In addition to contusions and extradural, subdural, subarachnoid, and intracerebral hemorrhages, closed head injury induces variable degrees of vasogenic edema that increases during the first 24 to 48 h and sometimes, small zones of infarction that have been attributed to vascular spasm caused by subarachnoid blood surrounding basal vessels. The frequency and importance of this type of secondary cerebral infarction have been debated. A retrospective imaging study by Marino and colleagues found that 17 of 89 patients had regions of stroke after moderate or severe head injury, a feature that had been pointed out by Adams and colleagues. Most were in the distribution of a major branch or penetrating cerebral vessel or in a watershed territory.
The presence of intracranial hypertension has also been associated with a higher incidence of infarction. Marmarou and colleagues demonstrated that brain swelling after head injury is essentially the result of edema and not of an increase in cerebral blood volume, as has long been postulated. In children, and in some cases in adults, the cerebral edema may be massive and lead to secondary brainstem compression.
With fractures of large bones, particularly the femur, with or without head injury, after 24 to 72 h there may be an acute onset of pulmonary symptoms (dyspnea and hyperpnea) followed by coma with or without focal signs or seizures. This sequence is a result of systemic fat embolism, first of the lungs and then of the brain. Cranial trauma is not required. In some cases the onset of pulmonary symptoms is associated with a petechial rash over the thorax, especially in the axillae and also in the conjunctivea and 1 in 3 cases is said to show fat globules in the urine. The specificity of the last of these findings has been questioned. Respiratory distress is the most important and often the only feature of the fat embolism syndrome, evident in the chest film as fluffy infiltrates in both lungs; however, cases have been reported without respiratory involvement.
In the brain, multiple small fat emboli cause widespread petechial hemorrhages and small infarctions, involving both white and gray matter and a few larger infarcts. Most patients with fat embolism recover spontaneously in 3 or 4 days, although a mortality rate of up to 10 percent is cited, usually related to underlying systemic and bony injuries. Treatment, aside from respiratory support, is supportive. Heparin, which had been used in the past, is not considered effective.
The physician first called on to examine a patient who has had a closed head injury will generally find one of three clinical conditions as indicated by the headings below, each of which is dealt with differently. It is usually possible to categorize the patient by assessing the mental and neurologic status when first seen and at intervals after the accident. The Glasgow Coma Scale has been used for almost 50 years as a rapid reference to accomplish this purpose (Table 34-1) but does not substitute for a fuller neurologic examination. The scale registers three aspects of neurologic function: eye opening, verbal response, and motor response to various stimuli. The scale uses a summed score from 3 to 15; a score of 7 or less is considered to reflect severe trauma and a poor clinical state, 8 to 12, moderate injury, and higher scores, mild injury. The scores provided by this scale correspond roughly with the outcome of the head injury as discussed further on, but its main utility is in recording sequential changes in the patient’s clinical state with an easily learned and reproducible tool.