sehrawat, SRF(H), CCRH Dr Archana Narang, Reader(NFSG), Dept. of Gynaecology
Hqrs., New Delhi and Obstetrics, Dr. B. R. Sur Homoeopathic Medical
College, Hospital and Research Centre, New Delhi
Dr. Saurav Arora, Independent Researcher, New Delhi
Tinea Dr. A. K. Prusty, RO(H)/S-3, Prof.(Dr.) L.K.Nanda, Chairman, SCCR, CCRH
Dr. Santi Adhikary, former SRF(H), Prof.(Dr.) Niranjan Mohanty, Member, SCCR, CCRH
RRI(H), Puri, Odisha Dr Sachin Junagade, Lecturer, Dept. Organon of Medicine,
MLDMHI, Palghar
Warts Dr. Renu Mittal, RO(H)/ S -3, Dr. Dr. Raj K. Manchanda, Director, Dte. of AYUSH, Govt. of
Sonal Pihal, JRF(H), CCRH Hqrs., NCT of Delhi
New Delhi Dr. Anand Kapse, Dept. of Organon of Medicine, MLDMHI,
Palghar
abbreviations
ACR American College of Rheumatology
ACT Assertive Community Treatment
ADASI Atopic Dermatitis Area and Severity Index
AD Atopic Dermatitis
ADSI Atopic Dermatitis Severity Index
AGEs Advanced Glycation End products
ASES American Shoulder and Elbow Surgeons shoulder score
ATTG Anti-tissue transglutaminase
BAI Beck Anxiety Inventory
BBCR Boger Boenninghausen’s Characteristics and Repertory
BCSS Basic Clinical Scoring System
B-IPQ Brief Illness Perception Questionnaire
BI-RADS Breast Imaging-Reporting and Data System
BIT Burrow Ink Test
BMI Body Mass Index
BMMP Benign Mucous Membrane Pemphigoid
BNSS Brief Negative Symptom Scale
BSE Breast Self-Examination
CAINS Clinical Assessment Interview for Negative Symptoms
CASS Clinical Assessment of Schizophrenic Syndromes
CBT Cognitive Behavioral Therapy
CCRH Central Council for Research in Homoeopathy
CDLQI Children’s Dermatology Life Quality Index
CDSS Calgary Depression Scale for Schizophrenia
CES Chronic Ear Survey
CGI-SCH Clinical Global Impression Schizophrenia
CHIK Chikungunya
CI Confidence Interval
CKD Chronic Kidney Disease
CMO Chief Medical Officer
CNS Central Nervous System
COMOT-15 Chronic Otitis Media Outcome Test 15 questionnaire score
COMQ-12 Chronic Otitis Media Questionnaire 12
COXs Cyclooxygenases
CRU(H) Clincial Research Unit (Homoeopathy)
CVD Cardiovascular disease
CWARTS Cutaneous WARTS
DALY Disability Adjusted Life Years
DASH Disabilities of the Arm Shoulder and Hand score
Quality and standard healthcare delivery is very important for the people of any country. To have
quality control and assurance, certain set standards are required to reach the target harmonized
healthcare delivery. Standard Treatment Guidelines (STGs), a systematically developed statement
designed to assist practitioners and patients in making decisions about appropriate healthcare for
specific clinical circumstances are one such document.
Standard Treatment Guidelines (STGs) have been in vogue in India only since recent times and are
gaining popularity among practitioners, owing to uniform guidelines. They have the advantage in
bringing together patients, healthcare providers, drug manufacturers and marketing agencies, and
above all, the policymakers and the legislative system of the country. The drawback in STGs lies in
the difficulties in their implementation on a large scale.
Homoeopathy is a holistic system of medicine wherein patients are treated with an individualistic
approach. Here the treatment given to each patient is tailored according to his/her need. Quality
control and assurance can be achieved by following uniform guidelines that are in consonance with
the available homoeopathic literature, modern medicine, research and day-to-day practices. In
pursuance to the mandate of the Ministry of AYUSH, Government of India, the Central Council for
Research in Homoeopathy has taken a lead and developed standard treatment guidelines for both
acute and chronic diseases.
The set of conditions included in STGs is not exhaustive; rather it is based on the conditions
recommended for management and treatment in day-to-day practice. It is emphasised that the
choices described here have the support of scientific evidence together with the collective opinion
of a wide group of recognised experts. Recommended treatments are primarily limited to the
medicines that were published in research papers, and/or conform to the opinion of experts as
well as experience in homoeopathic practice. It also covers medicines enlisted in essential drug list
(2012).
This document on standard treatment guidelines (STGs) is designed for use by homoeopaths at all
the levels delivering health services. The guidelines can also be used by general practitioners in
their private practice. The STGs are designed to be used as a guide to treatment choices and as a
reference book to help in the overall management of patients, including when to refer.
The research recommendations used have been rated on the following WHO ratings:
1) Evidence rating A — requires at least one randomised control trial as part of a body of scientific
literature of overall good quality and consistency addressing the specific recommendation.
2) Evidence rating B — requires the availability of well−conducted clinical studies, but no
randomised clinical trials on the topic of recommendation.
3) Evidence rating C — requires evidence obtained from expert committee reports or opinions and/
or clinical experience of respected authorities. This indicates an absence of directly applicable
clinical studies of good quality.
The contents of these treatment guidelines will undergo a process of continuous review, for which
comments or suggestions for improvement are welcome. Those comments or suggestions for
addition of diseases should include evidence of prevalence as well as a draft treatment guideline
using the format set out in this book.
To use these guidelines effectively, it is important that you become familiar with the contents; take
time to read the book and understand the contents and layout.
The contents of this book have been arranged in an alphabetical order. Within each section, outcomes
of the studies conducted both nationally and internationally have been identified. For each of these
disease states, the structuring of the information and guidelines has been standardised to include
a brief description of the condition or disease, common signs and symptoms, general management
followed homoeopathic treatment choices and flow chart of entire condition.
The book also incorporates the assessment scales used across the globe by researchers and to some
extent, by physicians in their practice can also be used for making homoeopathy evidence based
system of medicine.
Homoeopathic therapeutics have been suggested, which include the characteristic physical generals,
mental and particular symptoms related to the disease. The pattern has been adopted to emphasize
on holistic approach of homoeopathic treatment, which forms the fundamental basis of prescription.
Referral
These guidelines also have provision for referral of patients to other health facilities. Patients should
be referred when the prescriber is unable to manage the patient either due to lack of personal
experience or availability of appropriate facilities. Patients should be referred, in accordance with
agreed arrangements, where necessary diagnosis and support facilities exist. The patient should be
given a letter or note indicating the problem and what has been done so far, including laboratory
tests and treatment. When indicated for referral, minimal treatment must be given before the patient
reaches a physician/hospital of referral.
Introduction
A holistic model of health in Homoeopathy, taking an overview of the patients, including their
individual mind, body and spirit, life situation and other circumstances, is central in evolving a
curative approach to acute diseases and to some extent chronic diseases too. The holistic view uses
the totality and the constitution of each patient to find a remedy that suits him/her, rather than just
the disease. This is a paradigm shift from the conventional model of treatment approach, i.e., how
illness is viewed.2, 3
Selection of medicine
The medicine selected for each patient is tailored to person specific, taking into consideration4, 5
his/her mental make-up, physical symptoms, and characteristic particulars etc. In case of long term
illness, besides the above mentioned factors, age, occupation, previous illnesses and life circumstance
unique to that individual irrespective of the disease which he/she is suffering from, are also taken
into consideration; thus the dictum “Homoeopathy treats the patient but not the disease”.
Some organ specific medicines with their symptoms are described for each disease along with the
frequently prescribed polychrest medicines in homoeopathic management section. Person specific
or individualised medicine selected based on totality of symptom as written above is always to be
emphasized for effectiveness. In advance cases when mental symptoms are absent or paucity of
totality of symptoms, these rare medicines can be given which gives relief and paves the way to
surface the suppressed totality of symptoms for subsequent second prescription for annihilation
of disease. But these rare medicines should always be prescribed basing on their keynote symptom
which are given for each of the medicines in this book.
1 WHO. Homoeopathy: Overview and analysis of clinical research. December 2006 [unpublished]
2 Fritjof Capra. The Web of Life: A New Scientific Understanding of Living Systems university of Michigan : Anchor Books. 1996
3 David Owen. Principles and Practice of Homeopathy. Elsevier Ltd. Churchill Livingstone.2007
4 Carlston C. Classical Homoeopathy. Philadelphia, Pennsylvania; Elsevier sciences: 2003
5 Hahnemann, S. Organon of Medicine, 5 & 6 Ed. Delhi: Birla Publications, 2003
Selection of potency
After the appropriate medicine is selected, it is essential to decide the requisite potency, dose and
repetition which is imperative for optimum response and faster recovery in each case. Different types
of potencies such as centesimal/ decimal/ 50 millesimal potencies can be employed for treatment
of both acute and chronic diseases. However, selection of potency of the remedy is dependent on
various factors like susceptibility of the patient (high or low), type of disease (acute/chronic), seat/
nature and intensity of the disease, stage and duration of the disease and also the previous treatment
of the disease.6 In this context, given below are the basic rules as evolved through experience:
The closer the similarity a remedy bears to the picture presented by the patient, the higher is the
potency, provided no specific contra-indications to the use of high potencies exist in the case.
A prescription that is predominantly determined by the mental symptoms in a case, gives best
results when higher potencies are employed.
When prescribing for advanced pathological conditions, it is advised to begin the treatment of the
case with a remedy in lower potency.
The repetition of the remedy in regard to potency and dosage is almost as important as the selection
of the remedy itself. The selection of the remedy can hardly be said to be finished until the potency
and dosage have been decided upon. 5, 7,8
Centesimal scale
• Low potencies may be repeated frequently whereas high potencies are not to be frequently
repeated.
• In acute diseases, the medicine may be repeated at very short intervals of every 24, 12, 8, 4
hours or even every 5 minutes.
• In chronic cases, the medicine may be repeated at the interval of 14, 12, 10, 8 or 7 days.
• In chronic diseases resembling cases of acute diseases, the repetition may be made at still
shorter intervals. In these cases, either repeated doses of a low potency of the remedy are given
till the patient is cured or a single dose of high potency is administered followed by placebo till
recovery ensues.
LM scale
6 Close S. The Genius of Homeopathy: Lectures and Essays on Homeopathic Philosophy. New Delhi; B Jain Publishers; 183-211
7 Kent JT. Lectures on Homoeopathic Philosophy. North Atlantic Books, Washington; 1992
8 CCRH. A Handbook on Homoeopathy: Case Taking to Prescribing; New Delhi; CCRH: 2011
Remedy response
After the administration of the similimum, some results are expected. Further prescription largely
depends on the response of the patient to the remedy and proper interpretation of the remedy
response. The remedy response can be understood in respect to: aggravation, amelioration,
disappearance, no change/status quo and change in the order of the symptoms.
1. Aggravation
There are two types of aggravation, either of which may manifest. The first relates to an aggravation
of the disease condition, in which the patient becomes worse. Another type of aggravation is where
the symptoms of the patient are worse, but the patient feels better. Aggravation of symptoms may
manifest in the following manner after the administration of a medicine:
1.1. The aggravation is quick, short and strong with rapid improvement of the patient.
Interpretation: The response of the patient is satisfactory. There is no much tissue change, or
very superficial, if any. The potency was a bit higher. The medicine was most similar one. An
aggravation of this kind is very much reassuring
Prognosis: Very good
Follow-up action: Wait and watch
Interpretation: After a prolonged aggravation, the patient improves slowly. This indicates the
beginning of definite structural change in some organs but the disease has not progressed quite
so far. The medicine was right but the potency was high. Though there have been enough tissue
changes but the medicine would act for a very long time. The patient was on the borderline and
had the disease condition gone further, cure would have been impossible.
Prognosis: Favorable
Follow- up action: Not to disturb till the action of the medicine has exhausted.
Interpretation: The case is incurable since there has been enough irreversible tissue changes
in the patient. The medicine prescribed may or may not have been a correct one but the
potency was very high. The medicine was deep acting in nature, therefore, instead of helping
it has established destruction.
Prognosis: Bad
Follow up action: It necessitates immediate anti-doting. After re-case taking a more similar
medicine in low potency is to be given. Deep acting medicine and high potency should not be
used in chronic and doubtful cases especially where tissue-change may have occurred.
2. Amelioration
When the symptoms are ameliorated, the physician has to observe the pattern in greater detail
and note especially the sequence of events, the duration, etc. which will enable the physician
to judge whether the amelioration is long lasting or due to the palliation.
Interpretation: The medicine was the most similar one and the potency exactly fitted the case.
There was no organic disease or any tendency towards organic change. The trouble was only
a functional disorder. This is an example of highest order of cure, mostly in acute disease
conditions.
Prognosis: Very good
Follow up action: Wait and watch. Assessment to be done as per the nature of the disease. This
case may not require further repetition of medicine.
2.2 The amelioration comes first and the aggravation comes afterwards.
Interpretation:
A) In acute diseases:
1. High grade inflammatory action is present that organs are threatened by the rapid processes
going on. The infection is violent/virulent in nature.
B) In chronic disease:
1. The medicine was partially similar, or
2. There is a condition which interferes with the action of the remedy, or
3. Structural changes have occurred, or organs are destroyed or are in very precarious
condition.
2.4. A full-time amelioration of the symptoms, yet no special relief of the patient.
Interpretation: There are latent conditions (existing organic conditions) in a few patients that
prevent improvement beyond a certain limit. For e.g., a patient with one kidney or bigger part
of the lungs having been calcified / fibrosis. Hence the patient is curable only to a certain limit.
Suitable palliation has been brought about by the homoeopathic remedies.
Prognosis: Bad
Follow up action: Palliative medicine should be prescribed.
4. Change of Symptoms
Interpretation: The medicine was wrong. Greater number of such symptoms indicates towards
selection of a dissimilar medicine.
Prognosis: Bad
Follow up action: If the symptoms are not of serious nature we should wait till the new
symptoms pass off and the patient settles down to original state. After re-case taking a more
similar medicine is to be given. If the symptoms are of serious nature and threatening it has to
be antidoted.
Interpretation: The medicine has been very right. Appearance of old symptoms indicates that
the patient is curable.
Prognosis: Good.
Follow up action: The action of the medicine should not be disturbed. Only if the reestablished
symptom/discharge/eruption stays for pretty long time, the medicine may be repeated. Here
old symptom/diseases may come and go in the reverse order of their appearance (Following
Hering’s Law of Cure).
Interpretation: When the symptoms go from periphery to the centre, the remedy administered
was a wrong one.
Prognosis: Very bad.
Follow up action: It has to be antidoted at once. A more similar remedy has to be found out and
given.
In spite of best efforts in any disease condition, if a favorable response to the treatment is
not achieved, it is advised to refer the case as per the guidelines given in STGs for individual
disease.
Advantages of Homoeopathy
• Treatment with homoeopathic medicines is safe, effective and based upon natural substances.
With the use of single simple substance in micro-doses, medicines are not associated with any
toxicological effect and can be safely used for pregnant women and lactating mothers, infants
and children and in the geriatric population.
• Medicines, instead of having a direct action on the micro-organisms, act on the human system
(self-protective) to fight disease process. As such, no microbial resistance is known to develop
against homoeopathic drugs.
• The mode of administration of medicines is easy. There are no invasive methods and medicines
are highly palatable, thereby enhancing treatment compliance.
• Lack of diagnosis is not a hindrance for initiating treatment with homoeopathic medicines.
• Homoeopathic remedies are non-addictive and once relief occurs, the patient can easily stop
taking them.
• Treatment is cost-effective.
ACNE
CASE DEFINITION
Acne is a disease of the pilosebaceous units in the skin of the face, neck, chest and upper back that
causes non-inflammatory lesions - open (black) and closed (white) comedones, inflammatory lesions
(papules, pustules, nodules and cysts), and varying degrees of scarring and pigmentary changes.1,2
INCIDENCE2,3,4,5,6
Acne is estimated to affect 9.4% of the global population; also, it is the eighth most prevalent disease
worldwide. It is common in post-pubescent teens, with boys most frequently affected particularly
with more severe forms of the disease. According to the Global Burden of Disease (GBD) study, acne
vulgaris affects ~85% of young adults aged 12–25 years.
The exact incidence or prevalence of Acne in India is unclear due to insufficiency of published data.
Yet, for India with a population of more than a billion plus people and a significantly greater number
of young individuals, there are estimated 200–300 million acne sufferers.
Acne in a severe form is more common in males than in females, but the disease tends to be more
persistent in females with high incidence in urban as compared to the rural population, with a few
types leading to scar formation.
AETIOLOGY7,8,9
1. Genetic factors: Heredity plays an important role in the development of acne, with a family
history of acne being present in 70 percent of cases.
2. Endocrine factors: Circulating androgens must be present if acne is to appear.
1 Sutaria AH, Masood S, Schlessinger J. Acne Vulgaris. [Updated 2019 Dec 13]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls
Publishing;2020 [Cited on 2021 March 8]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459173/
2 Tan JKL, Bhate K. A global perspective on the epidemiology of acne. British Journal of Dermatology. Blackwell Publishing Ltd.2015; 172:3–12.
3 Thiboutot D, Gollnick H, Bettoli V, Dréno B, Kang S, Leyden JJ, et al. New insights into the management of acne: an update from the Global
Alliance to Improve Outcomes in Acne group. J Am Acad Dermatol. 2005;60(5): S1-50.
4 Kabba R, Bajaj AK, Thappa DM, Sharma R, Vedamurthy M, Dhar S, et al. Acne in India guidelines for management. Indian J Dermatol Venereol
Leprol.2009;75: S1-2.
5 Saxena K, Shah YM, Singh KK, Dutt S, Agrawal M, Singh N. Clinical profile of acne vulgaris in semiurban patients. Int J Res Dermatology.2018;4(1):23-28.
6 Ali FR, Al-Niaimi F. Acne vulgaris. Br J Hosp Med [Internet]. 2013;74(Sup5):C78–80 [Cited on 2021 March 8]. Available from: http://www.
magonlinelibrary.com/doi/10.12968/hmed.2013.74.Sup5.C78
7 Engler D, Farinha AM. Acne. South Africa Pharm J.2016;83(10):27–34.
8 Yentzer BA, Hick J, Reese EL, Uhas A, Feldman SR, Balkrishnan R. Acne vulgaris in the united states: A descriptive epidemiology.
Cutis.2010;86(2):94–99.
9 Kurokawa I, Danby FW, Ju Q, Wang X, Xiang LF, Xia L, et al. New developments in our understanding of acne pathogenesis and treatment. Exp
Dermatol. 2009;18(10):821–32.
3. Bacterial infection: Propionibacterium acnes are present in pilosebaceous follicles and may
play a major role in formation of acne pustules.
4. Physical and chemical factors: A variety of cosmetics, drugs, other chemicals, mechanical
factors and certain types of irradiation may be acnegenic.
5. Stress factors: Although stress has not been shown to cause acne, it can aggravate the
condition, possibly by inducing neurotic excoriation.
6. Diet: Dietary factors have little importance in acne but, occasionally, the intake of certain
foods may appear to be associated with a mild flare of the condition.
7. Fluid retention: One of the major causes of acne is inadequate intake of fluids. When the
body does not get enough water, it starts storing it, which leads to water retention. Excess
water builds up in between the tissues and in the spaces between the cells.
8. Weather and environment: Ultraviolet light is beneficial, and acne tends to improve slightly
in summer, although it can become much worse in hot, humid conditions found in the tropics.
9. Racial factors: These factors are of little importance although acne seems less common in
Japanese people.
10. Other factors: Premenstrual aggravation, Polycystic ovary disease, Vitamin B
supplementation, Obesity (has been found to be associated with an increased prevalence of
acne in people between the ages of 20–40 years) etc.
PATHOGENESIS10,11,12
The pathogenesis involved in the formation of acne lesions is multifactorial involving hormonal,
microbiological and immunological mechanisms and includes mainly four key pathogenic processes, viz.:
• altered follicular keratinization that leads to comedones
• increased and altered production of sebum secondary to hyperandrogenism, affecting the
sebaceous gland size
• follicular colonization, ductal hyperkeratosis, abnormality or proliferation of the microbial
flora especially Propionibacterium acnes; some studies have demonstrated that microbial
agents trigger immune mediator’s cytokine responses via Toll-like receptors (TLRs) that
recognize pathogen-associated molecular patterns conserved among microorganisms and
elicit immune responses
• complex inflammatory mechanisms that involve both innate and acquired immunity.
CLASSIFICATION OF ACNE
Acne vulgaris
Acne vulgaris: It is a chronic inflammatory disease of the pilosebaceous follicles, characterized by
comedones, papules, pustules, nodules, and often scars. It is described according to the severity of
the disease as follows:13
10 Burkhart CN, Gottwald L. Assessment of Etiologic Agents in Acne Pathogenesis. Skin Dermatology Clin.2007; 2(4):222–29.
11 Rosso JQ Del. A New Understanding of The Pathogenesis of Acne Vulgaris. J Drugs Dermatology.2013;12(8): S109 - S115
12 Kim J. Cunliffe Scientific Awards Review of the Innate Immune Response in Acne vulgaris: Activation of Toll-Like Receptor 2 in Acne Triggers
Inflammatory Cytokine Responses. Dermatology.2005;211(3):193–98.
13 James WD. Acne. N Engl J Med. 2005; 352(14):1463-72.
Severity Description
Comedones (noninflammatory lesions) are the main lesions. Papules and pustules
Mild
may be present but are small and few in number (generally <10)
Moderate numbers of papules and pustules (10–40) and comedones (10–40) are
Moderate
present. Mild disease of the trunk may also be present
Numerous papules and pustules are present (40–100), usually with many comedones
Moderately
(40–100) and occasional larger, deeper nodular inflamed lesions (up to 5). Widespread
severe
affected areas usually involve the face, chest, and back
Severe Nodulocystic acne and acne conglobata with many large, painful nodular or pustular
lesions are present, along with many smaller papules, pustules, and comedones
Acne conglobata: This is a mild form of cystic acne, characterized by numerous comedones and
large abscesses with interconnecting sinuses, cysts and grouped inflammatory nodules. Suppuration
is characteristic of acne conglobata.
Acne fulminans: Extremely severe cystic acne occurring in teenage boys. These undergo swift
suppurative degeneration, leaving ragged ulcerations, mostly on the chest and back.
Tropical acne: This is severe acne occurring in the tropics during the seasons when the weather is
hot and humid. Characteristically face is spared.
Acne aestivalis: Also known as Mallorca acne, this is also seasonal starting in spring, progressing
during summer, and resolving completely in the fall.
DIAGNOSIS
Acne vulgaris is primarily a clinical diagnosis. With the help of history and physical examination,
one can determine if there is an underlying factor responsible for the development of acne, such as
overuse of medication, chemicals or cosmetics and drugs which may be acnegenic. Endocrinological
abnormality such as excessive circulating androgens as seen in cases of polycystic ovarian syndrome
that leads to clinical features like seborrhea, hirsutism and androgenetic alopecia can also be one of
the identifying factors for diagnosis of acne. Hormonal assay including FSH, LH and circulating levels
of total and free serum testosterone, dihydroepiandrosterone should be tested in older women,
especially those with new-onset acne and other signs of androgen excess.
Figure 2: Acne vulgaris polymorphic eruption of comedones, papules, pustules, nodules, and cysts. B:
close up. Courtesy: Neena Khanna Illustrated synopsis of dermatology
and sexually transmitted diseases.
Different types or methods of classification of acne are known, viz; mild, moderate or severe
depending on the lesions that predominate in a given patient15 and also there is different classification
for children.16 The different grading system for evaluation and assessment are:
15 Moradi Tuchayi S, Makrantonaki E, Ganceviciene R, Dessinioti C, Feldman SR, Zouboulis CC. Acne vulgaris. Nat Rev Dis Prim [Internet]. 2015;
1:15029. [Cited on 2021 March 8] Available from: http://www.ncbi.nlm.nih.gov/pubmed/27189872
16 Kim W, Mancini AJ. Acne in childhood: An update. Pediatr Ann. 2013;42(10):418–27.
17 Adityan B, Kumari R, Thappa DM. Scoring systems in acne vulgaris. Indian J Dermatol Venereol Leprol. 2009;75(3):323–26.
18 Sharma RK, Dogra S, Singh A, Kanwar A. Epidemiological patterns of acne vulgaris among adolescents in North India: A cross-sectional study
and brief review of literature. Indian J Paediatr Dermatology. 2017;18(3):196-201.
19 Kamamoto CSL, Hassun KM, Bagatin E, Tomimori J. Acne-specific quality of life questionnaire (Acne-QoL): translation, cultural adaptation and
validation into Brazilian-Portuguese language. An Bras Dermatol. 2014; 89(1): 83–90.
20 Dreno B, Poli F, Pawin H, et al. Development and evaluation of a Global Acne Severity Scale (GEA Scale) suitable for France and Europe. J Eur
Acad Dermatol Venereol. 2011; 25:43–48.
DIFFERENTIAL DIAGNOSIS21,22
• Beard folliculitis: Pustules, papules or nodules which are present in perifollicular region,
comedones are absent.
• Acne keloidalis nuchae: Most often seen in black patients; lesions are typically localised
to the posterior neck, beginning as papules and pustules and may progress to confluent
keloids.
• Folliculitis(non-Gram-negative): Common condition manifesting as follicular based
erythematous papules and pustules.
• Rosacea: Presents with background erythema and telangiectasias (widened venules also
referred to as spider veins), and inflammatory papules and pustules. No comedones are
seen.
• Demodicidosis: It is caused by Demodex mites. Manifested by outbreaks of papular or
papulopustular lesions of the face.
• Keratosis pilaris: Dry, rough patches and tiny bumps, comedones absent.
• Seborrheic dermatitis: Poorly defined scaly lesions, less induration and no comedones
present.
COMPLICATIONS3,23,24
TREATMENT
General management
In spite of easy availability of different treatment modalities, the modern medicine itself accepts their
therapeutic shortcoming in successful treatment of acne, therefore, raising the need for efficient,
convenient and economical mode of treatment wherein lies the role of homoeopathic medicines.
Homoeopathic management
In homoeopathic literature, large number of medicines have been given for different presentations
of acne in different age groups. It has been evident from research conducted earlier that there is a
significant decrease in acne lesions after administration of homoeopathic remedies with a positive
21 Engler D, Farinha AM. Acne. South Africa Pharm J. 2016;83(10):27–34.
22 Poli F, Differential diagnosis of facial acne on black skin. International Journal of Dermatology. 2012; 51(1):24-26.
23 Jović A, Marinović B, Kostović K, Č� eović R, Basta-Juzbašić A, Bukvić Mokos Z. The Impact of Pyschological Stress on Acne. Acta Dermatovenerol
Croat. 2017;25(2):1133–41.
24 Gallitano SM, Berson DS. How Acne Bumps Cause the Blues: The Influence of Acne Vulgaris on Self-Esteem. International Journal of Women’s
Dermatology. Elsevier Inc. 2018;4(1):12–17.
impact on the overall health of the patient.25,26,27 Various observational studies have been done with
different medicines of homoeopathy. In Synthesis Repertory there are 200 remedies mentioned in
FACE chapter under the rubric Eruptions- acne.28 The frequently verified characteristic features of
some organospecific remedies are: Berberis aquifolium: Skin dry, rough, scaly with acne, pimples,
blotches, clears the complexion, eruptions on the scalp extending to the face and neck. Eugenia
jambos: Acne, simple and indurated. The pimples and some areas around are painful. Acne rosacea.
Eruptions on face of young women, especially during scanty menses. Kali bromatum: Acne of the
face; pustules. Bluish red pustular eruptions, on faces, chest, shoulders, leaves unsightly scars in
young fleshy persons of gross habits. Bovista: Acne worse in summers, due to use of cosmetics.
Ledum palustre: Red pimples on the forehead and cheeks, stinging pain when touched. Arsenicum
bromatum: Acne in young people. Acne rosacea, with violet papules on nose, worse in the spring.
Radium bromatum: Small pimples. Erythema and dermatitis, with itching, burning, swelling and
redness. Calcarea silicata: Pimples, comedones; very sensitive itching, burning, cold and blue.
The list of frequently prescribed polychrest medicines with their indications are given below:29,30,31
Natrum muriaticum Hot patient; poorly nourished, great • Acne puncata, comedones; vesicles
emaciation (marked on neck); losing with watery contents, burst and
flesh while living well; craving for salt; leave a thin scurf
aversion to bread and fatty things; • Face oily, shiny, as if greased
constipated; increased thirst; mapped • Worse at the seashore or form sea
tongue with red insular patches; air, heat of sun or stove
melancholic, sad, plays alone, irritable, • Better in the open air, cold bathing
cross, cries when spoken to; awkward,
hasty, drops things from nervous
weakness; disposition to weep without
cause, consolation aggravates
Psorinum Extremely chilly patient, wants to cover • Acne of all forms, simplex, rosacea
even in hottest summer weather; pale, worse during menses, from coffee,
delicate, sickly; scanty perspiration; fat, sugar, meat, when best selected
offensive discharges; wakes up at remedy fails or only palliates
night feeling hungry; anxious, fearful; • Worse from coffee, changes of
child is good all day while restless and weather, in hot sunshine, from cold
troublesome at night • Better from heat, warm clothing,
even in summer
Silicea terra Extremely chilly patient. All symptoms • Acne: eruptions; itches and burns
worse by cold except stomach complaints, only during day; acne solaris and
which are ameliorated. Profuse, offensive acne rosacea; pus offensive
discharges; sweats profusely especially • Worse from cold, during menses
on feet. Easy suppuration; glandular • Better from warmth
affinity; children with large heads
and distended abdomen; weak ankles,
slow in learning to walk; constipation;
obstinate, head strong, cries when
spoken kindly to, nervous, apprehensive.
Oversensitive, irritable and fearful
Tuberculinum Takes cold easily; tall, lean, thin, • Acne in tuberculous children
narrow- chested; active and precocious • Worse before a storm, dampness,
mentally but weak physically; emaciated early morning
with good appetite; family/ personal • Better in open air
history of tuberculosis; changeability of
symptoms. Obstinate and disobedient
children; irritable, fretful, desire to use
foul language; discontented, fear of dogs
Lab Investigations
• Hormonal assay like FSH, LH, Free
Serum Testosterone, USG pelvis in
case of PCOD
Improvement
Yes NO
Assess for
underlying cause
and treat with
Stop treatment and follow up Yes Improvement NO integrative care
intermittently
ADHESIVE CAPSULITIS
(FROZEN SHOULDER)
CASE DEFINITION
Adhesive capsulitis is characterized by pain and restricted movement of the shoulder, also referred
to as “frozen shoulder”.1 It is characterised by significant restriction of both active and passive
shoulder motion that occurs in the absence of a known intrinsic shoulder disorder.2 The condition
was initially termed ‘frozen shoulder’ by Codman in 1934 and later described as ‘adhesive capsulitis’
by Neviaser in 1945.3
INCIDENCE/ PREVALENCE4,5,6
Although the etiology of adhesive capsulitis has not been identified, there are a number of associated
factors:
• Having adhesive capsulitis on one side places an individual at risk (5%-34%) for opposite-arm
involvement, and can occur bilaterally simultaneously up to 14% of the time
• Individuals with type 1 or 2 diabetes mellitus
• Patients with Dupuytren’s disease
• Thyroid disease
• Lower body weight or lower Body Mass Index (BMI)
• Further associations include cardiac diseases, pulmonary diseases, parkinson’s disease and
stroke, hyperthyroidism, hypothyroidism, scleroderma or previous non-shoulder surgery
including cardiac surgery, thoracic, neck surgery or neurosurgery or shoulder trauma as rotator
cuff injury
1 Langford CA, Gilliland BC. Periarticular disorders of the extremities. In: Fauci AS, Braunwald E, Kasper D, Hauser S, Longo DL, Jameson JL, et al,
editors. Harrison’s Principles of Internal Medicine.17th ed. New York: Mc Graw Hill Education;2008: 2184-2186.
2 Chan HBY, Pua PY, How CH. Physical therapy in the management of frozen shoulder. Singapore Med J.2017;58(12):685-89.
3 Trachsel JM. Adhesive Capsulitis: A Case Study. Orthopaedic Nursing. 2009;28(6):279-83.
4 Uppal HS, Evans JP, Smith C. Frozen shoulder: A systematic review of therapeutic options. World J Orthop.2015;6(2):263-68.
5 Yuan X, Zhang Z, Li J. Pathophysiology of adhesive capsulitis of shoulder and the physiological effects of hyaluronan. European Journal of
Inflammation. 2017;15(3):239-43.
6 Kelley MJ, Shaffer MA, Kuhn JE, Michener LA, Seitz AL, Uhl TA, et al. Shoulder Pain and Mobility Deficits: Adhesive Capsulitis. Clinical Practice
Guidelines Linked to the International Classification of Functioning, Disability, and Health from the Orthopaedic Section of the American
Physical Therapy Association. Journal of Orthopaedic & Sports Physical Therapy.2013;43(5): A1-A31.
7 Wang K, Ho V, Hunter-Smith DJ, Beh PS, Smith KM, Weber AB. Risk factors in idiopathic adhesive capsulitis: a case control study. J Shoulder
Elbow Surg. 2013;22(7): 24–9.
8 Malavolta EA, Gracitelli MEC, Pinto GMR, da Silveira AZF, Assunc¸ão JH, Neto AAF. Asian ethnicity: a risk factor for adhesive capsulitis. Revista
Brasileira de Ortopedia .2018; 53(5):602–06.
9 Williams NS, Bulstrode CJK, O’Connell PR. Bailey & Love’s Short Practice of Surgery. 25th ed. London: Taylor and Francis Ltd; 2008.
• Night pain is often present in the affected shoulder and pain may interfere with sleep.
• The shoulder is tender to palpation, and both active and passive movements are restricted1
(elevation <100°, external rotation >50% restriction). 6
• Local tenderness is often felt anteriorly over the rotator interval.
• The pathognomonic sign of frozen shoulder is loss of external rotation, and this differentiates
it from rotator cuff disease.11
Clinical course
The clinical course of frozen shoulder can be divided into three stages as follows:2,10,11
1) Stage 1 – Painful phase: This can last for 2–9 months. The shoulder becomes increasingly painful,
especially at night, and the patient uses the arm less and less. The pain is often very severe
and may be unrelieved by analgesics. This phase is characterized by an acute synovitis of the
glenohumeral joint.
2) Stage 2 – Stiffening phase: This can last for 4–12 months and is associated with a gradual reduction
in the range of movement of the shoulder. The pain usually resolves during this period, although
there is commonly still an ache, especially at extremes of the reduced range of movement.
3) Stage 3 – Thawing phase: This lasts for a further 4–12 months and is associated with a gradual
improvement in the range of motion.
The clinical course runs over a period of 1–3 years, and the condition usually resolves without
any long-term sequelae.11 In some cases, it may persist and present symptoms like mild pain
which is the most common complaint2 or with some limitation of shoulder motion.1
COMPLICATIONS11
• Residual pain
• Residual stiffness
• Fracture of the humerus
• Rupture of the biceps tendon after shoulder manipulation
INVESTIGATIONS
Diagnosing adhesive capsulitis is primarily determined by history and physical examination, but
imaging studies can be used to rule out underlying pathology.
a) Radiographs are typically normal with adhesive capsulitis but can identify osseous
abnormalities, such as glenohumeral osteoarthritis.8 Radiographs of the shoulder show
osteopenia.1Arthrographic findings associated with adhesive capsulitis include a joint capsule
capacity of less than 10 to 12 mL and variable filling of the axillary and subscapular recess.8A
decrease of joint volume indicates shortening of the joint capsule.5
10 Jason JI, Sundaram SG, Subramani MV. Physiotherapy Interventions for Adhesive Capsulitis of Shoulder: A Systematic Review. Int J Physiother
Res. 2015;3(6):1318-25.
11 Mezian K, Coffey R, Chang KV. Frozen Shoulder. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021[cited 2021 March
2]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482162/
b) Magnetic resonance imaging (MRI) identifies abnormalities of the capsule and rotator cuff
interval in patients with adhesive capsulitis.8 MRI can depict thickening of the joint capsule
particularly in the axillary region and demonstrates thickening of the coracohumeral ligament.
c) Magnetic resonance arthrography (MRI) may show obliteration of the subcoracoid fat triangle,
resulting from shortening or fibrosis of the rotator interval capsule. Alteration of the synovium
can be shown by dynamic MRI enhanced with intravenous gadolinium administration.5
In the orthopaedic and rheumatologic community, there has been an increased interest in outcome
measures that capture the patient’s own perspective of their clinical status.12 There are several
outcome measures designed to assess patients with shoulder disorders:
The inclusion of at least one generic and one specific questionnaire has been recommended since
they complement each other.13 Most commonly used generic and multidimensional measures are
Medical Outcome Study Short Form- 36 (SF-36)18 and Euro Quality of Life (5D-5L)19. These tools are
an important (and often the only) way to obtain quantitative, meaningful assessments of the effect
of treatment on the quality of life and level of function experienced by patients.20
RED FLAGS21
12 Fernandes MR, Barbosa MA, Faria RM. Quality of life and functional capacity of patients with adhesive capsulitis: identifying risk factors
associated to better outcomes after treatment with nerve blocking. Rev Bras Reumatol. 2015;57(5):445–51.
13 Orthopaedic score [Internet]. London: Constant Shoulder Score [cited 2019 August 05]. Available from: http://www.orthopaedicscore.com/
scorepages/constant_shoulder_score.html
14 Michener LA, McClure PW, Sennett BJ. American Shoulder and Elbow Surgeons Standardized Shoulder Assessment Form, patient self-report
section: reliability, validity, and responsiveness. J Shoulder Elbow Surg. 2002;11(6):587-94.
15 The DASH Outcome Measure [Internet]. Toronto: The Disabilities of the Arm, Shoulder and Hand (DASH) Outcome Measure 2010 [Cited 2019
August 05]. Available from: http://www.dash.iwh.on.ca/sites/dash/files/downloads/DASH_questionnaire_2010.pdf
16 The DASH Outcome Measure Internet. Toronto. The Disabilities of the Arm, Shoulder and Hand (DASH) Outcome Measure 2010 [Cited 2019
August 05]. Available from: http://www.dash.iwh.on.ca/sites/dash/files/downloads/quickdash_questionnaire_2010.pdf
17 Roach KE, Budiman-Mak E, Songsiridej N, Lertratanakul Y. Development of a shoulder pain and disability index. Arthritis Care
Res.1991;4(4):143-49.
18 Research and Development (RAND) Internet. California: Medical Outcomes Study (MOS)The 36-Item Short Form Health Survey (SF-36) [Cited
2019 August 05].Available from: https://www.rand.org/content/dam/rand/www/external/health/surveys_tools/mos/mos_core_36item_survey.
pdf
19 EuroQOL Group [Internet]. Rotterdam: EQ-5D-5L 2009 [Cited 2019 August 05]. Available from: https://euroqol.org/eq-5d-instruments/eq-5d-
5l-about/
20 Plummer OR, Abboud JA, Bell JE, Murthi AM, Romeo AA, Singh P et al. A concise shoulder outcome measure: application of computerized
adaptive testing to the American Shoulder and Elbow Surgeons Shoulder Assessment. J Shoulder Elbow Surg.2019; 28:1273–80.
21 Rangan A, Goodchild L, Gibson J, Brownson P, Thomas M, et al. Frozen shoulder. Shoulder elbow; 2015:7(4):299-307.
DIFFERENTIAL DIAGNOSIS3,8
The following conditions should be considered in the differential diagnosis when a patient presents
with shoulder pain:
• Shoulder dislocation
• Osteoarthritis
• Impingement syndrome and rotator cuff tear
• Tumor
• Acute calcific tendonitis/ bursitis
MANAGEMENT
General management
The main objective of all treatments for adhesive capsulitis should be early pain relief and functional
restoration.6 While selecting a treatment method for adhesive capsulitis, it is extremely important
to consider the patient’s symptoms, stage of the condition, and recognition of different patterns of
motion loss.12
Patient education: Patients should be educated in the chronicity of this condition. If they know and
understand ahead of time that it can be several years before symptoms are completely resolved,
apprehension and a feeling of urgency for functional return may be decreased.22
Physiotherapy: There is a fair level of evidence for manual mobilisation techniques with exercise
for adhesive capsulitis.12 Passive mobilisation and capsular stretching are two of the most
used techniques. There are several adjuncts that are often used with physiotherapy including
extracorporeal shockwave therapy, electromagnetic stimulation, acupuncture and the use of lasers.
Homoeopathic management
The Homoeopathic Medical Repertory by Robin Murphy23 lists the following medicines under
rubric ‘frozen shoulder’: ferr., rhus-t., ruta, sang., thiosin. This repertory has 159 medicines under
the rubric ‘Pain, shoulders’ and 30 medicines under the rubric ‘Stiffness, shoulders. The number of
medicines in the Synthesis Repertory24 under the rubric ‘Pain, shoulders’ is 344 and under the rubric
‘Stiffness, shoulders’ is 59. There are a few studies showing encouraging results with homoeopathic
treatment.25,26
22 Manske RC, Prohaska D. Diagnosis and management of adhesive capsulitis. Curr Rev Musculoskelet Med.2008; 1:180–89.
23 Murphy R. Homoeopathic Medical Repertory. Second Indian Edition (Reprint). New Delhi: Indian Books & Periodicals
Publishers;2004:409-1635.
24 Schroyens F. Synthesis Repertory ver. 9.1. New Delhi: B Jain Publishers (Pvt. Ltd); 2002.
25 Magotra N, Sharma N, Michael J, Kundu N, Nath A, et al. Utility of homoeopathic medicines in treatment of frozen shoulder: An open,
observational clinical trial. National homoeo recorder.2018;4(14): 36.
26 Shwetha B. A Clinical study of adhesive capsulitis and its homeopathic treatment [dissertation on the internet]. Karnataka: Rajiv Gandhi
University of Health Sciences; 2010[Cited 2021 March 9]. Available from: http://52.172.27.147:8080/jspui/bitstream/123456789/4607/1/
Shwetha%20B.pdf
The organospecific remedies verified clinically and suggestive for adhesive capsulitis of shoulder
are:27,28Ammonium phosphoricum: Pain in shoulder joint. Acts well in patients with gout, uric acid
diathesis. Nodosities in finger joints. Asparagus officinalis: Rheumatic pain in back, especially near
shoulder and limbs. Pain at acromion process of left scapula under clavicle and down arm, with
feeble pulse. Chelidonium majus: Pain in arms, shoulders, hands, fingertips. Right side shoulder
and scapula affected with liver complaints. Elaps corallinus: Pressure between the shoulders. Pain
worse in wet weather, fears rain. Fagopyrum esculentum: Pain in shoulder, with pain along fingers.
Vehement itching in arms and legs, better by cold bathing. Ferrum muriaticum: Pain in right shoulder,
right elbow, and a marked tendency to cramps and round red spots on the cheeks. Granatum:
Pain around shoulders, as if heavy load had been carried. Guaiacum officinale: Rheumatic pain in
shoulders, arms and hand. Tearing and shooting in the shoulder-blades, and in the forearms. Sharp
stitches in the top of right shoulder. With stiffness worse by heat. Indium metallicum: Constant pain
in left shoulder, as if bruised. Intermitting pains in left shoulder with soreness extending down arm.
Muscles of left arm and shoulder feel flabby and soft; no power in arm. Ledum palustre: Throbbing
in the right shoulder. Pressure in the shoulder, worse motion, night; better cold application. Myrica
cerifera: Pain under shoulder-blades and back of neck, in all muscles, in hollow of right foot.
Natrium arsenicosum: Aching in arms; worse in shoulder. Joints stiff. With nasal catarrh and pain
at the root of nose. Primula veris: Right axillary muscles painful. Weight and lassitude in limbs,
especially shoulders. Radium bromatum: Sharp pains in shoulders, arms, hands and fingers. Arms
feel heavy. Cracking in shoulder; accompanied with skin complaints. Worse at night. Better open air,
continued motion, hot bath. Ranunculus bulbosus: Right side shoulder affected. Muscular pains
about margins of shoulder blades in women of sedentary employment, often burning pain in small
spots, worse wet stormy weather, evening, cold air.
The commonly prescribed medicines along with their indications are given in the following table:25,26,29
27 Boericke W. New Manual of Homoeopathic Materia Medica with Repertory.9th ed. New Delhi: B Jain Publishers Pvt Limited;2010.
28 Clarke JH. A Dictionary of Practical Materia Medica. Reprint edition. New Delhi: B Jain Publishers Pvt Limited; 2009.
29 Allen HC. Keynotes and Characteristics with Comparisons of some of the Leading Remedies of the Materia Medica with Bowel Nosodes.8th ed.
New Delhi: B Jain Publishers Pvt Limited;2013.
Calcarea Chilly patient; takes cold easily; fat, fair, • Rheumatoid pains after exposure to
carbonica flabby, distended abdomen; pale, weak, water. Sharp sticking pains as if parts
easily tired; head sweats profusely while were wrenched or sprained
sleeping; sour smelling discharges; longing • Arthritic nodosities
for fresh air; desire for eggs and indigestible • Worse in cold air, wet weather, cold
things, sweets; aversion to meat and milk; water, from washing, morning
fearful, shy, timid, slow and sluggish; feels • Better in dry weather, lying on painful
better when constipated side
Ferrum Chilly patient. Anemic and chlorotic, • Rheumatism of the shoulder. Cracking
metallicum with pseudo-plethora; who flush easily. in shoulder joint, left shoulder
Oversensitiveness. Vomiting after eating, • Shooting and tearing pain shoulder
after midnight. Intolerance to eggs joint, and in the arm, or pulling,
paralytic weakness and heaviness
• Worse at night, at rest, especially
while sitting still
• Better on walking slowly about, in
summer
Kalium Chilly patient. Kali pains are sharp and • Tearing pain in arms from shoulder
carbonicum cutting; nearly all are better by motion. to wrist, swelling of shoulder, with
Sweating, backache and weakness are pain
accompanying symptoms in most of diseases. • Cracking in shoulder joint when
Obstinate; hypersensitive to pain, noise and moving or raising arm
touch. Swelling over upper eyelid • Pain, as from blows and bruises,
under right shoulder joint
• Worse in cold weather, lying on left
and painful side
• Better in warm weather, during day
Lycopodium Hot patient; intellectually keen but physically • Heaviness of arms. Numbness and
clavatum weak; upper part of body emaciated, lower tearing pain in shoulder and elbow
part semi- dropsical; complexion pale, joints especially while at rest or at
dirty, sallow with deep furrows; looks old; night
recurrent respiratory and gastrointestinal • Rheumatic tension in right shoulder
affections; tendency for flatulent dyspepsia; joint. Cannot lie on painful side.
worse from 4pm - 8pm; right-sided • Better by motion, after midnight,
complaints or symptoms shift from right to from being uncovered
left; desire for warm foods and drinks, sweet;
dominating, cranky, lack of self-confidence,
precocious
Medorrhinum Hot patient. Chronic ailments due to • Rheumatism of top of shoulder and
suppressed gonorrhea. Time passes too arm; pains extend to fingers
slowly. Difficult concentration. Craving for • Worse when thinking of it, heat,
liquor, salt, sweets, warm drinks. Chronic covering, stretching, thunderstorm,
rheumatism. State of collapse and trembling least movement, from daylight to
all over. Ailments from daylight to sunset, sunset
heat, inland • Better at the seashore, damp weather
Nux vomica Chilly patient; thin; prone to indigestion; • Rheumatic pains, with sensation of
tongue coated yellowish in the posterior part; weakness in shoulders and arms,
constipation; with frequent unsuccessful soreness in shoulder joint
desire for stool. Oversensitive to all external • Drawing pain in arms, extending
impressions; noise, odors, light or music; from the shoulder to fingers, with
nervous disposition sensation as if the arms were asleep
• Loss of motion of the arm, esp. at
night
• Worse in morning, from touch, dry
weather, in cold air
• Better in evening, while at rest, lying
down, in damp, wet weather, hard
pressure
Phosphorus Tall, fast growing child with tendency • Rheumatic, tearing and lancinating
to stoop; haemorrhagic tendency. Chilly pains in shoulders, arms, and hands
patient; craving for salt, cold foods and (particularly in joints)
drinks. Oversensitive to external impressions; • Stitches in elbow and shoulder joints,
nervous and affectionate, anxious esp. stiffness in morning on washing, with
during thunderstorm pressure
• Worse in evening, before midnight,
lying on left or painful side, change
of weather, from getting wet in hot
weather
• Better by lying on right side, from
being rubbed
Rhus Chilly patient; body sore, bruised and stiff; • Tearing and burning sensation in
toxicodendron restless, can’t rest in any position; red shoulder, with paralysis of arm, pain
triangular tip of tongue; worse in damp, between shoulders on swallowing
cold, rainy weather, during rest and sleep, • Worse before a storm, at night, from
better by continued motion; increased thirst; getting wet while perspiring
great apprehension at night, sad, anxious; • Better in warm, dry weather,
weeping without knowing why wrapping up, change of position,
moving affected parts
Ruta graveolens All parts of the body are painful as if bruised. • Wrenching pain in the shoulder joint,
Feeling of intense lassitude, weakness and especially when arms are hanging
despair. Constipation from inactivity or down or when resting on them
impaction. Over-straining of ocular muscles. • Dull tearing pain in bones of arms
Eye strain followed by headache and elbow joints
• Worse on lying down, from cold, wet
weather
Sulphur Hot patient, kicks off the cloth at night; dirty, • Rheumatic pain in left shoulder;
filthy, does not want to be washed; lean, thin, drawing and tearing pain in arms and
stoop-shouldered; child who walks and sits hands
stooping; red orifices; desires sweets, sugar, • Stitching pain extending from
meat; when the best selected remedy fails to shoulder into chest on motion
improve • Pressure on shoulders as from a
weight
• Worse at rest, when standing,
warmth in bed, changeable weather
• Better in dry, warm weather, lying on
the right side
Clinical Features:
• Spontaneous often severe pain of sudden onset
• Night pain in the affected shoulder which interfere with sleep
• Shoulder tender on palpation
• Active and passive movements are restricted
• Pathognomonic sign of frozen shoulder- loss of external rotation
NO
Anxiety disorders
DIAGNOSIS1
Anxiety disorders differ from one another in the types of objects or situations that induce fear,
anxiety, or avoidance behaviour, and the associated cognitive ideation. Thus, while anxiety disorders
tend to be highly co-morbid with each other, they can be differentiated by close examination of the
types of situations that are feared or avoided and the content of the associated thoughts or beliefs.
