Medical Management of Cerebral Edema
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.
Cerebral edema, simply defined as an increase in brain water content (above the normal brain water content of approximately 80%) and invariably a re sponse to a primary brain insult, is commonly observed in a variety of brain injury paradigms, including TBI, SAH, ischemic stroke and ICH, primary and metastatic neoplasms, inflammatory diseases (meningitis, ventriculitis, cerebral abscess, and encephalitis), and severe toxic– metabolic derangements (hyponatremia and fulminant hepatic encephalopathy). In the clinical setting, cerebral edema is a frequent cause of morbidity and death in patients with neural injuries.
Cerebral edema has traditionally been classified into three major subtypes: cytotoxic, vasogenic, and interstitial (hydrocephalic) (see the Underlying Mechanisms of Edema Formation section for more details). This classification is highly simplistic, given that it pertains to complex pathophysiological and molecular mechanisms, but is valuable as a simple therapeutic guide for treatment of cerebral edema. Most brain insults involve a combination of these fundamental subtypes of edema, although one can predominate depending on the type and duration of injury. Cytotoxic edema results from swelling of the cellular elements (neurons, glia, and endothelial cells) because of substrate and energy failure, and affects both gray and white matter. This edema subtype is conventionally thought to be resistant to any known medical treatment. Vasogenic edema that results from breakdown of the BBB due to increased vascular permeability, as commonly encountered in TBI, neoplasms, and inflammatory conditions, predominantly affects white matter. This edema subtype is responsive to both steroid administration (no tably edema associated with neoplasms) and osmotherapy. Other causes of vasogenic edema include tissue hypoxia and water intoxication that maybe responsive to osmotherapy but resistant to steroid administration. Interstitial edema, a consequence of impaired absorption of CSF, leads to increases in transependymal CSF flow, resulting in acute hydrocephalus. This edema subtype is also not responsive to steroid administration, and its response to osmotherapy is debatable.
Most cases of brain injury that result in elevated ICP begin as focal cerebral edema. Consistent with the Monroe–Kellie doctrine as it applies to intracranial vault physiology, the consequences of focal (with or without ICP elevation) or global cerebral edema can be lethal and in clude cerebral ischemia from compromised regional or global CBF and intracranial compartmental shifts due to ICP gradients, resulting in compression of vital brain structures ('herniation' syndromes; Table 1 ). Prompt re cog nition of these clinical syndromes and institution of targeted therapies constitutes the basis of cerebral resuscitation. It is imperative to emphasize the importance of a pa tient displaying cerebral herniation syndrome without increments in global ICP; in these cases, elevations in ICP may or may not accompany cerebral edema, particularly when the edema is focal in distribution.
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.
Cerebral edema, simply defined as an increase in brain water content (above the normal brain water content of approximately 80%) and invariably a re sponse to a primary brain insult, is commonly observed in a variety of brain injury paradigms, including TBI, SAH, ischemic stroke and ICH, primary and metastatic neoplasms, inflammatory diseases (meningitis, ventriculitis, cerebral abscess, and encephalitis), and severe toxic– metabolic derangements (hyponatremia and fulminant hepatic encephalopathy). In the clinical setting, cerebral edema is a frequent cause of morbidity and death in patients with neural injuries.
Cerebral edema has traditionally been classified into three major subtypes: cytotoxic, vasogenic, and interstitial (hydrocephalic) (see the Underlying Mechanisms of Edema Formation section for more details). This classification is highly simplistic, given that it pertains to complex pathophysiological and molecular mechanisms, but is valuable as a simple therapeutic guide for treatment of cerebral edema. Most brain insults involve a combination of these fundamental subtypes of edema, although one can predominate depending on the type and duration of injury. Cytotoxic edema results from swelling of the cellular elements (neurons, glia, and endothelial cells) because of substrate and energy failure, and affects both gray and white matter. This edema subtype is conventionally thought to be resistant to any known medical treatment. Vasogenic edema that results from breakdown of the BBB due to increased vascular permeability, as commonly encountered in TBI, neoplasms, and inflammatory conditions, predominantly affects white matter. This edema subtype is responsive to both steroid administration (no tably edema associated with neoplasms) and osmotherapy. Other causes of vasogenic edema include tissue hypoxia and water intoxication that maybe responsive to osmotherapy but resistant to steroid administration. Interstitial edema, a consequence of impaired absorption of CSF, leads to increases in transependymal CSF flow, resulting in acute hydrocephalus. This edema subtype is also not responsive to steroid administration, and its response to osmotherapy is debatable.
Most cases of brain injury that result in elevated ICP begin as focal cerebral edema. Consistent with the Monroe–Kellie doctrine as it applies to intracranial vault physiology, the consequences of focal (with or without ICP elevation) or global cerebral edema can be lethal and in clude cerebral ischemia from compromised regional or global CBF and intracranial compartmental shifts due to ICP gradients, resulting in compression of vital brain structures ('herniation' syndromes; Table 1 ). Prompt re cog nition of these clinical syndromes and institution of targeted therapies constitutes the basis of cerebral resuscitation. It is imperative to emphasize the importance of a pa tient displaying cerebral herniation syndrome without increments in global ICP; in these cases, elevations in ICP may or may not accompany cerebral edema, particularly when the edema is focal in distribution.
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