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Edema pulmonar por presión negativa atípico con lesión miocárdica post-apendicectomía: reporte de un caso
Jingyuan Du1, Ting He2, Xuecong Wang3
1Cardiovascular Department, Bei Lun District People's Hospital, Beilun District, Ningbo, Zhejiang, China.
Rationale:
Negative pressure pulmonary edema (NPPE), an uncommon perioperative complication, primarily results from acute upper airway obstruction. While typically affecting young healthy patients with prominent respiratory manifestations, concurrent myocardial injury remains exceptionally rare. This case reports an atypical case of NPPE with biomarker-confirmed myocardial injury but absent respiratory symptoms.
Patient Concerns:
A 26-year-old male developed a significant hemodynamic derangement following extubation after an appendectomy. Immediately post-extubation, he exhibited transient hypertension (150/100 mm Hg) and tachycardia (100 bpm), which progressed to sustained hypotension (86/47 mm Hg) within 50 minutes, persisting for 3 hours. Notably, this occurred in the complete absence of respiratory symptoms such as dyspnea or frothy sputum.
Diagnoses:
The diagnosis of NPPE was confirmed by chest computed tomography showing pulmonary edema. Concurrent myocardial injury was biomarker-confirmed (troponin I 2.49 ng/mL; creatine kinase-myocardial band 7.85 ng/mL), despite unremarkable echocardiography and electrocardiography.
Interventions:
Initial management for transient hypertension and tachycardia included intravenous urapidil and esmolol. For subsequent sustained hypotension, fluid resuscitation was administered. Following diagnosis, treatment involved diuretics and corticosteroids.
Outcomes:
The patient's hemodynamic instability resolved, and his condition improved with the instituted therapy.
Lessons:
This case highlights that NPPE can present with occult myocardial injury without respiratory signs, necessitating serial cardiac biomarker monitoring in hemodynamically unstable patients. The underlying mechanism, while not directly proven here, may involve catecholamine surge, inflammatory cascades, and hypoperfusion.
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