3.3 Pulmonary Embolism, Pleural Effusion & Pneumothorax

Acute Pulmonary Embolism (PE)

Venous thromboembolism (VTE), encompassing deep vein thrombosis (DVT) and pulmonary embolism (PE), is a major cause of preventable hospital morbidity and sudden death. Caribbean inpatients with sickle cell disease, advanced malignancy, major orthopedic surgery, or prolonged immobility are at heightened risk.

Pathophysiology & Virchow's Triad

Venous thrombi typically originate in the deep venous plexuses of the lower extremities (iliofemoral veins) or pelvic veins. The development of thrombosis reflects Virchow's Triad:

1. Endothelial Injury: Trauma, surgery, central venous catheters, hyperhomocysteinemia.
2. Venous Stasis: Immobility, general anesthesia, prolonged air travel, obesity, heart failure.
3. Hypercoagulability: Factor V Leiden, prothrombin gene mutation, antiphospholipid syndrome, active malignancy, pregnancy, combined oral contraceptives, hormone replacement therapy, and sickle cell disease.

When a thrombus embolizes to the pulmonary arterial tree, it occludes vascular beds, triggering acute physiological sequelae:

• V/Q Mismatch: Occluded segments are ventilated but unperfused, creating alveolar dead space and arterial hypoxemia.
• Acute Right Ventricular Strain (Cor Pulmonale): Sudden elevation in pulmonary vascular resistance and RV afterload causes acute RV dilatation, increased wall tension, and right coronary artery hypoperfusion. RV free-wall ischemia leads to bowing of the interventricular septum into the left ventricle, impairing left ventricular filling, reducing cardiac output, and causing obstructive shock.

Clinical Presentation & Pre-Test Probability Stratification

Classic symptoms include sudden-onset pleuritic chest pain, dyspnea, tachypnea (> 20/min), tachycardia (> 100 bpm), hemoptysis, and unilateral leg swelling. Syncope is a warning for possible hemodynamic compromise or RV dysfunction; assess both promptly rather than inferring shock or a saddle location from syncope alone.

Wells Criteria for Pulmonary Embolism

• Interpretation (Two-Tier Model):
  • PE Unlikely (Score <= 4.0): Check high-sensitivity D-dimer. High negative predictive value (> 95%). If D-dimer is normal (< 500 ng/mL, or age-adjusted cutoff: age x 10 for age > 50), PE is safely ruled out without imaging. If D-dimer is elevated, proceed to imaging.
  • PE Likely (Score > 4.0): Proceed directly to diagnostic imaging; do not order D-dimer.

Diagnostic Investigations

• CT Pulmonary Angiography (CTPA): The definitive gold standard investigation of choice. Accurately demonstrates intraluminal filling defects.
• Ventilation-Perfusion (V/Q) Scintigraphy: Reserved for patients with severe renal impairment (eGFR < 30 mL/min), severe iodinated contrast allergy, or young pregnant patients with normal baseline chest radiographs (to minimize maternal breast radiation).
• Bedside Echocardiography: Indicated in unstable patients unable to travel to CT. Hallmarks of RV strain include RV dilatation (RV/LV ratio > 1.0) and McConnell's sign (severe hypokinesia of the mid-free RV wall with normal or hyperdynamic RV apical contraction).
• Electrocardiogram (ECG): Most commonly shows non-specific sinus tachycardia. The classic S1Q3T3 pattern (deep S wave in lead I, Q wave in lead III, T-wave inversion in lead III) reflects acute right heart strain but is present in only 15-20% of cases. Inverted T waves in leads V1-V4 and new right bundle branch block (RBBB) are additional strain markers.

