High altitude cerebral edema
Andrew M. Luks, Philip N. Ainslie, Justin S. Lawley, Robert C. Roach, Tatum S. Simonson in Ward, Milledge and West's High Altitude Medicine and Physiology, 2021
Described in 1913 by Ravenhill as “puna of the nervous type” and reintroduced in the English language literature by Fitch half a century later, high altitude cerebral edema (HACE) is perhaps the most feared acute altitude illness as it can be associated with substantial morbidity and mortality if not recognized and treated promptly. After reviewing the epidemiology and important clinical aspects of the disease, including the timing and onset, symptoms and signs, and diagnostic approach, this chapter addresses the current understanding of disease pathophysiology and best practices for prevention and treatment. Basic laboratory studies are typically normal in HACE, aside from the possibility of a mild, nonspecific leukocytosis. Patients with isolated HACE typically have normal plain chest radiographs, while those with concurrent HAPE manifest alveolar opacities consistent with pulmonary edema. The approach to prevention of HACE is the same as that used for other forms of acute altitude illness.
Hypertension and acute stroke
Chris Carter in Critical Care Nursing in Resource Limited Environments, 2019
Hypertension is a global concern, contributing to the burden of heart disease, stroke and kidney failure and premature death and disability. This chapter outlines the practical management of hypertension which may be undiagnosed or inadequately controlled leading to stroke. The cause of the hypertension will determine the treatment, for example hypertension due to pregnancy will be managed differently to sub-arachnoid haemorrhage with decompensation. The cause may be due to stress response, chronic hypertension, increased intra-cranial pressure or activation of neuroendocrine system. Severe hypertension may cause cerebral oedema, intracerebral haemorrhage and breakdown of the blood-brain barrier. Hypertension is a significant concern for low- to low-middle income countries, in addition to poorly diagnosed or inadequately controlled hypertension; by 2020 an estimated 1.15 billion hypertensive patients in low-income settings will require healthcare. Issues surrounding under-diagnosis and poor management may result in hypertensive patients only being identified during crises or acute conditions.
Pathobiology, aetiology, and genetics
Christos Tziotzios, Jesse Dawson, Matthew Walters, Kennedy R Lees in Stroke in Practice, 2017
Aetiology does not influence the hyperacute management of ischemic stroke, but establishing a cause is essential in order to reduce or prevent recurrence. There is ample epidemiological evidence of a genetic predisposition to stroke. Genome-wide association studies have identified a genetic locus on chromosome 12p13 to be associated with total, ischemic, and atherothrombotic stroke in white subjects. Gene therapy for stroke remains remote from clinical practice but gene markers may allow more effective screening and risk profiling and may play a role in the prevention and investigation of stroke. Cerebral oedema may also follow an ischemic stroke, and oedema may add to the neurological damage and injury. Atherosclerosis ranks among the disorders leading to stroke and transient ischemic attack. Severe heart failure and cardiomyopathy are also associated with myocardial dyskinesia that promotes mural thrombi. Embolism may accompany cardioversion, and the risk is higher shortly after development of atrial fibrillation.
Application of the cerebral edema monitor on cardiopulmonary bypass in infants
Published in Brain Injury, 2019
Jiaming Lan, Linfeng Wu, Xingqin Tan, Li Xiang, Chunbao Guo
A diagnostic accuracy study was adopted to evaluate the ability of Cerebral edema monitor by comparing the index test results with those of the reference standard. The serum levels of astrocyte S100 protein and neuron-specific enolase (NSE) were determined. Changes in the cerebral electrical impedance coefficient (CEIC) was detected with the BORN-BE monitor. The left- and right-sided CEIC values, serum levels of S100, and serum NSE in the CPB group significantly increased from the beginning to the end of the operation (P < .05). Furthermore, left and right-sided CEIC values, serum levels of S100, and serum NSE in the CPB-B group were significantly higher than those of the CPB-A group (P < .05). Detection rates of cerebral edema in the CPB-B group at the 24 h post-operative time point were significantly higher than those in the CPB-A group (P < .05). The degree of brain damage is positively correlated with the CPB and aortic cross-clamping. CEIC is a sensitive index reflecting brain damage during CPB in infants.
Diffusion tensor imaging of benign intracranial hypertension: absence of cerebral oedema
Published in British Journal of Neurosurgery, 2006
B. K. Owler, J. N. P. Higgins, A. Péna, T. A. Carpenter, J. D. Pickard
Cerebral oedema, it has been suggested, may have a role in the pathophysiology of benign intracranial hypertension (BIH). We applied diffusion tensor MR imaging (DTI), a technique able to detect cerebral oedema, to the study of patients with BIH. A quantitative regional analysis of diffusion parameters (trace and relative anisotropy) was conducted by comparing five BIH patients and six healthy controls. A small but significant increase in anisotropy accompanied by a small but significant decrease in trace was found in the putamen and head of the caudate nucleus. No significant changes were demonstrated in the thalamus, cerebral white matter or cortical regions. Our findings support other recent work that suggests cerebral oedema is not a factor in the pathogenesis of BIH.
Escin attenuates cerebral edema induced by acute omethoate poisoning
Published in Toxicology Mechanisms and Methods, 2011
Tian Wang, Na Jiang, Bing Han, Wenbo Liu, Tongshen Liu, Fenghua Fu, Delu Zhao
Organophosphorus exposure affects different organs such as skeletal muscles, the gastrointestinal tract, liver, lung, and brain. The present experiment aimed to evaluate the effect of escin on cerebral edema induced by acute omethoate poisoning. Sprague-Dawley rats were administered subcutaneously with omethoate at a single dose of 60 mg/kg followed by escin treatment. The results showed that escin reduced the brain water content and the amount of Evans blue in omethoate-poisoned animals. Treatment with escin decreased the levels of tumor necrosis factor-alpha (TNF-α), matrix metalloproteinase-9 (MMP-9), cyclooxygenase-2 (COX-2), and prostaglandin E2 (PGE2) in the brain. Escin also alleviated the histopathological change induced by acute omethoate poisoning. The findings demonstrated that escin can attenuate cerebral edema induced by acute omethoate poisoning, and the underlying mechanism was associated with ameliorating the permeability of the blood–brain barrier.