An Uncommon and Lethal Scenario: Neurogenic Pulmonary Edema, Impaired Left Ventricular Function, and Resistant Ventricular Fibrillation Following Grade 3 Subarachnoid Hemorrhage - a Unique Case Report.

doi:10.21203/rs.3.rs-5045135/v1

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Case Report

An Uncommon and Lethal Scenario: Neurogenic Pulmonary Edema, Impaired Left Ventricular Function, and Resistant Ventricular Fibrillation Following Grade 3 Subarachnoid Hemorrhage - a Unique Case Report.

https://doi.org/10.21203/rs.3.rs-5045135/v1

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Background: Neurogenic pulmonary edema (NPE) is a rare but serious complication of acute brain injuries, including subarachnoid hemorrhage (SAH). The early recognition and management of NPE in the context of SAH are crucial for improving patient outcomes. This case report discusses a fatal presentation of SAH complicated by acute NPE, cardiovascular compromise, and fatal arrhythmia.

Case Presentation: A previously healthy 40-year-old woman was urgently transferred to the Emergency Treatment Unit at Anuradhapura Teaching Hospital after experiencing sudden loss of consciousness, generalized seizures, and severe respiratory distress. Initial assessment revealed a blocked airway due to frothy secretions, labored breathing with low oxygen saturation, and hemodynamic instability. Neurological examination indicated a Glasgow Coma Scale score of 7. Point-of-care ultrasound (POCUS) and imaging studies confirmed pulmonary edema, reduced cardiac ejection fraction, and a Grade IV subarachnoid hemorrhage according to the Fisher scale. Despite aggressive medical interventions, including intubation, ventilation, and inotropic support, the patient’s condition deteriorated, leading to ventricular fibrillation and, ultimately, her demise.

Discussion: The case highlights the importance of early identification and prompt management of NPE in patients with SAH. The pathophysiology of NPE involves complex interactions between neurogenic, hemodynamic, and inflammatory factors, which can lead to rapid clinical decline. ECG changes, such as widespread ST-segment depression, may serve as early indicators of acute pulmonary complications in SAH patients. Multidisciplinary collaboration, standardized treatment protocols, and continuous quality improvement initiatives are recommended to enhance the management of similar cases.

Conclusion: This case underscores the critical need for heightened awareness and early intervention in the management of NPE associated with SAH. Timely, coordinated care may improve outcomes and reduce mortality in patients with this challenging clinical presentation.

Neurology

Neurosurgery

Critical Care & Emergency Medicine

Cardiac & Cardiovascular Systems

Pulmonology

Neurogenic Pulmonary Edema

Subarachnoid Hemorrhage

Fisher scale

Intracranial aneurysms

We present a rare and fatal case of subarachnoid hemorrhage complicated by acute neurogenic pulmonary edema, cardiovascular compromise, and fatal arrhythmia. A previously healthy 40-year-old woman was transferred to our tertiary care unit within an hour after experiencing a sudden loss of consciousness, generalized seizures, and acute respiratory distress.

Upon arrival, she exhibited a blocked airway due to excessive frothy secretions, labored breathing, and critically low oxygen saturation. Her cardiovascular status was compromised, with tachycardia, hypotension, and cold, clammy extremities. Neurologically, she had a significantly reduced Glasgow Coma Scale score.

Point-of-care ultrasound (POCUS) revealed pulmonary edema, a reduced ejection fraction, and other cardiac abnormalities. An electrocardiogram showed widespread ST-segment depression and sinus tachycardia. Arterial blood gas analysis indicated metabolic acidosis and elevated lactate levels, alongside signs of acute respiratory distress syndrome (ARDS) and electrolyte imbalances.

Despite initial stabilization efforts, her condition rapidly deteriorated, culminating in ventricular fibrillation and unsuccessful resuscitation. The complex interplay of subarachnoid hemorrhage, acute pulmonary edema, cardiac dysfunction, and severe metabolic disturbances led to a rapid decline, ultimately resulting in her unfortunate demise despite aggressive medical intervention.

A previously healthy 40-year-old woman was urgently transported to the Emergency Treatment Unit at Anuradhapura Teaching Hospital, a tertiary care facility, within an hour of the sudden onset of critical symptoms. Her ordeal began at a nearby divisional hospital after her family found her unresponsive, exhibiting generalized tonic-clonic seizures and severe respiratory distress. The local hospital managed her seizures before transferring her to Anuradhapura Teaching Hospital.

Upon arrival, a thorough assessment was conducted. The patient presented with a blocked airway, primarily due to a substantial accumulation of frothy nasal and oral secretions, producing a distinctive gurgling sound. Her breathing was visibly labored, with widespread crepitations in both lungs, a respiratory rate of 36, and an oxygen saturation (SpO2) as low as 60%. Immediate interventions included the placement of an oropharyngeal airway and administration of high-flow oxygen via a non-rebreather mask.

