After studying this note, you will be able to approach a patient with pericarditis, effusion, and tamponade in the Kenyan clinical setting. Remember to always check local protocols and drug dosages against the Kenya MoH guideline and your hospital formulary.

Pericarditis, effusion and tamponade

Definition

Pericarditis is inflammation of the pericardium, the double-layered sac surrounding the heart. Pericardial effusion is the accumulation of excess fluid within the pericardial space. Cardiac tamponade is a life-threatening condition where a significant pericardial effusion causes compression of the heart, impairing its ability to fill and pump blood effectively.

Anatomy and physiology you need

The pericardium consists of two layers: the visceral pericardium (epicardium) covering the heart surface and the parietal pericardium forming the outer sac. Between these layers is the pericardial space, normally containing a small amount of serous fluid (around 15-50 ml) that lubricates the heart's movements. The pericardium is a relatively inelastic sac.

Causes and risk factors

In our setting, causes are diverse and often overlap:

• Infectious:
  • Tuberculosis (TB): A major cause, especially in HIV-positive individuals. Can be primary pericardial TB or secondary to pulmonary TB.
  • Viral: Coxsackievirus, echovirus, influenza, HIV.
  • Bacterial: Pneumococcal, staphylococcal, streptococcal, meningococcal. Often secondary to pneumonia or sepsis.
  • Fungal: Less common, but consider in immunocompromised patients.
  • Malaria: While not a direct cause of pericarditis, severe malaria can lead to systemic inflammation and effusion.
• Inflammatory/Autoimmune:
  • Rheumatic fever: Post-infectious sequelae.
  • Systemic Lupus Erythematosus (SLE): Autoimmune inflammation.
  • Rheumatoid Arthritis: Less common than SLE.
• Malignancy:
  • Primary cardiac tumours: Rare.
  • Metastatic disease: Lung, breast, lymphoma, leukaemia.
• Trauma:
  • Blunt or penetrating chest trauma.
  • Post-cardiac surgery or procedures (Dressler's syndrome).
• Metabolic:
  • Uraemia: In patients with chronic kidney disease.
  • Hypothyroidism: Myxoedema.
• Medications:
  • Isoniazid (for TB prophylaxis/treatment).
  • Hydralazine, procainamide.
• Idiopathic: A significant proportion remain without a clear cause.
• Sickle Cell Disease: Can present with acute chest syndrome, which may involve pericardial inflammation or effusion.

Pathophysiology

Pericarditis: Inflammation of pericardium $\rightarrow$ Increased vascular permeability $\rightarrow$ Exudation of fluid, inflammatory cells, and proteins into pericardial space $\rightarrow$ Pericardial effusion.

Effusion: Accumulation of fluid $\rightarrow$ Increased intrapericardial pressure.

Cardiac Tamponade: Significant effusion $\rightarrow$ Intrapericardial pressure exceeds diastolic ventricular pressure $\rightarrow$ Impaired ventricular filling $\rightarrow$ Reduced stroke volume $\rightarrow$ Reduced cardiac output $\rightarrow$ Hypotension, shock. The inelastic pericardium limits the ability to accommodate large volumes of fluid, leading to rapid pressure increases. Right atrial and ventricular diastolic pressures rise first due to their lower filling pressures, leading to the characteristic haemodynamic compromise.

Clinical features

History questions that matter

• Pain character and modification: Is the pain sharp and retrosternal? Does it worsen on deep inspiration, coughing, or lying flat, and ease on leaning forward? (Pleuritic and positional features distinguish pericardial pain from ischemic pain).
• Systemic symptoms: Ask about fever, night sweats, significant weight loss, and chronic cough (strongly points to tuberculous pericarditis).
• Underlying disease history: Enquire about known HIV infection, previous TB treatment, chronic kidney disease (uremic pericarditis), or autoimmune conditions (e.g., SLE).
• Dyspnea and fatigue: Ask if breathlessness is progressive, orthopneic, or sudden. Rapid worsening with dizziness implies hemodynamic compromise from effusion or tamponade.

