Case Report: Neurogenic pulmonary edema coupled with myocardial damage following tenecteplase thrombolysis for acute ischemic stroke

Neurogenic pulmonary edema (NPE) is defined as an acute respiratory distress syndrome triggered by severe sympathetic discharge from acute compromise in the central nervous system. Due to the absence of specific diagnostic indicators, NPE is challenging to rapidly identify and accurately diagnose. We report a case of NPE coupled with myocardial damage following tenecteplase thrombolysis for acute ischemic stroke, explore the differential diagnosis of pulmonary edema after thrombolysis, and analyze multiple peripheral organ damage following ischemic stroke. A 61-year-old Chinese male presented with acute-onset aphasia and left-sided hemiparesis persisting for 3.25 h. Approximately one hour after tenecteplase thrombolysis, the patient developed acute respiratory distress. Arterial blood gas analysis demonstrated PaO₂ of 54 mmHg and PaCO₂ of 62 mmHg. Chest CT revealed patchy opacities with indistinct margins in the dorsal lung regions. Laboratory investigations revealed elevated levels of creatine kinase, creatine kinase-MB, B-type natriuretic peptide, and high-sensitivity troponin I. Echocardiogram demonstrated reduced left ventricular systolic function. The electrocardiogram exhibited ST-T segment abnormalities. Abnormal laboratory parameters indicative of hepatic and renal dysfunction were observed on admission day 2. Based on the clinical diagnosis of NPE, therapeutic interventions were initiated, including intravenous administration of furosemide, methylprednisolone sodium succinate, sodium nitroprusside, and piperacillin sodium/tazobactam sodium. The patient's clinical manifestations, laboratory parameters, and imaging findings improved significantly. Additionally, Takotsubo syndrome was considered as a potential comorbid condition. The hepatic and renal impairment were postulated to result from severe hypoxemia, and may also be modulated by neurohumoral mechanisms following massive cerebral infarction.

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Journal
Frontiers in Cardiovascular Medicine
Published
2026-02-17
DOI
https://doi.org/10.3389/fcvm.2026.1703463
Primary Topic
Takotsubo Cardiomyopathy and Associated Phenomena
Type
article
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article

Case Report: Neurogenic pulmonary edema coupled with myocardial damage following tenecteplase thrombolysis for acute ischemic stroke

Haixia Mo, Huijuan Shi, Huixin Yang, Xiaowei Li et al.
Frontiers in Cardiovascular Medicine
Takotsubo Cardiomyopathy and Associated Phenomena
article

Case Report: Neurogenic pulmonary edema coupled with myocardial damage following tenecteplase thrombolysis for acute ischemic stroke

Haixia Mo, Huijuan Shi, Huixin Yang, Xiaowei Li, Jiannan Chen
article en

Abstract

Neurogenic pulmonary edema (NPE) is defined as an acute respiratory distress syndrome triggered by severe sympathetic discharge from acute compromise in the central nervous system. Due to the absence of specific diagnostic indicators, NPE is challenging to rapidly identify and accurately diagnose. We report a case of NPE coupled with myocardial damage following tenecteplase thrombolysis for acute ischemic stroke, explore the differential diagnosis of pulmonary edema after thrombolysis, and analyze multiple peripheral organ damage following ischemic stroke. A 61-year-old Chinese male presented with acute-onset aphasia and left-sided hemiparesis persisting for 3.25 h. Approximately one hour after tenecteplase thrombolysis, the patient developed acute respiratory distress. Arterial blood gas analysis demonstrated PaO₂ of 54 mmHg and PaCO₂ of 62 mmHg. Chest CT revealed patchy opacities with indistinct margins in the dorsal lung regions. Laboratory investigations revealed elevated levels of creatine kinase, creatine kinase-MB, B-type natriuretic peptide, and high-sensitivity troponin I. Echocardiogram demonstrated reduced left ventricular systolic function. The electrocardiogram exhibited ST-T segment abnormalities. Abnormal laboratory parameters indicative of hepatic and renal dysfunction were observed on admission day 2. Based on the clinical diagnosis of NPE, therapeutic interventions were initiated, including intravenous administration of furosemide, methylprednisolone sodium succinate, sodium nitroprusside, and piperacillin sodium/tazobactam sodium. The patient's clinical manifestations, laboratory parameters, and imaging findings improved significantly. Additionally, Takotsubo syndrome was considered as a potential comorbid condition. The hepatic and renal impairment were postulated to result from severe hypoxemia, and may also be modulated by neurohumoral mechanisms following massive cerebral infarction.

Frontiers in Cardiovascular MedicineVol. 13
Hebei Medical University (CN), Third Hospital of Hebei Medical University (CN), First Hospital of Shijiazhuang (CN)
Good health and well-being
Openalex Percentile: Top 55%
Takotsubo Cardiomyopathy and Associated Phenomena
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