Acute Head Injury

Pathogenesis and Pathophysiology. Head injury (HI) accounts for a disproportionate share of morbidity and mortality in traumatized patients. The past two decades have witnessed a significant decline, however, in overall HI mortality from the mid-30 percent range in the 1970s to less than 20 percent in the 1990s. This improvement has paralleled an understanding of the secondary injury process and an appreciation that all neurological damage does not occur at the moment of insult but evolves over the ensuing hours and days from various biochemical and molecular derangements. This understanding has led to the development of aggressive treatment strategies to prevent intracranial pressure (ICP) elevations and ischemia. This understanding has led also to extensive clinical therapeutic trials to identify pharmacological neuroprotective agents. The structural injury to the brain at the time of impact is rarely the sole determinant of outcome. Hypoxia, hypotension, mass lesions, increased ICP, ischemia, free radical production, excitotoxicity, and loss of calcium homeostasis are also important.

The frequent occurrence and deleterious effects of the secondary insults of hypoxia and hypotension have long been known. y , y Mortality is doubled when these insults are superimposed on severe HI (.Fig 51-1 ), and, similarly, concomitant elevated ICP increases morbidity. y Considerable research has focused on the biochemical and molecular mechanisms of secondary injury. Although these events are multifactorial and interrelated, their timing sequence justifies consideration of each component ( . Fig 5.1-2 ).

The contribution of oxygen free radicals to secondary injury following HI is a subject of active research. [4 , y Free radicals generated by HI, including superoxide, hydroxyl, hydrogen peroxide, singlet oxygen, nitrous oxide, have the potential to damage proteins and the phospholipid components of cells and organelle membranes. Additionally, extensive membrane depolarization, induced by trauma, allows for a nonselective opening of the voltage-sensitive calcium channels and an abnormal accumulation of calcium within neurons and glia. Such calcium shifts are associated with activation of lipolytic and proteolytic enzymes, protein kinases, protein phosphatases, dissolution of microtubules, and altered gene expression. y Another method of abnormal calcium influx is via activation of excitatory amino acid receptors such as glutamate and aspartate. Excitotoxicity occurs in a widespread fashion after trauma, resulting in cell swelling, vacuolization, and death. y

Head injury can result in various types of primary injury occurring at the moment of impact including lacerations of the scalp, skull fractures, cortical contusions and lacerations, diffuse axonal injury, and intracranial hemorrhage. A coup contusion occurs at the site of impact in the absence of a fracture. A contrecoup contusion occurs in the brain diametrically opposite the point of impact. Acceleration/ deceleration forces may cause tearing of nerve fibers at the moment of impact, which is called shearing injury or diffuse axonal injury. Types of intracranial hematomas include extradural, subarachnoid, subdural, and intracerebral hematomas.

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