Neurogenic Pulmonary Edema Research Articles

Rerecognition of neurogenic pulmonary edema

Neurogenic pulmonary edema is a clinical complication caused by various central nervous system disorders.It includes a variety of pathogenic factors, however, over-activation of the sympathetic nerve is the main mechanism.The main clinical manifestations are dyspnea and hypoxemia, which may be accompanied by circulatory disorder.The respiratory support therapy and circulatory support therapy are the main treatment measures.It has the characteristics of rapid progress and high mortality, which should be obtained enough attention. Key words: Neurogenic pulmonary edema; Pulmonary edema,

Neurogenic Pulmonary Edema

Neurogenic Pulmonary Edema (NPE) is defined as the acute onset of dyspnea or a decrease in PaO2/FiO2 ratio, following an acute central nervous system (CNS) insult, in the absence of other obvious causes of lung injury. The most important cause of NPE is subarachnoid hemorrhage (SAH), followed by cerebraltrauma and epilepsy. The incidence of NPE after SAH in the literature may vary from 4 to 23% in greater studies, with SAH accounting for 43-73% of cases of NPE. It is postulated that an excessive adrenergic discharge would lead to pulmonary vasoconstriction and a rapid increase in pulmonary capillaryhydrostatic pressure, thus promoting fluid leakage to the alveolar space. NPE is generally treated in a supportive and conservative fashion, and patient management should be focused in the primary insult.

НЕЙРОГЕННЫЙ ОТЕК ЛЕГКИХ

Neurogenic pulmonary edema is one of the complications of acute cerebral diseases and traumas and it is accompanied by severe respiratory failure. It is associated with a high mortality level. There are several theories about neurogenic pulmonary edema development. The theory of the double hit is the most recent causing significant discussion. The theory is based on the pulmonary injury due to systemic inflammatory response when the glial tissue of the injured brain becomes the source of inflammatory mediators. A similar pathogenesis allows considering neurogenic pulmonary edema to be one of the forms of acute respiratory distress syndrome. It has diagnostic criteria common with acute respiratory distress syndrome, which are identified during acute cerebral injury and not associated with the other etiological factors. Currently, there are no effective prevention and treatment of neurogenic pulmonary edema. Support of respiratory exchange through artificial pulmonary ventilation is a major tool used for its management, which is recommended to be performed in compliance with protective ventilation principles. And some particular approaches of the preventive ventilation can be applied only with neuromonitoring.

Neurogenic Pulmonary Edema and Stunned Myocardium in a Patient With Meningioma

Neurogenic Pulmonary Edema and Stunned Myocardium in a Patient With Meningioma

死亡危重型手足口病临床特点分析

目的：探讨进入IV期危重型手足口病(Hand-mouth and foot disease, HFMD)死亡的临床特点、诊治经过及死亡分析，总结经验及教训。方法：采用回顾性分析方法对2009年1月至2014年12月昆明周边及地州转入我院救治19例危重型HFMD患儿的临床资料进行分析。结果：19例患儿来自农村，其中男性13例(68.42%)，女性6例(31.58%)，3岁以下16例，占84.21%，3岁以上3例，占15.79%。所有病例均有发热、惊跳、肢体抖动的表现。16例患儿入院时出现肺出血、呼吸循环衰竭的表现。17例患儿均出现白细胞总数及中性粒细胞、超敏C-反应蛋白升高，12例血糖升高。4例合并消化道出血，1例同时合并肾功能衰竭。病原学：18例EV71阳性，1例为其它未定型肠道病毒感染。结论：早期识别并及时治疗第2期HFMD病例，及时进行干预，避免进展为危重型HFMD，危重型HFMD主要由EV71病毒感染引起，致死率高，进入IV期危重型HFMD出现神经源性肺水肿、肺出血、呼吸循环衰竭、严重脑功能障碍等严重并发症，死亡率高。 Objective: To investigate clinical characteristics into the type of hand, foot and mouth disease in acute stage IV, and diagnosis and treatment of the death cases, summarizes the experiences and lessons. Methods: Retrospective analysis was used to study the 19 cases clinical data of critical HFMD in the area around Kunming from January 2009 to December 2014. Results: 19 cases were from countryside, 13 of which were boys (68.42%), 6 of were girls (31.58%), 16 under 3 years (84.21%) and 3 above 3 years of age (15.79%). All cases had fever, startle and limb jitter. Pulmonary hemorrhage and respiratory failure occurred in 16 cases. 17 cases of children pre-sented increased white cell count, neutrophilic granulocytes and hypersensitivity C-reactive protein, and 12 cases blood sugar were elevated. 4 cases were complicated with alimentary tract hemorrhage and 1 case was combined with Kidney function failure. Pathogeny: 18 cases of EV71 were positive，and another one is the other enterovirus infection. Conclusion: It was very critical to early identify and treat stage II HFMD to avoid the progression to severe HFMD which was mainly caused by EV71 virus. The stage IV HFMD appeared serious complication: Neurogenic pulmonary edema, pulmonary hemorrhage, respiratory failure, brain dysfunction, and so on. The fatality rate was very high.

