surviving patients (46%). TABLE 1 Decompressive bifrontal craniotomy in 13 survivors Age, Sex Preoperative Condition Etiology, Pathology Postop Status Consc. Respirations Pupils Motor Reflexes 20 M coma spont. bilat. dilated fixed bilat. decereb. rigidity areflexia, bilat. trauma, cerebral contusion self care, on rehab, R hemiparesis, Babinski speech normal 23 M resp. to pain spont. R dilated fixed, L hemiplegia bilat. hyperreflexia, trauma, cerebral edema
Raymond N. Kjellberg and Alberto Prieto Jr.
Raymond A. Clasen, Sylvia Pandolfi, Iris Laing and Donald Casey Jr.
I t is known that the cerebral edema associated with cryogenic brain lesions in the monkey can be reduced by systemic hypothermia. 4, 6 The experiments reported here were designed to determine whether increasing the body temperature would increase this type of edema. The relationship between this experimental model and human disease was considered in a previous paper. 10 Materials and Methods Focal areas of hemorrhagic necrosis were produced in the brains of rhesus monkeys by freezing through the intact skull. The animals were given 25 microcuries of I
Richard D. Penn and Diane Kurtz
M ass lesions within the intracranial cavity may cause damage due to local pressure, distortion of cerebral blood vessels and circulation, and cerebral edema. Measurement of these effects in man has been difficult and involves invasive techniques such as the intracarotid injection of radioactive tracers to determine regional blood flow and the implantation of intracranial pressure monitors. With the advent of computerized tomography (CT), many of these factors can now be studied in vivo non-invasively, and the precise size and location of a mass lesion and
Ahmed Raslan and Anish Bhardwaj
✓Cerebral edema is frequently encountered in clinical practice in critically ill patients with acute brain injury from diverse origins and is a major cause of increased morbidity and death in this subset of patients. The consequences of cerebral edema can be lethal and include cerebral ischemia from compromised regional or global cerebral blood flow (CBF) and intracranial compartmental shifts due to intracranial pressure gradients that result in compression of vital brain structures. The overall goal of medical management of cerebral edema is to maintain regional and global CBF to meet the metabolic requirements of the brain and prevent secondary neuronal injury from cerebral ischemia. Medical management of cerebral edema involves using a systematic and algorithmic approach, from general measures (optimal head and neck positioning for facilitating intracranial venous outflow, avoidance of dehydration and systemic hypotension, and maintenance of normothermia) to specific therapeutic interventions (controlled hyperventilation, administration of corticosteroids and diuretics, osmotherapy, and pharmacological cerebral metabolic suppression). This article reviews and highlights the medical management of cerebral edema based on pathophysiological principles in acute brain injury.
Harold A. Wilkinson, James G. Wepsic and George Austin
, Ackerman GL: Treatment of bromide intoxication with ethacrynic acid and mannitol diuresis. Ann Int Med 65: 749–752, 1966 2. Bakay L , Haque IU : Morphological and chemical studies in cerebral edema. J Neuropath Exp Neurol 23 : 393 – 418 , 1964 Bakay L, Haque IU: Morphological and chemical studies in cerebral edema. J Neuropath Exp Neurol 23: 393–418, 1964 3. Beks JWF , ter Weeme CA : The influence of urea and mannitol on increased intraventricular pressure in cold-induced cerebral oedema. Acta
A CT and biochemical study
Eugene A. Quindlen and Anita P. Bucher
correlated with the amount of preoperative cerebral edema shown on computerized tomography (CT) scans and with the histological type of the tumor. Human CNS tumors are an ideal model to study this association since, unlike tumors elsewhere in the body, it is usually possible to image the entire extent of the tumor and of the surrounding edema. Peritumoral edema is a significant cause of mortality and neurological morbidity in patients with primary or metastatic cerebral tumors. In addition, cerebral edema can complicate and delay various treatment options such as surgery
Alfonso Schettini, H. Robert Lippman and Edward K. Walsh
D ecompression of a supratentorial mass lesion, such as the evacuation of a subdural hematoma, may be complicated by a sudden increase in brain volume, intracranial hypertension, cerebral edema, and coma, and may occasionally lead to a fatal outcome. Although these processes have been attributed to brain congestion (hyperemia), the pathogenesis remains obscure. In the laboratory this condition has been experimentally reproduced by expanding a supratentorial extradural balloon. 7, 9, 17, 50, 52 Rapid decompression after a given period of brain compression can
Tetsuaki Teraura, John Stirling Meyer, Keizo Sakamoto, Kazuo Hashi, Peter Marx, Cornelia Sterman-Marinchesu and Seiji Shinmaru
A good part of the controversy about the pathogenesis of cerebral edema is due to lack of agreement on terminology as well as the grade of edema. Cerebral edema and brain swelling usually occur together but do not have the same meaning and the terms should not be used interchangeably. Significant degrees of brain swelling can occur unaccompanied by cerebral edema, primarily as a consequence of increased cerebral blood volume. As used in this communication, the terms have been arbitrarily assigned the following meanings: 1. “Cerebral edema”: increased
Patricia A. Tornheim and Robert L. McLaurin
S teroids have been shown, clinically and experimentally, to reduce cerebral edema associated with several forms of intracranial pathology. The response to these drugs in patients with brain tumors is often dramatic. For the head-injured patient with brain edema, however, beneficial effects from steroids are uncertain. Clinical and experimental studies have been conducted to evaluate possible anti-edema properties of steroids on cerebral edema of traumatic origin. The results of several clinical trials are inconclusive. From a number of laboratory studies
Sindhura Pisipati, Kyle A. Smith, Kushal Shah, Koji Ebersole, Roukoz B. Chamoun and Paul J. Camarata
. The long-term efficacy of LITT is currently under investigation in multiple applications including the treatment of primary and secondary tumors, and it appears to be a promising therapy for high-grade gliomas since associated survival has ranged from 6.9 to 30 months in various studies. 2 , 4 One of the drawbacks of using LITT is the development of significant cerebral edema, 12 which in patients harboring larger lesions can require prolonged courses of steroids and can be significant enough to warrant hyperosmolar therapy, extending hospital stays or even