Neurogenic pulmonary oedema

Reviewed and revised 17 August 2015

OVERVIEW

Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by the acute onset of pulmonary edema following a significant central nervous system (CNS) insult

• The etiology is thought to be a surge of catecholamines that results in cardiopulmonary dysfunction
• Generally under recognised

CAUSE

Inciting insult can be any acute CNS disorder, including:

• head injury
• intracranial and subarachnoid hemorrhage
• seizures
• tumors
• hydrocephalus
• spinal cord injury
• neurosurgical procedures

PATHOGENESIS

Proposed mechanism

• especially abrupt severe rise in ICP
• neuronal compression, ischemia or damage -> increased sympathetic discharge -> catecholamine surge -> increased SVR and decreased left ventricular contractility + alveolar-capillary leakage

Several theories have been proposed to explain how the catecholamine surge causes pulmonary edema:

• Neuro-cardiac (direct myocardial injury)
• Neuro-hemodynamic (ventricular compliance is indirectly altered by the abrupt increases in systemic and pulmonary pressures following CNS injury)
• “Blast theory” (acute (transient) rise in capillary pressure induces a degree of barotrauma capable of damaging the capillary-alveolar membrane, in addition to neuro-hemodynamic effects causing transudative pulmonary edema)
• Pulmonary venule adrenergic hypersensitivity (massive sympathetic discharge following CNS injury directly affects the pulmonary vascular bed, and that the edema develops regardless of any systemic changes)

CLINICAL FEATURES

Types

• early – minutes to hours after CNS insult
• delayed – 12 to 24 hours after CNS insult

Features

• highly variable
• mild SOB -> acute fulminating pulmonary oedema (acutely dyspneic, tachypneic, and hypoxic within minutes)
• sympathetic surge: fever, tachycardia, and hypertensive, and leukocytosis may occur
• often spontaneously resolve within 24 to 48 hours; may last longer if CNS insult persists/ recurs

INVESTIGATIONS

• bilateral hyperdense infiltrates similar to ARDS on CXR
• no tests specific for neurogenic pulmonary oedema
• identify CNS lesion (e.g. CT head)
• consider measurement of serum catecholamines

MANAGEMENT

• primarily supportive
• protective lung ventilation strategy with relative high PEP
• some advocate use of alpha-blockers (phentolamine and phenoxybenzamine) -> no high quality evidence available
• avoid excessive diuresis -> need to maintain systemic perfusion and cerebral blood flow
• treat underlying CNS insult (e.g. ICP control)

References and Links

LITFL

• CCC – Negative Pressure pulmonary oedema

Journal articles

• Davison DL, Terek M, Chawla LS. Neurogenic pulmonary edema. Crit Care. 2012 Dec 12;16(2):212. PMID: 22429697. [free full text]
• O’Leary R, McKinlay J. Neurogenic pulmonary oedema. Contin Educ Anaesth Crit Care Pain (2011) 11 (3): 87-92  [free full text]

FOAM and web resources

• UMEM Education Pearls — Non-Cardiogenic Pulmonary Edema