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  • Updated 10.27.2020
  • Released 10.27.2020
  • Expires For CME 10.27.2023

Cerebral edema

Introduction

Overview

Cerebral edema is excessive accumulation of fluid in the intracellular or extracellular spaces of the brain that increases pressure within the skull, leading to direct compression of the brain with impairment of function. Several neurologic disorders are associated with cerebral edema, particularly traumatic brain injury and large hemisphere infarction. Multiple methods of treatment are available, such as osmotherapy and decompressive craniotomy, but they are mostly nontargeted and address secondary effects. Treatments in development target the molecular pathways involved in the pathomechanism of cerebral edema. A personalized approach is needed to select the treatment(s) best suited for an individual patient.

Key points

• Cerebral edema is usually associated with various intracranial pathologies, traumatic brain injuries, ischemic strokes, and brain tumors and raises intracranial pressure.

• Early detection and management of cerebral edema is important.

• Several therapies are available for cerebral edema and current therapies such as osmotherapy and decompressive craniotomy address only secondary effects whereas new drugs in development target molecular mechanisms of cerebral edema.

• Aims of the treatment are reduction of intracranial pressure, neuroprotection, and addressing the cause if possible.

Historical note and terminology

Relationship between cerebral edema, intracranial hypertension, and functional outcome in traumatic brain injury was recognized in ancient Egyptian medicine as early as 3000 to 2500 BC. The Edwin-Smith Papyrus from the 17th century BC describes the use of neurologic examinations to classify head injury severity, identify intracranial hypertension, and determine prognosis for outcome (17). The word “edema” is Greek in origin, meaning swelling. Hippocrates recognized cerebral edema and described it in his work On Injuries of the Brain (04). In the following centuries, cerebral edema was linked to several other neurologic disorders. During the 18th century, cerebral edema was recognized as distinct from acute hydrocephalus, which was previously believed to be the underlying cause of all cases of excess intracranial water. Interest in cerebral edema was renewed in the 19th century with discovery of the blood-brain barrier. In early part of the 20th century, Harvey Cushing revived the 18th century Monro-Kellie doctrine, which states that during health, the volume occupied by the contents of the cranium must remain in dynamic equilibrium—the implication being that the fluid influx rate must equal the efflux rate. In 1965, electron microscopy was used to describe 2 different types of cerebral edema in a monograph on cerebral edema (01). A couple of years later, these subtypes were termed cytotoxic edema characterized by cellular swelling attributed to inhibited cell volume regulation and vasogenic edema defined by extravasation of fluid that contained plasma proteins and was attributed to vascular injury. Although the term “brain swelling” refers to increase in brain volume due to any cause, it is used synonymously with “cerebral edema”, which refers to abnormal accumulation of water within the brain tissue, as it is the main contribution to increase in volume. Cerebral edema is described as reversible or irreversible according to the treatability of the primary cause. Malignant cerebral edema is characterized by rapid neurologic deterioration associated with massive cerebral swelling, leading to transtentorial herniation and death or poor functional outcome.

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