Infective endocarditis is characterized by proliferation of microorganisms on the heart's endothelium, resulting in the development of vegetations, most commonly on the cardiac valves. It can be classified as either acute or subacute. Acute endocarditis follows a rapidly progressive course while subacute progresses more slowly. Common causative organisms include streptococci, enterococci, and staphylococci. It is diagnosed using the Duke's Criteria based on clinical evidence, laboratory findings, and echocardiographic imaging. Homeopathic treatment focuses on addressing the underlying susceptibility and constitutional symptoms of each individual patient.

1. Infective Endocarditis
Dr. Mohit Mathur

2. What is Infective endocarditis?
The condition is characterized by proliferation of microorganisms on
the endothelium of heart resulting in development of vegetations. The
cardiac valves (both native & prosthetic) are most commonly involved
but the infection can involve any region with endocardial defect.

3. Classification of Infective Endocarditis
infective endocarditis
Acute endocarditis:
it is a hectically febrile illness, rapidly
damages cardiac structures, hematogenously
seeds extracardiac sites, and, if untreated,
progresses to death within weeks.
Subacute endocarditis:
It follows an indolent course; causes structural
cardiac damage only slowly, if at all; rarely
causes metastatic infection; and is gradually
progressive unless complicated by a major
embolic event or ruptured mycotic aneurysm.

4. Aetiology of infective endocarditis
• The organisms commonly implicated are:
• Streptococcia, Pneumococci, Enterococci, Staphylococcus aureus,
Coagulase-negative staphylococci, Fastidious gram-negative
coccobacilli (HACEK group) (Haemophilus, Actinobacillus,
Cardiobacterium, Eikenella, and Kingella), Gram-negative Bacilli,
Candida spp., Polymicrobial/miscellaneous, Diphtheroids.

5. Pathophysiology
endothelial
injury
•at the site of impact of high-velocity jets or on the low pressure side of a cardiac structural lesion allows either direct infection by virulent organisms or the development of an uninfected platelet-fibrin thrombus—a
condition called nonbacterial thrombotic endocarditis (NBTE)
•The thrombus subsequently serves as a site of bacterial attachment during transient bacteremia
•Organisms that cause endocarditis generally enter the bloodstream from mucosal surfaces, the skin, or sites of focal infection.
Formation of
vegetations
•organisms proliferate and induce a procoagulant state at the site by eliciting tissue factor from adherent monocytes.
•Fibrin deposition, resulting from tissue factor initiation of the coagulation cascade, combines with platelet aggregation, stimulated by tissue factor and independently by proliferating microorganisms, ultimately leads to
generation an infected vegetation.
clinical
features
•clinical manifestations are the result of factors such as:
•release of cytokines
•damage to the intracardiac structures
•embolization of vegetation fragments
•hematogenous infection of extra cardiac sites
•deposition of immune complexes

6. Clinical manifestations
Constitutional features:
• Fever: In patients with subacute presentations, fever is typically low-
grade and rarely exceeds 39.4°C (103°F); in contrast, temperatures
between 39.4° and 40°C (103° and 104°F) are often noted in acute
endocarditis. Fever may be blunted or absent in patients who are
elderly or severely debilitated or who have marked cardiac or renal
failure.
• Chill, sweat, anorexia, weight loss, malaise

7. Cardiac manifestations
• Cardiac murmurs: murmurs may be due to predisposing cardiac
pathology. Valvular damage and ruptured chordae may result in new
regurgitant murmurs
• Congestive heart failure develops in 30 to 40% of patients; it is usually
a consequence of valvular dysfunction but occasionally is due to
endocarditis-associated myocarditis or an intracardiac fistula.
• Pericarditis
• Varying degrees of heart blocks

8. Noncardiac manifestations
• Musculoskeletal symptoms, including nonspecific inflammatory
arthritis and back pain.
• Hematogenously seeded focal infection may involve any organ but
most often is clinically evident in the skin, spleen, kidneys, skeletal
system, and meninges. Arterial emboli are clinically apparent in up to
50% of patients.

