Head Injury

Head trauma remains a major health predicament despite extensive preventive efforts. The magnitude of the problem can be appreciated by pointing out that approximately 2 million people suffer head injuries in the United States each year. Of these, approximately 100,000 die and almost as many are left with long-term disabilities. The cost of caring for these patients in the United States approaches $25 billion each year.

Over the past three decades general developments in the field of critical care have helped reduce mortality in patients with severe traumatic brain injury (TBI) (1). More recently, a number of developments that have focused specifically on the treatment of intracranial injuries have paralleled the growth of the field of neurological critical care. Evidence-based guidelines were developed in an effort to define and standardize the treatment of patients with severe TBI (2). Also, new devices have become available to monitor head-injured patients. Currently, our understanding of the pathophysiology of head injury is evolving. For example, the concept that ischemia is a major cause of ongoing injury in severe TBI is being questioned and mitochondrial dysfunction has been proposed as the cause of metabolic suppression of neuronal function after injury (3,4).

This chapter focuses on the intensive care unit (ICU) treatment of patients with severe head injury, defined generally as comprising those patients with a Glasgow Coma Scale (GCS) score less than 9 after initial resuscitation (the well-known GCS is shown in Table 12.1). Throughout the chapter reference is made to the TBI guidelines, which were developed jointly by the Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of Neurological Surgeons, and Joint Section on Neurotrauma and Critical Care (2) and updated in 2000 (5, 6, 7, 8, 9 and 10). This effort was undertaken to establish an evidence-based approach to guidelines for the treatment of patients with severe head injury. The literature was reviewed and the recommendations of these groups were classified as a:

1) Standard of care: high degree of clinical certainty, usually class I (prospective randomized controlled trial) evidence; 2) Guideline: moderate degree of clinical certainty, class II (observational, cohort, prevalence, and case-control studies) evidence; and 3) Options: unclear clinical certainty, class III (retrospective case series, registries, case reports, and expert opinion) evidence.

This approach, although perhaps omitting some nuances that should be known to neurointensivists and others interested in head trauma, is nonetheless the most comprehensive and well-considered summary of current thinking on the subject. Use is also made of the traumatic Coma Data Bank [a National Institutes of Health (NIH)-funded multicenter project to study patients with severe TBI] that should be familiar to all intensivists (11, 12, 13, 14 and 15).

PRIMARY AND SECONDARY CEREBRAL INJURY

Primary injuries, those that occur at the time of the trauma, can only be ameliorated by prevention. These include crushing or laceration of the brain and large hematomas. Secondary injury refers to the intracranial and systemic factors that cause ongoing and potentially reversible injury. In some instances the delineation is not quite so clear; for example, brain contusion and vascular injury have irreversible mechanical or necrotic, and partly reversible subcellular components, the latter being subsumed by the currently fashionable term “apoptosis” (16, 17 and 18). In order to provide rational and effective care, it is essential to understand the mechanisms responsible for secondary injury. To date, most ICU treatment has focused on the control of elevated intracranial pressure (ICP) and on maintaining adequate cerebral perfusion pressure (CPP) and there have been several unsuccessful trials of neuroprotective agents (19,20). The latter address the somewhat controversial concept that ischemia is an important cause of secondary damage after head injury. From these approaches we have learned that extremes of high ICP and low CPP are clearly harmful, but the importance of other factors within those other pressure limits remains uncertain. As we gain an understanding of the cause of metabolic depression in the pathophysiology of head injury, we may advance our ability to treat severe cases.

TABLE 12.1. Glasgow coma scale

Eye opening
	Spontaneous	4
	To voice	3
	To pain	2
	None	1
Verbal response
	Oriented	5
	Confused	4
	Inappropriate	3
	Incomprehensible sounds	2
	None	1
Motor response
	Obeys commands	6
	Localizes pain	5
	Withdraws to pain	4
	Flexion response to pain	3
	Extension response to pain	2
	None	1

Intracranial Pressure and Cerebral Perfusion Pressure

Intracranial hypertension occurs in approximately 40% of patients suffering persistent traumatic loss of consciousness (21), and mortality rises with increased ICP (22) (Chapters 2 and 3). These observations have led to the logical (but not necessarily valid) assumption that lowering ICP leads to improved outcome.

The manner in which elevated ICP causes neurological injury is incompletely understood. As discussed in Chapter 2, elevated ICP in the setting of low or normal blood pressure can result in a critical reduction in CPP and inadequate delivery of oxygen and glucose to maintain neuronal viability. The definition of this CPP threshold is discussed in the following. If this were the only manner by which elevated ICP caused injury, however, the problem could be overcome by simply raising blood pressure to sufficient levels. Analysis of the Traumatic Coma Databank supports the concept that intracranial hypertension is harmful even in the setting of adequate CCP. In a multiple regression analysis, elevated ICP remained an independent predictor of poor outcome after controlling for CPP, age, GCS motor score, and other factors (23,24).