Circulatory assessment revealed tachycardia with a heart rate of 120. Her extremities were cold and clammy, with a faint peripheral pulse. Blood pressure was 80/50 mm Hg, despite receiving two pints of normal saline boluses at the local hospital. She exhibited no signs of fever or external trauma. Neurological assessment showed a Glasgow Coma Scale (GCS) score of 7 (E2 V2 M3), bilateral upgoing plantar reflexes, and no focal neurological deficits.

Bedside point-of-care ultrasound (POCUS) revealed bilateral diffuse B-lines, indicative of pulmonary edema, a reduced ejection fraction, and an elevated ventricular rate. The inferior vena cava showed less than 50% collapsibility. An electrocardiogram (ECG) demonstrated widespread ST-segment depression in the anterior and inferior territories, along with sinus tachycardia.

Arterial blood gas analysis revealed metabolic acidosis with partial respiratory compensation, with a pH of 7.339, pCO2, HCO3- 15.2, and elevated lactate levels (Lactate 5.2). The patient met the criteria for acute respiratory distress syndrome (ARDS) with a PaO2/FiO2 ratio of 125, alongside electrolyte abnormalities, including elevated sodium (Na+ 153.1) and low potassium (K+ 2.8) levels.

Further laboratory investigations included Troponin I and CRP tests. Following initial management, a decision was made to intubate and ventilate the patient, initiate inotropic support, and proceed with diagnostic imaging. A non-contrast CT scan of the brain revealed a substantial subarachnoid hemorrhage without intraventricular extension or intracerebral hemorrhage. Additionally, the CT scan depicted the characteristic 'Star Sign' in the basal regions, consistent with a Fisher Grade hemorrhage. Chest X-rays showed diffuse interstitial pulmonary infiltrates in both lung fields, suggestive of acute pulmonary edema. Neurosurgical consultation led to a plan for urgent endovascular intervention, with a follow-up contrast-enhanced CT scan once the patient's condition stabilized.

While receiving inotropic support, the patient maintained a marginally acceptable mean arterial perfusion, aided by intravenous norepinephrine and dobutamine. Despite maximal respiratory support, she continued to experience persistently low oxygen saturation (SpO2).

Approximately one hour after initial stabilization and continuous reevaluation, the patient suddenly went into ventricular fibrillation. Despite three rounds of defibrillation, her condition did not improve, ultimately leading to asystole. Tragically, despite an hour-long, exhaustive resuscitation effort, the patient did not survive.

Neurogenic pulmonary edema (NPE) is a frequently overlooked yet significant consequence of acute brain injuries. Neglecting its recognition can lead to prolonged morbidity, making it crucial for healthcare providers to identify and adapt their clinical strategies accordingly. NPE is characterized by the onset of pulmonary edema in individuals experiencing acute brain injuries, thus necessitating specialized management in the care of patients with a range of cerebral conditions."(1) In our case, the patient exhibited the onset of Neurogenic Pulmonary Edema, confirmed by clinical signs such as frothy sputum, widespread bilateral lung crepitations, declining oxygen saturation levels, and corroborated by findings from lung ultrasound, chest X-ray, and arterial blood gas (ABG) analysis. This occurrence was concomitant with a Grade 3 Subarachnoid Hemorrhage, assessed at Grade IV on the Fisher scale. Subarachnoid hemorrhage (SAH) can lead to the development of acute pulmonary edema, with neurogenic pulmonary edema (NPE) being a distinct variant triggered by central nervous system injuries, such as SAH. NPE is characterized by a sudden accumulation of fluid in the lungs and can pose a life-threatening condition. Risk factors associated with NPE in SAH patients include vertebral artery dissection and a high initial World Federation of Neurosurgical Societies (WFNS) grade upon admission. Timely recognition and management of NPE are vital in mitigating adverse outcomes. Lung ultrasound has proven to be a valuable tool for accurately identifying pulmonary edema in SAH patients. In summary, acute pulmonary edema is a potential complication in subarachnoid hemorrhage patients, and NPE, with its specific characteristics, demands swift diagnosis and intervention. While vertebral artery dissection and severe WFNS grades upon admission are confirmed as significant risk factors for NPE, it's noteworthy that appropriate diagnosis and treatment can help reduce the risk of unfavorable outcomes, as there were no observed differences in neurological outcomes at discharge between groups. (2) (5)

The pathophysiology of this condition encompasses several intricate mechanisms. One proposed cause involves the overactive sympathetic discharge triggered by elevated intracranial pressure, subsequently causing alterations in pulmonary vascular pressure and fluid seepage. Additionally, the adrenergic surge induced by SAH can initiate a chain of reactions that contribute to the development of both neurogenic pulmonary edema (NPE) and stress-induced hemoconcentration. (3)

Hemodynamic alterations, including elevated extravascular lung water index and pulmonary vascular permeability index, have been documented in individuals experiencing both SAH and pulmonary edema. (4)

Furthermore, individuals with low-grade SAH are at a higher risk of experiencing acute cardiopulmonary complications, such as neurogenic pulmonary edema (NPE) and conditions resembling takotsubo cardiomyopathy. (6)(7)

The precise etiology of pulmonary edema in SAH patients can exhibit variability, with potential involvement of cardiac insufficiency and inflammatory processes. In summary, the pathophysiology of acute pulmonary edema in SAH is characterized by intricate interactions among neurogenic, hemodynamic, and inflammatory elements. In our case, the patient demonstrated hemodynamic instability and impaired left ventricular function, as evident in bedside 2D Echo findings.

