Many algorithms exist for the treatment of elevated ICP (Figure 1). These generally begin with safe, noninvasive interventions. If ICP continues to be elevated, progressively more aggressive treatments are applied. The variety of the algorithms that are available reflects the differences with which various centers embrace the individual treatments that make up those algorithms. Of note, use of steroids to treat TBI is not recommended.

Figure 1 Basic algorithm for the management of elevated intracranial pressure.

Computed Tomography Scanning

Repeat CT scanning should be considered if there is any suspicion that elevated ICP readings may be caused by a delayed or recurrent hematoma, by hydrocephalus or ventriculostomy malfunction, by a large infarction, and so on (Figure 2).

Figure 2 Postoperative computed tomography (CT) scans from a patient who had undergone evacuation of an acute subdural hematoma. Intracranial pressure readings remained elevated after surgery. CT scan revealed postoperative epidural hematoma, for which the patient had to be taken back to surgery.

Sedation and Paralysis

Sedation and analgesics may help to lower ICP, supplemented if needed by neuromuscular blockade.

Cerebrospinal Fluid Drainage

Persistently elevated ICP may respond to CSF drainage if a ventriculostomy has been inserted. The older practice of routinely changing a ventriculostomy catheter every 5–7 days to prevent infection does not seem to be justified by more recent studies,⁵ and some centers have reported leaving catheters in place for 2 weeks or even longer without an increase in infection rates. The subsequent development of antibiotic-coated ventriculostomy catheters seems to have had a considerable impact on lowering the incidence of ventriculostomy-related infections.⁶

Osmotic Diuretics

Administration of mannitol is often a useful step. Mannitol has an osmotic effect that pulls fluid from the brain into the vascular compartment. It also decreases blood viscosity, which enables cerebral arteries to constrict (and thereby lower intracerebral blood volume) without decreasing CBF because the decrease in viscosity facilitates adequate flow through the narrower artery.⁷ Hypertonic saline is receiving a great deal of interest as a possible surrogate or supplement to mannitol. Its use has become especially widespread among pediatric intensivists. Although preliminary reports are encouraging, more solid data are still pending about the optimal method of administration and about relative indications, contraindications, and adverse events.

Hyperventilation

Continued elevations of ICP may respond to judicious use of mild hyperventilation. Whenever possible, we attempt to use monitors of cerebral oxygenation to make sure that cerebral ischemia does not result from hyperventilation that is more aggressive than the brain can tolerate.

Barbiturate Coma

Persistent intracranial hypertension may respond to pentobarbital-induced coma.⁸ This treatment is effective at lowering ICP, but hypotension is a major problem. Prior to administering barbiturates, we usually insert a pulmonary artery catheter to ensure that intravascular volume is adequate. Likewise, we have pressors ready for immediate infusion if the blood pressure begins to decrease.

Decompressive Craniectomy

Intracranial hypertension that persists despite initiation of the treatments listed in Figure 1 is a serious problem. Decompressive craniectomy, in which a large part of the skull is temporarily removed so that the injured brain has room to swell, is currently a popular intervention. It seems clear that a large craniectomy can lower ICP, but uncertainty remains about whether it improves patient outcomes. It is possible that many of these operations are performed prematurely and/or with inadequate removal of bone (Figure 3). The complications of decompressive craniectomy can also be troubling, including development of contralateral subdural fluid collections and herniation of brain through the craniectomy defect (Figure 4).

Figure 3 Postoperative computed tomography (CT) scan from the patient whose initial CT scan is shown in Figure 1 of the previous chapter. The bone flap was not replaced, but the size of the craniectomy was too small to prevent subsequent midline shift.

Figure 4 Massive herniation of necrotic brain through a craniectomy defect.

Hypothermia

Another potential treatment is hypothermia. The results of the National Acute Brain Injury Study: Hypothermia demonstrated lack of effect when this treatment was applied indiscriminately to all patients.⁹ However, like decompressive craniectomy or any other intervention, it is likely that a specific subpopulation of TBI patients can benefit. The difficulty for investigators and clinicians lies in identifying patients for whom an intervention has the most optimal benefit:risk ratio.

Individualization of Treatment

Although most algorithms recommend that patients be treated according to the same sequence of interventions, patients are in fact unique. Ideally, treatments would be applied not according to an algorithm that forces all patients into the same pathway, but rather according to a patient’s particular metabolic picture. In terms of treating elevated ICP, patients with considerable amounts of cerebral edema might benefit most from osmotic diuretics, those with obstructed CSF flow may need a ventriculostomy, and those with elevated CBF might benefit from mild hyperventilation performed early in their course.

