Diastatic fracture involves a separation of bones at a suture line or a marked separation of bone fragments; both are usually visible on computed tomographic (CT) scans. Facial fracture may also play a role in head injuries. A blow to the lower jaw when the jaw is closed can cause the mandibular condyles to displace upward and backward against the base of the skull, leading to a concussion or a basilar skull fracture. Another type of facial fracture, which may or may not involve the cranium, is an orbital blowout fracture, which usually involves the floor of the orbit and is caused by blunt impact to the orbit and its contents.

Basilar skull fractures can occur when the mandibular condyles perforate into the base of the skull, but they most often result from extension of fractures of the calvaria. Basilar fractures often produce Battle’s sign (an oval-shaped bruise over the mastoid) or raccoon eyes (ecchymotic areas around the eyes).

The presence of depressed elements of a fracture may warrant specific diagnostic and therapeutic measures. If the depressed fracture is closed, the rationale for surgical correction is to evacuate any local mass if present, repair any dural lacerations to prevent cerebral herniation through the defect, and correct any cosmetic disfigurement caused by the depression. In general, if the depression on the tangential view of the skull is greater than the thickness of the skull, the dura is probably lacerated, and surgery is recommended. Depressions of a lesser degree, unless over the forehead, rarely necessitate surgical exploration.

A compound depressed skull fracture usually requires surgical debridement. If the injury has been caused by a blow to a static head, the patient’s level of consciousness is frequently well preserved, and no neurologic deficits may be seen. When a blow has been sustained to a moving head, consciousness is impaired.

Skull fractures can be the source of various complications, including intracranial infections, hematomas, air within the cranium, and meningeal and brain tissue damage. Traumatic pneumocephalus may occur if the frontal, ethmoid, or sphenoid sinuses or the mastoid processes are fractured. Air that has entered the skull locates in the epidural, subdural, subarachnoid, interventricular, or intercerebral space. Pneumocephalus seldom produces symptoms unless it is under tension and thus produces compression of the underlying brain tissue. The incidence rate of pneumocephalus and cerebral spinal fluid rhinorrhea with sella turcica fractures is small, but a high incidence rate of infection exists if this condition is present. Associated palsies of the oculi motor, trochlear, trigeminal, or abducens nerves may also be seen. ^{32.33. and 34.}

In general, temporal bone fractures can cause pneumocephalus if dural tearing occurs in conjunction with injury to the eustachian tube, the middle ear, or the mastoid process. The patient may have sensory neurologic hearing loss, otorrhagia, or cerebral spinal fluid rhinorrhea in the presence of a temporal bone fracture.

Subdural hematoma is a collection of blood between the brain surface and the dura. It may occur as a result of a contusion or laceration of the brain with bleeding into the subdural space, tearing of the veins that bridge the subdural space, or an extension of an intercerebral hematoma through the brain surface into the subdural space. Subdural hematoma might be unassociated with skull fracture. ^1,9,27,39

Subdural hematomas are classified as acute, subacute, or chronic, depending on the time elapsed between the injury and the appearance of signs and symptoms of neurologic dysfunction. As with other types of traumatic brain injury, the time course of development and the degree and rate of neurologic dysfunction depend on many factors. As a general rule, if dysfunction occurs within 24 hours, the hematoma is acute; if it occurs between 2 and 10 days, it is subacute; and if it occurs after 2 weeks, the hematoma is chronic. This particular classification is partially pathologic. The location of the hematoma and the amount of mass effect play important roles in determination of the timing of surgical intervention.

Elderly patients may have larger subdural hematomas with slowly developing symptoms because they have larger potential subdural spaces as a result of cerebral atrophy. In contrast, symptoms may be displayed rapidly and marked increases in intercranial pressure may develop in a younger patient with a small subdural space.

Subdural hematomas generally occur in children under the age of 2 years. Signs and symptoms include a bulging fontanel and a large head (because of separation of the sutures) and retinal hemorrhages (because of increased ICP). In the infant patient, a shock-like state may also develop because a relatively large blood volume loss may be caused by a subdural hematoma.

Acute subdural hematomas are usually associated with high morbidity and mortality rates, which reflects the usually severe nature of the associated injuries and the not-infrequent association of rapidly rising ICP resulting from the mass effect and development of cerebral edema. Two separate related pathophysiologic problems are cerebral contusion and edema and the presence of blood in the subdural space. The CT scan is valuable in determination of whether surgical intervention may be indicated. If the major problem contributing to poor neurologic status is the mass effect, then surgical intervention may be necessary. If the major problem is the cerebral injury, then corrective treatment should be directed toward the increased ICP.