The diagnostic criteria according to DSM V are:
1) Excessive anxiety and worry (apprehensive expectation), occurring more days than not for at
least 6 months, about a number of events or activities (such as work or school performance).
2) The individual finds it difficult to control the worry.
3) The anxiety and worry are associated with three (or more) of the following six symptoms (with
at least some symptoms having been present for more days than not for the past 6 months;
• Restlessness or feeling keyed up or on edge
• Being easily fatigued
• Difficulty in concentrating or mind going blank
• Irritability
• Muscle tension
• Sleep disturbance (difficulty in falling or staying asleep, or restless, unsatisfying sleep).
4) The anxiety, worry, or physical symptoms cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
5) The disturbance is not attributable to the physiological effects of a substance (e.g., a drug of
abuse, a medication) or another medical condition (e.g., hyperthyroidism).
6) The disturbance is not better explained by another mental disorder (e.g., anxiety or worry about
having panic attacks in panic disorder, negative evaluation in social anxiety disorder [social
phobia], contamination or other obsessions in obsessive-compulsive disorder, separation
from attachment figures in separation anxiety disorder, reminders of traumatic events in
posttraumatic stress disorder, gaining weight in anorexia nervosa, physical complaints in
somatic symptom disorder, perceived appearance flaws in body dysmorphic disorder, having a
serious illness in illness anxiety disorder, or the content of delusional beliefs in schizophrenia
or delusional disorder).
Panic Disorder
1) Recurrent unexpected panic attacks. A panic attack is an abrupt surge of intense fear or intense
discomfort that reaches a peak within minutes, and during which time four (or more) of the
following symptoms occur;
2) At least one of the attacks has been followed by 1 month (or more) of one or both of the following:
• Persistent concern or worry about additional panic attacks or their consequences (e.g.,
losing control, having a heart attack, “going crazy”).
• A significant maladaptive change in behaviour related to the attacks (e.g., behaviours
designed to avoid having panic attacks, such as avoidance of exercise or unfamiliar
situations).
3) The disturbance is not attributable to the physiological effects of a substance (e.g., a drug of
abuse, a medication) or another medical condition (e.g., hyperthyroidism, cardiopulmonary
disorders).
4) The disturbance is not better explained by another mental disorder (e.g., the panic attacks do
not occur only in response to feared social situations, as in social anxiety disorder: in response
to circumscribed phobic objects or situations, as in specific phobia: in response to obsessions,
as in obsessive-compulsive disorder: in response to reminders of traumatic events, as in post-
traumatic stress disorder: or in response to separation from attachment figures, as in separation
anxiety disorder).
1) Developmentally inappropriate and excessive fear or anxiety concerning separation from those
to whom the individual is attached, as evidenced by at least three of the following:
2) The fear, anxiety, or avoidance is persistent, lasting at least 4 weeks in children and adolescents
and typically 6 months or more in adults.
3) The disturbance causes clinically significant distress or impairment in social, academic,
occupational, or other important areas of functioning.
4) The disturbance is not better explained by another mental disorder, such as refusing to leave
home because of excessive resistance to change in autism spectrum disorder; delusions or
hallucinations concerning separation in psychotic disorders; refusal to go outside without a
trusted companion in agoraphobia; worries about ill health or other harm befalling significant
others in generalized anxiety disorder; or concerns about having an illness in illness anxiety
disorder.
1) Marked fear or anxiety about one or more social situations in which the individual is exposed
to possible scrutiny by others. Examples include social interactions (e.g., having a conversation,
meeting unfamiliar people), being observed (e.g., eating or drinking), and performing in front of
others (e.g., giving a speech).
2) The individual fears that he or she will act in a way or show anxiety symptoms that will be
negatively evaluated (i.e., will be humiliating or embarrassing: will lead to rejection or offend
others).
3) The social situations almost always provoke fear or anxiety.
4) The social situations are avoided or endured with intense fear or anxiety.
5) The fear or anxiety is out of proportion to the actual threat posed by the social situation and to
the socio-cultural context.
6) The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more.
7) The fear, anxiety, or avoidance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
8) The fear, anxiety, or avoidance is not attributable to the physiological effects of a substance (e.g.,
a drug of abuse, a medication) or another medical condition.
9) The fear, anxiety, or avoidance is not better explained by the symptoms of another mental
disorder, such as panic disorder, body dysmorphic disorder, or autism spectrum disorder.
10) If another medical condition (e.g., Parkinson’s disease, obesity, disfigurement from bums or
injury) is present, the fear, anxiety, or avoidance is clearly unrelated or is excessive.
Selective Mutism
1) Consistent failure to speak in specific social situations in which there is an expectation for
speaking (e.g., at school) despite speaking in other situations.
2) The disturbance interferes with educational or occupational achievement or with social
communication.
3) The duration of the disturbance is at least 1 month (not limited to the first month of school).
4) The failure to speak is not attributable to a lack of knowledge of, or comfort with, the spoken
language required in the social situation.
5) The disturbance is not better explained by a communication disorder (e.g., childhood-onset
fluency disorder) and does not occur exclusively during the course of autism spectrum disorder,
schizophrenia, or another psychotic disorder.
Agoraphobia
1) Marked fear or anxiety about two (or more) of the following five situations:
2) The individual fears or avoids these situations because of thoughts that escape might be
difficult or help might not be available in the event of developing panic-like symptoms or other
incapacitating or embarrassing symptoms (e.g., fear of falling in the elderly; fear of incontinence).
3) The agoraphobic situations almost always provoke fear or anxiety.
4) The agoraphobic situations are actively avoided, require the presence of a companion, or are
endured with intense fear or anxiety.
5) The fear or anxiety is out of proportion to the actual danger posed by the agoraphobic situations
and to the socio-cultural context.
6) The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more.
7) The fear, anxiety, or avoidance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
8) If another medical condition (e.g., inflammatory bowel disease, Parkinson’s disease) is present,
the fear, anxiety, or avoidance is clearly excessive.
9) The fear, anxiety, or avoidance is not better explained by the symptoms of another mental
disorder—for example, the symptoms are not confined to specific phobia, situational type; do
not involve only social situations (as in social anxiety disorder): and are not related exclusively
to obsessions (as in obsessive-compulsive disorder), perceived defects or flaws in physical
appearance (as in body dysmorphic disorder), reminders of traumatic events (as in post-
traumatic stress disorder), or fear of separation (as in separation anxiety disorder).
Specific Phobia
1) Marked fear or anxiety about a specific object or situation (e.g., flying, heights, animals, receiving
an injection, seeing blood).
2) The phobic object or situation almost always provokes immediate fear or anxiety.
3) The phobic object or situation is actively avoided or endured with intense fear or anxiety.
4) The fear or anxiety is out of proportion to the actual danger posed by the specific object or
situation and to the socio-cultural context.
5) The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more.
6) The fear, anxiety, or avoidance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
7) The disturbance is not better explained by the symptoms of another mental disorder, including
fear, anxiety, and avoidance of situations associated with panic-like symptoms.
8) Or other incapacitating symptoms (as in agoraphobia): objects or situations related to
obsessions (as in obsessive-compulsive disorder); reminders of traumatic events (as in post-
traumatic stress disorder); separation from home or attachment figures (as in separation
anxiety disorder); or social situations (as in social anxiety disorder).
Anxiety disorders due to other medical conditions
DIFFERENTIAL DIAGNOSIS1,6
Conditions Causes Differential features
Psychiatric conditions Major depressive disorder They exhibit high rates of dysphoric mood,
psychomotor retardation, suicidal ideation, guilt,
hopelessness and helplessness, as well as more work
impairment than patients with anxiety disorders
Acute stress disorder It does not persist for more than 4 weeks
Autism Spectrum Disorder Social anxiety and social communication deficits are
hallmarks of autism spectrum disorder
Medical conditions Parkinson’s disease, Multiple Many general medical conditions may present with
sclerosis, Hyperthyroidism, prominent anxiety symptoms. If not identified and
Hyperparathyroidism, properly addressed, these conditions may adversely
Seizure disorders, affect the treatment outcome of the anxious patient.
Pheochromocytoma, Appropriate laboratory tests or physical examinations
Vestibular dysfunctions, may be helpful in determining the etiological role of
Cardiopulmonary conditions another medical condition
Medications/ Cocaine, amphetamines, Anxiety disorders frequently occur in association
substances caffeine, cannabis, alcohol, with intoxication and withdrawal from several classes
barbiturates etc. of substances. A detailed history should be taken,
history of substance or medication (e.g., a drug of
abuse, exposure to a toxin) will be there
6 Cameron OG. The differential diagnosis of anxiety. Psychiatric and medical disorders. Psychiatr Clin North Am. 1985 Mar;8(1):3-23.
Yes
Due to the effects of a general Substance- induced
medical condition anxiety disorder
NO
Yes
Panic disorder with or
Due to the effects of a substance
without agoraphobia
NO
Yes
Recurrent unexpected panic attacks with or Social phobia (social
without agoraphobia anxiety disorder)
NO
Yes
Fear of humiliation or embarrassment in social
Specific phobia
Major depression with or performance situations
prominent anxiety
symptoms NO
Yes
Obsessive- compulsive
Yes Fear cued by object or situation
phobia
Accompanying Yes NO
symptoms of
depression Yes
Generalised anxiety
Obsessions or compulsions
disorder
NO
At least 4 weeks of 6- month period of excessive anxiety and worry Reexperiencing of event, Post-traumatic stress
mixed anxiety and plus associated symptoms increased arousal, and Yes
disorder
depression avoidance of stimuli
NO NO associated with traumatic
Yes
event
Yes
7
Kay J, Tasman A. Anxiety Disorders: Generalised Anxiety Disorder. Essentials of Psychiatry. England: John Wiley & Sons Ltd;2006: 642-644.
RED FLAGS8
• Demonstrating excessive distress out of proportion to the situation: crying, physical symptoms,
sadness, anger, frustration, hopelessness, embarrassment
• Easily distressed, agitated or angry when in a stressful situation
• Repetitive reassurance questions, “what if” concerns, inconsolable, won’t respond to logical
arguments
• Headaches, stomach aches, regularly too sick to do normal daily work
• Anticipatory anxiety, worrying hours, days, weeks ahead
• Disruptions of sleep with difficulty in falling asleep, frequent nightmares, difficulty in sleeping
alone
• Perfectionism, self-critical, very high standards that make nothing good enough
• Overly-responsible, people pleasing, excessive concern that others are upset with him or her,
unnecessary apologizing
• Demonstrating excessive avoidance: refuses to participate in expected activities
• Excessive time spent consoling about distress with ordinary situations.
Disorder-specific scales are available to better characterize the severity of each anxiety disorder and
to capture change in severity over time. For ease of use, particularly for individuals with more than
one anxiety disorder, these scales have been developed to have the same format (but different focus)
across the anxiety disorders, with ratings of behavioural symptoms, cognitive ideation symptoms,
and physical symptoms relevant to each disorder.1
Psychiatric evaluation and physical examination are necessary. It includes history of present illness,
current symptoms; past psychiatric history, general medical history and history of substance
use, personal history (e.g. psychological development, life events and response to those events),
social, occupational and family history; review of the patient’s medications; physical and mental
status examination and adequate diagnostic tool and criteria. Diagnose GAD according to ICD-10
(W.H.0,1992).
Anxiety should not be due to the other Axis I disorder (e.g. mood disorder, psychotic disorder, social
phobia, OCD, somatization disorder, hypochondriasis, PTSD) or a general medical condition (e.g.
hyperthyroidism) or substance use disorder (intoxication or withdrawal).
Patients experience excessive anxiety but many of them experience panic attacks, which may
worsen the clinical picture. The prolonged illness may cause depressive symptoms with emergence
of suicidality and substance abuse.
8 Chansky TE. Normal Anxiety and Red Flags [Internet]. 2019 [cited 2019 Feb 13]. Available from: http://tamarchansky.com/tools/normal-
anxiety-red-flags
Standard Treatment Guidelines In Homoeopathy 35
ANXIETY DISORDERS
Many may continue to function in their social and occupational lives with some impairment, others
may become severely incapacitated and give up their jobs and social duties. The impairment in
different areas can be assessed by self-administered visual analog scale.
The mental status examination is a structured assessment of the patient’s behavioural and cognitive
functioning. It includes descriptions of the patient’s appearance and general behaviour, level of
consciousness and attentiveness, motor and speech activity, mood and affect, thought and perception,
attitude and insight, the reaction evoked in the examiner, and, finally, higher cognitive abilities. The
specific cognitive functions of alertness, language, memory, constructional ability, and abstract
reasoning are the most clinically relevant. It should be done at the end of the overall evaluation
when the patient can be placed most at ease and when some degree of rapport has been established
between the examiner and the patient. The structured mental status examination should focus on
the following: Level of consciousness, Appearance and general behaviour, Speech and motor activity,
Affect and mood, Thought and perception, Attitude and insight, Examiner’s reaction to the patient,
Cognitive abilities (Attention, Language, Memory, Constructional ability and praxis and Abstract
reasoning).
PREVENTION
Studies show that early intervention is effective in reducing the development of Anxiety disorder21.
Following community and self-help approach can be helpful in reducing the impact of Anxiety
related disorder:4,22
• Stay active
• Regular exercise with healthy diet
• Stress identification and management techniques
• Get help early from a support groups (in-person or online) which can provide an opportunity
to share experiences and coping strategies
• Avoid alcohol, caffeine or drug use.
MANAGEMENT
General management
Anxiety disorders are the most prevalent psychiatric disorder and are associated with a high burden
of illness. Anxiety disorders are often under recognized and ignored in primary care. Treatment is
indicated when a patient shows marked distress or suffers from complications resulting from the
disorder.20
The goal of management is to provide relief in psychological and somatic symptoms and minimize
the impairment. This can be addressed in following ways:23
Psychotherapy
Cognitive behaviour therapy- Cognitive-Behavioural Therapy (CBT) is very helpful in providing relief
to the symptoms of anxiety disorder. All of these need the services of a specially trained counsellor/
psychotherapist to assess the needs of the patients and plan the nature of the intervention. Most of
the CBT begin with an assessment, Patient education and specific treatment planning. It typically
includes psychoeducation, self-monitoring, relaxation, problem solving and restructuring of worry
related distorted beliefs. The patient is gradually exposed to feared situation or bodily symptoms.
Cognitive therapy focuses on identifying, challenging, and then neutralizing unhelpful or distorted
thoughts underlying anxiety disorders. Exposure therapy focuses on confronting the fears underlying
an anxiety disorder to help people engage in activities they have been avoiding. Exposure therapy is
sometimes used along with relaxation exercises and/or imagery.13,24
Goals
• Psycho-education: Directs explanation of the symptoms and disorder to the patient and
the family. All patients with anxiety disorders require supportive talks and attention to the
emotional problems that are associated with the anxiety disorder. Psychoeducation includes
information about the physiology of the bodily symptoms of anxiety reactions and the
rationale of available treatment possibilities.25
• Monitoring of anxiety
• Cognitive restructuring: Corrects the hypothesized cognitive distortions and helps to identify
and counter fear of bodily sensations.
Long-term outcome is better when they are used in combination. Hypnosis, autogenic training, and
biofeedback or complementary medicine methods such as acupuncture, osteopathy, or homeopathy
are often recommended for the treatment of clinical anxiety.
The aim of management is to provide relief in psychological and somatic symptoms and minimize
the impairment. This can be addressed in following ways:
24 Huppert JD, Cahill SP, Foa EB. Anxiety Disorders: Cognitive-Behavioral Therapy. In: Sadock BJ, Sadock VA, Ruiz P, editors. Kaplan & Sadock’s
Comprehensive Textbook of Psychiatry. 9th ed. USA:Lippincott Williams & Wilkins; 2009:1915-1925
25 Bandelow B, Michaelis S, Wedekind D. Treatment of anxiety disorders. Dialogues Clin Neurosci. 2017;19(2):93-107.
• Establishing and maintaining a therapeutic alliance-The treatment of GAD may be long lasting,
hence the alliance is crucial. Understanding the life events, the extent and severity of symptoms
requires confiding and lasting therapeutic relationship. Attention to the patient’s worries and
fears are essential for long term gains.
• Monitoring the patient’s psychiatric status-The symptomatic improvement in psychological
and autonomic symptoms leads to greater confidence in the treating doctor. The anxiety goes
slowly with treatment and bursts of severe symptoms during the treatment need constant
monitoring.
• Pharmacotherapy-The drug treatment is done for 6-12 months, some evidence indicate that
treatment should be long term.
• Goals-Reduce psychological and autonomic symptoms and other co-morbid conditions.
Improve occupational and social functioning.
• The patient and family education-This seemingly unimportant aspect is most relevant to Indian
settings where awareness of psychiatric illness and its realization and need for treatment with
compliance is little. Many feel dejected, angry, isolated and may have suicidal ideas. Family and
the patient need to be told that this is like any other illness that needs treatment and success
depends on compliance.
• Relapse-The education that the illness is a chronic relapsing illness is essential and emergence
of anxiety with or without treatment should be promptly treated. Sudden discontinuation
may lead to emergence of withdrawal symptoms thus early recognition by the patient and the
family helps in prompt treatment.
• Stop treatment-Decision to stop treatment will depend on clinical response of the patients.
Usually the treatment is stopped in a tapering manner after at least 6 months stability of
clinical improvement and asymptomatic status of the patient. Before stopping the treatment,
the nature of illness, possibilities of recurrence, response to triggers and his/her ability to
cope with the situation should be discussed at length. Patient’s personal view should be
included in decision making of stopping the treatment. Patient should be encouraged to adapt
alternative methods of anxiety reduction like yoga, pranayama, relaxation techniques including
progressive muscular relaxation (PMR)/Shavasan etc. which can be mastered by him before
weaning off medicines.
Homoeopathic management
Homoeopathy can play a fundamental role in treating anxiety disorders. Constitutional homoeopathic
treatment with counselling can effectively manage this disease.
Mental symptoms such as anxiety, depression and insomnia are amongst the common reasons for
individuals to seek treatment with complementary therapies in general and homoeopathy in particular.
There are few researches done in Anxiety disorders26, 27,28,29,30 using homoeopathic intervention
which direct to its positive effects. Besides research, the enormous literatures and homoeopathic
textbooks have plenty of information pertaining to this condition.31,32,33,34 Homoeopathic medicines
along with counseling, psychotherapies shall be of immense help for recovery of the patients.
There are number of homeopathic medicines available in homeopathic literatures,35,36 which are
also supported by various researches20,21,22 for the treatment of anxiety disorders. Hahnemann has
also described about mental diseases and their management in Organon of Medicine37 in aphorisms
210 to 230. Synthesis repertory30 contains around 485 remedies under rubric ‘Anxiety’ along with
the various sub-rubrics under it.
Medicines like Arsenicum album and Aconitum napellus etc. are very useful in cases of panic attacks
or disorders. Keynote symptoms related to anxiety disorder of some frequently indicated medicines
are: Opium: Used in post-traumatic stress, also to overcome the fear. Calcarea arsenica: Great
mental depression. The slightest emotion causes palpitation of heart. Kali arsenicosum: Eyes had
a fixed look, face looked frightened and anxious; worse third day. Nervous depression and great
nervousness. Kali carbonicum: Alternating moods. Very irritable. Anxiety felt in the stomach.
Nitricum acidum: It is often employed when hate and mistrust are at their maximal expression.
Great anxiety about his disease, constantly thinking about his past troubles. Anxious in evening.
Apis mellifica: Despondent. Indicated with possessive jealousy. Whereas Aconite is helpful in acute
attack of Anxiety. Colocynthis: Can provide relief in a case of acute anger. Digitalis purpurea: When
there is anxiety about future, every shock strikes in the epigastrium. Cannabis indica: When there
is anxious depression, constant fear of becoming insane. Excessive loquacity.
26 Prabhu RL, Ruckmani A, Venkatesan D, Madhusudhanan N, Pavithra R. Anxiolytic effect of homeopathic preparation of Pulsatilla nigricans in
Swiss albino mice. Homeopathy. 2012; 101(3): 171-74.
27 Gelabert RZ. Clinical Study of the Effectiveness of Pluralist Homeopathy in Generalized Anxiety Disorder. Altern Integr Med. 2017; 6(4):250.
28 Magnani P, Conforti A, Zanolin E, Marzotto M, Bellavite P. Dose-effect study of Gelsemium sempervirens in high dilutions on anxiety-related
responses in mice. Psychopharmacology.2010; 210(4):533–545.
29 Coppola L, Montanaro F. Effect of a homeopathic-complex medicine on state and trait anxiety and sleep disorders: a retrospective
observational study. Homeopathy. 2013; 102(4): 254-61.
30 Marzotto M, Conforti A, Magnani P, Zanolin ME, Bellavite P. Effects of Ignatiaamara in mouse behavioural models.Homeopathy.2012;101(1): 57-67.
31 Allen HC. Keynotes and Characteristics with Comparisons of some of the Leading Remedies of the Materia Medica. 5th ed. Calcutta: Economic
Homoeo Pharmacy; 1983.
32 Boericke W. New Manual of Homœopathic Materia Medica and Repertory. 9th Reprinted Ed. New Delhi: B Jain Publishers (P) Ltd; 2005.
33 Hering C. The Guiding Symptoms of our Materia Medica. Reprint ed. New Delhi: B Jain Publishers (P) Ltd; 2010.
34 Kent JT. Repertory of the Homœopathic Materia Medica.6th ed. Reprint ed. New Delhi: B Jain Publishers (P) Ltd; 2011.
35 Murphy R. Homeopathic Medical Repertory - a Modern Alphabetical and Practical Repertory. 3rd ed. New Delhi: B Jain Publishers (P) Ltd;
2013.
36 Schroyens F. Synthesis –Repertorium Homeopathicum Syntheticum. 9.1st ed. New Delhi: B Jain Publishers (P) Ltd; 2012.
37 Hahnemann S. Organon of Medicine. 5th & 6th ed. New Delhi: B Jain Publishers (P)Ltd; 2008.
The commonly prescribed homoeopathic medicines and their indications are given below:
Aconitum napellus Physical and mental restlessness, • Sudden, intense anxiety attacks and
and fright; complains and tension for post-traumatic anxiety
caused by exposure to dry, cold • Great fear and anxiety of mind, with
weather, checked perspiration; great nervous excitability; afraid to go
tingling, coldness and numbness; out, to go into a crowd where there is
better in open air any excitement or gathering of many
people; to cross the street
• Countenance expressive of fear; life
is rendered miserable by fear; is
sure his/her disease will prove fatal;
predicts the day he/she will die
• Physical and mental restlessness
• Worse from music
Argentum nitricum Inco-ordination, loss of control and • Disease arises from unusual or long
want of balance everywhere, mentally continued mental exertion
and physically; trembling in affected • Mental anxiety ─ very impulsive;
parts; Great desire for sweets however always in a hurry but accomplishes
it aggravates; Splinter-like pains, nothing; in continual motion; he walks
Pains increase and decrease gradually; fast
Time passes slowly; Prematurely aged
• Fears to be late when there is plenty
look.; Impulsive; wants to do things in
of time. Apprehension when ready
a hurry. Fear of heights; Melancholic;
to go to church or opera, bringing on
apprehensive of serious disease; Worse
diarrhoea
from warmth in any form, at night,
from cold food, sweets, after eating at • Fearfulness and anxiety about many
menstrual period, from emotion, left things especially bridges, closed
side; Better from eructation; fresh spaces, heights, and personal health.
air; cold; pressure Fear of heights
Arsenicum album Chilly patient; rapid disproportionate • Mentally restless, but physically too
prostration; burning pains better by weak to move
heat (except headache); cadaveric • Dread of death when alone, or, going
odour of discharges and body; to bed. Thinks disease is incurable and
anxiety, anguish, fear for death and useless to take medicines
restlessness
• Attack of anxiety at night driving out
of bed. Anxiety for others- what will
happen when they cannot help me
• Anxiety- hypochondriac- little
symptoms will provoke a storm inside.
Anxiety – when anything is expected
of him. Anxiety when about to journey
by railroad or while in a train
• Worse after midnight
Ignatia amara Marked hyperaesthesia of all the • Mood swing. Easily offended. Silent
senses, and a tendency to clonic grief. Contradiction aggravates
spasms. Great contradiction; Worse • Bad effect of anger, grief or
in the morning, open air, after disappointed love. Broods in solitude
meals, coffee, smoking, liquids, over imaginary trouble
external warmth. Better while eating,
• Anguish, esp. in the morning on
change of position. Hysteric women,
waking, or at night, sometimes with
sensitive, easily excited nature women
palpitation of the heart
having mild disposition, quick to
perceive, rapid in execution • Anxious to do now this, now that,
impatience
Lycopodium clavatum Hot patient, intellectually keen • Any new challenge creates anxiety due
but physically weak; upper part of to lack of confidence. Constant fear of
body emaciated, lower part semi- breaking down under stress
dropsical; complexion pale, dirty, • Apprehensive. Inclined to laugh and
sallow with deep furrows; looks old; cry at same time. Head strong and
recurrent respiratory and gastro- haughty when sick
intestinal affections; tendency for
• Responsibility in work or relationships
flatulent dyspepsia; worse from
can create debilitating anxiety and
4pm- 8 pm; right sided complaints
fear of failure, which may manifest in
or symptoms shifts from right to left;
sexual difficulties, irritability, digestive
desire for warm foods and drinks,
complaints, and claustrophobia
sweet; dominating, cranky, lack of
self-confidence, precocious • Worse from heat or warm room, hot
air, bed
• Better by motion, after midnight, on
getting cold
Phosphorus Tall, fast growing child with tendency • Desire to be magnetized. Great
to stoop; hemorrhagic tendency; lowness of spirits, easily vexed
Chilly patient. Craving for salt, cold • Fearfulness, as if something were
foods and drinks. Oversensitive to creeping out of every corner, of
external impressions; Nervous and robbers. Ecstasy. Dread of death when
affectionate, anxious esp. during alone
thunderstorm
• Brain feels tired. Insanity, with
an exaggerated idea of one’s own
importance. Excitable, produces heat
all over. Restless, fidgety. Indifferent
• Worse from touch, physical or mental
exertion, twilight, change of weather,
evening, during a thunderstorm,
ascending stairs
• Better in dark, cold, open air, sleep
Silicea terra Extremely chilly patient; all symptoms • Restless, fidgety, starts at least noise.
worse by cold except stomach Anxious, yielding, faint hearted
complaints, which are ameliorated. • Fear of failure; literary work; pins,
Profuse, offensive discharges; sweats sharp objects. Lack self-confidence
profusely especially on feet. Easy and fearful of new undertakings,
suppuration; glandular affinity; large especially speaking in public. Overly
head and distended abdomen; weak anxious about trifles (obsessive)
ankles, slow in learning to walk;
• Persons overwork and exhaust
constipation; Obstinate, head strong,
themselves to avoid failure. Mental
cries when spoken kindly to, nervous,
labor very difficult. Desire to be
apprehensive, Oversensitive, irritable
magnetized
and fearful
• Worse in new moon, in morning, from
washing, during menses, uncovering,
lying down, damp, cold
• Better from warmth, wrapping up head,
summer, in wet or humid weather
Stramonium Painlessness of complaints; chorea, • Anxiety includes night terrors,
mania and fever delirium; young nightmares, or dark thoughts while
plethoric children, furious, malicious, awake. People scared of the dark or
fearful, desires light and company, being alone and are especially scared
worse in the dark and solitude by thoughts of monsters or mysterious
figures
• Imaginations tend to worsen the
anxiety. The person is anxious,
obsessive-compulsive, and feels
forsaken or alone in the wilderness;
but a mild demeanour may mask
violence of thought or action
• Worse on looking at bright or shining
objects, after sleep
• Better from bright light, company,
warmth
• For diagnosis of anxiety disorders, use criteria in the Diagnosis and Statistical Manual of Mental
Treat for
Disorders-5(refer text)
substance
• Take history of present illness, current symptoms; past psychiatric history, general medical history abuse /
and history of substance use, personal history, social, occupational and family history; review of the medical
patient’s medications; physical and mental status examination condition
• Blood, urine and other lab tests are used to diagnose any medical condition/medication/substance
abuse
Improvement
Continue follow-
up with regular Improvement
assessment
Yes NO
Re-assess and
select constitutional NO Yes
homoeopathic
medicine on the
basis of symptom Patient should Continue follow-
similarity be treated with up with regular
Continue follow- integrative assessment and
up with regular approach & high- taper off the dose
assessment level psychological of conventional
intervention medicine
and if required
hospitalization is to
Deterioration of be done
signs/ symptoms/
progressing to Improvement
chronicity- refer
chronic treatment NO Yes
APHTHOUS STOMATITIS
CASE DEFINITION1,2,3
Aphthous stomatitis is one of most common ulcerative diseases associated mainly with the oral
mucosa characterized by the extremely painful, recurring, solitary or multiple ulcers in the upper
throat and non-keratinized oral mucosa. These types of ulcers are usually small, multiple, ovoid or
round with circumscribed margins and gray or yellow floors and are encompassed by erythematous
halo.
INCIDENCE/ PREVALENCE4,5,6
Aphthous stomatitis affects approximately 20% of the general population. It is slightly more common
in girls and women as well as among affluent socioeconomic classes and countries. Age of onset
may be during childhood, but more commonly in the second and third decades of life, becoming
less common with advancing age. Aphthous stomatitis can be a manifestation of Behcet syndrome,
systemic lupus erythematosus, reactive arthritis, or inflammatory bowel disease (especially Crohn’s
disease).
CLASSIFICATION7,8,9,10
It is classified into three types of recurrent aphthous stomatitis (RAS) based on clinical manifestation-
Major recurrent aphthous stomatitis, Minor recurrent aphthous stomatitis and Herpetiform
aphthous ulcers.
1 Sharma D, Garg R. A Comprehensive Review on Aphthous Stomatitis, its Types, Management and Treatment Available. J Develop
Drugs.2018;7(2):188.
2 Alli BY, Erinoso OA, Olawuyi AB. Effect of sodium lauryl sulfate on recurrent aphthous stomatitis: A systematic review, J Oral Pathol Med.
2019;48:358–364.
3 Nattah SS, Konttinen YT, Enattah NS, Ashammakhi N, Sharkey KA, Häyrinen-Immonen R. Recurrent aphthous ulcers today: a review of the
growing knowledge. Int. J. Oral Maxillofac. Surg. 2004; 33: 221–234.
4 Plewa MC, Chatterjee K. Aphthous Stomatitis. StatPearls [Internet] 2020. [Cited 2020 Aug 24]. Available from: https://www.ncbi.nlm.nih.gov/
books/NBK431059/
5 Pederson A. Are recurrent oral apthous ulcers of viral etiology? Med Hypotheses.1991;36(3):206-210.
6 Queiroz SIML, Silva MVAD, Medeiros AMC, Oliveira PT, Gurgel BCV, Silveira � JDD. Recurrent aphthous ulceration: an epidemiological study of
etiological factors, treatment and differential diagnosis. An Bras Dermatol. 2018; 93(3):341-346.
7 Namrata M, Abilasha R. Recurrent Apthous Stomatitis. International Journal of Orofacial Biology.2017;1(2):43-47.
8 Rivera C. Essentials of recurrent aphthous stomatitis (Review), Biomedical Reports.2019;11(2):47-50.
9 Zain RB. Classification, epidemiology and aetiology of oral recurrent aphthous ulceration/stomatitis. Annal Dent Univ Malaya.1999; 6: 34 - 37.
10 Edgar NR, Saleh D, Miller RA. Recurrent Aphthous Stomatitis: A Review. J Clin Aesthet Dermatol.2017;10(3):26-36.
2) Minor Recurrent Aphthous Stomatitis: Minor RAS have been reported to constitute 70%–
87% of all forms of RAS. It manifests as recurrent, round, clearly defined, small, painful
ulcers with shallow necrotic centers, raised margins, and erythematous halos. These lesions
are 5–10 mm in diameter and have a gray-white pseudo-membrane. These lesions heal
within 14–10 days without scarring. The most common location is on nonkeratinized oral
mucosa (the labial and buccal mucosa and floor of the mouth). Lesions appear as single or
multiple ulcers but can be distinguished from other mucocutaneous diseases based on their
history, location, healthy appearance of adjacent tissues, and lack of distinguishing systemic
features.
3) Herpetiform aphthous ulcers: The least common form of RAS is herpetiform aphthous
ulcers, which afflict 5% to 10% of patients with RAS. It occurs more frequently in females,
and onset is often in adulthood. Multiple small clusters of pinpoint ulcers characterize this
rare form of RAS, and they occur throughout the oral cavity. They tend to be small (2–3
mm) and numerous (ranging from 10 to 100 ulcers) but can become confluent to produce
larger, plaque-form, irregular lesions. Lesions last 7–30 days and have the potential to scar.
Although these lesions are herpes like or herpetic form in nature, herpes simplex virus
(HSV) cannot be cultured from these lesions.
Figure 1: a) Major b) Minor c) Herpetiform RAS. Courtesy: Anu Shastri A., Srivastava R.
Etiopathogenesis, Diagnosis and Recent Treatment Modalities for Recurrent Aphthous Stomatitis: A
Review. International journal of contemporary medical research;2015.
The precise etiopathogenesis of aphthous stomatitis is not fully disclosed. The potential factors
responsible for aphthous ulcers are described below:
11 Parkhill AL. Oral Mucositis and Stomatitis Associated with Conventional and Targeted Anticancer Therapy.
Journal of Pharmacovigilance.2013;1(4).
12 Jurge S, Kuffer R, Scully C, Porter SR. Mucosal disease series. Number VI. Recurrent aphthous stomatitis. Oral Dis. 2006;12(1):1-21.
13 Lankarani KB, Sivandzadeh GR, Hassanpour S. Oral manifestation in inflammatory bowel disease: a review. World J
Gastroenterol.2013;19(46):8571-9.
14 Gualtierotti R, Marzano AV, Spadari F, Cugno M. Main Oral Manifestations in Immune-Mediated and Inflammatory Rheumatic Diseases. J Clin
Med. 2018;8(1):21.
15 Scully C, Hodgson T, Lachmann H. Auto-inflammatory syndromes and oral health. Oral Dis. 2008;14(8):690-699.
Disease Phases10
DIAGNOSIS
The diagnosis of RAS is based on history and clinical findings. There is no specific diagnostic test, but
there is a need to exclude other possible causes of recurrent ulcers as mentioned under aetiology
and risk factors.16
16 Scully C, Porter S. Oral mucosal disease: recurrent aphthous stomatitis. Br J Oral Maxillofac Surg.2008;46(3):198-206.
CLINICAL FEATURES16,17,18,19
1) Minor aphthae
The prodromal stage of ulceration is variable, but there is usually a sensation described as
“burning” or “prickling” for a short period before the ulcers appear.
• Number: There are typically 1-4 ulcers in each attack
• Duration: Each lesion lasts for 10 –14 days. The variability in times of recovery can
depend on the area affected or on whether superinfection occurred.
• Location: These are usually confined to the nonkeratinized parts of the mucosa and
therefore do not involve the hard palate or the gingiva.
• Scars: Heal without scarring.
2) Major aphthae
These lesions are deeper, larger and last longer than minor aphthae. As a result of the long periods
involved, there is a greater tendency to produce a heaped-up margin which, when a single ulcer is
seen, may lead to the suspicion that the lesion is malignant. These lesions cause substantial pain
associated with fever, dysphagia and malaise.
• Number: There are usually no more than one or two lesions in each attack.
• Duration: They persist longer than minor aphthae and can last for weeks or months.
• Location: They have a predilection for the posterior part of the mouth, particularly the
soft palate and pharyngeal wall or tonsillar fauces. In some patients, the tongue is the
site of predilection.
• Scars: Often leave a scar after healing.
3) Herpetiform aphthae
The herpetiform type, like the other forms of RAS, occurs usually on mobile mucosa and not on
attached mucosa like a true herpes infection. The age of onset of herpetiform aphthae is later than
the other types with initial episode usually presenting in the second or third decade of life.
• Number: The ulcers may number 50 or more, and although each individual ulcer rarely
exceeds 2 mm in diameter, groups of ulcers may coalesce to form compound ulcers with
irregular outlines.
• Duration: This type of cluster forming ulcers can take up to 7-14 days to heal but it can
vary depending upon period of intervals between recurrences.
• Location: Occurs usually on mobile mucosa.
• Scars: These ulcers do not leave scars after healing.
17 Femiano F, Lanza A, Buonaiuto C, Gombos F, Nunziata M, Piccolo S, et al. Guidelines for Diagnosis and Management of Aphthous Stomatitis.
The Pediatric Infectious Disease Journal.2007;26(8).728-732.
18 Kadir AS, Islam AM, Ruhan M, Mowla A, Nipun JN. Recurrent aphthous stomatitis: An overview, International Journal of Oral Health
Dentistry.2018;4(1):6-11.
19 Kramer IR, Pindborg JJ, Bezroukov V, Infirri JS. Guide to epidemiology and diagnosis of oral mucosal diseases and conditions. World Health
Organization. Community Dent Oral Epidemiol. 1980 ;8(1):1-26.
INVESTIGATIONS20
DIFFERENTIAL DIAGNOSIS12,18
Diagnosis Differential features
Carcinoma Painless ulcer with induration where the tissue feels firm and
thickened with fixation and loss of mobility with the surface
being nodular or ulcerated and the ulcer with raised/rolled
margin. In the later stages there may be a soft fungating mass
that bleeds readily
Leukoplakia White patch, or plaque, that cannot be characterized
clinically or pathologically as any other disease with variable
appearance. Lesions may be white, whitish-yellow or grey and
some appear homogeneous, while others are nodular, showing
white areas intermingled with red zones; this is often called a
nodular (speckled) leukoplakia
Leukoedema Seen typically on the buccal mucosa and has been described
as resembling an ill-defined ‘grey veil’ lying on the mucosa
Erythroplakia Bright red velvety plaques which cannot be characterized
clinically or pathologically as due to any other condition
Leukokeratosis nicotinapalati Specific lesion may occur in the palate of heavy pipe and
cigar smokers, particularly the former where the mucosa is
reddened which soon becomes greyish-white and present
with a wrinkled appearance
Lichen planus Oral lesions are seen with or without skin lesions. Skin lesions
are pruritic, purple, polygonal papules. Oral lesions occur in
two forms: (a)Reticular with white striae form on both sides.
(b) Erosive characterized by painful ulceration on the buccal
mucosa, gingiva or lateral tongue
Herpangina Coxsackie viral infection mostly affecting children, multiple
small vesicles appear on the faucial pillars, tonsils, soft palate
and uvula which rupture to form small ulcers
Herpetic Caused by herpes simplex virus and is of two types: primary
gingivostomatitis and secondary
20 Nair JR, Moots RJ. Behcet’s disease. Clin Med (Lond). 2017 ;17(1):71-77.
Hand, foot and mouth Viral infection affecting children. Oral lesions are seen on the
disease palate, tongue and buccal mucosa
Vincent infection (Acute necrotizing Causative organisms are fusiform bacillus and spirochaete,
ulcerative gingivitis) Borrelia vincentii. It starts at the interdental papillae and then
spreads to free margins of the gingivae which get covered with
necrotic slough
Tuberculosis, syphilis May present as chronic ulcers. Diagnosis confirmed by specific
and actinomycosis tests.
Moniliasis Caused by Candida albicans and occurs in two forms:
(Candidiasis) 1.Thrush which appears as white grey patches on the oral
mucosa and tongue.
2.Chronic hypertrophic candidiasis where the lesion appears
as white patch which cannot be wiped off
Erythema multiforme Disease of rapid onset involving the skin and mucous
membranes, either of which may be involved alone
Pemphigus vulgaris Autoimmune disorder with oral lesions is seen in 50% of the
cases and may precede skin lesions
Benign mucous membrane pemphigoid Autoimmune disorder and mucosal lesions involving cheek,
(BMMP) gingivae and palate
Drug allergy Systemic administration of drugs like penicillin, tetracycline,
sulfa drugs, barbiturates, phenytoin, etc. may cause erosive,
vesicular or bullous lesions in the oral cavity
Median rhomboid glossitis It is a developmental anomaly seen as red rhomboid area,
devoid of papillae, on the dorsum of tongue in front of foramen
caecum
Geographical tongue It is characterized by erythematous areas, devoid of papillae,
surrounded by an irregular keratotic white outline
RED FLAGS24
MANAGEMENT25,26
General management
Patient education is important to prevent recurrence of aphthous ulcerations.
• Practice good oral hygiene and avoid local trauma or oral hygiene products of known sensitivity
• Consider taking dietary supplements with iron, zinc, or vitamins B1, B2, B6, B12, or C if
vitamin or mineral deficiency is identified
• Avoid hard foods (e.g., hard toasted bread), all types of nuts (walnuts, hazelnuts, etc.),
chocolate, acid beverages or foods (fruits or citrus juices, tomato), salty foods, very spicy
foods and alcoholic and carbonated beverages
• Only individuals diagnosed with celiac disease should choose a gluten-free diet
• Avoid known trigger foods, emotional or physiologic stress whenever possible
• Supportive care including rest
• Increased fluid intake
• Reassurance that aphthae are not communicable.
Homoeopathic management
Homoeopathic medicines have scope in treatment of aphthous stomatitis as per the research
evidence.27 Several medicines are given in homoeopathic repertories for aphthous stomatitis. In
synthesis repertory28, 204 medicines are found in chapter MOUTH under the rubric Aphthae. The
frequently verified characteristic features of some organospecific remedies are: Digitalis purpurea:
Roughness, excoriation and scraping in the mouth and throat, with clammy taste. Kalium chloricum:
Acute ulceration and follicular stomatitis, aphthous and gangrenous. Entire mucus membrane of
mouth red, tumid, gray based ulcer. Profuse secretion of acrid saliva. Fetor. Sempervivum tectorum:
Tongue ulcerated bleeds easily, especially at night, much soreness of tongue with stabbing pains.
Muriaticum acidum: Tongue, pale, swollen, dry, leathery, paralyzed. Deep ulcers on tongue
accompanied with low fevers and great prostration. Mercurius corrosivus: Aphthae and ulcers
with burning, scalding sensation in mouth. Hydrastis: Ulceration of tongue, fissures toward the
edges. Zincum metallicum: Bloody taste. Blisters on tongue. Manganum aceticum: Tongue sore
and irritable with ulcers.
The following are few commonly prescribed homoeopathic medicines for aphthous stomatitis with
their indications, enlisted from experiences, and textbooks.29,30,31,32
25 Dhingra PL, Dhingra S, Dhingra D. Diseases of Ear, Nose and Throat & Head and Neck Surgery. 6th Ed. Haryana: Elsevier;2014. Chapter 43,
Common Disorders of Oral Cavity; p. 217-219
26 Belenguer-Guallar I, Jiménez-Soriano Y, Claramunt-Lozano A. Treatment of recurrent aphthous stomatitis. A literature review. J Clin Exp Dent.
2014;6(2): 168-74.
27 Mousavi F, Mojaver YN, Asadzadeh M, Mirzazadeh M. Homeopathic treatment of minor aphthous ulcer: a randomized, placebo-controlled
clinical trial. Homeopathy. 2009;98(3):137-141.
28 Schroyens F. Synthesis Repertory ver. 9.1; New Delhi: B Jain Publishers Pvt. Ltd.; 2002:307-08.
29 Allen HC. Allen’s keynotes Rearranged and classified with leading remedies of the materia medica and bowel nosodes.8th ed. New Delhi: B. Jain
Publishers (P) Ltd.;1997.
30 Boericke W. Boericke’s New Manual of Homoeopathic Materia Medica with Repertory.9th Ed. New Delhi: B. Jain Publishers; 2007.
31 Clarke JH. A Dictionary of Practical Materia Medica. 7th ed. New Delhi: B. Jain Publishers;2000.
32 Kent JT. Repertory of the Homoeopathic Materia Medica.6th American edition. New Delhi: Jain publishing co.;1978.
Arsenicum album Chilly patient; rapid disproportionate • Tongue dry, clean, and red; stitching
prostration; burning pains better by and burning pain in tongue; ulcerated
heat (except headache); cadaveric odour with blue color, dryness and burning
of discharges and body; anxiety, anguish, heat
fear of death and restlessness • Bloody saliva, metallic taste
and gulping up of burning water
• Fetor oris; taste bitter to water; sour,
foul, saltish and sweetish taste in
morning
• Worse after midnight, from cold, cold
drinks, or food, right side
• Better from heat, from warm drinks
Borax veneta Poorly nourished babies; dread • Aphthae in the mouth, on the tongue,
of downward motion in nearly all inside of the cheek; easily bleeding
complaints; nervous, frightened, when eating or touched; prevents
sensitive to sudden noises, cries out of child from nursing; with hot mouth,
sleep as if frightened, awakes suddenly dryness and thirst
dreaming and grasping sides of bed • Cracked and bleeding tongue,
without apparent cause salivation, especially during dentition
• Aphthous sore mouth; of old people
• Taste bitter, even saliva; Thrush
• Worse from smoking, touch, eating
salty or sour food, after menses
• Better by pressure
Carbo vegetabilis Chilly patient; disintegration and • Aphthae; bluish, blackish ulcers, with
imperfect oxidation is the keynote of the burning
remedy; Weak digestion, simplest food • Excoriation of the tongue, with
disagrees, eructation gives temporary difficulty in moving it
relief; patient may be almost lifeless, but • Tongue coated white or yellow
head is hot; coldness, breath cool, pulse brown, covered with aphthae
imperceptible; oppressed and quickened • Dryness and roughness of the mouth,
respiration, and must have air, must without thirst
be fanned hard very closely many • Scorbutic gums. Taste bitter, sour.
complaints. Persons who have never Increased saliva. Sore aphthous in the
fully recovered from the effects of some throat
previous illness. Aversion to darkness. • Worse in evening, at night and open
Fear of ghosts. Sudden loss of memory air, cold, from fat food, butter, coffee,
milk, wine
• Better from eructation, cold
Lycopodium Hot patient, intellectually keen but • Mouth waters. Blisters on tongue. Bad
clavatum physically weak; upper part of body odor from mouth
emaciated, lower part semi- dropsical; • Tongue dry without thirst, black,
complexion pale, dirty, sallow with deep cracked, swollen; oscillates to and fro
furrows; looks old; recurrent respiratory • Worse from heat or warm room, hot
and gastro-intestinal affections; air, bed
tendency for flatulent dyspepsia; worse • Better from warm food and drink, on
from 4 to 8 pm; right-sided complaints getting cold, from being uncovered
or symptoms shift from right to left;
desire for warm foods and drinks,
sweet; dominating, cranky, lack of self-
confidence, precocious
Mercurius solubilis Sensitive to changes of temperature. • Tongue heavy, thick, indented, moist
Profuse offensive perspiration. Tongue coating; yellow, flabby, feels as if
flabby with imprint of teeth. Increased burnt, with ulcers
salivation. Increased thirst for large • Stomatitis from taking chewing gum
quantity of water. Worse at night, in wet • Fetid odor from mouth, can smell it
damp weather all over room
• Great thirst, with moist mouth
• Taste sweetish, bread tastes sweet
• Worse in warm room
Nitricum acidum Chilly patient; takes cold easily; thin • Bleeding of gums
built; sickly; desires fat, craving for • Painful pimples on sides of tongue
lime, slate, pencil, papers and charcoal • Tongue clean, red and wet with center
and salt; disposed to diarrhea; strong furrowed
smelling urine; headstrong, irritable, • Salivation and fetor oris. Bloody saliva
fearful, vindictive • Worse in evening and at night, cold
climate, hot weather
• Better while riding in carriage
Sulphur Hot patient, kicks off cloth at night; dirty, • Vesicles, blisters, and aphthae in
filthy, does not want to be washed; lean, mouth and on tongue, sometimes
thin, stoop-shouldered; child walks and with burning pain, or with excoriating
sits stooping; red orifices; desires sweets, pain, when eating.
sugar, meat; when the best selected • Exfoliation of mucous membrane of
remedy fails to improve mouth.
