SUDEP in adults and children

Sudden unexpected death in epilepsy (SUDEP) represents an important cause of death in patients with epilepsy and it exceeds the expected rate of sudden death in the general population by nearly 24 times. We searched the electronic databases (Cochrane, EMBASE, Scopus, Medline, Pubmed) for studies related to etiology and risk stratification of SUDEP including data on Takotsubo cardiomyopathy (TKC) following seizures resulting in death or near death.: SUDEP is more common among males in the fourth decade of life. Risk for SUDEP is increased by early onset of seizures, low IQ, generalised tonic clonic seizures, nocturnal seizures and seizure frequency. Nonadherance to antiepileptic medications, absence of therapeutic drug level monitoring, presence of neuropathological lesions on imaging and certain subgroups like Dravet syndrome increase its risk. The risk for premature death in patients undergoing temporal lobe resection for drug resistant epilepsy decreased over time but remained above the standard population. Prolonged postictal electroencephalographic suppression was a risk factor for SUDEP in patients with generalised seizures which may indicate a cerebral electrical shutdown. Documented ictal/postictal hypoventilation, laryngeal spasm and cardiac rhythm abnormalities prior to SUDEP may suggest central apnea, neurogenic pulmonary edema, cardiac arrhythmia, or a combination of the above as a cause. Seizure triggered TKC does not seem to play a major role in the pathogenesis of SUDEP.

Neurogenic Pulmonary Edema Caused by Subarachnoid Hemorrhage: A Case Report

Neurogenic pulmonary edema is a serious and life-threatening complication caused by central nervous system diseases, excluding cardiogenic pulmonary edema, other causes of pulmonary edema, lung injury, etc. The lack of specific diagnostic criteria for NPE and the lack of awareness among clinicians often lead to underdiagnosis and misdiagnosis. The disease progresses rapidly with poor prognosis and high mortality [1]. In this paper, we report a patient with a ruptured right middle cerebral artery aneurysm causing subarachnoid hemorrhage, who developed neurogenic pulmonary edema and underwent elective aneurysm clamping under general anesthesia. The relevant perioperative management is reported as follows, and the anesthesia management of patients with neurogenic pulmonary edema is analyzed in the context of the relevant literature.

Neurogenic pulmonary edema in subarachnoid hemorrhage: relevant clinical concepts

Background Subarachnoid hemorrhage (SAH) continues to be a condition that carries high rates of morbidity, mortality, and disability around the world. One of its complications is neurogenic pulmonary edema (NPE), which is mainly caused by sympathetic hyperactivity. Due to the complexity of the pathophysiological process and the unspecificity of the clinical presentation, it is little known by general practitioners, medical students and other health care workers not directly related to the neurological part, making the management of this chaotic condition difficult. This review aims to present recent evidence on clinical concepts relevant to the identification and management of NPE secondary to SAH. Main body of the abstract NPE is defined as a syndrome of acute onset following significant central nervous system (CNS) injury. Its etiology has been proposed to stem from the release of catecholamines that produce cardiopulmonary dysfunction, with this syndrome being associated with spinal cord injury, cerebrovascular disorders, traumatic brain injury, status epilepticus, and meningitis. NPE has long been considered a rare event; but it may occur more frequently, mainly in patients with SAH. There are two clinical presentations of NPE: the early form develops in the first hours/minutes after injury, while the late form presents 12–24 h after neurological injury. Clinical manifestations consist of non-specific signs of respiratory distress: dyspnea, tachypnea, hypoxia, pink expectoration, crackles on auscultation, which usually resolve within 24–48 h in 50% of patients. Unfortunately, there are no tools to make the specific diagnosis, so the diagnosis is by exclusion. The therapeutic approach consists of two interventions: treatment of the underlying neurological injury to reduce intracranial pressure and control sympathetic hyperactivity related to the lung injury, and supportive treatment for pulmonary edema. Short conclusion SAH is a severe condition that represents a risk to the life of the affected patient due to the possible complications that may develop. NPE is one of these complications, which due to the common manifestation of a respiratory syndrome, does not allow early and accurate diagnosis, being a diagnosis of exclusion. Therefore, in any case of CNS lesion with pulmonary involvement, NPE should be suspected immediately.

