3.4 Venous Thromboembolism, Pleural Disease & Pneumothorax

3.4 Venous Thromboembolism, Pleural Disease & Pneumothorax

Acute pulmonary vascular emergencies and pleural space disorders represent life-threatening presentations frequently encountered in acute medicine. Rapid clinical risk stratification, prompt diagnostic imaging, and time-critical interventional procedures are vital to prevent fatal decompensation.

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1. Pulmonary Embolism (PE): Pathophysiology and Clinical Presentation

Pulmonary embolism occurs when an endogenous or exogenous thrombus—originating in over 90% of cases from the deep veins of the lower limbs or pelvis—migrates through the venous circulation into the pulmonary arterial bed. Obstruction of pulmonary arterial blood flow leads to ventilation-perfusion mismatch (increased dead space), reflex bronchoconstriction, neurohumoral vasoconstriction, acute right ventricular afterload increase, right ventricular dilatation, and potentially fatal circulatory collapse.

Risk Factors (Virchow's Triad)

1. Endothelial Injury: Recent major surgery (especially hip or knee arthroplasty, pelvic surgery), lower limb trauma, vascular cannulation.
2. Venous Stasis: Prolonged bed rest, hospital admission, long-distance travel, congestive heart failure, stroke with limb paresis.
3. Hypercoagulability: Active malignancy, pregnancy, combined oral contraceptive pill or hormone replacement therapy, inherited thrombophilias (Factor V Leiden, prothrombin gene mutation, antithrombin III deficiency), antiphospholipid syndrome.

Clinical Presentation and Findings

• Symptoms: Sudden-onset dyspnoea, pleuritic chest pain, haemoptysis (indicates pulmonary infarction), syncope or presyncope (indicates massive PE with acute right heart outflow obstruction).
• Physical Signs: Tachypnoea ($\text{RR} \ge 20\text{/min}$), tachycardia ($\text{HR} > 100\text{ bpm}$), unilateral painful leg swelling (DVT), cyanosis, hypotension (systolic $\text{BP} < 90\text{ mmHg}$), raised JVP, and right ventricular heave.
• Electrocardiogram (ECG): Sinus tachycardia is the most common finding. Classic signs of right ventricular strain include the $S_1Q_3T_3$ pattern (deep S wave in I, pathological Q wave in III, inverted T wave in III), T-wave inversions in leads V1–V4, and new right bundle branch block (RBBB).

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2. Two-Level Wells Score & Diagnostic Algorithm

NICE guidelines recommend evaluating all patients with suspected PE using the two-level Wells score:

Clinical Probability Stratification

• PE Unlikely ($\le 4\text{ points}$):

  • Perform a high-sensitivity D-dimer test.
  • Negative D-dimer: PE is safely ruled out; stop investigations and do not anticoagulate.
  • Positive D-dimer: Arrange an urgent CT Pulmonary Angiography (CTPA).

• PE Likely ($> 4\text{ points}$):

  • Arrange an immediate CTPA.
  • Critical Rule: If CTPA cannot be obtained immediately (e.g., scanner maintenance or night delays), administer interim therapeutic anticoagulation immediately while awaiting imaging.

Imaging Modalities: CTPA vs V/Q Scan

• CT Pulmonary Angiography (CTPA): Definitive first-line imaging modality of choice. Directly visualizes intraluminal filling defects in main, lobar, segmental, and subsegmental pulmonary arteries.
• Ventilation-Perfusion (V/Q) Scintigraphy: Preferred alternative if:
  1. Severe renal impairment (eGFR $< 30\text{ mL/min}$ where iodinated contrast is contraindicated).
  2. Severe documented iodinated contrast allergy.
  3. Normal baseline chest X-ray in pregnancy (delivers lower breast radiation dose than CTPA, although CTPA is preferred if the CXR is abnormal).