Pathogenesis of acute lung injury after traumatic brain injury

Background Traumatic brain injury(TBI) may be accompanied by lung injury and pulmonary dysfunction. The TBI patients with pulmonary complications tend to have prolonged stay in intensive care unit, poorer prognosis, and increased risk of death. Objective To review the manifestations and potential pathophysiological basis of lung injury after TBI. Content Some TBI patients develop pulmonary injury, including acute respiratory distress syndrome (ARDS), neurogenic pulmonary edema (NPE), and ventilator-associated pneumonia (VAP). Multiple processes that involve in the development of pulmonary injury following TBI include hyperactivity of sympathetic, but hypoactivity of parasympathetic nervous system, enhanced release of substance P, neuropeptide A, proinflammatory cytokines, and adhesion molecule-1, and activation of high-mobility group box-1-RAGE axis, etc. Reversal or blocking of these processes prevent or attenuate lung injury. Trend Further investigations are needed to determine the potential risk factors that affect the incidence of lung injury in TBI patients. The information is critical to develop appropriate intervention or prevention strategies to improve treatment for TBI. Key words: Traumatic brain injury; Lung injury

Determining Brain Death: Basic Approach and Controversial Issues.

Determining Brain Death: Basic Approach and Controversial Issues.

Risk factors for neurogenic pulmonary edema in patients with severe hand, foot, and mouth disease: A meta-analysis

ObjectiveTo investigate the risk factors for neurogenic pulmonary edema (NPE) in patients with severe hand, foot, and mouth disease (HFMD) and to provide evidence for the prevention and treatment of NPE. MethodsSeveral databases were searched (from inception to 2017) to identify case–control studies on risk factors for NPE among patients with severe HFMD. Data were analyzed via meta-analysis. The combined odds ratio (OR) and 95% confidence interval (CI) were calculated using fixed-effects and random-effects models, and a sensitivity analysis and evaluation of publication bias was also performed. ResultsA total of 14 studies involving 557 cases (severe HFMD with NPE) and 1450 controls (severe HFMD) were included. Results for the categorical variables were as follows: hyperglycemia (OR 10.25, 95% CI 4.82–21.76), tachycardia (OR 6.21, 95% CI 3.02–12.75), hypertension (OR 3.79, 95% CI 2.90–4.95), respiratory rhythm abnormality (OR 7.86, 95% CI 2.46–25.12), drowsiness (OR 8.11, 95% CI 4.26–15.44), vomiting (OR 8.96, 95% CI 3.83–20.96), limb tremors (OR 8.96, 95% CI 3.83–20.96), atypical rash (OR 4.27, 95% CI 2.83–6.45). No significant publication bias was found for the different factors. ConclusionsDrowsiness ranks first among risk factors for NPE in children with severe HFMD, followed by vomiting, tachycardia, hypertension, breathing rhythm changes, limb tremors, atypical rash, and hyperglycemia.

Hemoptisis en el espectro del edema pulmonar neurogénico

El edema pulmonar neurogénico es un diagnóstico de exclusión, cuya frecuencia de presentación no ha sido establecida, dada la falta de criterios diagnósticos bien validados que permitan realizar un abordaje inicial temprano en el paciente con un evento y/o insulto en el sistema nervioso central. Los dos principales mecanismos fisiopatológicos están dados por: aumento de la permeabilidad capilar y en la vasoconstricción pulmonar y sistémica que permiten la expresión radiológica de patrón de ocupación alveolar difusa con un sin número de diagnósticos diferenciales según el escenario clínico. Dado que el estatus convulsivo ha sido catalogado como la principal causa de edema pulmonar neurogénico; ante la presencia probable de estatus convulsivo inicial con hallazgos inespecíficos de edema pulmonar de etiología no cardiogénico y hemoptisis se expone un caso inusual de edema pulmonar neurogénico con resolución clínica y radiológica al cabo de 48 horas del cese completo de las crisis parciales, siendo esta última medida el principal objetivo de tratamiento en el paciente con dicha condición.