• Lips dry, bright red with burning pain
• Worse at rest, warmth in bed, washing,
in morning, night, from alcoholic
stimulants, periodically
• Better in dry, warm weather, lying on
right side
General management
Proper case history and physical examination
• Practice good oral hygiene
• Avoidance of local trauma or oral
hygiene products of known sensitivity
• Nutritional supplements such as
Vitamin B-12 capsules, vitamin D
capsules, folate tablets, or zinc tablets
Appropriate homoeopathic prescription for patients with RAS who have
according to the symptom similarity. Acute deficiency of vitamins and minerals
disease is to be treated with acute medicine • Avoid known trigger foods, emotional
and regular follow up and change of or physiologic stress whenever possible
medicine if no improvement in condition • Suggested supportive care includes
rest
• Increas fluid intake
RED FLAGS
Improvement
• Persistence of ulcers
more than 3 or 4 weeks
Yes NO • Ulcers with raised
border
• Ulcers which are deep
Reassess the case and and/or hard
prescribe appropriate • Persistent ulcers
homoeopathic medicine accompanied by lymph
node enlargement
• Signs of dehydration
• Ulcers in high-risk
Check for complete resolution patients such as
Yes Improvement
smokers and drinkers.
ATOPIC DERMATITIS
CASE DEFINITION1
Atopic dermatitis (AD) is a chronic, recurrent inflammatory skin disease, commonly having a
childhood onset and characterised by variably distributed pruritic eczematous lesions with flexural
predilection; mostly exhibited by patients with personal or family history of atopic diathesis [(i)
personal or family history of bronchial asthma, allergic rhinitis and conjunctivitis and/or atopic
dermatitis and /or (ii) predisposition to overproduction of immunoglobulin E (Ig E) antibodies].
Synonyms- Atopic dermatitis is sometimes called eczema, a term that also refers to a larger group
of skin conditions. Other names include “infantile eczema”, “flexural eczema”, “prurigo besnier”,
“allergic eczema”, and “neurodermatitis”.2,3,4,5
INCIDENCE/PREVALENCE6,7,8
AD affects 1%-20% of people worldwide. The clinical presentation often varies with age. AD is
seen in 3% of all infants, begins between 3 and 6 months of age. 50% of all those with AD present
within their first year of life and probably 85% present it by 5 years of age. Early childhood AD often
predisposes a child to later develop asthma and/or allergic rhinitis (hay fever).
The prevalence of AD in adults is about 1%-3%, and 10%-20% in children. Since 1960s, the
prevalence of AD has increased more than 3-fold. Its prevalence is lower in developing countries
than industrialized nations (2-3 fold). It affects about one-fifth of all individuals during their lifetime.
The etiology of AD is multifactorial and complex which is not completely understood. The factors
which play key roles in the development of atopic dermatitis are – genetic factor, impaired immune
response, defect in skin barrier including the role of filaggrin (FLG), environmental exposures, and
other eliciting and exacerbation factors.
1 Rajagopalan M, De A, Godse K, Krupa Shankar D S, Zawar V, Sharma N, et al. Guidelines on management of atopic dermatitis in India: An
evidence-based review and an expert consensus. Indian J Dermatol. 2019; 64 (3):166-81.
2 Bieber T. Atopic dermatitis. Ann Dermatol. 2010 17;22 (2):125-37.
3 Williams HC. Clinical practice. Atopic dermatitis. N Engl J Med. 2005;352 (22):2314-24.
4 Brown S, Reynolds NJ. Atopic and non-atopic eczema. BMJ. 2006;332 (7541):584-88.
5 Darsow U, Lübbe J, Taï�eb A, Seidenari S, Wollenberg A, Calza AM, Giusti F, Ring J. European Task Force on Atopic Dermatitis. Position paper on
the diagnosis and treatment of atopic dermatitis. J Eur Acad Dermatol Venereol. 2005; 19 (3):286-95.
6 Williams H, Robertson C, Stewart A, Aï�t-Khaled N, Anabwani G, Anderson R, et al. Worldwide variations in the prevalence of symptoms of
atopic eczema in the International Study of Asthma and Allergies in Childhood. J Allergy Clin Immunol. 1999; 103(1):125–138.
7 Sehgal VN, Khurana A, Mendiratta V, Saxena D, Srivastava G, Aggarwal AK. Atopic dermatitis; Etio-pathogenesis, An overview. Indian J
Dermatol. 2015;60 (4): 327-31.
8 Rajka G. Essential Aspects of Atopic Dermatitis. Berlin, Germany: Springer Verlag; 1989: 125-38.
9 Ogg G. Role of T cells in the pathogenesis of atopic dermatitis. Clin Exp Allergy. 2009; 39(3):310–6.
10 Mittermann I, Aichberger KJ, Bünder R, Mothes N, Renz H, Valenta R. Autoimmunity and Atopic Dermatitis. Current Opinion in Allergy and
Clinical Immunology.2004; 4 (5): 367-371.
11 McPherson T. Current Understanding in Pathogenesis of Atopic Dermatitis. Indian J Dermatol. 2016;61(6):649-655.
• Genetic factor
There is a clear genetic predisposition and is an important risk factor in atopic dermatitis. The
child is at increased risk to develop atopy, if either parent is affected and with the severity of the
complaint.
The immunological response of patients includes key roles of T cells, dendritic cells, innate
lymphoid cells, mast cells, and eosinophils. There are abnormalities in both adaptive and innate
immunity in children with AD.
Environmental factors, in addition to genetic factors, are the main drivers of change in disease
burden. Factors such as climate, urban versus rural setting, diet, breast feeding and time of
weaning, obesity and physical exercise or tobacco smoke and pollution etc. are implicated as
main predisposing factors. Even emotional stress may exacerbate the symptoms.
It is well established that emotional stressors and anxiety make the symptoms worse or trigger
the AD in an individual.12
DIAGNOSIS
Clinical presentation13
• Pruritus and scratching, pruritus being the hallmark of atopic dermatitis. Itching often precedes
the appearance of lesions; hence the concept that atopic dermatitis is “the itch that rashes.”
• Course is marked by exacerbations and remissions.
• Eczematous dermatitis (acute, subacute, or chronic) with typical morphology and age-specific
patterns.
• Personal or family history of atopy (allergic rhinitis, asthma, food allergies or eczema).
• Clinical course lasting longer than six weeks.
• Atopic dermatitis can be divided into three stages:
12 Suárez AL, Feramisco JD, Koo J, Steinhoff M. Psychoneuroimmunology of psychological stress and atopic dermatitis: pathophysiologic and
therapeutic updates. Acta Derm Venereol. 2012;92(1):7-15.
13 Khanna N. Illustrated Synopsis of Dermatology & Sexually Transmitted Diseases.4th ed. New Delhi: Elsevier;2011.
Three distinct patterns of AD as mentioned below have been recognized, depending on the age of
the patient:
Diagnostic Criteria14,15,16
The diagnosis of AD is mainly clinical based on signs and symptoms alone with very few laboratory
tests available for confirmation. Different forms of criteria are developed to aid in diagnosis, one of
which is mentioned below:
UK diagnostic criteria
The diagnostic criteria based on the work of Hanifin and Rajka are useful in classifying cases. It is
classified as major and minor.
Major criteria (3 or more) Minor criteria (3 or more)
• Presence of an itchy skin condition or • Xerosis (dry skin)
evidence of rubbing or scratching, plus three • Ichthyosis / hyperlinear palms/ keratosis pilaris
or more of the following: • IgE reactivity /Elevated serum IgE (Immediate skin
o Onset below 2 years (not used if test reactivity, Radio allegro sorbent test (RAST)
child is under 4 years) positive
o History of skin crease involvement • Early age of onset. Tendency for cutaneous infections
(including cheeks) in children under (especially S. aureus and Herpes simplex virus)
10 years • Tendency to non-specific hand/foot dermatitis
14 Eichenfield LF, Tom WL, Chamlin SL, Feldman SR, Hanifin JM, Simpson EL, et al. “Guidelines of care for the management of atopic dermatitis:
section 1. Diagnosis and assessment of atopic dermatitis”. Journal of the American Academy of Academy Dermatology. 2014; 70 (2):338 – 51.
15 Brenninkmeijer EE, Schram ME, Leeflang MM, Bos JD, Spuls PI. Diagnostic criteria for atopic dermatitis: a systematic review”. The British
Journal of Dermatology. 2018; 158 (4):754–65.
16 Williams HC, Burney PG, Pembroke AC, Hay RJ. “The U.K. Working Party’s Diagnostic Criteria for Atopic Dermatitis. III. Independent hospital
validation”. The British Journal of Dermatology.1994.131(3):406–16.
INVESTIGATIONS13,17
• IgE levels: Elevated total serum IgE (normal: <200IU/ml) and IgE antibodies specific to
antigens may be useful in diagnosing atopic state
• Eosinophil counts: Increased eosinophil may be present
DIFFERENTIAL DIAGNOSIS18,19,20
The differential diagnosis of AD in children and adults includes non-atopic dermatitis, seborrheic
dermatitis, allergic contact dermatitis, nummular dermatitis, psoriasis (palmoplantar), palmoplantar
pustulosis, scabies, lichen simplex chronicus, chronic actinic dermatitis, dermatophytosis,
dermatomyositis, pemphigus foliaceus, cutaneous T-cell lymphoma.
Typical atopic dermatitis is not difficult to diagnose because of its predilection for symmetric
involvement of face, neck, ante-cubital and popliteal fossae.
17 Vanecova J, Bukac J. The severity of atopic dermatitis and the relation to the level of total IgE, onset of atopic dermatitis and family history about
atopy. Food and Agricultural Immunology. 2016; 27(5): 734-741.
18 Brenninkmeijer EEA, Spuls PI, Legierse CM, Lindeboom R, Smitt JHS, Bos JD. Clinical differences between atopic and atopiform dermatitis. J Am Acad
Dermatol. 2008;58(3):407-14.
19 Novak N,Bieber T. Allergic and nonallergic forms of atopic diseases. J Allergy Clin Immunol.2003;112(2):252-62.
20 Charman C, Williams H. Outcome measures of disease severity in atopic eczema. Arch Dermatol. 2000;136(6):763-9.
Infantile Seborrheic • Onset during 1st days or weeks of life, absence of pruritus, and presence of
dermatitis greasy scaling on a yellow-red base; top of the scalp, axilla, and diaper area
are involved
• Atypical, seborrheic areas often not excoriated and not pruritic, no whitish
dermographism
• IgE level is usually normal; no Eosinophilia; food allergy and respiratory
allergy conditions rare
Irritant or allergic • Localized rash or irritation of the skin results from either exposure
contact dermatitis to allergens (allergic contact dermatitis) or irritants (irritant contact
dermatitis)
• Many substances can cause such reactions, including soaps, cosmetics,
fragrances, jewellery and plants. Only the superficial regions of the skin
(epidermis and the outer dermis) are affected
• Red, itchy rashes, burning pain; occurs at any age, mostly in adults; typical
morphology and localised distribution, pruritic, often excoriated caused by
direct contact with a substance or an allergic reaction to it
• Irritant dermatitis is usually confined to the area where the trigger touches
the skin and more painful than itchy, whereas allergic dermatitis may be
more widespread on the skin and more itching often itches. IgE level is
usually normal. Positive patch test
Nummular dermatitis • A chronic condition that causes coin-shaped spots on the skin; often itchy
with burning pain and well-defined; brown, pink, or red; may ooze clear
fluid or become dry and crusty; may have a personal or family history of
allergies, asthma, or atopic dermatitis and may result in one patch or
multiple patches of coin-shaped lesions
• Lasts for several months; not contagious; the skin may be red, scaly, or
inflamed around the lesions
Palmoplantar Pustulosis • A rare autoimmune chronic skin condition; smokers are more affected;
firstly, red and tender then blisters and pustules form on palms of hands and
soles of feet
• Can start as a small area and spread; common for them to come and go;
white or yellow pus in the pustules; after drying up, they can turn brown,
thick and scaly; deep and painful cracks on skin causes difficulty to walk or
perform other activities
Pemphigus foliaceus • An acquired superficial blistering skin disease; intact bullae are rarely
found; skin lesions that are often distributed in seborrheic areas can mimic
acute/ subacute eczema; body’s immune system produces immunoglobulin
G (IgG) autoantibodies that target the intercellular adhesion glycoprotein
desmoglein-1 (dsg-1)
Following measurement scales are used for assessing the severity and outcome of atopic
dermatitis:
COMPLICATIONS/RED FLAGS
21 Streiner DL, Norman GR. Health Measurement Scales: A Practical Guide to Their Development and Use. 2nd ed. New York: Oxford University Press;1995.
22 Finlay AY. Measurement of disease activity and outcome in atopic dermatitis. Br J Dermatol. 1996;135 (4):509-15.
23 Finlay AY. Quality of life assessments in dermatology. Semin Cutan Med Surg.1998;17(4):291–96.
24 McKenna SP, Doward LC. Quality of life of children with atopic dermatitis and their families. Curr Opin Allergy Clin Immunol. 2008; 8 (3):
228–31.
Standard Treatment Guidelines In Homoeopathy 69
ATOPIC DERMATITIS
MANAGEMENT
General management
AD adversely affects social interactions and personal relationships. Notably, pruritus can be
intractable and lead to significant emotional distress and sleep loss. Therefore, treatments for AD
need to rapidly control symptoms of the disease and improve quality of life. Given the chronic and
relapsing nature of the disease, its general management should focus on the following strategies:
• Identification and avoidance of triggering and/or aggravating factors that exacerbate itching,
such as woollen clothes, emotional stress, and uncomfortable climatic conditions.
• Emotional stress, anxiety and depression can provoke itching, and scratching exacerbates
AD. Such patients with emotional or psychological problems should asked to relax.
• Psychological support and counselling can be helpful to break the itch-scratch cycle, especially
in adolescents and young adults.
Due to limited understanding of the etiopathology of childhood prevalence of AD, the prevention is
focused on the management of both predisposing and exacerbating risk factors.25,26
Homoeopathic management
Homoeopathy medicines can offer practical benefit in the treatment of AD.27,28,29,30,31,32,33,34,35 Several
clinical research studies and case studies36,37,38,39 have shown that homoeopathic treatment has
a positive therapeutic effect in AD with improvement in the health-related quality of life of such
patients.
25 Flohr C. Recent perspectives on the global epidemiology of childhood eczema. Allergol Immunopathol (Madr). 2011;39 (3):174–82.
26 Flohr C, Nagel G, Weinmayr G, Kleiner A, Strachan DP, Williams HC. Lack of evidence for a protective effect of prolonged breastfeeding on
childhood eczema: lessons from the International Study of Asthma and Allergies in Childhood (ISAAC) Phase Two. Br J Dermatol. 2011;165
(6):1280–89.
27 Rossi E, Bartoli P, Bianchi A, Da Frè M. Homeopathy in paediatric atopic diseases: long-term results in children with atopic dermatitis.
Homeopathy. 2012;101(1):13-20.
28 Jose MM, Pedrera-Zamorano JD. Statistical comments on Homeopathy in paediatric atopic diseases: long-term results in children with atopic
dermatitis. Homeopathy. 2016; 105 (4): 356.
29 Hughes R, Ward D, Tobin AM, Keegan K, Kirby B. The use of alternative medicine in pediatric patients with atopic dermatitis. Pediatr
Dermatol. 2007;24 (2):118–120.
30 Siebenwirth J, Lüdtke R, Remy W, Rakoski J, Borelli S, Ring J. Effectiveness of a classical homeopathic treatment in atopic eczema. A
randomised placebo-controlled double-blind clinical trial. Forsch Komplemented. 2009;16(5):315-23.
31 Witt CM, Brinkhaus B, Pach D, Reinhold T, Wruck K, Roll S, Jackel T, Staab, D, Wegscheider K, Willich SN. Homoeopathic versus Conventional
Therapy for Atopic Eczema in Children: Medical and Economic Results. Dermatology. 2009; 219 (4): 329–40.
32 Roll S, Reinhold T, Pach D, Brinkhaus B, Icke K, Staab D, Jäckel T, Wegscheider K, Willich SN, Witt CM. Comparative effectiveness of
homoeopathic vs. conventional therapy in usual care of atopic eczema in children: long-term medical and economic outcomes. PLoS
One.2013;8(1):54973.
33 Keil T, Witt CM, Roll S, Vance W, Weber K, Wegscheider K, Willich SN. (2008) Homoeopathic versus conventional treatment of children with
eczema: A comparative cohort study. Complement Ther Med.2008 ;16(1):15–21.
34 Schäfer T, Riehle A, Wichmann HE, Ring J. Alternative medicine in allergies - prevalence, patterns of use, and costs. Allergy. 2002; 57 (8):694–
700.
35 Becker-Witt C, Lüdtke R, Weisshuhn TER, Willich SN.Diagnoses and treatment in homeopathic medical practice. Forsch Komplementärmed
Klass Naturheilkd. 2004;11 (2):98–103.
36 Witt CM, Lüdtke R, Willich SN. Homeopathic treatment of children with atopic eczema: A prospective observational study with Two years
follow-up. Acta Derm Venereol. 2009; 89 (2): 182–83.
37 Eizayaga JE, Eizayaga JI; Prospective observational study of 42 patients with atopic dermatitis treated with homeopathic medicines.
Homeopathy. 2012.101(1):21-7.
38 Parveen S. Homoeopathic treatment in a case of co-morbid atopic dermatitis and depressive disorder.Indian J Res Homoeopathy.2016 ;10 (1):
75-82.
39 Nwabudike CL. Atopic Dermatitis and Homeopathy. Our Dermatol Online. 2012; 3 (3): 217-20.
There are about 183 medicines mentioned in Synthesis repertory40 under rubric “Eczema-atopic”
in Skin chapter. Out of 183 medicines, three medicines (Graphites, Rhus toxicodendron and Sulphur)
are in 1st grade and 26 in 2nd grade. AD is an illness with varying locations, varying states and
stages of pathology with different rates of progress showing predominant skin symptoms. In this
condition, different factors like age, occupation, previous illnesses and life circumstance unique to
the individual patient are taken into consideration by constructing the totality of symptoms.
As per homoeopathic concept of diseases, AD is a psoric or pseudo-psoric disease and its treatment
plan differs considerably in acute and chronic cases. The miasmatic load can move to sycotic
with consequential thickening of lesions; could also move to tubercular if one observes repeated
secondary bacterial infections. Chronic cases require comparatively longer period of treatment
by the indicated constitutional medicines. Several changes in plan of treatment may be necessary
before complete alleviation of symptoms.41,42
A particular difficulty is posed in patients of AD who are on suppressive medication, either local
ointments or oral medication. Advise to cease this medication may result in a sudden flare up of
itching and other manifestations. This may need some remedies selected based on the presenting
symptoms to take care of the distressing symptoms before moving on to the constitutional, deep-
acting remedy.
The frequently verified characteristic features of some organospecific remedies are: Arsenicum
iodatum: Chilly, cannot endure cold, debilitating night-sweats, eczema of the beard; watery,
oozing, itching; worse, washing. The discharge may be fetid, watery, and the mucous membrane
is always red, angry, swollen; itches and burns. Dry, scaly, itchy. Marked exfoliation of skin in the
form large scales. Calcarea sulphurica: Purulent exudations in or upon the skin. Skin affections
with yellowish scabs. Many little matterless pimples under the hair, bleeding when scratched. Dry
eczema in children. Cicuta virosa: Eczema; no itching, exudation forms into a hard, lemon-colored
crust with burning pain. Elevated eruptions, as large as peas. Suppressed eruption causes brain
disease. Worse, from touch everything appears strange and terrible. Confounds present with the
past; desire for unnatural things, like coal. Caladium seguinum: The skin has a rough, dry feeling
Itching, burning rash (forearm and chest), alternating with asthma. Violent itching on various parts.
Croton tiglium: Pure idiopathic eczema, such as usually appears in children. Eczema over whole
body to soles of feet, face and genitalia intense itching; stinging, smarting pains but scratching is
painful. Vesicles; confluent oozing, exuding offensive moisture., worse by very gentle scratching.
Manganum aceticum: Chronic eczema associated with amenorrhoea worse at menstrual period,
menopause. Pix liquida: Cracked skin; itching intolerably, bleeds on scratching, eruptions on back
of hand. Vinca minor: Great sensitiveness of skin, with redness and soreness from slight rubbing;
eczema of head and face, pustules itching, burning and offensive odor, matting hair together, plica
40 Schroyens F. The Essential Synthesis. Indian Edition. New Delhi: B. Jain Publishers(P) Ltd; 2012.
41 Hahnemann S. Organon of Medicine. Combined Fifth & Sixth Edition. Dudgeon Re and Boericke W (Translators). New Delhi: B. Jain Publishers
(P) Ltd; 1921.
42 Kent JT. Lectures on Homoeopathic Philosophy. Reprint edition. New delhi: B. Jain Publishers(P) Ltd.; 2013.
polonica. Jugulans cineria: Pustules. Eczema, especially on lower extremities, sacrum and hands.
Erythema and erysipelatous redness. Kalium arsenicum.: Intolerable itching, worse undressing.
Dry, scaly, wilted. Acne; pustules worse during menses. Chronic eczema; itching worse from warmth,
walking, undressing. Sulphur iodatum: Obstinate skin affections, notably in barber’s itch and acne.
Weeping eczema. Viola tricolor: Eczema impetigonoides of the face, Intolerable itching, eruptions,
particularly over face and head, with burning, itching; worse at night. Thick scabs, which crack and
exude a tenacious yellow pus.
43 Boericke W. Boericke’s new manual of Homoeopathic Materia Medica. 3rd revised and augmented ed. New Delhi: B. Jain Publishers Pvt. Ltd.;2007.
44 Allen HC. Allen’s Keynotes- Rearranged and classified with leading remedies of the Materia Medica and bowel nosodes. 10th Reprint ed. New
Delhi: B. Jain Publishers Pvt. Ltd.;2006.
45 Clarke JH. A Dictionary of Practical Material Medica. Reprint ed. New Delhi: B Jain Publishers Pvt. Ltd.; 2007.
46 Kent J.T. Lectures on Homoeopathic Materia Medica. Reprint ed. New Delhi: B. Jain Publisher’s (P) Ltd.;2011.
47 Herring C. The Guiding Symptoms Of our Materia Medica. Reprint ed. New Delhi: B. Jain Publishers (P) Ltd.;1989.
Arsenicum album Chilly patient; rapid disproportionate • Eczema-Dry, papular, rough, scaly eruption,
prostration; burning pains better by itching of skin, if scratched a sore, bleeding,
heat (except headache); cadaveric odour burning sensation is left
of discharges and body; anxiety, anguish, • Associated with pustules and ulcers with
fear of death and restlessness offensive discharges.
• Worse from cold, cold drinks or food
• Scratching feels better from heat
Bacillinum Taciturn, sulky, snappish, fretty, irritable, • It has been found in eczematous condition of
morose, depressed and melancholic. the margins of the eyelids a strong indication
Fretful ailing, whines and complains; for it
mind given to be frightened, particularly • An inter-current for patients who have a
by dogs, having a personal or family personal or family history of chest affections
history of chest affections patients; • Worse at night and early morning, cold air
tendency to swelling of neck glands
Calcarea carbonica Chilly patient; takes cold easily; fat, • Eczema, thin moist scabs upon head, with
fair, flabby, distended abdomen; pale, swollen cervical glands; eczema behind
weak, easily tired; head sweats profusely ears
while sleeping; sour smelling discharges; • Hard eczematous vesicles on backs of
longing for fresh air; desire for eggs and hands. Itch-like phagedenic blisters on
indigestible things, sweets, aversion index fingers. Nettle rash; better in cold air
to meat and milk; fearful, shy, timid, • Petechial eruptions. Itching on various
slow and sluggish; feels better when parts of body
constipated • Spots glistening through skin, itching
terribly; when scratching,
• Worse from exertion, mental or physical,
cold in every form, water, washing, moist
air, wet weather, during full moon
• Better in dry climate and weather
Dulcamara Chilly patient; prone to excessive mucus • Humid eruptions on face, genitals, hands,
secretions; worse in cold, damp, rainy arms around the menstrual period
weather; restless and irritable • Thick, brown-yellow crusts, bleeding when
scratched
• Worse at night
• Better from moving about, external warmth
Patient meets Haanifin and Rajka criteria for diagnosis of Atopic dermatitis (Refer text)
• Skin care- advice for general management for appropriate skin Skin care
care to prevent exacerbations and improve quality of life
• Lifestyle changes- maintain good hygiene • Use oil-based fragrance-free
• Education (Learning how to recognize flares facilitates timely moisturizers to keep the skin
treatment) hydrated during remissions
• Avoidance of irritants and food allergens • Bath at least once a day with
• Identification and avoidance of proven allergens lukewarm water but avoid soap
• Psychological counselling
• Wear cotton dress; avoid wool
Yes No
Continue homoeopathic treatment with individualised Re-assess the case and give appropriate homoeopathic
homoeopathic medicine medicine based on symptoms similarity
BREAST FIBROADENOMA
CASE DEFINITION1,2
Fibroadenomas are common benign lesions of the breast that usually present as a single breast mass
in young women. These are solid, round, rubbery lumps that move easily when pushed. They are
assumed to be aberrations of normal breast development or the product of hyperplasic processes,
rather than true neoplasm.
INCIDENCE/PREVALENCE3,4,5,6,7
• Fibroadenoma is the most common benign tumour of the breast under age 30 years. They
usually arise in the fully developed breasts between 15-25 years of age.
• In the adolescent population, the overall incidence of fibroadenoma is 2.2% and accounts for
68% of all breast masses and 44%–94% of biopsied breast lesions.
• More than 70% of fibroadenomas present as a single mass, and 10%–25% of fibroadenomas
present as multiple masses.
• They are more frequent among women in higher socio-economic classes and in dark-skinned
populations.
AETIOLOGY and RISK FACTORS2,8,9
• The exact etiology of fibroadenoma is unknown. However, several studies show that estrogen
influences the development of fibroadenomas.
• Females who take oral contraceptives before 20 years of age tend to suffer from fibroadenoma
at higher rates than the general population.
• Family history of breast cancer in first-degree relatives was reported by some investigators to
be related with increased risk of developing these tumours.
• There is substantial agreement between the risk factors for fibroadenoma and breast cancer.
The characteristics known to increase risk of breast cancer were also found to increase the risk
of fibroadenoma.
• Late menarche, more children, and larger childhood body size were also found to reduce
fibroadenoma risk.
• Consumption of large quantities of vitamin C was found to be associated with reduced risk of
fibroadenoma.
1 Greenberg R, Skornick Y, Kaplan O. Management of breast fibroadenomas. J Gen Intern Med.1998 Sep;13(9):640-5.
2 World Health Organization. The ICD-10 classification of mental and behavioural disorders: Clinical descriptions and diagnostic guidelines
[Internet];1992 [Cited 2020 October 5]. Available from: https://icdlist.com/icd-10/D24.1
3 NLM(U.S.). Fibroadenoma of the Breast [Internet]; 2020 [Cited 2020 July 14]. Available from: http://www.nlm.nih.gov/medlineplus/ency/
article/007216.htm
4 Santen R, Mansel R. Benign Breast disorders. N Engl J Med.2005; 353(3):275-85.
5 Lee M, Soltanian HT. Breast fibroadenomas in adolescents: current perspectives. Adolesc Health Med Ther.2015;6:159-63.
6 Chang DS, McGrath MH. Management of benign tumors of the adolescent breast. PlastReconstr Surg. 2007; 120(1):13-19
7 Sainsbury RC. TheBreast. In: Russell RCG, Williams NS, Bullstrode CJK, editors. Bailey and Love’s Short Practice of Surgery, 24th ed. London:
Edward Arnold; 2004. p. 834.
8 Ajmal M, Van Fossen K. Breast Fibroadenoma. [Updated 2020 Jul 26]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing;
2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK535345
9 Li J, Humphreys K, Ho PJ, Eriksson M, Darai-Ramqvist E, Lindström LS, Hall P, Czene K. Family History, Reproductive, and Lifestyle Risk Factors
for Fibroadenoma and Breast Cancer. JNCI Cancer Spectr. 2018 Dec 10;2(3):051.
PATHOLOGY8,10
Fibroadenomas are of two types:
• Intracanalicular- Includes proliferation of stromal cells compressing epithelial cells into
clefts
• Pericanalicular- Includes proliferation of stromal cells around epithelial structures
On gross examination, the tumours are encapsulated, and they have a homogenous gray-white
appearance on a cut section. On microscopy, they have an epithelial and a stromal component. There
is presence of foam cells and apocrine cells and an absence of excessive mitotic activity or anaplasia.
Calcification may also be present. The basement membrane also remains intact in fibroadenoma
which reflects its benign feature. They arise from hyperplasia of a single lobule and usually grow up
to 2-3 cm in size.
TYPES8,11,12,13
Complex fibroadenoma
These are subtypes of fibroadenomas harbouring one or more complex features, including epithelial
calcifications, papillary apocrine metaplasia, sclerosing adenosis, and cysts larger than 3 mm.
Approximately, 16% of fibroadenomas have been reported as complex. Complex fibroadenomas
tend to occur in older patients and are often smaller than simple fibroadenomas. The risk of invasive
breast cancer is increased in women with complex fibroadenomas.
Giant (Juvenile) fibroadenoma
Giant (juvenile) fibroadenoma of the breast is an uncommon variant of fibroadenoma in adolescents
and young women with rapid growth and large size. Giant fibroadenomas are benign tumours, but
their rapid growth and large size together with their rarity may determine difficulties in the clinical
approach. Moreover, giant fibroadenomas must be excised in all cases to exclude a phyllodes tumour
and to prevent deformity later.
Phyllodes tumour
A stromal tumour of the breast can be either benign or malignant. It is not a fibroadenoma; therefore,
it needs to be watched closely.
DIAGNOSIS1,10,14
Clinical presentation
• Fibroadenomas are usually single lumps, but there may be several lumps affecting both
breasts
10 Grube BJ, GiulianoAE. Benign breast diseases. In: Bereck JS, editor. Novak’s Gynecology. 13thed. Philadelphia, USA: Lippincott Williams and
wilkins;2002:543-565.
11 Gobbi D, Dall’Igna P, Alaggio R, Nitti D, Cecchetto G. Giant fibroadenoma of the breast in adolescents: report of 2 cases. J Pediatr Surg. 2009
Feb; 44(2):39-41.
12 Sklair-Levy M, Sella T, Alweiss T, Craciun I, Libson E, Mally B. Incidence and management of complex fibroadenomas. AJR Am J Roentgenol.
2008 Jan; 190 (1): 214-8.
13 Dupont WD, Page DL, Parl FF, Vnencak-Jones CL, Plummer WD Jr, Rados MS, et al. Long-term risk of breast cancer in women with
fibroadenoma. N Engl J Med. 1994;331(1):10–15.
14 Cerrato F, Labow BI. Diagnosis and management of fibroadenomas in the adolescent breast. Semin Plast Surg. 2013 Feb;27(1):23-5.
• Lumps may be easily moveable under the skin; firm, painless, and rubbery
• They have smooth, well-defined borders
• They may grow in size, especially during pregnancy
• Fibroadenomas often get smaller after menopause.
Fibroadenomas are usually diagnosed by:
Breast Self-Examination (BSE)15
It helps in early detection of breast disease. Most breast diseases are first detected by the patient
rather than the physician. The woman should inspect her breasts while standing or sitting before a
mirror, looking for any asymmetry, skin dimpling, or nipple retraction. She should carefully palpate
her breasts with the fingers of the opposite hand. Finally, she should lie down and again palpate each
quadrant of the breast, as well as the axilla. Pre-menopausal women should examine their breasts
monthly during the week after menses.
Best time to do:
• Once a month
• 10 days after your menstrual period
• If not menstruating, pick a certain day-such as the first day of each month
• If on hormones then do it 1-2 days after withdrawal bleeding.
Step 1:
Begin by looking at your breasts in the mirror with your
shoulders straight and your arms on your hips.
Here’s what you should look for:
If breasts are of usual size, shape, and color
If breasts are evenly shaped without visible distortion or
swelling
If you see any of the following changes, bring them to your
doctor’s attention:
Dimpling, puckering, or bulging of the skin
A nipple that has changed position or an inverted
nipple (pushed inward instead of sticking out)
Redness, soreness, rash, or swelling
Step 2:
Raise your arms and look for the same changes. Look for
any dimpling of skin or in-drawing nipple
15 Breastcancer.org. Breast Self-Exam [internet]; 2019[cited 2020 Mar 11]. Available at: https://www.breastcancer.org/symptoms/testing/
types/self_exam
Standard Treatment Guidelines In Homoeopathy 81
BREAST FIBROADENOMA
Step 3:
While you’re at the mirror, look for any signs of fluid coming
out of one or both nipples (this could be a watery, milky, or
yellow fluid or blood)
Step 4:
Next, feel your breasts while lying down, using your right hand
to feel your left breast and then your left hand to feel your
right breast. Use a firm, smooth touch with the first few finger
pads of your hand, keeping the fingers flat and together. Use a
circular motion, about the size of a quarter
Cover the entire breast from top to bottom, side to side — from
your collar bone to the top of your abdomen, and from your
armpit to your cleavage. Follow a pattern to be sure that you
cover the whole breast. You can begin at the nipple, moving in
larger and larger circles until you reach the outer edge of the
breast. You can also move your fingers up and down vertically,
in rows, as if you were mowing a lawn. This up-and-down
approach seems to work best for most women. Be sure to
feel all the tissues from the front to the back of your breasts:
for the skin and tissues just beneath, use light pressure; use
medium pressure for tissues in the middle of your breasts; use
firm pressure for the deep tissues in the back. When you’ve
reached the deep tissues, you should be able to feel down to
your ribcage
Step 5:
Finally, feel your breasts while you are standing or sitting.
Many women find that the easiest way to feel their breasts is
when their skin is wet and slippery, so they like to do this step
in the shower. Cover your entire breast, using the same hand
movements described in Step 4
INVESTIGATIONS8,10,16,17,18
Type Findings
Ultrasonography USG is the primary imaging modality for younger women and pregnant or lactating
(USG) patients. USG is better than mammography at identifying tumours within dense
breast tissues. Fibroadenomas appear as circumscribed, homogeneous, oval,
hypoechoic masses that may have gentle lobulations; a smooth, thin, echogenic
capsule; variable acoustic enhancement; and homogeneity
Mammography Indications for mammography screening:
1) Age of 40 years for the general population
2) Age of 25–30 years for BRCA1 carriers and untested relatives of BRCA
carriers
3) Symptomatic women of 35 years or above with lump or other clinical
evidence of breast Ca
4) Search for occult primary tumour in patients presenting with metastasis.
5) Screening mammography should not be used in pregnant women. While
breastfeeding, the tissues in breasts may appear dense on a mammogram,
making it hard to interpret
Findings
Well-circumscribed discrete, oval mass, hypodense or isodense of breast glandular
tissue to a mass with macro-lobulation or partially obscured margins. Involuting
fibroadenomas in older, typically post-menopausal patients may contain
calcification, often producing the classic, coarse popcorn calcification appearance
Magnetic resonance Breast MRI is useful when multiple breast biopsies would not be feasible for multiple
imaging (MRI) lesions. They typically appear as circumscribed, oval masses and are isointense or
hypointense
Aspiration cytology- Cytology is essential to exclude malignancy, if conservative treatment is considered
Core biopsy, FNAC and is helpful in identifying a benign lesion. Firm nodular mass with smear showing
benign tight clusters and sheets of breast duct epithelial cells with uniform small
round nuclei. No inflammatory component seen and no cytological evidence of
atypia or malignancy
COMPLICATIONS12
Fibroadenoma shows an elevated risk of breast carcinoma compared with women of similar age in
the general population; malignant transformation from fibroadenoma to cancer is rare. The risk of
developing breast carcinoma has been found to be higher in patients with complex fibroadenoma
than in those with non-complex fibroadenomas.
DIFFERENTIAL DIAGNOSIS8,19
• Juvenile fibroadenoma
• Low grade phyllodes tumour
16 Jackson VP, Rothschild PA, Kreipke DL, Mail JT, Holden RW. The spectrum of sonographic findings of fibroadenoma of the breast. Invest
Radiol. 40 -34:)1(21; 1986.
17 Wilkinson S, Anderson TJ, Rifkind E, Chetty U, Forrest AP. Fibroadenoma of the breast: a follow-up of conservative management. Br J
Surg. 1-390:)4(76; 1989.
18 Agrawal A, Tripathi P, Sahu A, Daftary J. Breast screening revisited. J Family Med Prim Care.2014;3(4):340-4.
19 Stanford Medicine, Surgical pathology criteria. Fibroadenoma of breast[internet];2005[cited 2006 May 27]. Available from:http://
surgpathcriteria.stanford.edu/breast/fibroadenoma/differentialdiagnosis.html
Patients who present with breast masses should undergo a medical evaluation, which includes:
RED FLAGS13
• Any lesion being followed which significantly increases in size or develops atypical features on
imaging (should undergo repeat biopsy are to be considered for excision biopsy)
• Mass becoming non-mobile, hard, enlarging, tender, fixed to overlying skin or nipple areolar
complex
• Associated with axillary or supra-clavicular lymphadenopathy
• Complex fibroadenomas (Fibroadenomas with cysts, sclerosing adenosis, epithelial calcifications,
or papillary apocrine changes are classified as complex)
• Fibroadenomas with proliferative disease, or a family history of breast cancer
• Juvenile fibroadenomas that are typically growing rapidly
• Giant fibroadenomas
MANAGEMENT 6,20,21,22,23,24,25
The natural history of fibroadenoma varies from individual to individual. In some patients
fibroadenomas may remain dormant without any change in size. In most of the patients, there may be
slowly waxing and waning of sizes without associated pain or skin changes. Usually, fibroadenomas
show spontaneous regression in 10%–40% of population during observation.
20 Sainsbury JR, Nicholson S, Needham GK, Wadehra V, Farndon JR. Natural history of the benign breast lump. Br J Surg. 2-1080:)11(75; 1988.
21 Dixon JM, Dobie V, Lamb J, Walsh JS, Chetty U. Assessment of the acceptability of conservative management of fibroadenoma of the breast. Br J
Surg. 1996;83(2):264-5.
22 Carty NJ, Carter C, Rubin C, Ravichandran D, Royle GT, Taylor I. Management of fibroadenoma of the breast. Ann R Coll Surg Engl. 1995 Mar;
77(2):127-30.
23 Grady I, Gorsuch H, Wilburn-Bailey S Long-term outcome of benign fibroadenomas treated by ultrasound-guided percutaneous excision.
Breast J. 2008;14(3):275-8.
24 Kaufman CS, Littrup PJ, Freman-Gibb LA, Francescatti D, Stocks LH, Smith JS, et al. Office-based cryoablation of breast fibroadenomas:
12-month followup. J Am Coll Surg. 2004; 198(6):914-23.
25 Sperber F, Blank A, Metser U, Flusser G, Klausner JM, Lev-Chelouche D. Diagnosis and treatment of breast fibroadenomas by ultrasound-
guided vacuum- assisted biopsy. Arch Surg. 2003; 138(7):796-800.
Usually, other than regular observation, there is no role for allopathic medication under conservative
treatment. Surgical excision is considered for patients. However, distortion of shape and texture
of the breast, scarring of breast tissue and recurrence of disease after surgery, lumpectomy make
breasts look smaller are the prime cause due to which patients opt for alternative treatments. If
conservative management of fibroadenoma is to be advocated, physical examination, sonography,
and Fine Needle Aspiration Cytology should all be performed, and their results should be compatible
with fibroadenoma. The flow of management of the patient as per the age group, i.e., above or below
35 years is given in Figure 1 and 2.
HOMOEOPATHIC MANAGEMENT26,27,28,29,30
Individualized homoeopathy has a role in the treatment of fibroadenoma. By proper case taking
and eliciting the totality of symptoms after considering the symptomatology, including mind and
disposition, physical generals, predisposition, relevant past/personal/family history of the patient,
miasmatic background etc., the correct similimum can be determined the regression/ resolution of
fibroadenoma as well as prevention of its recurrence.
The most probable dominant miasm behind fibroadenoma of breast is sycotic miasm. A few research
studies9,24,25 have shown positive role of homoeopathic treatment in regression of fibroadenoma.
It is suggested that the constitutional homoeopathic treatment may be given as the first‑line of
treatment in cases as per the above algorithms. In cases with paucity of characteristic expressions,
we can think of specific medicines.
In Synthesis repertory medicines for breast fibroadenoma are found in chapter CHEST, 55 medicines
are given under rubric ‘tumor-mammae’.31 The frequently verified characteristic features of some
organospecific remedies are: Scrophularia nodosa: Very useful in the dissipation of breast tumors,
nodosities in the breasts. Chimaphila umbellata: This remedy cures both atrophy or hypertrophy.
Plethoric young women with large breasts. Painful tumors of mammae, with sharp pain through it,
not ulcerated with undue secretion of milk. Calcarea fluorica: Remedy for hard, stony glands; hard
knots in the female breast. Lapis albus: Affections of glands, glands have a certain elasticity and
pliability about them. Persistent burning and stinging pain in mammae with hardening of glands
but not like stony hardness of Calc fl. and Cistus. Iodium: Dwindling of mammary glands, nodosities
on the skin of mammae. Hydrocotyle asiatica: Cellular proliferation in any part, hypertrophy and
induration of connective tissues. Asterias rubens: Nodes and induration of mammary gland, dull
aching, neuralgic pain in this region. Tumors with lancinating pain-mostly left side. Axillary gland
swollen, hard and knotted. Flabby lymphatic constitution with red face. The commonly prescribed
constitutional homoeopathic medicines along with their indications are as follows:
26 Parveen S. Individualized homoeopathic treatment of breast fibroadenoma: A case report. Indian J Research in Homoeopathy 2018;12(1):
46-52.
27 Kumar S, Mohan CK, Sugathan NV, CV C. A case of left mammary fibroadenoma successfully cured by homoeopathic therapy. Research on
Chronic Diseases. 2019; 2(2): 49-54.
28 Boericke W. Pocket Manual of Homoeopathic Materia Medica and Repertory.3rd revised & Augmented ed. New Delhi: B. Jain Publishers (P)
Ltd.;2007.
29 Gupta G, Naveen G, Madhu C. Fibroadenoma of breast: A sonomammographical supported clinical study on the effect of homoeopathic drugs.
Homoeopathy for all.2003;4(48):37-45.
30 Shukla P, Misra P, Misra RK, Jain RK, Shukla R, Manchanda R. Homoeopathic Management of Breast Fibroadenoma —An Open Label, Single
Arm, Observational Trial. Homoeopathic Links. 2020;33(2):90–98.
31 Schroyens F. Synthesis Repertory ver. 9.1. New Delhi: B Jain Publishers Pvt. Ltd.; 2002.
Pulsatilla nigricans Hot patient; marked changeability • Nodes in the breast are accompanied by
of symptoms; aversion to fatty foods, menstrual irregularity, amenorrhoea
warm foods and drinks; dislikes butter; • Worse from heat
thirstless with great dryness of mouth;
• Better from cold applications
tongue coated yellow or white; worse
towards evening and in warm room,
better in open air, by slow, gentle
motion and cold applications; desire
for company, mild, gentle, affectionate,
yielding, weeping disposition
Bryonia alba Hot patient; dry; excessively thirsty, • Stony heaviness of breasts
tendency to constipation, all symptoms • Stitching pains aggravates on motion
worse from least motion; and relief
• Pain in breasts at menstrual period.
from absolute rest; tongue dry, parched,
cracked, thickly white coated; nervous, • Breasts hot and painful hard
desire to be in one position quietly, not • Abscess of mammae
to be carried; desires open air • Worse from warmth, touch
• Better by lying on painful side,
pressure, rest
Silicea terra Extremely chilly patient; all symptoms • Hard lumps in breast
worse by cold except stomach • Nipples very sore; ulcerate easily;
complaints, which are ameliorated; drawn in
Profuse, offensive discharges; sweat
• Fistulous ulcers of breast. Discharge of
profuse especially on feet; easy
blood from the vagina, every time the
suppuration; affinity for glands; large
child is nursed
head and distended abdomen; weak
ankles, slow in learning to walk; • Worse during menses, lying down, left
constipation; obstinate, head strong, side, cold
cries when spoken kindly to, nervous, • Better from warmth
apprehensive, oversensitive, irritable
and fearful
Phytolacca Fatty; soreness; restlessness; prostration; • Has powerful effect on fibrous and
decandra right-sided affections; profound osseous tissues
prostration; tendency to glandular • Mammae hard and very sensitive
indurations and inflammation; worse at
• Tumours of the breasts with enlarged
night, better in dry warm weather
axillary glands
• Breast is hard and painful and of a
purple hue
• Irritable breasts, before and during
menses
• Worse on motion, right side
• Better from warmth, rest
Conium maculatum Chilly patient, perspires during sleep; • Stitching pain in nipples. Wants to
desires salt; glandular affection; press the breasts hard with the hand
emotionally closed, flat or hard people, • Breasts enlarged and painful before
mental dullness or confusion; debility of and during menses
mind and body; generally aggravation • Stony hard glandular induration after
from suppression of sexual desire; the bruises and injuries to breasts
complaints of conium originates slowly • Worse on lying down, before and
and progressively during menses, bodily or mental
exertion
• Better by motion, pressure
Calcarea carbonica Chilly patient; takes cold easily; fat, fair, • Breast’s tender and swollen before
flabby, distended abdomen; pale, weak, menses
easily tired; head sweats profusely while • Tendency for lymphatic glandular
sleeping; sour smelling discharges; enlargement
longing for fresh air; desire for eggs • Hot swelling breasts
and indigestible things, sweets aversion • Deficient lactation, with distended
to meat and milk; fearful, shy, timid, breasts in lymphatic women
slow and sluggish; feels better when • Worse from exertion, mental or
constipated physical
• Better by lying on painful side
Sepia officinalis Chilly patient; tall, thin built with yellow • Induration of the breast
saddle across upper part of cheeks • Shooting in mammae, excoriation
and nose, big belly; dry flabby skin. of nipple, nipple cracked across the
Predisposed to take cold at change of crown
weather. Desire for sour food which • Worse on left side
aggravates. Cheerful, active when well • Better by exercise, pressure, warmth
but indifferent and quarrelsome when of bed, hot applications, drawing
sick self-absorbed, sad, weeping and limbs up
indolent
Women younger than 35 yrs of age Women older than 35 yrs of age
Fibroadenoma
red flags
• Any lesion significantly Persistence Resolution
increases in size or
develops atypical
features
• Mass becoming non- Increased size in regular Static or reduction
mobile, hard, enlarged, follow ups/ new lumps / in size with no
tender, fixed to associated pain or nipple complications
overlying skin or nipple discharge
areolar complex
• Associated with axillary
or supraclavicular
lymphadenopathy
• Complex Consider for standard
fibroadenomas care/integrative Homoeopathic treatment
approach and routine follow-ups
• Fibroadenomas with
proliferative disease, or till complete regression
family history of breast
cancer.
• Juvenile fibroadenomas
growing rapidly
• Giant fibroadenomas Stop treatment
Fibroadenomas that are not removed /surgically removed/ resolved under homoeopathic treatment should
be followed up with ultrasound studies every 6 months for 2 years. If they are not increasing in size /
reappearing over this time, further follow-up or treatment is unnecessary
CHIKUNGUNYA
CASE DEFINITION1,2
Chikungunya fever (CHIKF) is an arthropod-borne viral disease transmitted by Aedes aegypti and
Aedes albopictus mosquitoes. CHIKF is characterized by fever, headache, rash, and debilitating
polyarthralgia, with an incubation period of 3–7 days.
