Suspected neurogenic pulmonary edema after subarachnoid hemorrhage: a brain–heart–lung diagnostic challenge

Abstract

Background Neurogenic pulmonary edema (NPE) is an acute pulmonary complication after severe central nervous system injury. Its diagnosis is challenging when respiratory deterioration coincides with cardiac abnormalities capable of causing pulmonary congestion. Case presentation A 66-year-old man with hypertension and diabetes mellitus presented with sudden dyspnea, hypoxemia, tachypnea, bilateral fine crackles, and an irregular tachyarrhythmia. Non-contrast brain computed tomography showed focal right temporoparietal subarachnoid hemorrhage. Serial electrocardiograms demonstrated atrial fibrillation with rapid/variable ventricular response with elevated high-sensitivity troponin I. Echocardiography showed a left ventricular ejection fraction of 71%, global normokinesis, no regional wall-motion abnormality, concentric left ventricular hypertrophy, and diastolic dysfunction. Initial chest radiography showed increased bronchovascular markings without cardiomegaly or bilateral infiltrates. The patient received respiratory, cardiovascular, and neurological treatment, underwent urgent craniectomy and evacuation, and subsequently developed progressive hemodynamic deterioration with recurrent cardiac arrest and death. Conclusions The close temporal relationship between subarachnoid hemorrhage and abrupt hypoxemic respiratory distress supported a working diagnosis of suspected NPE. Preserved ventricular systolic function made severe systolic pump failure less likely, but it did not exclude a cardiogenic contribution. Atrial fibrillation, hypertension, concentric left ventricular hypertrophy, and diastolic dysfunction therefore remained clinically relevant competing explanations.

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BibTeX RIS

BibTeX

@article{kasvana2026suspected,
  title = {{Suspected neurogenic pulmonary edema after subarachnoid hemorrhage: a brain–heart–lung diagnostic challenge}},
  author = {Kasvana Kasvana and Syilvia Cendy Enike and Nikita Tan and Yohanes Firmansyah and Puja Laksana Maqbul},
  journal = {The Egyptian Journal of Bronchology},
  year = {2026},
  month = oct,
  doi = {10.1186/s43168-026-00706-0},
  url = {https://doi.org/10.1186/s43168-026-00706-0},
  note = {CC BY},
}

RIS

TY  - JOUR
TI  - Suspected neurogenic pulmonary edema after subarachnoid hemorrhage: a brain–heart–lung diagnostic challenge
AU  - Kasvana Kasvana
AU  - Syilvia Cendy Enike
AU  - Nikita Tan
AU  - Yohanes Firmansyah
AU  - Puja Laksana Maqbul
PY  - 2026
DA  - 2026/10/25
JO  - The Egyptian Journal of Bronchology
DO  - 10.1186/s43168-026-00706-0
UR  - https://doi.org/10.1186/s43168-026-00706-0
AB  - Background Neurogenic pulmonary edema (NPE) is an acute pulmonary complication after severe central nervous system injury. Its diagnosis is challenging when respiratory deterioration coincides with cardiac abnormalities capable of causing pulmonary congestion. Case presentation A 66-year-old man with hypertension and diabetes mellitus presented with sudden dyspnea, hypoxemia, tachypnea, bilateral fine crackles, and an irregular tachyarrhythmia. Non-contrast brain computed tomography showed focal right temporoparietal subarachnoid hemorrhage. Serial electrocardiograms demonstrated atrial fibrillation with rapid/variable ventricular response with elevated high-sensitivity troponin I. Echocardiography showed a left ventricular ejection fraction of 71%, global normokinesis, no regional wall-motion abnormality, concentric left ventricular hypertrophy, and diastolic dysfunction. Initial chest radiography showed increased bronchovascular markings without cardiomegaly or bilateral infiltrates. The patient received respiratory, cardiovascular, and neurological treatment, underwent urgent craniectomy and evacuation, and subsequently developed progressive hemodynamic deterioration with recurrent cardiac arrest and death. Conclusions The close temporal relationship between subarachnoid hemorrhage and abrupt hypoxemic respiratory distress supported a working diagnosis of suspected NPE. Preserved ventricular systolic function made severe systolic pump failure less likely, but it did not exclude a cardiogenic contribution. Atrial fibrillation, hypertension, concentric left ventricular hypertrophy, and diastolic dysfunction therefore remained clinically relevant competing explanations.
SN  - 1687-8426
SN  - 2314-8551
ER  -

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