Neurogenic pulmonary edema

Neurogenic
pulmonary oedema. Endotracheal tube with the distal tip to the right main bronchus, needs to be adjusted. Bilateral extensive patchy air space opacities with air bronchogram. No obvious Kerley B lines or pleural effusions. No pneumothorax.
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Neurogenic
pulmonary oedema. Large subarachnoid haemorrhage along with intraparenchymal haematoma in the right basifrontal lobe. Diffuse cerebral oedema with effacement of basal cisterns and cortical sulci bilaterally.
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Neurogenic pulmonary edema is an etiological subtype of non-cardiogenic pulmonary edema, classified as a subtype of the acute respiratory distress syndrome by the Berlin definition.

The diagnosis of neurogenic pulmonary edema is based on the occurrence of edema after a neurologic event/insult and the exclusion of other plausible causes.

Epidemiology

The incidence of neurogenic pulmonary edema is difficult to estimate, with the majority of published studies regarding this entity being case report level data. Noted associations include:

  • viral encephalitis
    • particularly with enterovirus-71
  • subarachnoid hemorrhage 
    • marked variability in reported incidence, ranging from 7% to 78% in fatal cases secondary to aneurysmal rupture
  • traumatic brain injury 
  • seizures

Clinical presentation

Two distinct syndromes have been described based on the time course elapsed from the inciting event, both presenting with signs and symptoms of respiratory distress (e.g. dyspnea, tachypnea, crackles) with subsequent progression to hypoxemic respiratory failure;

  • "early" or "acute" neurogenic pulmonary edema (most common)
    • occurs within the first 4 hours in the majority (71.4%) of patients
    • association with younger patients and higher serum glucose
    • spontaneous resolution within 48–72 hours
  • "delayed" neurogenic pulmonary edema
    • onset within 12-24 hours
    • similar time course

Pathology

It characteristically presents within minutes to hours following a neurologic insult and usually resolves within 72 hours.

The exact pathophysiology is unclear but is thought to be the result of an adrenergic response leading to increased pulmonary hydrostatic pressure and increased lung capillary permeability .

Radiographic features

Plain radiograph

On chest radiographs, there are nonspecific, bilateral, rather homogeneous airspace consolidative appearances with an apical predominance is thought to the present in about half of cases .

See also

Siehe auch:
und weiter:
Assoziationen und Differentialdiagnosen zu neurogenes Lungenödem:
Lungenödem
 
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