Pulmonary embolism, effusions and pneumothorax

Key Takeaways

  • Use D-dimer in an appropriate probability pathway rather than indiscriminately.

  • Shock with suspected PE requires immediate senior assessment and a reperfusion decision.

  • Secondary spontaneous pneumothorax can be serious despite a small radiographic size.

Last updated: October 2026

Acute Pulmonary Embolism: Clinical Presentation & Risk Scoring

Venous thromboembolism (VTE), encompassing deep vein thrombosis (DVT) and pulmonary embolism (PE), is a major cause of preventable hospital morbidity and mortality. In acute PE, occlusion of the pulmonary arterial bed increases pulmonary vascular resistance, inducing acute right ventricular (RV) afterload strain, RV dilatation, interventricular septal flattening, and subsequent left ventricular underfilling leading to obstructive shock.

Clinical Presentation and Electrocardiography

  • Symptoms & Signs: Dyspnoea (most common symptom, present in >80%> 80\%), pleuritic chest pain, tachypnoea, tachycardia, cough, haemoptysis, and lower extremity swelling or pain. Syncope occurs in massive central PE due to sudden transient RV outflow obstruction.
  • Electrocardiography (ECG): Normal ECG is found in up to 25% of cases. The most frequent abnormality is sinus tachycardia. Signs of acute right ventricular strain include T-wave inversions in anterior/inferior leads (V1-V4, II, III, aVF), new incomplete or complete right bundle branch block (RBBB), and the classic S1Q3T3 pattern (deep S wave in lead I, pathological Q wave in lead III, and inverted T wave in lead III). While S1Q3T3 is specific for RV strain, it is present in only 10% to 15% of patients.

Pre-Test Probability & Diagnostic Algorithm

Diagnostic pathways combine clinical scoring, D-dimer testing, and definitive cross-sectional imaging.

  • Wells Score for PE:

    • Clinical signs and symptoms of DVT (+3.0+3.0 points)
    • Alternative diagnosis less likely than PE (+3.0+3.0 points)
    • Heart rate >100 bpm> 100\text{ bpm} (+1.5+1.5 points)
    • Immobilisation or surgery within the prior 4 weeks (+1.5+1.5 points)
    • Previous objectively confirmed DVT or PE (+1.5+1.5 points)
    • Haemoptysis (+1.0+1.0 point)
    • Active malignancy treated within 6 months or receiving palliative care (+1.0+1.0 point)
    • Scoring Tier: PE unlikely ≤4.0\le 4.0 points; PE likely >4.0> 4.0 points.
  • Pulmonary Embolism Rule-out Criteria (PERC): Applied exclusively when clinical probability is low. All 8 criteria must be met to rule out PE without blood testing: age <50 years< 50\text{ years}, heart rate <100 bpm< 100\text{ bpm}, oxygen saturation ≥95%\ge 95\% on room air, no prior DVT/PE, no recent trauma or surgery (<4 weeks< 4\text{ weeks}), no haemoptysis, no exogenous oestrogen use, and no unilateral leg swelling.

  • Age-adjusted D-dimer: For an appropriate patient older than 50 with non-high probability, an assay using a standard 500 microgram/L FEU threshold may use age × 10 microgram/L FEU. Confirm the laboratory assay and units; FEU and DDU are different. A negative result is useful only within the validated pathway.

Cut-off=Age×10 μg/L\text{Cut-off} = \text{Age} \times 10\ \mu\text{g/L}

This avoids unnecessary computed tomography in elderly patients with physiologically elevated baseline fibrin degradation products.


Diagnostic Imaging & Hemodynamic Risk Stratification

Cross-Sectional Imaging Modalities

  1. Computed Tomography Pulmonary Angiography (CTPA): The primary diagnostic modality of choice. Directly visualises intraluminal filling defects down to subsegmental branches and evaluates RV strain (RV/LV diameter ratio >0.9> 0.9).
  2. Ventilation-Perfusion (V/Q) Scintigraphy: Evaluates mismatch between lung ventilation and perfusion. Indicated when CTPA is contraindicated:
    • Severe renal impairment calls for balancing contrast risk against the danger of missing PE; it is not an absolute ban on CTPA. V/Q is an alternative when suitable.
    • Severe, documented anaphylactic reaction to iodinated intravenous contrast
    • Pregnant patients with a normal baseline chest X-ray (V/Q delivers lower radiation dose to maternal breast tissue than CTPA, reducing lifetime maternal breast cancer risk)