9. Neurological manifestations
• Neurologic symptoms, most often resulting from embolic strokes,
occur in up to 40% of patients.
• Other neurologic complications include aseptic or purulent
meningitis, intracranial hemorrhage due to hemorrhagic infarcts or
ruptured mycotic aneurysms, seizures, and encephalopathy.
• Microabscesses in brain and meninges occur commonly in S. aureus
endocarditis.

10. Renal manifestations
• hypocomplementemic glomerulonephritis and renal dysfunction.
• Embolic renal infarcts cause flank pain and hematuria but rarely
cause renal dysfunction.

11. Other features
• Digital clubbing, splenomegaly,
• Peripheral manifestations- Osler’s nodes (painful tender swelling at
finger tips, probably as a result of vasculitis)
• Petechial haemorrhages in skin and mucous membrane; subungual
haemorrhages in finger & toe nails, Janeway lesions, Roth’s
spots(white centred retinal hemorrhages)

12. Laboratory investigations
• Duke’s Criteria is widely employed for diagnosis of infective endocarditis. It is
based on clinical, laboratory and echocardiographic evidence. Documentation of
two major criteria or one major criteria and three minor criteria or five minor
criteria allows a clinical diagnosis of definite infective endocarditis:
• Major criteria:
• Positive blood culture
• Echocardiographic evidence of endocardial involvement (oscillating intracardiac mass on
valves, abscess etc)
• Minor criteria:
• Predisposing heart condition or iv drug use
• Fever> 38.0°C(>100.4°F)
• Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm,
intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions
• Immunologic phenomena: glomerulonephritis, Osler’s nodes, Roth’s spots, rheumatoid factor
• Microbiologic evidence: positive blood culture but not meeting major criterion as noted
previouslya or serologic evidence of active infection with organism consistent with infective
endocarditis

13. Other investigations
• Complete blood count
• creatinine measurement,
• chest radiography and electrocardiography.
• The erythrocyte sedimentation rate, C-reactive protein level,
circulating immune complex titer, and rheumatoid factor
concentration are commonly increased in endocarditis.
• Cardiac catheterization is useful primarily to assess coronary artery
patency in older individuals who are to undergo surgery for
endocarditis.

14. Homoeopathic management
Though Infective endocarditis involves endocardium but it has systemic
manifestations. In majority of patients a definite predisposing factor
exist which makes the patient susceptible to this infection. Effective
homoeopathic treatment relies on exploration of the underlying
susceptibility and prominent constitutional features of patient.
The treatment should be reviewed at short intervals by repeat
echocardiography, blood culture & serum inflammatory markers.
Patient with hectic fever and positive blood cultures may need
admission for constant monitoring.
In case of injection drug abusers treatment can be difficult because of
risk of repeated bacteraemia.

15. As far as therapeutic medication is concerned, several remedies are
available to treat endocarditis that can be selected on the basis of
predisposing cause, constitutional features and modalities of the
patient. The commonly prescribed medicines are:
Abrotanum, Acetic Acid, Arsenicum Album, Aurum Metallicum, Aurum
Muriaticum, Cactus Grandiflora, Calcarea Carbonicum, Colchicum, Kali
Iodatum, Kalmia, Lachesis, Naja, Phosphorus, Spigelia, Spongia &
Veratrum Viride.

16. Important clinical rubrics for infective
endocarditis:
• Boger Boenninghausen Characteristics & Repertory (BBCR),
Chest(Inner), Heart and region of, inflammation
• Boericke’s repertory, Circulatory system, Inflammation (Endocarditis)
• Kent’s Repertory, Chest, Inflammation, Endocardium
• Complete Repertory- heart & circulation- inflammation- heart,
carditis: endocardium
• Kent repertory, chest, murmurs
• Kent’s Repertory, generalities, inflammation, internally
• Kent’s Repertory, septicaemia
• Kent’s Repertory, fever, septic fever

17. Thank you