Neurogenic Pulmonary Edema Following Acute Subarachnoid Hemorrhage: A Case Report and Review of Emergency Management

Abstract

Neurogenic pulmonary edema (NPE) is a rare, life-threatening condition characterized by the accumulation of fluid in the lungs following acute central nervous system (CNS) injury. This case report discusses a 42-year-old woman who presented to the emergency department with sudden onset of severe headache followed by syncope. She was later found unconscious and experienced multiple episodes of seizures and respiratory distress. Initial chest X-ray (CXR) revealed clear lung fields, but two hours later, bilateral alveolar opacities indicative of pulmonary edema were noted. Brain computed tomography (CT) confirmed the presence of subarachnoid hemorrhage (SAH).

NPE typically presents with symptoms similar to other causes of pulmonary edema, including dyspnea, frothy sputum, and wheezing. It often follows conditions such as epileptic seizures, traumatic brain injury, or intracranial hemorrhage. In this case, a significant amount of frothy sputum was observed during endotracheal intubation, further supporting the diagnosis of NPE. The primary focus of treatment for NPE involves managing the underlying CNS injury while providing adequate supportive care, such as oxygenation, mechanical ventilation, and intracranial pressure (ICP) monitoring.

This case highlights the importance of rapid diagnosis and management of NPE in patients with acute CNS injuries. Early recognition and intervention are essential to prevent severe respiratory compromise and improve clinical outcomes. Physicians should be mindful of NPE as a potential complication in patients presenting with neurological emergencies.

Introduction

Neurogenic pulmonary edema (NPE) is an uncommon but severe form of pulmonary edema that arises as a consequence of acute central nervous system (CNS) injury. This condition is characterized by the sudden accumulation of fluid in the lungs, leading to respiratory distress, often following traumatic brain injuries, subarachnoid hemorrhages (SAH), or seizures.^1,2 The exact pathophysiology of NPE is not fully understood, but it is thought to involve a surge in catecholamine release following CNS injury, resulting in increased pulmonary vascular permeability and fluid leakage into the alveoli.³

NPE can mimic other causes of pulmonary edema, such as cardiogenic or non-cardiogenic causes, and is often diagnosed based on clinical context and radiological findings. Timely recognition of NPE is critical, as its management primarily focuses on treating the underlying neurological insult while providing supportive care for the respiratory system.⁴ Delay in diagnosis or treatment can lead to worsening respiratory failure and poorer outcomes.

Case Report

A 42-year-old woman with no known underlying medical conditions was brought to the emergency department (ED) after collapsing at a convenience store while using an ATM. Witnesses reported that she experienced a sudden onset of severe headache followed by syncope. Upon arrival at the ED, she regained consciousness and complained of a persistent, severe headache.

On physical examination, the patient was weak and in visible distress. Her Glasgow Coma Scale (GCS) score was E4M6V5, indicating mild impairment of consciousness. Muscle power was decreased in all limbs, with an upper extremity strength of 3/5 bilaterally and lower extremity strength of 3/5 bilaterally. The rest of her physical examination was unremarkable. Initial laboratory workup revealed no abnormalities, with a white blood cell (WBC) count of 9,400/uL and normal arterial blood gas (ABG) values, except for mild hypercapnia (pH: 7.32, pCO₂: 50.3 mmHg, HCO¯: 25.5 mmol/L).

A chest X-ray (CXR) performed at the time of arrival showed clear lung fields (Fig. 1). Shortly after two hours, the patient's condition deteriorated, she experienced multiple episodes of generalized seizures and respiratory distress. During intubation for airway protection, a large amount of whitish frothy sputum was observed, further raising suspicion for pulmonary edema. Repeat CXR after intubation revealed bilateral alveolar opacities, suggestive of pulmonary edema (Fig. 2).

Fig. 1.

Initial chest X-ray showed bilateral clear lung fields.

Fig. 2.

Chest X-ray after two hours showed bilateral increased alveolar opacities.

A non-contrast computed tomography (CT) scan of the brain was performed, revealing SAH in the prepontine cisterns, which caused by right posterior inferior cerebellar artery aneurysm rupture (Fig. 3). Based on the clinical presentations and imaging findings, a diagnosis of NPE secondary to acute SAH was made. The patient's respiratory condition required mechanical ventilation, and she was closely monitored in the intensive care unit (ICU).

Fig. 3.

Brain CT revealed prepontine cisterns subarachnoid hemorrhage (SAH).

After admission, the patient received stent assisted coiling for cerebral aneurysm and external ventricular drain with intracranial pressure monitoring. After surgery and hospitalization, the patient's condition improved and she was successfully discharged.

Discussion

NPE is a rare but serious condition that results from acute CNS injuries. The hallmark symptoms of NPE are respiratory distress, frothy sputum, and pulmonary infiltrates on imaging.^5,6

The occurrence of NPE following SAH is well-documented, with studies estimating that it can affect 2% to 4% of patients with SAH.² The release of catecholamines in response to SAH can increase pulmonary capillary pressure and lead to non-cardiogenic pulmonary edema.^3,7 In this case, the SAH was located in the prepontine cisterns, which is a significant region for autonomic control, potentially triggering an exaggerated sympathetic response. This catecholamine surge, sometimes referred to as a "sympathetic storm," is thought to be central to the development of NPE.^1,4

Management of NPE centers on addressing the underlying CNS injury and providing supportive care for the respiratory system. In this patient, early endotracheal intubation and mechanical ventilation were crucial for maintaining oxygenation and preventing further respiratory decline. Intracranial pressure (ICP) monitoring and measures to control the effects of the SAH were also key components of treatment.⁸ While the main focus was on managing the CNS injury, aggressive respiratory support was essential to mitigate the effects of NPE.

This case highlights the importance of considering NPE in the differential diagnosis of acute respiratory distress in patients with CNS injuries. Emergency physicians must be vigilant in recognizing this condition because the rapid progression of pulmonary edema can lead to severe respiratory compromise. Early intubation and ventilatory support can significantly improve outcomes, but the ultimate prognosis depends on the extent of the underlying neurological injury.

In conclusion, NPE should be suspected in any patient with acute CNS trauma who develops respiratory distress, especially in the presence of frothy sputum and bilateral pulmonary infiltrates. Prompt recognition and treatment, including stabilization of the CNS injury and supportive care, are crucial to preventing further complications and ensuring better patient outcomes.