Clinical Significance and Prognostic Effect of Serum 25-hydroxyvitamin D Concentrations in Critical and Severe Hand, Foot and Mouth Disease

Objective: To examine the association of serum 25-hydroxyvitamin D [25(OH)D] concentrations with critical and severe hand, foot and mouth disease (HFMD) and assess the clinical significance and prognostic effect of 25(OH)D concentrations in children with HFMD. Methods: This is a prospective observational study. The 138 children with HFMD were divided into common (49 cases), severe (52 cases), and critical (37 cases) HFMD groups. Another 59 healthy children undergoing outpatient medical examinations during the same period were chosen as the control group. Serum 25(OH)D concentrations were measured in all the subjects, and each group was subdivided by serum 25(OH)D concentration into 25(OH)D normal (≥30 ng/mL); insufficiency (20–29.9 ng/mL), and deficiency (<20 ng/mL) groups. The pediatric critical illness score (PCIS) was recorded for the critical and severe HFMD group upon admission to the pediatric intensive care unit (PICU). Children with critical and severe HFMD were also monitored for blood lactate (LAC), serum calcium ions (Ca++), D-dimer (DD), lactate dehydrogenase (LDH), and creatine kinase-MB (CK-MB) levels; the incidences of brainstem encephalitis, neurogenic pulmonary edema, and circulatory failure; and the 14-day mortality rate. Results: Serum 25(OH)D concentrations were generally low in all groups. The critical HFMD group showed a significantly lower serum 25(OH)D mean concentration (20.0 ± 8.4 ng/mL) and a higher proportion of deficiency (18%) compared with the control group (28.1 ± 6.6 ng/mL, 8%), common (29.5 ± 8.1 ng/mL, 10%) and severe (31.9 ± 9.7 ng/mL, 8%) HFMD groups (p < 0.05). In the critical and severe HFMD groups, the 25(OH)D deficiency group had lower PCISs than the 25(OH)D normal and insufficiency groups (p < 0.05); and had higher values than the latter two groups for LAC, LDH, CK-MB and DD; and the incidences of brainstem encephalitis, neurogenic pulmonary edema, circulatory failure, and mortality (p < 0.05). The death group showed significantly lower serum 25(OH)D concentrations and PCISs than the survival group (p < 0.05) and had higher LAC, LDH, CK-MB and DD levels and higher incidences of brainstem encephalitis, neurogenic pulmonary edema, and circulatory failure (p < 0.05). Logistic regression analysis revealed that the serum 25(OH)D concentration was an independent factor that influenced mortality in children with critical and severe HFMD. Conclusions: In this study, we find the serum 25(OH)D concentrations are substantially reduced in children with critical and severe HFMD and are associated with the severity of HFMD. The serum 25(OH)D concentrations may have clinical value for determining the progression of critical HFMD and predicting the risk of death. Further evidence is needed before it can be stated that 25(OH)D concentrations have clinical value in HMFD diagnosis.

Management of Neurogenic Pulmonary Edema and Differential Hypoxemia in an Adult Supported on Venoarterial Extracorporeal Membrane Oxygenation

Management of Neurogenic Pulmonary Edema and Differential Hypoxemia in an Adult Supported on Venoarterial Extracorporeal Membrane Oxygenation

Coronary fat embolism following subarachnoid hemorrhage: an experimental study.

