Neurogenic Pulmonary Edema in a 22-Year-Old Male Secondary to a Ruptured Cerebellar Arteriovenous Malformation: A Case Report.
- 1Anesthesiology, HCA Florida Westside Hospital, Plantation, USA.
- 2Osteopathic Medicine, Nova Southeastern University Dr. Kiran C. Patel College Of Osteopathic Medicine, Fort Lauderdale, USA.
- 3Anesthesiology and Critical Care, HCA Florida Westside Hospital, Plantation, USA.
Abstract
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, fourth-ventricular 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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BibTeX
@article{collins2026neurogenic,
title = {{Neurogenic Pulmonary Edema in a 22-Year-Old Male Secondary to a Ruptured Cerebellar Arteriovenous Malformation: A Case Report.}},
author = {Michael Dylan Collins and Amit Sharma and Aaron Hacker and Imani Thornton},
journal = {Cureus},
year = {2026},
month = oct,
doi = {10.7759/cureus.117635},
url = {https://europepmc.org/article/MED/42999619},
note = {CC BY},
}
RIS
TY - JOUR
TI - Neurogenic Pulmonary Edema in a 22-Year-Old Male Secondary to a Ruptured Cerebellar Arteriovenous Malformation: A Case Report.
AU - Michael Dylan Collins
AU - Amit Sharma
AU - Aaron Hacker
AU - Imani Thornton
PY - 2026
DA - 2026/10/08
JO - Cureus
DO - 10.7759/cureus.117635
UR - https://europepmc.org/article/MED/42999619
AB - 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, fourth-ventricular 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.
SN - 2168-8184
ER -