Infective Endocarditis

Infective Endocarditis

1. Definition
   Infective endocarditis (IE) is a microbial infection of the inner lining of the heart, most often the heart valves. It is a serious condition that can rapidly damage cardiac structures and needs urgent treatment.

2. Synonyms (if any)
   Bacterial endocarditis – used when the infection is known to be caused by bacteria; the term emphasizes the bacterial origin but otherwise refers to the same disease.

3. Causes / Etiology

• Staphylococcus aureus – highly virulent, often produces acute IE after skin or intravenous catheter entry.
• Viridans group streptococci – less aggressive, usually follows dental procedures and produces sub‑acute IE.
• Enterococci – common after genitourinary manipulation; may cause either acute or sub‑acute forms.
• Fungi (Candida, Aspergillus) – occur in immunocompromised patients or those on long‑term antibiotics; tend to give chronic, indolent disease.
• Rare viruses (herpes simplex, CMV) – can seed the endocardium in severely immunosuppressed hosts.
  Each organism gains access to the bloodstream through a portal of entry (skin, oral cavity, urinary tract) and then adheres to damaged endocardium.

4. Types / Classification
   Acute infective endocarditis
   ‑ Definition: Sudden onset, high‑grade fever, rapid valve destruction.
   ‑ Causes: Mostly Staphylococcus aureus, sometimes Gram‑negative bacilli.
   ‑ Clinical features: Toxic appearance, new murmur, embolic phenomena within days.
   ‑ Duration: Days to a few weeks if untreated.
   ‑ Difference from chronic: Faster progression, more severe systemic toxicity.

Sub‑acute (chronic) infective endocarditis
‑ Definition: Insidious onset, low‑grade fever, gradual valve damage.
‑ Causes: Viridans streptococci, Enterococcus spp., HACEK organisms.
‑ Clinical features: Weight loss, night sweats, small peripheral lesions (Janeway lesions, Osler nodes).
‑ Duration: Weeks to months before diagnosis.
‑ Difference from acute: Slower symptom development, less dramatic systemic signs, more likely to produce large vegetations that embolise later.

5. Pathophysiology / Pathology – step by step

6. Endothelial injury – turbulent flow or pre‑existing valve disease damages the endocardial surface, exposing underlying collagen.

7. Platelet‑fibrin thrombus formation – the damaged area attracts platelets and fibrin, creating a sterile nidus.

8. Microbial adhesion – circulating microorganisms bind to the thrombus via surface adhesins.

9. Colonisation and vegetation growth – organisms multiply, producing a mass of organisms, fibrin, and inflammatory cells (vegetation).

10. Embolisation – fragments of vegetation break off and travel to distant organs, causing infarcts or septic emboli.

11. Immune response – circulating immune complexes may deposit in skin, kidney (glomerulonephritis) and cause systemic manifestations.

12. Clinical Features
    General (both acute and chronic)
    ‑ Fever, chills, sweats, fatigue, anorexia, weight loss.
    Acute IE specific
    ‑ High‑grade fever, rapid onset of new murmur, signs of sepsis, early heart failure.
    Chronic IE specific
    ‑ Low‑grade fever, night sweats, small peripheral lesions (Janeway lesions – painless erythematous macules; Osler’s nodes – painful nodules), splinter haemorrhages, prolonged malaise.
    Relevance – recognizing the pattern of lesions helps differentiate acute from sub‑acute disease and guides early investigation.

13. Complications
    Acute complications
    ‑ Severe valvular regurgitation → acute heart failure.
    ‑ Septic emboli to brain, spleen, kidney → stroke, infarction, abscess.
    ‑ Septic shock and multi‑organ failure.
    Chronic complications
    ‑ Progressive valve scarring → stenosis or chronic regurgitation.
    ‑ Mycotic aneurysms in cerebral vessels.
    ‑ Immune‑complex glomerulonephritis.
    Importance – many complications are life‑threatening; early detection can reduce mortality.