Subarachnoid hemorrhage (SAH) can lead to neurogenic pulmonary edema (NPE), and chylomicron metabolism may be altered unfavorably in acute lung injury. This study aimed to investigate the possible effect of NPE on the development of coronary fat embolism. This study was conducted on 27 rabbits, 5 of which were used as the control (n=5). Experimental SAH was induced in 15 of the animals by injecting homologous blood into the cisterna magna, and the remaining 7 animals were administered only isotonic saline solution (Sham, n=7) in the same manner under general anesthesia. After 21 days, all the animals were euthanized, and their hearts, lungs, and brains underwent histopathological examination. Six animals died of SAH during the experiment, and foamy hemorrhagic parenchymal lesions and intra-alveolar hemorrhage were observed in their lungs. The histopathologic findings revealed minimal changes in the lungs, heart, and brains of the surviving animals; however, an abundant amount of fat globules was found in the coronary arteries of the six nonsurviving animals. There was a meaningful difference between the number of occluded coronary arteries with fatty globules in the surviving and nonsurviving animals (P<.001). However, the difference between the survivors and the isotonic-saline-injected group was not meaningful (P>.05). Coronary fat embolism was an important mortality factor following SAH (P<.005). In SAH-induced NPE, the leakage of chylomicrons into the systemic circulation may lead to coronary fat embolism, which has not yet been reported in the literature.

Severe respiratory failure and traumatic brain injuries: What do we know?

Extracorporeal membrane oxygenation (ECMO) is a form of mechanical circulatory support that can be lifesaving in people with potentially reversible heart or lung injuries. ECMO is nearly always used urgently, when all other treatment options for cardiopulmonary injury have failed and high mortality is otherwise expected. Standard ECMO treatment involves venous drainage from the femoral vein or left atrium with artificial extra-circulatory oxygen exchange. Return to the body is through the same veins (veno-venous) or arterial system via the femoral artery or ascending aorta (veno-arterial). Compared with cardiopulmonary bypass circuit, ECMO is transportable, smaller, closed to the atmosphere, and can treat a patient for several days to weeks. Neurological consequences of severe respiratory failure and its different management strategies in adults are likely common but uncharacterized and poorly described in the reviewed literature. Development of severe respiratory failure (SRF) occurs in 20–25% of patients with isolated severe traumatic brain injury (TBI) and is associated with a threefold increase in mortality, or patients remaining in a vegetative state.1 It has been attributed mostly to aspiration, infection, neurogenic pulmonary edema, and release of pro-inflammatory mediators into the systemic circulation causing ultrastructural damage in type II pneumocyte.2 This decreases the pulmonary tolerance of subsequent mechanical stress due to mechanical ventilation. Actually, some data suggest that the main feature of ALI/ARDS in brain-injured patients is the presence of a poor oxygenation (reduced PaO2/FiO2 ratio) accompanied by a moderate increase in the elastance of the respiratory system even though these patients had a normal chest X-ray. Ventilatory support for such patients could be difficult with a lot of challenges to keep optimal oxygenation and acceptable level of blood carbon dioxide. It involves the application of positive end-expiratory pressure (PEEP) to recruit collapsed alveoli, improve arterial oxygenation, and reduce elastance of the respiratory system. Although improving oxygenation is a key factor for optimizing O2 delivery to the brain, clinical studies provide contradictory information on the use of PEEP in patients with acute lung injury (ALI) complicating severe brain injury. Furthermore, we tend to use higher tidal volumes in patients with acute brain injury because mild hypocapnia is a key factor in the clinical management of raised intracranial pressure, which is a frequent abnormality in such patients;3,4 this would be an injurious ventilator strategy and may present a further relevant inflammatory stimulus. Moreover, it has been shown that the use of high tidal volumes for the first 48 h after ICU admission is associated with the development of ventilator-induced lung injury.4 In addition, one of the recognized methods in improving oxygenation in SRF patients is the use of prone position, because it improves the lung mechanics and augments oxygenation. Studies have demonstrated that patients with unstable intracranial pressure (ICP) have higher ICP in the horizontal position sideways. Therefore, the recommended position for this patient cohort is a 30-degree head-up tilt combined with a straight head position.4 Furthermore, TBI patients who require ECMO support for their SRF will need full anticoagulation, as the circuit poses considerable derangement in the hemostatic system with increased platelet consumption and a higher risk of intracranial bleeding. There have been several reports of ECMO without anticoagulation therapy, but so far with no evidence or good literature to support this notion.5 Although some controversy and difficulties exist, it seems that multiorgan clinical approach instead of single-organ approach represents the optimal way in clinical management of patients with ALI/SRF and TBI.

