Clinical Vignette

An otolaryngologist requested an expeditious neurologic evaluation of a very vigorous octogenarian who was so fit that he downhill skied 3 weeks earlier; this patient reported recent-onset sense of “spinning vertigo” and cloudiness of vision, precipitated by sudden standing or neck extension. Additionally, he was experiencing new-onset headaches that were becoming increasingly severe and were awakening him from his sleep. Concomitantly he was having difficulty with mental concentration and hand coordination, as well as a feeling of “weak legs.” On further questioning, he recalled that 7 weeks earlier he had slipped on the ice, striking his occiput, while helping to push an auto out of a snow bank.

On examination, he had moderately severe difficulty performing tandem gait (something most healthy 70-year-olds often cannot perform, but this was probably abnormal in this athletic man). The remainder of his neurologic examination was normal. Head computed tomography (CT) demonstrated large biparietal subdural hematomas. Bilateral craniotomies were performed, draining both hematomas. Except for a few focal motor sensory seizures, occurring only in the immediate postoperative period and responding well to phenytoin, his recovery was otherwise excellent.

Comment: This gentleman presented a classic history for subdural hematoma. Initially he had disregarded a moderately significant closed head injury as there were no immediate sequelae other than for a modest scalp contusion. He was symptom-free for 5 weeks. This patient’s initial symptoms were not very impressive because his brain compensated well. Despite a careful neurologic examination, the tandem ataxia was his only neurologic abnormality. This could easily be dismissed as appropriate for age; however, the entire clinical picture was classic for a subdural hematoma until proven otherwise as defined by the CT scans.

General Principles of Head Injury Care

The initial management of severe head injuries, as for any serious trauma victim, includes the “ABC” evaluation for Airway, Breathing, and Circulation and a careful general and neurologic examination.

• A—airway: Suction to free pharynx from blood and other material; intubate after cervical spine evaluation.

• B—breathing: Evaluate rate, rhythm, and breath sounds; ventilate to raise PaO₂ and reduce PaCO₂ (to lower intracranial pressure [ICP]); monitor arterial blood gas levels.

• C—circulatory status: Start intravenous infusion of normal saline solution, followed by blood if indicated; obtain immediate laboratory work and x-rays; administer steroids and phenytoin, plus pressor agent if required (shock rarely due to head injury alone; search for cause).

Concomitantly, the patient’s general level of responsiveness must be assessed using the Glasgow Coma Scale (Fig. 59-1). The lowest possible score of 3 means that individuals have no ability to open the eyes, no motor response to verbal command or direct stimuli, and no verbal response to the physician’s questions, giving a score of 1 or nil for each of the three components. The highest possible score is 15. Soft tissue injuries are commonly associated with more severe head injuries. A complete examination of the exterior surface of the face and head is vital. Blood loss can be extensive given the location of blood vessels within the dense connective tissue of the scalp, which decreases retraction of cut vessels and promotes bleeding.

Figure 59-1 Glasgow Coma Scale.

Skull Fractures

These can be located in the calvaria (vault) and/or the basal skull. Fractures of the cranial vault carry a 20 times greater incidence of intracranial hematoma in comatose patients and a 400 times greater incidence in conscious patients. Basal skull fractures, often difficult to identify on head CT, can present with pathognomonic signs, including raccoon or Panda bear eyes, battle signs (ecchymosis over the mastoid), and cerebrospinal fluid (CSF) leakage from the nose, throat, or ears (Fig. 59-2). Most leaks resolve spontaneously. Persistent leaks necessitate operative treatment (Fig. 59-3).

Figure 59-2 Basilar Skull Fractures.

Figure 59-3 Signs Suggesting Need for Operation.

Depressed fractures, and those along the temporal bone, are more commonly associated with injury to the brain or blood vessels. A fracture line across the middle meningeal artery may predispose to an epidural hematoma. Open fractures with their communication between the intracranial vault and the external environment are associated with higher risks of spinal fluid leaks and infection (Fig. 59-4).

Figure 59-4 Compound Depressed Skull Fractures.

Extra-Axial Traumatic Brain Injuries

Traumatic Subarachnoid Hemorrhage

This is the most common sequela of TBI and is typically associated with other types of intracranial lesions. Subarachnoid hemorrhage (SAH) can range from clinically insignificant to fatal. These SAH blood products can obstruct CSF reabsorption, leading to increased intracranial pressure (ICP) with hydrocephalus. Treatment of SAH often involves placement of ventricular drains and shunting systems for secondary hydrocephalus.

Epidural Hematomas

These represent an acute blood collection contained between the dura and inner table of the skull. These occur in approximately 2% of TBIs (Fig. 59-5). Epidural hematomas (EHs) most commonly develop in the temporal and parietal regions; 90% of EH are associated with a skull fracture. Arterial lacerations, particularly of the middle meningeal artery (Fig. 59-6) or, less commonly, venous injuries, initiate the formation of hematomas. Contiguous lacerations of the dura mater allow this blood into the epidural space.

Figure 59-5 Epidural Hematoma.

Figure 59-6 Meningeal Arteries and Dura Mater.

Immediately after the closed head injury, the patient “typically” experiences an initial but relatively brief loss of consciousness secondary to the primary concussive injury. This is then followed by a lucid interval with return of wakefulness. Subsequently, as the torn vessels leak, an epidural hematoma develops and enlarges, leading to a rapid lapse into coma. Sometimes this entire process may transpire from injury, to transient loss of consciousness, and to a brief period of a “paradoxically reassuring alertness,” only to have a devastating, often irreversible, coma develop within just 1 hour after the blunt head injury (see Fig. 59-3). However, this classic presentation occurs in less than one third of affected individuals. The actual rate of symptom progression depends on the type of associated brain injuries, their etiology, and the subsequent precise rate of blood accumulation within the epidural space.

Cranial CT imaging usually demonstrates a hyperdense, biconvex collection between the skull and brain (Fig. 59-7). On occasion, the initial CT is normal as the hematoma has yet to develop to a size that is definable. Thus when the patient is “at risk,” it is essential to be prepared to repeat the CT scan at the slightest change in clinical status. Once the EH is identified, emergency surgical evacuation is indicated. Any failure to recognize an epidural hematoma has a most significant mortality depending on patient age, time of treatment, hematoma size, and associated injuries.