14. Investigations / Diagnosis
    Routine tests
    ‑ Blood cultures (three sets from different sites, 1 h apart) – to isolate the causative organism.
    ‑ Complete blood count – often shows leukocytosis or anemia of chronic disease.
    Specific tests
    ‑ Transthoracic echocardiogram (TTE) – first‑line imaging to detect vegetations, abscesses, valve dysfunction.
    ‑ Transesophageal echocardiogram (TEE) – higher sensitivity, especially for prosthetic valves or small vegetations.
    Confirmatory tests
    ‑ Modified Duke criteria – combines clinical, microbiological and echocardiographic findings to confirm IE.
    ‑ MRI/CT brain – if neurological symptoms suggest embolic stroke.

15. Differential Diagnosis (key points)

• Acute rheumatic fever – shares fever and murmur but has migratory arthritis, erythema marginatum, and Jones criteria.
• Non‑infective (marantic) endocarditis – sterile vegetations seen in malignancy; blood cultures remain negative.
• Libman‑Sacks endocarditis (SLE) – vegetations are small, verrucous, and occur on both sides of valve leaflets; associated with positive ANA.

10. Management / Treatment
    General management
    ‑ Hospital admission, cardiac monitoring, and supportive care (oxygen, IV fluids, analgesia).
    ‑ Strict aseptic technique for all invasive procedures to prevent further seeding.

Modern medicine treatment
‑ Empiric intravenous antibiotics started after first blood cultures (e.g., vancomycin + gentamicin + ceftriaxone) pending sensitivities.
‑ Tailor antibiotics to organism and susceptibility; typical duration 4–6 weeks for native valves, longer for prosthetic valves.
‑ Indications for surgery: refractory heart failure, uncontrolled infection, large mobile vegetations (>10 mm) or embolic events. Valve repair or replacement is performed accordingly.

Diet and lifestyle advice
‑ High‑protein, calorie‑dense diet to counteract catabolism and weight loss.
‑ Adequate fluid intake to maintain renal perfusion, especially when on nephrotoxic antibiotics.
‑ Avoid alcohol and smoking as they impair immune response and increase embolic risk.

11. Homeopathic Therapeutics (8 remedies, each with 7–8 points)

1. Streptococcinum
‑ Causation: After streptococcal throat infection or dental sepsis.
‑ Characteristic symptoms: Low‑grade fever, sore throat, feeling of a “lump” in throat.
‑ Modalities: Worse from cold air, better from warm drinks.
‑ Mental state: Irritable, anxious about health.
‑ Thirst and appetite: Thirst for warm water, appetite reduced.
‑ Discharges: Thin, yellow sputum if chest involved.
‑ Physical generals: Small painless erythematous spots on palms (Janeway‑like).
‑ Constitution: Young adults with recent sore throat; helps by targeting the streptococcal origin of the vegetation.

2. Pyrogenium
‑ Causation: Septicemia with high fever after wound infection.
‑ Characteristic symptoms: Burning fever, chills, feeling of heat in the body.
‑ Modalities: Worse from movement, better when lying still.
‑ Mental state: Restless, fearful of death.
‑ Thirst and appetite: Great thirst for cold water, appetite poor.
‑ Discharges: Foul‑smelling purulent exudate from any infected site.
‑ Physical generals: Rapid pulse, flushed face.
‑ Constitution: Patients with overwhelming infection; helps by reducing toxic fever.

3. Sanguis rubrum
‑ Causation: Blood‑borne infection, especially after dental extraction.
‑ Characteristic symptoms: Weakness, pallor, bleeding gums.
‑ Modalities: Worse from cold, better from warmth.
‑ Mental state: Depressed, feels “heavy” in chest.
‑ Thirst and appetite: Thirst for warm drinks, appetite low.
‑ Discharges: Bloody sputum or urine if emboli involve lungs/kidney.
‑ Physical generals: Small petechiae on skin, splinter haemorrhages.
‑ Constitution: Persons with a tendency to bleed easily; helps by improving blood quality and reducing vegetative growth.

