INTERNS THESIS TOPIC

Name of Intern:

Sr. No Name of Subject Thesis Topic

1. Practice of Medicine Pancreatitis

2. Obgy Infertility

3. Surgery Otitis

4. Community Medicine RHD

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Sr. No Topic Page No.

1. Introduction

2. Epidemiology

3. Aetiology

4. Pathophysiology

5. Sign and Symptoms

6. Clinnical Course

7. Diagnosis

8. Management

9. Homeopathic Management

10. Cases
1. Introduction to RHD

What is rheumatic heart disease?

Rheumatic heart disease is a condition in which the heart
valves have been permanently damaged by rheumatic
fever. The heart valve damage may start shortly after
untreated or under-treated streptococcal infection such as
strep throat or scarlet fever. An immune response causes
an inflammatory condition in the body which can result in
on-going valve damage.

Who is at risk?
Rheumatic fever mostly affects children and adolescents in low-
and middle-income countries, especially where poverty is
widespread and access to health services is limited. People
who live in overcrowded and poor conditions are at greatest
risk of developing the disease.

Where rheumatic fever and rheumatic heart disease are

endemic, rheumatic heart disease is the principal heart disease
seen in pregnant women, causing significant maternal and
perinatal morbidity and mortality. Pregnant women with
rheumatic heart disease are at risk of adverse outcomes,
including heart arrythmias and heart failure due to increased
blood volume putting more pressure on the heart valves. It is
not uncommon for women to be unaware that they have
rheumatic heart disease until pregnancy.

Despite it being eradicated in many parts of the world, the

disease remains prevalent in sub-Saharan Africa, the Middle
East, Central and South Asia, the South Pacific, and among
immigrants and older adults in high-income countries,
especially in indigenous peoples.
2. Epidemiology
About 33 million people are affected by rheumatic heart
disease with an additional 47 million
having asymptomatic damage to their heart valves. As of 2010
globally it resulted in 345,000 deaths, down from 463,000 in
1990.
In Western countries, rheumatic fever has become fairly rare
since the 1960s, probably due to the widespread use of
antibiotics to treat streptococcus infections. While it has been
far less common in the United States since the beginning of the
20th century, there have been a few outbreaks since the
1980s. The disease is most common among Indigenous
Australians (particularly in central and northern
Australia), Māori, and Pacific Islanders, and is also common
in Sub-Saharan Africa, Latin America, the Indian Subcontinent,
the Middle East, and North Africa.
Rheumatic fever primarily affects children between ages 5
and 17 years and occurs approximately 20 days after strep
throat. In up to a third of cases, the underlying strep infection
may not have caused any symptoms.
The rate of development of rheumatic fever in individuals with
untreated strep infection is estimated to be 3%. The incidence
of recurrence with a subsequent untreated infection is
substantially greater (about 50%).The rate of development is
far lower in individuals who have received antibiotic treatment.
Persons who have suffered a case of rheumatic fever have a
tendency to develop flare-ups with repeated strep infections.
The recurrence of rheumatic fever is relatively common in the
absence of maintenance of low dose antibiotics, especially
during the first three to five years after the first episode.
Recurrent bouts of rheumatic fever can lead to valvular heart
disease. Heart complications may be long-term and severe,
particularly if valves are involved. In countries in Southeast-
Asia, sub-saharan Africa, and Oceania, the percentage of
people with rheumatic heart disease detected by listening to the
heart was 2.9 per 1000 children and by echocardiography it
was 12.9 per 1000 children. Echocardiographic screening
among children and timely initiation of secondary antibiotic
prophylaxis in children with evidence of early stages of
rheumatic heart disease may be effective to reduce the burden
of rheumatic heart disease in endemic regions.

Acute rheumatic fever is caused by the body’s autoimmune

response to a group A streptococcal infection, classically
pharyngitis. Rheumatic heart disease refers to the long-term
cardiac damage caused by either a single severe episode or
multiple recurrent episodes of acute rheumatic fever. It is
rheumatic heart disease that remains a significant worldwide
cause of morbidity and mortality, particularly in resource-poor
settings. Improved living conditions and widespread treatment
of superficial group A streptococcal infections have meant
acute rheumatic fever/rheumatic heart disease are now rare in
developed countries although some Indigenous populations
living in wealthy nations are adversely affected.

Acute rheumatic fever largely affects children between the ages

of 5–14 years with risk factors for acute rheumatic
fever/rheumatic heart disease including age, sex,
environmental influences that increase exposure to group A
streptococcal infections, and host susceptibility. Since
rheumatic heart disease results from cumulative damage, the
peak prevalence of clinically symptomatic rheumatic heart
disease occurs between the ages of 20–40 years. Conservative
estimates indicate between 275,000 and 345,000 deaths occur
each year from rheumatic heart disease with global burden of
disease figures in 2013 calculating at least 32.9 million
prevalent rheumatic heart disease cases. In 2015, rheumatic
heart disease was ranked as the 43rd leading cause of years of
life lost and is attributed to an annual 1.8 million years lived
with disability and 9 million lost disability-adjusted life years.
More
than 75% of the world’s children are currently living in countries
where rheumatic heart disease remains endemic.

Effective rheumatic heart disease prevention, control, and

management warrants prioritization if World Health
Organization global targets to reduce premature deaths from
cardiovascular diseases by 25% by 2025 are to be achieved.

