Closed Head Injury Treatment & Management

Updated: May 04, 2022
  • Author: Leonardo Rangel-Castilla, MD; Chief Editor: Brian H Kopell, MD  more...
  • Print

Medical Care

Intracranial hypertension is a common neurologic complication among patients who are critically ill. Intracranial hypertension is the common pathway in the presentation of traumatic head injury. The underlying pathophysiology of increased ICP is a topic of intense basic and clinical research; this has led to advances in our 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.

An anticonvulsant regimen should be started for patients with moderate or severe head injury. Administration should cease if no seizure activity occurs within the first 7 days after injury. For patients who have seizure activity during this time period, or who have undergone surgical procedures, one may opt to continue anticonvulsants for 6-12 months.

Consultations should be obtained as necessary for other accompanying injuries (eg, plastic surgeons for facial lacerations), with awareness that the patient's closed head injury takes precedence over all other non–life-threatening injuries.

Normal values of intracranial pressure

For 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 children are not well established. Normal values are less than 10-15 mm Hg for adults and for older children, 3-7 mm Hg for young children, and 1.5-6 mm Hg for term infants. Intracranial pressure can be subatmospheric in newborns. Patients with ICP values greater than 20-25 mm Hg require treatment in most circumstances. Sustained ICP values greater than 40 mm Hg indicate severe, life-threatening intracranial hypertension.

Cerebral dynamics overview

Cerebral perfusion pressure (CPP) depends on mean systemic arterial pressure (MAP) and ICP and 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 maintains normal cerebral blood flow (CBF), with CPP ranging from 50 to 150 mm Hg. At CPP values less than 50 mm Hg, the brain may not be able to compensate adequately and CBF may fall 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), the ability of the brain to autoregulate pressure 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 vasoconstriction of cerebral vessels and may reduce ICP. When pressure autoregulation is impaired or absent, ICP decreases and increases with changes in CPP. [64]

Treatment considerations

Elevate the head of the patient to 30° (this may be the least invasive method of lowering ICP). Some researchers have demonstrated improved ICP control with elevation (head of bed) to 45°, but evidence from use of multimodality monitoring has suggested 30° head elevation for maximum benefit. [21] Note that head elevation may reduce cerebral perfusion, even as it lowers ICP.

Provide hyperventilation. The goal is to maintain PaCO2 between 35 and 45 mm Hg. Judicious hyperventilation helps to reduce PaCO2 and causes cerebral vasoconstriction. [7]  Note that aggressive hyperventilation may exacerbate cerebral ischemia to the point that secondary brain injury may occur. One study shows that patients who were hyperventilated to a PCO2 level of 25 mm Hg had worse outcomes than those kept at a nearly normal PCO2 level. [57] In addition, for most patients, hyperventilation is not necessary to control ICP. [29, 65, 66, 67] Hyperventilation reduces ICP only temporarily, progressively losing effectiveness after 16 hours of continuous use. [68]

Consider administering mannitol. This agent 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. [69, 70] Mannitol is also considered a free radical scavenger. [71] Administration of this drug to patients with severe TBI both with jugular bulb oxygen saturation [72] and with multimodal brain monitoring [73] suggests a potential change in the internal milieu that would improve cerebral oxygenation.

Check serial serum osmolarity levels to maintain osmolarity no greater than 315-320 mOsm/kg H2O to avoid acute renal failure. Some studies have raised concern that early use of mannitol can lead to hypotension, with an associated worse outcome. [74] For this reason, patients treated with mannitol must be kept euvolemic with isotonic fluid resuscitation as required.

Some evidence suggests that barbiturates may be effective in lowering refractory ICP; however, such administration often causes depressed myocardial function and CPP. [51] These drugs often have associated morbidity and do not significantly change outcomes. [75, 76]

  • Barbiturate-induced coma with electroencephalographic (EEG) burst suppression is often a "last ditch effort" to reduce ICP and should be reserved for patients with refractory ICP who are unresponsive to other measures. One may even consider decompressive craniectomy before using barbiturates. Barbiturate serum levels represent a poor estimation of therapeutic effect and should not be followed for treatment purposes. For this reason, all patients should have EEG monitoring for induced burst suppression. A loading dose of pentobarbital can be administered as a 10-mg/kg bolus (over 30 minutes), 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.

Give special attention to preventing hypotension. [20, 31] Data from the Traumatic Coma Data Bank (TCDB) reveal that hypotension in patients with severe TBI increases mortality from 27% to 50%. [21] Traditional management has included fluid restriction to minimize cerebral edema, but this practice may be dangerous for 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 serum sodium level and osmolarity are within normal limits. [21] However, treating patients with 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 risk of fluid overload. [77, 78] The ultimate goal in treating patients with closed head injuries is to maintain a state of euvolemia. For a euvolemic patient who is hemodynamically stable, two-thirds maintenance of isotonic solution is recommended. Hypotonic fluids should be avoided because they may decrease serum osmolarity and increase brain swelling.