4. Ferrum phosphoricum
‑ Causation: Early inflammatory stage of infection, after minor trauma.
‑ Characteristic symptoms: Low‑grade fever, fatigue, slight headache.
‑ Modalities: Worse from exertion, better from rest.
‑ Mental state: Indecisive, easily distracted.
‑ Thirst and appetite: Slight thirst, appetite diminished.
‑ Discharges: Thin, watery nasal discharge if upper airway involved.
‑ Physical generals: Warm skin, mild tachycardia.
‑ Constitution: Children or young adults with early infection; helps by modulating the initial inflammatory response.

5. Kali mur
‑ Causation: Mucous membrane infection after prolonged cough or sinusitis.
‑ Characteristic symptoms: Thick yellowish sputum, sore throat, hoarseness.
‑ Modalities: Worse from cold, better from warm drinks.
‑ Mental state: Irritable, impatient.
‑ Thirst and appetite: Thirst for warm liquids, appetite reduced.
‑ Discharges: Thick, yellow‑green sputum.
‑ Physical generals: Enlarged cervical lymph nodes, low‑grade fever.
‑ Constitution: Patients with chronic respiratory infections; helps by clearing mucous and reducing bacterial load.

6. Natrum mur
‑ Causation: Salt‑loss state after prolonged vomiting or diarrhoea, leading to weakened immunity.
‑ Characteristic symptoms: Weakness, dizziness, craving for salty foods.
‑ Modalities: Worse from heat, better from cool environment.
‑ Mental state: Confused, forgetful.
‑ Thirst and appetite: Thirst for cold water, appetite variable.
‑ Discharges: Watery diarrhoea if gut involved.
‑ Physical generals: Dry skin, low blood pressure.
‑ Constitution: Elderly or debilitated patients; helps by restoring electrolyte balance and supporting immune function.

7. Apis mellifica
‑ Causation: After insect bite or allergic reaction that predisposes to secondary infection.
‑ Characteristic symptoms: Burning pain, swelling, red welts.
‑ Modalities: Worse from heat, better from cool compresses.
‑ Mental state: Restless, anxious, wants to be alone.
‑ Thirst and appetite: Thirst for cold water, appetite poor.
‑ Discharges: Watery, sometimes bloody discharge from wound.
‑ Physical generals: Swollen, hot, red skin patches resembling Janeway lesions.
‑ Constitution: Persons with hypersensitivity; helps by reducing local inflammation and preventing spread.

8. Lachesis
‑ Causation: After venomous bite or severe allergic reaction leading to circulatory collapse.
‑ Characteristic symptoms: Intense throbbing pain, feeling of constriction in chest.
‑ Modalities: Worse from heat, better from cool air.
‑ Mental state: Jealous, suspicious, fear of being harmed.
‑ Thirst and appetite: Thirst for cold drinks, appetite very low.
‑ Discharges: Bloody sputum if pulmonary emboli occur.
‑ Physical generals: Bluish discoloration of lips, weak pulse.
‑ Constitution: Individuals with a tendency to develop large vegetations and emboli; helps by improving circulation and reducing clot formation.

12. Prognosis
    Outcome depends on organism virulence, speed of diagnosis, presence of heart failure or embolic events, and patient’s baseline health. Early appropriate antibiotics and timely surgery improve survival; delayed treatment markedly increases mortality.

13. Prevention
    ‑ Antibiotic prophylaxis (e.g., amoxicillin 2 g oral 1 h before dental work) for patients with prosthetic valves, previous IE, or certain congenital heart diseases.
    ‑ Meticulous oral hygiene and regular dental check‑ups to reduce bacteremia from dental sources.
    ‑ Avoidance of non‑sterile intravenous lines and prompt treatment of skin infections.
    These measures markedly lower the incidence of IE in high‑risk groups.

14. Diet
    Recommended foods:
    ‑ Fresh fruits, vegetables, whole grains and lean protein – provide antioxidants and nutrients needed for tissue repair and immune competence.
    Avoided foods:
    ‑ High‑sugar sweets, excessive salt, and saturated‑fat rich fast foods – they can impair immune response, promote inflammation and worsen hypertension that stresses the heart.