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

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


CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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