The case definition of Chikungunya fever as proposed by the World Health Organization (WHO) is
described below:
Suspected case
A suspected case involves a patient presenting with acute onset of fever, usually with chills/rigors,
that lasts for 3-5 days with pain in multiple joints/swelling of extremities that may continue for
weeks to months.
Probable case
A probable case is characterized by conditions that support a suspected case (see above) along with
one of the following conditions:
Confirmed case
Chikungunya fever is confirmed if the patient meets one or more of the following findings irrespective
of the clinical presentation:
INCIDENCE/PREVALENCE
1 Suhrbier A, Jaffar-Bandjee MC, Gasque P. Arthritogenic alphaviruses—an overview. Nat Rev Rheumatol. 2012; 8(7):420–9.
2 World Health Organization. Guidelines for Prevention and Control of Chikungunya Fever [Internet]. 2009 [Cited 2020March 04]. Available
from: https://apps.who.int/iris/bitstream/handle/10665/205166/B4289.pdf?sequence=1&isAllowed=y
AETIOLOGY3
Chikungunya virus is an arthropod-borne virus (arbovirus) that belongs to the family Togaviridae
and to the genus Alphavirus. The virus is related to the Semliki Forest antigenic complex, a group of
viruses that may be associated with joint symptoms in humans.
• In the sylvatic cycle, Aedes mosquitoes transmit the disease to primates, rodents, and birds
• Humans get infected when traveling in forested areas
• In the urban cycle, the mosquitoes transmit the disease among humans.
RISK FACTORS4,5,6
Once a person has been infected, he or she is likely to be protected from future infections.
3 Higgs S, Vanlandingham D. Chikungunya virus and its mosquito vectors. Vector Borne Zoonotic Dis. 2015;15(4):231-40.
4 Dhimal M, Gautam I, Joshi HD, O’Hara RB, Ahrens, Kuch U. Risk Factors for the Presence of Chikungunya and Dengue Vectors (Aedes aegypti
and Aedes albopictus), Their Altitudinal Distribution and Climatic Determinants of Their Abundance in Central Nepal. PLoS Negl Trop Dis.
2015; 9(3): e0003545.
5 Moizéis RNC, Fernandes TAAM, Guedes PMM, Pereira HWB, Lanza DCF, Azevedo JWV, et al. Chikungunya fever: a threat to global public health.
Pathog Glob Health. 2018; 112(4): 182–194.
6 Guidelines for containment of chikungunya and dengue epidemic outbreaks [Internet]. [Cited 2020 March 4]. Available from: https://nvbdcp.
gov.in/WriteReadData/l892s/GUIDELINES_FOR_CONTAINMENT_OF_DENGUE_FEVER%20_AND_CHIKUNGUNYA_EPIDEMICS.pdf
PATHOGENESIS7
Figure 1:Skin is a major portal of entry (1), and resident structural cells encounter the virus delivered
by the mosquito (Aedes species), together with immunoregulatory proteins from mosquito’s saliva.
The local immune response (2 and 3) is critical but does not prevent the virus from spreading to
other organs, such as joints (4), skeletal muscles, heart, kidney, liver, and, more rarely, the brain.
Chikungunya virus (CHIKV) mainly targets fibroblasts (4). Macrophages can also be infected and may
represent a potential reservoir in tissue sanctuaries. Hence, CHIKV may be protected from the robust
innate and adaptive immune responses. Ballooned macrophages in synovial tissues are classically
associated with viral persistence and, allegedly, contribute to a chronic inflammatory response.
These events may drive arthralgia (inflammatory nociception) for months to years and can evolve
to arthritis in some patients (6). Rhabdomyolysis, hepatitis, myocarditis, and neuropathology’s may
be observed in the more severe cases in adults, while neonates infected at birth may be at risk of
encephalitis andand death.Courtesy: Gasque P et al. Chikungunya Pathogenesis: From the Clinics to
the Bench.
7 Gasque P, Bandjee MCJ, Reyes MM, Viasus D. Chikungunya Pathogenesis: From the Clinics to the Bench. The Journal of Infectious Diseases.
2016; 214(5): 446–48.
DIAGNOSIS
Clinical presentation2,8,9
• After an incubation period of 4-7 days, there is a sudden onset of flu-like symptoms which may
include headache, nausea, vomiting, muscle pain, joint swelling, or skin rashes. The rash are
mostly of the pruriginous maculopapular type on the chest but bullous or other forms can also
be seen and at times may desquamate.
• Symptoms usually last for 3–7 days after being bitten by an infected mosquito.
• Severe joint and body pain: This type of pain is frequent and keeps increasing as the days pass.
Sometimes, the joints also get swelled up. The joint pain may persist for months.
• Appearance of rashes usually on limbs and trunks and also known to cause rashes on entire
body which keep coming back frequently.
• Redness of eye: This typically means that one is likely to suffer from conjunctivitis and face
difficulty in looking towards the light.
• Bleeding: The person suffering from this disease is at a high risk of suffering from bleeding.
Haemorrhage may occur at times.
• Residual arthritis, with morning stiffness, swelling and pain on movement may persist for weeks
or months after recovery.
• Although rare, the infection can result in meningoencephalitis (swelling of the brain), especially
in newborns and those with pre-existing medical conditions.
• Chikungunya disease does not often result in death, but the symptoms can be severe and
disabling.
INVESTIGATIONS10
Three main laboratory tests are used for diagnosing Chikungunya fevers:
• Virus isolation (viral RNA detection)
• Serological tests (IgM capture ELISA most sensitive)
• Molecular technique of polymerase chain reaction (PCR)
• Specimen is usually blood or serum but in neurological cases with meningo-encephalitic feature
CSF may also be sent as specimen
Investigations Findings
Blood test
o CBC o Decreased lymphocyte
o ESR o Increased
o Liver enzymes o Mild elevation
Serology IgM Chik (positive)
PCR CHIK RT-PCR (positive)
8 Simon F, Javelle E. Chikungunya Virus Infections. The New England Journal of Medicine. 2015;373(1):93-5.
9 National Vector Borne Disease Control Programme. Chikungunya fever—national guidelines[internet].[Cited 2020 march 04]. Available from:
https://nvbdcp.gov.in/index4.php?lang=1&level=0&linkid=489&lid=3766
10 Chang K, Hsieh HC, Tsai JJ, Lin WR, Lu PL, Chen YH. Diagnosis and management of imported Chikungunya fever in Taiwan: a case report.
Kaohsiung J Med Sci. 2010; 26(5):256–60.
Fever with or without arthralgia is a very common manifestation of several other diseases. Some of
the diseases which can be considered in differential diagnosis are:
Dengue Fever Severe low back pain with purpuras or active bleeding might suggest dengue fever.
Confirmatory laboratory diagnosis is possible.
Clinical signs and Chikungunya fever Dengue fever
symptoms
1 Onset of fever of Acute Gradual
40°C
2 Duration of fever 1-2 days 5-7 days
3 Maculopapular ra Frequent Rare
sh
4 Presence of Rare Common
shock and severe
haemorrhage
5 Arthralgia Frequent and lasting over a month Infrequent and short
duration
Laboratory
parameters
1 Leukopenia Frequent Infrequent
2 Thrombocytopenia Infrequent Frequent
Malaria Patient can present with high fevers and may also complain of joint pains. Periodicity
of fever and alteration of consciousness / seizures should prompt diagnosis for malaria
Leptospirosis Severe myalgia localized to calf muscles with conjunctival congestion/ or subconjunctival
haemorrhage with or without oliguria or jaundice in a person with history of skin contact
to contaminated water would suggest Leptospirosis
Rheumatic fever More common in the children and presents with fleeting (migratory) polyarthritis
predominantly affecting the large joints. Modified Jones criteria should be the basis for
diagnosis. Raised ASO titre and a history of recurrent sore throat are other points to be
noted
Reactive In general, any arthritis that follows a febrile gastrointestinal or genitourinary infection
arthritis (triggering microbes) is considered a reactive acute inflammatory arthritis if it lasts less
than six months. The hallmark feature is enthesitis where collagenous structures such
as tendons and ligaments inserting into bones are involved. Oral mucosal ulcers are seen
Serum sickness Polyarthritis may be associated with a serum sickness type/reaction caused by vaccine,
illness medication or other viral infections
Rickettsial Can present with fever, rash and joint pains. Confirmed by serology
disease
COMPLICATIONS11,12,13,14
• Persistent severe arthralgias- lead to long-term disability and loss of workdays
• Neurological- Encephalopathy and encephalitis, Myelopathy and myelitis, Acute disseminated
encephalomyelitis, Guillain-Barré syndrome
• Ocular complications- retinal detachment, intra-retinal haemorrhage, and branch retinal artery
occlusion
• The burden on the economy in terms of loss of productivity and income is estimated to be
significant
RED FLAGS16
• Persistent severe arthralgias
• Neurological- Encephalopathy and encephalitis
• Myelopathy and myelitis, Acute disseminated encephalomyelitis
• Ocular complications- retinal detachment, intra-retinal haemorrhage, and branch retinal artery
occlusion
• Guillain-Barré syndrome.
PREVENTION15
• Minimizing vector population: Elimination of breeding places of Aedes mosquitoes by removal
of water containing receptacles, space spraying of insecticide, residual application on surfaces
where the mosquito is likely to alight and use of larvicide.
• Minimize the vector-patient contact: Use mosquito repellents on skin and clothing, when
indoors, staying in well-screened areas. Use bed nets if sleeping in areas that are not screened
or air-conditioned. When working outdoors during day times, wearing long-sleeved shirts and
long pants to avoid mosquito bite.
• Reporting to the nearest public health authority: for the prevention of epidemic.
MANAGEMENT
General management16
• Treatment of Chikungunya fever is symptomatic and supportive. Adequate fluid intake must be
ensured.
• Chikungunya fever is usually self-limiting and resolves with time. Symptomatic treatment is
recommended after excluding other more dangerous diseases.
11 Das T, Jaffar-Bandjee MC, Hoarau JJ, Krejbich Trotot P, Denizot M, Lee-Pat-Yuen G. Chikungunya fever: CNS infection and pathologies of a re-
emerging arbovirus. Prog Neurobiol. 2010;91(2):121-9.
12 Fourie ED, Morrison JG. Rheumatoid arthritic syndrome after chikungunya fever. S Afr Med J. 1979;56(4):130-2.
13 Krishnamoorthy K, Harichandra kumar KT, Kumari AK, Das LK. Burden of chikungunya in India: estimates of disability adjusted life years
(DALY) lost in 2006 epidemic. J Vector Borne Dis. 2009; 46(1):26-35.
14 Mehta R, GerardinP, de Brito CAA, Soares CN, Ferreira MLB, Solomon T. The neurological complications of chikungunya virus: A systematic
review. Rev Med Virol. 2018; 28(3): p. 1978.
15 World health organization. Outbreak and spread of chikungunya. WHO Weekly epidemiological record. 2007; 82(47):409-416.
16 Central Council for Research in Homoeopathy . Epidemics- IMR project[Internet]. [Cited 2020 March 4]. Available from: https://www.
ccrhindia.nic.in/admnis/admin/showimg.aspx?ID=6475
• There is no vaccine currently available for Chikungunya. Supportive care with rest is indicated
during the acute joint symptoms.
• Movement and mild exercise tend to improve stiffness and morning arthralgia, but heavy
exercise should be avoided as these may exacerbate rheumatic symptoms.
Homoeopathic management
Given the limited number of options for providing any relief in conventional medicine, homeopathy
has emerged as an extremely effective mode of treatment for chikungunya infections. Homeopathy
provides effective and safe pain relief in these patients while keeping the range of fever low. It is
important to remember that in this condition the severity of muscle, joint pains and headache can
be severe. Initially indicated acute homoeopathic remedies may give relief which may be followed
by constitutional remedy in order to get rid of post-fever arthralgia.
In synthesis repertory17, rubric ‘Pain-fever’ in chapter EXTREMITIES can be found. The homoeopathic
literature mentions several medicines like Belladonna, Eupatorium perfoliatum, Bryonia alba,
Phosphorus etc. as effective medicines for the disease. Studies18,19,20 conducted on this disease have
been able to validate a few of the medicines which are usually prescribed for chikungunya.
The frequently verified characteristic feature of one of the specific remedy for Chikungunya is:
Polyporus pinicola: Intermittent, remittent fever, pain in back, ankles and legs.
The list of frequently prescribed polychrest medicines with their indications are given below:21,22
17 Schroyens F. Synthesis Repertory ver. 9.1. New Delhi: B Jain Publishers Pvt. Ltd.; 2002.
18 Nair KRJ, Gopinadhan S, Roja V, Nayak D, Oberai P, Singh H, et al. Homoeopathic Genus Epidemicus ‘Bryonia alba’ as a prophylactic during an
outbreak of Chikungunya in India: A cluster -randomised, double -blind, placebo- controlled trial. Indian J Res Homoeopathy.2014;8(3):160-5.
19 Wadhwani G.G. Homeopathic drug therapy Homeopathy in Chikungunya Fever and Post-Chikungunya Chronic Arthritis: an observational
study. Homeopathy. 2013; 102(3):193-198.
20 Rejikumar R, Dinesh RS. A Study on the Prophylactic Efficacy of Homoeopathic Preventive Medicine Against Chikungunya Fever[internet].
[Cited 2020 March 6]. Available at: https://www.similima.com/pdf/efficacy-chikunguna-kerala.pdf.
21 Boericke W. Boericke’s New Manual of Homoeopathic Materia Medica with Repertory: Third Revised & Augmented Edition based on Ninth
Edition. New Delhi: B. Jain Publishers(P) Ltd.; 2007.
22 Allen HC. Keynotes and Characteristics with Comparisons of some of the Leading Remedies of the Materia Medica. New Delhi: B. Jain
Publishers(P) Ltd.;2007.
Belladonna Congestion is the keynote of the medicine; • A high feverish state, with
dryness, bright redness, burning heat, great comparative absence of toxemia.
pain and fullness or swelling, rush of blood Cold limbs and hot head
to head or face, throbbing of carotids; great • High fever with burning heat. No
sensitiveness especially of special senses; thirst with fever. Joints swollen, red,
pains that come and go suddenly; excited shining with red streaks radiating
mental state, delirium, restless sleep, • Shooting, or tearing, aching pains in
convulsive movements; dryness of mouth the limbs
and throat with aversion to water; dilated • Bruise-like pains in the joints and
pupils bones
• Rheumatic pains (in the joints) flying
from one place to another
• The pains are aggravated, chiefly at
night, and in the afternoon towards
three or four o’clock, touch, jar, lying
down
• Better in semi-erect posture
• Fever Exposure in
Resident Resident in an area of
• Incapacitating arthralgia in an area Yes an area of No
Yes chikungunya
• Not explained by other where the chikungunya transmission
conditions vector is transmission? in past 2
present? weeks
Yes No
Possible case
NEGATIVE
CASE
Test for CHIK
NEGATIVE CASE
CONFIRMED CASE
Homoeopathic treatment of
case according to symptoms
• Give homoeopathic
medicines as per
indications + adequate
red flags
rest
• Persistent severe • Continue follow-up
arthralgias
• Neurological- Encephalopathy and
encephalitis
• Myelopathy and myelitis, Acute
disseminated encephalomyelitis
Improvement
• Guillain-Barré syndrome
• Ocular complications- retinal
detachment, Intra-retinal No Yes
haemorrhage, and branch retinal
artery occlusion.
Consider for integrative Continue with
treatment homoeopathic treatment
CHRONIC SUPPURATIVE
OTITIS MEDIA
CASE DEFINITION1,2
Chronic suppurative otitis media (CSOM) is persistent inflammation of the middle ear or mastoid
cavity, characterised by recurrent or persistent ear discharge (otorrhoea) over 2–6 weeks through a
perforation of the tympanic membrane.
INCIDENCE/PREVALENCE3,4 5
• CSOM is a highly prevalent disease especially in childhood and leads to significant morbidity
worldwide.
• The world’s wide prevalence of CSOM is 65-330 million people mainly in developing countries;39-
200 million (60%) people suffer from clinically significant hearing impairment. The prevalence
of CSOM in India is 7.8%.
AETIOLOGY4,6
• In CSOM, the bacteria may be aerobic, e.g., Psedomonas aeruginosa, Escherichia coli, S. aureus,
Streptococcus pyogenes, Proteus mirabilis, Klebsilla species or anaerobic, e.g, Bacteroids, pepto
streptococcus, Proprioni bacterium). The bacteria are infrequently found in the skin of the
external auditory canal, but may proliferate in the presence of trauma, inflammation, laceration
or high humidity.
• Ascending infections via the eustachian tube like infection from tonsils, adenoids, and infected
sinus may be the cause of CSOM.
RISK FACTORS7
• Genetic disposition
• Allergy to ingestions (milk, eggs, fish, etc.), atopy
• Upper respiratory tract infections (with pharyngeal reflux, with snoring)
• History of acute otitis media or recurrent otitis media
• Second-hand smoke
• Medication during pregnancy, inadequate antibiotic treatment
• Indoor cooking
• Low economic status, overcrowding
• Overweight
1 Kumari MS, Madhavi J, Krishna NB, Meghanadh KR, Jyothy A. Prevalence and associated risk factors of otitis media and its subtypes in South
Indian population Egyptian Journal of Ear, Nose, Throat and Allied Sciences. 2016; 17(2): 57-62.
2 Jose A. Chronic suppurative otitis media. BMJ clinical evidence. 2007.
3 Bhutta MF, Thornton RB, Kirkham LS, Kerschner JE, Cheeseman MT. Understanding the aetiology and resolution of chronic otitis media from
animal and human studies. Disease Models & Mechanisms. 2017;10(11):1289-1300.
4 World Health Organization. Chronic suppurative otitis media: burden of illness and management options. [Internet] Geneva: World Health
Organization. 2004 [cited 2021 March 19]. Available from: https://apps.who.int/iris/handle/10665/4294.
5 Mittal R, Lisi CV, Gerring R, Mittal J, Mathee K, Narasimhan G et al. Current concepts in the pathogenesis and treatment of chronic suppurative
otitis media. J Med Microbiol. 2015;64(10):1103–1116.
6 Dhingra PL. Diseases of Ear, Nose, Throat &Head and Neck Surgery. 6th. India: Elsevier publishers; 2014.
7 Zhang Y, Xu M, Zhang J, Zeng L, Wang Y, et al. Risk Factors for Chronic and Recurrent Otitis Media–A Meta-Analysis.PLoS ONE. 2014; 9(1): p. 86397.
Standard Treatment Guidelines In Homoeopathy 107
CHRONIC SUPPURATIVE OTITIS MEDIA
3. Central perforation.
4. Middle ear mucosa. It is seen when the perforation is large. Normally, it is pale pink and moist.
When inflamed, it looks red, oedematous and swollen. Occasionally, a polyp may be seen.
2. Atticoantral type: It is also called unsafe or dangerous type. It involves posterosuperior part of
the cleft and is associated with an attic or a marginal perforation. This disease is often associated
with a bone eroding process such as cholesteatoma, granulations or osteitis. Risk complications
are high in this variety.
A. Pathogenesis
1. Cholesteatoma.
2. Osteitis and granulation tissue- Osteitis involves outer attic wall and posterior-superior margin
of the tympanic ring. A small of granulation tissue surrounds the area of ostetitis and may even
fill the attic, antrum, posterior tympanum and mastoid. A fleshy red polypus may be seen filling
the meatus.
3. Ossicular necrosis- It is common in this type of disease. Destruction may be limited to the long
process of incus or may also involve stapes super structure, handle of malleus, or the entire
ossicular chain. Therefore, hearing is loss is always greater than in tubotympanic type.
4. Cholesterol granuloma- They are composed of granulation tissue with foreign body giant cells
surrounding the cholesterol crystals.
1. Ear discharge- Usually scanty, but always foul smelling due to bone destruction.
2. Hearing loss- Cholestatoma, having destroyed the ossicles leads to hearing loss mostly conductive
but sensorium element may also be added.
3. Bleeding- It may occur from granulation or the polyp, when cleaning the ear.
4. Perforation- It is either attic or posteriosuperior marginal type.
5. Retraction pocket- An invagination of tympanic membrane is seen in the attic or posterior-
superior are of pars tensa.
6. Cholestatoma- Pearly- white flakes of cholestatoma can be sucked from the retraction pockets.
DIAGNOSIS 4,9
• Signs and symptoms (like hearing loss, aural discharge, headache, itching in auditory canal)
• Complete otoscopic examination (the integrity of tympanic membrane and the attic for exclusion
of cholesteatoma)
9 Bareeqa SB, Ahmed SI. Comment to Empirical Therapy for Chronic Suppurative Otitis Media. Clin Med Insights Ear Nose Throat. 2018;
11:1179550618810226.
INVESTIGATIONS 5
Investigation Findings
Otoscopy • It may reveal presence of cholesteatoma, its site and extent,
evidence of bone destruction, granuloma, condition of ossicles, and
pocket of discharges
Tuning fork tests and Audiogram • These are essential for assessment and to confirm the degree and
type of hearing loss
X -ray of Mastoid (Lateral View) • It indicates extent of bone destruction and degree of mastoid
pneumatization
CT Scan of temporal bone • It reveals bone erosion from cholesteatoma, ossicular erosion,
involvement of petrous apex and sub-periosteal abscess
MRI • If intratemporal or intracranial complications are suspected, it can
reveal dural inflammation, sigmoid sinus thrombosis, labyrinthitis
and extradural and intracranial abscess
DIFFERENTIAL DIAGNOSIS10
COMPLICATIONS4,15,16
B. Intracranial
1. Extradural abscess
2. Subdural abscess
3. Meningitis
4. Brain abscess
5. Lateral sinus thrombophlebitis
6. Otitic hydrocephalus
RED FLAGS5
PROGNOSIS 5,18
It depends upon:
MANAGEMENT
General management17
• Keep the ear dry. Avoid water entering the ear while bathing, swimming, and performing such
activities with water.
• Aural toilet, keeping the chronically draining ear clean and dry as much as possible. Techniques
include in-office mopping with cotton swabs, suctioning to remove discharge and debris, and
placing an ear wick to stent open an oedematous canal.
• Detect hearing loss and manage accordingly.
• Managing weight and other co-morbidities which may maintain the condition for long period.
• Counseling to the parents: information regarding risk factors needs to be told to the parents;
teaching the correct method of breast feeding and burping after meals.
• Treating upper respiratory tract infections in time.
Homoeopathic management
Homoeopathic management targets the patient suffering from CSOM, and medicine is selected based
upon the presenting complaints, relevant past/family/personal/ treatment history, physical general
& mental symptoms of the individual patient. Homeopathy for CSOM patients has been shown to be
effective.18,19
In synthesis repertory20, 88 medicines for CSOM are found in chapter EAR under the rubric
‘Inflammation-media’. The frequently verified characteristic features of some organospecific remedies
are: Dulcamara: Middle ear catarrh (otitis media, otorrhea). Worse from cold in general, damp
weather, night. Kali sulphuricum: Eustachian deafness. Discharge of yellow matter (otorrhea).
Thiosinaminum: Catarrhal deafness with cicatricial thickening. Subacute suppurative otitis media,
formation of fibrous bands impending free movement of the ossicles.
Aurum Worse in cold air, getting cold. Many • Caries of ossicula and mastoid
metallicum complaints only in winter. Syphilitic affection • Obstinate and foetid otorrhea after
of bones profound melancholy. Oversensitive scarlatina
to pain, smell, taste, hearing, touch • External meatus bathed in pus
• Pain worse at night and drive to
despair
17 Standard treatment guidelines, Armed Forces Medical College. Pune: Excell Prints;2007: 107-112.
18 Hasan, N., Ahmed, S., Zaman, S., Ferdousi, S., Khaleque, M. A., & Bari, L. CSOM Causing Tympanic Membrane Perforation and Impaired Hearing:
Improved by Homeopathy. Journal of Advances in Medicine and Medical Research. 2017;21(2):1-9.
19 Panchajani R. A clinical study on miasmatic approach in management of patients with chronic suppurative otitis media[dissertation].
Kulasekharam, Tamil nadu: Sarada Krishna Homoeopathic Medical College;2019[cited 2021 March 19]. Available from: http://repository-
tnmgrmu.ac.in/10745/
20 Schroyens F. Synthesis Repertory ver. 9.1. New Delhi: B Jain Publishers Pvt. Ltd.; 2002
21 Boericke W. Boericke’s New Manual of Homeoeopathic Materia Medica with Repertory: third revised & Augmented Edition Based on Ninth
edition. New Delhi: B. Jain publishers(P)Ltd.: 2007.
22 Allen HC. Allen’s Keynotes- Rearranged and classified with leading remedies of the Materia Medica and bowel nosodes. 10th Reprint edition.
New Delhi: B. Jain Publishers (P) Ltd;2006.
Calcarea Chilly patient; takes cold easily; fat, fair, • Scrofulous inflammation with
Carbonica flabby, distended abdomen; pale, weak, mucopurulent otorrhea and enlarged
easily tired; head sweats profusely while glands
sleeping; sour smelling discharges; longing • Perversion of hearing, hardness of
for fresh air; desire for eggs and indigestible hearing
things, sweets aversion to meat and milk; • Polyps which bleed easily
fearful, shy, timid, slow and sluggish; feels • Worse from cold in every form, water,
better when constipated washing, moist air, wet weather
• Better in dry climate and weather,
lying on painful side
Causticum Chilly patient. Burning, rawness and soreness • Ringing, roaring, pulsating noises with
are characteristic. Intensely sympathetic. deafness
Paralysis of single part. Aversion to sweets. • Words and steps re-echo
Better damp, wet, weather • Chronic otitis media
• Accumulation of ear wax.
• Worse in dry, cold winds, in clear
fine weather, cold air, from motion of
carriage
• Better from warmth
Capsicum Persons with light hair, blue eyes, nervous • Burning, stinging in ears, swelling and
annuum but stout and plethoric habit. Home sickness. pain behind the ears-inflammation of
Burning and smarting sensation, as from mastoid
cayenne pepper. General uncleanliness of • Tenderness over the petrous bone
the body. Marked thirst; but drinking causes extremely sore and tender to touch
shuddering. Worse open air, uncovering (caries)
• Otorrhea and mastoid disease before
suppuration
• Better from heat
Hepar sulph Extremely chilly patient; hypersensitive (to • Discharges of fetid pus from the ears
cold, pain), Faints easily; scrawny; Glandular (Otorrhea)
constitution; Profuse sweat; Irritable; • Whizzing and throbbing in ears, with
difficult to please, slow to act hardness of hearing (Tinnitus)
• Mastoiditis. Sensitive to touch and
draft
• Worse from dry cold winds, cool air,
lying on painful side
• Better in damp weather, from
wrapping head up, from warmth
Kali Chilly patient. Susceptible to cold, fat, • Swollen, with tearing pains
bichromicum chubby, short necked, shifting pains (otitis),sharp stitches in the left ear
Aversion and intolerance to meat, desires • Thick, yellow, stringy, fetid discharges
sour things. Worse from cold, open air, hot (otorrhea)
weather; Better from motion, pressure • Perforation of the septum
• Polypus
• Better from heat
Lycopodium Hot patient, intellectually keen but physically • Thick yellow offensive discharges
clavatum weak; upper part of body emaciated, lower • Otorrhraea and deafness with or
part semi- dropsical; complexion pale, without tinnitus; after scarlatina
dirty, sallow with deep furrows; looks old; • Humming and roaring with hardness
recurrent respiratory and gastro-intestinal of hearing
affections; tendency for flatulent dyspepsia; • Every noise causes a peculiar echo in
worse from 4- 8 pm; right-sided complaints the ear
or symptoms shifts from right to left; • Worse from heat or warm room, hot
desire for warm foods and drinks, sweet; air
dominating, cranky, lack of self- confidence, • Better by motion, after midnight, on
precocious getting cold, from being uncovered
Mercurius Sensitive to changes of temperature Profuse • Thick, yellow discharges, fetid, bloody
solubilis offensive perspiration Tongue flabby with (otorrhea)
imprint of teeth. Increased salivation • Otalgia, sticking pains
Increased thirst for large quantity of water. • Worse from warmth of bed, at night
Worse at night, in wet damp weather
Psorinum Extremely chilly patient, wants to cover even • Raw, red, oozing scabs around the ears
in hottest summer weather; pale, delicate, • Sore pain behind the ears
sickly; scanty perspiration; offensive • Chronic otorrhea
discharges; wakes up at night feeling • Very fetid pus from ears, brownish,
hungry; anxious, fearful, child is good all day offensive
while restless and troublesome at night • Worse from changes of weather, in hot
sunshine, from cold.
• Better from heat, warm clothing, even
in summer
Pulsatilla Hot patient; marked changeability of • Sensation as if something was being
nigricans symptoms; aversion to fatty foods, warm forced outward
foods and drinks, dislikes butter; thirstless • Hearing difficult, as if the ear were
with great dryness of mouth; tongue coated stuffed. Diminished acuteness of
yellow or whitish; worse towards evening hearing
and in warm room, better in open air, by slow, • Otorrhea. Thick, bland discharge;
gentle motion and cold applications; desire offensive odor. Catarrhal Otitis
for company, mild, gentle, affectionate, • Otalgia, worse at night.
yielding, weeping disposition • Worse from heat, lying on left or on
painless side
Silicea terra Extremely chilly patient; all symptoms worse • Fetid discharge (otorrhea)
by cold except stomach complaints, which are • Caries in the mastoid
ameliorated Profuse, offensive discharges; • Loud-pistol-like retort
sweats profusely especially on feet Easy • Sensitive to noise
suppuration; glandular affinity; large head • Roaring in ears (tinnitus)
and distended abdomen; weak ankles, slow • Worse in morning, from washing,
in learning to walk; constipation. Obstinate, during menses, uncovering, lying
head strong, cries when spoken kindly down, damp, lying on, left side
to, nervous, apprehensive, Oversensitive, • Better from warmth, wrapping up head,
irritable and fearful summer, in wet or humid weather
Sulphur Hot patient, kicks off the cloth at night; dirty, • Whizzing in ears (tinnitus)
filthy, does not want to be washed; lean, thin, • Bad effects from the suppression of
stoop-shouldered; child who walks and sit otorrhea
stooping; red orifices; desires sweets, sugar, • Deafness preceded by exceedingly
meat; when the best selected remedy fails to sensitive hearing
improve • Catarrhal deafness
• Worse at rest, warmth in bed, washing,
bathing, in morning, night, periodically
• Better in dry, warm weather, lying on
right side
Thuja Chilly patient; with illusions & fixed ideas. • Chronic Otitis; discharge purulent
occidentalis Unhealthy skin with tendency for warty (otorrhea)
growths; oily/ greasy sweat, face and stool; • Creaking when swallowing
perspiration on uncovered parts. Complaints • Polypi
worse from cold, warm air and damp humid • Worse at night, from heat of bed,
atmosphere and chronic complaints better vaccination.
during a cold • Better on left side
Clinical presentations
• Recurrent persistent ear discharges
(otorrhea) over 2-6 weeks
• Bleeding from the ear
• Thickened granular middle ear mucosa
• Hearing impaired
RED FLAGS
Improvement
• Persistent headache
• Vertigo
• Facial weakness
Yes No
• A listless child refusing to
take feeds and easily going
to sleep
• Fever, nausea and vomiting
indicate intracranial
infection
• Irritability and neck
Follow up for 6 weeks Consider for integrative
rigidity suspects
care
meningitis
• Diploia
• Mastoiditis (if there is
postauricular swelling or
tenderness)
CASE DEFINITION1
Diabetic foot ulcer (DFU) is defined as a foot affected by ulceration that is associated with neuropathy
and /or peripheral arterial disease of the lower limb in a patient with diabetes mellitus(DM).
INCIDENCE/PREVALENCE2,3,4
• Global prevalence of diabetic foot is 6.3%. It is usually more prevalent in males than in females,
and more prevalent in type 2 diabetics than in type 1 diabetics.
• Diabetic foot is found to be more prevalent in diabetic patients who are old, have a low body mass
index, long duration of diabetes mellitus, and have more hypertension, diabetic retinopathy, and
smoking history.
ETIOPATHOGENESIS5,6,7
Diabetic neuropathy is the common factor in almost 90% of diabetic foot ulcers. Nerve damage in
diabetes mellitus affects the motor, sensory, and autonomic fibers. Motor neuropathy causes muscle
weakness, atrophy, and paresis. Sensory neuropathy leads to loss of the protective sensation of pain,
pressure, and heat. Autonomic dysfunction causes vasodilation and decreased sweating, resulting in
loss of skin integrity, providing a site vulnerable to microbial infection. Even minor injuries, especially
when complicated by infection, increase the demand for blood in the foot, and an inadequate blood
supply may result in foot ulceration, potentially leading to limb amputation. The majority of foot
ulcers are of mixed etiology (neuroischemic), particularly in older patients.
RISK FACTORS8,9
The following factors increase the risk of DFU or amputation in the patients:
• Previous amputation
• Previous history of DFU
• Peripheral neuropathy
• Foot deformity
• Diabetic nephropathy specially end stage renal disease
1 Alexiadou K, Doupis J. Management of Diabetic Foot Ulcers. Diabetes Ther. 2012; 3(1): 4.
2 Zhang P, Lu J, Jing Y, Tang S, Zhu D, Bi Y. Global epidemiology of diabetic foot ulceration: a systematic review and meta-analysis. Journal
Annals of Medicine. 2017;49(2):106-116.
3 Tesfaye S, Stevens LK, Stephenson JM, Fuller JH, Plater M, Ionescu-Tirgoviste C, et al. Prevalence of diabetic peripheral neuropathy and its
relation to glycaemic control and potential risk factors: the EURODIAB IDDM Complications Study. Diabetologia. 1996;39(11):1377–1384.
4 Kumar S, Ashe HA, Parnell LN, Fernando DJ, Tsigos C, Young RJ, et al. The prevalence of foot ulceration and its correlates in type 2 diabetic
patients: a population-based study. Diabet Med. 1994;11(5):480–484.
5 Bowering CK. Diabetic foot ulcers. Pathophysiology, assessment, and therapy. Can Fam Physician. 2001; 47:1007–1016.
6 Prompers L, Huijberts M, Apelqvist J, Jude E, Piaggesi A, Bakker K, et al. High prevalence of ischaemia, infection and serious comorbidity in
patients with diabetic foot disease in Europe. Baseline results from the Eurodiale study. Diabetologia. 2007; 50:18–25.
7 Boulton AJ. The diabetic foot: grand overview, epidiomology and pathogenesis. Diabetes Metab Res Rev. 2008;24(1): 3-6.
8 Ahmad W, Khan IA, Ghaffar S, Al-Swailmi FK, Khan I. Risk factors for diabetic foot ulcer. J Ayub Med Coll Abbottabad.2013;25(1-2):16-8.
9 Iraj B, Khorvash F, Ebneshahidi A, Askari G.Prevention of diabetic foot ulcer.Int J Prev Med. 2013;4(3):373-6.
CLASSIFICATION
However, the International Working Group on the Diabetic Foot (IWGDF) recommended guidelines
and classifications in 2019 which are widely accepted. These are Wagner- Meggit, University of
Texas, SINBAD and WIfI out of which SINBAD is the most practical system of classification to be
implemented.18
DIAGNOSIS
A good history and physical examination can clinch the diagnosis. It includes duration of DM,
neuropathic and peripheral vascular disease symptoms, previous ulcers or amputations and any
other complication of DM like retinopathy or nephropathy.
10 Wagner FW. The dysvascular foot: a system for diagnosis and treatment. Foot and Ankle.1981;2(2): 64-122.
11 Calhoun JH, Jeff Cantrell J, Cobos J, Lacy J, Valdez RR, Hokanson J, et al. Treatment of Diabetic Foot Infections: Wagner Classification, Therapy,
and Outcome. foot and ankle.1988; 9(3):101-106.
12 Lavery LA, Davis KE, Berriman SJ, Braun L, Nichols A, Kim PJ, et al. WHS guidelines update: Diabetic foot ulcer treatment guilelines. Wound
repair and regeneration. 2016; 24(1):112-126.
13 Foster A, Edmonds M. Simple staging system: a tool for diagnosis and management. Diabet Foot.2000; 3(2):56-62.
14 Game F. Classification of diabetic foot ulcers. Diabetes Metab Res Rev. 2015;32 (Suppl 1):186-194.
15 Schaper NC. Diabetic foot ulcer classification system for research purposes: a progress report on criteria for including patients in research
studies. Diabetes Metabolism Research and Reviews. 2004;20(S1):590-595.
16 Tentolouris N. Introduction. In: Katsilambros N, Eleftherios D, Konstantinos M, Tentolouris N, Panagiotis T, editors. Atlas of the diabetic foot.
2nd ed. Singapore: John Wiley & Sons ltd.; 2010:1-10.
17 Jain AKC. “A new classification of diabetic foot complication: a simple and effective teaching tool”. Journal of Clinical and Diagnostic Research.
2014;8(12): NC07-NC09.
18 Schaper NC, Netten JJV, Apelqvist J, Bus SA, Hinchliffe RJ, Lipsky BA, IWGDF Editorial Board. Practical guidelines on the prevention and
management of diabetic foot disease (IWGDF 2019 update). Diab Metab Res Rev. 2020; 36(S1): e3266
Physical examination
• The foot ulcer needs to be examined carefully in terms of location, size, shape, depth, base
and margins; also in terms of perception of superficial pain (pinprick), temperature sensation
(using a two-metal rod), light sensation (using the edge of a cotton-wool twist), pressure (using
the Semmes–Weinstein 5.07 monofilament) and the vibration perception using a tuning fork
and/or a biothesiometer. The examination of position sense (proprioception) and deep tendon
reflexes (Achilles tendon, patellar) is also essential.19
• The foot should be carefully inspected for abnormalities like dry skin, fissures, deformities,
and callosities. An increase in temperature might suggest inflammation (redness, warmth,
tenderness, purulent secretions and fever). 20
• The location, size, shape, depth, base and margins of the ulcer should be examined clinically.
Diagnosing a soft tissue infection in patient with diabetes is sometimes difficult, as the signs of
inflammation of the overlying ulcer may be absent.21
• Palpation of foot pulses is crucial in the diabetic foot. The assessment of the femoral and popliteal
pulses is equally important, because without sufficient inflow into the leg, neuro-ischaemic
ulceration remains a high risk. If either the dorsalis pedis pulse or the posterior tibial pulse
can be felt, then significant ischemia of the foot is unlikely. Checking both feet for increased
temperature is also important. Warm or hot areas may indicate infection, a fracture or acute
Charcot foot.17
• Simple wound measurement: This is a crude measurement. Surface wound area is calculated by
multiplying the maximum perpendicular length by the maximum width of the wound bed and
is typically recorded in cm.2
• Wound planimetry: This measurement can be carried out using a mechanical planimeter or by
using an appropriate software package and a digital image.
• Stereo photogrammetry and light techniques: The advantages of digital imaging are that it
facilitates unique calibration at each wound measurement and subjective wound tracing is
eliminated.
19 Makrilakis K. Diabetic neuropathy. In: Katsilambros N, Eleftherios D, Konstantinos M, Nicholas T, Panagiotis T, editors. Atlas of the diabetic
foot. 2nd ed. Singapore: John Wiley & Sons ltd. 2010: 11-20.
20 Armstrong DG, Holtz-Neiderer K, Wendel C, Mohler MJ, Kimbriel HR, Lavery LA. Skin temperature monitoring reduces the risk for diabetic
foot ulceration in high-risk patients. Am J Med 2007;120(12): 1042-1046.
21 Tudhope L. The Diabetic foot recognition and principles of management. CME. 2009;27(7):312-16.
22 Flanagan M. Wound Measurement: can it help us to monitor progression to healing?. Journal of Wound Care. 2003;12(5):189-194.
23 Lagan KM, Dusoir AE, McDonagh SM, Baxter GD. Wound Measurement: The comparative reliability of direct versus photographic tracings
analysed by planimetry versus digitising techniques. Archives of Physical Medicine and Rehabilitation. 2000; 81(8):1110-1116.
INVESTIGATIONS24,25,26
DIFFERENTIAL DIAGNOSIS27
24 Lobmann R, Kayser R, Kasten G, Kasten U, Kluge K, Neumann W, et al. Effects of preventative footwear on foot pressure as determined by
pedobarography in diabetic patients: a prospective study. Diabet Med. 2001;18(4): 314-319.
25 Mayfield JA, Sugarman JR. The use of the Semmes-Weinstein monofilament and other threshold tests for preventing foot ulceration and
amputation in persons with diabetes. J Fam Pract. 2000;49(11): 17-29.
26 Rogers LC, Frykberg RG, Armstrong DG, Boulton AJM, Edmonds M, Van GH, et al. The Charcot Foot in Diabetes. Diabetes Care. 2011; 34(9):
2123–2129.
27 Lautenschlager S, Eichmann A. Differential diagnosis of leg ulcers. In: Hafner J, Ramelet A-A, Schmeller W, Brunner UV, editors. Management of
leg ulcers. Current Problems in Dermatology, vol. 28. Basel, Switzerland: S. Karger AG;1999:257-270.
28 Nayak C, Singh V, Singh K, Singh H, Gupta J, Ali MS, et al. A prospective observational study to ascertain the role of homeopathic therapy in the
management of diabetic foot ulcer. Indian Journal of Research in Homoeopathy. 2012;6(1,2):22-31.
29 Wukich DK, Raspovic KM. Assessing Health-Related Quality of Life in Patients with Diabetic Foot Disease: Why Is It Important and How Can
We Improve?2017 Roger E. Pecoraro Award Lecture. Diabetes Care. 2018;41(3):391-397.
30 Jain AK. A new classification of diabetic foot complications: a simple and effective teaching tool. The Journal of diabetic foot complications.2012;4(1):1-5.
COMPLICATIONS31
• Wet gangrene
• Abscess
• Tinea pedis
• Osteomyelitis
• Cellulitis
• Necrotizing fasciitis
PREVENTION9
Diabetes mellitus is a chronic metabolic disease, which affects the vascular system extensively
throughout the body. The metabolic complications of DM should be treated concomitantly with
no bias in treating one metabolic complication over others. The metabolic diseases secondary to
DM should be controlled and the target values should be kept below the recommended standard.
As a result, the preventive measures should be taken in order to control the neuropathy and
Peripheral artery disease, which are the main causes of DFU. The preventive measures and
management of diabetic complications consist of the following:
• Lifestyle modifications
• Blood pressure control
• Lipid management
• Glycemic control
• Smoking cessation
• Annual comprehensive foot examination
Nail and skin care
• Diabetic patients should examine their feet daily. The maceration especially between the toes
is usually caused by fungal infection and should be observed carefully. It is recommended to
use a mirror in order to better observe the plantar surface of the foot. In case, if the diabetic
patient’s vision is compromised due to retinopathy or the patient is unable to perform the
daily examination of own feet, another individual who is fully trained should do the task for
the patient.
• The feet should be washed and dry at least once a day. It is important to dry spaces between
the toes very carefully.
• The temperature of the water used for rinsing the foot should be less than 37 centigrade. It
is recommended to use the elbow or forearm in order to estimate the temperature of water.
This method helps to prevent accidental burning of the extremities due to characteristic
glove stocking neuropathy in diabetic patients.
• The diabetic patients, especially the ones with sensory neuropathy, should not use the
heating pads over their bodies. It is also recommended to warn the patients not to place
their feet close to the heaters during winter.
31 Jain ACK. Type 1 diabetic foot complications. The Journal of Diabetic Foot Complications. 2016;8(1):17-22.
• All the patients especially those with diabetic neuropathy or high risk diabetic foot should
use footwear both indoors and outdoors. It is recommended to wear special shoes with
adequate size when the patient is walking indoor on the carpet. The use of the shoes without
stockings in diabetic patients should be discouraged. In patients with neuropathy, it is also
recommended to use the footwears with enclosed frontal part in order to prevent the minor
trauma to the fore foot.
• It is recommended to observe and physically examine inside the patient’s shoes on a daily
basis. This recommendation is given to detect any external objects inside the shoes and to
look for pressure effect on different surfaces of the patient’s feet. The lateral engorgement of
the shoes is an indication of pressure exerted by the first and fifth metatarsals.The swelling
observed in the frontal part of the shoes is caused by the pressure of distal phalanges of the
first digit.
• Diabetic patients, due to autonomic neuropathy, present with increased perspiration in the
upper body and decreased perspiration in lower extremity. As a result, the dryness of the
plantar surfaces of the feet and heels is common. The minor trauma combined with the
dry skin creates cracks which facilitate the entrance of microorganisms into the skin and
consequently foot infection is inevitable. It is recommended to apply lubricants containing
urea or salicylates which can penetrate the dry and hyperkeratosis skin. However, the use
of lubricants in the inter-digital spaces is discouraged.
• In diabetic patients, it is recommended to change and put on clean socks daily.
• The patients should be discouraged wearing tight socks and the seams should be towards
outside.It is not advisable to wear stockings up to the knees.
• Especially in female diabetics, any kind of manipulation of the nails is not recommended.
The nails should not be cut in a rounded fashion.
• The patient should not use any kind of chemical substances or commercial pads or plasters
in order to treat the calluses of the feet.
RED FLAGS32
MANAGEMENT
General management12,18,33
Standard care for DFU is provided by ensuring glycemic control, adequate perfusion, local
wound care, regular debridement, off-loading of the foot, control of infection and management
32 NHS Devon CCG. Diabetes Footcare Guidelines [Internet].2015[cited 2020 March 7]. Available from: https://northeast.
devonformularyguidance.nhs.uk/referral-guidance/northern-locality/endocrinology/diabetes-footcare-pathway
33 Lipsky BA, Berendt AR. Hyperbaric Oxygen Therapy for Diabetic Foot Wounds. Diabetes Care. 2010; 33(5): 1143–1145.
of comorbidities. All the diabetic patients should undergo comprehensive foot examination once a
year. The goal of this examination is to determine the risk factors that may result in foot ulcer and
consequently amputation of the affected organ.
Foot care
i) Shake and wipe shoes from inside before they are worn
ii) Shoes (with closed toes)to be worn at all times, indoors and out to avoid injury
iii) Socks to be changed every day
iv) Shoes to be designed and fitted by a footwear specialist
Non-pharmacological treatment
Hyperbaric Oxygen (HBO) has been found to be a useful adjunctive therapy for DFUs and is associated
with decrease in amputation rates.
Homoeopathic management
Diabetic foot ulcer is the result of multiple factors preceding over a period. Homoeopathic remedy
selection should be based on totality of symptoms including characteristic particulars related to
ulcer.
Research studies have shown that patients with diabetic foot ulcer and some cases of gangrene
have improved under homoeopathic treatment.34,35,36,28 Synthesis repertory37 contain more than 50
medicines under rubric “Ulcer-foot” and the Ulcer rubric in skin section contain number of sub-
rubrics which characterizes the ulcer.
The frequently verified characteristic features of some organospecific remedies are: Anthracinum:
Ulceration, sloughing, and intolerable burning. When Arsenic or best selected remedy fails to relieve
the burning pain of ulcer. Graphites: Ulcers discharging a glutinous fluid, thin and sticky. Tarentula
cubensis: Senile ulcers. Pain and inflammation predominate. Burning and stinging pain with
purplish hue, prostration. Intermittent septic chills. Mezereum: Ulcer itch and burn, surrounded
by vesicles and shining, fiery red areola. Ulcers with thick, yellowish white scabs, under which thick
yellow pus collects. Calendula officinalis mother tincture can be used for regular dressing of the
ulcer for maintaining hygiene and to prevent any superadded infections.
34 Ali MS, P Hima Bindu. A Case of Diabetic Foot Gangrene. Indian J Res Homoeopathy. 2007; 1(1):42-51.
35 Ali M S, P Hima Bindu. A Case of Diabetic Foot Ulcer: Homoeopathic Treatment could avoid Amputation. The Homoeopathic Heritage. 2009;
34(8):35-38.
36 Mahesh S, Mallappa M, Vithoulkas G. Five case studies of gangrene, preventing amputation through Homoeopathic therapy. Indian J Res
Homoeopathy;2015.9(2):114-22.
37 Schroyens F. Synthesis Repertory Ver. 9.1. New Delhi : B Jain Publishers Pvt. Ltd; 2002
The list of frequently prescribed polycrest medicines with their indications are given below:38,39,40
Medicines General Indications Characteristic particulars
Arsenicum Chilly patient; rapid disproportionate • Skin dry, ulcers hard on the edges
album prostration; burning pains better by heat • Stinging, burning with proud flesh, turning
(except headache); cadaveric odour of black, flat, pus thin, ichorous suppuration,fetid
discharges and body; anxiety; anguish, fear of smell,bleeding, putridity and bluish-green
death and restlessness colour of the ulcers
• Want of secretion in the ulcers. Ulcers in a
form of wart.