Examination findings and mechanisms

• Pericardial friction rub: High-pitched, superficial, scratchy sound heard best at the left lower sternal border with the patient leaning forward in end-expiration. It is generated by friction between inflamed, roughened visceral and parietal pericardial layers. It has up to three components per cardiac cycle (atrial systole, ventricular systole, rapid ventricular filling).
• Beck's triad (cardiac tamponade):
  • Hypotension with narrow pulse pressure: Compression limits ventricular filling, slashing stroke volume.
  • Elevated jugular venous pressure (JVP): High intrapericardial pressure prevents venous return to the right atrium; characteristically displays an absent or attenuated y-descent because early ventricular filling is prevented.
  • Muffled heart sounds: Fluid layer acts as an acoustic insulator dampening acoustic transmission.
• Pulsus paradoxus: An exaggerated inspiratory drop in systolic blood pressure (>10 mmHg). During inspiration, increased venous return distends the right ventricle within a non-distensible pericardial space; the interventricular septum bulges into the left ventricle, reducing left ventricular filling, stroke volume, and systolic output.
• Tachycardia and tachypnea: Compensatory autonomic responses to sustain cardiac output when stroke volume is fixed, and to counter poor systemic perfusion.
• Ewart’s sign: Dullness and bronchial breathing below the left scapula caused by a massive effusion compressing the base of the left lung.
• Peripheral signs: Hepatomegaly, ascites, and lower limb edema appear in subacute effusions or effusive-constrictive disease due to prolonged venous congestion.

Differential diagnosis

Investigations

Diagnosis and severity

Diagnostic criteria

Diagnosis of acute pericarditis requires at least two of the following four criteria:

1. Characteristic pericardial chest pain (sharp, positional, pleuritic).
2. Pericardial friction rub on auscultation.
3. New widespread ST-segment elevation and/or PR-segment depression on ECG.
4. New or worsening pericardial effusion on imaging.

Severity stratification

• Mild / Uncomplicated acute pericarditis: Hemodynamically stable, small or absent effusion, normal inflammatory markers resolving with standard anti-inflammatory therapy, no myocardial involvement (troponin negative).
• High-risk features (warrants admission and urgent workup):
  • High fever (>38°C) or subacute onset (raises suspicion of TB or bacterial etiology).
  • Moderate-to-large pericardial effusion.
  • Failure to respond to non-steroidal anti-inflammatory therapy within 7 days.
  • Myopericarditis (troponin elevation, ventricular dysfunction).
  • Immunosuppression (advanced HIV disease).
• Cardiac tamponade (medical emergency): Presence of effusion coupled with hemodynamic instability: pulsus paradoxus (>10 mmHg), chamber collapse on echocardiography (specifically right ventricular diastolic collapse), severe hypotension, and shock. Requires immediate pericardiocentesis.

Management

Immediate Stabilisation

• Cardiac Tamponade (Medical Emergency):
  • Immediate volume expansion with normal saline bolus to increase right-sided filling pressures and temporise cardiac output while preparing intervention.
  • Avoid positive pressure ventilation and vasodilators or diuretics, which drop preload and induce arrest.
  • Emergency pericardiocentesis: subxiphoid approach under ultrasound guidance. If ultrasound is unavailable in extremis, insert needle at $45^\circ$ angle aiming toward the left shoulder while aspirating.
  • Send fluid for microscopy, GeneXpert MTB/RIF, Gram stain, culture, and cytology.
• Acute Pericarditis / Stable Effusion:
  • Bed rest and exercise restriction until symptom resolution and inflammatory markers normalise.
  • Screen for high-risk features warranting admission: fever, subacute course, large effusion, immunosuppression (advanced HIV), trauma, or failure of response to anti-inflammatory therapy.

