4.4 Acute Lung Injury, Embolism & Pleural Disorders

Acute Respiratory Distress Syndrome (ARDS)

ARDS is diagnosed using the Berlin definition, which requires all of the following:

• Acute onset — within one week of a known clinical insult (sepsis, aspiration, pneumonia, trauma, pancreatitis, transfusion)
• Bilateral opacities on chest imaging not fully explained by effusions, lobar/lung collapse, or nodules
• Respiratory failure not fully explained by cardiac failure or fluid overload — an objective assessment (e.g., echocardiogram) is used to rule out hydrostatic pulmonary edema when no clear risk factor is present
• Oxygenation impairment measured by the PaO2/FiO2 (P/F) ratio with PEEP or CPAP ≥5 cmH2O

A key distinguishing point from cardiogenic pulmonary edema: in ARDS, pulmonary artery occlusion (wedge) pressure is typically normal or low (≤18 mmHg) because the underlying process is inflammatory capillary leak, not left heart failure.

Management centers on lung-protective ventilation: low tidal volume (approximately 6 mL/kg predicted body weight), plateau pressure kept below 30 cmH2O to limit ventilator-induced lung injury, and permissive hypercapnia (tolerating a higher PaCO2 to avoid injuriously high pressures/volumes). Adjuncts for moderate-to-severe ARDS include prone positioning, conservative fluid management, neuromuscular blockade in select severe cases, and ECMO when conventional ventilation fails.

Pulmonary Embolism (PE)

PE classically presents with sudden-onset dyspnea, pleuritic chest pain, tachycardia, tachypnea, and sometimes hemoptysis or a sense of impending doom. Risk factors follow Virchow's triad: venous stasis (immobility, long flights, post-surgical state), hypercoagulability (malignancy, pregnancy, oral contraceptives, inherited thrombophilia), and endothelial injury (trauma, prior DVT, central lines).

A massive PE can obstruct right ventricular outflow enough to cause obstructive shock: hypotension, jugular venous distension, tachycardia, and signs of acute RV strain on echocardiogram (RV dilation, septal bowing). This is a distinct shock category from cardiogenic, hypovolemic, or distributive shock—the pump itself is fine, but flow is mechanically blocked.

Diagnosis: CT pulmonary angiography is the gold standard; D-dimer is useful only to help rule out PE in low-probability patients (a negative result in low-risk patients argues against PE, but a positive result is nonspecific). The Wells score stratifies pretest probability. Treatment is anticoagulation for most patients; thrombolytics or catheter/surgical embolectomy are reserved for massive PE with hemodynamic instability, since the bleeding risk of thrombolysis must be weighed against the risk of the clot itself.

Pleural Space Complications

Chest Tube Principles

• Tidaling (fluid rise/fall in the water seal chamber with respiration) confirms the tube is patent and the system is functioning; absence of tidaling means either the lung has fully reexpanded or the tube is obstructed/kinked.
• Continuous bubbling in the water seal chamber that persists (beyond the initial period of lung reexpansion) indicates an air leak—check tubing connections and the insertion site before assuming it is coming from the pleural space itself.
• Never clamp a chest tube without a specific order and close supervision—clamping a tube that is still draining air can rapidly cause a tension pneumothorax.
• Avoid routine stripping or milking of tubing, which creates dangerous negative pressure spikes.
• Keep the collection system below chest level at all times and monitor drainage volume/color; notify the provider for sudden increases, a change to frank blood, or drainage exceeding roughly 200 mL/hr, which may indicate active bleeding.

Pneumonia and Pulmonary Hypertension

Pneumonia (community- or hospital-acquired) presents with fever, productive cough, pleuritic pain, crackles, and a new infiltrate on chest imaging; it is a leading trigger for sepsis and ARDS in progressive care patients. Pulmonary hypertension (elevated mean pulmonary artery pressure at rest) causes progressive right ventricular strain and, over time, right heart failure; management includes treating the underlying cause and, in select patients, pulmonary vasodilator therapy.

PE Risk Stratification

Not every PE requires the same intensity of treatment. PE is generally stratified as:

• Low-risk (submassive without dysfunction) — hemodynamically stable, no RV strain — anticoagulation alone
• Submassive (intermediate-risk) — hemodynamically stable but with evidence of RV strain (echo findings, elevated troponin/BNP) — closer monitoring, anticoagulation, thrombolytics considered case-by-case
• Massive (high-risk) — sustained hypotension or shock from RV failure — thrombolytics or embolectomy considered emergently

This stratification is why two patients with the same clot burden on CT can receive very different treatment plans — the hemodynamic and RV-function picture, not just the presence of a clot, drives urgency.

ARDS Complications to Monitor

Beyond the acute oxygenation failure, ARDS carries meaningful risk of ventilator-associated lung injury (barotrauma/volutrauma from high pressures or volumes, which lung-protective ventilation is specifically designed to prevent), ventilator-associated pneumonia from prolonged intubation, and right ventricular strain from elevated intrathoracic pressures and hypoxic pulmonary vasoconstriction. Nutrition, early mobility when feasible, sedation minimization, and daily assessment of readiness to reduce ventilator support all remain part of ARDS bundle care even while the primary focus stays on lung-protective settings.