• Swelling of the foot with burning, hard, shining
with burning vesicles of blue-blackish colour
on the instep.
• Corrosive and ulcerous vesicles on the soles
of the feet and on the toes. Fatigue in legs and
feet
• Worse in wet weather, from cold, seashore,
right-side
Calcarea Chilly patient; takes cold easily; fat, fair, • Flaccidity of the skin. Skin excoriated in
carbonica flabby, distended abdomen; pale weak, easily several places, unhealthy, every injury tends to
tired; head sweats profusely while sleeping; ulceration, even small wounds suppurate and
sour smelling discharges; longing for fresh do not heal
air; desire for eggs and indigestible things, • Ulcers deep fistulous, carious. Ulcers with too
sweets; aversion to meat and milk; fearful, little pus
shy, timid, slow and sluggish; feels better • Cramps in calves of legs, soles of feet and toes
when constipated chiefly on extending the legs
• Burning in soles of feet. Coldness and numbness
of feet especially at night in bed
• Worse from ascending, cold in every form,
water, washing, moist air, wet weather, standing
• Better in dry climate and weather, lying on
painful side
Carbo Chilly patient; distintegration and imperfect • Painless ulcers of the fingers and toes. Fetid
vegetabilis oxidation is the keynote of the remedy; ulcers with burning pains and discharge of
patient may be almost life less, but the corrosive and bloody pus
head is hot; coldness, breath cool, pulse • Torpor and insensibility of legs and feet.
imperceptible, oppressed and quickened Aneurism in hamstring muscles with tensive
respiration, and must have air, must be pain and pulsation. Cramps in legs and soles of
fanned hard very closely; Persons who have feet especially at night. Perspiration of the feet
never fully recovered from the effects of some • Redness and swelling of the toes with shooting
previous illness; aversion to darkness; Fear of pain as if they had been frozen.
ghosts; Sudden loss of memory • Senile gangrene which begins in toes and
extends upwards. Affected parts are bluish
• Worse in open air,warm damp weather
• Better from cold
38 Boericke W. Boericke’s New Manual of Homoeopathic Materia Medica with Repertory: Third Revised & Augmented Edition based on Ninth
Edition. New Delhi: B. Jain Publishers (P) Ltd.;2007.
39 Allen HC. Keynotes and Characteristics with Comparisons of some of the Leading Remedies of the Materia Medica. New Delhi: B. Jain
Publishers(P) ltd.;2007.
40 Clarke JH. A Dictionary of Practical Materia Medica.1st Reprint edition. New Delhi: B. Jain Publishers(P) ltd.;2005.
Kali Chilly patient; susceptible to cold, fat, chubby, • Ulcer dry, oval, have an overhanging edges,
bichromicum short necked, shifting pains; aversion and a bright red inflammed areola, hard base,
intolerance to meat; desires sour things; movable on subjacent tissues, dark spot in
worse from cold, open air, hot weather, better the center, after healing the cicatrix remain
from heat depressed
• Ulcers corrode and become deeper without
spreading in circumference
• Punched out deep ulcers with regular edges.
Ulcers especially painful in cold weather.
Ulcers on previously inflammed feet
• Worsen from undressing
Lachesis mutus Hot patient; thin and emaciated; hemorrhagic • Skin bluish or bluish-black or purplish around
diathesis; great sensitiveness to touch; hot the ulcers. Hot perspiration
flushes and perspiration; Desires oysters, • Ulcers surrounded by pimples, vesicles and
alcohol, farinaceous food, all complaints other small ulcers
worse after sleep; loquacious, jumps from one • Ulcers with great sensitiveness to touch,
idea to another; jealous, suspicious, indolent uneven bottom, ichorous, offensive discharge
when touched
• Gangrenous ulcers, wounds with inflammatory
fever, weak, quick and intermittent pulse
• Worse on left side, in the spring, warm bath,
pressure or constriction
• Better from appearance of discharges, warm
applications
Lycopodium Hot patient, intellectually keen but physically • Skin ulcerates, tendency to become chapped
clavatum weak; upper part of body emaciated, lower • Mercurial ulcers, bleeding ulcers with shooting
part semi-dropsical; complexion pale, dirty, pains which burn while being dressed
sallow with deep furrows; looks old; recurrent • Fistulous ulcers with callous, red edges,
respiratory and gastro-intestinal affections; reversed and shining. Great dryness of the
tendency for flatulent dyspepsia; worse from skin
4.00-8.00 pm; right sided complaints or • Abscesses beneath skin worse warm
symptoms shifts from right to left; desire for applications
warm foods and drinks, sweets; dominating, • Worse from heat or warm room, hot air, bed
cranky, lack of self-confidence, precocious • Better by motion,on getting cold, from being
uncovered
Mercurius Sensitive to change of temperature; profuse • Skin is always moist and yellow in color.
solubilis offensive perspiration; tongue flabby with General tendency to free perspiration but
imprint of teeth; increased salivation, patient is not relieved thereby
increases thirst for large quantity of water; • Ulcers irregular, spreading, shallow, bleeding,
worse at night, in wet damp weather with burning on edges, hard and swollen on
edges with bloody or corroding pus
• Phagedenic and chancrous ulcers. Wounds
ulcerate easily and become gangrened
• Worse from lying on right side, from
perspiration, warm room and warm bed
Nitric acid Seat of action of the remedy is outlets of the • Complaints from punctured wounds. Wounds
body where the mucous membrane and skin and ulcers with lancinations as by splinters or
meet; sticking pain as from splinter; acts best with burning pains especially when they are
on the dark complexioned and past middle touched, and which bleed easily
life; Pains appear and disappear quickly; • Mercurial and carious ulcers. Ulceration of
Persons who have chronic diseases and take bones and rachitis
cold easily and disposed to diarrhoea; Better • Ulcers with sanious, sanguineous and
from carriage riding corrosive suppuration.
• Limbs become cold and as if frozen in a
moderately old temperature
• Worse from cold climate,hot weather
Phosphorus Tall, fast growing child with tendency to • Burning sensation in legs and feet. Ulcers on
stoop; haemorrhagic tendency; chilly patient; legs with surrounding small pustules. Paralytic
craving for salt, cold foods and drinks; feeling in feet.Numbness of tips of toes.
oversensitive to external impressions; Nervous • Pain as from ulceration in soles when walking.
and affectionate, anxious especially during Shocks in feet day and night before going to
thunderstorm sleep
• Pale skin
• Fistulous ulcers. Large ulcers surrounded by
small ones. Ulcers bleed on appearance of
menses
• Bruised pain in periosteum of tibia and
gangrenous periosteum of tibia
• Worse from touch, change of weather, from
getting wet in hot weather, lying on left or
painful side, ascending stairs
• Better from lying on right side, cold, open air,
washing with cold water, sleep
Pulsatilla Hot patient; Marked changeability of • Pain as from subcutaneous ulceration in legs
nigricans symptoms; aversion to fatty foods, warm and soles of feet. Complaints are worse when
foods and drinks, dislikes butter; thirstlessness hanging the feet down
with great dryness of mouth; tongue coated • Suppurating wounds with thick pus, too
yellow or whitish; worse towards evening and profuse and yellow
in warm room, better in open air, by slow, • Shining redness, hardness and itching round
gentle motion and cold application; desire for ulcers with bleeding, shooting, burning and
company, mild, gentle, affectionate, yielding, gnawing pains
weeping disposition • Deep or fistulous ulcers where there is much
swelling around
• Inflamed or putrid ulcers. Varices in legs and
feet
• Worse from heat warm room, lying on left or
on painless side when allowing feet to hang
down
• Better in open air, motion, cold applications
Sepia Chilly patient; tall, thin built with yellow • Ulcers on instep. Stiffness in heels and joints
saddle across upper part of cheeks and nose, of feet, as from contraction
big belly; dry flabby skin. Predisposed to take • Pricking and burning sensation of feet.
cold at change of weather. Desire for sour Tingling and numbness in soles of feet
food which aggravates. Cheerful, active when • Profuse or suppressed perspiration of feet.
well but indifferent and quarrelsome when Stinging in the heels
sick self-absorbed, sad, weeping and indolent • Tension in tendoachilies. Ulcers on heel arising
from corrosive vesicles. Indolent ulcers on
joints and tips of toes. Deformity of toenails
• Worse from washing, laundry-work,
dampness, left side, after sweat, cold air,
• Better from pressure, warmth of bed, hot
applications, drawing limbs up, cold bathing,
after sleep
Silicea terra Extremely chilly patient; all symptoms worse • Every injury tends to suppurate and ulcerate.
by cold except stomach complaints, which are Small wounds heal with difficulty
ameliorated; profuse, offensive discharges; • Corrosive ulcer on heels with itching.
sweats profusely especially on feet; easy Ulceration of great toe with shooting pain. In
suppuration; glandular affinity; large head growing toenails
and distended abdomen; weak ankles, slow in • Abscess which does not break but burrow
learning to walk; constipation obstinate, head under the skin. Ulcers burning, scabby, indolent,
strong, cries when spoken kindly to, nervous, when circumscribed with redness, very high,
apprehensive, oversensitive, irritable and hard ulcers with proud flesh and corroding pus
fearful • Ulcers smell offensive. Cancerous ulcers,
inflammation, softening and ulceration of bones
• Worse from washing, uncovering, lying down,
damp, lying on, left side
• Better from warmth, wrapping up head,
summer, in wet or humid weather
Sulphur Hot patient, kicks off the clothes at night; • Skin dry, rough, scaly with voluptuous
dirty, filthy, does not want to be washed; itching- feels so good to scratch
lean, thin, stoop shouldered; child who walks • Ulcers with elevated margins, surrounded by
and sit stooping; red orifices; desires sweets, itchy pimples, red or bluish areola, bleeding
sugar, meat; when the best selected remedy readily, and secreting a fetid and sanious or
fails to improve yellow thick pus
• Fistulous ulcers, proud flesh in the ulcers.
Burning sensation in feet, wants to find a cool
place for them, puts them out of bed
• Worse at rest, when standing, warmth in bed,
washing, bathing,periodically
• Better in dry, warm weather, lying on right
side, from drawing up affected limbs
Secale Hot patient, anaemia, coldness, numbness, • Skin shrivelled, mottled, dusky-blue tinge
cornutum petechiae, mortification and gangrene, • Dry gangrene, developing slowly
useful in old people with shrivelled skin-thin, • Varicose ulcers, burning sensation, better by
scrawny old women, excessive appetite and cold
thirst, craves acids, excessive smokers • Skin feels cold to touch yet covering is not
tolerated
• Great aversion to heat
• Worse from heat, warm covering
• Better from cold, uncovering, rubbing,
stretching out limbs
RED FLAGS
• Sepsis
• Critical lower limb
Improvement ischaemia with
necrosis, pain or
ulceration
• Rapidly
Yes No deteriorating
ulceration or
necrosis
DIABETIC NEUROPATHY
CASE DEFINITION1
Diabetic neuropathy (DN) refers to various types of nerve damages associated with diabetes mellitus.
DN encompasses multiple different disorders involving proximal, distal, somatic, and autonomic
nerves. It may be acute and self-limiting or a chronic, indolent condition.
INCIDENCE/PREVALENCE2,3,4
Factors leading to the development of diabetic neuropathy are not understood completely; some of
the most commonly associated factors are as follows:
1 Vinik A, Casellini C, Nevoret ML. Diabetic Neuropathies. [Updated 2018 Feb 5]. In: Feingold KR, Anawalt B, Boyce A, et al., editors. Endotext
[Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000. Available from: https://www.ncbi.nlm.nih.gov/books/NBK279175/
2 Trivedi S, Pandit A, Ganguly G, Das SK. Epidemiology of peripheral neuropathy: An Indian perspective. Ann Indian Acad Neurol. 2017;
20(3):173-84.
3 Bansal V, Kalita J, Misra UK. Diabetic neuropathy. Postgrad Med J. 2006; 82(964): 95–100.
4 Hicks CW, Selvin E. Epidemiology of Peripheral Neuropathy and Lower Extremity Disease in Diabetes. Curr Diab Rep. 2019;19(10):86.
5 Liu X, Xu Y, An M, Zeng Q. The risk factors for diabetic peripheral neuropathy: A meta-analysis. PLoS One. 2019; 14(2): e0212574.
CLASSIFICATION6,7
PATHOGENESIS8
The pathogenesis of diabetic neuropathy is complex and is mainly marked by metabolic and
vascular factors. Causative factors include persistent hyperglycemia, microvascular insufficiency,
oxidative and nitrosative stress, defective neurotrophism, and autoimmune-mediated nerve
destruction. Although nerve fiber loss is accepted as the genesis of insensitivity in Diabetic Peripheral
Neuropathy (DPN), the pathophysiological explanation behind neuropathic pain in diabetes mellitus
is poorly understood.
DIAGNOSIS9
The diagnosis of DPN can only be made after a careful clinical examination.
Patients with type 1 diabetes mellitus for 5 or more years and all patients with type 2 diabetes
mellitus should be assessed annually for DSPN using medical history and simple clinical tests.
Clinical tests
Clinical presentation9
• The most frequent presentation of DPN is the symmetrical sensory pain/impairment that
affects lower limbs earlier than the upper limbs in a classic stocking and gloves’ appearance.
• Other symptoms to suggest DPN include atypical pain, altered sensations, numbness,
sensation of pins and needles, hot or burning sensations. More interestingly, painful
symptoms could happen in diabetic patients with or without neuropathy.
• Neuropathic motor dysfunction symptoms include muscle weakness, poor balance and falls.
• Signs of neuropathy tested at the bedside include vibration sensation and altered
proprioception, which reflect large-fibre function.
6 Tesfaye S, Boulton AJM, Dyck PJ, Freeman R, Horowitz M, Kempler P, et al. Diabetic Neuropathies: Update on Definitions, Diagnostic Criteria,
Estimation of Severity, and Treatments. Diabetes Care. 2010; 33(10): 2285–2293.
7 Assessing diabetic peripheral neuropathy in primary care. Best Practice Journal; 2014:61:37-47.
8 Juster-Switlyk K, Smith AG. Updates in diabetic peripheral. F1000Researc. 2016;5(F1000 Faculty Rev):738.
9 Hamed E, Monem MA. A review of diabetic peripheral neuropathy management given recent guidelines updates. Arch Gen Intern. Med.
2018;2(4):1-5.
• Also, impairment of pain, light touch, and temperature which reflects small fibres-functions,
any of which could present as an early sign of neuropathy.
• Motor signs include wasting and decreased reflexes.
• Motor and sensorimotor neuropathy symptoms and signs are all reported and recognised
as complications of diabetes mellitus.
INVESTIGATIONS10
Investigations are needed for DPN to exclude any other underlying pathology and severity of disease.
Some of the investigations are:
RED FLAGS 16
DIFFERENTIAL DIAGNOSIS17
COMPLICATIONS8,18
Insensitivity or loss of pain leads to foot ulceration and a host of unintentional serious injuries
or infections. Patients who have lost feelings in their hands cannot sense temperature and often
burn themselves while cooking or ironing, and also have difficulty in handling small objects.
Those who have lost sensation in their feet often sustain puncture wounds, friction wounds and
burns that can become infected and/or ulcerated and lead to gangrene, amputation.
PREVENTION19
Early detection and control of diabetes mellitus and coexisting risk factors for neuropathy (e.g.,
smoking, alcohol abuse, hypertension) can prevent, delay, or slow the progression of diabetic
neuropathy.
17 Pop-Busui R, Boulton AJM, Feldman EL, Bril V, Freeman R, Malik RA. Diabetic Neuropathy: A Position Statement by the American Diabetes
Association. Diabetes Care. 2017; 40(1): 136–154.
18 Tesfaye S, Selvarajah D. Advances in the epidemiology, pathogenesis and management of diabetic peripheral neuropathy. Diabetes Metab Res
Rev. 2012;28(1):8-14.
19 Aring AM, Jones DE, Falko JM. Evaluation and prevention of Diabetic Neuropathy. American Family Physician. 2005;71(11):2123-2128.
MANAGEMENT17,18,20
General management
Patients of diabetes mellitus for a long period, may present with neuropathic symptoms such as-
classic stocking and gloves’ appearance, atypical pain, altered sensations, numbness, sensation
of pins and needles, hot or burning sensations etc. They should be advised to maintain their
blood sugar levels, by lifestyle changes such as regular physical activities and diet management.
Some activities of daily life such as walking, normal work, relationship with others, sleep
have been found to be effective in patients with DN.21 Plant-based (vegetarian diet) dietary
interventions, vitamin B12 intake, changes in nutritional habits and food preparations, effective
dietary education etc. typically improve glycemic control and prevent the onset of diabetes
mellitus as well as its complications as DN.22,23
Homoeopathic management
Diabetic neuropathy is a chronic disease and deep acting constitutional homoeopathic medicine
is needed. The similimum selected on the basis of totality of symptoms of patients suffering
from diabetic neuropathy will not only alleviate the symptoms of neuropathy but also control
the blood glucose levels.
The research studies and case reports in diabetic neuropathy have shown beneficial role of
homoeopathic treatment in these cases.15,24,25 Homoeopathic literature gives many remedies for
this disease condition. The main diagnostic symptoms of DPN (Numbness, Insensibility foot;
Formication, Delusions senses of, Prickling, Senses hyperacute, Painlessness of complaints
usually painful) were converted into corresponding rubrics and repertorised using ‘Complete
Repertory’. The following are the medicines enlisted against any of these rubrics (in grade 3) are :
Sulphur, Lycopodium, Rhus toxicodendron, Nux vomica, Phosphoric acid, Phosphorus, Arsenicum
album, Conium maculatum, Cocculus, Opium, Secale cornutum, Rhododendron, Platinum
metallicum, Graphites and Stramonium.
20 Bhadada SK, Sahay RK, Jyotsna VP, Agrawal JK. Diabetic Neuropathy: Current Concepts. Journal, Indian Academy of Clinical
Medicine.2001;2(4):305-318.
21 Yo M, D’Silva L, Martin K, Sharma N, Pasnoor, LeMaster JW, et al. Pilot Study of Exercise Therapy on Painful Diabetic Peripheral Neuropathy.
Pain Med. 2015; 16(8):1482-89.
22 Bunner AE, Wells CL, Gonzales J, Agarwal U, Bayat E, Barnard ND. A dietary intervention for chronic diabetic neuropathy pain: a randomized
controlled pilot study. Nutr Diabetes. 2015;5(5); e158.
23 Sun Y, Lai MS, Lu CJ. Effectiveness of vitamin B12 on diabetic neuropathy: systematic review of clinical controlled trials. Acta Neurol Taiwan.
2005;14(2):48-54.
24 Mehra P, Sharma B, Baig H, Raveendar C, Prasad RVR, Rao MP, et al. Efficacy of homoeopathic treatment for diabetic distal symmetric
polyneuropathy: A multicentric randomised double-blind placebo-controlled clinical trial. Explore (NY). 2020 May 22; S1550-
8307(20)30163-4
25 Pomposelli R, Piasere V, Andreoni C, Costini G, Tonini E, Spalluzzi A, et al. Observational study of homeopathic and conventional therapies in
patients with diabetic polyneuropathy. Homeopathy. 2009 Jan;98(1):17-25.
The list of frequently prescribed medicines with their characteristic indications are given below:26
26 Boericke W. New Manual of Homoeopathic Materia Medica with Repertory. 3rd revised and augmented edition based on 9th edition. New
Delhi; B. Jain Publishers; 2007.
Arsenicum album Chilly patient; rapid disproportionate • Burning all over the body at night;
prostration; burning pains better by burning, prickling, stitching pain in
heat (except headache); cadaveric the extremities
odour of discharges and body; • Numbness of both the feet and soles;
anxiety, anguish, fear for death and aggravates while sitting
restlessness • Worse wet weather, from cold, right
side
Calcarea carbonica Chilly patient; takes cold easily; fat, • Burning in soles.
fair, flabby, distended abdomen; • Cold, damp feet; feel as if damp
pale, weak, easily tired; head stockings were worn
sweats profusely while sleeping; • Sharp sticking, as if parts were
sour smelling discharges; longing wrenched or sprained
for fresh air; desire for eggs • Weakness of extremities
and indigestible things, sweets; • Worse from exertion, ascending,
aversion to meat and milk; fearful, cold in every form, water, washing,
shy, timid, slow and sluggish; feels moist air, wet weather, standing
better when constipated • Better dry climate and weather, lying
on painful side
Nux vomica Chilly patient; thin, prone to • Paresis of arms, with shocks
indigestion; tongue coated yellowish • Legs numb; feels paralyzed; sensation
in the posterior part; oversensitive of sudden loss in power of arms and
to all external impressions; noise, legs, in the morning
odors, light or music nervous • Worse morning, touch, dry weather,
disposition cold
• Better in evening, while at rest, in
damp, wet weather, strong pressure
Conium maculatum Troubles at the change of life, old and • Fingers and toes numb
bachelors; with a type of weakness, • Muscular weakness especially of
languor, local congestions, and lower extremities
sluggishness. Vertigo, when lying • Worse lying down, turning or rising in
down and when turning over in bed. bed
Tumors, piercing pains; worse at
night. Better, while fasting, in the
dark, from letting limbs hang down,
motion and pressure
Plumbum metallicum The blood, alimentary and nervous • Paralysis of single muscle
systems are the special seats of • Stinging and tearing in limbs, also
action. Progressive muscular twitching and tingling, numbness,
atrophy. Mental depression. pain or tremor
Abdomen retracted. Constipation;
stools hard, lumpy, black with
urging and spasm of anus. Worse,
at, night, motion. Better, rubbing,
hard pressure, physical exertion
Nitricum acidum Chilly patient. Offensive • Sensation of band around the head,
discharges especially urine, around the bones.
feces and perspiration. Sensitive • Excessive physical irritability
to noise, pain, touch, jar. Pain • Worse evening and night, cold climate,
sharp, sticking, pricking as from hot weather
splinters, suddenly appearing and • Better while riding in carriage
disappearing
Natrium muriaticum Hot patient; poorly nourished, great • Palms hot and perspiring
emaciation (marked on neck); • Numbness and tingling in fingers and
losing flesh while living well; craving lower extremities. Ankles weak and
for salt; aversion to bread and fatty turn easily
things; constipated; increased thirst; • Great weakness and weariness.
mapped tongue with red insular Oversensitive to all sorts of influences
patches; melancholic, sad, plays • Worse warm room, lying down about
alone, irritable, cross, cries when 10 a m, at seashore, heat
spoken to; awkward, hasty, drops • Better open air, cold bathing, lying on
things from nervous weakness; right side, tight clothing
disposition to weep without cause,
consolation aggravates
Carboneum Sluggishness of mind. Dementia • Peripheral neuritis cramps in limbs
sulphuratum alternating with excitement. Ski, • Lightening like pain with cramps.
anaesthesia, burning, itching, Anaesthesia of arms and hands,
sensitive patients worse cold with unsteady, tottering feet insensible
wasted muscles and skin • Worse bathing, sensitive to warm,
damp, weather
• Better in open air
Clinical presentation
• Clinical history of diabetes mellitus
• Muscular symptoms: muscle weakness, poor balance and falls
• Sensory symptoms: altered proprioception, paraesthesia, impaired
sensation of pain, light touch, and temperature
Confirm diabetic neuropathy with blood sugar levels, evaluation scales and
nerve conduction test if feasible
Start individualized homeopathic treatment along with Start individualized homeopathic treatment along with
lifestyle modification and continue earlier treatment lifestyle modifications
RED FLAGS
• Atypical progression of
neuropathy
• Relative lack of coexistent
retinopathy or neuropathy
• Failure to achieve adequate
control of dysaesthesia
• Secondary problems
Improvement
Yes No
Yes No
Yes Improvement No
GOUT
CASE DEFINITION1,2,3
INCIDENCE/ PREVALENCE4,5,6,7
• The general prevalence of gout is 1–4% in the general population. In western countries, it occurs
in 3–6% men and 1–2% women. Prevalence rises up to 10% in men and 6% in women more than
80 years old.
• In India, approximately 0.12-0.19% population is affected by gout with male preponderance.
Polyarticular gout is more frequent in the elderly and females. Initial presentation is predominantly
monoarticular with the ankle joint being the commonest to be involved. But overall, the first
metatarsophalangeal (MTP) joint is the commonest joint affected with > 90% having this joint
involvement at some point of the disease.
• The reported male to female ratio is approximately 7:1 to 9:1 but in people over the age of 65
this ratio is reduced to 3:1.
• Hyperuricaemia: Most important risk factor for the development of gout (Normal range for
serum urate levels is 2.0-7.0 mg/dl in men and 2.0-6.0 mg/dl in women).
• Genetic factors: Familial clustering is often evident in common primary gout.
• Dietary factors: Dietary factors like intake of meat, seafood, sugar-sweetened soft drinks, and
foods high in fructose.
• Alcohol consumption: Alcohol consumption especially beer and hard liquor increases the risk
of incidence gout.
• Obesity: BMI is significantly associated with risk for gout. Obesity increases serum urate by
eliciting both increased production and decreased renal excretion of urate.
• Acute gouty attack: Classically, it produces an acute mono-arthritis of rapid onset, often
waking patients from sleep, reaching a peak within 24 to 48 hours. The pain is intense,
and patients often cannot wear socks or touch bedsheets during flare-ups with marked
exacerbation of pain even at the simple touch. The affected joints become red, shiny and
tender in a few hours. The most affected joints are big toe also known as podagra (50% of
initial attacks), foot, ankle, mid tarsal, knee, wrist, finger, and elbow. Acute flares also occur
in periarticular structures, including bursae and tendons.
• Inter-critical period: During the period between acute attacks the patient is asymptomatic
even if monosodium Urate (MSU) deposition may continue to increase silently.
• Chronic tophaceous gout: It is characterized by the deposition of solid MSU crystal aggregates
in various locations including joints, bursae, and tendons as tophi. Tophaceous gout may
lead to significant morbidity and, if untreated, can cause prominent joint damage and
marked functional impairment.
The signs and symptoms of gout almost always occur suddenly, and often at night. They include:
• Intense joint pain- Gout usually affects the large joint of your big toe, but it can occur in any
joint. Other commonly affected joints include the ankles, knees, elbows, wrists and fingers. The
pain is likely to be most severe within the first four to 12 hours after it begins.
• Lingering discomfort- After the most severe pain subsides, some joint discomfort may last from
a few days to a few weeks. Later attacks are likely to last longer and affect more joints.
• Inflammation and redness- The affected joint or joints become swollen, tender, warm and red.
• Limited range of motion- As gout progresses, you may not be able to move your joints normally.
INVESTIGATIONS15,16
Identification of urate crystals in fluid from an affected joint is the definitive diagnostic test for the
diagnosis of gout. In practice, this test is applied to only a minority of patients. Guidelines exist for
clinical diagnosis without joint aspiration. Other tests which may be considered are:
Test Comment
Serum urate concentration Level may go down in few cases during an acute attack (serum uric
acid levels ≤6 mg/dL)
Full blood count To exclude myeloproliferative disorders; raised white cell count may
indicate septic arthritis
Renal function Hyperuricaemia can occur in renal failure
Fasting lipids, glucose, and thyroid Hyperlipidaemia, diabetes mellitus, hypothyroidism, and possibly
functions hyperthyroidism are associated with gout
Urinary urate excretion Some authorities advise measuring this if the serum urate
concentration is >0.8 mmol/l because of risk of renal stone formation
Acute gout
Chronic gout
DIFFERENTIAL DIAGNOSIS21
• Septic arthritis
• Trauma
• Active arthritis
• Pseudogout
• Rheumatoid arthritis
• Psoriatic arthritis.
COMPLICATIONS22,23
17 Singh JA, Taylor WJ, Simon LS, Khanna PP, Stamp LK, McQueen FM, et al. Patient-reported outcomes in chronic gout: a report from OMERACT
10. J Rheumatol. 2011;38(7):1452–1457.
18 Janssen CA, Voshaar MAHO, Klooster PMT, Jansen TLTA, Vonkeman HE, Laar MAFJVD. A systematic literature review of patient-reported
outcome measures used in gout: an evaluation of their content and measurement properties. Health and Quality of Life Outcomes.
2019;17(1):63.
19 Janssen CA, Voshaar MAHO, Klooster PMT, Vonkeman HE, Laar MAFJVD. Development and validation of a patient-reported gout attack
intensity score for use in gout clinical studies. Rheumatology. 2019; 58(11):1928-1934.
20 Lee W, Teng GG, Kok JC, Santosa A, Lim AYN, Wee H‐L. Validity and reliability of the Gout Impact Scale in a multi‐ethnic Asian population. Int J
Rheum Dis. 2019; 22(8): 1427– 1434.
21 Engel B, Just J, Bleckwenn M, Weckbecker K. Treatment Options for Gout. Dtsch Arztebl Int. 2017;114(13):215–222.
22 Zhong M. Research on Complications of Gout and Prevention. In: 2nd International Conference on Social Science, Public Health and Education
(SSPHE 2018). Advances in Social Science, Education and Humanities Research.2019;196:255-257. [Cited on 2019 September 4] Available
from: file:///C:/Users/lenovo/AppData/Local/Temp/61.pdf
23 Sam SE, Thomas TE, Abraham E. A review on gout. World Journal of Pharmaceutical Research. 2016;5(6):634-647.
• Formation of tophi
• Joint damage
• Renal diseases like renal stones, chronic kidney disease
• Cardiovascular diseases like coronary heart disease, stroke
• Glucose intolerance and diabetes mellitus
• Retinopathy.
RED FLAGS24
• Uncontrollable pain
• Joint destruction
• Constitutional features such as fever, weight loss and malaise
• Renal failure.
MANAGEMENT19,25
General management
Lifestyle and dietary recommendations for gout patients should consider overall health benefits
and risk, since gout is often associated with the metabolic syndrome and an increased future
risk of cardiovascular disease (CVD) and mortality. Some of the measures are:
• Overweight patients should aim for a normal weight but should not crash-diet or follow protein-
rich diets such as the atkins diet.
• Reduced-fat foods and vegetarian sources of protein should be integrated into the diet.
• Protein-rich foods such as meat and yeast should be avoided.
• Patients known to suffer from gout and kidney stones should be instructed to consume sufficient
fluids (>2 L /day).
• Consumption of alcohol, particularly beer and spirits, should be reduced. Patients should be
encouraged to refrain from consuming alcohol on at least 3 days per week.
• Sugar-sweetened beverages should be avoided. Fructose inhibits uric acid excretion by the
kidneys.
Homoeopathic management 26,27
Research studies indicate that homoeopathic medicines play a considerable role in not only
alleviating the serum uric acid in gout but also a significant role in improving the well-being,
activity and quality of life of patients with gout, without any adverse effects. A few studies have
been done showing the effects of homoeopathic medicines in hyperuricemia.28,29
24 Schroeder K. The 10-minute clinical assessment. [Internet]. 2nd ed. Malden, MA: Wiley-Blackwell, 2016 [cited on 2019 September 4 ].
Available from: https://www.worldcat.org/title/10-minute-clinical-assessment/oclc/966128564/viewport
25 Choi HK. A prescription for lifestyle change in patients with hyperuricemia and gout. Curr Opin Rheumatol. 2010 Mar;22(2):165-72.
26 Boericke W. Pocket manual of homoeopathic materia medica with repertory. New Delhi: B. Jain Publishers; 2007.
27 Allen HC. Allen’s Key Notes and characteristics of the material medica with nosodes. New Delhi: B. Jain Publishers;1986.
28 Saha S, Sarkar P, Chattopadhyay R, Saha S. An open-label prospective observational trial for assessing the effect of homoeopathic medicines in
patients suffering from gout. Indian J Res Homoeopathy.2019;13(4):236-43.
29 Deep A, Kumar A. Homoeopathic management of hyperuricemia in primary gout: A randomised single blind placebo controlled study.
International journal of homoeopathic sciences.2020;4(1):73-77.
Homoeopathic constitutional simillimum improves the quality of life of patients, along with
reducing the intensity of pain, and reducing the disease activity. The homoeopathic consultation
process is a very detailed, elaborate and a personalized process; the entire process of case
taking, case receiving has a definite therapeutic effect on the patient with gout.
The therapeutic strategy for the management of gout would depend among other factors, upon
the stage of the disease and if the patient is consuming allopathic medication which would
interfere with the expressions of the symptoms of the disease. Anamnesis would help trace the
original unmodified picture of the disease and establish the evolutionary stages through which
the patient has traversed. This would enable the physician to become clear about the miasmatic
diagnosis as well as the state of the susceptibility at the point of time.
Therapeutic strategies might thus call for one of the following actions:
a. Initiating treatment with an acute/specific medicine based on the existing symptom to take
care of the acute exacerbations which are inevitable when the suppressive medication is
withdrawn.
b. Use of the intercurrent remedy based on the appreciation of the miasmatic blocks
encountered. Here the pre-dominant miasm is sycotic maism.
c. Introducing the chronic medicine after the complete withdrawal of the allopathic medication
or when the symptom totality clearly points to its use or the improvement has stopped after
relief obtained by specific homoeopathic medicine.
In Synthesis repertory30, 208 medicines are found in chapter EXTREMITIES under the rubric
‘Pain-joint-gouty’. The homoeopathic literature has rich source of medicines for all stages of gout.
There are few rare remedies also which can be used during acute exacerberation condition. The
frequently verified characteristic features of some specific remedies are: Uric acid: Gout with gouty
eczema, lipoma. Ammonium phosphoricum: Chronic gout, uric acid diathesis, nodosities in joints
of fingers and at the back of hands. Coldness from least draft of air. Ammonium benzoicum: Remedy
for albuminuria, especially in patients with gout diathesis. Gout, with deposits in joints. Arnica
montana: Gout with extreme soreness. Great fear of being touched or approached. Sprained and
dislocated feeling. Soreness after over exertion. Formic acid: Gout, chronic myalgia, muscular pain
and soreness. Appears suddenly, worse right side, motion, better pressure. Urtica urens: Gout
and uric acid diathesis, pain of acute gout. Worse from snow air, cool moist air, touch. Chininum
sulphuricum: Polyarticular gout, acute articular rheumatism.
Indications of frequently prescribed medicines for the management of gout are given below:31
30 Schroyens F. Synthesis Repertory ver. 9.1. New Delhi: B Jain Publishers Pvt. Ltd.; 2002.
31 Allen HC. Allens Keynotes rearranged and classified with leading remedies of the Materia Medica and bowel nosodes. 9th ed. New Delhi: B Jain
Publishers Pvt Ltd;2017.
Lycopodium clavatum Hot patient, intellectually keen but • Chronic gout with chalky deposits
physically weak; upper part of body in the joints
emaciated, lower part semi- dropsical; • Pain in the heels on treading, as if
complexion pale, dirty, sallow with deep from a pebble
furrows; looks old; recurrent respiratory • Right foot hot, left cold
and gastro-intestinal affections; • Worse from heat or warm room,
tendency for flatulent dyspepsia; hot air, bed
worse from 4 pm - 8 pm; right sided • Better by motion, on getting cold,
complaints or symptoms shift from right from being uncovered
to left; desire for warm foods and drinks,
sweet; dominating, cranky, lack of self-
confidence, precocious
Pulsatilla nigricans Hot patient; marked changeability • Drawing tensive pain with
of symptoms; aversion to fatty foods, restlessness and chilliness
warm foods and drinks, dislikes butter; • Pain in limbs shifting rapidly
thirstless with great dryness of mouth; • Boring pain in heels towards
tongue coated yellow or whitish; worse evening; suffering from letting the
towards evening and in warm room, affected limb hang down
better in open air, by slow, gentle • Pains appear suddenly leaves
motion and cold applications; desire gradually
for company, mild, gentle, affectionate, • Worse lying on left or painless side
yielding, weeping disposition
Rhododendron Rheumatic and gouty symptoms well • Gouty inflammation of great toe
marked. Rheumatism in the hot season. joint
Dread of storm, particularly afraid of • Rheumatic tearing pain in all limbs,
thunderstorm. Worse before a storm is especially right side
a true guiding symptom. Cannot sleep • Worse at rest at night towards
until legs are crossed. Electric shock like morning and in stormy weather
pains • Better, after the storm breaks,
warmth
Homoeopathic medicine on the basis • Clinical assessment with personal history of Diabetes
of acute totality or individualised mellitus, Hypertension, Thyroid disorders etc
homoeopathic medicine as per need of the • General physical examination
case to be prescribed. • Renal function test, S. uric acid
Followed by detailed history with • Advice FBC, CRP, Lipid profile,Blood culture, RA
investigations. Factor, BSF & PP, Thyroid profiles etc. to rule out
co-morbidities
Improvement No
General management
Confirm Gout • Control of weight (without
Reassess case and if pain is taking much of proteins)
intense then give integrative • Reduce fat foods and
care and advice patient to vegetarian sources of
Yes follow up in intercritical period protein should be integrated
into the diet
• Protein-rich foods should be
Continue acute
avoided
homoeopathic medicine • Start individualized homoeopathic treatment • Consume sufficient
till acute phase persists • Advice for lifestyle modifications fluids(>2 L /day)
• Consumption of alcohol
should be reduced.
• Sugar-sweetened beverages
should be avoided
Improvement
MIGRAINE
The name ‘migraine’ originally comes from the Greek word hemicrania, meaning ‘half of the head’,
representing one of the most striking features of the condition that in many cases pain only affects
one half of the head. The pain is generally throbbing in nature, and typically made worse by any
form of movement or even modest exertion. The pain of migraine is typically accompanied by other
features such as nausea, dizziness, extreme sensitivity to lights, noises, and smells, lack of appetite,
disturbances of bowel function, and so on.
INCIDENCE /PREVALENCE2,3,4
• Migraine is ranked as the third most prevalent disorder and seventh-highest specific cause of
disability worldwide and represents one-third of all neurological disease burden with more
than 50% of neurological Years lived with disability (YLD) or 22.9% of global YLDs.
• Migraine is also a paroxysmal headache that affects almost 10% of adults around the world.
• It is experienced at some point by over 20% of women and over 10% men.
• Globally, migraine is the most common type of headache among individuals aged 20-40 year old,
with the highest occurrence being around the age of 40, known to be the age of the maximum
workforce.
The etiology of migraine is largely unknown, however several factors which may be associated with
migraine are:
PATHOPHYSIOLOGY 6,8
There are different theories regarding the pathophysiology for migraine. Migraine without aura is
considered as a neurobiological disorder and pain is believed to result from activity within trigeminal
nucleus resulting in release of vasoactive neuropeptides, particularly calcitonin gene-related peptide
(CGRP), neurokinin A, and substance P, from perivascular axons. The released neuropeptides interact
with dural blood vessels to promote vasodilatation and dural plasma extravasations, resulting in
perivascular inflammation. Orthodromic conduction alone trigeminovascular fibres transmits pain
impulses to the trigeminal nucleus caudalis where the information is relayed further to higher
cortical pain centres.
Cortical spreading depression (CSD), a slow, self-propagating wave of neuronal and glial
depolarization is the neuro-physiological phenomenon likely involved with the pathophysiology
of the migraine aura. Mutations in gene CACNA1A of calcium voltage gated (50%) and SCN1A of
Na+ /K+ ATPase (20%) have tendency to suffer from migraine. The platelet hypothesis involves
abnormal platelet activation with relevant characteristics like: they do not adhere to one another
unless precipitated; certain stimuli (catecholamines, thromboxane A2 and ADP) when aggregate
release a portion of contents (e.g. Serotonin, adenosine and its phosphate derivatives). This platelet
hyperaggregability forms micro-emboli that lodge in microvasculature releasing their contents
which cause changes in vasomotor tone which induce tissue response leading to migraine pain.
DIAGNOSIS 9,10,11
There are two main types of migraine: migraine without aura (MO), and migraine with aura (MA).
Many people have both; MO is at least three times as common as MA. Only about 20% of migraine
sufferers experience aura, usually (but not invariably) before the headache starts.
A positive diagnosis is based on the typical clinical picture that does not require any further
investigations to exclude alternative explanations for a patient’s symptoms.
Clinical presentation
The clinical presentation of migraine may vary from patient to patient, and from one attack to
another in same patient. It may occur in three clinical phases:
8 Hadjikhani N, Vincent M. Neuroimaging clues of migraine aura [Internet]. The Journal of Headache and Pain 20. [Internet] 2019 [cited on
2021 March 10]. Available from: file:///C:/Users/A/Downloads/Hadjikhani-Vincent 2019_Article_NeuroimagingCluesOfMigraineAur.pdf
9 DeMaagd G. The Pharmacological Management of Migraine, Part 1 Overview and Abortive Therapy. P T. 2008; 33(7):404–416.
10 The International Classification of Headache Disorders 3rd edition [Internet]. 2013 [Cited on 2020 March 19]. Available from: https://ichd-3.
org/1-migraine/
11 Weatherall MW. The diagnosis and treatment of chronic migraine. Ther Adv Chronic Dis. 2015; 6(3):115–123.
1. The pre-headache phase includes the premonitory phase and the migraine aura. This phase may
precede the headache by hours to days, affecting up to 20% to 60% of patients. Features of
the premonitory phase are both physical and somatic, compared with the aura phase, which
manifests with more neurological features.
2. During the headache phase the migraine itself usually presents with throbbing, pulsatile pain
in the fronto-temporal region, usually lasting from 4 to 72 hours. The pain may vary in severity
from mild to severe. Other clinical features include nausea, vomiting, autonomic symptoms,
nasal congestion, and lacrimation.
3. The resolution (post-dromal) phase consists of fatigue and irritability, lasting a day or two; this
is sometimes referred to as the “migraine hangover.”
Although these three phases characterize the stages of migraine, many patients do not present in
such a typical fashion; they might experience only some of these clinical features.
12 Muthyala N, Qadrie ZL, Suman A. Migraine & Migraine Management: A Review. Pharma Tutor 2018;6(4):8-17.
Standard Treatment Guidelines In Homoeopathy 159
MIGRAINE
INVESTIGATIONS11
Almost everyone with migraine needs no investigation. The goal of investigating is to exclude other
causes of migraine like symptoms, not to confirm migraine.
• Screen out hypertension and depression
• Erythrocyte sedimentation rate (ESR) to rule out temporal arteritis
• Chest X-ray in smokers to consider metastatic cancer
• CT scan to rule out SOL (space occupying lesions), malignancy.
EVALUATION AND ASSESSMENT
• ID-Migraine, a three-item screening test13
• Migraine-Specific Quality of Life Survey14
• Migraine Disability Assessment Scale (MIDAS)15
• Migraine Severity Scale16
• Global Assessment of Migraine Severity (GAMS)2
• The Visual Aura Rating Scale (VARS)17
• Headache Impact Test -6 (HIT-6)18
DIFFERENTIAL DIAGNOSIS 19,20
• Tension type headache
• Cluster headache
• Medication overuse headache (MOH).
Headache Tension-type
Migraine (with or without aura) Cluster headache
feature headache
Unilateral (around the
Pain eye, above the eye and
Bilateral Unilateral or bilateral
location along the side of the
head/face)
Variable (can be sharp,
Pressing/tightening Pulsating (throbbing or banging in
Pain quality boring, burning,
(non-pulsating) young people aged 12–17 years)
throbbing or tightening)
13 Lipton RB, Dodick D, Sadovsky R, Kolodner K, Endicott J, Hettiarachchi J, et al. A self-administered screener for migraine in primary care The
ID Migraine validation study. Neurology. 2003;61(3):375-82.
14 Jhingran P, Davis SM, LaVange LM, Miller DW, Helms RW. MSQ: Migraine- Specific Quality-of-Life Questionnaire. Further investigation of the
factor structure. Pharmacoeconomics. 1998;13(6):707-17.
15 Stewart WF, Lipton RB, Kolodner K, Liberman J, Sawyer J. Reliability of the migraine disability assessment score in a population-based sample
of headache sufferers. Cephalalgia. 1999;19(2):107-14.
16 El Hasnaoui A, Vray M, Richard A, Nachit-Ouinekh F, Boureau F, MIGSEV Group. Assessing the severity of migraine: development of the
MIGSEV scale. Headache. 2003;43(6):628–35.
17 Eriksen MK, Thomsen LL, Olesen J. The Visual Aura Rating Scale (VARS) for migraine aura diagnosis. Cephalalgia. 2005;25(10):801-10.
18 Yang M, Rendas-Baum R, Varon SF, Kosinski M. Validation of the Headache Impact Test (HIT-6™) across episodic and chronic migraine
Cephalalgia. 2011;31(3):357–367.
19 Elrington G. Migraine: Diagnosis and Management. J Neurol Neurosurg Psychiatry. 2002;72(2):ii10–ii15.
20 National Institute for Health and Care Excellence. London: Headaches in over 12s: diagnosis and management Clinical guideline [Internet].
2012 [Cited 2019 August 06]. Available from: https://www.nice.org.uk/guidance/cg150
Headache Tension-type
Migraine (with or without aura) Cluster headache
feature headache
Pain
Mild or moderate Moderate or severe Severe or very severe
intensity
Not aggravated by Aggravated by, or causes
Effect on
routine activities of avoidance of, routine activities of Restlessness or agitation
activities
daily living daily living
Unusual sensitivity to light and/
or sound or nausea and/or
vomiting. Aura symptoms can On the same side as
occur with or without headache the headache: red and/
and are fully reversible; develop or watery eye, nasal
Other over at least 5 minutes, last 5−60 congestion and/or runny
symptoms None minutes. Typical aura symptoms nose, swollen eyelid,
include visual symptoms such as forehead and facial
flickering lights, spots or lines and/ sweating, constricted
or partial loss of vision; sensory pupil and/or drooping
symptoms such as numbness and/ eyelid
or sensation of pins and needles;
and/or speech disturbance
4–72 hours in adults;
Duration
30 minutes–continuous 1–72 hours in young people aged 15–180 minutes
of headache
12–17 years
Once Once every
every other day to
≥ 15 days other day 8 per
≥ 15 days
per month to 8 times day, with
Frequency of <15 days < 15 days per per month
for more per continuous
headache per month month for more than
than 3 day, with remission for
3 months
months remission <1 month in
for > 1 a 12-month
month period
Episodic Chronic Episodic Chronic
Episodic Chronic
tension- tension- migraine migraine
Diagnosis cluster cluster
type type (with or (with or
headache headache
headache headache without aura) without aura)
COMPLICATIONS 9
• Status migrainosus
• Migrainous infarction
• Migraine aura-triggered seizure.
PREVENTION16
RED FLAGS 21
• Thunderclap headache
• Positional headache
• Headaches initiated by exertion
• New headaches (especially if older than 50 years of age or conditions such as cancer, blood
clotting disorder)
• Substantial change in headache pattern
• Constant headache always in the same location of the head
• Worrisome neurologic symptoms
• Headache that never goes away
• Systemic symptoms.
MANAGEMENT
General management 9,11
• Migraine treatment depends on the duration and severity of pain, associated symptoms, degree
of disability, and initial response to therapy. To maintain a headache diary is helpful.
• Medical conditions like stroke, myocardial infarction, epilepsy, affective and anxiety disorders,
and some connective tissue disorders are more common in people with migraine. Regular health
check ups should be done to identify underlying cause.
• Avoid triggering factors/risk factors such as sleep patterns, emotional status, stress etc. to
decrease the frequency of episodes of migraine.
• Non-drug therapies include biofeedback, behavior modification, and psychosocial interventions,
including relaxation and stress management, acupuncture, applications of heat and cold, impulse
magnetic-field therapy, photic stimulation, and physical approaches (e.g., aerobic exercise,
isometric neck exercises, and chiropractic manipulations).
Homoeopathic management
Migraine falls into the category of chronic disease. It is essentially paroxysmal in nature and
precipitated by various causative modalities. This chronic illness has acute exacerbations in its
course. So, there is a prominent role of detailed case taking which will unfold the person behind
suffering. It will be crucial to identify various attributes of the person, the stressors at work, family,
society level and other physical causative factors like weather change, etc. which can be understood
properly and managed.
Acute exacerbations can be managed by various acute medicines like Glonoine selected after proper
data collection about attacks of migraine and analysing the symptom picture manifested by the
patient before, during and after the attacks. But the chronic individualized constitutional medicines
given after the acute attack will help in reducing the frequency of acute attacks and will modify the
intensity of further acute paroxysms of headache.
21 Schwedt TJ. Headache “Red Flags”. [Internet] American migraine foundation [Internet]. 2015 [Cited 2020 March 19]. Available from: https://
americanmigrainefoundation.org/resource-library/headache-red-flags-when-to-see-your-doctor/
Homoeopathic intervention has been found to have encouraging results in terms of decrease in the
frequency, severity, and duration of migraine attacks.22,23,24
In Synthesis repertory25, medicines for migraine in the chapter HEAD under the rubric ‘Migraine’ (see
Pain) mentions 767 remedies. The frequently verified characteristic features of some organospecific
remedies are: Cedron: Pain from temple to temple across eyes. Pain over whole right side of face,
coming on about 9 am; worse working on rising from bed, dizzy, cannot see to light a candle and
could not tell when it was lighted. Whole body seems numb with headache. Periodicity is a marked
symptom. Chinninum sulphuricum: Pain in forehead and temples, increasing gradually at noon,
of malarial origin, with vertigo and pulsation. Worse left side. Inability to remain standing. Iris
versicolor: Frontal headache, with nausea. Scalp feels constricted. Right temple especially affected.
