Head Injury Treatment & Management

Updated: Sep 29, 2016
  • Author: David A Olson, MD; Chief Editor: Stephen A Berman, MD, PhD, MBA  more...
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Medical Care

Acute management

In the setting of acute head injury, give priority to the immediate assessment and stabilization of the airway and circulation. Despite the fact that prehospital intubation has become common, at least one study has reported a higher rate of mortality in patients intubated in the field than in those intubated in the hospital setting. In this study, however, more critically ill patients required in-field intubation. [27]

Following stabilization, direct attention to prevention of secondary injury. Keep mean arterial pressures above 90 mm Hg; arterial saturations should be greater than 90%. Urgent CT scanning is a priority.

Next, focus attention on reducing intracranial pressure, since elevated intracranial pressure is an independent predictor of poor outcome. If the intracranial pressure rises above 20-25 mm Hg, intravenous mannitol, CSF drainage, and hyperventilation can be used. Hypertonic saline has also been used in lieu of mannitol to lower intracranial pressure, but a recent meta-analysis found no evidence of diminished mortality or improved ICP control with this treatment. [95]  More definitive studies are obviously needed. [96] If the intracranial pressure does not respond to these conventional treatments, high-dose barbiturate therapy is permissible, despite the fact that no evidence currently suggests that barbiturate treatment actually improves outcomes. (Its blood pressure–lowering effects may be detrimental.) [10]

Interestingly, a 2008 study utilizing the National Trauma Data Bank retrospectively uncovered a 45% reduction in survival in patients who underwent intracranial pressure monitoring. [97] These results had been called into question because of a dearth of clinical and neuroimaging data, but a 2012 prospective study of 2134 patients with severe traumatic brain injury found improved 2-week survival in patients who underwent ICP monitoring compared to those who were not monitored. Nevertheless, the non-monitored patients may have had a more grave prognosis to start with because they were significantly older and more likely to have had pupillary abnormalities, factors which could have impacted the treating physicians' decision to implement ICP monitoring. [98]

Another approach used by some clinicians is to focus primarily on improving cerebral perfusion pressure as opposed to intracranial pressure in isolation. One study reported that 80% of patients with severe head injuries experienced recoveries with no or little disability after volume expansion, mannitol, CSF drainage, and vasopressors were used to maintain a cerebral perfusion pressure of at least 70 mm Hg. [99] Other studies have found higher perfusion pressures were associated with more complications and have recommended maintaining a cerebral perfusion pressure of 50-70 mm Hg. [100]

The question whether saline or albumin fluid resuscitation would maximize cerebral perfusion pressure and lead to improve outcomes lead to a large, double-blind, randomized controlled study of 460 patients with Glasgow Coma Scale scores < 13 who also had abnormal head CT scan results. A post-hoc 2-year follow-up demonstrated increased mortality in those receiving albumin as opposed to saline. [101]

Although hypothermic therapy initially appeared promising, and despite the fact that hypothermia decreases intracranial pressure, a large randomized study of 392 patients with head injuries recently demonstrated that hypothermic therapy does not improve outcomes. In addition, a post-hoc analysis found that the rewarming of patients with head injury who arrived in the emergency department already hypothermic was likely detrimental. [102] Furthermore, a current review of 23 randomized, controlled trials concluded that this therapy was of no benefit. [103]

Although acute hypothermic treatment has been found to worsen outcomes in patients with diffuse head injuries, it may improve outcomes in patients with surgically-evacuated hematomas. This indicates a potential benefit in this subgroup; however, further prospective studies are needed. [104]  Current opinion holds that therapeutic hypothermia administration should be reserved only for clinical trials. [105]

Head injury induces a hypermetabolic state and early nutritional interventions may be as critical as cerebral perfusion pressure. Parental or enteral feedings reduced mortality by at least 50% in one study when given early in the course of severe head injury. [106]

As mentioned previously, head injury may alter coagulation parameters, and this can raise the risk of deep venous thrombosis to as much as 15% if no pharmacologic prophylaxis is given within the first 48 hours. [107] The risk of extension of intracranial bleeding needs to be balanced with the benefits of thromboembolic prevention. A retrospective review suggested that early prophylaxis is safe because there was no difference between intracranial hemorrhage progression in patients with head injury who received enoxaparin or heparin within the first 3 days versus later in the course of their hospitalization. [108] Further studies, of course, are required.

Steroids have demonstrated no benefit in the treatment of acute head injury. A 2004 multicenter European randomized trial of steroids versus placebo found a higher mortality after only 2 weeks in the steroid-treated patients. [109]

Phenytoin has demonstrated efficacy in controlling early posttraumatic seizures, but mortality rates, surprisingly, were unaffected by this benefit. In 1 study, approximately 2.5% of patients treated with phenytoin had an allergic reaction to the drug during the first 2 weeks of therapy. [110] A trial of valproate in early seizure prophylaxis showed a trend toward an increased mortality rate. Because of its relatively benign side-effect profile, levetiracetam has been increasingly employed to prevent post-traumatic seizures, but its efficacy has not been empirically validated. [111] Anticonvulsant therapy, if used, should be discontinued after 1–2 weeks unless further seizures supervene. [112]

Finally, as stated previously, neuroprotective agents mostly have failed to improve the outcomes of patients with brain injury. However, the calcium channel blocker nimodipine was successful in reducing rates of death and severe disability when instituted acutely in patients with head injuries and traumatic subarachnoid hemorrhages, despite its failure to improve outcomes in 2 large trials of patients with all types of traumatic intracranial injuries. [113]

Although numerous synthetic neuroprotective agents are under development, several existing substances have shown promise, but other agents have been disappointing.

