Endocarditis and pericardial emergencies

Infective Endocarditis (IE): Microbiology, Diagnosis, and Management

Infective endocarditis is a microbial infection of the endocardial surface of the heart, most commonly targeting cardiac valves.

Microbial Etiology

• Staphylococcus aureus: Leading pathogen in Australia ($30\%\text{ to }40\%$ of cases). Acute, fulminant, destructive course causing rapid leaflet perforation and perivalvular abscess. Dominant organism in intravenous drug use (IVDU) and healthcare-associated infections.
• Viridans Group Streptococci (S. oralis, S. mitis, S. sanguinis): Oral commensals classically causing subacute endocarditis on pre-existing abnormal/damaged valves following dental procedures.
• Enterococcus faecalis: Typically affects older adults following genitourinary or gastrointestinal instrumentation.
• Staphylococcus epidermidis (Coagulase-Negative Staphylococci): Leading pathogen in prosthetic valve endocarditis occurring within 12 months of surgery; produces adherent biofilm.
• Streptococcus gallolyticus (formerly S. bovis): Strongly associated with occult colorectal adenomas and carcinoma; isolation mandates prompt colonoscopy.
• Culture-negative endocarditis: Prior antibiotics and fastidious organisms such as Coxiella and Bartonella warrant specialist microbiology. HACEK organisms can grow in modern routine blood cultures; they are not inherently always culture-negative. Exposure history, serology and molecular testing complement repeated cultures.

Right-Sided Endocarditis in IVDU

• Primarily affects the tricuspid valve ($> 70\%$ of cases), predominantly caused by S. aureus.
• Presents with high swinging fevers and recurrent septic pulmonary emboli (pleuritic chest pain, cough, haemoptysis, multiple peripheral nodular cavitary lung lesions on imaging).
• Peripheral stigmata (splinter haemorrhages, Osler nodes, Janeway lesions) are typically absent because septic emboli lodge in the pulmonary circulation rather than the systemic arterial bed.

Modified Duke Criteria for Diagnosis

Diagnosis is established with 2 Major, 1 Major + 3 Minor, or 5 Minor criteria:

• Major Criteria:
  1. Blood Cultures Positive for IE: Typical microorganisms consistent with IE from 2 separate blood cultures, or persistently positive blood cultures drawn $> 12\text{ hours}$ apart, or a single positive culture for Coxiella burnetii (or Phase I IgG titre $> 1:800$).
  2. Evidence of Endocardial Involvement on Imaging: Echocardiography demonstrating oscillating intracardiac vegetation, perivalvular abscess, new partial dehiscence of a prosthetic valve, or new pathological valvular regurgitation.
• Minor Criteria:
  1. Predisposition: Heart condition (prosthetic valve, prior IE, bicuspid valve) or intravenous drug use.
  2. Fever: Temperature $\ge 38.0^\circ\text{C}$.
  3. Vascular Phenomena: Major arterial emboli, septic pulmonary infarcts, mycotic aneurysms, intracranial haemorrhage, conjunctival splinter haemorrhages, Janeway lesions (painless, flat erythematous macules on palms/soles).
  4. Immunological Phenomena: Glomerulonephritis, Osler nodes (painful, raised violaceous nodules on finger/toe pads), Roth spots (retinal haemorrhages with pale fibrin centres), positive rheumatoid factor.
  5. Microbiological Evidence: Positive blood culture not meeting major criteria, or serological active infection.

Diagnostic & Therapeutic Pathway (local antimicrobial guidance)

1. Blood Cultures: Draw three independent sets of peripheral blood cultures from separate venepuncture sites with at least 30 to 60 minutes between draws prior to commencing antibiotics (unless the patient is in fulminant septic shock).
2. Echocardiography: Transthoracic echocardiography (TTE) is rapid first-line imaging. Transoesophageal echocardiography (TOE) is the gold standard (sensitivity $> 90\%$) and is mandatory for evaluating prosthetic valves, perivalvular abscesses, or when clinical suspicion remains high despite a non-diagnostic TTE.
3. Empirical Antibiotic Regimens:
   • Native valve infection: Obtain multiple cultures promptly before antibiotics if stable. Unstable sepsis needs immediate treatment. Empirical IV therapy is selected with infectious diseases using valve type, acquisition, renal function, allergy and local resistance; do not mandate a nephrotoxic gentamicin combination for every native-valve case.
   • Prosthetic valve infection: Urgent infectious-diseases/cardiology review, cultures and echocardiography are needed. Biofilm-directed treatment and surgery decisions depend on the organism and complications. Rifampicin is not indiscriminately added before cultures and control of bacteraemia.
4. Indications for Urgent Cardiac Surgery:
   • Heart failure / cardiogenic shock from severe acute valvular regurgitation.
   • Uncontrolled infection (persistent positive blood cultures $> 7\text{ to }10\text{ days}$ despite targeted antibiotics, fungal endocarditis).
   • Perivalvular extension (abscess, pseudoaneurysm, fistula, new conduction block indicating aortic root abscess infiltrating the AV node).
   • Large mobile vegetations ($> 10\text{ mm}$), especially following an embolic event.