Definitive Medical Therapy

Surgical Interventions

• Pericardial window / Subxiphoid pericardiotomy: Indicated for recurrent or loculated effusions, diagnostic biopsy, or purulent pericarditis.
• Complete Pericardiectomy: Definitive treatment for established chronic constrictive pericarditis with marked symptoms (NYHA III/IV).

Monitoring and Follow-Up

• Acute phase: Continuous cardiac telemetry, serial blood pressure (watching for narrow pulse pressure and pulsus paradoxus), and repeat bedside ultrasound to detect re-accumulation.
• Follow-up: Clinical review with repeat transthoracic echocardiogram at 6–8 weeks to assess for late constriction or chronic effusion.

Contraindications and Safety

• Anticoagulants (heparin, warfarin): Strictly contraindicated in acute pericarditis without a vital separate indication; markedly increases risk of converting serous fluid into a fatal haemopericardium.
• Steroids in undifferentiated disease: Avoid empirical steroid monotherapy in TB-endemic settings; induces rapid dissemination of untreated tuberculous infection.

Complications and Prognosis

• Cardiac Tamponade: Can cause sudden obstructive shock, electromechanical dissociation, and death.
• Recurrent Pericarditis: Occurs in up to one-third of patients not prescribed colchicine.
• Chronic Constrictive Pericarditis: Fibrocalcific encasement impeding diastolic filling. High risk in tuberculous and purulent etiologies.
• Prognosis: Excellent for idiopathic/viral pericarditis. TB pericarditis carries significant mortality, particularly with delayed drainage or advanced HIV coinfection.

High-Yield Exam Points

• The "Clear Lungs" Clue: Tamponade presents with raised JVP and hypotension without pulmonary crackles (isolated right-heart filling failure), unlike cardiogenic shock from acute myocardial infarction.
• The Diuretic Error: Administering furosemide to a patient with tamponade because of elevated JVP and oedema is a fatal mistake; removing preload collapses the cardiac chambers.
• ECG Look-alike: ST-elevation in acute pericarditis is diffuse and concave upwards ("saddle-shaped") with PR depression. ST-elevation in STEMI is localised to a coronary territory, convex upwards, and lacks diffuse PR depression.
• Beck's Triad: Low arterial pressure, elevated jugular venous pressure, and muffled heart sounds. Frequently incomplete in clinical practice; absence does not rule out tamponade.
• Bedside Examination Trigger: An examiner will ask you to demonstrate pulsus paradoxus: inflate the cuff until no sounds are heard, deflate slowly; note the pressure when sounds appear on expiration, then the lower pressure when sounds are heard continuously throughout inspiration. A difference exceeding 10 mmHg is abnormal.

Clinical Case

A 28-year-old man presents with a two-week history of worsening exertional dyspnoea, progressive abdominal distension, and low-grade fevers. He reports night sweats and unquantified weight loss over two months. On examination, blood pressure is 94/70 mmHg, pulse is 114 bpm, respiratory rate is 24/min, and oxygen saturation is 96% on room air. The jugular venous pressure is markedly elevated to the angle of the jaw. Chest auscultation reveals clear lung fields bilaterally, but heart sounds are faint. The liver is tender and enlarged 4 cm below the costal margin with moderate ascites.

Questions and Model Answers

1. What is the most immediate life-threatening physiological state in this patient? Cardiac tamponade secondary to a large pericardial effusion. The elevated JVP, muffled heart sounds, tachycardia, and low pulse pressure represent Beck's triad and obstructive shock.

2. Which initial bedside diagnostic test must be performed immediately, and what key feature establishes the diagnosis? Bedside transthoracic echocardiography (point-of-care). Key feature: late diastolic right ventricular collapse or early right atrial systolic collapse during expiration, alongside a large pericardial fluid collection.