Rheumatic fever and rheumatic heart disease are diseases of

poverty and economic disadvantage. In developing areas of
the world, severe disease caused by group A Streptococcus
(GAS; eg, ARF, rheumatic heart disease, glomerulonephritis,
and invasive infections) is estimated to affect over 33 million
people and is the leading cause of cardiovascular death during
the first five decades of life . ARF can occur at any age,
although most cases occur in children 5 to 15 years of age .
Worldwide, based upon conservative estimates, there are
approximately 470,000 new cases of ARF and 275,000 deaths
attributable to rheumatic heart disease each year . Most cases
occur in low- and middle-income countries and among
Indigenous groups .
Regions with the highest rates are likely to have the least
accurate data with substantial underreporting.

The mean incidence of ARF is 19 per 100,000 school-aged

children worldwide, but it is lower (≤2 cases per 100,000
school-aged children) in the United States and other
developed countries . In many low- and middle-income
countries and in certain Indigenous populations, such as those
in Australia and New Zealand, the incidence of ARF is
substantially higher, with some of the highest rates reported in
Indigenous Australians at 153 to 380 cases per 100,000
children aged 5 to 14 years .
3. Aetiology

Overview

Rheumatic heart disease is cardiac inflammation and scarring

triggered by an autoimmune reaction to infection with group A
streptococci. In the acute stage, this condition consists of
pancarditis, involving inflammation of the myocardium,
endocardium, and epicardium. Chronic disease is manifested
by valvular fibrosis, resulting in stenosis and/or insufficiency.
Rheumatic fever is rare before age 5 years and after age 25
years; it is most frequently observed in children and
adolescents. The highest incidence is observed in children
aged 5-15 years and in underdeveloped or developing
countries where antibiotics are not routinely dispensed for
pharyngitis and where compliance is low.
4. Pathophysiology

Rheumatic fever is a systemic disease affecting the connective

tissue around arterioles, and can occur after an untreated strep
throat infection, specifically due to group A
streptococcus (GAS), Streptococcus pyogenes. It is believed to
be caused by antibody cross-reactivity. This cross-reactivity is
a type II hypersensitivity reaction and is termed molecular
mimicry. Usually, self reactive B cells remain anergic in the
periphery without T cell co-stimulation. During a streptococcal
infection, mature antigen-presenting cells such as B cells
present the bacterial antigen to CD4+T cells which differentiate
into helper T2 cells. Helper T2 cells subsequently activate the B
cells to become plasma cells and induce the production of
antibodies against the cell wall of Streptococcus. However the
antibodies may also react against the myocardium and joints,
[12]
producing the symptoms of rheumatic fever. S. pyogenes is
a species of aerobic, cocci, gram-positive
bacteria that are non-motile, non-spore forming, and forms
chains and large colonies.
S. pyogenes has a cell wall composed of
branched polymers which sometimes contain M protein,
a virulence factor that is highly antigenic. The antibodies which
the immune system generates against the M protein may cross-
react with heart muscle cell protein myosin, heart
muscle glycogen and smooth muscle cells of arteries,
inducing cytokine release and tissue destruction. However, the
only proven cross-reaction is with perivascular connective
tissue. This inflammation occurs through direct attachment of
complement and Fc receptor-mediated recruitment of
neutrophils and macrophages. Characteristic Aschoff bodies,
composed of swollen eosinophilic collagen surrounded by
lymphocytes and macrophages can be seen on light
microscopy. The larger macrophages may become Anitschkow
cells or Aschoff giant cells. Rheumatic valvular lesions may
also involve a cell-mediated immunity reaction as these lesions
predominantly contain T-helper cells and macrophages.
In rheumatic fever, these lesions can be found in any layer of
the heart causing different types of carditis. The inflammation
may cause a serofibrinous pericardial exudate described as
"bread-and-butter" pericarditis, which usually resolves without
sequelae. Involvement of the endocardium typically results
in fibrinoid necrosis and wart formation along the lines of
closure of the left-sided heart valves. Warty projections arise
from the deposition, while subendocardial lesions may induce
irregular thickenings called MacCallum plaques.

Rheumatic heart disease

Pathophysiology of rheumatic heart disease

showing an (right of image), as seen in rheumatic heart disease. .