Lung maladies following aneurysmal subarachnoid haemorrhage

AbstractPulmonary complications are common in patients with aneurysmal subarachnoid haemorrhage. It is associated with adverse outcome in the form of higher incidence of vasospasm, poor neurological outcome, longer length of stay and higher mortality. These patients are at high risk for ventilator associated pneumonia. Preventive measures, early detection and timely appropriate treatment is important. Acute respiratory distress is common in patients with subarachnoid haemorrhage. Measures to minimize the second hit to the vulnerable lungs is crucial. Low tidal volume ventilation, application of PEEP and prone ventilation should be used with special emphasis to avoid hypercarbia and increase in intracranial pressure. Activation of sympathetic nervous system, release of catecholamine and damage to pulmonary endothelium can lead to neurogenic pulmonary edema. Treatment of underlying cause and supportive care is helpful. These patients are at high risk of deep vein thrombosis and pulmonary embolism. Measures to prevent deep vein thrombosis and administration of pharmacological prophylaxis when safe, needs to be considered.

Application of transpulmonary thermodilution monitoring (PiCCO) in patient with neurogenic pulmonary edema and acute obstructive hydrocephalus due to a central neurocytoma: A case report

Abstract Neurogenic pulmonary edema (NPE) is an acute life-threatening complication associated with many forms of central nervous system injury. Its pathophysiology is still debated. We report a patient with acute obstructive hydrocephalus due to a central neurocytoma who also had NPE, for which serial transpulmonary thermodilution monitoring (PiCCO) was performed. Insertion of the PiCCO, which provides information about the patient's cardiac output, preload status and amount of lung water, revealed a high pulmonary vascular permeability index (PVPI) and low global end-diastolic volume (GEDV) without cardiac dysfunction, indicating permeability edema, which led to our changing the therapeutic strategy. Using PiCCO monitoring to balance the preload and extent of pulmonary edema enabled achievement of an optimal cardiac preload for organ perfusion, resulting in normalization of pulmonary edema by day 2. PiCCO facilitates understanding of the mechanism of NPE, guiding the management of fluid balance and the choice of vasopressors in patients with life-threatening NPE.

Could cardiac biomarkers predict neurogenic pulmonary edema in aneurysmal subarachnoid hemorrhage?

Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by the acute onset of pulmonary edema after a significant central nervous system (CNS) insult. NPE occurs as a result of release of catecholamines into the blood immediately after aneurysm rupture. The aim of this study is to investigate the connection between the value of cardiac biomarkers on admission and incidence of NPE in patients with aneurysmal subarachnoid hemorrhage (SAH). A total of 262 SAH patients (162 women, 100 men) were prospectively included in the study. Clinical characteristics, electrocardiographic (ECG) changes, serum cardiac and inflammatory biomarkers were measured on admission and on the day of development of NPE. These data were analyzed in order to predict the development NPE. Nineteen patients (7.25%) developed NPE. Comparison revealed that patients who subsequently developed NPE, sustained more severe SAH. Cardiac damage was more severe in these patients, as represented by significantly higher mean values of all examined cardiac biomarkers (P = 0.000), except for troponin I value that was significantly lower (P = 0.000). Multivariate regression analysis revealed that elevated troponin I (OR, 4.980; 95% CI, 1.27-19.49; P = 0.021) and white blood cell count (OR, 22.195; 95% CI, 3.99-123.50; P = 0.000) are predictors of NPE. Significantly higher values of cardiac biomarkers were observed in SAH patients complicated with NPE. Elevated values of cardiac biomarkers appear to play an active role in prediction of NPE, although white blood cell count may be involved in the prediction of NPE. There is an influence of SAH therapy on predictors of NPE.

A Possible Case of Neurogenic Pulmonary Edema in a Sheep following Intracranial Surgery

