Closed Head Injury Treatment & Management

Updated: Feb 24, 2016
  • Author: Leonardo Rangel-Castilla, MD; Chief Editor: Brian H Kopell, MD  more...
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Medical Care

Intracranial hypertension is a common neurologic complication in patients who are critically ill. Intracranial hypertension is the common pathway in the presentation of traumatic head injury. The underlying pathophysiology of increased intracranial pressure (ICP) is the subject of intense basic and clinical research, which has led to advances in the understanding of the physiology related to ICP. Few specific treatment options for intracranial hypertension have been subjected to randomized trials, however, and most management recommendations are based on clinical experience.

Normal values of intracranial pressure

In healthy individuals with closed cranial fontanelles, central nervous systems contents, including brain, spinal cord, blood, and cerebrospinal fluid (CSF), are encased in a noncompliant skull and vertebral canal, constituting a nearly incompressible system. In the average adult, the skull encloses a total volume of 1450 mL: 1300 mL of brain, 65 mL of CSF, and 110 mL of blood. The Monroe-Kellie hypothesis states that the sum of the intracranial volumes of blood, brain, CSF, and other components is constant, and that an increase in any one of these must be offset by an equal decrease in another.

The reference range of ICP varies with age. Values for pediatric subjects are not as well established. Normal values are less than 10-15 mm Hg for adults and older children, 3-7 mm Hg for young children, and 1.5-6 mm Hg for term infants. ICP can be subatmospheric in newborns. ICP values greater than 20-25 mm Hg require treatment in most circumstances. Sustained ICP values of greater than 40 mm Hg indicate severe, life-threatening intracranial hypertension.

Cerebral dynamics overview

Cerebral perfusion pressure (CPP) depends on the mean systemic arterial pressure (MAP) and ICP, which is determined by the following relationship:

CPP = MAP – ICP where MAP = (1/3 systolic BP) + (2/3 diastolic BP)

As a result, CPP can be reduced from an increase in ICP, a decrease in blood pressure, or a combination of both factors. Through the normal regulatory process called pressure autoregulation, the brain is able to maintain a normal cerebral blood flow (CBF) with a CPP that ranges from 50-150 mm Hg. At CPP values less than 50 mm Hg, the brain may not be able to compensate adequately, and CBF falls passively with CPP.

After injury, the ability of the brain to autoregulate may be absent or impaired. When CPP is within the normal autoregulatory range (50-150 mm Hg), this ability of the brain to pressure autoregulate also affects the response of ICP to a change in CPP. When pressure autoregulation is intact, decreasing CPP results in vasodilation, which allows the CBF to remain unchanged. This vasodilation can result in an increase in ICP. Likewise, an increase in CPP results in the vasoconstriction of cerebral vessels and may reduce ICP. When pressure autoregulation is impaired or absent, ICP decreases and increases with changes in CPP. [57]

Perhaps the least invasive method of lowering ICP is to elevate the head of the patient to 30°. Some researchers have demonstrated improved ICP control with elevation (head of bed) to 45°, but recent evidence from using multimodality monitoring has suggested a 30° head elevation for maximum benefits. [26] Note that head elevation may reduce cerebral perfusion, even as it lowers ICP.

Hyperventilation became a popular means of reducing ICP in the 1970s. However, recent studies raise concern that aggressive hyperventilation exacerbates cerebral ischemia. One study shows that patients who were hyperventilated to a PCO2 level of 25 mm Hg had worse outcomes than patients who were kept at a nearly normal PCO2 level. [50] In addition, in most patients, hyperventilation is not necessary to control ICP. [58, 59, 33, 60] Currently, hyperventilation (PCO2 of 30-35 mm Hg) is recommended to reduce ICP for only a short period, as a temporizing measure while other methods of ICP control are initiated. Hyperventilation reduces ICP only temporarily, progressively losing effectiveness after 16 hours of continuous use. [61]

Mannitol probably has several mechanisms of action. One obvious mechanism is through osmotic diuresis via drawing edema from the cerebral parenchyma. This usually takes 15-30 minutes, and the effect usually lasts 1.5-6 hours. Another mechanism is by immediate plasma expansion and decreased blood viscosity, thereby improving blood flow and eventually resulting in intracranial vasoconstriction in an attempt to maintain constant blood flow. This vasoconstriction ultimately leads to decreased intracranial volume (Monroe-Kelly hypothesis) and decreased ICP. [62, 63] Mannitol is also considered a free radical scavenger. [64] Administration of this drug in severe traumatic brain injury patients studied both with jugular bulb oxygen saturation [65] as well as with multimodal brain monitoring [66] suggests a potential change in the internal milieu that would improve cerebral oxygenation.

Serial serum osmolarity levels must be checked to maintain an osmolarity of no greater than 315-320 mOsm/kg H2 O to avoid acute renal failure. Some studies have raised concern that the early use of mannitol can lead to hypotension, with an associated worse outcome. [67] For this reason, patients treated with mannitol must be kept euvolemic with isotonic fluid resuscitation as required.