Patients with closed head injury are prone to acute coagulopathies. These coagulopathies are often the result of release of thromboplastin and tissue-activating protein from injured brain tissue. Release of these proteins leads to abnormal intravascular clotting, which consumes clotting factors, platelets, and fibrinogen and ultimately results in elevated prothrombin time (PT) and activated partial thromboplastin time (aPTT). For patients with acute intracranial hemorrhage, these coagulopathies must be addressed and corrected promptly.

  • Fresh frozen plasma (FFP) transfusions until coagulopathy is corrected is the preferred method. This is especially true for individuals who are taking anticoagulants (eg, warfarin) and are at high risk of continued bleeding. Winter and colleagues showed that prophylactic FFP administration in individuals with closed head injury confers no benefit. [79] 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.

  • Use rFVIIa to treat patients with coagulation disorders, those who have experienced trauma, and those 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 widespread use of rFVIIa, and 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 this drug, rFVIIa is clearly an agent with tremendous promise. [80] In placebo-controlled trials, off-label use of rFVIIa in high doses increased the risk of arterial events but not venous thromboembolic events, particularly among older patients. [81] Until more clinically significant data emerge, caution should be exercised when rFVIIa is used in off-label settings. [82]

Pyrexia commonly occurs in patients with head injuries, possibly because of posttraumatic inflammation, direct damage to the hypothalamus, or secondary infection. Fever should be avoided, as it increases cerebral metabolic demand and affects ICP. [7]  While the source of the infection is sought, maintain body temperature in a normothermic range with acetaminophen.

  • The most common cause is fever secondary to underlying infection. Less common is unexplained fever or "neurogenic" fever, which is estimated to occur in approximately 8% of patients who have head injuries with pyrexia. [83] 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. [84, 85] These changes may further compromise the injured brain and may worsen neuronal damage. For this reason, the source of the fever must be identified and corrected.
  • Despite sound physiologic justification for treating fever in brain-injured patients, no evidence indicates that doing so improves outcome.

Hyperglycemia has 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. [86]

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 for patients whose blood pressure is difficult to control. Corticosteroids have been used occasionally but have no proven benefit for patients with severe head injuries. [76]

  • Effective treatment of intracranial hypertension involves 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. [64]

Surgical Care

As a general rule, indications for surgery include any intracranial mass lesion that causes significant or progressive neurologic 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, it is advisable to operate on these patients as soon as possible.

Before operating, one must always consider the patient's condition and must 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 neurologic 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 than initial CT scan findings in evaluating his or her intracranial status.

Some authors have suggested a decompressive craniotomy/craniectomy (ie, removal of a bone flap with or without dural opening) to provide more space for the brain to expand, for treatment of uncontrollable ICPs before irreversible ischemic brain damage has occurred. The role of decompressive craniotomy/craniectomy in the absence of compressive pathology (such as subdural hematoma) for patients with closed head injuries has not been well documented. However, most authors agree that children benefit more from decompressive craniotomy/craniectomy than adults, and some authors are advocates of very early decompressive craniotomy/craniectomy for uncontrollable ICP in children. [87] It seems clear that older individuals, particularly those older than 50 years, do less well with elective decompressive craniotomy/craniectomy. [88, 89]

One study investigated complications associated with use of a dural substitute, the Neuro-Patch, during decompressive craniectomy. Results suggest that it has not been found to increase the incidence of neurosurgical site infection and hydrodynamic complications, including subdural hygroma and CSF 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. [90]

Despite inclusion of a relatively small number of patients, a meta-analysis of 2 randomized, controlled trials convincingly and strongly suggests that early induction of hypothermia to and below 35°C for 48 hours before or soon after craniotomy improves outcomes for patients with intracranial hematoma after severe TBI. This study is trendsetting rather than definitive, and confirmation by a prospective clinical trial is required. [91]

Despite the poor overall prognosis of patients with closed head injury and bilateral fixed and dilated pupils, one study suggests that good recovery may be possible if an aggressive surgical approach is taken, particularly for those with extradural hematoma. Of 82 patients who underwent surgery for extradural or subdural hematoma, among those with extradural hematoma the mortality rate was 29.7%, with a favorable outcome seen in 54.3%. For patients with acute subdural hematoma, the mortality rate was 66.4%, with a favorable outcome in 6.6%. [92]



Historically, physicians believed that patients with closed head trauma should be on NPO status. However, this thinking has changed, and the current goal for patients with TBI is to provide nutrition as soon as possible after injury. The consequences of hypermetabolism, hypercatabolism, and altered immune function are part of the response to traumatic head injury. Once a person with acute TBI develops this hyperdynamic state, 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 often is not tolerated by the patient with head injury. Parenteral nutritional support can be given to these patients without worsening of cerebral edema. [93]