Severity Stratification & Acute Management

  • Massive (High Risk): Clinical Criteria: Sustained hypotension (systolic BP<90 mmHg\text{BP} < 90\text{ mmHg} for ≥15 min\ge 15\text{ min}), obstructive shock, or cardiac arrest; Primary Therapeutic Strategy: Immediate Systemic Thrombolysis (Alteplase 100 mg100\text{ mg} IV over 2 hrs) + Unfractionated Heparin
  • Submassive (Intermediate Risk): Clinical Criteria: Normotensive, but exhibits both RV dysfunction (CT/echo) and myocardial injury (elevated troponin/BNP); Primary Therapeutic Strategy: Therapeutic Anticoagulation (LMWH or DOAC) + Continuous HDU/ICU monitoring for decompensation
  • Low Risk: Clinical Criteria: Normotensive, normal RV function, normal cardiac biomarkers; Primary Therapeutic Strategy: Early discharge on Direct Oral Anticoagulant (Apixaban or Rivaroxaban)

Pharmacotherapy of Venous Thromboembolism

  • Direct Oral Anticoagulants (DOACs): First-line therapy for non-high-risk PE. Apixaban (10 mg10\text{ mg} bd for 7 days, then 5 mg5\text{ mg} bd) or Rivaroxaban (15 mg15\text{ mg} bd with food for 21 days, then 20 mg20\text{ mg} daily) do not require initial heparin lead-in.
  • Anticoagulant selection: DOACs suit many stable patients, including selected patients with cancer. LMWH is used in pregnancy and may be preferable with particular cancer or bleeding risks. Kidney function, liver disease, antiphospholipid syndrome, interactions and planned procedures alter the choice.

Pleural Effusions: Transudates vs Exudates

Pleural effusions occur when pleural fluid formation exceeds physiological lymphatic clearance. Diagnostic thoracentesis is performed to differentiate transudative from exudative processes.

Light's Criteria

A pleural effusion is classified as an exudate if it meets at least one of the following three criteria:

  1. Pleural Fluid ProteinSerum Protein>0.5\frac{\text{Pleural Fluid Protein}}{\text{Serum Protein}} > 0.5
  2. Pleural Fluid LDHSerum LDH>0.6\frac{\text{Pleural Fluid LDH}}{\text{Serum LDH}} > 0.6
  3. Pleural Fluid LDH >23×> \frac{2}{3} \times upper limit of normal laboratory serum LDH

If none of these criteria are met, the effusion is a transudate.


Pneumothorax: Classification and Emergency Intervention

Pneumothorax is the presence of air within the pleural cavity leading to lung collapse.

Primary vs Secondary Spontaneous Pneumothorax

  • Primary spontaneous pneumothorax: In a stable patient with minimal symptoms, a conservative pathway can be appropriate even for a larger radiographic pneumothorax. Decide using symptoms, physiological stability, reliable follow-up and local pleural guidance rather than a 2-cm cut-off alone. Give oxygen for hypoxaemia, not routinely to a normoxic patient. Breathlessness or instability may require aspiration or a small-bore drain.
    • Management: If small (<2 cm< 2\text{ cm} rim at the level of the hilum on erect CXR) and minimally symptomatic: observe, administer high-flow oxygen (accelerates air reabsorption fourfold), and discharge with outpatient review. If large (≥2 cm\ge 2\text{ cm}) or breathless: simple needle aspiration with a 16−18G16-18\text{G} cannula. If aspiration fails (>2.5 L> 2.5\text{ L} air aspirated without resistance or persistent large pneumothorax), insert a small-bore (10−14 Fr10-14\text{ Fr}) chest tube.
  • Secondary Spontaneous Pneumothorax (SSP): Occurs in patients with underlying lung pathology (most commonly COPD with bullous disease, cystic fibrosis, or necrotising pneumonia). Because physiological reserve is compromised, SSP requires lower thresholds for intercostal catheter insertion.

Tension Pneumothorax: Immediate Decompression

Tension pneumothorax is a purely clinical diagnosis that occurs when a 'one-way valve' pleural tear permits air entry during inspiration but prevents egress during expiration. Rising intrapleural pressure collapses the ipsilateral lung, shifts the mediastinum to the contralateral side, compresses the superior and inferior vena cava, obstructs venous return, and precipitates acute obstructive shock and pulseless electrical activity (PEA) arrest.

