Key result
Tenecteplase thrombolysis linked to neurogenic pulmonary edema and myocardial damage in an ischemic stroke case.
Why the study?
Neurogenic pulmonary edema is challenging to rapidly identify and accurately diagnose due to the absence of specific diagnostic indicators.
Case Report (n=1)
No
This case highlights the potential for severe neurogenic pulmonary edema and myocardial damage (potentially Takotsubo syndrome) following acute ischemic stroke and tenecteplase thrombolysis, emphasizing the need for rapid recognition and multidisciplinary management.
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Warrants vigilance for cardiopulmonary complications after tenecteplase in stroke; hypothesis-generating and requires confirmation in larger cohorts.
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.
Li et al. (2026) conducted a case report in acute ischemic stroke (n=1). tenecteplase thrombolysis was evaluated on development of neurogenic pulmonary edema coupled with myocardial damage following tenecteplase thrombolysis. Tenecteplase thrombolysis in a 61-year-old male with acute ischemic stroke was followed by neurogenic pulmonary edema with myocardial damage, evidenced by ABG PaO2 54 mmHg, elevated CK (1286 U/L), CK-MB (33 U/L), BNP, hs-TnI, and LVEF 41%.
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