Therapeutic Management

• Hemodynamically Unstable (Massive PE): Defined by sustained systolic BP < 90 mmHg, drop >= 40 mmHg for > 15 minutes, or cardiogenic shock.
  • Immediate Systemic Thrombolysis: Administer recombinant tissue plasminogen activator (Alteplase / rtPA 100 mg IV infusion over 2 hours; or, under specialist resuscitation protocols for extreme instability, 0.6 mg/kg over 15 minutes, maximum 50 mg).
  • Cautious fluid resuscitation (<= 500 mL crystalloid; excessive volume worsens RV dilatation and ischemia), inotropic support with norepinephrine, and unfractionated heparin.
  • Surgical or catheter-directed embolectomy if thrombolysis is contraindicated (active internal bleeding, recent hemorrhagic stroke).
• Hemodynamically Stable (Submassive & Low-Risk PE):
  • Direct Oral Anticoagulants (DOACs) are frontline therapy: Apixaban 10 mg BD for 7 days then 5 mg BD, or Rivaroxaban 15 mg BD for 21 days then 20 mg OD (neither requires heparin lead-in).
  • Alternatives: Low Molecular Weight Heparin (LMWH, Enoxaparin 1 mg/kg BD) bridging to Warfarin (target INR 2.0 - 3.0), or LMWH monotherapy in pregnancy.
  • Duration: 3 months for provoked transient risk factor; extended/indefinite for unprovoked or recurrent VTE.

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Pleural Effusion: Transudate vs. Exudate Differentiation

A pleural effusion represents an abnormal accumulation of fluid in the pleural space. Differentiating between a transudative and an exudative process is the vital first diagnostic step.

Light's Criteria (Gold Standard)

A pleural effusion is classified as an EXUDATE if at least one of the following three criteria is fulfilled:

1. Pleural fluid protein / Serum protein ratio > 0.5
2. Pleural fluid LDH / Serum LDH ratio > 0.6
3. Pleural fluid LDH > 2/3 the upper limit of normal for serum LDH (typically > 200 IU/L)

(If none of these criteria are met, the effusion is classified as a transudate).

Etiological Breakdown

• Transudates (Intact Pleura, Hydrostatic / Oncotic Imbalance):
  • Congestive Heart Failure (most common transudate; elevated pulmonary capillary hydrostatic pressure)
  • Cirrhosis with hepatic hydrothorax (peritoneal fluid transudation through diaphragmatic defects)
  • Nephrotic syndrome (decreased oncotic pressure due to severe hypoalbuminemia)
  • Peritoneal dialysis, severe malnutrition, myxedema
• Exudates (Local Pleural Inflammation / Increased Capillary Permeability):
  • Parapneumonic effusions and Empyema
  • Malignancy (bronchogenic carcinoma, metastatic breast cancer, lymphoma)
  • Pulmonary embolism with pulmonary infarction
  • Tuberculosis pleurisy (lymphocyte-predominant, high adenosine deaminase ADA > 40 U/L)
  • Autoimmune diseases (rheumatoid pleuritis with very low glucose < 1.6 mmol/L, SLE)
  • Acute pancreatitis (elevated pleural fluid amylase)

Diagnostic Thoracentesis & Parapneumonic Effusion Management

Any unexplained pleural effusion (> 10 mm depth on ultrasound or lateral decubitus CXR) warrants diagnostic thoracentesis with biochemical, cytological, and microbiological evaluation.

Clinical Pearl: Measure pH promptly in non-purulent fluid. In suspected infection, pH <=7.20 supports drainage, but pH >7.20 alone does not establish a simple effusion. Use ultrasound to confirm safe access; initial infection drainage is usually through a small-bore tube (<=14 Fr). Reassess persistent fever or residual collections for additional drainage, intrapleural therapy or surgical review.

Pneumothorax: Classification & Emergency Interventions

Pneumothorax is the presence of air within the pleural cavity, leading to loss of negative intrapleural pressure and partial or complete lung collapse.