Chronic rheumatic heart disease (RHD) is characterized by

repeated inflammation with fibrinous repair. The cardinal
anatomic changes of the valve include leaflet thickening,
commissural fusion, and shortening and thickening of the
tendinous cords. It is caused by an autoimmune reaction to
Group A β-hemolytic streptococci (GAS) that results in valvular
damage.[16] Fibrosis and scarring of valve
leaflets, commissures and cusps leads to abnormalities that
can result in valve stenosis or regurgitation. The inflammation
caused by rheumatic fever, usually during childhood, is
referred to as rheumatic valvulitis. About half of patients with
rheumatic fever develop inflammation involving valvular
endothelium. The majority of morbidity and mortality associated
with rheumatic fever is caused by its destructive effects on
cardiac valve tissue. The pathogenesis of RHD is complex and
not fully understood, but it is known to involve molecular
mimicry and genetic predisposition that lead to autoimmune
reactions.
Molecular mimicry occurs when epitopes are shared between
host antigens and Streptococcus antigens. This causes an
autoimmune reaction against native tissues in the heart that
are incorrectly recognized as "foreign" due to the cross-
reactivity of antibodies generated as a result of epitope sharing.
The valvular endothelium is a prominent site of lymphocyte-
induced damage. CD4+ T cells are the major effectors of heart
tissue autoimmune reactions in RHD. Normally, T cell
activation is triggered by the presentation of bacterial antigens.
In RHD, molecular mimicry results in incorrect T cell activation,
and these T lymphocytes can go on to activate B cells, which
will begin to produce self-antigen-specific antibodies. This
leads to an immune response attack mounted against tissues
in the heart that have been misidentified as pathogens.
Rheumatic valves display increased expression of VCAM-1, a
protein that mediates the adhesion of lymphocytes. Self-
antigen-specific antibodies generated via molecular mimicry
between human proteins and streptococcal antigens up-
regulate VCAM-1 after binding to the valvular endothelium.
This leads to the inflammation and valve scarring observed in
rheumatic valvulitis, mainly due to CD4+ T cell infiltration.
While the mechanisms of genetic predisposition remain
unclear, a few genetic factors have been found to increase
susceptibility to autoimmune reactions in RHD. The dominant
contributors are a component of MHC class II molecules, found
on lymphocytes and antigen-presenting cells, specifically
the DR and DQ alleles on human chromosome 6. Certain allele
combinations appear to increase RHD autoimmune
susceptibility. Human leukocyte antigen (HLA) class II allele
DR7 (HLA-DR7) is most often associated with RHD, and its
combination with certain DQ alleles is seemingly associated
with the development of valvular lesions. The mechanism by
which MHC class II molecules increase a host's susceptibility to
autoimmune reactions in RHD is unknown, but it is likely related
to the role HLA molecules play in presenting antigens to T cell
receptors, thus triggering an immune response. Also found on
human chromosome 6 is the cytokine TNF-α which is also
associated with RHD. High expression levels of TNF-α may
exacerbate valvular tissue inflammation, contributing to RHD
pathogenesis. Mannose-binding lectin (MBL) is an inflammatory
protein involved in pathogen recognition. Different variants of
MBL2 gene regions are associated in RHD. RHD-
induced mitral valve stenosis has been associated with MBL2
alleles encoding for high production of MBL. Aortic valve
regurgitation in RHD patients has been associated with
different MBL2 alleles that encode for low production of
MBL. Other genes are also being investigated to better
understand the complexity of autoimmune reactions that occur
in RHD.
5. Sign and Symptoms

The disease typically develops two to four weeks after a throat

infection. Symptoms include: fever, painful joints with those
joints affected changing with time, involuntary muscle
movements, and occasionally a characteristic non-itchy rash
known as erythema marginatum. The heart is involved in about
half of the cases. Damage to the heart valves usually occurs
only after multiple attacks but may occasionally occur after a
single case of RF. The damaged valves may result in heart
failure and also increase the risk of atrial fibrillation
and infection of the valves.

A recent history of strep infection or rheumatic fever is key to

the diagnosis of rheumatic heart disease. Symptoms of
rheumatic fever vary and typically begin 1 to 6 weeks after a
bout of strep throat. In some cases, the infection may have
been too mild to have been recognized, or it may be gone by
the time the person sees a doctor.

These are the most common symptoms of rheumatic fever:

 Fever
 Swollen, tender, red and extremely painful joints —
particularly the knees and ankles
 Nodules (lumps under the skin)
 Red, raised, lattice-like rash, usually on the chest, back,
and abdomen
 Shortness of breath and chest discomfort
 Uncontrolled movements of arms, legs, or facial muscles
 Weakness
Symptoms of rheumatic heart disease depend on the degree of
valve damage and may include:

 Shortness of breath (especially with activity or when

lying down)
 Chest pain
 Swelling
6. Clinical course

The Jones criteria were introduced in 1944 as a set of clinical

guidelines for the diagnosis of RF. The manifestations of RF in
the Jones criteria were divided into major and minor categories.
Suggested major manifestations were least likely to lead to an
improper diagnosis and included carditis, joint symptoms,
subcutaneous nodules, and chorea. Historical evidence of RF
or RHD also constituted a major manifestation. Minor
manifestations were considered suggestive of RF but were not
sufficient for the diagnosis and included clinical signs such as
fever and erythema marginatum, and laboratory markers of
inflammation. Presence of 2 major or 1 major and 2 minor
manifestations provided reasonable evidence of rheumatic
activity. However, because a previous history of definite RF or
RHD was considered a major criterion, presence of minor
manifestations was sufficient to establish the diagnosis of RF
recurrence.

To improve specificity, these guidelines have been periodically

modified. In the first modification, objectively identifiable arthritis
replaced joint symptoms as a major manifestation and
arthralgia was assigned to the minor category. The history of
previous RF or RHD was downgraded to the minor category
and therefore documentation of a major manifestation became
necessary for the diagnosis of recurrence of RF. On the other
hand, erythema marginatum was recommended as a major
criterion. Most importantly, the evidence of preceding group A
β-hemolytic streptococcal pharyngitis was added to the list of
minor manifestations in the modified Jones criteria. The
evidence of a prior streptococcal infection was considered
essential for the diagnosis of RF in the 1965 revision of the
Jones Criteria, and it was suggested that exclusion of clinical
syndromes of nonstreptococcal origin will further increase the
accuracy of the criteria. The increase in specificity adversely
affected the sensitivity, and 25% of the RF cases diagnosed by
modified criteria could not be diagnosed by revised Jones
criteria. Such cases usually presented in the relatively late
phase of the disease or with delayed manifestations of RF,
when antistreptococcal antibody titers suggestive of preceding
streptococcal infection had already normalized. Therefore, the
late manifestations of RF were subsequently exempted from
the requirement of elevated antistreptococcal antibody titers.

