Perioperative Management of Subarachnoid Hemorrhage

Spears, Julian; Macdonald, R. Loch; Weir, Bryce

doi:10.1016/b978-1-4160-5316-3.00366-x

Cited by 6 publications

(4 citation statements)

References 208 publications

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“…Other causes of neurological deterioration after aneurysmal subarachnoid hemorrhage include rebleeding, vasospasm, intraventricular hemorrhage, intracerebral hemorrhage, increased intracranial pressure and edema, seizures, hypoxia, and metabolic disturbances, e.g., hyponatremia. The pathogenesis of hydrocephalus is multifactorial and is related to the obstruction of cerebrospinal fluid (CSF) circulation either within the ventricular system or in the subarachnoid space (Spears et al 2011 ). Although pathophysiology of this condition is not fully understood, hydrocephalus after SAH can be treated effectively using current treatment methods.…”

Section: Introductionmentioning

confidence: 99%

Predictors of shunt-dependent hydrocephalus following aneurysmal subarachnoid hemorrhage: a pilot study in a single Egyptian institute

Aboul-Ela

El-Din

Zaater

et al. 2018

Egypt J Neurol Psychiatry Neurosurg

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BackgroundAcute hydrocephalus can cause neurological deterioration after aneurysmal subarachnoid hemorrhage (aSAH). Predicting which patient would require shunting is challenging.MethodsThis prospective study was conducted upon twenty patients who suffered acute hydrocephalus due to subarachnoid hemorrhage of ruptured aneurysms. Surgical or non-surgical management of hydrocephalus was conducted. Glasgow Coma scale (GCS) was assessed, and hydrocephalus was graded by bicaudate index. Fisher grade was determined from CT scan. Aneurysm site was determined by conventional or CT angiography. Either surgical clipping or endovascular coiling of aneurysms was performed.ResultsInitially, 3 (15%) patients had emergency CSF diversion on admission due to poor GCS on arrival. Initially, the remaining 17 patients were managed conservatively. Five patients did not require any intervention. Twelve patients had external ventricular drainage placement, 4 were weaned, and 8 failed weaning. High bicaudate index (> 0.2) correlated with shunting. Aneurysm site correlated well with shunting (ACoA or PCoA).ConclusionsPatients with fair GCS can be managed conservatively. Any deterioration warrants shifting to CSF diversion. Higher bicaudate index will usually need CSF diversion. The value of Fisher carries no significant value. Aneurysm location (ACoA or PCoA) correlates with an increased incidence of ventriculoperitoneal shunt placement.

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Section: Introductionmentioning

confidence: 99%

Predictors of shunt-dependent hydrocephalus following aneurysmal subarachnoid hemorrhage: a pilot study in a single Egyptian institute

Aboul-Ela

El-Din

Zaater

et al. 2018

Egypt J Neurol Psychiatry Neurosurg

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“…Cerebral blood flow (CBF) decreases in the first days. Another important factor to point out is that intracranial pressure (ICP) arises, with the issue of an altered cerebral auto-regulation, worsening the already adverse cellular environment, and facilitating processes like edema, ischemia, and cell death [ 2 ].…”

Section: Reviewmentioning

confidence: 99%

“…The pathophysiology described behind the rupture of an aneurysm usually occurs in association with the presence of comorbidities such as hypertension, tobacco smoking, sedentary lifestyle, and so on. After one of these aneurysms burst, blood passes through the blood-brain barrier, producing disturbances on self-regulatory mechanisms, electrolytes, abnormal pressure upon specific areas, which in general leads to the neurologic symptoms showed in these patients [ 2 ]. The pathognomonic characterization described in SSH includes the worst headache ever, but it is understood that a wide variety of symptoms may be displayed, such as dizziness, diplopia, sensory or motor disturbance, seizures, and memory disturbances, amongst others [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Understanding Cognitive Deficit After Subarachnoid Hemorrhage: A Memory Focused Approach

