4.3 Pulmonary Embolism & Thoracic Emergencies

Pulmonary Embolism (PE)

A Pulmonary Embolism (PE) occurs when a thrombus (most commonly originating from deep vein thrombosis in the lower extremities) dislodges, travels through the venous system and right side of the heart, and occludes a pulmonary artery or one of its branches. Less common causes include fat emboli (from long bone fractures), air emboli, or amniotic fluid emboli.

Pathophysiology and Hemodynamic Consequences

The primary pathophysiologic consequence of a PE is increased pulmonary vascular resistance (PVR) due to mechanical obstruction and release of vasoconstrictive mediators (e.g., serotonin, thromboxane). This leads to increased right ventricular (RV) afterload. In severe cases, the acute increase in RV afterload causes RV dilation and dysfunction, shifting the intraventricular septum toward the left ventricle (LV). This septal shift impairs LV filling (preload), leading to a significant decrease in cardiac output and systemic hypotension, a condition known as obstructive shock. Concurrently, obstruction of the pulmonary vasculature creates dead-space ventilation (V/Q mismatch), leading to severe hypoxemia.

Clinical Presentation and Risk Stratification

The clinical presentation is highly variable. Symptoms may include acute onset dyspnea, pleuritic chest pain, cough, hemoptysis, and syncope (a harbinger of massive PE). Tachycardia and tachypnea are the most common vital sign abnormalities.

Patients must be risk-stratified to guide management:

• Massive PE (High-Risk): Defined by systemic hypotension (systolic BP < 90 mm Hg for > 15 minutes, or requiring vasopressors) not explained by other causes, pulselessness, or profound bradycardia.
• Submassive PE (Intermediate-Risk): Hemodynamically stable (normotensive) but evidence of RV dysfunction (on echocardiogram or CT angiography) or myocardial necrosis (elevated troponin or BNP).
• Low-Risk PE: Hemodynamically stable with no evidence of RV strain or biomarker elevation.

Diagnosis

The diagnostic approach depends on the patient's hemodynamic stability and clinical probability (using tools like the Wells Score or Geneva Score).

• CT Pulmonary Angiography (CTPA): The gold standard imaging modality for diagnosing PE in hemodynamically stable patients.
• Ventilation-Perfusion (V/Q) Scan: Utilized in patients who cannot undergo CTPA (e.g., severe renal impairment, contrast allergy).
• Echocardiography (Transthoracic or Transesophageal): Crucial in the unstable patient (where transport to CT is unsafe) to rapidly assess for RV dysfunction (e.g., McConnell's sign) or direct visualization of a clot in transit.
• D-Dimer: Highly sensitive but lacks specificity. Useful for ruling out PE in patients with a low clinical probability.

Management Strategies

The foundation of PE treatment is systemic anticoagulation, initiated immediately upon high clinical suspicion while awaiting diagnostic confirmation.

• Initial Anticoagulation: Options include low-molecular-weight heparin (LMWH), unfractionated heparin (UFH - preferred in renal failure or if interventions are planned), or direct oral anticoagulants (DOACs - for low-risk patients).
• Thrombolytic Therapy (Systemic Fibrinolysis): Indicated for patients with massive PE (high-risk) presenting with shock or hypotension. Alteplase (tPA) accelerates clot lysis, rapidly reducing PVR and improving hemodynamics. It carries a significant risk of major hemorrhage, including intracranial bleeding. The use of thrombolytics in submassive PE is controversial and reserved for cases demonstrating rapid clinical deterioration.
• Catheter-Directed Therapy (CDT): Catheter-directed thrombolysis or mechanical embolectomy is an option for patients with massive or high-risk submassive PE who have absolute contraindications to systemic thrombolysis or have failed medical therapy.
• Surgical Embolectomy: Considered in massive PE when thrombolysis is contraindicated, CDT is unavailable, or there is a clot in transit in the right heart.
• Inferior Vena Cava (IVC) Filter: Indicated only when anticoagulation is absolutely contraindicated (e.g., active major bleeding) or when recurrent PEs occur despite therapeutic anticoagulation.

Thoracic Emergencies

Pneumothorax

A pneumothorax is the accumulation of air in the pleural space, leading to partial or complete lung collapse.

• Spontaneous Pneumothorax: Occurs without antecedent trauma. Primary (PSP) typically affects tall, thin, young males without underlying lung disease. Secondary (SSP) occurs in patients with pre-existing lung pathology (e.g., COPD bleb rupture, cystic fibrosis, Pneumocystis jirovecii pneumonia).
• Traumatic Pneumothorax: Results from blunt or penetrating chest trauma or iatrogenic causes (e.g., central line placement, thoracentesis, mechanical ventilation).

Tension Pneumothorax

A tension pneumothorax is a life-threatening medical emergency. Air enters the pleural space during inspiration but cannot escape during exhalation (a one-way valve effect). The accumulating air rapidly increases intrathoracic pressure, collapsing the ipsilateral lung, shifting the mediastinum away from the affected side, compressing the contralateral lung, and severely impairing venous return to the heart, leading to rapid cardiovascular collapse and obstructive shock.

• Clinical Signs: Severe dyspnea, tachycardia, hypotension, tracheal deviation (away from the injured side), distended neck veins (JVD), and absent breath sounds and hyperresonance to percussion on the affected side.
• Management: Requires immediate needle decompression (typically 14g angiocatheter in the 2nd intercostal space mid-clavicular line, or 4th/5th ICS anterior axillary line) without waiting for radiographic confirmation. This converts a tension pneumothorax into a simple pneumothorax. Needle decompression must be followed immediately by the insertion of a definitive chest tube (tube thoracostomy).

Hemothorax

A hemothorax is the accumulation of blood in the pleural space, most commonly resulting from blunt or penetrating chest trauma causing lacerations to the lung parenchyma, intercostal vessels, or internal mammary artery.

• Clinical Signs: Hypovolemic shock (tachycardia, hypotension), decreased breath sounds, and dullness to percussion on the affected side.
• Management: Rapid volume resuscitation and insertion of a large-bore chest tube (32F-40F) to drain the blood, re-expand the lung, and monitor ongoing blood loss.
• Indications for Urgent Thoracotomy: Immediate evacuation of > 1,500 mL of blood upon chest tube insertion, or continuous output of > 200 mL/hr for 2-4 hours, or the patient remains hemodynamically unstable despite resuscitation.