In the setting of RF, diagnosis of a primary episode of carditis is

based on presence of a significant apical systolic and/or basal
diastolic murmur(s), clinical presence of pericarditis, or
unexplained congestive heart failure. Pericarditis and
congestive heart failure almost never occur in the absence of
valvular involvement. In a recurrence of RF, rheumatic cardiac
involvement almost invariably occurs if the initial episode of RF
involved the heart. The term mimetic carditis was introduced to
explain this phenomenon. For the diagnosis of carditis in a
recurrence of RF, the revised Jones criteria recommended
demonstration of evidence either of pericarditis or an obvious
change in previous clinical cardiac findings. Changes in the
cardiac findings included appearance of a new murmur and
change in the previous murmurs or an obvious increase in
cardiac size in the clinical context of RF. The diagnosis of
rheumatic carditis by Jones criteria becomes difficult when
carditis is the isolated manifestation of RF. This is true
especially when carditis is subclinical, when it is apparent but
supportive noncarditic criteria for diagnosis of RF are not
fulfilled, or when the previous cardiac findings are not known
for documentation of interval change in cardiac findings during
the recurrence of disease. These difficulties led to a major
change in the 1992 update of Jones criteria wherein the
previous history of RF or RHD was excluded from the list of
minor manifestations, limiting the applicability of the Jones
criteria only to primary episodes of RF. This change
represented a return to the intent of the original proposal of
Jones, which did not require strict application of the criteria for
the diagnosis of a recurrence of RF.
The diagnosis of carditis therefore remains a problem, and the
solution is obviously not the formulation of yet another set of
clinical criteria. The development of laboratory aids of
incremental diagnostic use is desirable. Because valvulitis
constitutes the sine qua non of rheumatic carditis,
echocardiographic documentation of valvular regurgitant
lesions should, theoretically, be of significant help.
7. Diagnosis

People with rheumatic heart disease will have or recently had a

strep infection. A throat culture or blood test may be used to
check for strep.

They may have a murmur or rub that may be heard during a

routine physical exam. The murmur is caused by the blood
leaking around the damages valve. The rub is caused when the
inflamed heart tissues move or rub against each other.

Along with a complete medical history and physical exam, tests

used to diagnose rheumatic heart disease may include:

 Echocardiogram (echo). This test uses sound waves to

check the heart's chambers and valves. The echo sound
waves create a picture on a screen as an ultrasound
transducer is passed over the skin overlying the heart.
Echo can show damage to the valve flaps, backflow of
blood through a leaky valve, fluid around the heart, and
heart enlargement. It’s the most useful test for
diagnosing heart valve problems.
 Electrocardiogram (ECG). This test records the strength
and timing of the electrical activity of the heart. It shows
abnormal rhythms (arrhythmias or dysrhythmias) and can
sometimes detect heart muscle damage. Small sensors
are taped to your skin to pick up the electrical activity.
 Chest X-ray. An X-ray may be done to check your lungs
and see if your heart is enlarged.
 Cardiac MRI. This is an imaging test that takes detailed
pictures of the heart. It may be used to get a more
precise look at the heart valves and heart muscle.
 Blood tests. Certain blood tests may be used to look for
infection and inflammation.
Modified Jones criteria were first published in 1944 by T.
Duckett Jones, MD. They have been periodically revised by
the American Heart Association in collaboration with other
groups. According to revised Jones criteria, the diagnosis of
rheumatic fever can be made when two of the major criteria,
or one major criterion plus two minor criteria, are present
along with evidence of streptococcal infection: elevated or
rising antistreptolysin O titre or Anti-DNase B. A recurrent
episode is also diagnosed when three minor criteria are
present. Exceptions are chorea and indolent carditis, each of
which by itself can indicate rheumatic fever. An April 2013
review article in the Indian Journal of Medical Research stated
that echocardiographic and Doppler (E & D) studies, despite
some reservations about their utility, have identified a massive
burden of rheumatic heart disease, which suggests the
inadequacy of the 1992 Jones' criteria. E & D studies have
identified subclinical carditis in patients with rheumatic fever, as
well as in follow-ups of rheumatic heart disease patients who
initially presented as having isolated cases of Sydenham's
chorea. Signs of a preceding streptococcal infection include:
recent scarlet fever, raised antistreptolysin O or other
streptococcal antibody titre, or positive throat culture. The last
revision of 2015 suggested variable diagnostic criteria in low-
risk and high-risk populations to avoid overdiagnosis in the first
category and underdiagnosis in the last one. Low-risk
populations were defined as those with acute rheumatic fever
annual incidence ≤2 per 100 000 school-aged children or all-
age rheumatic heart disease prevalence of ≤1 per 1000. All
other populations were categorised as having a moderate or
high risk.
Major criteria