Alfonso¹,

Aftab²,

Hamadneh³

et al. 2020

Cureus

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Aneurysmal subarachnoid hemorrhage (aSAH) is a prevalent condition affecting a large portion of the population, many of them still in productive ages. Memory impairment is a common factor amongst those patients. Memory exerts a pivotal role in productivity. That is why it is important to understand how it can be affected in post-aSAH patients. There are certain areas most affected in cases of memory disturbances, as well as its functional connections with crucial cerebral regions. Active research on functional magnetic resonance and diffusion tension imaging is used to identify compromised areas within the brain. There are suggested factors regarding poor performance, such as cerebrospinal fluid drainage and new infarction areas, which should be addressed properly to benefit these patients and simultaneously help them return to a productive and functional life.

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“…Cardiac Troponin I release occurs frequently after SAH and has been associated with a neurogenic form of myocardial injury 14 . Elevated Troponin I has been reported in up to 68% of SAH patients 15 . Troponin elevation, usually modest, is an early and specific marker for cardiac involvement after SAH 16,17 and its levels peak about two days after SAH.…”

Section: Introductionmentioning

confidence: 99%

Troponin I Changes in Patients with Subarachnoid Hemorrhage

Sarker¹,

Hoque²,

Khan³

et al. 2018

TAJ: J of Teachers Assoc

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Background : Subarachnoid hemorrhage (SAH) is a catastrophic neurological event. Aside from its neurological morbidities, SAH is associated with significant medical complications. Cardiac manifestations are common and can impact morbidity and mortality in SAH patients. Myocardial enzyme release occur frequently after Subarachnoid hemorrhage that reflect adverse intracranial events .These changes often are unrecognized or misinterpreted, potentially placing patients at risk for inappropriate management.Objective : The aim of this study was to assess Troponin I changes after acute SAH and these changes were compared with neurological severity. The result of the study might be helpful for better understanding diagnostic and therapeutic implications of acute neurocardiogenic injury after SAH.Patients and methods : This cross sectional descriptive study was conducted over 30 patients with SAH in medicine, neuromedicine and intensive care unit of Rajshahi Medical College Hospital during the period of January 2015 to December 2016. Predictor variables reflecting demographic (age, sex, occupation), hemodynamic (pulse, systolic and diastolic blood pressure) and neurological (WFNS score) informations were recorded. We evaluated their cTnI level, which had been measured at admission. A cTnI level above 0.12 ng/ml was defined as an indicator of cardiac injury following SAH.Results : Out of 30 patients 26.7% were both in between 40-49 years and 60-69 years age group & 50% were male and 50% were female. Among the risk factors 60% of patient had history of hypertension, 40% smoking, 10% Diabetes mellitus and 3.3% alcohol abuse. On admission the mean GCS was 12.53±2.69,. The most frequently occurring WFNS grading were grade 1 and grade 4 (both were 43.3% of patients). Out of Thirty, 43.3% of patients demonstrated elevations of Troponin I. WFNS score ≥ 3 (92.3%, p = <0.001) significantly correlated with elevated Troponin I concentration.Conclusion : serum troponin I reveal a higher incidence of myocardial injury in patients with SAH. The present study also demonstrates that raised serum cTnI is associated with more severe neurological injury. These findings support a neurocardiogenic cause of cardiac injury after SAH.TAJ 2014; 27(2): 39-43

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Perioperative Management of Subarachnoid Hemorrhage

Cited by 6 publications

References 208 publications

Predictors of shunt-dependent hydrocephalus following aneurysmal subarachnoid hemorrhage: a pilot study in a single Egyptian institute

Predictors of shunt-dependent hydrocephalus following aneurysmal subarachnoid hemorrhage: a pilot study in a single Egyptian institute

Understanding Cognitive Deficit After Subarachnoid Hemorrhage: A Memory Focused Approach

Troponin I Changes in Patients with Subarachnoid Hemorrhage

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