Sick headache, worse rest; begins with a blur before eyes, after relaxing from a mental strain.
Onosmodium virginianum: Chiefly left-sided migraine; occipito-frontal pain in the morning on
waking. Pain in the eyeballs between orbit and the ball, extending to the left temple.
The list of frequently prescribed polychrest medicines with their indications are given below26,27
Cocculus indicus Unmarried and childless women, sensitive • Headache in nape and occiput;
and romantic girls, etc. Spasmodic and extending to the spine; as if tightly
paretic affections, notably those affecting bound by a cord; with nausea, as if at
one-half of the body. All the symptoms are sea; at each menstrual period
worse riding in a carriage or on shipboard; • Sick headache from carriage, boat or
seasickness. Time passes too quickly. train riding
Aversion to food, drink, tobacco • Prosopalgia in the afternoon with wide
radiations of pain
• Pain worse from lying on back of head,
emotional disturbance
22 Walach H, Lowes T, Mussbach D, Schamell U, Springer W, Stritzl G, et al. The long-term effects of homeopathic treatment of chronic headaches:
one-year follow-up and single case time series analysis. Br Homeopath J. 2001;90(2):63-72.
23 Muscari-Tomaioli G, Allegri F, Miali E, Pomposelli R, Tubia P, Targhetta A, et al. Observational study of quality of life in patients with headache,
receiving homeopathic treatment. Br Homeopath J. 2001;90(4):189-97.
24 Witt CM, Lüdtke R, Willich SN. Homeopathic treatment of patients with migraine: a prospective observational study with a 2-year follow-up
period. J Altern Complement Med. 2010;16(4):347-55.
25 Schroyens F. Synthesis Repertory ver. 9.1; New Delhi: B Jain Publishers Pvt. Ltd.; 2002.
26 Boericke W. Boericke’s New manual of Homoeopathic Materia Medica with Repertory: Third Revised & Augmented Edition based on Ninth
Edition. New Delhi: B. Jain Publishers(P) Ltd.; 2007.
27 Allen HC. Allens Keynotes rearranged and classified with leading remedies of the Materia Medica and bowel nosodes, 9th ed. New Delhi: B Jain
Publishers Pvt Ltd; 2017.
Lachesis mutus Hot patient; thin and emaciated; • Headache, pressing or bursting pain in
hemorrhagic diathesis; great sensitiveness temples; dreads to go to sleep because
to touch; hot flushes and perspiration; she awakens with such a headache
desires oysters, alcohol, farinaceous • With headache, flickering, dim vision
foods; all complaints worse after sleep; and very pale face
loquacious, jumps from one idea to another,
jealous, suspicious, indolent • Worse from motion, pressure, stooping,
lying, after sleep
• Better from onset of a discharge
Nux vomica Chilly patient; thin, prone to indigestion; • Headache in occiput or over eyes,
tongue coated yellowish in the posterior with vertigo; brain feels turning in a
part; constipation with frequent circle
unsuccessful desire for stool. Bad effects of • Pressing pain in vertex, as of a nail
spiced food, alcohol, loss of sleep, mental driven in
over exertion. oversensitive to all external
impressions: noise, odors, light or music; • Frontal headache, with desire to press
nervous disposition the head against something
• Congestive headache associated with
haemorrhoids
• Better in damp, wet weather, from
hard strong pressure
Sepia officinalis Chilly patient; tall, thin built with yellow • Headache: in terrific shocks; at
saddle across upper part of cheeks and menstrual nisus, with scanty flow; in
nose; big belly; dry flabby skin. Predisposed delicate, sensitive, hysterical women;
to take cold from change of weather. Desire pressing, bursting pain
for sour food which aggravates. Irregular • Worse from motion, stooping, mental
menses. Cheerful, active when well but labor
indifferent and quarrelsome when sick,
self-absorbed, sad, weeping and indolent • Better by external pressure, continued
hard motion
Silicea terra Extremely chilly patient; all symptoms • Chronic sick headaches, since some
worse by cold except stomach complaints, severe disease of youth; ascending
which are ameliorated. Profuse, offensive from nape of neck to the vertex, as if
discharges; sweats profusely especially on coming from the spine and locating in
feet. Easy suppuration; glandular affinity; one eye, especially the right
large head and distended abdomen; • Worse from draught of air or
weak ankles, slow in learning to walk; uncovering the head
constipation. Obstinate, head strong,
cries when spoken kindly to, nervous, • Better from pressure wrapping up
apprehensive, oversensitive, irritable and warmly, profuse urination
fearful
Sulphur Hot patient, kicks off the cloth at night; • Sick headache every week or every two
dirty, filthy, does not want to be washed; weeks; prostrating, weakening; with
lean, thin, stoop-shouldered; child who hot vertex and cold feet
walks and sits stooping; red orifices; desires • Beating, throbbing headache
sweets, sugar, meat; when the best selected
remedy fails to improve • Worse from stooping
Syphilinum Utter prostration and debility in the • Linear pains from temple, across, or
morning. Pains from darkness to daylight; from eyes backwards
decrease and increase gradually. Syphilitic • Stupefying cephalgia
affections. Loss of memory, apathetic,
hopelessness of recovery, confusion • Pain increases and decreases gradually
• Worse at night, from sun down to
sunrise
Headache one-sided
Lifestyle or preventive measures
• Encourage regular meals, adequate
hydration, sleep, and exercise
• Encourage activities of relaxation such
as mindfulness, yoga, or meditation
• With Aura • Avoid specific triggers if known
Symptoms as nausea, dizziness,
extreme sensitivity to lights, noises,
smells, lack of appetite, etc.
• Without Aura
No other symptom accompanies
RED FLAGs
• Thunderclap headache
Evaluation through homeopathic case • Positional headache
taking and assessment scales • Headaches initiated by
exertion
• New headaches (especially
if older than 50 years of
age)
• Substantial change in
Start Homoeopathic treatment along
headache pattern
with general management
• Constant headache always
in the same location of the
head
• Worrisome neurologic
symptoms
• Headache that never goes
away
Yes Improvement No • Systemic symptoms
POST-OPERATIVE PAIN
CASE DEFINITION
Pain is defined as “an unpleasant sensory and emotional experience associated with actual or
potential tissue damage or described in terms of such damage.”1 Post-operative pain is defined
as acute pain, resulting from surgery, surgical procedures or trauma. It can be physiological or
pathological and involve inflammatory reactions.2
CLASSIFICATION
Post-operative pain is generally classified into acute and chronic pain. Acute post-operative pain is
defined as “pain occurring in surgical patients following a procedure”.3 If, after a surgical procedure,
the resulting pain continues for at least two months, and other causes of the pain have been excluded,
then this is termed as chronic post-operative pain.4
INCIDENCE/PREVALENCE
• More than 80% of patients who undergo surgical procedures experience acute post-operative
pain and approximately 75% of those with post-operative pain report the intensity as moderate,
severe, or extreme.5,6
• In India, only 30% of patients who undergo surgery report adequate post-operative pain relief.7
1 Merskey H, AlbeFessard D, Bonica JJ, Carmon A, Dubner R, et al. Pain terms: a list with definitions and notes on usage. Recommended by the
IASP subcommittee on taxonomy. Pain Rep. 1979;6:249–52.
2 Masigati HG, Chilong KS. Postoperative pain management outcomes among adults treated at a tertiary hospital in Moshi, Tanzania. 2014;
16(1):47-53.
3 American society of anesthesiologists task force on acute pain management. Practice guidelines for acute pain management in the
perioperative setting: an updated report by the American society of anesthesiologists task force on acute pain management. Anesthesiology.
2012;116(2):248-73.
4 Macare WA. Chronic pain after surgery. Br J Anaesth. 2001; 87(1): 88-98.
5 Apfelbaum JL, Chen C, Mehta SS, Gan TJ: Postoperative pain experience: Results from a national survey suggest postoperative pain continues
to be undermanaged. Anesth Analg. 2003; 97(2):534-540.
6 Gan TJ, Habib AS, Miller TE, White W, Apfelbaum JL. Incidence, patient satisfaction, and perceptions of postsurgical pain: Results from a US
national survey. Curr Med Res Opin. 2014; 30 (1):149-160.
7 Vijayan R. Managing acute pain in the developing world. Pain Clin Updat. 2011;19(3):1-7.
8 Poleshuck EL, Katz J, Andrus CH, Hogan LA, Jung BF, Kulick DI, et al. Risk factors for chronic pain following breast cancer surgery: a
prospective study. J Pain. 2006; 7(9): 626–34.
9 Hanley MA, Jensen MP, Smith DG, Ehde DM, Edwards WT, Robinson LR. Pre-amputation pain and acute pain predict chronic pain after lower
extremity amputation. J Pain. 2007; 8(2): 102–9.
10 Meyhoff CS, Thomsen CH, Rasmussen LS, Nielsen PR. High incidence of chronic pain following surgery for pelvic fracture. Clin J Pain. 2006;
22(2): 167–72.
11 Bar-El Y, Gilboa B, Unger N, Pud D, Eisenberg E. Skeletonized versus pedicled internal mammary artery: impact of surgical technique on post
CABG surgery pain. Eur J Cardiothorac Surg. 2005; 27(6): 1065–9.
12 Lavand’ homme P. ‘Why me?’ The problem of chronic pain after surgery. Br J Pain. 2017; 11(4): 162-165.
13 Pluijms WA, Steegers MAH, Verhagen AFTM, Scheffer GJ, Wilder-Smith OHG. Chronic post-thoracotomy pain: a retrospective study. Acta
Anaesthesiol Scand. 2006; 50(7): 804–8.
• Inadequately controlled pain negatively affects quality of life, function, and functional recovery,
risk of post-surgical complications, risk of persistent postsurgical pain,14,15 prolonged hospital
stays and overcrowding of wards, which consequently, adversely affect the quality of health
care.16
The intensity, quality and duration of post-operative pain is affected mainly by:
INTENSITY OF PAIN19
Based on intensity and duration, pain can be either severe, moderate or mild.
• Severe pain lasting more than 48 hours- generally seen after- surgical procedures of epigastrium,
thorax, kidneys, hemorrhoids, rectum, major joints and bones with the exception of hips and
spinal surgery.
• Severe pain lasting less than 48 hours- seen after cholecystectomy, prostatectomy, abdominal
hysterectomy, and cesarean section.
• Moderate pain lasting more than 48 hours- seen in heart surgery, hip surgery, surgery of the
larynx and pharynx.
• Moderate pain of shorter duration- seen after operations like appendectomy, inguinal hernia
repair, vaginal hysterectomy, mastectomy, intervertebral disc surgery.
• Mild pain- seen in minor operations, such as gynecological procedures.
14 Kehlet H, Jensen TS, Woolf CJ. Persistent postsurgical pain: Risk factors and prevention. Lancet 2006; 367 (9522):1618-1625.
15 Roger Chou, Gordon DB, de Le-Casasola OA, Rosenberg JM, Bickler S, Brennan T, et al. Management of Postoperative Pain: A Clinical Practice
Guideline From the American Pain Society, the American Society of Regional Anesthesia and Pain Medicine, and the American Society of
Anesthesiologists’ Committee on Regional Anesthesia, Executive Committee, and Administrative Council. The Journal of Pain.2016;17(2):131-
157.
16 Masigati HG, Chilonga KS. Postoperative pain management outcomes among adults treated at a tertiary hospital in Moshi, Tanzania. Tanzan J
Health Res. 2014;16(1):47-53.
17 Gerbershagen HJ, Aduckathil S, van Wijck AJM, Peelen LM, Kalkman CJ, Meissner W. Pain intensity on the first day after surgery: a prospective
cohort study comparing 179 surgical procedures. Anesthesiology. 2013;118(4):934-44.
18 Malek J, Ctrnacta E, Kurzova A. Patients’ perioperative worries and experiences. RozhlChir. 2004;83(8):406-10.
19 Málek J, Š� evčí�k P. Postoperative Pain Management [Internet]. Third updated edition Mladáfronta a.s., MeziVodami 1952/9;2017 [cited
2020 Mar 6]. Available from: https://www.coursehero.com/file/64426398/125136f77e1b7daf7565bd6653026c35-Postoperative-Pain-
Management-170518pdf/
EFFECTS OF PAIN
Positive
Acute pain plays “positive” role by providing a warning sign of tissue damage and inducing
immobilization to allow appropriate healing.19
Negative
DIAGNOSING PAIN19
Proper diagnosis of the type and intensity of pain is crucial for an adequate and targeted treatment
of post-operative pain. The examination of post-operative pain includes medical history, physical
examination, and specific evaluation of pain. During physical examination, one must not only focus
on the site of maximum tenderness, but also on distant structures, which may be associated with
the pain. Pain intensity, location, medical treatments, number of episodes, onset, position, quality,
radiation, severity etc. can provide important diagnostic clues to known the mechanism of pain and
decide personalized management.
A widely used method for assessing pain is the PQRST20,21 method, which is easy to remember and a
valuable tool to accurately describe, assess and document a patient’s pain.
PQRST
P= Provocation/Palliation
20 Kernicki JG. Differentiating chest pain: advanced assessment techniques. Crit Care Nurs. 1993; 12(2):66–76
21 Gordon D. Acute pain assessment tools. Current Opinion in Anaesthesiology. 2015;28(5):565-569.
Q = Quality/Quantity
Patient may be asked the following for assessing the quality/quantity of pain for diagnostic reasons:
Use words to describe the pain such as sharp, dull, stabbing, burning, crushing, throbbing, nauseating,
shooting, twisting or stretching.
R = Region/Radiation
It’s important to understand the location, and radiation of the pain. Ask the patient:
S = Severity
• How severe is the pain on a scale of 0 to 10, with zero being no pain and 10 being the worst pain
ever?
• Does it interfere with activities?
• How bad is it at its worst?
• Does it force you to sit down, lie down, slow down?
• How long does an episode last?
T = Timing
Sometimes, knowing when the pain started can be diagnostically important. One may ask:
Assessment of pain is a vital element in effective management of the post-operative pain. Following
general recommendations and principles for successful pain management may be followed for
evaluation:19
• Assess pain both at rest and on movement to evaluate patient’s functional status.
• Assess the effect of a given treatment (before and after intervention).
• In the surgical Post Anaesthesia Care Unit (PACU), or other circumstances where pain is intense;
evaluate, treat, and re-evaluate frequently (e.g., every 15 minutes initially, then every 1-2 hours,
as pain intensity decreases).
• In the surgical ward, evaluate, treat, and re-evaluate regularly (e.g., every 4-8 hours)- both
intensity of pain and patient’s response to treatment.
• Define maximum pain score above which pain relief is offered (the intervention threshold). For
example, verbal ratings score of 3 at rest and 4 on moving, on a 10-point scale.
• Pain and response to treatment, including adverse effects, should be documented clearly in easily
accessible forms, such as the vital sign sheet. This is useful for treatment, good communication
between staff, auditing and quality control.
• Patients who have difficulty in communicating their pain require particular attention. This
includes patients who are cognitively impaired, severely emotionally disturbed, children,
patients who can not speak the local language, and patients whose level of education or cultural
background differ significantly from that of their health care team.
• Unexpected intense pain, particularly if associated with altered vital signs (hypotension,
tachycardia, or fever), is immediately evaluated. New diagnoses, such as wound dehiscence,
infection, or deep venous thrombosis, should be considered.
• Immediate pain relief, without asking for a pain rating, is given to patients with pain, who are
not sufficiently focused to use a pain rating scale.
• Family members are involved when required.
A. Facial expressions: This scale is suitable for patients where verbal communication is a problem.
Faces Pain Scale Revised22,23, Wong-Baker FACES pain rating scale24 and Oucher scale25 are
usually used in post-operative pain assessment.
B. Verbal rating scale (VRS): The patient is asked to rate his/her pain on a five-point scale as “none,
mild, moderate, severe or very severe”, Four-point VRS 26, Seven-point Graphic Rating Scale27,
and a Six-point Present Pain Inventory (PPI).28,29
22 Bieri D, Reeve RA, Champion GD, Addicoat L, Ziegler JB. The faces pain scale for the self-assessment of the severity of pain experienced by
children: Development, initial validation, and preliminary investigation for ratio scale properties. Pain. 1990;41(2):139-150.
23 Faces Pain Scale - Revised (FPS-R) [Internet]. 2001 [Cited on 2020 January 17] Available from: http:// www.iasp pain.org/files/Content/
Content Folders/Resources 2/FPSR/FPS-R_English.pdf
24 Wong DL, Baker CM. Pain in children. Comparison of assessment scales. Pediatr Nurs. 1988;14(1):9-17.
25 Beyer JE, Denyes MJ, Villarruel AM. The creation, validation, and continuing development of the Oucher: A measure of pain intensity in
children. J Pediatr Nurs. 1992;7(5):335-346.
26 Closs SJ, Barr B, Briggs M, Cash K, Seers K. A comparison of five pain assessment scales for nursing home residents with varying degrees of
cognitive impairment. J Pain Symptom Manage. 2004;27(3):196-205.
27 Bergh I, Sjostrom B, Oden A, Steen B. An application of pain rating scales in geriatric patients. Aging Clin Exp Res. 2000;12(5): 380-387.
28 Gagliese L, Katz J. Age differences in postoperative pain are scale dependent: A comparison of measures of pain intensity and quality in
younger and older surgical patients. Pain. 2003;103(1-2):11-20.
29 Melzack R, Katz J, Coderre TJ. Methods of postoperative pain control. Cah Anesthesiol. 1992;40(5):309-315.
C. Numerical rating scale (NRS): This consists of a simple 0 to 5 or 0 to 10 scale which correlates to
no pain at zero and worst possible pain at 5 (or 10).30,31
D. Visual analogue scale (VAS): This consists of an ungraduated, straight 100 mm line marked at
one end with the term “ no pain” and at the other end “the worst possible pain”.32,33,34
E. Post-operative Quality of Recovery Scale (PQRS): This questionnaire is an accepted tool used for
self-assessment of patients’ quality of recovery after surgery. It addresses multiple domains,
including nociception, emotion, day to-day activities, cognition and satisfaction and each domain
comprises a series of questions.35
1. Morbidity
Inadequately managed postoperative pain is usually associated with both physiological and
psychological dysfunction.36,37 Changes can occur in diverse organ systems, including the
cardiovascular (coronary ischemia, myocardial infarction), pulmonary (hypoventilation, decreased
vital capacity, pulmonary infection), gastrointestinal (reduced motility, ileus, nausea, vomiting),
and renal (increases in urinary retention and sphincter tone, oliguria) systems. A negative impact
may also be seen on immune function, the muscular system, coagulation, and wound healing, and
negative psychological effects, such as demoralization and anxiety.38
Postoperative pain also adversely affects physical functioning, recovery, and quality of life39, 40 and its
impact is correlated with the severity of pain.41
The consequences of poorly controlled pain during or after surgery may also include adverse effects
of and toxicity related to anesthetic/analgesic medications, particularly if required for prolonged
30 Morrison RS, Ahronheim JC, Morrison GR, Darling E, Baskin SA, Morris J, et al. Pain and discomfort associated with common hospital
procedures and experiences. J Pain Symptom Manage. 1998;15(2):91-101.
31 Gagliese L, Weizblit N, Ellis W, Chan VWS. The measurement of postoperative pain: A comparison of intensity scales in younger and older
surgical patients. Pain. 2005;117(3):412-420.
32 DeLoach LJ, Higgins MS, Caplan AB, Stiff JL. The visual analog scale in the immediate postoperative period: intrasubject variability and
correlation with a numeric scale. Anesth Analg. 1998; 86(1):102–6.
33 Gudex C, Dolan P, Kind P, Williams A. Health state valuations from the general public using the Visual Analogue Scale. Quality of Life Research.
1996; 5(6): 521-531.
34 Flaherty SA. Pain measurement tools for clinical practice and research. Journal of the American Association of Nurse Anesthetists. 1996;
64(2): 133-140.
35 Royse CF, Newman S, Chung F, Stygall J, McKay RE, Boldt J, et al. Development and feasibility of a scale to assess postoperative recovery: the
post-operative quality recovery scale. Anesthesiology. 2010;113(4):892-905.
36 Breivik H. Postoperative pain management: why is it difficult to show that it improves outcome? Eur J Anaesthesiol. 1998;15(6):748–751.
37 Joshi GP, Ogunnaike BO. Consequences of inadequate postoperative pain relief and chronic persistent postoperative pain. Anesthesiol Clin
North America. 2005;23(1):21–36.
38 Gan TJ. Poorly controlled postoperative pain: prevalence, consequences, and prevention. Journal of Pain Research. 2017;10:2287–2298.
39 VanDenKerkhof EG, Hopman WM, Reitsma ML, Goldstein DH, Wilson RA, Belliveau, et al. Chronic pain, healthcare utilization, and quality of life
following gastrointestinal surgery. Can J Anaesth. 2012;59(7):670–680.
40 Peters ML, Sommer M, de Rijke JM, Kessels F, Heineman E, Patijin J, et al. Somatic and psychologic predictors of long-term unfavorable
outcome after surgical intervention. Ann Surg. 2007;245(3):487–494.
41 Wu CL, Naqibuddin M, Rowlingson AJ, Lietman SA, Jermyn RM, Fleisher LA. The effect of pain on health-related quality of life in the immediate
postoperative period. AnesthAnalg. 2003;97(4):1078–1085.
periods or at elevated doses to relieve pain. Although opioid analgesics remain the mainstay of
postoperative pain therapy for efficacy, their use may be limited by potentially harmful effects.
Common opioid-related AEs include respiratory depression, nausea, vomiting, pruritus, and bowel
dysfunction, which have been associated with a substantial burden on quality of life.42
Inadequate pain relief has been shown to result in increased length of stay, time to discharge,
readmission rates, and time before ambulation all of which can increase cost of care.43,44
MANAGEMENT
Two main approaches can be adopted for managing post-operative pain: Use of pharmacological
intervention, and non-pharmacological approach.45 The non-pharmacological methods are non-
drug methods used to relieve pain. This can be divided into two main groups:
1. Psychological methods
a) Humour or Laughter is the most effective way of relieving pain compared to other self-
initiated noninvasive methods.46 Laughter has been described as internal jogging, promoting
hope and optimism. Its use as a method of pain relief in the immediate post-operative period
is not well documented.
b) Relaxation is widely researched as a psychological method of acute pain control. Distress,
which is part of the psychological perception of pain, is commonly reduced through the
use of relaxation techniques even though the perceived level of pain remains the same.
Results have shown relaxation to reduce muscular tension and increase comfort levels
in postoperative patients as well as reduce the amount of analgesia used in the first 24 h
postoperatively.47
c) Distraction is not designed to make the pain disappear but rather to make it more bearable,
by replacing it with another focus of attention, thus increasing pain tolerance.48
d) Music has also been suggested as a means of reducing patients’ isolation and anxiety.49
e) Guided imagery, a technique in which an experienced practitioner helps a patient provoke
a state of mind or mental images in the absence of that stimuli, through metaphor and
storytelling. It helps to elicit a physiological response, through modulations at the level of
42 Dahan A, Aarts L, Smith TW. Incidence, reversal, and prevention of opioid-induced respiratory depression. Anesthesiology. 2010;112(1):
226–238.
43 Twersky R, Fishman D, Homel P. What happens after discharge? Return hospital visits after ambulatory surgery. Anesth Analg. 1997;84(2):319–324.
44 Coley KC, Williams BA, DaPos SV, Chen C, Smith RB. Retrospective evaluation of unanticipated admissions and readmissions after same day
surgery and associated costs. J Clin Anesth. 2002;14(5):349–353.
45 Czarnecki ML, Turner HN, Collins PM, Doellman D, Wrona S. Procedural Pain Management: A position statement with clinical practice
recommendations. Pain Management Nursing. 2011;12(2): 95–111.
46 Fritz D J. Noninvasive pain control methods used by cancer outpatients. Oncology Nurses Forum (suppl) 1988:108.
47 Flaherty GG, Fitzpatrick JJ. Relaxation technique to increase comfort levels of postoperative patients; a preliminary study. Nursing Research.
1978;27(6): 352-355.
48 McCaffery M. Nursing approaches to nonpharmacological pain control. International Journal of Nursing Studies. 1990;27(1):1-5.
49 Magill-Levreault L. Music Therapy in Pain and Symptom Management. J Palliat Care. 1993; 9(4):42-8.
the autonomic nervous system, such effects would result in changes of the cardiovascular,
respiratory, nervous, endocrine and even immune system.50
f) Cognitive behavioral therapy (CBT) helps to develop important set of coping skills intended
to improve psychological functioning, including behavioral activation, structured relaxation
exercises, recalling and scheduling of pleasurable events, dogmatic assertive communication,
and behavior pacing aiming to avoid prolongation and/or exacerbation of flares of pain.51
g) Hypnosis is phenomena which includes change in consciousness and memory, and
susceptibility to suggestions, reactions, and thoughts. It is applied in perioperative care
procedures to induce a non-pharmacological sedation and reduces anxiety.19
2) Physical approaches
a) Cold increases the threshold of pain, reduces local swelling and muscle spasm. It is used for
a limited period of time after tooth extraction, small surgical procedures on the knee; minor
incisions, etc. Long-term application is unpleasant and may cause trauma.19
b) Heat relaxes muscle spasms and improves joint mobility. It is not used in the treatment of
acute post-operative pain, as it increases the risk of bleeding and edema formation.52
c) Immobilization reduces pain, but prolonged immobilization is not desirable due to an
increased risk of deep venous thrombosis, pressure sores, muscle wasting, and complex
regional pain syndrome.19
d) Massage mechanically improves blood supply, lymphatic drainage, reduces sensitization of
tissues, and has an overall positive psychological effect.53, 54
e) Transcutaneous electrical nerve stimulation (TENS) is a method based on the gate control
theory of pain. Using skin electrodes, nerve fibers are stimulated by a defined electrical
current. TENS has been used as an adjuvant method, which may lead to reduced consumption
of analgesics after surgery, enhanced rehabilitation, improved lung function, blood perfusion
in both the stimulated and distant dermatomes, and increased patient satisfaction with the
treatment. TENS is effective mainly in treating mild pain, e.g., after inguinal hernia repair and
laparoscopic cholecystectomy, but not after open cholecystectomy. Disadvantages include
the need to purchase the device, use of electrodes and patient education.55
f) Rehabilitation improves post-operative course, shortens recovery time and hospital stay
and prevents complex regional pain syndrome.19
50 El Geziry A, Toble Y, Al Kadhi F, Pervaiz M, Al Nobani M. Non-Pharmacological Pain Management. In: Pain Management in Special
Circumstances [Internet]. 2018 [cited on 2021 March 16]. Available from: https://www.intechopen.com/books/pain-management-in special-
circumstances/non-pharmacological-pain-management
51 Hayes SC, Luoma JB, Bond FW, Masuda A, Lillis J. Acceptance and commitment therapy: Model, processes and outcomes. Behaviour Research
and Therapy. 2006;44(1):1-25.
52 Chandler A, Preece J, Lister S. Using heat therapy for pain management (clinical practice). Nursing Standard. 2002;17(9):40-2.
53 Kutner JS, Smith MC, Corbin L, Hemphill L, Benton K, Mellis BK, et al. Massage therapy versus simple touch to improve pain and mood in
patients with advanced cancer: A randomized trial. Annals of Internal Medicine. 2008;149(6):369-79.
54 Ward CW. Non-pharmacologic methods of postoperative pain management. Med Surg Matters. 2016;25(1):9-10
55 Carroll D, Tramèr M, McQuay H, Nye B, Moore A. Transcutaneous electrical nerve stimulation in labour pain: a systematic review. Br J Obstet
Gynaecol. 1997;104(2):169-75.
g) Acupuncture has been used for around 5000 years, and it is considered one of the world’s
oldest arts of an empiric body healing. Basically, acupuncture works by putting the needle in
specific region of the body, which stimulates the nerve. Each needle will cause no discomfort
to little discomfort to the patient, but it will produce a small injury at the insertion area which
will stimulate the body and the immune system to increase circulation, wound healing, pain
modulation and pain analgesia.56
Homoeopathic management
The Complete Repertory61 enlists 25 medicines for managing post-operative pains under the
rubric ‘GENERALITIES - PAIN - operations, after’, ‘PAIN- neuralgic - operations, after surgical’ and
‘WOUNDS - painful - operation, after’. Similar rubrics are also found in different chapters such as
Eyes, Ears, Nose, Teeth, Throat, Chest, Abdomen and back in different repertories such as Clarke’s
Clinical Repertory, Phatak and Synthesis repertories.
56 White A, Editorial Board of Acupuncture in Medicine. Western medical acupuncture: A definition. Acupuncture in Medicine. 2009;27(1):33-5.
57 Robertson A, Suryanarayanan R, Banerjee A. Homeopathic Arnica montana for post-tonsillectomy analgesia: A randomised placebo control
trial. Homeopathy. 2007;96(1):17–21.
58 Lannitti T, Morales-Medina JC, Bellavite P, Rottigni V, Palmieri. Effectiveness and safety of Arnica montana in post-surgical setting, pain, and
inflammation. Am J Ther. 2016;23(1):e184–197.
59 Mazzocchi A, Montanaro F. Observational study of the use of Symphytum 5CH in the management of pain and swelling after dental implant
surgery. Homeopathy. 2012;101(4):211–216.
60 Hostanska K, Rostock M, Melzer J, Baumgartner S, Saller R. A homeopathic remedy from Arnica, marigold, St. John’s wort and comfrey
accelerates in vitro wound scratch closure of NIH 3T3 fibroblasts. BMC Complement Altern Med. 2012;12:100.
61 Zandvoort RV. Complete Repertory 2019. Available from: https://www.completedynamics.com/; last accessed on Oct 15, 2020.
62 Allen HC. Allen’s Keynotes- Rearranged and classified with leading remedies of the Materia Medica and Bowel Nosodes. 10th edition. New
Delhi: B. Jain Publishers (P) Ltd; 2005.
63 Boericke W. New Manual of Homeopathic Materia Medica with Repertory. Third Revised & Augmented Edition. New Delhi: B. Jain Publishers
(P) Ltd; 2007.
64 Phatak SR. Materia Medica Of Homoeopathic Medicines. 2nd edition. New Delhi: B. Jain Publishers (P) Ltd; 1999.
Pain immediately after surgical procedure Post-operative pain continues for more than two months
Diagnosis of pain
• Using PQRST scale
• Facial Expression Scale (Children and
elderly patients)
Yes Improvement No
Red flagS
• Extreme heat of
Partial relief of pain site
complaints • Shiny redness
• Pus formation
• High fever
RHEUMATOID ARTHRITIS
CASE DEFINITION1,2
INCIDENCE / PREVALENCE
• RA affects approximately 0.3–1% of the adult population worldwide with a peak onset of the
disease between 40 years and 70 years of age and the prevalence rises with age.3
• It can also afflict young children even before the age of 16 years, referred to as juvenile RA (JRA),
which is similar to RA except that rheumatoid factor is not found.4
• It occurs more commonly in females than in males with a ratio of 3:1.2
ETIOLOGY1,2,5
RISK FACTORS6
Increased risk Decreased risk
• Female sex • Fish and omega 3 fatty acid consumption
• Exposure to tobacco smoke • Moderate alcohol intake
• Air pollution • Healthy diet
1 Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo DL, Jameson JL, editors. Harrison’s Principles of Internal Medicine.17th edition vol. 2. New
York: McGraw Hill; 2008: p. 1968-77.
2 Colledge NR, Walker BR, Ralston SH, editors. Davidson’s principle & practice of Medicine. 22nd ed. New York: Churchill Livingstone, Elsevier,
London. 2014: p 1096- 1103.
3 Løppenthin K, Esbensen B A, Østergaard M, Ibsen R, Kjellberg J, Jennum P. Morbidity and mortality in patients with rheumatoid arthritis
compared with an age- and sex-matched control population: A nationwide register study. J Comorb. 2019; 9: 223.
4 Bullock J, Rizvi SAA, Saleh AM, Ahmed SS, Do DP, Ansari RA, et al. Rheumatoid Arthritis: A Brief Overview of the Treatment. Med Princ Pract.
2018;27(6):501–507.
5 Scherer HU, Haupl T, Burmester GR. The etiology of rheumatoid arthritis. Journal of Autoimmunity [Internet]. 2019 [Cited on 2021 March 8].
Available from: https://doi.org/10.1016/j.jaut.2019.102400
6 Deane KD, Demoruelle MK, Kelmenson LB, Kuhn KA, Norris JM, Holers VM. Genetic and environmental risk factors for rheumatoid arthritis.
Best Pract Res Clin Rheumatol. 2017; 31(1): 3–18.
PATHOGENESIS7
Rheumatoid arthritis (RA) is characterized by persistent joint inflammation leading to cartilage and
bone damage, disability and eventually resulting in systemic complications. The progression of the
disease may lead to loss of functionality, reduce quality of life and enhance morbidity and mortality.
RA pathogenesis is the result of a complex interaction between genetic and environmental factors,
inducing the aberrant activation of innate and adaptative immune system which cause the breakdown
of immune tolerance, autoantigen presentation with antigen specific T and B cells activation and
aberrant inflammatory cytokines production.
The initial disease stage of RA is associated with alteration of immune system with consequent
production of autoantibodies, targeting various molecules including modified self-epitopes. In the
following stages of the disease, both the innate (e.g., dendritic cells, macrophages and neutrophils) and
adaptive immune cells (e.g., B and T lymphocytes) contribute to the amplification and perpetuation
of the chronic inflammatory state. The cascade of events leads to synovitis, proliferation of synovia
and cartilage and subchondral bone destruction. 8 (Figure 1)
The intestinal tract is another mucosal organ implicated in the pathogenesis of RA because dysbiosis
in RA patients can result from the abundance of certain rare bacterial lineages. It is well documented
that gut microbiota may contribute to the pathogenesis of RA via multiple molecular mechanisms.8
Stages in pathogenesis of RA
7 Calabresi E, Petrelli F, Bonifacio AF, Puxeddu I, Alunno A. One year in review 2018: pathogenesis of rheumatoid arthritis. Clin Exp Rheumatol.
2018; 36(2): 175-184.
8 Guo Q, Wang Y, Xu D, Nossent J, Pavlos NJ, Xu J. Rheumatoid arthritis: pathological mechanisms and modern pharmacologic therapies. Bone
Res. 2018; 6: 15. Available from: https://doi.org/10.1038/s41413-018-0016-9
DIAGNOSIS1,2,4
The clinical diagnosis of RA is largely based on signs and symptoms of a chronic inflammatory
arthritis, with laboratory and radiographic results. 2010 American College of Rheumatology criteria
(ACR) is used for early diagnosis of RA.
The presence of radiographic joint erosions or subcutaneous nodules may confirm the diagnosis in
the later stages of the disease.
These criteria do not take into account whether the patient has rheumatoid nodules or radiographic
joint damage because these findings occur rarely in early RA..
Criterion Score
Joint affected
1 large joint 0
2-10 large joints 1
1-3 small joints 2
4-10 small joints 3
>10 joints including at least one small joint 5
Serology
9 Sanchez PC, Novarro PR. Physiology and pathology of Autoimmune Diseases: Role of CD4+T cells in Rheumatoid Arthritis. Intechopen.
In: Rezaei N, editor. Physiology and pathology of immunology. [Internet]. 2017 [Cited on 2021 March 8]. Available from: http://dx.doi.
org/10.5772/intechopen.70239
Clinical presentation1,2,4
The typical presentation is with pain, swelling and morning stiffness affecting the small joints of
hands, feet, and wrists. The most frequently involved joints are wrists, metacarpophalangeal (MCP)
and proximal interphalangeal (PIP) joints. However, distal interphalangeal (DIP) joint involvement
may occur in RA, but it usually is a manifestation of co-existent osteoarthritis.4 Flexor tendon
tenosynovitis is a frequent hallmark of RA and leads to decreased range of motion, reduced grip
strength, and ‘trigger’ fingers.1
Signs/ Symptoms
• Joint pain
• Early morning joint stiffness lasting for more than 1 hour that eases with physical activity
• Joint tenderness
• Swelling of joint
• Redness of joint
• Limited range of motion.
RA may result in a variety of extra-articular manifestations during its clinical course, even prior to
the onset of arthritis. Some extra-articular manifestations are as follows:1,2,10
Extra-articular manifestations
• Systemic • Fever
• Weight loss
• Fatigue
• Susceptibility to infection
• Musculoskeletal • Muscle wasting
• Tenosynovitis
• Bursitis
• Osteoporosis
• Haematological • Anaemia
• Thrombocytosis
• Neutropenia
• Eosinophilia
• Lymphoma
• Neurological • Cervical myelopathy
• Peripheral neuropathy
• Cervical cord compression
• Occular • Keratoconjunctivitis sicca
• Episcleritis
• Scleritis
• Lymphatic • Felty syndrome
• Splenomegaly
• Cardiac • Pericarditis
• Myocarditis
• Endocarditis
• Ischemic heart disease
• Pulmonary • Nodules
• Pleural effusion
• Bronchiolitis
• Interstitial lung disease
• GI • Vasculitis
• Endocrine • Hypoandrogenism
• Skin • Rheumatoid nodules
• Purpura
• Pyoderma gangrenosum
10 Das S, Padhan P. An Overview of the Extraarticular Involvement in Rheumatoid Arthritis and its Management. J Pharmacol Pharmacother.
2017;8(3):81–86.
INVESTIGATIONS 1,2,11
Investigation Findings
RF (Rheumatoid Factor) • Positive
• RF is a relatively good biomarker for establishing the
diagnosis of RA.
ACPA (Anti- Citrullinated Peptide Antibody) • Positive
• It is highly sensitive and specific serological marker of RA.
CRP (C-Reactive Protein) Elevated
ESR (Erythrocyte Sedimentation Rate) Elevated
X-ray It shows reduced joint space, erosion of articular margins,
subchondral cysts, juxta-articular rarefaction, soft tissue
shadow at the level of the joint because of joint effusion or
synovial hypertrophy, deformities of hand and fingers.
MRI (Magnetic Resonance Imaging) Detects erosions earlier than an X-ray
Ultrasound Ultrasound (US) is able to provide high resolution multiplanar
images of soft tissue, cartilage and bone profiles.
Disease activity is based on validated scales which are obtained from the tender joint count, swollen
joint count, global patient assessment, physician global assessment, and/or marker of inflammation.
These are:
DAS28-ESR (Disease Activity Score): The Disease Activity Score (DAS) 28 is a scoring of 28 tender
or swollen joints, a patient global assessment, and a physician global assessment on VAS (in
mm), along with ESR.
DAS28-CRP (Disease Activity Score): The Disease Activity Score (DAS) 28 is a scoring of 28 tender
or swollen joints, a patient global assessment, and a physician global assessment, along with CRP.
11 Šenolt L, Grassi W, Szodoray P. Laboratory biomarkers or imaging in the diagnostics of rheumatoid arthritis? BMC Med. 2014;12:49.
12 Nakajima A, Aoki Y, Terayama K, Sonobe M, Takahashi H, Saito M, et al. Health assessment questionnaire-disability index (HAQ-DI) score at the
start of biological disease-modifying antirheumatic drug (bDMARD) therapy is associated with radiographic progression of large joint damage
in patients with rheumatoid arthritis. Mod Rheumatol. 2017; 27(6):967-972.
13 Heaney A, Stepanous J, Rouse M, McKenna SP. A Review of the psychometric properties and use of the Rheumatoid Arthritis Quality of Life
Questionnaire (RAQoL) in Clinical Research. Current Rheumatology Reviews. 2017;13(3):197-205.
14 Machold KP. Prevention and cure of rheumatoid arthritis: is it possible? Best Prac Res Clin Rheumatol. 2010;24(3):353-361.
15 Muñoz JGB, Giraldo RB, Santos AM, Bello-Gualteros JM, Rueda JC, Saldarriaga EL, et al. Correlation between rapid-3, DAS28, CDAI and SDAI as
a Measure of Disease Activity in a Cohort of Colombian Patients with Rheumatoid Arthritis. Clin Rheumatol [serial online]. 2016;36(5). DOI:
10.1007/s10067-016-3521-5
16 Canhao H, Rodrigues AM, Gregorio MJ, Dias SS, Gomes JAM, Santos MJ, et al. Common Evaluations of Disease Activity in Rheumatoid Arthritis
Reach Discordant Classifications across Different Populations. Front med [serial online]. 2018; 5:40. DOI: 10.3389/fmed.2018.00040
Simplified Disease Activity Index (SDAI): This includes the sum of tender and swollen joint counts
[28 joints] and patient and physician global assessments and CRP.
Clinical Disease Activity Index (CDAI): The sum of tender and swollen joint counts [28 joints] and
patient and physician global assessments. This helps to generate specific cut-off values that are
used to classify RA as in remission or in a low, moderate, or high activity state.
Routine Assessment of Patient Index Data 3 (RAPID3): It is a measure of physical function, pain
and global status, and is used mostly by US rheumatologists in clinical practice.
American College of Rheumatology (ACR) criteria for percentage improvement in involved joint
count (e.g., ACR 20, ACR 50, and ACR 70).
RED FLAGS17
• Cardiovascular disease (especially hypertension, atrial fibrillation, sinus tachycardia with right
bundle branch block, infective endocarditis or myocardial infarction)
• Lung disease (interstitial lung disease, asthma, pulmonary fibrosis and infection, e.g.,
tuberculosis)
• Gastrointestinal disease (e.g., cholelithiasis, gastritis, peptic ulcer disease, diverticular disease,
and hemorrhoidal disease)
• Osteoporosis or osteopenia (reduced bone mineral density)
• Malignancies.
COMPLICATIONS1,2,18
• Infections
• Chronic anemia
• Gastrointestinal cancers
• Pleural effusions
• Osteoporosis
• Heart disease
• Sicca syndrome
• Felty syndrome
• Lymphoma.
MANAGEMENT
General management1,2,4,20,21
The main goal is to control inflammation, relieve pain and reduce disability associated with rheumatoid
arthritis. Management of the patient with rheumatoid arthritis can be divided into two parts:
Non-pharmacological treatment19,20
1. Patient education: Educating patient about the disease condition and methods for managing the
condition via healthy lifestyle behaviors.
19 Cunningham NR, Zuck SK. Nonpharmacologic Treatment of Pain in Rheumatic Diseases and Other Musculoskeletal Pain Conditions. Curr
Rheumatol Rep. 2013; 15(2): 306.
20 King M. Management of Edema. J Clin Aesthet Dermatol. 2017;10(1):E1-4.
2. Rest
3. Exercise: Exercises can improve and maintain range of motion of the joints.
4. Physiotherapy: This consists of:
(i) Use of splints and braces for correction of joint deformities and to provide joint support
5. Occupational therapy: Role of occupational therapy is to help the patient cope with his
occupational requirements in the most comfortable way, by modifying them.
6. Nutrition and dietary therapy: Weight loss may be recommended for overweight and obese
people to reduce stress on inflamed joints. Obesity is a risk factor for more rapid progression of
joint damage. This should be explained to obese patients and strategies must be offered on how
to lose and maintain an appropriate weight.
Homoeopathic management
Research studies indicate that homoeopathic medicines may play a considerable role in reducing
the symptoms of joint inflammation, frequency, duration and severity of the attacks in rheumatoid
arthritis and delay the onset of complications.21,22,23
Homoeopathic constitutional similimum improves the quality of life of patients with RA by reducing
intensity of pain, limiting disability and reducing disease activity.24 Thus the general improvement
of the patients limits the need of analgesics and DMARDs in RA. There are many medicines available
in the homoeopathic literature which can be selected based on presenting totality of each case for
the treatment of RA.
In Synthesis repertory25, 302 medicines are found in chapter EXTREMITIES under the rubric ‘Pain-
rheumatic’. The frequently verified characteristic features of some organospecific remedies are:
Actea spicata: Rheumatic pains in small joints, wrist, fingers, ankles, toes. Swelling of joints from
slight fatigue. Wrist swollen, red, worse by motion. Calcarea fluorica: Chronic synovitis of knee
joint. Worse during rest, change of weather, better warm application. Caulophyllum: Special affinity
for the smaller joints, severe drawing, erratic pain and stiffness in small joints, fingers, toes, ankles
etc. Guaiacum officinale: Rheumatic pain in shoulders, arms and hands; immovable stiffness. Worse
in heat, cold weather. Stellaria medica: Rheumatism, darting, shifting pains in all parts; stiffness of
joints; parts sore to touch; worse by motion. Formica rufa: Rheumatic pains, stiff and contracted
21 Gibson RG, Gibson S, MacNeill AD, Buchanan WW. Homoeopathic therapy in rheumatoid arthritis: evaluation by double blind clinical
therapeutical trial. Br J Clin Pharmacol. 1980;9(5):453–9.
22 Andrade LE, Ferraz MB, Atra E, Castro A, Silva MS. A randomized controlled trial to evaluate the effectiveness of homeopathy in rheumatoid
arthritis. Scand J Rheumatol. 1991;20(3):204–8.
23 Gibson RG, Gibson SL, MacNeill AD, Gray GH, Dick WC, Buchanan WW. Salicylates and homoeopathy in rheumatoid arthritis: preliminary
observations. Br J Clin. Pharmacol. 1978; 6(5): 391-395.
24 Rao P, Nagalakshmi PM. Immunological studies on Rheumatoid Arthritis treated with Homeopathic drugs: Results of the Pilot Study. Indian
Journal of Research in Homoeopathy. 2008;2(4):42-49.
25 Schroyens F. Synthesis Repertory ver. 9.1. New Delhi: B Jain Publishers Pvt. Ltd.; 2002.
joints, pains worse by motion and better by pressure. Lithium carbonicum: Rheumatism of small
joints. Chronic rheumatism connected with heart lesions. Rheumatic nodes. Better by hot water.
26 Clarke JH. A Dictionary of Practical Materia Medica, large edition, New Delhi: B Jain Publishers Pvt Ltd;2005
27 Boericke W. Pocket Manual of Homoeopathic Materia Medica & Repertory, 9th ed. New Delhi: B Jain Publishers (P) Ltd.: 2008
28 Allen HC. Allens Keynotes rearranged and classified with leading remedies of the Materia Medica and bowel nosodes, 9th ed. New Delhi: B Jain
Publishers Pvt Ltd;2017.
Colchicum Colchicum is best known as a remedy in • Joints stiff and feverish; shifting
autumnale gout and rheumatism. It affects markedly rheumatism
the muscular tissues, periosteum, and • Parts are red, hot, swollen, with tearing
synovial membranes of the joints. There pains
is always great prostration, internal • Inflammation of great toe, gout in heel,
coldness, and tendency to collapse. Bad cannot bear to have it touched or moved
effects from suppressed sweat. The smell • Knees strike together, can hardly walk
of food causes nausea even to fainting, • Hot oedematous swelling and coldness of
especially fish the legs and feet, with acute pain during
movement
• Worse in the evening and at night
• Better by stooping
Pulsatilla nigricans Hot patient; marked changeability of • Sharp, jerking, and drawing pains in
symptoms; aversion to fatty foods, warm shoulder joint as well as in the arms,
foods and drinks, dislikes butter; thirstless hands and fingers
with great dryness of mouth; tongue • Sensation of tension and swelling and
coated yellow or whitish; worse towards wrenching pain in joints of elbows, hands
evening and in warm room, better in and fingers, with rigidity
open air, by slow, gentle motion and cold • Pain in limbs, shifting rapidly; tensive
applications; desire for company, mild, pain, letting up with a snap
gentle, affectionate, yielding, weeping • Knees swollen, with tearing, drawing
disposition pains
• Feet red, inflamed, swollen. Legs feel
heavy and weary
• Worse on beginning to move, lying on left
side, from letting the affected limb hang
down
• Better in the open air, cold applications.
Medorrhinum Weak memory. Time passes too slowly; • Legs heavy, ache all night, cannot keep still
cannot speak without weeping; loses the • Burning of hands and feet
thread of conversation. State of collapse • Finger joints enlarged, puffy
and trembling all over; wants to be • Restless, better clutching hands
fanned all the time. Intense restless and • Painful stiffness of every joint in the body
fidgety legs and feet. Very thirsty. Craving • Deformity of finger joints, large puffy
for liquor, salt, sweets, warm drinks knuckles, swelling and painful stiffness of
ankles
• Worse when thinking of it, from least
movement, from daylight to sunset
• Better at the seashore, lying on stomach, in
damp weather
No Improvement Yes
Red flags
• Cardiovascular disease
Symptoms persist No symptoms
• Lung diseases
• Gastrointestinal disease
• Osteoporosis or
osteopenia Re-assess the case and give Stop treatment and
• Malignancy appropriate homoeopathic monitor regularly
treatment
SCABIES
CASE DEFINITION1
Scabies is a parasitic infestation of the skin caused by the mite Sarcoptes scabiei var. hominis. In
developed countries, scabies outbreaks are common in residential and nursing care homes where
they cause significant morbidity and distress.