 Joint manifestations are the unique clinical signs that

have different implications for different population-risk
categories : Only polyarthritis (a temporary migrating
inflammation of the large joints, usually starting in the
legs and migrating upwards) is considered as a major
 criterion in low-risk populations, whereas monoarthritis,
polyarthritis and polyarthralgia (joint pain without
swelling) are all included as major criteria in high-risk
populations.
 Carditis: Carditis can involve the pericardium
(pericarditis which resolves without sequelae), some
regions of the myocardium (which might not provoke
systolic dysfunction), and more consistently the
endocardium in the form of valvulitis. Carditis is
diagnosed clinically (palpitations, shortness of breath,
heart failure, or a new heart murmur) or by
echocardiography/Doppler studies revealing mitral or
aortic valvulitis. Both of clinical and subclinical
carditis are now considered a major criterion.
 Subcutaneous nodules: Painless, firm collections of
collagen fibers over bones or tendons. They commonly
appear on the back of the wrist, the outside elbow, and
the front of the knees.
 Erythema marginatum: A long-lasting reddish rash that
begins on the trunk or arms as macules, which spread
outward and clear in the middle to form rings, which
continue to spread and coalesce with other rings,
ultimately taking on a snake-like appearance. This rash
typically spares the face and is made worse with heat.
 Sydenham's chorea (St. Vitus' dance): A characteristic
series of involuntary rapid movements of the face and
arms. This can occur very late in the disease for at least
three months from onset of infection.
Minor criteria

 Arthralgia: Polyarthralgia in low-risk populations and

monoarthralgia in others. However, joint manifestations
cannot be considered in both major and minor
categories in the same patient.
 Fever: ≥ 38.5 °C (101.3 °F) in low-incidence
populations and ≥ 38 °C (100.4 °F) in high-risk
populations.
 Raised erythrocyte sedimentation rate (≥60 mm in the
first hour in lox-risk populations and ≥30 mm/h in
others) or C reactive protein (>3.0 mg/dL).
 ECG showing a prolonged PR interval after accounting
for age variability (Cannot be included if carditis is
present as a major symptom)
8. Management

The management of rheumatic fever is directed toward the

reduction of inflammation with anti-inflammatory
medications such as aspirin or corticosteroids. Individuals with
positive cultures for strep throat should also be treated
with antibiotics.
Aspirin is the drug of choice and should be given at high doses.
One should watch for side effects like gastritis and salicylate
poisoning. In children and teenagers, the use of aspirin and
aspirin-containing products can be associated with Reye's
syndrome, a serious and potentially deadly condition. The
risks, benefits, and alternative treatments must always be
considered when administering aspirin and aspirin-containing
products in children and teenagers. Ibuprofen for pain and
discomfort and corticosteroids for moderate to severe
inflammatory reactions manifested by rheumatic fever should
be considered in children and teenagers.
Vaccine
No vaccines are currently available to protect against S.
pyogenes infection, although research is underway to develop
one.[42] Difficulties in developing a vaccine include the wide
variety of strains of S. pyogenes present in the environment
and the large amount of time and people that will be needed for
appropriate trials for safety and efficacy of the vaccine.[43]
Infection
People with positive cultures for Streptococcus
pyogenes should be treated with penicillin as long as allergy is
not present. The use of antibiotics will not alter cardiac
involvement in the development of rheumatic fever. Some
suggest the use of benzathine benzylpenicillin.
Monthly injections of long-acting penicillin must be given for a
period of five years in patients having one attack of rheumatic
fever. If there is evidence of carditis, the length of therapy may
be up to 40 years. Another important cornerstone in treating
rheumatic fever includes the continual use of low-dose
antibiotics (such as penicillin, sulfadiazine, or erythromycin) to
prevent recurrence.
Inflammation
While corticosteroids are often used, evidence to support this is
poor.[1] Salicylates are useful for pain.
Steroids are reserved for cases where there is evidence of an
involvement of the heart. The use of steroids may prevent
further scarring of tissue and may prevent the development of
sequelae such as mitral stenosis.
Heart failure
Some patients develop significant carditis which manifests
as congestive heart failure. This requires the usual treatment
for heart failure: ACE inhibitors, diuretics, beta blockers,
and digoxin. Unlike typical heart failure, rheumatic heart failure
responds well to corticosteroids.

Specific treatment for rheumatic heart disease will be

determined by your physician based on:
 your overall health and medical history
 extent of the disease
 your tolerance for specific medications, procedures,
or therapies
 expectations for the course of the disease
 your opinion or preference
Since rheumatic fever is the cause of rheumatic heart disease,
the best treatment is to prevent rheumatic fever from occurring.
Penicillin and other antibiotics can usually treat strep throat (a
streptococcus A bacterial infection) and stop acute rheumatic
fever from developing.
Persons who have previously contracted rheumatic fever are
often given continuous (daily or monthly) antibiotic treatments,
possibly for life, to prevent future attacks of rheumatic fever
and lower the risk of heart damage.
Antibiotic therapy has sharply reduced the incidence and
mortality rate of rheumatic fever/rheumatic heart disease. To
reduce inflammation, aspirin, steroids, or non-steroidal
medications may be given. Surgery may be necessary to repair
or replace the damaged valve.
9. Homeopathic Management
Rheumatic heart disease is a serious complication of rheumatic
fever. It refers to the chronic heart valve damage that can
develop years after a bout of rheumatic fever, often leading to
heart failure if left untreated.
Rheumatic fever is an inflammatory autoimmune disease that
can develop as a result of inadequately treated strep throat or
scarlet fever. When this happens, the immune system responds
abnormally with chronic inflammation and the gradual deposit
of calcium crystals in and around the valves of the heart.
Rheumatic fever is most common in children and adolescents.
Although strep throat is common in the United States,
rheumatic fever is considered rare is most developed countries.