One mechanism, albeit indirect, through which elevated ICP may cause damage is by the creation of pressure gradients. When bilateral ICP monitors were placed in patients with unilateral mass lesions the difference in ICP between hemispheres was as high as 15 mm Hg (25,26). These gradients develop as a result of the dural reflections that divide the intracranial space into a number of compartments, and occasionally by asymmetric ventricular enlargement. These pressure gradients can produce tissue shifts and eventually herniation and coma.

Cerebral Blood Flow and Metabolism

Ischemia

Disturbances of cerebral blood flow (CBF) following severe TBI has been the focus of
considerable attention and has led to the assumption that ischemia was a major cause of secondary brain injury. This concept should be viewed in the context of pathologic studies performed in the 1970s; ischemic neuronal damage was a common finding in the brains of patients who died following TBI (27,28). However, the population studied was skewed because only patients whose initial injury was severe enough to be fatal were included. In addition, the pathologic findings could have resulted from systemic hypotension, hypoxia, or aggressive hyperventilation. Some regions of ischemia were attributed to vasospasm, a phenomenon that has been difficult to corroborate and is not reflected in the more global reduction in flow summarized below. Thus, the frequency of ischemia in patients who survive with present-day treatment, the time period during which it occurs, its contribution to secondary injury, and its impact on outcome are not known.

Physiologic studies performed 20 or more years ago found hemispheric CBF to be moderately reduced in most patients 1 to 2 days after TBI (29,30), whereas others reported hyperemic hemispheric flow (normal or elevated CBF in comatose patients) in over 50% of patients studied within 96 hours of trauma. More recent studies performed during the first few hours after injury found hemispheric CBF to be low in most cases (24,31). In studies performed very early after injury (average of 3.1 hours), Bouma and coworkers (32) reported global or regional CBF of <18 mL/100 g per minute (considered to be a critical level for ischemic damage) in one third of patients. Subsequent studies that included patients with mass lesions (33) also found regional CBF below this threshold in almost 30% of patients studied within 4 hours, and in 20% of patients studied 4 to 8 hours after injury. Furthermore, low blood flow was associated with poor outcome (34).

Several studies of global cerebral metabolic rate for oxygen (CMRO₂) using simultaneous sampling of arterial and jugular venous blood have reported low global CMRO₂ (29,34, 35 and 36). CMRO₂ also was found to correlate with the level of consciousness (35,36) and outcome (23).

The oxygen/lactic acid index, derived from arterial and jugular venous blood, also has been used to define cerebral ischemia (37,38). Some caution needs to be exercised in the interpretation of lactate levels because increased brain lactate production can occur in the presence of adequate CBF and oxygen delivery (39,40). In addition, increased levels of lactate also may result from the accumulation of white blood cells following TBI (41, 42 and 43), or reduced clearance of lactate caused by low CBF.

The arteriovenous difference in oxygen content (a-vDO₂) has been used to assess for global ischemia following TBI. Normal values for a-vDO₂ range from approximately 4.5 vol% to 9 vol% (44, 45, 46 and 47). When ischemia was defined as a-vDO₂ <10 vol% Obrist found evidence of ischemia in only one of 75 TBI patients (35).

Recently, a number of studies have suggested an alternative explanation for reduced CBF following TBI. There is a growing body of evidence that following TBI, subarachnoid hemorrhage (48), and intracerebral hemorrhage (49), metabolic suppression may be the primary event and this is followed by a passive fall in CBF. Using a number of experimental models of TBI, investigators have found impaired mitochondrial function (4,50), which results in diminished ATP production. Preliminary positron emission tomography (PET) studies in TBI patients have suggested that there may be a compensatory rise in glucose use (51). Recently, biopsies from a small series of patients with severe TBI also demonstrated impaired mitochondrial function, and some have proposed that mitochondrial function may be used as a surrogate efficacy measure for preclinical studies of head injury (50).

If it is confirmed that mitochondrial function is impaired following TBI, it will fundamentally affect how TBI patients are treated. Current approaches to treatment focus on improving CBF and delivery of energy substrates (oxygen and glucose). If the limiting factor in ATP synthesis is the inability of the
mitochondria to use oxygen, then improving delivery may not have much impact. Instead treatment strategies should be directed toward improving mitochondrial function.

TABLE 12.2. Computed tomography classification system of head injury

Diffuse injury I	No visible pathology seen on computed tomography
Diffuse injury II	Cisterns are present with shift 0-5 mm. No high- or mixed-density lesion >25 cc. May include bone fragments and foreign bodies
Diffuse injury III (swelling)	Cisterns compressed or absent. Shift 0-5 mm. No high- or mixed-density lesion >25 cc
Diffuse injury IV (shift)	Shift >5 mm. No high- or mixed-density lesion >25 cc
Evacuated mass lesion	Any lesion surgically evacuated
Nonevacuated mass lesion	High- or mixed-density lesion >25 cc not surgically evacuated
From Marshall SB, Klauber MR, Van Berkum C, et al. The diagnosis of head injury requires a classification based on computed axial tomography. J Neurotrauma 1992;9:S287-S292, with permission.

