P015: NEUROGENIC PULMONARY EDEMA POST CEREBRAL INFARCT WITH HEMORRHAGIC CONVERSION
Aaron Hacker, DO1; Keyan Shasti, BS2; Elham Shams, MS, MHS2; Edward Parker, DO1; 1Westside Hospital; 2Nova Southeastern University
Neurogenic pulmonary edema following cerebral ischemia is an acute respiratory distress syndrome (ARDS) with clinical characteristics that include acute onset, apparent pulmonary interstitial fluid infiltration and rapid resolution. We present a case of neurogenic pulmonary edema occuring post craniotomy for cerebral ischemia with hemorragic conversion in a young african american female. The pathophysiology of NPE revolves around sympathetic stimulation and uncontrolable release of catecholamines, which cause contraction of resistance vessels. Subsequent increases in systemic vascular resistance leads to fluid shifts into pulmonary circulation, while pulmonary circulation overload results in increased pulmonary capillary pressure with subsequent alveolar injury and inflammation.We present the case of a young African American female who underwent craniotomy for an ischemic cerebral accident with hemorrhagic conversion and developed neurogenic pulmonary edema (NPE) in the postoperative period. The patient had a past medical history of recently diagnosed atrial fibrillation (AF) for which she refused ablation.
Preoperatively, the patient was managed with aspirin and subcutaneous heparin for thromboembolic prophylaxis. She was also started on intravenous nicardipine and labetalol for blood pressure control. General anesthesia was induced with propofol and fentanyl and maintained with sevoflurane
Intraoperative monitoring included invasive arterial blood pressure, central venous pressure. Transcranial Doppler monitoring of cerebral blood flow velocity was not available. The patient underwent a right frontal craniotomy for evacuation of the intracerebral hemorrhage. Intraoperative course was uneventful, and the patient was extubated in the operating room.
Postoperatively, the patient developed respiratory distress with increasing oxygen requirements and bilateral pulmonary infiltrates on chest radiography consistent with NPE. The patient was reintubated and transferred to the intensive care unit (ICU) for further management.
The management of NPE involves optimizing oxygenation, reducing airway resistance, and controlling pulmonary hypertension. The patient was managed with mechanical ventilation, positive end-expiratory pressure, and inhaled nitric oxide for pulmonary vasodilation. The patient also received intravenous diuretics and fluid restriction to reduce pulmonary congestion.
NPE is a rare complication of central nervous system injury, including traumatic brain injury and stroke. The pathophysiology of NPE is not fully understood but is thought to be related to an increase in sympathetic nervous system activity, leading to increased pulmonary capillary pressure and permeability.
The presence of AF in this patient may have contributed to the development of NPE. AF is associated with a higher risk of stroke and is a known risk factor for NPE. The decision to refuse AF ablation may have contributed to the development of this complication.
In conclusion, this case report highlights the challenges of managing a young African American female with NPE following craniotomy for an ischemic cerebral accident with hemorrhagic conversion. The perioperative management of this patient required a multidisciplinary approach involving the anesthesia team, neurosurgeons, and critical care specialists. Early recognition and management of NPE are essential for successful outcomes in high-risk patients undergoing complex procedures. Further research is needed to better understand the pathophysiology and risk factors for NPE in patients with central nervous system injury.