Rheumatic fever systemic, febrile disease that is inflammatory

& non-suppurative in nature & variable in severity, duration &
sequelae.
It is acute febrile illness following streptococcal sore throat &
characterised by fleeting arthritis, pancarditis, leucocytosis &
raised ESR.

Following a streptococcal infection the patient will experience

the sudden occurrence of fever & joint pain; this is the most
common type of onset. Rheumatic fever may occur without any
sign or symptom of joint involvement. Acute rheumatic
fever usually affects children (5-15years) or young adults.

Rheumatic heart disease describes a group of short-term

(acute) and long-term (chronic) heart disorders that can occur
as a result of rheumatic fever. One common result of
rheumatic fever is heart valve damage. This damage to the
heart valves may lead to a valve disorder.
Rheumatic fever
Rheumatic fever is an inflammatory disease that may affect
many connective tissues of the body, especially those of the
heart, joints, brain or skin. It usually starts out as a strep throat
(streptococcal) infection. Anyone can get acute rheumatic
fever, but it usually occurs in children between the ages of 5
and 15 years. About 60% of people with rheumatic fever
develop some degree of subsequent heart disease.
Every part of the heart, including the outer sac (the
pericardium), the inner lining (the endocardium) and the valves
may be damaged by inflammation caused by acute rheumatic
fever. However, the most common form of rheumatic heart
disease affects the heart valves, particularly the mitral valve. It
may take several years after an episode of rheumatic fever for
valve damage to develop or symptoms to appear.
Symptoms
Symptoms of heart valve problems, which are often the result
of rheumatic heart disease, can include: chest pain, excessive
fatigue, heart palpitations (when the heart flutters or misses
beats), a thumping sensation in the chest, shortness of breath,
and swollen ankles, wrists or stomach
HOMOEOPATHIC REMEDIS
ARSENICUM ALBUM 30-- Palpitation , pain and dyspnea.
Rheumatic heart of cigarette smokers and tobacco chewers
AURUM MET 30- Pain in the heart and a feeling as if the heart
stopped beating for two or three seconds. Rheumatism with
hypertension
CACTUS GRANDIFLORUS 3X- Pain in the heart with feeling
of construction in it. Vertigo and low blood pressure
KALI NITRICUM 30- Violent stitch in the heart with steady with
steady but weak pulse
KALMIA LAT 30- Heartrheumatism of tobacco smokers and
chewers . Pains are so sharp as if he will not be able to take
the next breath. Pain travels to shoulder blades
LACHESIS 200- Rheumatic pains of heart specially during
menopause. Constricted feeling around the heart
NATRIUM IOD 30- Incipient rheumatic endocarditis. Vertigo
and dyspnea
RANUNCULUS BULBOSUS Q- 10-15 drops a dose relieves
various kinds of pains and rheumatic pains in the chest walls ,
in the ribs, sternum, heart, muscular tissue and shoulder
blades when these are worse in cold air and atmospheric
changes SPIGELIA 30- Rheumatic carditis with trembling pulse
SPONGIA 30- Rheumatism with asthmatic symptoms
SUMBUL 30- Aching and numbness of the left arm with pain in
the heart and hypochondrial regions

Case Study
This is a case of 52 years female suffering from Rheumatic
Valvular Heart Disease with Severe Mitral stenosis i.e. 0.7
cm2 along with H/O systemic embolism.
Her reports on 18th Dec 2004 were:
  Rheumatic valvular heart disease.
 Critical mitral stenosis. MVA 0.7 sqcm.
 Grade IV mitral regurgitation.
 Tiny thrombosis in left atrial appendage.
 Moderate PH.
This patient had (Lt) atrial thrombosis & systemic
thromboembolism which is the cause of 25% deaths in this
condition.
She was diagnosed as R.H.D. since 2002. As her condition
was critical, she was advised initially for the mitral balloon
valvuloplasty, but afterwards her consultant cardiologist also
refused for surgery as she had (Lt) atrial thrombosis (because
of that she had H/O unconsciousness for 9-10 times in
past.) which was crucial and he didn’t want to take risk. She
was advised to continue with medicines only. So, the patient &
her relatives gave up all the hopes of getting cured.
Severe mitral stenosis occurs when the opening is reduced to
1 cm2. At this stage, a mean LAP of 25 mm Hg is required to
maintain a normal cardiac output. With progressive stenosis,
critical flow restriction reduces left ventricular preload and
output. The increase in LAP also enlarges the left atrium and
raises pulmonary vascular pressures. The resulting pulmonary
congestion and reduced cardiac output can mimic primary left
ventricular failure. As the disease evolves, chronic elevation of
the LAP eventually leads to pulmonary hypertension, tricuspid
and pulmonary valve incompetence, and secondary right heart
failure.
The mitral valve orifice is normally about 4 cm2 in diastole.
Thromboembolism — Frequent complication of mitral
stenosis with an embolic event, most commonly cerebral.
Most emboli originate from the left atrium. The most common
site for embolism from this site is the cerebral circulation, but
any organ may be involved, especially spleen, kidneys, and
the coronary circulation, resulting in a myocardial infarction.
Emboli can also arise from the right atrium when there is
pulmonary hypertension and right ventricular and atrial
dilatation. Emboli from this site lead to pulmonary embolism
and infarction.
CASE NO.1
Date of Examination

