Introduction

Traumatic brain injury is a leading cause of disability and death in developed countries and increasingly in developing countries. The annual death rate from traumatic brain injury ranges from 14 to 30 per 100 000 population. Persons at the highest risk of brain injury are aged between 15 and 24 years, with the incidence in males being two to three times greater than that in females. The cost to society is great given the lost potential productivity of these usually young individuals, in addition to the need for prolonged support by family and community for those with persistent disability.

A number of clinical classifications of brain injury have been developed to help understand the pathology and predict outcome. The most widely used is the Glasgow Coma Scale (GCS). Although the postresuscitation GCS score correlates well with outcome, it does not provide the clinician with a morphological picture of the underlying brain injury.

Morphologically, brain injury may be broadly classified as either focal or diffuse, although these terms are not mutually exclusive. Focal injury implies intracerebral hemorrhage, subdural hematoma, or epidural hematoma; diffuse injury generally refers to clinical and surrogate radiographic manifestations of diffuse axonal injury. Diffuse axonal injury classically consists of focal lesions in the dorsolateral quadrants of the midbrain or the corpus callosum, and microscopic damage to axons. The distinction between focal and diffuse injury is clinically important in that focal injuries are potentially amenable to surgical intervention.

Over the past two decades, the concept of primary and secondary brain injury has acquired greater significance. Primary brain injury refers to damage that occurs at the moment of injury and includes brain contusion or laceration, diffuse axonal injury, epidural hemorrhage, and subdural hemorrhage. Secondary injury is caused by events that follow the initial brain insult and adversely affect outcome. Secondary injury can be due to secondary insults or to secondary processes that are set in motion by the initial trauma. Secondary insults include hypotension leading to reduced cerebral perfusion, brain edema, delayed hematomas, elevated intracranial pressure, hyperthermia, seizures, hyperglycemia, infections, and iatrogenic misadventures. These can be avoided or attenuated by careful attention to detail. These secondary insults should be distinguished from secondary processes that occur at a biochemical level in the brain in the minutes, hours, and days following injury.

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