Emergency War Surgery NATO Handbook: Part IV: Regional Wounds and Injuries: Chapter XXII: Craniocerebral Injury

Mechanisms of Injury

United States Department of Defense

An understanding of the mechanisms and pathophysiology of injury is necessary for successful treatment. The mechanisms of injurv call be divided into the primary events occurring at the time of impact, and the secondary events that develop over subsequent hours to days (Table 12).

Primary open injuries disrupt neurons, glia, and blood vessels. Primary closed injuries produce parenchymal damage through the shearing of axons and capillaries, particularly in the white matter, and through small pectechial hemorrhages. These may coalesce over the first week after injury into delayed focal hematomas.

Secondary brain injuries occur as a result of systemic and intracranial processes following the primary brain injury. The brain can be protected from secondary injury by prompt recognition of such systemic events as hypoxia, hypotension, hypercarbia, hyponatremia, and other forms of electrolyte imbalance. Secondary injury of intracranial origin can be reduced by the prompt detection and treatment of hematomas and of waves of intracranial pressure elevation that accompany loss of cerebrovascular autoregulation, cerebral edema, seizures, and infection.

The causes of death after head injury can be divided into those occurring in the acute phase within a few hours of injury and those occurring in the subacute phase within a few days of injury. In the acute phase, massive sympathetic and parasympathetic discharges give rise to cardiac arrhythmias, low cardiac output, and respiratory difficulties due to ventilation/perfusion mismatches.

Patients who survive the immediate effects of coma-producing injury develop a hyperdynamic cardiovascular and metabolic condition caused by a preponderance of sympathetic overactivity. Cardiac output is often elevated to twice normal by a combination of arterial hypertension, a reduction in systemic vascular resistance, and tachycardia. The metabolic rate of the body is increased to 1.5 times normal. This state lasts 5-10 days. Dehydration therapy for the purpose of preventing cerebral edema may lead to cardiovascular collapse and should be avoided.

Death in the subacute phase is usually due to the enlargement of an intracranial mass in the form of a hematoma or parenchymal swelling. In response to increasing intracranial pressure, the temporal lobe(s) herniate through the tentorial notch, or the cerebellar tonsils herniate through the foramen magnum, causing damage to the cardiovascular and respiratory centers. The time required for casualty evacuation and triage results in the majority of neurosurgical care being delivered in the subacute phase of injury. Initial care is directed toward the prompt recognition, treatment, and prevention of secondary injuries, particularly those due to hypoxia and to focal intracranial hematomas. Definitive neurosurgical treatment is best carried out by specialist teams in fully-equipped hospital facilities.  

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