It is highly likely that each of these ICP-lowering treatments represents the optimal intervention for a certain type of patient. Our weakness lies in our inability to identify which treatment represents the best intervention for a given patient at that particular time in a patient’s course. Part of this weakness is explained by the fact that clinical trials in severe TBI have generally enrolled all severe TBI patients, regardless of their pathophysiologic picture. A treatment that may be beneficial in only certain types of patients might not be proven “effective” in a clinical trial because of the background noise from all the other patients who do not benefit. Targeted trials are more difficult to perform, but there appears to be a great need for the type of information that they can provide.

Failure of Intracranial Pressure Prophylaxis

Another important lesson that has been learned over and over again is that treatments for elevated ICP cannot be applied proactively. Doing so is not beneficial and, in fact, may cause harm in many cases. Our natural inclination as clinicians is to try to prevent ICP from rising by aggressively instituting treatments known to lower ICP; we worry that waiting until ICP rises may subject patients to the risk of harm. However, over the years, prophylactic use of hyperventilation, barbiturate coma, pharmacologic paralysis, hypothermia, or blood pressure elevation has been shown in class I or class II studies to have no benefit and, in many cases, to have significant risks. Thus, the best we can do at this time is to monitor patients carefully, to focus on the ABCs (airway, breathing, and circulation) and on prevention of secondary insults, and to intervene promptly when ICP elevation or another adverse event occurs.

Guidelines

Various guidelines for the management of brain-injured patients have enjoyed widespread circulation. Properly constructed, guidelines summarize a review of the literature with a weighting of that literature based on the quality of the design and execution of the reviewed studies. Methodologically solid studies are given a higher classification than trials that are poorly conceived or carried out. The resulting recommendations are weighted accordingly.

Not surprisingly, most clinical decisions have little in the way of randomized, prospective, controlled trials to support them. At the same time, such well-constructed trials are usually designed to answer a specific question in a specific population, and with specified outcome measures. Generalizability of findings to a larger population is often problematic.

These limitations of guidelines suggest that it is unwise to follow their recommendations blindly. Instead, a much more reasoned approach is to integrate evidence-based guidelines with a particular physician’s judgment and experience, with a particular patient’s situation, and with the particular aspects of the environment in which care is being delivered. This approach should avoid unthinking adherence to guidelines while, at the same time, ensuring that they receive serious and appropriate consideration.

Failure of Clinical Trials

Millions of dollars and countless hours of effort have been poured into clinical trials to test drugs and other treatments that were designed to improve outcome after TBI. These have all failed. Analysis of these trials and recommendations for improving the design of future trials have become dynamic fields of inquiry, but such considerations are beyond the scope of this chapter. The lesson learned from these failures is that, for the time being, we must continue to focus on the basics of patient care instead of placing unjustified optimism in the development of a single pharmacologic “cure” for TBI.

MORBIDITY AND COMPLICATIONS

Traumatic brain-injured patients are prone to the same complications as any other trauma patients. These include infections of the respiratory tract, urinary tract, and other body systems, as well as infections of therapeutic devices like central and peripheral venous catheters and arterial lines. Deep venous thrombosis, decubitus ulcers, myocardial infarction, and loss of lean body mass are just a few of the many other adverse events that may develop during a critically ill patient’s prolonged stay in an ICU.

For the most part, these complications are managed just as they would be in a patient without a brain injury. A common temptation is to blame unusual developments on the brain injury by ascribing them to a “central process.” However, that must be a diagnosis of exclusion that is appropriate only after a thorough work-up has eliminated more likely sources.

Some complications are unique to the brain-injured patient. Elevated ICP and its management have already been discussed. Excessive and inappropriate sedation not only impairs accurate neurologic assessment of a patient, but may also unnecessarily subject a patient to the risks of sedation and of a lengthened stay in the ICU.

Prophylaxis against seizures is currently recommended for the first week after injury. After that time, anticonvulsants may be discontinued in patients who have not had a seizure. If seizures occur in a patient who is already receiving anticonvulsants, serum levels of the drug should be checked. Options include administering a bolus and increasing the maintenance dose of the drug, or adding a second agent. The optimal duration of seizure treatment in these patients remains unclear, but certainly treatment is reasonable for at least several months and probably longer.