Although some evidence suggests that barbiturates may be effective in lowering refractory ICP, such administration often causes depressed myocardial function and CPP. [45] These drugs often have an associated morbidity and do not significantly change outcome. [68, 11]

A barbiturate-induced coma with EEG burst suppression is often a "last ditch effort" to reduce the ICP and should be reserved only for patients with refractory ICP who are unresponsive to other measures. One may even consider decompressive craniectomy prior to the use of barbiturates. Barbiturate serum levels are a poor estimate of therapeutic effect and should not be followed for treatment purposes. For this reason, all patients should have EEG monitoring to monitor for induced burst suppression. A loading dose of pentobarbital can be administered as a 10 mg/kg bolus (over 30 min), followed by 5 mg/kg/h for 3 doses, titrated to a low level of bursts per minute (2-5). Barbiturates are contraindicated in hypotensive patients.

One must give special attention to preventing hypotension. [25, 35] Data from the Traumatic Coma Data Bank (TCDB) reveal that hypotension in patients with severe TBI increases the mortality rate from 27% to 50%. [26] Traditional management has included fluid restriction in order to minimize cerebral edema, but this practice may be dangerous in patients who already have intravascular volume depletion.

Cerebral edema may occur regardless of the amount of intravenous fluid administered, and hypervolemia, per se, does not cause brain edema if the serum sodium level and osmolarity are within normal limits. [26] However, managing patients who have closed head injuries with liberal amounts of hypotonic intravascular fluid may cause intracerebral hemorrhages to blossom. Smaller amounts of hypertonic solutions may be equally effective without the risk of fluid overload. [69, 70] The ultimate goal of the management of patients with closed head injuries is to maintain a state of euvolemia. In a euvolemic patient who is hemodynamically stable, two-thirds maintenance of isotonic solution is recommended. Avoid hypotonic fluids because they may decrease serum osmolarity and increase brain swelling.

In addition, patients with closed head injuries are prone to acute coagulopathies. These coagulopathies are often the result of release of thromboplastin and tissue-activating protein from injured brain tissue. The release of these proteins leads to abnormal intravascular clotting, which consumes clotting factors, platelets, and fibrinogen and ultimately results in elevated PT and aPTT. In patients with acute intracranial hemorrhages, these coagulopathies must be addressed and corrected promptly.

Fresh frozen plasma (FFP) transfusions until the coagulopathy is corrected is the preferred method. This is especially true for individuals who are taking anticoagulants (eg, warfarin) and who are at high risk of continued bleeding. Winter and colleagues have shown that prophylactic FFP administration in individuals with closed head injuries is of no benefit. [71] Vitamin K plays an important role in correcting the coagulopathy; however, it usually takes 24-48 hours to be activated. During this interval, the patient's intracranial hemorrhage is likely to worsen. Recombinant activated factor VII (rFVIIa) is a relatively new pharmaceutical agent developed for use in patients with hemophilia in whom inhibitors to clotting factors VIII or IX have developed.

The use of rFVIIa in neurosurgery has lagged behind its use in other fields, although the body of literature on such uses is growing. Various uses are pertinent to the neurosurgeon, including the treatment of patients with coagulation disorders, those patients who have experienced trauma, and those patients with perioperative hemorrhage, intracerebral hemorrhage, or subarachnoid hemorrhage. rFVIIa is a safe and effective agent with the potential to revolutionize the treatment of neurosurgical patients with hemorrhage. Cost is a major impediment to the widespread use of rFVIIa, and some evidence suggests that its use in the neurosurgical population may be subject to higher risk than in other populations studied thus far. Although further study is needed to better delineate the safety and efficacy of the drug, rFVIIa is clearly an agent with tremendous promise. [72] In placebo-controlled trials, the off-label use of rFVIIa in high doses increased the risk of arterial events but not venous thromboembolicevents, particularly among older patients. [73] Until more clinically significant data emerge, caution should be exercised when using rFVIIa in off-label settings. [74]

Pyrexia commonly occurs in patients with head injuries, possibly because of posttraumatic inflammation, direct damage to the hypothalamus, or secondary infection. The most common cause is fever secondary to an underlying infection. Less common is an unexplained fever or "neurogenic" fever estimated to occur in approximately 8% of patients who have head injuries with pyrexia. [75] Regardless of the cause of the elevated temperature, pyrexia alone increases metabolic expenditure, glutamate release, and neutrophil activity, while causing blood-brain barrier breakdown.

Pyrexia is also thought to exacerbate oxygen radical production and cytoskeletal proteolysis. [76, 77] These changes may further compromise the injured brain and worsen neuronal damage. For this reason, the source of the fever must be identified and corrected.

Although the source of the infection is sought, maintain body temperature in a normothermic range with acetaminophen. However, despite sound physiological justification for treating fever in brain-injured patients, no evidence indicates that doing so improves outcome.