INCIDENCE/PREVALENCE2,3,4,5,6,7,8
• The burden of scabies is greater in resource-poor tropical regions, especially in children (5-10 %),
adolescents, and elderly people.
• Scabies has been recognised as a “neglected tropical disease” (NTD) by the World Health
Organisation.
• Worldwide, scabies is responsible for 0.07% of the total burden of diseases. Prevalence estimates
in the recent scabies-related literature range from 0.2% to 71%.
• It causes significant global morbidity, with an estimated 300 million cases annually.
• In India, the incidence of scabies ranges from 13% to 59% in rural and urban areas.
• Scabies mites burrow into the top layer of the epidermis where the adult female lays eggs. The
eggs hatch in 3-4 days and develop into adult mites in 1-2 weeks. After 4–6 weeks, the patient
develops an allergic reaction to the presence of mite proteins and faeces in the scabies burrow,
causing intense itching and rashes. Most individuals are infected with 10-15 mites.2
• Transmission: The microscopic scabies mites are almost always transmitted by direct prolonged
skin-to-skin contact with a person who is already infested. An infected person can spread scabies
even if he or she has no symptoms. Humans are the source of infestation; animals do not spread
human scabies.9
• It is an intensely itchy dermatosis caused by the mite Sarcoptes scabiei. Scabies presents within
two to six weeks of initial infestation, but reinfestation can provoke symptoms within 48 hours.10
1 Chandler DJ, Fuller LC. A Review of Scabies: An Infestation More than Skin Deep. Dermatology. 2019;235(2):79-90.
2 World Health Organization. Neglected Tropical Disease: Scabies and other ectoparasites [Internet].2012 [Cited on 2020 September 14)
Available from: https://www.who.int/neglected_diseases/diseases/scabies-and-other-ectoparasites/en/
3 World Health Organization. Epidemiology and management of common skin diseases in children in developing countries [Internet]. 2005
[Cited on 2021 March 04]. Available from: https://apps.who.int/iris/handle/10665/69229
4 Engelman D, Kiang K, Chosidow O, McCarthy J, Fuller C, Lammie P, et al. Toward the Global Control of Human Scabies: Introducing the
International Alliance for the Control of Scabies. PLoSNegl Trop Dis. 2013; 7(8): e2167.
5 Banerji A. Scabies. Paediatr Child Health. 2015;20(7):395-398.
6 Karimkhani C, Dellavalle RP, Coffeng LE, Flohr C, Hay RJ, Langan SM, et al. Global skin disease morbidity and mortality: An update from the
Global Burden of Disease Study 2013. JAMA Dermatology. 2017;153(5):406–12.
7 Karimkhani C, Colombara DV, Drucker AM, Norton SA, Hay R, Engelman D, et al. The global burden of scabies: a cross-sectional analysis from
the Global Burden of Disease Study 2015. Lancet Infect Dis. 2017;17(12):1247-1254.
8 Nair PA, Vora RV, Jivani NB, Gandhi SS. A Study of Clinical Profile and Quality of Life in Patients with Scabies at a Rural Tertiary Care Centre. J
ClinDiagn Res. 2016;10(10): WC01-WC05.
9 Centers for Disease Control and Prevention guideline. Scabies [Internet]. 2010 [Cited on 2020 August 14] Available from: https://www.cdc.
gov/parasites/scabies/gen_info/index.html
10 Johnston G, Sladden M. Scabies: diagnosis and treatment. BMJ. 2005;331(7517):619-622.
• Scabies affects all age groups and both sexes, but the most vulnerable age groups are young
children and the elderly in resource-poor communities who are especially susceptible to scabies
as well as to the secondary complications of infestation (Figure 1).11,12
Figure 1: Life cycle image of mite Sarcoptes scabiei var. hominis. Courtesy: Scabies: Centers for Disease Control and
Prevention guideline:2010.
RISK FACTORS11,13,14,15
• Scabies is transmitted by close personal contacts. Infants and children are therefore particularly
liable to infection from close physical contact with other children and adults at home and at
school.
11 World Health Organization. Scabies epidemiology [Internet]. 2017 [Cited on 2020 September 18]. Available from: http://www.who.int/
lymphatic_filariasis/epidemiology/scabies/en/
12 Chosidow O. Clinical practice. Scabies. The New England Journal of Medicine. 2006;354(16):1718–172.
13 FDRE MOH. Scabies Outbreak Preparedness and Response Plan [Internet]. 2015 [Cited on 2020 September 14]. Available from: https://www.
humanitarianresponse.info/sites/www.humanitarianresponse.info/files/documents/files/fmoh_scabies_response_plan-_29_dec_2015.docx_.
pdf
14 Raza, N, Qadir, SNR, Agha H. Risk factors for scabies among male soldiers in Pakistan: case-control study. EMHJ. 2009;15(5):1105-1110.
15 Sara J, Haji Y, Gebretsadik A. Scabies Outbreak Investigation and Risk Factors in East Badewacho District, Southern Ethiopia: Unmatched
Case Control Study. Dermatology Research and Practice [Internet]. 2018 [Cited on 2021 March 9]. Available from: https://doi.
org/10.1155/2018/7276938
• It is reported that overcrowded living conditions, sleeping together, sharing of clothes, sharing
of towels, poor hygiene practices, malnutrition, and travel to scabies outbreak areas are common
risk factors for scabies.
• Outbreaks can occur among elderly people in nursing homes and can be transmitted to nursing
staff. Transmission between adults is often by sexual contact.
DIAGNOSIS 1,2,9,10,12,16,17,18,19
• Pruritus is the hallmark of scabies regardless of age which develops 6-8 weeks after the exposure.
• Severe itching (pruritus), especially at night, is the earliest and most common symptom of
scabies.
• The most common presenting lesions are papules, vesicles, pustules, and nodules.
• The pathognomonic sign is the burrow; a short, wavy, scaly, grey line on the skin surface. These
burrows appear as tiny raised and crooked (serpiginous) greyish-white or skin-colored lines on
the skin surface.
• History of itching in several family members over the same period is almost pathognomonic.
• Individuals with crusted scabies present with thick, exfoliating crusts that may be more
widespread, including the face.
• Itching and rash may affect much of the body or be limited to common sites such as between the
fingers, wrist, axilla, elbow, groins, penis, nipple, waist, buttock, shoulder blades; in infants and
young children, the palms, soles and head (face, neck and scalp) are more commonly involved.
• Infants and small children may have a more widespread rash, including involvement of the
palms, soles of the feet, ankles, and sometimes the scalp. Inflammatory scabies nodules may be
seen, particularly on the penis and scrotum of adult males and around the breasts of females.
16 Khanna N. Illustrated synopsis of dermatology and sexually transmitted diseases. 4th edition; India: Reed Elsevier India pvt limited;
2011:p.288.
17 Burkhart CN, Burkhart CG. Scabies, other mites, and pediculosis. In: Wolff K, Goldsmith L, Katz S, Gilchrest B, Paller AS & Leffell D,
editors. Fitzpatrick’s Dermatology in General Medicine, 8th Edition. New York: McGraw-Hill; 2011:p.2570.
18 Walton SF, Currie BJ. Problems in Diagnosing Scabies, a Global Disease in Human and Animal Populations.Clinical Microbiology Reviews.
2007;20(2):268-279.
19 Leung V, Miller M. Detection of scabies: A systematic review of diagnostic methods. Can J Infect Dis Med Microbiol. 2011;22(4):143-146.
COMPLICATIONS
Post-scabetic pruritus, secondary bacterial infection (esp. Streptococcus pyogenes) due to disruption
of skin barrier, nodular scabies or pseudo-lymphoma, acute post-streptococcal glomerulonephritis,
rheumatic heart disease, acute renal damage, impetigo and septicaemia.
INVESTIGATIONS15
• Skin scrapings are central to diagnosis and involve the application of one or two drops of
mineral oil to a suspected lesion, which is then scraped or shaved with a scalpel or a microscope
slide. The specimens are examined directly under a low-power light microscope. A small number
of mites on an infected individual can often negate or delay a diagnosis.
• ‘Burrow Ink Test’ (BIT) in which fountain pen ink is gently rubbed on a suspicious site. Excess
ink is wiped off with an alcohol swab, making the burrow visible as a wavy ink-filled line in the
stratum corneum where the mite has tunnelled.
• Epiluminescence microscopy using a dermatoscope, is the technique which relies on
identifying a triangular structure, which corresponds to the anterior section of the mite including
the mouth part and the two pairs of front legs.
• Classic scabies: Impetigo, furunculosis, eczema, bites (mosquitoes, midges, fleas, lice, bedbugs,
chiggers, other mites), tinea corporis, paronychia, papular urticarial and other allergic reactions,
20 Monsel G, Delaunay P, Chosidow O. Arthropods. In: Griffiths C, Barker J, Bleiker T, Chalmers R, Creamer D, editors. Rook’s textbook of
dermatology. 9th ed. Hoboken: Wiley & Sons;2016: p.201.
21 Currier R, Walton S, Currie B. Scabies in animals and humans: history, evolutionary perspectives, and modern clinical management. Annals of
the New York Academy of Sciences. 2011; 1230:E50-60.
22 Hardy M, Engelman D, Steer A. Scabies- A clinical Update. Focus. The Royal Australian College of General Practitioners. 2017; AFP 46 (5):264-
268.
RED FLAGS16
PREVENTION 29,30
• Early detection and implementation of infection control measures are keys in preventing further
transmission.
• Avoid direct skin-to-skin contact with an infected person or with items such as clothing or
bedding used by an infected person.
• All household members and other potentially exposed persons should be treated at the same
time as the infested person, to prevent possible re-exposure and re-infestation.
• Treatment usually is recommended for members of the same household, particularly for those
who have prolonged skin-to-skin contact.
23 Davis JS, McGloughlin S, Tong SY, Walton SF, Currie BJ. A novel clinical grading scale to guide the management of crusted scabies. PLoSNegl
Trop Dis. 2013;7(9): e2387.
24 Elman S, Hynan LS, Gabriel V, Mayo MJ. The 5-D itch scale: a new measure of pruritus. Br J Dermatol. 2010;162(3):587-93.
25 Reich A, Bożek A, Janiszewska K, Szepietowski JC. 12-Item Pruritus Severity Scale: Development and Validation of New Itch Severity
Questionnaire. Biomed Res Int [Internet].2017 [Cited on 9 March 2021]. Avilable from: https://www.hindawi.com/journals/
bmri/2017/3896423/
26 Morgan M, McCreedy R, Simpson J, Hay RJ. Dermatology quality of life scales- a measure of the impact of skin diseases. Br J Dermatol.
1997;136(2):202-206.
27 Basra MK, Sue-Ho R, Finlay AY. The Family Dermatology Life Quality Index: measuring the secondary impact of skin disease. Br J Dermatol.
2007;156(3):528-538.
28 Pereira MP, Ständer S. Assessment of severity and burden of pruritus. Allergol Int. 2017;66(1):3-7.
29 Centre for disease control and prevention. Parasites: Prevention & control, CDC Scabies- Prevention and Control [Internet]. 2010 [Cited on:
2020 August 14]. Available from: https://www.cdc.gov/parasites/scabies/prevent.html
30 Ministry of Health, Malaysia. Guideline for Management of Scabies in Adults and Children [Internet]. 2015 [Cited on 2020 August 14]
Available from: file:///C:/Users/USER/Downloads/Guideline%20For%20Management%20Of%20Scabies%20In%20Adults%20And%20
Children.pdf
MANAGEMENT 1,21,23
General management
• Patients with scabies and their close physical contacts, even without symptoms, should receive
treatment at the same time. Prescriptions must be provided for all household members and
sexual partners.
• Avoid wearing damp clothes as the mites can thrive and multiply if favorable conditions are
provided.
• Bedding or clothing worn or used next to the skin anytime during the three days before treatment
should be machine-washed using hot water at high temperature (>50°C) and dried or kept in
a plastic bag for up to 72 hours, because mites that are separated from the human host will die
within this time period.
• Mattresses should be thoroughly vacuumed, ironed or steam cleaned, paying particular attention
to the seams.
• Where possible, amenities such as toilets and chairs should not be shared.
• To avoid scratching the skin hard as that can lead to the secondary skin infections.
• Patient and family members should use fresh, clean bedding and clothing to avoid recurrence.
• School children with scabies should be given leave from school and should be notified of the
case. Parents of other children who may have been exposed to children with scabies should be
notified by a letter from the school.
Homoeopathic management
The totality of various characteristic signs and symptoms exhibited by the patient leads to the similar
remedy. The homoeopathic concept of health is ‘holistic’ and ‘individualistic’.31
For this individualisation of the patient, the ‘totality of symptoms’ which is not merely the numerical
aggregate of all the symptoms but includes the idea or plan which unites them in a special manner
to give them its characteristic form.32 The miasmatic background of each case must be taken into
consideration while selecting the remedy. Hahnemann has considered psora responsible for the
production of scales, crusts, and pruritus.33
Some medicines that can be specifically useful in treatment of scabies are: Anthrakokali: Papular
eruptions with a vesicular tendency, especially on the scrotum. Croton tiglium: Intense itching
but scratching is painful. Worse during summer, touch, at night and in the morning, washing. Rhus
venenata: Itching relieved by hot water. Selenium: Dry scaly eruptions with itching. Itching around
ankles and folds of skin, between fingers; in palms.
31 Hahnemann S. Organon of Medicine. 3rd Indian Reprint. Calcutta: Economic Homoeo Pharmacy; 2012.
32 Close S. The Genius of Homoeopathy. Reprint ed. New Delhi: B Jain Publ (P) Ltd; 1995.p.153-4,194.
33 Hahnemann S. The Chronic Diseases Their Peculiar nature and Their Homoeopathic cure.14th Impression, vol-I. New Delhi: B. Jain Publishers
(P) Ltd;2014: p.39.
Psorinum Extremely chilly patient, wants to cover • Patients lack immunity, catch infections
even in hottest summer weather; pale, very quickly, and recover slowly
delicate, sickly; scanty perspiration; • Blisters exude pus with extreme itching
offensive discharges; wakes up at night which is worse at night and warmth of bed
feeling hungry; anxious, fearful, child is • The skin complaints tend to return every
good all day while restless and troublesome winter
at night • Scalp is dry, scaly or moist, suppurating
eruptions
• Skin inactive, dry & dirty look
• Worse from changes of weather, cold
• Better in heat, warm clothing, in summers
Sepia Chilly patient; tall, thin built with yellow • Indicated in scabies where the lesions are
saddle across upper part of cheeks and yellowish brown and scaly
nose, big belly; dry flabby skin. Predisposed • Most common affected areas are bends of
to take cold at change of weather. Desire the elbows and knees
for sour food which aggravates. Irregular • Worse from washing
menses. Cheerful, active when well but • Better by exercise, warmth of bed
indifferent and quarrelsome when sick, self-
absorbed, sad, weeping and indolent
Causticum Dark-complexioned and rigid-fibered • Indicated when scabies affects the webs of
persons. Restlessness at night, with fingers and folds of skin with itching and
tearing pains in joints and bones, and soreness
faint-like sinking of strength. Emaciation • Worse from becoming cold, from getting
due to disease, worry, etc, and of long wet or bathing
standing. Intense sympathy for suffering of
others. Burning, rawness, and soreness are
characteristic. Worse: dry, in clear
fine weather. Better, in damp, wet weather
34 Allen HC. Keynotes and characteristics with comparisons of the leading remedies of the Materia Medica; 11th impression, New Delhi: B. Jain
Publishers Pvt. Ltd; 2012.
35 Boericke W. Pocket manual of homoeopathic Materia Medica. Reprint ed. New Delhi B. Jain Publishers Pvt. ltd;1998.
Graphites Chilly patient, takes cold easily; fatty; • Lesions crack and ooze a clear or sticky
pale; tendency to skin affections and yellowish discharge when scratched
constipation; lumpy, thick, hard; history • Unhealthy skin and every little injury
of delayed menstruation; skin and glands; suppurate
dislikes sweets; cautious, indecisive and • Cracks or fissures in ends of fingers,
lazy nipples, of anus & between the toes
• Worse from warmth, at night
• Better in dark, from wrapping up
Hepar Extremely chilly patient; hypersensitive • Unhealthy skin, every little injury
sulphuris (to cold, pain), Faints easily; scrawny; suppurates
Glandular constitution; Profuse sweat; • Great sensitiveness to slightest touch,
Irritable; difficult to please, slow to act burning, stinging, easily bleeding
• Worse from dry cold winds
• Better from warmth, damp weather,
wrapping up head
General management
• All bed linens and clothes Start homoeopathic
worn next to skin to be treatment and advise general
washed in hot water management
• Do not scratch the skin
hard
• Nails must be clipped to
avoid scratching
• Patient must be isolated
for first 24 hours of
treatment No Improvement Yes
• Treat all the household
members at the same
time
• School going children
Continue homoeopathic
may take leave from Re-assess and change the
treatment
school prescription/ potency/
repetition if required
RED FLAGS
• Secondary skin infections
• Acute glomerulonephritis Improvement Yes Check for complete resolution
• Eczematisation
• Crusting of skin
No
SCIATICA SYNDROME
case DEFINITION1,2
Sciatica Syndrome is a set of symptoms including pain caused by general compression or irritation
of one of five spinal nerve roots of each sciatic nerve or by compression or irritation of the left or
right or both sciatic nerves. Sciatica is a set of symptoms rather than a diagnosis for what is irritating
the root of the nerve to cause the pain.
INCIDENCE/PREVALENCE 2,3,4
Exact data on the incidence and prevalence of sciatica are lacking. In general, an estimated 5%-
10% of patients with low back pain have sciatica, whereas the reported lifetime prevalence of low
back pain ranges from 49% to 70%. The annual prevalence of disc related sciatica in the general
population is estimated at 2.2%.
• No gender predominance.
• Occurs in fourth to fifth decade and then declines; rarely seen before the age of 20 years unless
due to trauma.
• No association with body height has been established except in the age group 50 to 60 years.
• Genetic predisposition: more significant in monozygotic; individuals under 40 years.
• Physical activity increases incidence in those with prior sciatica symptoms.
• Occupational: subject to physically awkward positions or strenuous physical activity (e.g.,
machine operators, truck drivers).
• Smoking and mental stress can be other risk factors.
AETIOLOGY 2,3
Any condition that may structurally impact or compress the sciatic nerve may cause sciatica
symptoms. The most common cause of sciatica is a herniated or bulging lumbar intervertebral disc.
• Spondylolisthesis
• Lumbar or pelvic muscular spasm and/or inflammation
• Spinal or paraspinal mass including malignancy
1 National Guideline Centre (UK). Low Back Pain and Sciatica in Over 16s: Assessment and Management. London: National Institute for Health
and Care Excellence (UK) [Internet]. 2016 [cited on 11 March 2021]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK401577/
2 Davis D, Arvind, Maini K, Vasudevan A. Sciatica. StatPearls Publishing [Internet]. 2020 [Cited on 8 March 2021]. Available from: https://www.
ncbi.nlm.nih.gov/books/NBK507908/
3 Stafford MA, Peng P, Hill DA. Sciatica: a review of history, epidemiology, pathogenesis, and the role of epidural steroid injection in
management. British Journal of Anaesthesia. 2007;99(4):461-73.
4 Koes BW, van Tulder MW, Peul WC. Diagnosis and treatment of sciatica. BMJ. 2007; 334(7607): 1313–1317.
Clinical presentation2,4,5
Physical examination6
• Patrick sign
• Straight leg raising (SLR) test
• Crossed SLR sign
• Reverse SLR sign.
INVESTIGATIONS4, 5, 6
Diagnostic imaging is only useful if the results influence further management. In acute sciatica the
diagnosis is based on history taking and physical examination. Imaging may be indicated at this
stage only if there are indications or “red flags” signs (mentioned below).
• Plain X-ray of the lumbar spine: helps to rule out fracture, spondylolisthesis, malignant
infiltration of a vertebral body.
• Non-contrast CT scan, especially using spiral scanning techniques, can provide helpful images
of the disc protrusion and/or narrowing of the exit foramina.
• MRI: investigation of choice if available, since soft tissues are well imaged.
• Electromyography: used to access the functional integrity of the peripheral nervous system.
COMPLICATIONS/RED FLAGS4
• Malignancies
• Osteoporotic fractures
• Radiculitis
• Cauda equina syndrome.
DIFFERENTIAL DIAGNOSIS3
• Epidural abscess
• Epidural hematoma
• Tumor
• Pott’s Disease, also known as spinal tuberculosis
• Piriformis syndrome.
PREVENTION2, 3, 4
• Advise to stay active and continue daily activities; a few hours of bed rest may provide some
symptomatic relief but does not result in faster recovery.
• Use of hot or cold packs for comfort and to decrease inflammation.
• Avoidance of inciting activities or prolonged sitting/standing.
• Practicing good, erect posture.
• Engaging in exercises to increase core strength.
• Gentle stretching of the lumbar spine and hamstrings.
• Regular light exercises such as walking, swimming, or aquatherapy.
• Use of proper lifting techniques.
Most cases of sciatica resolve in less than 4 to 6 weeks with no long-term complications even if no
medical therapy is sought. In more severe cases or cases where the neurologic deficit is present,
the patient may have a more prolonged course of recovery. However, recovery is still excellent.
Some studies have shown that poor occupational mechanics, psychological depression, and poor
socioeconomic situations lead to an increased chance of chronic, recurrent sciatica.
MANAGEMENT2, 3, 5, 6
General management
• To do back strengthening exercises and avoid physical maneuvers (likely to strain the lumbar
spine).
• Non-pharmacological management include acupuncture, spinal manipulation, traction therapy,
physical therapy, behavioural treatment, multidisciplinary treatment.
• Deep tissue massage may be helpful in some cases.
Homoeopathic management11,12,13
Homoeopathy with its huge armamentarium of medicines and holistic approach can prove beneficial
in such cases. The homoeopathic medicines have well defined side affinity, aggravating and
ameliorating factors and can bring relief in the acute pain and paresthesis. In Synthesis repertory14,
medicines for sciatica syndrome 225 medicines are found in chapter EXTREMITIES under the rubric
‘Pain-lower limb-sciatic nerve’. High ranking medicines for right-sided sciatica - Dioscorea villosa,
Lachesis mutus, Lycopodium clavatum, Phytolacca decandra, Tellurium.
High ranking medicine for left-sided sciatica -Ammonium muriaticum, Kali bichromicum. The
specific medicines verified clinically and suggestive for sciatica syndrome are: Arsenicum album:
Cold damp cellars aggravate or bring on complaints of Sciatica. Burning pains, relieved by heat.
Gnaphalium polycephalum: Intense pain along the sciatic nerve with a feeling of numbness.
Hypericum perforatum: Lancinating pain in lower limbs (sciatica), neuritis with tingling, burning
pain, numbness and flossy skin. Iris versicolor: Sciatica, sudden shooting, causing lameness, feels
as if was wrenched. Pain extending to popliteal space, better from violent motion. Lac vaccinum
defloratum: Violent rectal and sciatic pains following every effort at defection. Lyssinum: Dull
pain in left sciatic nerve, returning periodically. Worse sight or sound of running water or pouring
water. Phytolacca decandra: Sciatica, pain involves the right leg especially the outer side of the
thigh, aggravation damp weather. Aching, soreness, restlessness, prostration, are general guiding
symptoms. Sepia: Sciatica with lancinating stitches, must get out of bed for relief. Pain worse from
rising, better from slow walking. Sciatica, better during pregnancy. Tellurium metallicum: Pain in
sacrum, passing into right thigh down the sciatic nerve, worse when pressing at stool, coughing,
laughing, also when lying on the affected side. Valeriana officinalis: Sciatica, pain aggravates when
standing and letting foot rest on floor.
11 Allen HC. Keynotes and Characteristics with Comparisons of Some of The Leading Remedies of The Materia Medica with Bowel Nosodes.
Eighth Edition. New Delhi: B. Jain Publishers (P) Ltd.; 2002.
12 Homeopathic Therapeutics for Sciatica. Hompath Software, last update on 18/12/2018, last seen on September 04, 2019.
13 Kent JT. Repertory of homoeopathic materia medica. Enriched Indian ed. New Delhi: B Jain Publishers (P) Ltd; 2007.
14 Schroyens F. Synthesis Repertory ver. 9.1. New Delhi: B Jain Publishers Pvt. Ltd.; 2002.
The medicines with indications for treatment of sciatica are mentioned below:11,15
Lac caninum The keynote symptom is, erratic pains, • Sciatica- right sided
alternating sides. Great weakness and • Backache: intense, unbearable,
prostration. Sore throat, diphtheria and across supra-sacral region,
rheumatism. Feels as if walking on air, extending to right natis and right
or of not touching the bed when lying sciatic nerve
down • Spine aches from base of brain to
coccyx, very sensitive to touch or
pressure
• Worse by rest and on first moving
Lachesis mutus Hot patient; thin and emaciated; • Sciatica, right-sided, pain as from a
hemorrhagic diathesis; great hot iron
sensitiveness to touch; hot flushes and • Worse after sleep
perspiration; Desires oysters, alcohol, • Better by appearance of discharge
farinaceous food, all complaints worse
after sleep; loquacious, jumps from one
idea to another, jealous, suspicious,
religious and indolent
Rhus toxicodendron Chilly patient; sore, body bruised and • Muscular rheumatism, sciatica, left
stiff; restless, can’t rest in any position; side
red triangular tip of tongue; worse in • Numbness and formication, after
damp, cold, rainy weather, during rest overwork and exposure
and sleep, better by continued motion; • Lameness, stiffness and pain on first
increased thirst; great apprehension at moving after rest, or on getting up in
night, sad, anxious; weeping without the morning
knowing why • Worse at night
• Better by walking or continued
motion
15 Boericke W. New manual of Homoeopathic Materia Medica with Repertory. Third Revised, Augmented Edition based on Ninth Edition. New
Delhi: B. Jain Publishers(P) Ltd.; 2007.
Radiating pain
Yes No
Red flags
• Malignancies
Start homoeopathic • Osteoporotic fractures
treatment along with lifestyle • Radiculitis
management • Cauda equina syndrome.
Yes Improvement No
SCHIZOPHRENIA
INCIDENCE/PREVALENCE2,3,4
• In 2017, there were an estimated 1.1 million new cases and a total of 19.8 million cases of
schizophrenia globally.
• About 0.3% to 0.7% of people are affected by schizophrenia during their lifetimes.
• It is equally prevalent in men and women. The onset is earlier in men than in women. The peak
ages of onset are 10-25 years for men and 25-35 years for women. When the onset occurs after
45 years, the disorder is characterized as late-onset schizophrenia.
Burden5
• Despite its relatively low prevalence, it is associated with significant health, social, and economic
concerns.
• Individuals with schizophrenia have an increased risk of premature mortality (death at a
younger age than the general population).
• Co-occurring medical conditions, such as heart disease, liver disease, and diabetes mellitus,
contribute to the higher premature mortality rate among individuals with schizophrenia. Possible
reasons for this excess early mortality are increased rates of these medical conditions and
under-detection and under-treatment of them.
• An estimated 4.9% of people with schizophrenia die by committing suicide, a rate that is far
greater than the general population, with the highest risk in the early stages of illness.
• Approximately, half of individuals with schizophrenia have co-occurring mental and/or
behavioral health disorders.
• Financial costs associated with schizophrenia are disproportionately high relative to other
chronic mental and physical health conditions, reflecting both “direct” costs of health care as
well as “indirect” costs of lost productivity, criminal justice involvement, social service needs,
and other factors beyond health care.
1 Madhivanan S, Jayaraman K, Daniel SJ, Ramasamy J. Symptomatic Remission in Schizophrenia and its Relationship with Functional Outcome
Measures in Indian Population. J Clin Diagn Res. 2017 Jan;11(1):VC05-VC07.
2 GBD 2017 Disease and Injury Incidence and Prevalence Collaborators. Global, regional, and national incidence, prevalence, and years lived
with disability for 354 diseases and injuries for 195 countries and territories, 1990–2017: a systematic analysis for the Global Burden of
Disease Study 2017. The Lancet. 2018;392 (10159): 1789–1858.
3 Sadock BJ, Sadock VA, Ruiz P. Kaplan and Sadocks Synopsis of Psychiatry Behavioral Sciences /Clinical Psychiatry. Eleventh ed. New Delhi:
Wolter Kluwer [India] Pvt Ltd; 2018.
4 Global Burden of Disease Collaborative Network. Global Burden of Disease Study 2017 (GBD 2017) Results. Seattle, United States: Institute for
Health Metrics and Evaluation (IHME); 2018.
5 National Institute of Mental Health. Schizophrenia [Internet]. 2018 [Cited Feb 11,2020]. Available from: https://www.nimh.nih.gov/health/
statistics/schizophrenia.shtml
• Environmental factors: Season of birth – late winters/ early spring/ summers have been linked
to the incidence of schizophrenia. Children growing in an urban environment are more prone to
schizophrenia. Other factors are: exposure to influenza epidemics, maternal starvation during
pregnancy, Rhesus factor incompatibility, and excess of winter births.
• Genetic and physiological: There is a strong genetic contribution in determining risk for
schizophrenia. The concordance rates of schizophrenia for monozygotic twins have been found
to be about 40 to 50%, and heritability estimates are around 80%.
• Birth and pregnancy complication hypotheses: Infants born with a history of pregnancy or birth
complications are at increased risk of developing schizophrenia as adults.
• First degree biological relatives of persons with schizophrenia have a ten times greater risk for
developing the disease than the general population.
• Biochemical factors: Dopamine, Serotonine, Nor-epinephrine, GABA, Neuropeptides, Glutamate,
Acetyl choline and Nicotine are impaired in schizophrenia.
• Age: The mean ages of onset for schizophrenia is below 45 years in men and women.
• Marital status: Reports have shown higher rates of schizophrenia for unmarried than for married
patients.
TYPES OF SCHIZOPHRENIA10
• Paranoid/ Paraphrenic type: This is the commonest type of schizophrenia. The clinical
picture is dominated by relatively stable, often paranoid, delusions, usually accompanied by
hallucinations. Disturbances of affect, volition and speech, and catatonic symptoms, are not
prominent.
• Disorganized/ Hebephrenic type: A form of schizophrenia in which affective changes are
prominent, delusion and hallucinations fleeting and fragmentary, behavior irresponsible and
unpredictable and mannerisms common. Shallow mood with often giggling or self-satisfied,
self-absorbed smiling.
• Catatonic type: Prominent psychomotor disturbances are essential and dominant features and
may alternate with extreme hyperkinesis and stupor or automatic obedience and negativism.
Constrained attitude and postures may be maintained for long periods.
• Undifferentiated/Atypical type: Condition meeting the general diagnostic criteria for
schizophrenia but not conforming to any of above subtypes or exhibiting the features of more
than one of them without a clear predominance of a particular set of diagnostic characteristics.
6 American Psychiatric Association: Diagnostic And Statistical Manual of Mental Disorders. 5th ed. Arlington VA. American Psychiatric
Association; 2013.
7 Gejman PV, Sanders AR, Duan J. The role of genetics in the etiology of schizophrenia. Psychiatr Clin North Am. 2010;33(1):35-66.
8 Chou IJ, Kuo CF, Huang YS, Grainge MJ, Valdes AM, See LC, et al. Familial Aggregation and Heritability of Schizophrenia and Co-aggregation of
Psychiatric Illnesses in Affected Families. Schizophr Bull. 2017;43(5):1070-1078.
9 Karlsgodt KH, Sun D, Cannon TD. Structural and Functional Brain Abnormalities in Schizophrenia. Curr Dir Psychol Sci. 2010;19(4):226-231.
10 World Health Organization. The ICD-10 classification of mental and behavioural disorders: Clinical descriptions and diagnostic guidelines.
10th Revision. Geneva: World Health Organization; 2019.
DIAGNOSIS
Diagnostic criteria
11 Ahuja N. A short text book of Psychiatry. In: Schizophrenia. 6th ed. New Delhi: Jaypee publishers; 2006:57-73.
12 Morrens M, Hulstijn W, Sabbe B. Psychomotor slowing in schizophrenia. Schizophr Bull. 2007;33(4):1038-53.
Standard Treatment Guidelines In Homoeopathy 223
SCHIZOPHRENIA
DIFFERENTIAL DIAGNOSIS3,6
Schizophreniform disorder and brief These disorders are of shorter duration than schizophrenia;
psychotic disorder in schizophreniform disorder, the disturbance is present for
less than 6 months, and in brief psychotic disorder, symptoms
are present for at least 1 day but less than 1 month
Delusional disorder Delusional disorder can be distinguished from schizophrenia
by the absence of the other symptoms characteristic of
schizophrenia (e.g., delusions, prominent auditory or visual
hallucinations, disorganized speech, grossly disorganized or
catatonic behaviour, negative symptoms)
Schizotypal personality disorder Schizotypal personality disorder may be distinguished
from schizophrenia by sub threshold symptoms that are
associated with persistent personality features.
Obsessive-compulsive disorder and body They are present with poor or absent insight, and the
dysmorphic disorder preoccupations may reach delusional proportions. But
these disorders are distinguished from schizophrenia by
their prominent obsessions, compulsions, preoccupations
with appearance or body odor, hoarding, or body-focused
repetitive behaviours
Post-traumatic stress disorder Post-traumatic stress disorder may include flashbacks
that have a hallucinatory quality, and hypervigilance may
reach paranoid proportions. But a traumatic event and
characteristic symptom features relating to reliving or
reacting to the event are required to make the diagnosis
Autism spectrum disorder or communication These disorders have deficits in social interaction with
disorders repetitive and restricted behaviours and other cognitive and
communication deficits
Substance/medication-induced psychotic Individuals with substance/medication-induced psychotic
disorder disorder may present with symptoms characteristic of
for schizophrenia. The substance/medication-induced
psychotic disorder can usually be distinguished by the
chronological relationship of substance use to the onset
and remission of the psychosis in the absence of substance
use
Medical or Neurological
• Epilepsy The medical evaluation should be done including a complete
• CNS infections medical and family history, laboratory investigations
• Brain tumors
• Dementia of Alzheimer’s type
• Vit B12 deficiency
• Endocrinopathies
• Fabry’s disease
• Heavy metal poisoning
• Homocystinuria
• Huntington’s disease
• Pellagra
• Pick’s disease
• Systemic lupus erythematosus
• Wernicke’s Korsakoff syndrome
• Wilson’s disease
A comprehensive assessment of the patient and his/her caregivers needs to be carried out.
The cornerstones of this assessment are detailed history taking and physical and mental state
examinations. Efforts should be made to obtain information from all sources, especially the family.
The scales are mainly used to monitor the severity of positive and negative symptoms and track
treatment response in schizophrenics and they are:
PREVENTION10,17,18
Primary Prevention: Essentially involves education programmes about the association of obstetric
complications and the increased risk of schizophrenia. Interventions related to primary prevention
can be delivered to the general population or to different target populations.
Secondary Prevention: Involves intervention at the prodromal phase. It aims to modify the course
of an illness by early intervention. Early intervention can result in reduction in morbidity and better
quality of life for the patients and their families. Possible risk faced by prodromal patients, such as
unnecessary stigmatisation, and the role of drug treatment during intervention at this stage.
Tertiary Prevention: Drug and psychosocial intervention are indicated as part of tertiary prevention
to prevent further disability in the illness. It aims to reduce the burden of established disorder by
optimizing treatment and rehabilitation.
• Presence of suicidal behavior which puts the life of the patient at risk
• Presence of severe agitation or violence which puts the life of others at risk
• Refusal to eat which puts the life of the patient at risk
• Severe malnutrition
• Patient unable to care for self to the extent that she/he requires constant supervision or support
• Catatonia
• Presence of general medical or comorbid psychiatric conditions which make management
unsafe and ineffective in the outpatient setting
• Lack of social support
• Poor drug compliance.
17 Lee C, McGlashan TH, Woods SW. Prevention of Schizophrenia. CNS Drugs 19. 2005:193–206.
18 Brown AS, McGrath JJ. The prevention of schizophrenia. Schizophr Bull. 2011;37(2):257-61.
MANAGEMENT 3,10,14,19
Treatment options for management of schizophrenia can be broadly classified as:
A. Psychosocial interventions
These increase social abilities, self-sufficiency, practical skills, and interpersonal communication
in schizophrenia patients. The goal is to enable persons who are severely ill to develop social and
vocational skills for independent living. Emphasis should be given to psychosocial therapies like:
Family interventions
Persons with schizophrenia and their families who have ongoing contact with each other
should be offered a family intervention, the key elements of which include a duration of at least
9 months, illness education, crisis intervention, emotional support, and training in how to cope
with illness symptoms and related problems.
Some common elements are:
• Engagement of the family early in the treatment process in a “no fault” atmosphere
• Education about schizophrenia (the vulnerability-stress model, risk factors)
• Variation in prognosis, rationale for various treatments, suggestions for coping with the disorder
• Communication training directed at enhancing the clarity of communication and improving the
exchange of both positive and negative feedback within the family
• Problem-solving training aimed at improving ways of managing everyday
• Problems, coping with stressful life events, and planning to deal with
• Anticipated stressors, by generalizing problem-solving skills
• Crisis intervention at times of extreme stress or when signs of relapse are evident.
Supported employment
Persons with schizophrenia who have the goal of employment should be offered supported
employment, the key elements of which include individualized job development, rapid placement
emphasizing competitive employment, ongoing job support, and integration of vocational and
mental health services.
Assertive community treatment
Systems of care serving persons with schizophrenia should include a program of assertive
community treatment (ACT). This intervention should be provided to individuals who have any
of the following characteristics: high risk for repeated hospitalizations, difficulty remaining in
traditional services, or recent homelessness. The key elements of ACT include a multidisciplinary
team (including a psychiatrist), a shared caseload among team members, direct service provision
by team members, a high frequency of patient contact, low patient-to-staff ratios, and outreach
to patients in the community.
19 Dixon LB, Dickerson F, Bellack AS, Bennett M, Dickinson D, Goldberg RW, et al. Schizophrenia Patient Outcomes Research Team (PORT). The
2009 schizophrenia PORT psychosocial treatment recommendations and summary statements. Schizophr Bull. 2010;36(1):48-70.
Skills training
Persons with schizophrenia who have skill deficits such as problems with social skills or
activities of daily living should be offered skills training. The key elements of this intervention
include behaviorally based instruction, modeling, corrective feedback, and contingent social
reinforcement. Clinic-based skills training should be supplemented with practice and training
in the individual’s day-to-day environment.
Cognitive behavioral therapy
Persons with schizophrenia who have residual psychotic symptoms while receiving adequate
pharmacotherapy should be offered adjunctive cognitive behaviorally oriented psychotherapy.
The key elements of this intervention include a shared understanding of the illness between the
patient and therapist, the identification of target symptoms, and the development of specific
cognitive and behavioral strategies to cope with these symptoms.
Token economy interventions
Systems of care that deliver long-term inpatient or residential care should provide a behavioural
intervention based on social learning principles. The key elements of this intervention, often
referred to as a token economy, are contingent positive reinforcement for clearly defined target
behaviours, individualized treatment approach, and the avoidance of punishing consequences.
Individual supportive therapy
A supportive empathic relationship between patients and professionals, in which good listening
promotes a lasting therapeutic alliance is an essential part of good practice. Additional elements
could include support and advice, encouraging continued engagement, treatment-adherence
and healthy lifestyles. Efforts to minimize stress may also be beneficial. Individual support
along with medication is the most commonly practiced treatment in schizophrenia. Patients
and families consistently rank individual support as among the most highly valued services
offered to patients with schizophrenia.
Group therapies
They use a group context to provide patient with opportunities for mutual support, the sharing
of common experiences, feedback about their social behaviors, a setting to practice new social
skills, and an efficient educational forum to learn about schizophrenia and its treatment.
Psychoeducation
Psychoeducation may be considered both for the patient and family members. The aim is to
educate the patient and family about the illness. Simple and brief explanations about the nature
of the patient’s illness, treatments, likely side effects, likely length of treatment etc. can be
offered. Relatives also need to be given time to confront the painful fact of the illness, and what
it entails for the patient and the family as a whole. Treatment adherence will be another main
objective at this stage. Prior to every session, feedback of the previous sessions may be taken
and psychoeducation is to be tailored to the needs of the patient and the caregivers.
B. Lifestyle and dietary modifications
All the patients are to be advised for a change in the lifestyle and diet to reduce the risk of metabolic
side effects and cardiovascular morbidity and mortality. These include physical exercises, dietary
modifications and abstinence from smoking.
C. Rehabilitation
Rehabilitation programmes need to be culturally moulded and adapted to the needs of patients and
their families. Relatively simple and inexpensive strategies can form a part of the overall psychosocial
intervention package.
Homoeopathic management
Homoeopathy is a useful treatment option in psychiatric cases as it treats patient holistically taking
mind and body into account. A few studies20,21,22 were conducted which proved the effectiveness of
homoeopathic medicines in schizophrenia in untreated cases and anti-psychotic treatment resistant
cases.
Patients who are on conventional anti-psychotic treatment frequently experience side effects before
they experience clinical improvement. The patients who are on homoeopathic medicines do not
have any side effect.
Hahnemann has described mental disease as one-sided disease (Aph. 210-230) where there is
derangement of mind and disposition. The disease is psoric in origin and chronic in nature.
• These cases are difficult to perceive and manage as these are mostly one-sided mental diseases.
• In non-psychotic patients, the mind or the consciousness often prohibits the free expression of
the subconscious. But in these patients, it goes one step further – it creates a false ‘reality’ with
their pathological delusions and feelings, an additional layer upon their subconscious. When
we give them the free space to traverse their inner journey, it becomes difficult to differentiate
between the common pathological symptoms and PQRS symptoms. E.g., Delusions of being
20 Oberoi P, Gopinadhan S, Sharma A, Nayak C, Goutham K. Homoeopathic management of Schizophrenia: A Prospective, no comparative, open
label observational study. IJRH. 2016:10(2):108-18.
21 Janardhanan NK, Gopinadhan S, Pramanik MS, Shaw R, Blachandran VA, Kurup TN, et al. Behavioral disorders. Series 1: Clinical Research
studies; New Delhi; Central Council for Research in Homoeopathy: 2008.p.1-14.
22 Balachandran VA. Homoeopathic management of Schizophrenia- an analytical report. CCRH Quarterly Bulletin. 1996; 18:15-8.
23 Bodman F. Insights into homoeopathy. England: Beaconsfield publishers;1990.
persecuted or being followed are common pathological symptoms in mental diseases and yet
they can be characteristic too. So how do we separate the common from the characteristic
symptoms?
• In such cases, the paucity of symptoms also poses a hurdle to complete the totality of symptoms.
So, the importance of objective assessment from observation of physicians, relatives or caregivers
is always important.
• Homoeopathy focuses on the individualistic qualities of the person for which the understanding
of the person is most important. So, in such cases, it is always important to make an attempt
to understand the “schizophrenic person not the schizophrenia” which is available before the
symptoms started or during the lucid phases.
• Physical symptoms play an important role in formulating the totality of symptoms and treating
mental diseases. Bodman has mentioned in his write up related to the importance of physical
concomitants in cases of mental illnesses.
Hahnemann in Organon of Medicine has mentioned that if the mental disease is very acute and
violent, then an acute medicine like Aconite, Belladonna, Stramonium, Hyoscyamus etc. should be
given first, later followed by a deep acting anti-psoric medicine.24
Many homoeopathic medicines described in literature 22,25,26 have predominant mental symptoms
akin to schizophrenia. In Synthesis repertory27, total 36 medicines for schizophrenia are found in
chapter MIND under the rubric ‘Schizophrenia’.
According to the study conducted by CCRH at Central Research Institute [H], Kottayam, Kerala,
India, Sulphur, Lycopodium, Natrum mur, Pulsatilla and Phosphorus were found to be the most
useful medicines in treating schizophrenia patients. Some small medicines for the symptoms of
schizophrenia are: Absinthium: Delirium with hallucinations and loss of consciousness. Cerebral
irritation, hysterical and infantile spasms. Crocus sativus: Anger with violence followed repentance,
pleasant mania. Sudden changes from hilarity to melancholy. Eupionum: Sensation as if the whole
body was made of jelly. Intense sweat from the slightest exertion. Moschus: Uncontrollable laughter,
anxiety with palpitations. Remedy for hysteria and nervous paroxysms, fainting fits and convulsions,
catalepsy, etc. Scutellaria laterifolia: Nervous sedative, where nervous fear predominates. Inability
to fix attention. Confusion. Valeriana officianalis: Hallucinations at night. Changeable disposition.
However, considering the totality of symptoms of the patients many other drugs are also indicated
for schizophrenia.
24 Dudgeon RE. Organon of Medicine. Reprint edition. Indian Books and Periodicals Publishers. 2004.
25 Boericke W., Boericke’s New Manual of Homoeopathic Materia Medica with Repertory: Third Revised and Augmented edition based on ninth
edition. New Delhi: B Jain Publishers;2010.
26 Allen.H.C. Allen’s Keynotes- Rearranged and classified with leading remedies of the Materia Medica and bowel nosodes. 10th reprint edition.
New Delhi: B. Jain Publishers [P] Ltd.;2006.
27 Schroyens F. Synthesis Repertory ver. 9.1. New Delhi: B Jain Publishers Pvt. Ltd.; 2002.
Hyoscyamus Increased cerebral activity • Fears: being alone; poison; being bitten; being
without inflammation; no control sold; to eat or drink; to take what is offered;
over urine and bowel; convulsions suspicious of some plot
and twitching especially of the • Lascivious mania: immodesty, will not be
tongue; jealousy, loquacious, covered, kicks off the clothes, exposes the
irritable, fear of being left person; sings obscene songs; lies naked in bed
alone; of running water even and chatters
on hearing it; insects; snakes, of • Delirium with restlessness, jumps out of bed,
shinning objects, fire, glass, etc; tries to escape; makes irrelevant answers;
aggravation at night thinks he is in the wrong place; talks of
imaginary doings, but has no wants and makes
no complaints
• Worse from mental affections, jealousy, unhappy
love
Sulphur Hot patient, kicks off the cloth at • Movement in abdomen as of a child
night; dirty, filthy, does not want • Delusions, thinks rags beautiful things, that he
to be washed; lean, thin, stoop- is immensely wealthy.
shouldered; child who walks and • Worse warmth in bed, washing, bathing,
sit stooping; red orifices; desires changeable weather
sweets, sugar, meat; when the best • Better in dry, warm weather
selected remedy fails to improve
• For diagnosis of schizophrenia, use criteria in the Diagnosis and Statistical Manual of
Mental Disorders-5 or ICD-10 (refer text)
• Comprehensive assessment of patient & caregivers, complete history, physical
examination, mental state examination, symptom evaluation, basic investigations
to rule out any other medical or neurological condition, assessment of ongoing
treatments, psychological testing for cognitive functions, neuroimaging etc. to be done
Yes Improvement No
Deterioration of signs/
symptoms
• Revaluate the diagnosis
Continue follow-up with • Reassess the case and
assessment tools and select homoeopathic red flags
taper off conventional similimum • Suicidal behavior
medications gradually • Check for medication • severe agitation or
compliance violence
• Refusal to eat
• Severe malnutrition
• Patient unable to self care
• Catatonia
Pseudo non-responses due True non- response • Presence of general
to poor compliance- evaluate medical or comorbid
causes, address the same & psychiatric conditions
ensure compliance • Lack of social support
• Poor drug compliance
Refer to higher
Yes Improvement No centre
SUBCLINICAL
HYPOTHYROIDISM
CASE DEFINITION1,2
INCIDENCE/PREVALENCE
• The incidence of SCH varies between 4 and 10% depending upon the gender, age and population.3,4
• In different prevalence studies from India subclinical hypothyroidism is found to be around
10.95% and 11.3% in general population and more in females in comparison to males. 5,6
CLASSIFICATION1
ETIOLOGY7,8,9,10
The etiology of SCH is same as that of overt hypothyroidism. It is most often triggered by chronic
lymphocytic thyroiditis (goitrous Hashimoto’s thyroiditis and atrophic thyroiditis), an autoimmune
disorder of the thyroid gland that is the most common cause of decreased thyroid hormone
production in patients with acquired mild, subclinical, or overt hypothyroidism.2
Thyroid- related causes Systemic causes
Hashimoto’s thyroiditis (most common cause) Diabetes mellitus
Iodine deficiency Celiac disease
Overtreatment of Graves’ disease Chronic renal failure
Transient neonatal hyperthyrotropinemia Syndromes (e.g., Turner syndrome, Down
syndrome etc.)