Abstract Objective: To describe presentation, treatment and outcome of a sheep that developed acute respiratory distress after intracranial surgery. Case summary: A 3-year-old female crossbred sheep weighing 64 kg was anaesthetized for intracranial surgery as a part of a research project. Premedication and induction of anesthesia were uneventful as well as tracheal intubation. Anesthesia was maintained with isoflurane in a 50% mixture of oxygen and air, fentanyl (5-15 μg kg-1h-1) and lidocaine (1.8 mg kg-1h-1). During anesthesia, an increased alveolar-arterial oxygen gradient was calculated on the basis of arterial blood gas analysis: inspiratory fraction of oxygen was increased and a recruitment manoeuvre was performed. After 210 minutes of anesthesia, the sheep was let recover with oxygen supplementation under monitoring of pulse-oxymetry, capnography, inspired and expired oxygen, temperature and invasive blood pressure. At tracheal extubation no signs of regurgitation or aspiration were noticed. Twenty-five minutes later, the sheep showed deterioration of neurological status and clonic seizure responsive to diazepam. After transient tachycardia, blood pressure rose acutely and sinus bradycardia followed. Severe tachypnea started in few minutes accompanied by loud respiratory noises and harsh diffuse crackles on both sides of the thorax. Foamy blood nasal exudates discharged from the nostrils. Neurogenic pulmonary edema as a sequel of increased intracranial pressure was suspected and treated with intravenous mannitol (0.5 gkg-1) and furosemide (4 mgKg-1). Hypoxemia was successfully managed with oxygen supplementation. Motor and cognitive functions improved progressively and were deemed normal within 12 hours from the episode, when arterial partial pressure of oxygen was 11.7 kPa (88 mmHg) at room air. New information provided: Severe pulmonary complications may be observed after iatrogenic neurological injury in sheep. Neurogenic pulmonary edema should be taken into account among the differential diagnoses of abrupt respiratory distress following seizure.

Chapter 3 - Neuropulmonology

Neuropulmonology refers to the complex interconnection between the central nervous system and the respiratory system. Neurologic injury includes traumatic brain injury, hemorrhage, stroke, and seizures, and in each there are far-reaching effects that can result in pulmonary dysfunction. Systemic changes can induce impairment of pulmonary function due to changes in the core structure and function of the lung. The conditions and disorders that often occur in these patients include aspiration pneumonia, neurogenic pulmonary edema, and acute respiratory distress syndrome, but also several abnormal respiratory patterns and sleep-disordered breathing. Lung infections, pulmonary edema - neurogenic or cardiogenic - and pulmonary embolus all are a serious barrier to recovery and can have significant effects on outcomes such as hospital course, prognosis, and mortality. This review presents the spectrum of pulmonary abnormalities seen in neurocritical care.

Flos Farfarae Inhibits Enterovirus 71-Induced Cell Injury by Preventing Viral Replication and Structural Protein Expression.

Enterovirus 71 (EV71) infection can cause airway symptoms, brainstem encephalitis, neurogenic shock, and neurogenic pulmonary edema with high morbidity and mortality. There is no proven therapeutic modality. Flos Farfarae is the dried flower bud of Tussilago farfara L. that has been used to manage airway illnesses for thousands of years. It has neuro-protective activity and has been used to manage neuro-inflammatory diseases. However, it is unknown whether Flos Farfarae has activity against EV71-induced neuropathy. The current study used both human foreskin fibroblast (CCFS-1/KMC) and human rhabdomyosarcoma (RD) cell lines to test the hypothesis that a hot water extract of Flos Farfarae could effectively inhibit EV71 infection. The authenticity of Flos Farfarae was confirmed by HPLC-UV fingerprint. Through plaque reduction assays and flow cytometry, Flos Farfarae was found to inhibit EV71 infection ([Formula: see text]). Inhibition of viral replication and protein expression were further confirmed by reverse transcription polymerase chain reaction (RT-PCR) and quantitative RT-PCR (qRT-PCR), and western blot, respectively. The estimated IC[Formula: see text]s were 106.3[Formula: see text][Formula: see text]g/mL in CCFS-1/KMC, and 15.0[Formula: see text][Formula: see text]g/mL in RD cells. Therefore, Flos Farfarae could be beneficial to inhibit EV71 infection by preventing viral replication and structural protein expression.

Systemic Complications Following Aneurysmal Subarachnoid Hemorrhage.

Many systemic complications follow aneurysmal subarachnoid hemorrhage and are primarily due to sympathetic nervous system activation. These complications play an important role in the overall outcome of patients. The purpose of this review is to provide an update on the diagnosis, pathophysiology, and management of systemic complications specifically associated with aneurysmal subarachnoid hemorrhage. Special focus has been made on systemic complications that occur more frequently in patients with aneurysmal subarachnoid hemorrhage compared to other stroke subtypes and in the neurocritical care patient population. These complications include neurogenic pulmonary edema, electrocardiographic changes, troponin elevation, neurogenic stunned myocardium, hyponatremia, and anemia.