Postoperative Pulmonary Oedema

Postoperative pulmonary oedema is excess fluid in the alveoli and interstitium, from raised hydrostatic pressure (cardiogenic or fluid overload) or increased capillary permeability (non-cardiogenic).

Epidemiology. Reported in about 1% to 3% of major noncardiac surgery, with higher rates after vascular surgery and in heart failure. Onset ranges from minutes (negative pressure oedema) to 24 to 72 hours (fluid mobilisation). Figures are imprecise.

Causes.

• Cardiogenic: left ventricular failure, myocardial ischaemia, arrhythmia, valve disease, and fluid or transfusion overload.
• Non-cardiogenic: negative pressure (post-obstructive) oedema, transfusion related acute lung injury, acute respiratory distress syndrome, aspiration, neurogenic oedema, re-expansion and reperfusion oedema.

Risk factors. Heart failure, renal failure, aortic or vascular surgery, net positive balance over 3 L, transfusion, sepsis, older age, and laryngospasm or airway obstruction at emergence.

Pathophysiology.

Cardiogenic oedema follows raised left atrial pressure that overcomes oncotic forces. Postoperative sodium and water retention, vasoconstriction, diastolic dysfunction and mobilisation of third space fluid on days 2 to 3 contribute.

Negative pressure oedema follows forced inspiration against a closed glottis, producing very negative intrathoracic pressure, which raises venous return and afterload and injures capillaries. Hypoxia and catecholamines add to it.

Permeability oedema reflects inflammatory endothelial injury.

Dyspnoea, orthopnoea, tachypnoea, frothy pink sputum, bibasal crackles, wheeze, third heart sound, raised jugular venous pressure, peripheral oedema, hypoxaemia, oliguria, and hypertension early or hypotension in shock.

Red flags.

• Cardiogenic shock.
• Ischaemic ECG change or chest pain.
• Saturation under 90% on oxygen over 60%.
• Sustained arrhythmia.
• Onset during or soon after transfusion.
• Unilateral oedema after drainage of effusion or pneumothorax.

Investigations.

• ECG and serial high sensitivity troponin.
• B-type natriuretic peptide over 100 ng/L or N-terminal pro-B-type peptide over 300 ng/L supports cardiac cause (postoperative values rise non-specifically).
• Chest radiograph: bat wing shadowing, septal lines, upper lobe diversion; normal heart size favours negative pressure oedema.
• Lung ultrasound with 3 or more B-lines in several zones.
• Echocardiography for ejection fraction, valves, regional wall motion and right heart.
• Blood gas, urea, electrolytes, fluid balance and weight.

Differential diagnosis.

• Pneumonia.
• Aspiration.
• Pulmonary embolism.
• Acute respiratory distress syndrome.
• Transfusion related lung injury (fever, hypotension, within 6 hours) versus circulatory overload (hypertension, raised pressures).
• Atelectasis.
• Pneumothorax.

General. Sit upright, give oxygen to saturation 94% to 98% (88% to 92% if hypercapnic risk), and apply CPAP 5 to 10 cmH2O or non-invasive ventilation. Stop maintenance fluids, restrict intake, catheterise, and treat ischaemia, arrhythmia and precipitants.

Cardiogenic oedema.

• Furosemide: 40 mg IV slowly (no faster than 4 mg/min); give 40 to 80 mg if already on diuretics; repeat 80 mg after 1 hour if the response is poor; usual daily maximum 200 mg; monitor urine output, potassium, magnesium and creatinine; larger doses are needed in renal impairment and caution is required in hypovolaemia.
• Glyceryl trinitrate: 10 to 20 microgram/min IV, increased by 5 to 10 microgram/min every 5 to 10 minutes; maximum 200 microgram/min; continue while blood pressure stays high; monitor blood pressure continuously; avoid with systolic pressure under 110 mmHg (under 90 mmHg is an absolute contraindication), recent phosphodiesterase-5 inhibitor use and severe aortic stenosis.
• Cardiogenic shock: inotropes or vasopressors in critical care with echocardiography.

Negative pressure oedema. Relieve the obstruction, give oxygen and CPAP, and ventilate with positive end expiratory pressure if needed. Diuretics are rarely required. It usually resolves in 12 to 48 hours.

Transfusion reactions. For transfusion related lung injury stop the transfusion, give supportive care and avoid diuretics if hypotensive. For circulatory overload stop the transfusion and give furosemide.

Monitoring. Continuous ECG and saturation, hourly urine output, daily weight, electrolytes and creatinine.

Referral and escalation. Critical care or high dependency for non-invasive ventilation, shock or refractory hypoxaemia. Cardiology for ischaemia, valve disease or new heart failure. Notify the transfusion service of suspected transfusion related lung injury.