Classification

• Primary Spontaneous Pneumothorax (PSP): Occurs without preceding trauma or underlying lung disease. Classically affects tall, slender young males (15-30 years). Caused by the spontaneous rupture of subpleural apical blebs or bullae. Cigarette smoking increases risk more than 20-fold.
• Secondary Spontaneous Pneumothorax (SSP): Occurs in the presence of pre-existing lung pathology—most commonly COPD/emphysema, pulmonary tuberculosis, asthma, cystic fibrosis, Marfan syndrome, or Pneumocystis jirovecii pneumonia. Carries higher morbidity and mortality because the patient lacks baseline pulmonary reserve.
• Traumatic / Iatrogenic: Rib fractures, penetrating trauma, subclavian central line insertion, thoracentesis, lung biopsy, or barotrauma from positive pressure mechanical ventilation.

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Tension Pneumothorax: Clinical Diagnosis & Immediate Resuscitation

Tension pneumothorax is a true, life-threatening surgical and medical emergency that arises when a disruption in the lung parenchyma or chest wall creates a one-way ball-valve mechanism. Air enters the pleural space during inspiration but cannot escape during expiration.

Pathophysiological Cascade

• Intrapleural pressure progressively exceeds atmospheric pressure -> Complete collapse of the ipsilateral lung -> Severe mediastinal shift toward the contralateral side -> Compression of the contralateral lung and downward flattening of the diaphragm -> Severe kinking and compression of the superior and inferior vena cava -> Catastrophic reduction in venous return (preload) -> Severe drop in cardiac output, profound obstructive shock, pulseless electrical activity (PEA), and death.

Emergency Clinical Diagnosis (DO NOT DELAY FOR CHEST X-RAY)

Tension pneumothorax is an exclusively clinical diagnosis. Delaying treatment to obtain a chest X-ray is medical negligence.

• Severe, rapidly worsening respiratory distress and agitation
• Severe hypotension and tachycardia
• Tracheal deviation away from the affected side (contralateral deviation)
• Distended neck veins (elevated JVP) due to superior vena cava compression
• Hyperresonance to percussion and absent breath sounds over the affected hemithorax
• Cyanosis and diaphoresis

Life-Saving Intervention

1. Immediate Emergency Needle Decompression:
   • Insert a large-bore cannula (14-16 gauge, minimum length 4.5-5 cm) into the second intercostal space in the midclavicular line (or the fourth/fifth intercostal space in the anterior axillary line) on the affected side.
   • Escaping air may be heard, but confirm effectiveness by improved breathing and circulation. If compromise persists, reassess catheter position/patency and proceed promptly to definitive pleural drainage; a hiss alone does not prove successful treatment.
2. Immediate Formal Tube Thoracostomy:
   • Needle decompression must be followed immediately by formal chest tube insertion (20-28 Fr) placed in the 5th intercostal space anterior to the midaxillary line within the 'safe triangle' (bounded by the anterior border of latissimus dorsi, the lateral border of pectoralis major, and the level of the 5th intercostal space), connected to an underwater seal drainage system.

Spontaneous Pneumothorax Management Algorithms

• Primary Spontaneous (PSP):
  • Minimally symptomatic, clinically and radiologically stable adults may be managed conservatively regardless of size, after observation and confirmation they can mobilize comfortably. Provide analgesia, oxygen if hypoxaemic, return precautions and early follow-up; arrange repeat imaging until resolution.
  • Consider ambulatory drainage where expertise, support and follow-up are available. For patients unsuitable for conservative or ambulatory care, offer needle aspiration or a small-bore chest drain after discussion. Reassess after aspiration; persistent breathlessness, instability or failure of lung expansion warrants drainage rather than discharge.
• Secondary Spontaneous (SSP):
  • Due to limited physiological reserve, all patients with SSP require hospital admission.
  • If large (> 2 cm) or patient is breathless: Immediate intercostal chest tube insertion connected to an underwater seal. If small (1-2 cm) and asymptomatic: needle aspiration, but chest drain is frequently needed.