  • Clinical Signs: Severe respiratory distress, cyanosis, unilateral absence of breath sounds and hyperresonance to percussion, marked hypotension, tachycardia, jugular venous distension, and tracheal deviation away from the affected hemithorax. Never delay treatment to perform a chest X-ray.
  • Immediate Needle Decompression: Perform emergent decompression using a large-bore cannula (14−16G14-16\text{G}, at least 4.5−5 cm4.5-5\text{ cm} length to traverse the chest wall):
    • Second intercostal space in the midclavicular line (just superior to the 3rd rib to avoid the neurovascular bundle), OR
    • Fourth or fifth intercostal space in the anterior axillary line (now increasingly preferred in adult trauma and Australian resuscitation guidelines due to thinner chest wall anatomy in this region).
  • Definitive Management: Immediate subsequent insertion of an intercostal catheter (chest tube) attached to an underwater seal drainage system within the safe triangle (bounded by the anterior border of latissimus dorsi, the lateral border of pectoralis major, and the horizontal level of the 5th intercostal space).

Primary references (checked 7 October 2026): NSW trauma pathway.

Test Your Knowledge

A 28-year-old tall, slender male presents to the emergency department with sudden-onset left-sided pleuritic chest pain and dyspnoea that began while resting at home. On examination, he is in mild discomfort with a respiratory rate of 18 breaths/min, heart rate 78 bpm, blood pressure 122/74 mmHg, and SpO2 98% on room air. Trachea is midline. Breath sounds are slightly diminished at the left apex. An erect chest X-ray reveals a 1.4 cm rim of air between the left lung margin and the chest wall at the level of the hilum. What is the most appropriate initial management?

A

Observation, analgesia, return precautions and reliable outpatient follow-up

B

Immediate emergency needle decompression

C

Insertion of a large-bore intercostal drain

D

Immediate thoracoscopic surgery

Test Your Knowledge

A 62-year-old woman is admitted with an unprovoked proximal DVT diagnosed yesterday. She has no recent surgery, intracranial disease or bleeding history. She develops sudden breathlessness, diaphoresis, and syncope upon standing. On examination, she is pale and clammy. Blood pressure is 74/46 mmHg, heart rate is 126 bpm, respiratory rate is 32 breaths/min, and oxygen saturation is 86% on room air. ECG reveals sinus tachycardia with T-wave inversions across V1 to V4. Bedside transthoracic echocardiography demonstrates severe right ventricular dilatation, severe hypokinesia of the right ventricular free wall, and bowing of the interventricular septum into the left ventricle. What is the most appropriate immediate medical intervention?

A

Administer 3 litres of 0.9% normal saline rapidly via two large-bore peripheral cannulae

B

Perform immediate systemic thrombolysis with intravenous alteplase 100 mg over 2 hours

C

Commence therapeutic subcutaneous enoxaparin 1.5 mg/kg once daily as monotherapy

D

Transfer to the radiology suite for a formal ventilation-perfusion lung scan

Test Your Knowledge

A 58-year-old male with a history of chronic alcohol-related liver cirrhosis presents with progressive exertional breathlessness and abdominal distension. A diagnostic thoracentesis of a large right-sided pleural effusion yields clear straw-coloured fluid. Laboratory investigation reveals: pleural protein 18 g/L (serum protein 62 g/L), pleural LDH 72 IU/L (serum LDH 180 IU/L; upper limit of normal serum LDH is 220 IU/L). Applying Light's criteria, how should this effusion be classified?

A

Exudative effusion resulting from acute bacterial parapneumonic infection

B

Exudative effusion secondary to metastatic peritoneal carcinomatosis

C

Transudative effusion resulting from altered hydrostatic or oncotic pressure gradients

D

Malignant chylothorax resulting from direct thoracic duct rupture

Test Your Knowledge

A 22-year-old unrestrained driver is brought to the resuscitation bay following a high-speed motor vehicle collision. He is severely agitated, cyanotic, and in profound respiratory distress. Vital signs: blood pressure 68/40 mmHg, heart rate 142 bpm, respiratory rate 38 breaths/min, and SpO2 78% on high-flow oxygen. Clinical examination reveals absent breath sounds and tympanitic percussion over the right hemithorax, marked jugular venous distension to the angle of the jaw, and trachea displaced to the left side. What is the immediate emergency action required?

A

Obtain an immediate portable upright chest X-ray to confirm the diagnosis

B

Perform rapid sequence intubation with high levels of positive end-expiratory pressure

C

Administer 2 units of uncrossed O-negative packed red blood cells through a rapid infuser

D

Perform immediate chest decompression using the local trauma technique

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