3. What is the most probable underlying etiology in this setting, and what diagnostic steps should follow decompression? Tuberculous pericarditis. Fluid aspirated from pericardiocentesis should be sent for GeneXpert MTB/RIF, mycobacterial culture, cytology, and adenosine deaminase (ADA).

Practice Questions

Question 1

A 34-year-old woman with known systemic lupus erythematosus presents with chest pain relieved by leaning forward. Her ECG demonstrates widespread concave ST-segment elevation. Which of the following treatments provides the strongest protection against disease recurrence?

A. Prednisolone monotherapy B. Colchicine combined with an NSAID C. Morphine combined with aspirin D. Warfarin combined with paracetamol

Answer: B. Colchicine combined with an NSAID Explanation: Colchicine halts microtubule assembly in leukocytes and, when combined with high-dose NSAIDs, dramatically reduces the rate of recurrent pericarditis compared to NSAID monotherapy or corticosteroids.

Question 2

A 42-year-old man with advanced HIV presents with dyspnoea and tachycardia. Bedside ultrasound shows a massive circumferential pericardial space with right ventricular diastolic collapse. The team prepares for pericardiocentesis. Which supportive medication is strictly contraindicated prior to drainage?

A. Intravenous normal saline B. Intravenous furosemide C. Supplemental oxygen D. Intravenous peripheral vasopressors

Answer: B. Intravenous furosemide Explanation: Patients with tamponade depend critically on high systemic venous filling pressures (preload) to fill the compressed ventricles; diuretics drop venous return and can cause immediate cardiovascular collapse.

Question 3

An examiner asks a student to distinguish acute pericarditis from an acute anterior ST-elevation myocardial infarction (STEMI) on a 12-lead ECG. Which finding specifically points towards acute pericarditis?

A. Pathological Q waves in leads V1 to V4 B. Convex ST elevation with reciprocal changes in inferior leads C. PR-segment depression in lead II with PR elevation in lead aVR D. New-onset left bundle branch block

Answer: C. PR-segment depression in lead II with PR elevation in lead aVR Explanation: Atrial subepicardial injury causes PR-segment depression in limb and precordial leads with reciprocal PR elevation in lead aVR, which is highly specific for acute pericarditis and absent in STEMI.

Question 4

A 25-year-old man is admitted with tuberculous pericardial effusion. Diagnostic and therapeutic drainage yield straw-coloured fluid positive on GeneXpert for rifampicin-susceptible Mycobacterium tuberculosis. HIV testing is negative. Which regimen offers the most comprehensive medical therapy to prevent constriction?

A. Four-drug anti-TB therapy alone B. Four-drug anti-TB therapy plus adjunctive tapered oral corticosteroids C. Intravenous broad-spectrum cephalosporin and high-dose ibuprofen D. Immediate pericardiectomy with four-drug anti-TB therapy

Answer: B. Four-drug anti-TB therapy plus adjunctive tapered oral corticosteroids Explanation: In HIV-negative patients with confirmed tuberculous pericarditis, adding a tapering course of systemic corticosteroids to anti-TB chemotherapy reduces the incidence of constrictive pericarditis and hospitalisation.

Question 5

A 50-year-old woman on haemodialysis develops pleuritic chest pain and a pericardial friction rub. Her doctor considers initiating therapeutic anticoagulation for concurrent deep vein thrombosis. Why must systemic therapeutic anticoagulation be avoided or delayed?

A. Anticoagulants accelerate the rate of pericardial calcification B. Anticoagulation inactivates the anti-inflammatory action of aspirin C. There is a high risk of transforming serous pericarditis into a fatal haemopericardium D. Uraemic toxins degrade heparin, rendering it clinically ineffective

Answer: C. There is a high risk of transforming serous pericarditis into a fatal haemopericardium Explanation: The inflamed, friable pericardial microvasculature easily bleeds under systemic anticoagulation, rapidly causing haemorrhagic conversion, rapid effusion enlargement, and fatal cardiac tamponade.

Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.