The question of ischemia remains unresolved at present. If present it is most likely limited to the first few hours following injury. During that period maintaining adequate blood pressure is essential (see the following) and management of elevated ICP is appropriate. Whether continuing to aggressively treat ICP and CPP in the subsequent days is useful is uncertain; such efforts should be integrated with the patient’s overall clinical status.

PROGNOSTICATING AND CLASSIFYING HEAD TRAUMA

Computed Tomography Classification

Early classifications of computed tomography (CT) findings in TBI separated patients with intracerebral clots or large contusions from those with little or no obvious intracranial pathology. The hematomas were further classified as epidural, subdural, or intracerebral. It appears, however, that patients without intracerebral mass lesions are a not homogeneous group and that examination of the cisterns and the position of normally midline structures yields additional prognostic information. A new scheme (52), which has become widely adopted, categorizes CT finding by the six categories listed in Table 12.2.

TABLE 12.3. Outcome based on computed tomography (CT) classification of head injury

		Discharge Glasgow outcome score
Intracranial diagnosis	Percent of category	Good/moderate	Vegetative	Dead
Diffuse injury I	7.0	62	29	10
Diffuse injury II	24	35	52	14
Diffuse injury III	21	16	50	34
Diffuse injury IV	4	6	38	56
Evacuated mass	37	23	38	39
Nonevacuated mass	5	11	36	53
Brainstem injury	1	0	33	67
TOTAL	100	26	42	33
From Marshall SB, Klauber MR, Van Berkum C, et al. The diagnosis of head injury requires a classification based on computed axial tomography. J Neurotrauma 1992;9:S287-S292, with permission.

When applied to the Traumatic Coma Databank population this classification provides prognostic information as summarized in Table 12.3.

Early Prognostic Factors

Systemic insults that occur prior to the patient’s arrival in the Emergency Department have a profound influence on outcome. A prospective multicenter study (53) of 717 TBI
patients identified the impact of prehospital hypoxia or hypotension on outcome. The major findings are summarized in Table 12.4. The special attention that should be afforded to early hypotension and hypoxia have been corroborated by other studies. To a large extent these problems occur prior to hospitalization and it has never been clarified if they are avoidable or simply reflect the degree of injury and parallel systemic injuries. Nonetheless, these systemic alterations should be attended to as quickly as possible.

A number of clinical and x-ray features that can be assessed shortly after arrival in the Emergency Department also provide important prognostic information. Three clinical variables have been consistently identified (not surprisingly) as independent predictors of outcome in severe TBI: age, postresuscitation GCS motor score, and pupillary reactivity (54,55). Analyses using a prediction tree (56) and neural network (57) have produced similar results. Radiologic factors that provide prognostic information include the condition of the basal cisterns (normal, partial, or complete obliteration) and the presence of mass lesions and midline shift (58,59). In patients with civilian gunshot wounds, additional poor prognostic factors include presence of subarachnoid or intraventricular blood (12).

SPECIFIC CRANIAL INJURIES

Skull Fracture

Skull fractures are classified as simple (linear), comminuted, depressed, or basilar. They are considered either closed or open, depending on whether there is an overlying scalp laceration. Skull fractures seen on plain radiographs suggest significant underlying pathology and should be followed up with a CT scan. Most skull fractures are linear and usually are located in the temporoparietal region, overlying the middle meningeal artery. Open depressed skull fractures usually are surgically debrided. When appropriate, this is accompanied by elevation of the depressed skull fragments, repair of any underlying dural laceration, and evacuation of any accompanying hematoma.

TABLE 12.4. Impact of prehospital hypotension and hypoxia on outcome

Secondary insult	n	Good or moderate disability (%)	Severe disability or vegetative (%)	Dead (%)
None	456	11	22	27
Hypoxia (PaO₂ <60)	78	45	22	33
Hypotension (SBP <90)	113	26	14	60
Both	52	6	19	75
TOTAL CASES	699	43	20	37
SBP, systolic blood pressure.
From Chesnut RM, Marshall LF, Klauber MR, et al. The role of scondary brain injury in determining outcome from severe head injury. J Trauma 1993;34:216-222, with permission.

Hemotympanum, raccoon eyes (bilateral periorbital ecchymosis), Battle’s sign (superficial ecchymosis over the mastoid process), otorrhea, or rhinorrhea usually indicate a basilar skull fracture. It is important to note that Battle’s sign generally takes more than 12 hours to appear. Rhinorrhea is seen with fractures of the frontal bone and otorrhea with fractures of the middle fossa that extend into the middle ear. It is important not to plug the external ear but rather to allow free egress of CSF to reduce the risk of infection. Prophylactic antibiotics are not generally recommended because they can select for more aggressive organisms (60,61). Most CSF leaks resolve spontaneously in 7 to 10 days; otorrhea resolves spontaneously in a higher percentage of cases than rhinorrhea. Basilar skull fractures may be confirmed on the routine CT cuts traversing the base of the skull, but definitive diagnosis often requires thin cuts through that region.

Only gold members can continue reading. Log In or Register to continue