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Acute Pericarditis & Cardiac Tamponade

Acute Pericarditis

• Etiology: Idiopathic or viral ($> 85\%$ of cases in Australia: enteroviruses, Coxsackievirus, adenovirus, SARS-CoV-2); post-myocardial infarction (early perilesional vs late autoimmune Dressler syndrome occurring 2 to 10 weeks post-MI); autoimmune (SLE, rheumatoid arthritis); uraemia; malignancy; tuberculosis.
• Clinical Presentation: Sharp, retrosternal, pleuritic chest pain that is aggravated by deep inspiration, coughing, and lying flat, and relieved by sitting upright and leaning forward. A superficial, high-pitched scratching pericardial friction rub is heard best with the diaphragm along the left lower sternal border during held expiration.
• 12-Lead ECG Evolution: Widespread, diffuse concave ST-segment elevation across multiple vascular territories (all leads except aVR and V1) accompanied by widespread PR-segment depression. Reciprocal ST depression and PR elevation are seen exclusively in lead aVR.
• First-Line Pharmacotherapy (Australian Guidelines):
  • High-dose Non-Steroidal Anti-Inflammatory Drugs: Ibuprofen ($600\text{ to }800\text{ mg}$ TDS) or aspirin ($650\text{ to }1000\text{ mg}$ TDS) for 1 to 2 weeks with a proton pump inhibitor.
  • Colchicine: $500\text{ mcg}$ once or twice daily (dose-adjusted for weight and renal function) for 3 months. Colchicine halves the recurrence rate and is mandatory adjunctive therapy.
  • Systemic Corticosteroids: Reserved strictly for NSAID intolerance, pregnancy, or refractory autoimmune pericarditis. Premature steroid use promotes recurrent disease.

Cardiac Tamponade

• Pathophysiology: Rapid accumulation of pericardial fluid under pressure exceeding intracardiac chamber pressures, resulting in compression of the cardiac chambers in diastole, impaired venous return, and catastrophic drop in stroke volume.
• Beck's Triad:
  1. Hypotension with narrow pulse pressure
  2. Jugular Venous Distension (elevated JVP with prominent $x$-descent and absent $y$-descent)
  3. Muffled / distant heart sounds
• Pulsus Paradoxus: An exaggerated inspiratory fall in systemic systolic blood pressure $> 10\text{ mmHg}$ during normal quiet respiration.
• ECG Signs: Sinus tachycardia, low QRS voltage throughout all leads ($< 5\text{ mm}$ in limb leads), and electrical alternans (beat-to-beat alternation of QRS amplitude and axis caused by the heart pendulously swinging within a large fluid effusion).
• Emergency Interventions:
  • Urgent bedside echocardiography confirms the diagnosis: right ventricular early diastolic collapse, right atrial late systolic collapse, and dilated, non-collapsing inferior vena cava (IVC plethora).
  • Definitive Treatment: Immediate emergency bedside echocardiogram-guided pericardiocentesis or surgical subxiphoid pericardial window. Rapid intravenous crystalloid infusion provides temporary preload support while equipment is prepared.
• Tamponade: Urgent expert drainage is definitive treatment. Positive pressure can reduce venous return and cause collapse, so maintain spontaneous ventilation when feasible and plan airway intervention with haemodynamic support. Necessary lifesaving ventilation is not absolutely forbidden.

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Clinical comparison: Differentiating Acute Pericarditis, STEMI, and Cardiac Tamponade

• Chest Pain Quality: Acute Pericarditis: Sharp, pleuritic; relieved leaning forward; ST-Elevation MI (STEMI): Crushing, heavy pressure; radiates to jaw/arm; Cardiac Tamponade: Dull ache or painless dyspnoea/fatigue
• ECG ST Segments: Acute Pericarditis: Widespread concave ST elevation across leads; ST-Elevation MI (STEMI): Localized convex ("tombstone") ST elevation; Cardiac Tamponade: Low voltage QRS; Electrical alternans
• ECG PR Segments: Acute Pericarditis: Widespread PR depression; PR elevation in aVR; ST-Elevation MI (STEMI): Normal PR segments; Cardiac Tamponade: Normal PR segments
• Reciprocal Changes: Acute Pericarditis: None (except ST depression in aVR); ST-Elevation MI (STEMI): Prominent reciprocal ST depression opposite leads; Cardiac Tamponade: Absent
• Physical Examination: Acute Pericarditis: High-pitched triphasic pericardial friction rub; ST-Elevation MI (STEMI): $S_3 / S_4$ gallop; clear lungs or pulmonary crackles; Cardiac Tamponade: Beck's triad (hypotension, raised JVP, muffled sounds)
• Pulsus Paradoxus: Acute Pericarditis: Absent; ST-Elevation MI (STEMI): Absent; Cardiac Tamponade: Present (inspiratory SBP drop $> 10\text{ mmHg}$)
• Primary Treatment: Acute Pericarditis: High-dose NSAIDs plus Colchicine; ST-Elevation MI (STEMI): Emergent reperfusion (Primary PCI or TNK); Cardiac Tamponade: Immediate decompressive pericardiocentesis

Primary references (checked 7 October 2026): Heart Foundation ACS resources.