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

## TL;DR

A 61-year-old man developed neurogenic pulmonary edema and heart damage after stroke treatment with tenecteplase, highlighting the need for careful monitoring of multi-organ effects.

## Contribution

This case report highlights the rare but serious complications of NPE and myocardial damage following tenecteplase use in acute ischemic stroke.

## Key findings

- The patient developed acute respiratory distress and elevated cardiac biomarkers after tenecteplase thrombolysis.
- Therapeutic interventions led to significant clinical and laboratory improvement.
- Hepatic and renal dysfunction were likely due to hypoxemia and neurohumoral mechanisms.

## 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.