Closed head, non-penetrating injuries are injuries related to a blow to the head. 1.5 million people each year incur a closed head injury, 75% of which are classified as mild. However, each year approximately 50,000 individuals die from head injuries and more than 100,000 suffer permanent disability. The severity of the injury is initially judged by assessing the so- called Glasgow Coma Scale (GCS) which assesses eye, motor, and verbal abilities. A score of 13-15 indicates a mild injury, a score of 9-12 indicates moderate injury, and a score of 8 or less indicates severe injury. Concussion where there is no loss of consciousness is considered a mild injury.
Causes: The number one cause of head injuries is road accidents. Drivers, passengers, pedestrians, and cyclists are the victims. Other causes include assaults, injuries incurred in sporting events, falls from mechanical slips, conditions that produce dizziness, vertigo, or syncope, and falls associated with drug or alcohol-induced altered states.
Pathophysiology: There have been great advances recently in the understanding of the pathologic process that results from a closed head injury. Depending on the severity of the blow the following structural findings may be present as noted clinically or by imaging: linear or depressed skull fractures, subgaleal hematomas ("goose eggs"), intracranial hemorrhage, cerebral edema, diffuse axonal injury (DAI), or no findings at all. Intracranial hemorrhages may include Sudbury hematoma, epidermal hematomas, intracerebral hemorrhage, or subarachnoid hemorrhage. The recent use of amyloid precursor protein staining has enabled clinicians to identify axonal injury which is often responsible for memory and cognitive impairment, and sometimes vegetative states associated with coma.
Neurochemical changes occur after traumatic brain injury. There is a release of free radicals as cell membranes break down. Together with free lipids and other chemical mediators such as prostaglandins and thromboxane, these substances produce severe inflammation which leads to swelling and ultimate cell and neuron death.
History: It is most important to ascertain whether or not the patient lost consciousness. Generally, the prognosis is worst when a patient has lost consciousness since there is a greater risk that the mediators of brain inflammation are produced in this setting. It is also important to elicit the type and mechanism of injury, as these also have some prognostic importance. Patients who are injured by assault or from a falling object have a much greater risk of poorer vocational outcomes than patients sustaining the typical acceleration/deceleration injuries that occur in motor vehicle accidents, because the former mechanism is associated with greater axonal damage. Note if the patient is alert, oriented and focused when conversing. If not, then this lapse in lucidity may portend a serious intracranial injury. Also, it must be ascertained whether or not the patient is on anticoagulant therapy. Those that are are at much greater risk for bleeding.
Physical: The GCS is the mainstay for the initial neurological assessment in close head injury. Next, a complete neurological exam should be performed. External examination should rule out several telltale signs of serious internal head injury, namely: battle's sign and raccoon eyes (to rule out a basilar skull fracture), hemotympanum (blood behind the ear drum), oto- or rhinorrhea (cerebrospinal fluid coming from the ear or nose), or abnormal pupil size or reactivity (indicative of a space occupying bleed causing impending brain herniation). Focal motor abnormalities such as weakness of the extremities, impaired reflexes, or posturing are indicators of severe brain injury. Finally, a thorough mental status exam must be performed to assess memory (vs. amnesia), cognition and judgment.
Lab and Imaging Studies: Low serum sodium levels (hyponatremia) occurs in up to 50% of moderately and severely head injured patients because of SIADH (syndrome of inappropriate anti diuretic hormone). Also, low serum magnesium levels are noted in all degrees of head injury including mild forms. In fact, some recent animal studies have shown that early administration of magnesium has attenuated experimental brain injury. Elevated serum neuron- specific enolase and protein S-100 B are excellent prognostic markers and correlate with persistent cognitive impairment after 6-12 months in patients with both minor and severe head injuries. Alcohol and illicit drug levels should be checked when indicated to rule out mental status changes cause by these substances rather than head injury.
Computerized tomography (CT) is the main imaging technique used in the immediate acute setting. This study is sometimes followed up with an MRI (magnetic resonance imaging) if the CT is equivocal or if there is a need to rule out axonal injury (DAI). All patients with loss of consciousness or focal neurological findings should undergo CT. Behavioral disorders, memory and other cognitive dysfunction correlates with abnormalities of the cingulate gyrus metabolism that can be picked up by PET scanning (positive emission tomography). Also, mild head injury can produce elevated choline/creatine ratios that can be picked up on proton magnetic resonance spectroscopy (the MRI in these patients is normal).
Treatment: The acute management of closed head injury is governed by the severity of injury. Airway and circulatory stabilization always comes first. If the injury is severe, attention should be focused on making an immediate imaging diagnosis of the injury. If there is an intracranial bleed, a neurosurgeon might elect to decompress it immediately. If there is no bleed but the patient is neurologically impaired, then reducing intracranial pressure is of paramount importance. If an intracranial pressure monitor shows a pressure above 20-25 mm HG, intravenous mannitol, CSF drainage, and hyperventilation must be utilized. At the same time, efforts should be made to improve cerebral perfusion pressure (CPP) to a level greater than 70 mm Hg which is associated with a much better outcome than when the CPP is lower. This is done with volume expansion and vasopressors. Seizures can be controlled with barbiturates and dilantin. Also, some studies show that the calcium channel blocker, nimodipine, will reduce the death and disability rate in some head injured patients. Magnesium also may be effective, as previously mentioned. Finally, cannabinoids (marijuana, THC) is in phase III trials for traumatic brain injury because it has been found to protect against excitotoxicity.
Long term management of moderate and severe head injury in complex and often frustrating and requires a team approach. Medications are necessary to control spasticity or dystonia. Cognitive impairment may improve with some experimental treatments including levodopa and methylphenidate.
Special Issues - Mild Head Injury: Typically, these injuries are associated with mild symptoms and mild cognitive impairments and resolve within 3 months of injury. Symptoms include headache, numbness, tingling, ringing in the ears, neck soreness, dizziness, a dissociative feeling, forgetfulness, confusion, irritability, emotional liability, and an inability to concentrate. Patients who have persistent complaints often are those to be malingers. A recent review of mild head injury found that 33-47% of patients in litigation were malingerers. On the other hand, some studies show that following mild head injury, only 54-79% of patients are able to return to their jobs. One study showed that after one year, 26% had moderate disability and 3% had severe disability. The most commonly reported persistent symptoms were irritability, fatigue, attention and memory disorders, and neuropsychological dysfunction, including depression. Post-traumatic headaches are also of special concern because they tend to be disabling. The mechanism involves the production of substances seen in migraine conditions: catecholamines and excitatory amino acids. Some studies show, however, that they resolve without treatment and persist as a function of analgesic overuse. These studies show that 75% of patients benefit from cessation of their pain medications.
Medical-Legal Issues: All head injured patients are potential litigants because of the persistent and disabling nature of the condition. Physicians must document cases meticulously and should substantiate the mechanism of injury, the extent of injury, the physical, emotional and cognitive consequences of the injury, delineate the treatment, and discuss the progress of the patient and the prognosis. All of these patient should be evaluated by numerous specialists who share and coordinate their findings in support of a team approach to the patient.
This article reproduced with permission of AFMS, Inc.