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3. Management of Pulmonary Embolism

Haemodynamically Stable PE

• First-Line Pharmacotherapy: Direct Oral Anticoagulants (DOACs) are first-line per NICE guidelines:
  • Apixaban: $10\text{ mg}$ BD for 7 days, then $5\text{ mg}$ BD maintenance.
  • Rivaroxaban: $15\text{ mg}$ BD for 21 days, then $20\text{ mg}$ OD maintenance.
  • Advantage: Single-agent oral therapy without the need for initial low-molecular-weight heparin (LMWH) bridging or INR monitoring.
• Alternative Anticoagulation (Special Populations):
  • Low-Molecular-Weight Heparin (LMWH, e.g., Dalteparin or Enoxaparin): Preferred during pregnancy (DOACs and warfarin are teratogenic/contraindicated). For active cancer, NICE NG158 (2020, updated 2023) now offers a DOAC (apixaban or rivaroxaban) first, with LMWH if a DOAC is unsuitable (for example high-risk gastrointestinal or genitourinary tumours, or interacting chemotherapy).
  • Unfractionated Heparin (IV UFH): Preferred in severe renal impairment ($\text{CrCl} < 15\text{ mL/min}$) or extreme bleeding risk due to short half-life and reversibility with protamine.
• Duration of Anticoagulation:
  • Provoked PE (identifiable transient risk factor e.g., major surgery, immobilisation): 3 months, then stop if the provoking factor has resolved.
  • Unprovoked PE: at least 3 months, then consider continuing long-term (NICE NG158) if bleeding risk is acceptable and the person agrees, using a bleeding-risk tool to support the decision.
  • Active cancer: 3–6 months, then review whether to continue. Antiphospholipid syndrome needs long-term warfarin (DOACs are avoided, especially in triple-positive disease).

Massive PE (Haemodynamically Unstable PE)

• Defined by systolic blood pressure $< 90\text{ mmHg}$, a drop in systolic BP of $\ge 40\text{ mmHg}$ for $> 15\text{ minutes}$, or cardiac arrest.
• Immediate Intervention: Intravenous systemic thrombolysis with Alteplase (recombinant tPA) ($50\text{ mg}$ bolus in cardiac arrest, or $100\text{ mg}$ infused over 2 hours) combined with unfractionated heparin and aggressive hemodynamic resuscitation.
• If thrombolysis is contraindicated or fails, consider catheter-directed mechanical thrombectomy or surgical pulmonary embolectomy.

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4. Pleural Effusion: Transudate vs. Exudate & Light's Criteria

A pleural effusion is an abnormal accumulation of fluid in the pleural space between the visceral and parietal pleura.

Pathophysiological Distinction

• Transudate (Pleural Protein $< 30\text{ g/L}$): Driven by elevated hydrostatic pressure or decreased oncotic pressure with intact pleural membranes. Pleural surfaces are disease-free.
  • Causes: Congestive heart failure (most common), liver cirrhosis with ascites (hepatic hydrothorax), nephrotic syndrome, severe hypoalbuminaemia, peritoneal dialysis.
• Exudate (Pleural Protein $> 30\text{ g/L}$): Driven by increased vascular permeability secondary to local pleural inflammation, infection, or malignant infiltration.
  • Causes: Parapneumonic effusions / empyema, bronchogenic carcinoma, pleural metastases (breast, ovary), pulmonary embolism, tuberculosis, connective tissue disease (rheumatoid arthritis, SLE), pancreatitis.

Light's Criteria (For Borderline Protein: $25\text{--}35\text{ g/L}$)

When pleural fluid protein is in the borderline zone, Light's criteria reliably separate exudates from transudates. Fluid is classified as an EXUDATE if at least one of the following three criteria is fulfilled:

$\frac{\text{Pleural Fluid Protein}}{\text{Serum Protein}} > 0.5$

$\frac{\text{Pleural Fluid LDH}}{\text{Serum LDH}} > 0.6$

$\text{Pleural Fluid LDH} > \frac{2}{3} \times \text{Upper Limit of Normal for Serum LDH}$

Complicated Parapneumonic Effusion and Empyema

A parapneumonic effusion develops secondary to underlying pneumonia. It progresses in three stages: uncomplicated $\rightarrow$ complicated $\rightarrow$ empyema (frank pus).