Name
Address

Age Sex Religion

Occupation Marital Status

History of the Patient

A) Chief Complaints:

B) History of present Complaint :

C) Past History :

D) Family History :
E) Drug History :

F) History of Allergy :

G) Personal History :

H) Gynaecological & Obstetrical History:

a. Monarch and Menopause

b. L.M.P.

c. Menstrual History :

i. Time Duration :

ii. Quantity :

iii. Character of blood :

 iv. Other Peculiarities :

d. Leucorrhoea :

i. Time :

ii. Quantity :

iii. Character of blood :

iv. Other Peculiarities :

e. Obstetrical History :

f. Contraceptive procedure advocated by the patient ,if any

I) Homeopathic Generalities :

a) Physical General Symptoms

i. Diet :

ii. Appelite :

iii. Desire :

iv. Aversion :

v) Intolerance :
 vi) Thirst :

i. Urine :

ii. Stool :

iii. Sleep :

iv. Dreams :

v. Sweat :

vi. Thermal Reaction :

vii. Physical Makeup :

b). Mental General Symptoms :

Examination of the patient:

I General Survey :

Decubitus :

Build :

Nutrition :

Face :

Tongue :
Pallor :

Icterus :

Cyanosis :

Clubbing :

Oedema :

Pigmentation/Eruptions :

Temperature :

Pulse :

Respiratory :

Blood Pressure :

Weight/Height :

Gait :

II. Local Examination :

Inspection :

Palpation :

Percussion :
Auscultation :

C. Systematic Examination :

SUMMARY OF THE CASE :

A. Diagnosis :-

1.Different Diagnosis

2.Provisional Diagnosis

B. Investigation :-

C. Final Diagnosis :-

D. Characteristic Totality :-
E. Analysis of Symptoms :

F. Evaluation of Symptoms :

G. Points of favour of Miasms :

II. Miasmatic Diagnosis :

I. Symptoms taken for reportorization :

J. Repertorial Analysis :

L. Advice :

M. Followup :
CASE NO.2
Date of Examination

Name
Address

Age Sex Religion

Occupation Marital Status

History of the Patient

A) Chief Complaints:

B) History of present Complaint :

C) Past History :
D) Family History :

E) Drug History :

F) History of Allergy :

G) Personal History :

H) Gynaecological & Obstetrical History:

a. Monarch and Menopause

b. L.M.P.

c. Menstrual History :

i. Time Duration :
 ii. Quantity :

iii. Character of blood :

iv. Other Peculiarities :

d. Leucorrhoea :

i. Time :

ii. Quantity :

iii. Character of blood :

iv. Other Peculiarities :

e. Obstetrical History :

f. Contraceptive procedure advocated by the patient ,if any

I) Homeopathic Generalities :

a) Physical General Symptoms

i. Diet :

ii. Appelite :

iii. Desire :
 iv. Aversion :

v) Intolerance :

vi) Thirst :

i. Urine :

ii. Stool :

iii. Sleep :

iv. Dreams :

v. Sweat :

vi. Thermal Reaction :

vii. Physical Makeup :

b). Mental General Symptoms :

Examination of the patient:

I General Survey :

Decubitus :

Build :

Nutrition :
Face :

Tongue :

Pallor :

Icterus :

Cyanosis :

Clubbing :

Oedema :

Pigmentation/Eruptions :

Temperature :

Pulse :

Respiratory :

Blood Pressure :

Weight/Height :

Gait :

II. Local Examination :

Inspection :
Palpation :

Percussion :

Auscultation :

C. Systematic Examination :

SUMMARY OF THE CASE :

A. Diagnosis :-

1.Different Diagnosis

2.Provisional Diagnosis

B. Investigation :-

C. Final Diagnosis :-
D. Characteristic Totality :-

E. Analysis of Symptoms :

F. Evaluation of Symptoms :

G. Points of favour of Miasms :

II. Miasmatic Diagnosis :

I. Symptoms taken for reportorization :

J. Repertorial Analysis :

L. Advice :

M. Followup :
CASE NO.3
Date of Examination

Name
Address

Age Sex Religion

Occupation Marital Status

History of the Patient

A) Chief Complaints:

B) History of present Complaint :

C) Past History :
D) Family History :

E) Drug History :

F) History of Allergy :

G) Personal History :

H) Gynaecological & Obstetrical History:

a. Monarch and Menopause

b. L.M.P.

c. Menstrual History :
 i. Time Duration :

ii. Quantity :

iii. Character of blood :

iv. Other Peculiarities :

d. Leucorrhoea :

i. Time :

ii. Quantity :

iii. Character of blood :

iv. Other Peculiarities :

e. Obstetrical History :

f. Contraceptive procedure advocated by the patient ,if any

I) Homeopathic Generalities :

a) Physical General Symptoms

i. Diet :

ii. Appelite :
 iii. Desire :

iv. Aversion :

v) Intolerance :

vi) Thirst :

i. Urine :

ii. Stool :

iii. Sleep :

iv. Dreams :

v. Sweat :

vi. Thermal Reaction :

vii. Physical Makeup :

b). Mental General Symptoms :

