Key result
Ruptured cerebellar AVM triggers fatal neurogenic pulmonary edema with potential naloxone and aspiration contributions.
Why the study?
Neurogenic pulmonary edema is a rare acute pulmonary complication following severe central nervous system insults, requiring early recognition and careful differential diagnosis.
Case Report (n=1)
This case highlights the difficulty of differentiating neurogenic pulmonary edema from other superimposed mechanisms, such as naloxone-associated edema or aspiration, following an acute catastrophic brain injury.
May prompt NPE consideration in hypoxemic failure after cerebellar AVM; leaves open need for prospective incidence data.
Neurogenic pulmonary edema (NPE) is an acute form of pulmonary edema that can follow a severe central nervous system insult.We describe a 22-year-old man who developed profound hypoxemic respiratory failure during presentation with a ruptured right cerebellar arteriovenous malformation (AVM).Emergency medical personnel found him unresponsive with agonal respirations after he had taken an unidentified medication for a severe headache.Because opioid toxicity was initially suspected, he received 2 milligrams (mg) of intranasal naloxone, with transient improvement in breathing.In the ED, he had pinpoint pupils, depressed consciousness, crackles, and a high oxygen requirement.After an additional 1 mg of intravenous naloxone, he became markedly hypoxemic and hypotensive, with copious pink frothy secretions, and required tracheal intubation and vasopressor support.Toxicology testing detected cannabinoids but not opioids.Computed tomography demonstrated an 18.7 milliliter (mL) right cerebellar hemorrhage, fourthventricular and basal-cistern mass effect, tonsillar herniation, an underlying AVM, and extensive bilateral pulmonary consolidation.An external ventricular drain was placed, but planned decompressive surgery was aborted when prone positioning caused severe oxygen desaturation and pulmonary secretions.Despite neurocritical and respiratory support, cerebral perfusion imaging later showed absent intracranial blood flow.The clinical pattern was most consistent with NPE caused by the catastrophic posterior fossa hemorrhage.Naloxone-associated pulmonary edema and aspiration were contributing considerations; the temporal deterioration after the second dose does not establish causation.This case emphasizes early recognition of pulmonary complications after acute brain injury and careful, evidence-based attribution when several mechanisms are plausible.
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Collins et al. (2026) conducted a case report in Neurogenic pulmonary edema (n=1). Ruptured cerebellar arteriovenous malformation and naloxone administration was evaluated on Clinical outcome (pulmonary edema and survival). A 22-year-old male developed fatal neurogenic pulmonary edema triggered by a ruptured cerebellar arteriovenous malformation, with naloxone administration and aspiration as potential contributing factors.
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