Neurogenic pulmonary edema

Changed by Andrew Murphy, 6 Jun 2020

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Neurogenic pulmonary oedema (NPE) is is an aetiological subtype of non-cardiogenic pulmonary oedema, classified as a subtype of the acute respiratory distress syndrome by the Berlin definition.

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

Epidemiology

The incidence of neurogenic pulmonary oedema 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 (SAH)
    • marked variability in reported incidence, ranging from 7% to 78% in fatal cases secondary to aneurysmal rupture 5,8
  • traumatic brain injury (TBI)
  • 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" NPEneurogenic pulmonary oedema (most common)
    • occurs within the first 4 hours in the majority (71.4%) of patients 9
    • association with younger patients and higher serum glucose 6
    • spontaneous resolution within 48–72 hhours 5
  • "delayed" NPEneurogenic pulmonary oedema
    • 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 of is unclear, but itis thought to relate to an adrenergic response leading to increased pulmonary hydrostatic pressure and increased lung capillary permeability 2.

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 4.

See also

  • -<p><strong>Neurogenic pulmonary oedema</strong> (NPE) is an aetiological subtype of <a href="/articles/non-cardiogenic-pulmonary-oedema-2">non-cardiogenic pulmonary oedema</a>, classified as a subtype of the <a title="Acute respiratory distress syndrome" href="/articles/acute-respiratory-distress-syndrome-1">acute respiratory distress syndrome</a> by the Berlin definition.</p><p>The diagnosis of neurogenic pulmonary oedema is based on the occurrence of oedema after a neurologic event/insult and the exclusion of other plausible causes.</p><h4>Epidemiology</h4><p>The incidence of neurogenic pulmonary oedema is difficult to estimate, with the majority of published studies regarding this entity being case report level data. Noted associations include:</p><ul>
  • +<p><strong>Neurogenic pulmonary oedema</strong> is an aetiological subtype of <a href="/articles/non-cardiogenic-pulmonary-oedema-2">non-cardiogenic pulmonary oedema</a>, classified as a subtype of the <a href="/articles/acute-respiratory-distress-syndrome-1">acute respiratory distress syndrome</a> by the Berlin definition.</p><p>The diagnosis of neurogenic pulmonary oedema is based on the occurrence of oedema after a neurologic event/insult and the exclusion of other plausible causes.</p><h4>Epidemiology</h4><p>The incidence of neurogenic pulmonary oedema is difficult to estimate, with the majority of published studies regarding this entity being case report level data. Noted associations include:</p><ul>
  • -<a title="Subarachnoid hemorrhage" href="/articles/subarachnoid-haemorrhage">subarachnoid hemorrhage</a> (SAH)<ul><li>marked variability in reported incidence, ranging from 7% to 78% in fatal cases secondary to aneurysmal rupture <sup>5,8</sup>
  • +<a href="/articles/subarachnoid-haemorrhage">subarachnoid hemorrhage</a> <ul><li>marked variability in reported incidence, ranging from 7% to 78% in fatal cases secondary to aneurysmal rupture <sup>5,8</sup>
  • -<li>traumatic brain injury (TBI)</li>
  • +<li>traumatic brain injury </li>
  • -<li>"early" or "acute" NPE (most common)<ul>
  • +<li>"early" or "acute" neurogenic pulmonary oedema (most common)<ul>
  • -<li>spontaneous resolution within 48–72 h <sup>5</sup>
  • +<li>spontaneous resolution within 48–72 hours <sup>5</sup>
  • -<li>"delayed" NPE<ul>
  • +<li>"delayed" neurogenic pulmonary oedema<ul>
  • -</ul><h4>Pathology</h4><p>It characteristically presents within minutes to hours following a neurologic insult and usually resolves within 72 hours.</p><p>The exact pathophysiology of is unclear, but it thought to relate to an adrenergic response leading to increased pulmonary hydrostatic pressure and increased lung capillary permeability <sup>2</sup>.</p><h4>Radiographic features</h4><h5>Plain radiograph</h5><p>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 <sup>4</sup>.</p><h4>See also</h4><ul>
  • +</ul><h4>Pathology</h4><p>It characteristically presents within minutes to hours following a neurologic insult and usually resolves within 72 hours.</p><p>The exact pathophysiology of is unclear but is thought to relate to an adrenergic response leading to increased pulmonary hydrostatic pressure and increased lung capillary permeability <sup>2</sup>.</p><h4>Radiographic features</h4><h5>Plain radiograph</h5><p>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 <sup>4</sup>.</p><h4>See also</h4><ul>
  • -<a href="/articles/non-cardiogenic-pulmonary-oedema-mnemonic-1">NOT-CARDIAC</a>: mnemonic for non cardiogenic pulmonary oedema</li>
  • +<a href="/articles/non-cardiogenic-pulmonary-oedema-mnemonic-1">NOT-CARDIAC</a>: a mnemonic for non-cardiogenic pulmonary oedema</li>

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