Examination of the patient:

I General Survey :

Decubitus :

Build :
Nutrition :

Face :

Tongue :

Pallor :

Icterus :

Cyanosis :

Clubbing :

Oedema :

Pigmentation/Eruptions :

Temperature :

Pulse :

Respiratory :

Blood Pressure :

Weight/Height :

Gait :

II. Local Examination :

Inspection :
Palpation :

Percussion :

Auscultation :

C. Systematic Examination :

SUMMARY OF THE CASE :

A. Diagnosis :-

1.Different Diagnosis

2.Provisional Diagnosis

B. Investigation :-

C. Final Diagnosis :-
D. Characteristic Totality :-

E. Analysis of Symptoms :

F. Evaluation of Symptoms :

G. Points of favour of Miasms :

II. Miasmatic Diagnosis :

I. Symptoms taken for reportorization :

J. Repertorial Analysis :

L. Advice :

M. Followup :
CASE NO.4
Date of Examination

Name
Address

Age Sex Religion

Occupation Marital Status

History of the Patient

A) Chief Complaints:

B) History of present Complaint :

C) Past History :
D) Family History :

E) Drug History :

F) History of Allergy :

G) Personal History :

H) Gynaecological & Obstetrical History:

a. Monarch and Menopause

b. L.M.P.
 c. Menstrual History :

i. Time Duration :

ii. Quantity :

iii. Character of blood :

iv. Other Peculiarities :

d. Leucorrhoea :

i. Time :

ii. Quantity :

iii. Character of blood :

iv. Other Peculiarities :

e. Obstetrical History :

f. Contraceptive procedure advocated by the patient ,if any

I) Homeopathic Generalities :

a) Physical General Symptoms

i. Diet :
 ii. Appelite :

iii. Desire :

iv. Aversion :

v) Intolerance :

vi) Thirst :

i. Urine :

ii. Stool :

iii. Sleep :

iv. Dreams :

v. Sweat :

vi. Thermal Reaction :

vii. Physical Makeup :

b). Mental General Symptoms :

Examination of the patient:

I General Survey :

Decubitus :
Build :

Nutrition :

Face :

Tongue :

Pallor :

Icterus :

Cyanosis :

Clubbing :

Oedema :

Pigmentation/Eruptions :

Temperature :

Pulse :

Respiratory :

Blood Pressure :

Weight/Height :

Gait :

II. Local Examination :

Inspection :
Palpation :

Percussion :

Auscultation :

C. Systematic Examination :

SUMMARY OF THE CASE :

A. Diagnosis :-

1.Different Diagnosis

2.Provisional Diagnosis

B. Investigation :-
C. Final Diagnosis :-

D. Characteristic Totality :-

E. Analysis of Symptoms :

F. Evaluation of Symptoms :

G. Points of favour of Miasms :

II. Miasmatic Diagnosis :

I. Symptoms taken for reportorization :

J. Repertorial Analysis :

L. Advice :

M. Followup :
CASE NO.5
Date of Examination

Name
Address

Age Sex Religion

Occupation Marital Status

History of the Patient

A) Chief Complaints:

B) History of present Complaint :

 C) Past History :

D) Family History :

E) Drug History :

F) History of Allergy :

G) Personal History :

H) Gynaecological & Obstetrical History:

a. Monarch and Menopause

b. L.M.P.
 c. Menstrual History :

i. Time Duration :

ii. Quantity :

iii. Character of blood :

iv. Other Peculiarities :

d. Leucorrhoea :

i. Time :

ii. Quantity :

iii. Character of blood :

iv. Other Peculiarities :

e. Obstetrical History :

f. Contraceptive procedure advocated by the patient ,if any

I) Homeopathic Generalities :
 a) Physical General Symptoms
i. Diet :

ii. Appelite :

iii. Desire :

iv. Aversion :

v) Intolerance :

vi) Thirst :

i. Urine :

ii. Stool :

iii. Sleep :

iv. Dreams :

v. Sweat :

vi. Thermal Reaction :

vii. Physical Makeup :

b). Mental General Symptoms :

Examination of the patient:
I General Survey :

Decubitus :

Build :

Nutrition :

Face :

Tongue :

Pallor :

Icterus :

Cyanosis :

Clubbing :

Oedema :

Pigmentation/Eruptions :

Temperature :

Pulse :

Respiratory :

Blood Pressure :

Weight/Height :

Gait :
II. Local Examination :
Inspection :

Palpation :

Percussion :

Auscultation :

C. Systematic Examination :

SUMMARY OF THE CASE :

A. Diagnosis :-

1.Different Diagnosis

2.Provisional Diagnosis
B. Investigation :-

C. Final Diagnosis :-

D. Characteristic Totality :-

E. Analysis of Symptoms :

F. Evaluation of Symptoms :

G. Points of favour of Miasms :

II. Miasmatic Diagnosis :

I. Symptoms taken for reportorization :

J. Repertorial Analysis :

L. Advice :

M. Followup :