• Indications for Immediate Intercostal Chest Drain Insertion:
  1. Frankly purulent or turbid fluid (pus).
  2. Pleural fluid $\text{pH} < 7.20$.
  3. Low pleural glucose ($< 3.3\text{ mmol/L}$) or very high $\text{LDH} > 1000\text{ IU/L}$.
  4. Positive microbiological culture or Gram stain.

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5. Pneumothorax: Classification and Management Algorithms

Pneumothorax is the presence of air within the pleural cavity, disrupting the negative intrapleural pressure that maintains lung inflation.

1. Tension Pneumothorax: Emergency Resuscitation

• Mechanism: A "one-way valve" laceration in the visceral or parietal pleura allows air into the pleural space during inspiration but prevents exit during expiration. Intrapleural pressure exceeds atmospheric pressure, causing total lung collapse, contralateral mediastinal shift, compression of the vena cava, obstructed venous return, and cardiac arrest.
• Clinical Signs: Severe respiratory distress, cyanosis, tachycardia, profound hypotension, distended neck veins (raised JVP), tracheal deviation away from the affected side, hyperresonance to percussion, and absent breath sounds on the affected side.
• Emergency Action: Never delay for a chest radiograph! Perform immediate needle thoracostomy / decompression using a large-bore cannula ($14\text{--}16\text{ gauge}$) inserted into:
  • The 2nd intercostal space in the mid-clavicular line (traditional site), OR
  • The 4th or 5th intercostal space in the anterior axillary line.
  • An immediate rush of air confirms decompression; leave the cannula in place and immediately perform definitive intercostal chest drain insertion.

2. Spontaneous Pneumothorax (BTS Guidelines)

Spontaneous pneumothorax is subdivided into Primary Spontaneous Pneumothorax (PSP, occurring in individuals without underlying clinical lung disease) and Secondary Spontaneous Pneumothorax (SSP, occurring in individuals with pre-existing lung pathology, most commonly COPD, asthma, or cystic fibrosis).

Primary Spontaneous Pneumothorax (PSP)

• Classically affects young, tall, slender males, especially smokers (including cannabis), secondary to rupture of subpleural apical blebs.
• Size is still measured on an erect chest X-ray (rim of 2 cm or more at the hilum is "large"), but the British Thoracic Society (BTS) 2023 guideline bases management on symptoms and high-risk features rather than size alone.

BTS 2023 Approach to Spontaneous Pneumothorax

1. High-risk characteristics (any of): haemodynamic instability, significant hypoxia, bilateral pneumothorax, underlying lung disease (i.e. SSP), age 50 or over with a significant smoking history, or haemothorax. These patients usually need a chest drain (small-bore, 14 French or less, is preferred).
2. No high-risk characteristics, minimal symptoms: conservative management is appropriate regardless of size, with safety netting and outpatient review (repeat X-ray at about 2–4 weeks).
3. No high-risk characteristics, symptoms needing intervention: choose with the patient between ambulatory management (an ambulatory pleural device, where specialist follow-up is available), needle aspiration (16–18 gauge cannula) or a chest drain. If needle aspiration fails, a chest drain or ambulatory device follows.

Secondary Spontaneous Pneumothorax (SSP)

• Occurs in patients with underlying lung disease (COPD, severe asthma, pulmonary fibrosis, cystic fibrosis). Because of poor respiratory reserve, even small pneumothoraces can cause respiratory failure.
• SSP is itself a high-risk characteristic: patients are admitted, and most need a chest drain; needle aspiration or an ambulatory device may be considered in selected stable patients, and conservative observation only for very small, minimally symptomatic SSP. Give oxygen to the patient's target saturation (88–92% if at risk of hypercapnia).
• Persistent air leak or failure to re-expand (around 3–5 days of drainage) needs early respiratory and thoracic surgical referral; surgery is also offered after a second ipsilateral or first contralateral pneumothorax, and in high-risk occupations (pilots, divers).