1 Pearce SH, Brabant G, Duntas LH, Monzani F, Peeters RP, Razvi S, et al. 2013 ETA Guideline: Management of Subclinical Hypothyroidism. Eur
Thyroid J. 2013;2(4):215-28.
2 Cooper DS, Biondi B. Subclinical thyroid disease. Lancet. 2012; 379(9821):1142–1154.
3 Canaris GJ, Manowitz NR, Mayor G, Ridgway EC. The Colorado thyroid disease prevalence study. Arch Intern Med. 2000;160(4):526–534.
4 Vanderpump MP, Tunbridge WM, French JM, Appleton D, Bates D, Clark F, et al. The incidence of thyroid disorders in the community: a twenty-
year follow-up of the Whickham Survey. Clin Endocrinol. 1995; 43(1):55–68.
5 Unnikrishnan AG, Kalra S, Sahay RK, Bantwal G, John M, Tewari N. Prevalence of hypothyroidism in adults: An epidemiological study in eight
cities of India. Indian J Endocr Metab. 2013;17(4):647-52.
6 Deshmukh V, Behl A, Iyer V, Joshi H, Dholye JP, Varthakavi PK. Prevalence, clinical and biochemical profile of subclinical hypothyroidism in
normal population in Mumbai. Indian J Endocr Metab. 2013;17(3):454-9.
7 Arrigo T, Wasniewska M, Crisafulli G, Lombardo F, Messina MF, Rulli I, et al. Subclinical hypothyroidism: the state of the art. J Endocrinol
Invest. 2008;31(1):79–84.
8 Cooper DS. Clinical practice. Subclinical hypothyroidism. N Engl J Med. 2001;345(4):260–265.
9 Garber JR, Cobin RH, Gharib H, Hennessey JV, KleinI, Mechanick JI, et al. Clinical practice guidelines for hypothyroidism in adults:
cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Thyroid OffJ Am Thyroid Assoc.
2012;18(6):988-1028.
10 Basaria S, Cooper DS. Amiodarone and the thyroid. Am J Med. 2004;118(7):706 –714.
DIAGNOSIS
Clinical Presentation11,12,13,14
The type of symptoms people relates to SCH include those of overt hypothyroidism:
• Fatigue, muscle cramps, cold sensitivity, dry skin, voice changes, and constipation.
• Other symptoms include poor memory, slowed thinking, weak muscles, puffy eyes, anxiety, and
depression
• Goitre-is the most common clinical sign, reported to be twice as prevalent as observed in the
general population2
• Weight gain- especially in children
• Increased cholesterol levels, especially in adult population15
• Impaired growth velocity
• Anemia and weakness
• Sleepiness
• Impaired psychomotor and cognitive development
Careful history taking which includes family, personal & medical history.
INVESTIGATIONS2,16
Physical examinations
11 Rapa A, Monzani A, Moia S, vivenze D, Bellone S, Petri A, et al. Subclinical hypothyroidism in children and adolescents: a wide range of clinical,
biochemical, and genetic factors involved. J Clin Endocrinol Metab. 2009; 94(7):2414–2420.
12 Wu T, Flowers JW, Tudiver F, Wilson JL, Punyasavatsut N. Subclinical thyroid disorders and cognitive performance among adolescents in the
United States. BMC Pediatric. 2006;6:12.
13 Vanderpump MP, Tunbridge WM, French JM, Appleton D, Bates D, Clark F, et al. The development of ischemic heart disease in relation to
autoimmune thyroid disease in a 20-year follow-up study of an English community. Thyroid. 1996;6(3):155–60.
14 Ajmani NS, Sarbhai V, Yadav N, Paul M, Ahmad A, Ajmani AK. Role of thyroid dysfunction in patients with menstrual disorders in tertiary care
center of walled city of Delhi. J Obstet Gynaecol India. 2016;66(2):115-9.
15 Marwaha RK, Tandon N, Garg MK, Kanwar R, Sastry A, Narang A, et al. Dyslipidemia in subclinical hypothyroidism in an Indian population.
Clin Biochem. 2011;44(14-15):1214-7.
16 Kabadi UM. Subclinical hypothyroidism- Natural course of the syndrome during a prolonged follow-up study. Arch Intern Med.
1993;153(8):957-61.
Local examination
• Thyroid gland should be palpated as per WHO guidelines (finger rolling method from behind)
for grading and consistency of thyroid gland.
Laboratory tests
• Serum TSH is the single best test for screening. TSH value above the normal upper limit in
the presence of normal thyroid hormone levels should raise the suspicion of SCH. Follow up of
the confirmed case should be done after 4-6 weeks. The measurement of serum TSH and fT4
should be repeated every 3–4 months once the TSH is within normal limits.
• Antithyroglobulin antibodies (TG-Abs) and anti-thyroperoxidase antibodies (TPO-Abs) titer to
be checked for; also used for cases of carcinoma. It should not be repeated often in follow-up.
• Thyroid ultrasonography should be performed whenever available.
DIFFERENTIAL DIAGNOSIS17,18,19
There are several non-thyroid factors which can transiently elevate TSH and lead to misdiagnosis
as subclinical hypothyroidism. These consist of the following situations:
Recovery from non-thyroidal illness: During the period of recovery from non-thyroidal illness,
where a momentarily raised serum TSH level is detected after a stage of TSH repression.
Pituitary lesions: Pituitary TSH-producing adenomas, thyroid hormone resistance, and rare
TSH receptor mutations. In patients with pituitary TSH producing adenomas or thyroid
hormone resistance, the high TSH is associated with raised serum free T4 and/or T3 levels. On
the contrary, subjects with subclinical hypothyroidism have normal free T4 levels. Patients with
TSH resistance due to abnormality in the TSH receptor have high serum TSH values and normal
or low serum free T4 and T3 levels.
Adrenal deficiency: Non-diagnosed and untreated adrenal deficiency.
Rheumatoid factors may result in some hindrance in immunometric tests.
Medications: Amiodarone, metoclopramide, amphetamine etc.
Chronic renal failure
COMPLICATIONS20,21,22,23
• Systemic symptoms of hypothyroidism
• Progression to overt hypothyroidism
17 Gosi SK, Garla VV. Subclinical Hypothyroidism. StatPearls [Internet]. 2020 [cited on 18 March 2021]. Available from: https://www.ncbi.nlm.
nih.gov/books/NBK536970/
18 Després N, Grant AM. Antibody interference in thyroid assays: a potential for clinical misinformation. Clin Chem. 1998; 44(3):440-54.
19 Ayala AR, Danese MD, Ladenson PW. When to treat mild hypothyroidism. Endocrinol Metab Clin North Am. 2000; 29(2):399-415.
20 Duntas LH, Wartofsky L. Cardiovascular risk and subclinical hypothyroidism: focus on lipids and new emerging risk factors. What is the
evidence? Thyroid. 2007;17(11):1075–84.
21 Roberts LM, Pattison H, Roalfe A, Franklyn J, Wilson S, Hobbs FDR, et al. Is subclinical thyroid dysfunction in the elderly associated with
depression or cognitive dysfunction? Ann Intern Med. 2006;145(8):573–81.
22 Christ-Crain M, Meier C, Huber PR, Staub J-J, Müller B. Effect of l-thyroxine replacement therapy on surrogate markers of skeletal and cardiac
function in subclinical hypothyroidism. Endocrinologist. 2004;14(3):161–6.
23 Klein RZ, Haddow JE, Faix JD, Brown RS, HermosRJ, Pulkkinen A, et al. Prevalence of thyroid deficiency in pregnant women. Clin Endocrinol
(Oxf). 1991;35(1):41–6.
MANAGEMENT
General management1,7,24
The BMJ clinical practice guidelines25 issued a strong recommendation against thyroid hormones
in adults with SCH [elevated TSH levels and normal free T4 (thyroxine) levels] because there were
no important benefits from treatment and in addition, possibility of harms cannot be ruled out.
Guidelines recommend treatment only when people are younger, symptomatic, a woman wanting
to be pregnant which has implication on mother and baby or have other indications for prescribing
(such as cardiovascular disease or antibodies to thyroid peroxidase). Clinicians should monitor the
progression or resolution of the thyroid dysfunction. Management of SCH depends on many factors:
age, other prevailing diseases, comorbidities etc. and presence of symptoms or no symptoms. The
target of treatment is to lower the patient’s serum TSH levels within the normal reference values and
prevent any complications. As the average serum TSH for the general population is approximately
1.4 mU/L, with 90 % of population with serum TSH values <3.0 mU/L, several physicians propose a
clinical TSH target of 0.5-2.5 mU/L in young and middle-aged persons. Once SCH has been diagnosed,
a repeat thyroid function test is desirable and should be re-checked within 8–12 weeks along with
thyroid autoantibodies. When abnormal serum TSH concentration has been reached, TSH should be
analysed again after 3-6 months and then every year.
Homoeopathic management
Homeopathic intervention has been found to be effective in various endocrine diseases. The
homeopathic treatment should be designed on the basis of symptomatology of the patient; physical
findings; constitution; past/personal/ family/treatment history of the patient etc. There are very
24 Fatourechi V, Lankarani M, Schryver PG, Vanness DJ, Long KH, Klee GG. Factors influencing clinical decisions to initiate thyroxine therapy for
patients with mildly increased serum thyrotropin (5.1-10.0 mIU/L). Mayo Clin Proc. 2003;78(5):554–60.
25 Bekkering GE, Agoritsas T, Lytvyn L, Heen AF, Feller M, Moutzouri E, et al. Thyroid hormones treatment for subclinical hypothyroidism: a
clinical practice guideline. BMJ. 2019; 365:12006.
In Synthesis repertory30, 41 medicines are found in chapter GENERAL under the rubric
‘Hypothyroidism’. The frequently verified characteristic features of some organospecific remedy is:
Thyroidinum: Marked sensitiveness to cold. Hypothyroidism after acute diseases, i.e., weakness.
Easy fatigue, weak pulse, tendency to fainting, palpitation, cold hands and feet, low blood pressure,
chilliness and sensitive to cold, craving for large amount of sweets.
The list of frequently prescribed polychrest medicines along with their indications can be
summarized as:31,32
Medicines General indications
Calcarea carbonica Chilly patients; takes cold easily; fat, fair, flabby, distended abdomen; pale, weak, easily
tired; head sweat profusely while sleeping; sour smelly discharges; longing for fresh air;
desire for eggs and indigestible things, sweets. Aversion to meat and milk; fearful, shy,
timid, slow and sluggish; feels better when constipated. Forgetful, confused. Pituitary
and thyroid dysfunction
Calcarea Sensitive to both cold and heat; tendency to the formation of abscesses; muscles are
sulphuricum flabby; disposed to hemorrhages. Thick yellow discharges from the mucous membranes.
Absent minded; irritable; easily angered. The external throat is swollen; the glands are
enlarged and painful
Carcinosinum Thin, delicate looking, fine skin and dark complexion or “Café au lait” hue, light -
colored eyes with pigmented moles. Strong family history of cancer, tuberculosis and
other chronic illnesses; history of pneumonia, mumps, adenoids, typhoid, etc.; history
of paternal control in childhood; affectionate, loving, sensitive to other’s suffering,
sympathetic to animals, fond of them, passionate, fastidious, fearful, sensitive to
reprimands
Causticum Chilly patient; sad, hopeless; intensely sympathetic. Skin is dirty white sallow, with
warts, especially on the face. Children are slow to walk. Burning, rawness and soreness
are characteristic stress incontinence. Restless legs at night. Worse from dry, cold
winds, clear, fine weather; better in damp, wet weather, warmth
Kali carbonicum Chilly patient; puffiness, weakness, backache and profuse perspiration; worse in
the morning 2am-4a.m.; excessive flatulence; distended stomach as if it would burst
Intolerance to cold weather. Hypothyroidism. Constipation; large difficult stool
26 Ghare P, Jadhav AB, Patil AV. A clinical study to see the effect of thyroidinum, a homoeopathic preparation on thyroid peroxidase antibody in
subclinical hypothyroidism of age group between 18-70 years. Int J Health Sci Res. 2020; 10(2):18-22.
27 Chauhan VK, Manchanda RK, Narang A, Marwaha RK, Arora S, Nagpal L, et al. Efficacy of homeopathic intervention in subclinical
hypothyroidism with or without autoimmune thyroiditis in children: an exploratory randomized control study. Homeopathy. 2014; 103(04):
224-231.
28 Bhattacharya P, Giri S, Ghosh B, Banerjee A. Symptomatic Subclinical Hypothyroidism Treated with Homoeopathy: Case Reports.
Homœopathic Links. 2020; 33(02): 120-125.
29 Narang A, Marwaha RK, Khanna VK. Evidence to evaluate the efficacy of homoeopathic treatment in Sub-Clinical Hypothyroidism (SCH). Asian
journal of homoeopathy. 2007;1(1):10-13.
30 Schroyens F. Synthesis Repertory ver. 9.1. New Delhi: B Jain Publishers Pvt. Ltd.; 2002.
31 Boericke W. New Manual of Homoeopathic Materia Medica with Repertory: Third Revised & Augmented Edition based on Ninth Edition. New
Delhi: B. Jain Publishers(P) Ltd.; 2007.
32 Allen HC. Keynotes and Characteristics with Comparisons of some of the Leading Remedies of the Materia Medica with Bowel Nosodes. Eighth
Edition. New Delhi: B Jain Publishers Pvt Limited; 2013.
TINEA
CASE DEFINITION
“Tinea”, the Latin name for worm, describes the serpentine appearance of the skin lesions.1 These
are superficial infections caused by a dermatophyte is known as dermatophytosis or ringworm. This
term is a misnomer because worms are not involved.2
INCIDENCE/PREVALENCE
• Dermatophytes (keratinophilic fungi) are the most common cutaneous fungal infections seen in
humans affecting skin, hairs and nails with a considerable morbidity.3
• According to World Health Organization (WHO), the prevalence rate of superficial mycotic
infection worldwide has been found to be 20-25%.
• Its prevalence varies in different countries. It is more prevalent in tropical and subtropical
countries like India where the heat and humidity are high for most part of the year.4,5
i. Trichophyton
ii. Microsporum
iii. Epidermophyton
According to habitat pattern, geophilic organisms originate in the soil and only sporadically infect
humans by direct contact with the soil. Zoophilic species are usually found on animals but can infect
humans also. Transmission may occur through direct contact with a specific animal species or
indirectly when animal hair is carried on clothing. Anthropophilic species have adapted to humans
as host. They are transmitted from person to person via direct contact or fomites.
1 Hay RJ. Dermatophytosis and other superficial mycoses. In: Mandell GL, Bennet JE, Dolin R, eds. Mandell, Douglas and Bennett’s principles and
practice of infectious diseases. 7th ed. Churchill Livingstone Elsevier; 2010:3345-55.
2 Verma S, Heffernan MP. Superficial fungal infection: Dermatophytosis, onychomycosis, tinea nigra, piedra. In: Wolff K, Goldsmith LA, Katz SI,
Gilchrest BA, Paller AS, Leffell DJ, editors. Fitzpatrick’s dermatology in general medicine. 7th ed. Mc Graw-Hill; 2008:1807-21.
3 Noble SL, Forbes RC, Stamm PL. Diagnosis and management of common tinea infections. Am Fam Physician. 1998; 58: p.163–74, 177-8.
4 World Health Organisation. Epidemiology and management of common skin diseases in children in developing
countries [Internet]. 2005 [Cited on 2021 March 9]. Available from: https://apps.who.int/iris/bitstream/handle/
10665/69229/WHO_FCH_CAH_05.12_eng.pdf;jsessionid=ABEC5463F0910536AE385E4796F878FB?sequence=1
5 Kumar K, Kindo AJ, Kalyani J, Anandan S. Clinico-mycological profile of dermatophytic skin infection in a tertiary care centre. Sri Ramachandra
Journal of Medicine. 2007;1(2):12-15.
CONTRIBUTING FACTORS1,2
a) Socio-economic conditions
b) Personal hygiene /Lifestyle– public showering, occlusive clothing.
c) Climate (hot and humid climate favours infection)
d) Living environment or type of population
e) Individual’s susceptibility
f) Poorly controlled diabetes mellitus
g) Age/obesity
h) Immunosuppression, i.e., chemotherapy, steroids, organ transplant, AIDS etc.
i) Migration of people.
PATHOGENESIS
• Dermatophytes are keratinophilic fungi which do not invade beyond the epidermis because
of their dependence on keratin for nutrition and fungistatic properties of transferrin and β
globulin in human serum.6
• These fungi cause inflammation due to permeation of the metabolic products of the fungus into
the skin or due to induction of delayed hypersensitivity.7,8
• The gross appearance of the lesion is an outer ring of active, progressing infection, with central
healing.9 Infection may proceed more deeply from superficial involvement and a variety of
pathologic changes can occur depending on the fungus, the site of infection, and the immune
status of the host.10
• Stratum corneum, hair and nails are attractive substrates for these fungi due to their low density
of bacterial inhibitors and competitors.
• The clinical appearance and behaviour of a fungal infection of the skin depends partly on the
host response.
• The clinical reactions may also be influenced by the type of dermatophyte.
CLINICAL FEATURES
a) Typical lesion
• A typical lesion of tinea is an annular or arcuate plaque which spreads centrifugally (away from
the centre).
• The edge is active, showing papulo-vesiculation, pustulation and scaling, while the centre is
usually relatively clear. (Figure 1,2)
6 Marks JG, Miller JJ. Looking bill & Mark’s Principles of Dermatology. 4thEd.India: Elsevier 2009. Rashes with epidermal involvement: 124-130.
7 Khanna N. Illustrated synopsis of dermatology and sexually transmitted diseases. 4th edition. India: Reed Elsevier; 2011:p.288.
8 Marks R. Roxburgh’s common skin diseases. 17th edition. New York: Oxford university press; 2003:39-40.
9 Patricia M. Bailey & Scott’s Diagnostic Microbiology. 13th ed. St. Louis, Missouri: Elsevier Publishers;2014: p.734.
10 Manson P, Cook GC, Zumla AI, Hay RJ.Manson’s tropical diseases. 22nd Ed. London: Elsevier publishers;2008:p.1190.
• In chronic lesion, there may be nodules, hyperpigmentation and even lichenification (thickening,
hyperpigmentation and increased skin markings) in the centre.
Figure 2:(a and b) Large sized, erythematous patches with active border over the gluteal regions and
legs. Courtesy: Verma et al. Indian J Dermatol 2017.
b) Sites of Infection-In 1910, Sabouraud, and the Father of Modern Medical Mycology classified
dermatophytosis as:
Tinea capitis is predominantly seen in pre-pubertal children. Tinea cruris occurs only in adults
especially the males and not in children. Tinea pedis and Tinea unguium are more common among
adults.11,12
11 Merz G. William, Hay J. Roderick. Topley and Wilson’s Microbiology and Microbial Infections. 10th ed. Arnold Publishers; 2005:p.223.
12 Longo DL, Kasper DL, Jameson JL, Fauci AS, Hauser SL, Loscalzo J. Harrison’s principles of internal medicine. 18th ed. New York: Mc Graw-Hill;
2012:p.350.
DIAGNOSIS8,9,10
(Figures-Courtesy: Khanna N. Illustrated synopsis of dermatology and sexually transmitted diseases.; 4th
edition; 2011)
252 Standard Treatment Guidelines In Homoeopathy
TINEA
DIFFERENTIAL DIAGNOSIS8,13
13 Sahoo AK, Mahajan R. Management of tinea corporis, tinea cruris, and tinea pedis: A comprehensive review. Indian Dermatol Online J.
2016;7(2):77-86.
Tinea pedis (Erythema, scale, fissures, maceration; itching between toes extending to sole, borders, and
occasionally dorsum of foot; may be accompanied by tinea manuum [“one-hand, two-feet” involvement] or
onychomycosis)
Contact dermatitis Distribution may match footwear; usually spares
interdigital skin
Dyshidrotic eczema “Tapioca pudding” vesicles on lateral aspects of
digits; often involves hands
Foot eczema May have atopic history; usually spares interdigital
skin
Juvenile plantar dermatosis Shiny taut skin involving great toe, ball of foot, and
heel; usually spares interdigital skin
Psoriasis Involvement of other sites; gray or silver scales; nail
pitting; 70% of affected children have family history
of psoriasis2
Tinea capitis (one or more patches of alopecia, scales, erythema, pustules, tenderness, pruritus, with cervical
and sub-occipital lymphadenopathy)
Alopecia areata Discrete patches of hair loss with no epidermal
changes (i.e., no scale); total loss of hair or fine
miniature hair growth; “exclamation point”
appearance of hair; no crusting; no inflammation;
possible nail pitting
Atopic dermatitis Personal history or family history of atopy; less
often annular; lymphadenopathy uncommon;
alopecia less common
Bacterial scalp abscess Alopecia less likely; hair pluck is painful
Psoriasis Gray or silver scales; nail pitting; 70% of affected
children have family history of psoriasis2; involvement
of other sites
Seborrheic dermatitis Greasy scale; typical distribution involving nasolabial
folds, hairline, eyebrows, post-auricular folds, chest.
Alopecia uncommon; lymphadenopathy uncommon
Trichotillomania No scale; commonly involves eyelashes and
eyebrows; hairs of varying lengths
Tinea unguium (Onychomycosis), discoloured (white, yellow, brown), thickened nail with subungual
keratinous debris and possible nail detachment; often starting with great toe but can involve any nail
Other nail dystrophies, most commonly associated with Appearance can be indistinguishable from
repeated low-grade trauma, psoriasis, or lichen planus onychomycosis; may have other manifestations of
alternate diagnosis
Tinea versicolor/Pityriasis versicolor is a frequent, benign, superficial fungal infection of the skin. It belongs
to Malassezia-related diseases. Clinical features of pityriasis versicolor include either hyperpigmented
or hypopigmented finely scaly macules. The most frequently affected sites are trunk, neck, and proximal
extremities.14
14
14 Karray M, McKinney WP. Tinea (Pityriasis) Versicolor. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing [Internet]. 2020
[Cited on 9 March 2021]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482500/
COMPLICATIONS 8
• Cicatricial alopecia: It may cause permanent hair loss especially seen in tinea capitis.
INVESTIGATIONS2,8
• Potassium hydroxide (KOH) scraping: Simple, inexpensive, quick and sensitive test.
• Cultures: Cultures need to be done when clinical suspicion is strong and KOH mount is negative
or when it is necessary to identify the fungal species. Sabouraud medium is used. Microscopic
morphology of microconidia and macroconidia, along with surface topography and pigmentation
are used for species identification.
• Wood’s light: It is useful method of screening outbreaks of Tinea capitis in schools. Shine
Wood’s light on the scalp (tinea capitis) shows a green fluorescence.
• Dermatophyte test medium: Scales from the advancing border, subungal debris or affected
hair embedded in the medium.
• Histopathology special stains: Hyphae cannot be visualized in the keratin with H&E, so
special stains like periodic acid- schiff (fungal cell wall appears pink to red purple) and grocott’s
methenamine silver (fungal cell wall appears black or dark brown for all fungi) are needed.
• Dermatology life quality index (DLQI): A simple practical questionnaire technique for routine
clinical use. The patients with skin diseases are asked about the impact of their disease and its
treatment on their lives.
• Dermatology quality of life scales (DQOLS): It assesses the impact of skin conditions on
patients’ psychosocial state and everyday activities.
15 Finlay AY. Quality of life assessments in dermatology. Semin Cutan Med Surg.1998;17(4):291-6.
16 Morgan M, McCreedy R, Simpson J, Hay RJ. Dermatology quality of life scales-a measure of the impact of skin diseases. Br J Dermatol.
1997;136(2):202-206.
17 Anderson R, Rajagopalan R. Responsiveness of the Dermatology-specific Quality of Life (DSQL) instrument to treatment for acne vulgaris in a
placebo-controlled clinical trial. Qual Life Res. 1998;7(8):723-734.
18 Chren MM, Lasek RJ, Sahay AP, Sands LP. Measurement properties of Skindex-16: a brief quality-of-life measure for patients with skin
diseases. J Cutan Med Surg. 2001;5(2):105-110.
• Dermatology specific quality of life (DSQL): A new tool which has been developed to
address the effects of skin disease and its treatment on physical and social functioning and self-
perception.
• Skindex-16: An accurate, sensitive, but brief quality-of-life outcome measure is needed for
study of dermatologic care.
RED FLAGS8,10,19
MANAGEMENT
General management
• Advice against wearing tight garments such as jeans, leggings, and jeggings.
• Wearing loose, cotton garments. Avoid use of synthetic clothes.
• Discourage sharing of bed linen (if feasible), towels and clothes. Regular washing of towels and
bed linen.
• Taking regular showers. Wearing clothes only after thoroughly drying the body.
• Washing clothes and bed linen in hot water and then sunning them. Sunlight is known to destroy
dermatophytes. In the absence of sunlight, ironing the clothes would be beneficial.
• Drying of clothes inside out. Wearing well dried inner garments after about 3–4 days of washing
if ironing is not possible.
• Washing infected clothes separately.
• Instructing patients with tinea cruris to wear “boxer shorts” instead of the tight-fitting ones that
hug the groin and cut into it.
• Removing waistband, wristband, etc.
• Preferring non-occlusive footwear.
• Dusting, wet mopping or vacuuming the house followed by cleaning with detergent so as to
reduce the spore load in the immediate environment.
• Keeping area dry.
Homoeopathic management
The homoeopathic concept of treatment is ‘holistic’ and ‘individualistic’.20 The totality of characteristic
signs and symptoms exhibited by the patient leads to the selection of similar remedy.
19 Al Hasan M, Fitzgerald SM, Saoudian M, Krishnaswamy G. Dermatology for the practicing allergist: Tinea pedis and its complications. Clin Mol
Allergy. 2004;2(1):5.
20 Hahnemann S. Organon of Medicine. 3rd Indian Reprint. Calcutta: Economic Homoeo Pharmacy; 2012.
The miasmatic background of the case must be taken into consideration, while selecting the
similimum. Hahnemann has considered Psora responsible for the production of Tinea.21 J.C. Burnett
called ringworm a “sub tuberculosis” state22 and later J.H. Allen mentioned it as a mixed miasmatic
state of “syco-psoric”.23
Antimiasmatic intercurrrent remedies may be given in cases of obstacle to the action of the similimum.
Intercurrent antimiasmatic remedy is to be selected on the basis of anti miasmatic totality indicated
by the system.
The frequently verified characteristic features of some organospecific remedies are: Tellurium
metallicum: Itching of hands and feet; ringworm on lower extremities; barber’s itch; craving for
apples; odour of body and sweat offensive and garlic like; discharges are acrid. Viola tricolor: Eruptions
over face and head with burning pain, itching; worse at night, in winter. Hydrocotyle asiatica: Dry
eruptions, circular spots with scaly edges, esp. on soles. Copious perspiration. Ranunculus bulbosus:
Burning pain and intense itching. Horny skin; fingertips and palms chapped. Worse in cold air.
Chrysarobinum: Ringworm. Vesicular or squamous lesions, crust formation, itching of thighs, legs
and ears; foul smelling discharges from ears. Radium bromatum: Itching all over the body, burning
of skin as on fire. Better by hot bath. Bacillinum burnett: Ringworms with fine white scales; falling of
hair in spots on scalp and face; worse at night, cold air; often used as an intercurrent.
Indications of a few important constitutional medicines with their indications are given below:24,25,26
21 Hahnemann S. The Chronic Diseases Their Peculiar nature and Their Homoeopathic cure. 14th Impression, vol-I. New Delhi: B. Jain Publishers
(P) Ltd;2014: p.39.
22 Burnett J.C. Ringworm. Calcutta: A.P. Homoeo Library. 2003; p.118.
23 Allen JH. The chronic Miasms with Repertory. Revised edition. 1998; New Delhi: B. Jain publishers Pvt. Ltd; 2007: p.94.
24 Allen HC. Keynotes and characteristics with comparisons of the leading remedies of the Materia Medica. 11th Ed. New Delhi: B. Jain Publishers
Pvt. Ltd; 2012.
25 Boericke W. Pocket manual of homoeopathic Materia Medica. Reprint ed. New Delhi: B. Jain Publishers Pvt. ltd; 1998.
26 Gupta R, Manchanda RK: Textbook of Dermatology for Homoeopathy. 1st edition. New Delhi: B. Jain Publishers (P) Ltd;2005:78-88.
Petroleum Adapted to persons with light hair • Itching, redness; skin cracked, rough,
and skin; irritable, quarrelsome bleeding; dry or moist. cracked tips of
disposition; easily offended at trifles; fingers fissured
vexed at everything; Heat and burning • All eruption itches violently
of soles of feet and palms of hands; • Cannot rest until he scratches the skin
Sweat and moisture of external off, when the part becomes moist,
genitals, both sexes; Painful, itching bloody, raw and inflamed
chilblains and chapped hands worse in • Skin symptoms are worse in winter,
cold weather, carriage riding, during a dampness
thunderstorm, in winter • Better in warm air, summer
Dulcamara Chilly patient; skin affections brought • Ringworm, especially on face, scalp,
on or worse by exposure to cold damp genitals and hands
rainy weather; restless and irritable • Tinea circinata
• Thick, brown and yellow crusts, bleed
when scratched
• Skin eruptions brought on in cold
wet weather but relieved by cold
applications
Sepia Officinalis Chilly patient; tall, thin built with • Eruptions more on flexures of the body-
yellow saddle across upper part of elbows, knees, face, hands and anterior
cheeks and nose, big belly; dry flabby surface of body
skin. Predisposed to take cold at change • Herpes circinatus (tinea corporis) in
of weather. Desire for sour food which isolated spots on upper part of body
aggravates Cheerful, active when well • Ringworm-like eruption every spring
but indifferent and quarrelsome when • Itching of skin; of various parts; of
sick self-absorbed, sad, weeping and external genitalia; is not better by
indolent scratching and is apt to change to
burning
• Better from warmth of bed, hot
applications
Investigations
• Potassium hydroxide
Diagnosis confirmedby
(KOH) Scraping
clinical findings
• Cultures
General management
• Wood’s Light
• Wearing loose, cotton • Dermatophyte test
garments; avoid tight clothing medium
• Discouraging sharing of bed Evaluation and assessment • Histopathology
linen special stains
• Dermatology life quality index (DLQI)
• Taking regular showers
• The dermatology quality of life scales
• Washing clothes separately
(DQOLS)
and bed linen in hot water
• The dermatology specific quality of life
and then sunning them,
(DSQL)
drying them inside out
• Skindex
• Instructing patients with
tinea cruris to wear “boxer
shorts”
• Preferring non-occlusive
footwear Start homoeopathic treatment &
• Dusting, wet mopping or advice for general management
vacuuming the house
• Keeping area dry
red flags
Improvement • If secondary bacterial
infection occurs
• Permanent hair loss
Yes No • Association with
other conditions like
diabetes mellitus
• Lower extremity
cellulitis
Conventional/ integrated
care to be initiated
WARTS
CASE DEFINITION1,2
Warts are common dermatological lesions caused by skin epithelial cells’ infection with Human
Papilloma Virus (HPV). The thickening of the epidermis with scaling and an upward extension of the
dermal papillae containing prominent capillaries give them their ‘wary’ or verrucous appearance.
INCIDENCE/PREVALENCE3,4
• Warts are common worldwide and affect approximately 10% of the population.
• Warts may occur at any age, but are unusual in infancy and early childhood; prevalence increases
among school-aged children and peaks at 12 to 16 years.
• A study conducted in India showed that warts were most commonly seen in the age group of 10
to 14 years (41.95%) in children, whereas in adults, the most common age group was 14 to 20
years (46.03%) and the average age at presentation was 11.5 years.
There are over 100 subtypes of the HPV, but only a few types can cause skin warts at selective
anatomical sites. However, with skin contact, the HPV can be transferred to any part of the body.
• Warts spread by direct or indirect contact due to impairment of the epithelial barrier function, by
trauma (including mild abrasions), maceration or both, which greatly predispose to inoculation
of virus in the skin.
• Plantar warts are commonly acquired from swimming pool or shower room floors, whose
rough surface abrade moistened keratin from infected feet and help to inoculate virus into the
softened skin of others.
• Common hand warts may spread widely round the nails in those who bite their nails or periungual
skin; over habitually sucked fingers in young children, and to the lips and surrounding skin in
both cases.
• Occupational handlers of meat, fish and poultry have high incidence of hand warts, attributed to
cutaneous injury and prolonged contact with wet flesh and water.
• Shaving may spread warts over the beard area.
• Genital warts have high infectivity as the thinner mucous surface is more susceptible to
inoculation of virus than thicker keratinized skin.
1 Zandi S, Zadeh RA, Yousefi SR, Gharibi F. Promising New Wart Treatment: A Randomized, Placebo-Controlled, Clinical Trial. Iranian Red
Crescent Med J. 2016; 18(8): e19650.
2 Marks JG, Miller JJ. Epidermal Growths. In: Looking bill& Marks’ Principles of Dermatology. 4th ed. India: Elsevier; 2009: p.51-56.
3 Al Aboud AM, Nigam PK. Wart (Plantar, Verruca Vulgaris, Verrucae). NCBI Bookshelf. A service of the National Library of Medicine, National
Institutes of Health: Stat Pearls Publishing [Internet]. 2019 [cited on 2021 March 20] Available from: https://www.ncbi.nlm.nih.gov/books/
NBK431047/
4 Rook, Wilkinson, Ebling. Viral infections. Textbook of Dermatology. 6th edition, Vol II. USA: Wiley-Blackwell. 2016: p. 1031-1044.
5 Leung L. Treating common warts – options and evidence. Clinical. Reprinted from Australian Family Physician.2010;39(12):933-37.
PATHOGENESIS2,6,7
• HPV is a double-stranded DNA virus that infects and replicates in keratinizing cells in the
epidermis. With a minor breach in the epithelial surface, HPV enters the epithelial cells via
putative surface receptors and proliferates. This results in persistent viral infection with
metaplasia of keratinocytes, which gradually accumulate keratohyalin granules and are sloughed
off.
• As these virally infected keratinocytes are not destroyed, the HPV virions are rarely exposed to
the langerhans cells of the skin, and therefore, evade being cleared by systemic immunity. This
facilitates the viral persistence and continual growth of the warts.
• Usually there is an incubation period of 1-20 months, in which viral DNA is established in host
cell without integration within the host cell genome.
• Cell-mediated immunity appears to contribute to the regression of warts; in immuno-deficient
hosts (e.g., those with organ transplants or epidermo-dysplasia verruciformis), warts may
reactivate or persist.
DIAGNOSIS
Clinical Presentation7,8,9,10,11
Warts may adopt a variety of patterns depending on the anatomical location or morphology,
associated with other skin diseases, on the causative agent, duration, immunologic status, family
history, treatment history. The different types of warts with their causative factor, location and
appearance are given below:
Types Causative Location Appearance Figures
factor
Common HPV-1, -2, Hands but also Smooth, skin-coloured, scaly, or
warts -4, -27, -57, often on the face rough, spiny papules or nodules
(Verruca -63 and genitals often more easily felt than
Vulgaris) seen. As the lesion enlarges,
an irregular hyperkeratotic
surface develops with the
classic ‘warty’ appearance.
They are more often multiple
than single. Pain is rare
6 Longworth MS, Laimins LA. Pathogenesis of human papillomavirus in differentiating epithelia. Microbiol Mol Biol Rev. 2004;68(2):362-372.
7 Hunter JAA, Savin JA, Dahl MV. Infections. In Clinical Dermatology. 2nded.London: Blackwell Science Ltd;1989: p.172-175.
8 Borrie P. Virus Diseases. In: Roxburgh’s Common Skin Diseases. 14thed. London: The English Language Book Society and H.K. Lewis& Co.
Ltd.;1961; p.91-92
9 James WD, Berger TG, Elston DM. Andrews’ Diseases of the Skin Clinical Dermatology. 10th ed. Philadelphia, USA: Saunders Elsevier; 2006.
10 Androphy. EJ, Kirnbauer R. Human Papilloma Virus infections. In: Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, Wolff K (ed).
Fitzpatrick’s Dermatology in General medicine. 8th ed (2). USA: McGraw-Hill Companies; 2012: p.2421-2433.
11 Dinulos JGH. Warts [Internet] MSD Manual professional version. 2019 [cited 2020 Feb 19]. Available from: https://www.msdmanuals.com/
en-in/professional/dermatologic-disorders/viral-skin-diseases/warts
Plane warts HPV-3, -10, Face and eyebrows Smooth, flat-topped papules,
(Flat warts -28 and41 and back of the skin coloured or light brown;
or Verruca hands they become inflamed as they
Plana) resolve spontaneously. Lesions
are multiple, painless, arranged
along a scratch line. There is
a tendency for the warts to
koebnerize, forming linear,
slightly raised, papular lesions
INVESTIGATIONS2,12,13,14
• Warts are usually diagnosed by their clinical appearance, but a histological examination may
need to be performed for warts resistant to treatment and for verrucous lesions in immuno-
compromised individuals.
• A cardinal sign of warts is the absence of skin lines crossing their surface and the presence of
pinpoint black dots (thrombosed capillaries) or bleeding when warts are shaved.
• Distinctive large keratinocytes (koilocytes) with small pyknotic nuclei surrounded by clear
cytoplasm are found in the upper layers of the epidermis.
• Typing of HPV based on DNA homology is a technique currently available in only a few
laboratories.
12 Sterling JC, Gibbs S, Hussain SSH, Mohd Mustapa MF, Handfield-Jones SE. British Association of Dermatologists’ guidelines for the
management of cutaneous warts. British Journal of Dermatology. 2014;171(4):696-712.
13 Corey L. Warts and Molluscum Contagiosum, Viral Diseases. In: Petersdorf RG, Adams RD, Braunwald E, Isseslbacher KJ, Martin JB, Wilson JD
(ed) Harrison’s Principles of Internal Medicine.10th ed. Singapore: McGraw-Hill International Book Company; 1983:p-1174-1175.
14 Lipke MM. An Armamentarium of Wart Treatments. Clin Med Res. 2006;4(4): 273-293.
When clinically assessing skin lesions, the following steps are useful to aid diagnosis:15
• Inspect the patient: Where on the body are the lesions? How many lesions are there? If there are
multiple lesions, do they follow a pattern or are they on a specific area?
• Describe the lesions: What is the largest diameter of lesion? What is ther colour? Are there
any secondary changes, e.g. lichenification, crusting, excoriation (scratch marks), ulceration,
erosion, fissure (thin crack), hypertrophy (increase in skin) or granuloma? Is there a clear
defined border? Is it regular?
• Palpate the lesion: Feel the surface, consistency, mobility, tenderness and temperature (use
gloves to prevent infection)
• Check the patient’s overall health: Examine the nails, scalp, hair and mucous membranes. Is there
any lymphadenopathy? Does the patient have fever?
DIFFERENTIAL DIAGNOSIS8,11
15 Akram S and Zaman H. Warts and verrucas: assessment and treatment. The Pharmaceutical Journal. 2015; 294 (7867):662-664.
16 Hogendoorn GK, Bruggink SC, Hermans KE, Kouwenhoven STP, Quint KD, Wolterbeek R, et al. Developing and validating the Cutaneous WARTS
(CWARTS) diagnostic tool: a novel clinical assessment and classification system for cutaneous warts. British Journal of Dermatology. 2018;
178(2):527–534.
17 Shanler SD, Powala C, Shields A, Bradshaw M, Schnyder J. Rater Reliability Testing of the Physician Wart Assessment for Common Warts: A
noninterventional, observational study. Journal of the American Academy of Dermatology. 2019; 81(4): AB263.
COMPLICATIONS13,14,18
PREVENTION19
HPV is contagious, people with warts should take following steps to avoid spreading the virus:
RED FLAGS16
• Patients presenting with any of the above symptoms should be referred to a dermatologist for
further assessment (e.g., biopsy and histological studies).
MANAGEMENT
General management12,20
There is no single treatment that is 100% effective, and different types of treatment may need to be
combined. Recurrences are common with almost all the treatment modalities. There is a possibility
of spontaneous regression if left untreated. Warts in adults, in those with a long duration of infection
and in immuno-suppressed patients are less likely to resolve spontaneously and are more recalcitrant
to treatment. Different types of warts and those at different sites may need differing treatments. The
ideal aims of treatment of warts are to remove the warts with no recurrence or scars and to induce
life-long immunity.
The general indications for treatment are: location, size, number and type, pain, interference with
function, emotional discomfort, cosmetic embarrassment, age and risk of malignancy. An immune
response is usually essential for clearance. Immunocompromised individuals may never show wart
clearance. Highest clearance rates for various treatments are usually in younger individuals who
have a short duration of infection.
Homoeopathic management
Warts are classified under one sided-diseases, as external local malady and are included under miasm
sycosis. Although warts are local diseases, they are treated with internal remedies which arebased on
comprehensive understanding of the patient; i.e. constitutional and anti-miasmatic treatment.
Research studies in homoeopathy have shown encouraging results for treatment of warts.21,22,23,24 In
homoeopathic literature25,26,27,28 large number of medicines have been documented for different
type of warts. Various studies21,22,23,24 (both observational and RCTs) have shown the effectiveness
of homoeopathic medicines in verruca vulgaris, verruca plana and verruca plantaris. Some of the
most frequently used medicines with positive results are: Thuja occidentalis, Ruta graveolens,
Calcarea carbonica, Dulcamara, Antimonium crudum, Causticum, Nitric acid, Natrum muriaticum,
Opium.
20 Sterling JC, Handfield-Jones S, Hudson PM, British Association of Dermatologists. Guidelines for the management of cutaneous warts. British
Journal of Dermatology. 2001;144(1):4-11.
21 Kainz JT, Kozel G, Haidvogl M, Smolle J. Homoeopathic versus placebo therapy of children with warts on the hands: a randomized, double-
blind clinical trial. Dermatology.1996;193(4):318-320.
22 Labrecque M, Audet D, Latulippe LG, Drouin J. Homeopathic treatment of plantar warts. Canadian Medical Association Journal. 1992: 146(10):
1749–1753.
23 Manchanda RK, Mehan N, Bahl R, Atey R. Double Blind Placebo Controlled Clinical Trials of Homoeopathic Medicines in Warts and Molluscum
Contagiosum. [Internet]. New Delhi Dilli Homoeopathic Anusandhan Parishad. [cited on 2020 Feb 19]. Available from: http://homeo.
delhigovt.nic.in/wps/wcm/connect/doit-homeopathy/Homeopathy/Home/Clinical+Studies+And+Publications/Warts
24 Gupta R, Bhardwaj OP, Manchanda RK. Homoeopathy in the treatment of warts. British Homeopathic Journal. 1991; 80(2):108-111.
25 Boericke W. Boericke’s New Manual of Homoeopathic Materia Medica with Repertory: Third Revised & Augmented Edition based on Ninth
Edition. New Delhi: B. Jain Publishers (P) Ltd.; 2007.
26 Das RBB. Miscellaneous. Select your remedy. 21st Revised ed. Delhi: B. Jain Publishers (P) Ltd; 2003: p.573-574.
27 HC Allen. Keynotes and Characteristics with Comparisons of some of the Leading Remedies of the Materia Medica. New Delhi: B. Jain
Publishers (P) Ltd.;1997.
28 Lilienthal S. Homoeopathic Therapeutics. Reprint edition. New Delhi: B. Jain Publishers (P) Ltd.; 2004.
In Synthesis repertory29, 136 medicines are found in chapter SKIN under the rubric ‘Warts’. The
frequently verified characteristic features of some organospecific remedies are: Anagallis: Possesses
power of softening flesh and destroying warts. Natrium sulphuricum: Sycotic excrescences, wart-
like red lumps all over the body. Worse in damp weather. Staphysagria: Fig warts pedunculated.
Better from warmth. Cinnabaris (Mercurius Sulphuratus Ruber): Prepuce swollen; warts on it,
which bleed easily. Sabina: Fig warts with intolerable itching and burning. Worse from heat and
warm air. Kalium muriaticum: Warts on the hands. Sepia officianalis: Warts on margin of prepuce,
on the body, large hard black warts. Magnesium sulphuricum: Warts on entire face. Ferrum
picricum: Multiple warts. Hands covered with warts, specific for corns. Natrium carbonicum:
Warts on palms of hands; sore to touch.
The frequently prescribed polycrest medicines for warts with their indications are given below:
Thuja Chilly patient; with illusions and fixed ideas. • Warts on cheeks, upper lips, neck,
occidentalis Unhealthy skin with tendency for warty hand, fingers, nose, head, chin, wart-
growths; oily/ greasy sweat, face and stool; like excrescences upon mucous
perspiration on uncovered parts. Complaints and cutaneous surfaces, sycotic
worse from cold, warm air and damp humid cauliflower excrescences
atmosphere and chronic complaints better • Fig warts, bleeding warts, large, seedy,
during a cold smelling like old cheese or herring
brine, pedunculated, hard, dark-
coloured, horny, broad conical, easily
splitting from their edge on their
surface, ulcerated, itching, indented,
small, oozing moisture
• Dry skin, with brown spots, nails
crippled, brittle and soft
Calcarea Chilly patient; takes cold easily; fat, fair, • Warts on arms, hands, fingers and
carbonica flabby, distended abdomen; pale, weak, easily face, neck, and upper extremities
tired; head sweats profusely while sleeping; • Fig-warts, smelling like old cheese,
sour smelling discharges; longing for fresh ulcerating warts, inflamed warts,
air; desire for eggs and indigestible things, itching warts small, horny, painful
sweets aversion to meat and milk; fearful, shy, stinging warts
timid, slow and sluggish; feels better when
constipated
29 Schroyens F. Synthesis Repertory ver. 9.1. New Delhi: B Jain Publishers Pvt. Ltd.; 2002.
Causticum Chilly patient. Burning, rawness and soreness • Warts on eyelids, eyebrow, face; on the
are characteristic. Intensely sympathetic. nose
Paralysis of single part. Aversion to sweets. • Fleshy warts close to nails, tips of
Better damp, wet, weather fingers and hands, back of the tongue,
jagged
• Painful warts, large, pedunculated,
horny warts
• Warts exuding moisture and bleeding
easily
Antimonium Chilly patient. Excessive irritability and • Warts on the soles of feet and palms of
crudum fretfulness with thickly coated white tongue. hands, horny warts
For children and old people with tendency
to grow fat. Aggravated by heat and cold
bathing. Desire for acids pickles
Nitricum Chilly patient. Offensive discharges especially • Warts on the hands, on face, eyelids,
acidum urine, feces and perspiration. Sensitive to neck, sternum, arms, hands, fingers,
noise, pain, touch jar. Pain sharp, sticking, lips, pedunculated warts, large jagged
pricking as from splinters, suddenly appearing • Cauliflower-like warts, bleeds when
and disappearing touched, bleed on washing, oozing,
moist painful, sticking, and pricking
Dulcamara Chilly patient. Complaints during hot days • Warts on fingers, (palmar surface)
and cold nights towards the close of summer. hands and face, fleshy, small, hard
Discharges thick yellow mucoid. Aggravation horny, pedunculated, flat, large,
in cold in general, damp, rainy weather smooth, liable to eruption
Natrum Hot patient; poorly nourished, great • Warts on palms of hands, bleeding,
muriaticum emaciation (marked on neck); losing flesh painful, old warts with cutting pain
while living well; craving for salt; aversion
to bread and fatty things; constipated;
increased thirst; mapped tongue with red
insular patches; melancholic, sad, plays
alone, irritable, cross, cries when spoken to;
awkward, hasty, drops things from nervous
weakness; disposition to weep without cause,
consolation aggravates
Ruta All parts of the body are painful as if bruised. • Warts on the palms of hands with sore
graveolens Feeling of intense lassitude, weakness and pains flat, smooth
despair. Constipation from inactivity or
impaction. Over straining of ocular muscles.
Eye strain followed by headache.
Sulphur Hot patient, kicks off the cloth at night; dirty, • Warts on the hands of onanists, arms,
filthy, does not want to be washed; lean, thin, hands, fingers, under the eyes, old,
stoop-shouldered; child who walks and sit inflamed, small, painful, hard, horny
stooping; red orifices; desires sweets, sugar,
meat; when the best selected remedy fails to
improve.
No Improvement Yes
No Improvement Yes
Red flags
Consider for integrative care
• Sudden increase in size,
change in appearance or
color of the wart. Intolerable
pain
• Interference in daily activities
• Lack of mirror image lesion in
any of the four quadrants of
the body); irregular border;
two or more colours in the
lesion
• Diameter more than 7mm.