Acute pulmonary edema is a recognized occurrence in individuals with subarachnoid hemorrhage (SAH) and often presents alongside notable electrocardiographic (ECG) alterations. Research has underscored the prevalence of ECG abnormalities in SAH patients and their potential to exacerbate clinical outcomes. These ECG changes in SAH patients can stem from autonomic neural stimulation originating in the hypothalamus or elevated levels of circulating catecholamines. Manifestations of these ECG changes may encompass T wave irregularities, ST segment shifts, and QT interval prolongation. Elevated levels of cardiac biomarkers, such as troponin I, have been detected in SAH patients experiencing pulmonary edema. Furthermore, ECG anomalies, including atypical Q or QS waves and nonspecific ST- or T-wave deviations, hold promise as predictive indicators of the onset of neurogenic pulmonary edema (NPE) within a 24-hour timeframe in adult patients with spontaneous SAH. Hence, ECG changes can serve as valuable indicators of acute pulmonary edema in patients afflicted by subarachnoid hemorrhage. (8)(9) In this particular case, the patient exhibited widespread ST segment depressions in the anterior and inferior regions, ultimately culminating in refractory ventricular fibrillation. ECG changes in patients with SAH can be attributed to two potential mechanisms: autonomic neural stimulation stemming from the hypothalamus and elevated levels of circulating catecholamines. Hypothalamic stimulation may lead to ECG changes without concomitant myocardial damage, whereas elevated catecholamine levels have been associated with QT-interval prolongation and myocardial injury. (10)The most effective treatments for subarachnoid hemorrhage in patients with aneurysms encompass a range of options, including endovascular treatment, surgical intervention, and medication therapy. Both single-stage and multiple-stage endovascular treatments have demonstrated safety and effectiveness, especially in patients with multiple intracranial aneurysms (MIAs) and concurrent subarachnoid hemorrhage (11).

Staged surgical treatment, which involves initially clipping the ruptured aneurysm and subsequently addressing intact aneurysms in a later phase, has yielded favorable treatment outcomes (12).To aid in recovery and neuroprotection for SAH patients, medications such as nimodipine, dexmedetomidine, SSRIs, and DL-3-n-butylphthalide have been prescribed (13).

In cases of vertebral artery dissecting aneurysms (VADAs), procedures like endovascular coil trapping and flow alteration have proven effective in preventing rerupture (14). Moreover, delayed treatment of bystander aneurysms in SAH patients has exhibited safety and efficacy, with no observed growth or bleeding during follow-up (15).

Based on the presented case, it is crucial to signify the importance of early recognition and prompt, coordinated multi-organ support in managing similar cases. The following steps are recommended:

1. Enhanced Surveillance and Training: Regular training programs should be implemented for healthcare professionals to increase awareness and recognition of neurogenic pulmonary edema, particularly in the context of neurological emergencies like subarachnoid hemorrhage, even though it is a relatively rare phenomenon.

2. Interdisciplinary Collaboration and Multidisciplinary Team Management: Foster collaboration among neurologists, neurosurgeons, intensivists, pulmonologists, and emergency medicine specialists to enable rapid decision-making and timely implementation of appropriate interventions.

3. Standardized Protocols: Develop and disseminate standardized protocols for the assessment, monitoring, and management of patients presenting with subarachnoid hemorrhage and acute neurogenic pulmonary edema. These protocols should cover a comprehensive range of diagnostic approaches, ventilation strategies, and hemodynamic support.

4. Quality Improvement Initiatives: Establish ongoing quality improvement initiatives to regularly evaluate and enhance the effectiveness of these protocols, ensuring they remain aligned with the latest evidence-based practices.

5. Patient and Family Education: Educate patients and their families about the potential complications associated with subarachnoid hemorrhage and the importance of seeking prompt medical attention. This can lead to earlier intervention and improved outcomes.

By implementing these recommendations, healthcare systems can improve their preparedness and responsiveness to cases of neurogenic pulmonary edema, potentially leading to better patient outcomes and reduced mortality in similar situations.

Conflict of interest statement

All the authors declare they do not have any conflict of interest.

Consent was obtained from the spouse of the patient.

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The authors declare no competing interests.

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An Uncommon and Lethal Scenario: Neurogenic Pulmonary Edema, Impaired Left Ventricular Function, and Resistant Ventricular Fibrillation Following Grade 3 Subarachnoid Hemorrhage - a Unique Case Report.

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