Rebleeding or delayed intracranial bleeding can be catastrophic (see Figure 2). Some of these events may be caused by suboptimal surgical technique in which inadequate time was spent ensuring that hemostasis was present. Often, however, patients may have a pre-existing history of liver disease, and the trauma itself can predispose to a coagulopathic state. Aggressive use of fresh frozen plasma and sometimes platelets may help achieve hemostasis in patients with persistent diffuse oozing. Recent reports describing the successful use of recombinant factor VIIa in such cases have generated considerable interest.

MORTALITY

Many studies in the trauma literature report outcomes in terms of patient mortality at hospital discharge. This choice of outcome measure is often driven by the data contained in a hospital’s trauma registry. Such an endpoint is an understandable choice for reports about chest and abdominal injuries, from which patients tend to either recover reasonably well or die soon after admission from their initial injuries or from subsequent complications.

Unfortunately, mortality rate at hospital discharge is a poor outcome measure for TBI. Survival is not considered to be a good outcome if a patient will remain in a persistent vegetative state. Most TBI studies have considered death, persistent vegetative state, or severe disability to be a poor outcome, whereas good recovery or moderate disability has been viewed as a good outcome. These outcome categories are based on the Glasgow Outcome Scale (GOS) (Table 1). In addition or instead of the GOS, some studies use more detailed instruments to assess outcome, especially if data are sought about less obvious measures, such as neuropsychological function.

Table 1 Glasgow Outcome Scale

Score	Category	Description
5	Good recovery (GR)	Able to live and work independently despite minor disabilities.
4	Moderate disability (MD)	Able to live independently despite disabilities. Can use public transportation, work with assistance/supervision, and so on.
3	Severe disability (SD)	Conscious but dependent on others for self-care. Often institutionalized.
2	Persistent vegetative state (PVS)	Not conscious, but may appear “awake.”
1	Death (D)	Self-explanatory.

The timing of outcome assessment is important. A patient who begins to recover quickly may have a high level of function upon discharge from the acute care hospital, which may take place just a week or two after injury. Another patient who is transferred early to a long-term care facility or to a rehabilitation hospital may have a low level of function upon leaving the acute care hospital. Yet at 6 months after injury, both these patients may have comparable levels of function if the second patient makes gradual progress. Recovery from brain injury may continue for several years. For practical reasons, most TBI studies collect outcome data at 6 months.

Some recent studies report quite good outcomes after TBI, with mortality rates of approximately 20% or lower. However, many of these studies did not enroll patients with a Glasgow Coma Scale score of 3, with fixed and dilated pupils, or with other findings to suggest that they were unlikely to have a good recovery. The Traumatic Coma Data Bank, which enrolled all patients who presented to four academic centers, included 753 patients. Approximate outcomes were as follows: 27% good recovery, 16% moderate disability, 16% severe disability, 5% persistent vegetative state, and 36% mortality.¹⁰ Current experience suggests that these percentages remain valid today. However, these data were collected in the 1980s. Because of subsequent advances in emergency medical services systems and in neurocritical care, it might be interesting to collect such data again to see if these advances have resulted in a noticeable improvement in outcomes.

Penetrating Brain Injury

Most penetrating brain injuries are caused by gunshot wounds to the head. The vast majority of these result in death before the patient ever reaches the hospital, and most studies indicate that the majority of patients who reach the hospital alive proceed to die. On the other hand, among survivors, there is a reasonable likelihood of reaching a good outcome.

Some authors recommend that heroic measures not be instituted in patients with a GCS score of 3 or 4, and perhaps for a score of 5 as well. Others, however, report that good outcomes can occasionally be attained by patients whose initial neurologic examination was quite poor. Thus, they advocate uniformly aggressive resuscitation and stabilization of these patients. The extent of surgical intervention that is necessary varies from extensive craniotomy and reconstruction to simple debridement that can be accomplished at the bedside.

It is important to remember that the possibility of organ donation represents the only good thing that can come from many of these often tragic cases.

CONCLUSIONS AND ALGORITHM

Figure 5 lists some basic principles and goals in the management of TBI patients. As always, the main goal remains the avoidance of secondary insults. The best monitor is a reliable neurologic examination repeated at regular intervals. Patients who do not obey commands may require monitoring of ICP and other parameters to facilitate prompt detection of adverse metabolic events. Generic algorithms are available for the treatment of intracranial hypertension (see Figure 1). Patient-specific interventions may supplement or replace these algorithms if monitoring data suggest the existence of particular pathophysiologic patterns in given patients.