An epidural hematoma is the collection of blood, usually arterial, between the skull and the dura. Epidural hematomas are classified as acute or subacute. An acute epidural hematoma that is arterial in origin generally produces symptoms within a few hours. Subacute epidural hematomas are venous in origin and take a long-er time to produce symptoms. These hematomas are associated with linear skull fractures in 90% of patients, but they may also occur as a result of blunt injuries in which no evidence of fracture is seen. ⁹ The classic symptoms displayed with epidural hematoma are transient loss of consciousness, recovery with a lucid interval during which neurologic status returns to normal, and the secondary onset of headache and a decreasing level of consciousness. As a result of the initial injury, the middle meningeal artery may tear and cause traumatic unconsciousness. Spasm and clotting then occur in the middle meningeal artery, and the bleeding stops. During the next several hours, the artery gradually bleeds, and a hematoma is formed, stripping the dura from the inside of the skull. Once a headache with a decreasing level of consciousness becomes obvious, the secondary rise in ICP has already occurred, and distortion of the brain with significant mass effect occurs. Because compensatory mechanisms of the inner cranial space have already been exhausted, the patient’s neurologic status rapidly deteriorates. The patient experiences a downhill course, usually with dilation of the ipsilateral pupil because of third-nerve compression by the herniating temporal structures, progressive unconsciousness with weakness or decerebration of either the contralateral extremities or the ipsilateral extremities, Cheyne-Stokes respirations, and, if no treatment is initiated, loss of pupillary reflexes, caloric responses, bradycardia, and death. Thus, identification of the epidural hematoma in the earliest possible stage, when a headache and drowsiness are the only symptoms, and transfer of the patient for immediate neurosurgical intervention are extremely important. ^1,39 The classic history and clinical progression, however, is only seen in one third of patients with epidural hematomas. Another third are unconscious from the time of injury, and the final third are never unconscious. In children, bradycardia and early papilledema may be the only warning signs. ^3,4

Cerebral hemorrhagic contusions frequently occur in patients, particularly adults, after traumatic brain injury. Of the patients who die of traumatic brain injury, 75% have contusions at autopsy. Hemorrhagic contusions are infrequently seen in children, but areas of localized decreased density on a CT scan may represent nonhemorrhagic contusions or possibly local ischemia. ^1,9,14,16

Generally, no surgical intervention is recommended for cerebral contusions because brain matter cannot be removed in areas of the brain that control motor, sensory, or visual functioning. If, however, the contusion occurs over the frontal or temporal lobes, with significant edema and shift, surgical removal of contused portions of the brain is feasible. When a temporal lobe contusion is present and signs of herniation are seen, surgical excision of the temporal lobe may be beneficial. Generally, patients with contusion are treated with medical control of elevated ICP.

Movement of one section of brain tissue over or against another section causes tears in blood vessels, which leads to contusions or intracerebral hematomas. Most intra-cerebral hematomas are found in the frontal and temporal lobes, usually very deep, and are associated with necrosis and hemorrhage. The anatomic relationship between these areas and irregularities of the skull has already been discussed. Intracerebral hematomas are readily identified on the CT scan. The clinical picture may vary from no neurologic defect to deep coma.

When a person is shot at close range, evidence of smoke may be visible on the skin. When the muzzle of the gun is somewhat farther from the scalp but still close, evidence of powder burns may exist. A bullet striking the skull can cause great destruction of the underlying brain tissue.

Although some of the energy of impact may be dissipated by the shattering of bones and soft tissues, the impact on the brain after a bullet penetrates the skull is still great. The bullet’s ability to destroy tissues is directly related to its kinetic energy at the moment of impact. The degree of damage to the brain depends primarily on the muzzle velocity of the bullet and the distance between the gun and its target.

A bullet that passes through the head produces a larger defect on the inner table of the skull than that produced on the outer table. High-velocity bullets cause extensive injury to the brain and cranium. The entrance wound is usually smaller than the exit wound, but a great deal of variation in size may be seen. Multiple linear fractures that radiate from either the entrance or exit wound are common. Some fractures may be far away from the trajectory of the bullet, particularly in thin bones. The transport team should describe the wounds but not attempt to determine whether they are entrance or exit wounds.

Injuries to the major cerebral arteries, veins, or venous sinuses can occur in any of the bullet’s intra-cranial passages. Cerebral injuries cause an immedi-ate but transitory increase in ICP. The eventual ICP depends on the degree of intracranial bleeding, which may be profuse even in the absence of injury to major vessels. Secondary cerebral edema causes a delayed increase in ICP. Damage to the hemisphere causes loss of autoregulation, falling cerebral blood flow, an increase in cerebral blood volume and ICP, and eventually, brain death.

Intracranial hematomas are frequently associated with penetrating wounds to the brain. If the bullet passes close to or transverses the ventricle, an intraventricular hematoma may result.

Infection is seen often in injuries caused by shell fragments because these fragments are more likely than bullets to carry dirt, hair, and bone fragments into the brain. Infections develop most often from retained bone fragments, improper closure of the scalp and dura, and delay of definitive surgery beyond 48 hours.

Whenever the skull has been penetrated, a risk of intracranial infection exists. The injury should be managed to minimize that risk. All patients with penetrating injuries should receive tetanus prophylaxis.

Most stab wounds are caused by assaults with sharp instruments such as knives, scissors, and screwdrivers or when the patient (often a child) falls on a stick or sharp toy. The best method is to transport the patient with a stab wound with the object immobilized, secured, and left in place.

If the penetrating object has been removed, determination of exactly where penetration of the skull occurred may be difficult, particularly if entry occurred at the eyelid or sclera. When the patient arrives at the hospital, the area of injury is explored and debrided, as with an open injury.