Hyperglycemia has also been shown to have a detrimental effect on induced brain ischemia. Clinical trials support the correlation between hyperglycemia and poor overall outcome in patients with head injuries and recommend that euglycemia be maintained at all times. [78]

Some patients with severe head injuries may develop hypertension, either from an exacerbation of a chronic process or as a result of the head injury. Keep systolic blood pressure less than 180 mm Hg, particularly in patients who have an intracranial hemorrhage. This value requires adjustment for patients with a history of uncontrolled hypertension. If possible, avoid nitroprusside because it is a cerebral vasodilator and may actually increase ICP. A nicardipine grip is preferred in patients whose blood pressure is difficult to control. Corticosteroids have occasionally been used but have no proven benefit for patients with severe head injuries. [11]

Effective treatment of intracranial hypertension involves the meticulous avoidance of factors that precipitate or aggravate increased ICP. When ICP becomes elevated, ruling out new mass lesions that should be surgically evacuated is important. Medical management of increased ICP should include sedation and paralysis, drainage of CSF, and osmotherapy with either mannitol or hypertonic saline. For intracranial hypertension refractory to initial medical management, barbiturate coma, hypothermia, or decompressive craniectomy should be considered. Steroids are not indicated and may be harmful in the treatment of intracranial hypertension that results from TBI. [57]


Surgical Care

As a general rule, indications for surgery include any intracranial mass lesion that causes significant or progressive neurological compromise, particularly a decreased level of consciousness. The overall outcome of individuals with an intracranial lesion that causes significant mass effect is improved with rapid decompression; therefore, operating on these patients as soon as possible is advisable.

Before operating, one must always consider the patient's condition and refrain from relying solely on radiographic evidence. For example, some patients with severe cerebral atrophy (eg, elderly patients) may accommodate a large intracranial hemorrhage, whereas most young individuals may experience neurological deficits with relatively smaller intracranial hemorrhages. Note that some intracranial hemorrhages may be actively bleeding during the initial head CT scan; what may appear as relatively small on the initial scan may actually become quite significant in a short period of time. In this case, the patient's physical examination findings are more valuable in evaluating his or her intracranial status than the initial head CT scan findings.

Some authors have suggested a decompressive craniotomy (ie, removal of a bone flap with or without dural opening) to provide more space for the brain to expand, for the treatment of uncontrollable ICPs before irreversible ischemic brain damage has occurred. The role of decompressive craniotomy in the absence of compressive pathology (such as subdural hematoma) in patients with closed head injuries has not been well documented. Most authors, however, agree that children benefit more from decompressive craniotomies than adults, and some authors are advocates of very early decompressive craniotomies for uncontrollable ICP in children. [79] It seems clear that older individuals, particularly those older than 50 years, do less well with elective decompressive craniotomies. [80, 81]

One study investigated complications associated with the use of a dural substitute, the Neuro-Patch, during decompressive craniectomy. Results suggested that it has not been found to increase the incidence of neurosurgical site infection and hydrodynamic complications, including subdural hygroma and cerebrospinal fluid leakage, following decompressive craniectomy or cranioplasty for severe TBI. However, patients with the Neuro-Patch more often encounter extra-axial hematoma at the site of craniectomy, which forms a compressive lesion on the adjacent brain. [82]

A metaanalysis of 2 randomized controlled trials, despite a relatively small number of patients, convincingly and strongly suggested that the early induction of hypothermia to and below 35°C for 48 h before or soon after craniotomy improves outcomes in patients with intracranial hematomas after severe traumatic brain injury. The study is trendsetting rather than a recommendation and requires confirmation by a prospective clinical trial. [83]

Despite the poor overall prognosis of patients with closed head injury and bilateral fixed and dilated pupils, one study suggested that a good recovery may be possible if an aggressive surgical approach is taken, particularly those with extradural hematoma. Of 82 patients who underwent surgery for extradural or subdural hematoma, in those with extradural haematoma, the mortality rate was 29.7%, with a favorable outcome seen in 54.3%. In patients with acute subdural haematoma, the mortality rate was 66.4%, with a favorable outcome seen in 6.6%. [84]



Obtain consultations as necessary for other accompanying injuries (eg, plastic surgeons for facial lacerations), realizing that the patient's closed head injury takes precedence over all other non—life-threatening injuries once the patient is stabilized.



Before, physicians thought that patients with closed head trauma should be on NPO status. Now, the new modality is to provide nutrition as soon as possible. The consequences of hypermetabolism, hypercatabolism, and an altered immune function are part of the response to traumatic head injury. Once a person with acute traumatic brain injury develops this hyperdynamic state, the resultant excessive protein breakdown ensues. This can lead to malnutrition. Lack of nutrient supplementation in these patients is associated with increased morbidity and mortality. Enteral nutrition is the preferred mode of feeding but is often not tolerated in the patient with head injury. Parenteral nutritional support can be given to these patients without worsening cerebral edema. [85]



The patient should be prescribed bed rest.