Combined neurogenic pulmonary edema and atypical takotsubo cardiomyopathy in a patient with ischaemic stroke: a unique case report

Background Neurogenic pulmonary oedema (NPE) and Takotsubo cardiomyopathy are rare complications of ischaemic stroke. They are considered to be due to an excess catecholamine release after sympathetic nervous stimulation following stroke onset. Among the different types of Takotsubo cardiomyopathy, apical ballooning is recognized as the typical form, but 3 atypical patterns have been described (midventricular, basal and focal) which are more commonly observed in patients with neurological disorders. Case summary A 78-year-old woman was treated with intravenous alteplase and underwent mechanical thrombectomy for ischaemic stroke. During the procedure, her respiratory condition quickly worsened requiring invasive mechanical ventilation because of a wide and persistent reduction of the inspiratory oxygen fraction/arterial partial oxygen pressure ratio (FiO2/PaO2). Transthoracic echocardiography revealed moderate left ventricular systolic dysfunction with akinesis of the septal-apical and inferior-apical segments. Coronary angiography excluded obstructive lesions and/or evidence of acute plaque rupture. Ventriculography confirmed akinesis/dyskinesis of the inferior segment of the left ventricular apex associated with normal kinesis of the remaining segments. Chest X-ray revealed an infiltrative shadow on both lungs. After 24 hours from NPE onset, her respiratory function improved and she was finally discharged on day 7 without neurological defects. Left ventricular systolic dysfunction was reversible and ejection fraction normalized in 3 months. Discussion It is a very rare case of simultaneous NPE and Takotsubo cardiomyopathy following ischaemic stroke. Moreover, it is unique in that it is the first observation of NPE associated with an atypical pattern of Takotsubo cardiomyopathy, which is more frequent in patients with neurological disorders. A rapid recognition and treatment are essential for patient survival.

Faktor Faktor Risiko terjadinya Pneumonia pada Stroke Akut di RSUP Dr Hasan Sadikin Bandung

Risk Factors of Pneumonia in Acute Stroke at Hasan Sadikin Hospital Bandung Abstract Background and Objective:Pneumonia is the most common non neurological complications in acute stroke (22%) that increase mortality rate, length of stay and hospitalization cost. It is necessary to identified risk factors for pneumonia including neurogenic pulmonary edema (NPE) for better prevention and early intervention. The purpose of this study is to determine risk factors of pneumonia (including NPE) in acute stroke patients at Hasan Sadikin General Hospital Bandung. Subject and Methods: Prospective observational descriptive study, consecutive sampling method, during September – October 2019. Primary data collected from acute stroke patients such as stroke severity, type, location and size of stroke, treatment during hospitalizataion, comorbidities (including NPE). Pneumonia was diagnosed based on Central for Disease Control Prevention (CDC) criteria, NPE based on Davison criteria. Results: 30 patients (28.3%) with pneumonia in acute stroke patients. Pneumonia were commonly found in NGT insertion (90%), dysphagia (64,71%), total anterior circulation infarct (TACI) (61,54%), large infarct size (61,54%), GCS 9-12 (50%) and NIHSS 16-20 (50%). NPE only found in 6,60% acute stroke patients, 57,14% of them developed pneumonia. Conclusions: Pneumonia in acute stroke patients is more often found in NGT insertion, dysphagia, TACI location, large infarct size, lower GCS and more severe stroke degree.

Abstract P444: Myocardial Infarction and Subarachnoid Hemorrhage. Frequency and Impact on Outcome

Introduction/background: Subarachnoid hemorrhage is known to be associated with systemic complications including neurogenic pulmonary edema and Talkotsubo cardiomyopathy. We set to establish the frequency of myocardial infarction (MI) and its impact on outcome among patients with subarachnoid hemorrhage (SAH) Methods: We analyzed the data from Nationwide Inpatient Sample (2005-2014) for all subarachnoid hemorrhage (ICH) patients. Myocardial infraction (MI) was identified using the International Classification of Disease, 9th Revision, Clinical Modification codes. Baseline characteristics, discharge outcomes (mortality, moderate to severe disability at dischagre, length of stay and in-hospital charges) were compared between the two groups. Results: Of the 325923 patients with SAH, 12720 (3.90%) had in-hospital myocardial infraction. SAH patients with MI were older (64.6 years versus 59.0 years, P <.0001) compared to SAH patients without MI but there was no difference in-term of proportion of females between the two groups. The in-hospital mortality was also higher (49.8% versus 23.9%, p≤.0001) among patients with MI in both univariate and multivariate analysis (OR = 1.75 (1.59 -1.93), P<.0001) after adjusting for potential confounders. SAH patients with MI had higher (68.5% versus 40.9%, P <.0001) proportion of moderate to severe disability at discharge compared to ones without. Similarly, mean length of in-hospital stay (13.2 days versus 11.8 days, P <.0001) and mean hospital charges ($188845 versus $150062, P <.0001) were also higher in SAH patients with MI Conclusions: While MI was reported in only 3.9% of SAH cases it had a significant impact on outcome with a one fold increase in morality and about 75% increase risk of severe disability.