Because of its excitotoxic blocking properties, magnesium chloride has been used to reduce cortical injury in experimentally brain-injured rats. Unfortunately, a human double-blind study of 499 patients with moderate or severe head injury failed to show benefit; the magnesium-treated patients actually did worse. One potential confounder in this study was vigilance and aggressive repletion of hypomagnesemia in controls. [114]

Although promising in rodents, in a recent pair of randomized, controlled multicenter studies, the neurosteroid progesterone showed no beneficial effect on functional outcomes in patients with acute traumatic brain injury. [115, 116, 117, 118]

The first trial, the double-blind PROTECT (Progesterone for the Traumatic Brain Injury, Experimental Clinical Treatment) III study in patients with severe to moderate acute traumatic brain injury, found no significant difference in favorable outcomes between treatment and placebo groups; the trial was halted after enrollment of 882 of 1140 planned participants. [115]  Subjects in the progesterone group had higher rates of phlebitis or thrombophlebitis than those in the placebo group. In the second study, SYNAPSE (the Study of a Neuroprotective Agent, Progesterone, in Severe Traumatic Brain Injury), 1195 patients with severe traumatic brain injury were assigned to receive either progesterone or placebo. [116]  Similar rates of favorable outcomes and mortality were observed in the two groups.

Experimental brain injury creates permeability in mitochondrial membranes, which contributes to cell death by causing calcium effluxes and energy depletion. Cyclosporin inhibits mitochondrial permeability and has been used in a phase II study of patients with traumatic brain injuries. Further trials are planned. [119]

More conventional agents have also included propranolol in a large, non-randomized prospective trial. When initiated within the first 24 hours in patients with moderate to severe head injuries, propranolol significantly reduced mortality, presumable by blocking the catecholamine surge that accompanies the initial injury. [120]  A recent randomized trial of erythropoetin also showed promising effects with 33% of treated severely head-injured patients exhibiting a good recovery compared to only 13% of controls. [121]

Cannabinoids also protect against excitotoxicity, but disappointingly, in a recent phase 3 trial, dexanabinol, a weak N -methyl-D-aspartic acid (NMDA) antagonist, showed no efficacy in outcome improvement when given within 6 hours to patients with severe closed head injuries. [122] More encouraging but less rigorous was a retrospective analysis of traumatic brain-injured patients that found decreased mortality among those patients with THC in their urine compared to those without this substance. [123]

Rosuvastatin given in the acute phase of moderate head injury significantly reduced amnesia in a double-blind placebo-controlled study of 34 patients. [124]

Animal studies of some health food supplements may lead to new directions. The dietary supplement creatine, when fed to rats for 4 weeks prior to an experimental brain injury, reduced cortical damage by 50%, primarily through stabilizing mitochondrial functioning. [125]  Furthermore, an open-label study of children and adolescents with traumatic brain injuries reported not only a shortened duration of post-traumatic amnesia but also reduced subjective symptoms in those treated with oral creatine for 6 months compared to those not treated. [126]  Melatonin is a free-radical scavenger, and when injected early in brain-injured rats, it significantly reduced levels of lipid breakdown products. [127]

Long-term management

Hypertonicity from spasticity or dystonia with attendant muscle spasms is often disabling. Although dantrolene, baclofen, diazepam, and tizanidine are current oral medication approaches to this problem, baclofen and tizanidine are customarily preferred because of their more favorable side effect profiles.

When using these agents, careful evaluation of functional status and symptom relief is a priority since adverse effects such as sedation may be pronounced.

Intrathecal baclofen is a newer approach with reported efficacy and minimal adverse effects. One study of 17 patients with traumatic brain injuries showed improved motor tone and decreased muscle spasms with intrathecal baclofen, but whether these benefits will translate into improved functioning remains unknown. [128]

Botulinum toxin also has shown promise in decreasing hypertonia in patients with head injuries, primarily by improving passive range of motion rather than by decreasing functional disability. [129, 130]

Solid data on cognitive enhancing medications for patients with head injury are lacking. Typically, only small numbers of subjects have been used and demonstrable functional improvement has been only marginally convincing.

Despite these drawbacks, one double-blind, placebo-controlled study of methylphenidate demonstrated improved motor outcomes and attention in patients with head injuries during active treatment, but only 6 patients completed each 30-day treatment arm. [131] A 2006 double-blind, placebo-controlled study of 18 patients with closed head injuries treated with a single dose of 20 mg of methylphenidate achieved significant improvement in reaction times on a working memory test, but no other cognitive tasks significantly benefited. [132]

Donepezil treatment significantly improved visual and verbal memory as well as attentional deployment in 18 patients with head injuries of all levels of severity in a 2004 double-blind, placebo-controlled study. [133] Other less rigorous studies have also reported cognitive improvements in donepezil-treated, head-injured patients. [134]

Anecdotal reports exist of dramatic alerting responses to both levodopa and methylphenidate in patients with vegetative or comatose states. Levodopa treatment has also resulted in improvement in patients with akinesia and rigidity secondary to traumatic substantia nigral damage. [135] Furthermore, levodopa has even produced qualitative cognitive improvements in a small number of head-injured patients. [136]

Emotional lability and the pathologic laughing and crying associated with pseudobulbar palsy reportedly have responded rapidly and exquisitely to not only selective serotonin reuptake inhibitors but also possibly to dextromethorphan with quinidine. [137, 138]  Sertraline has shown efficacy in depression in mild head injury. [139] Treat other possible psychiatric complications of head injury on a patient-by-patient basis, since no extensive pharmacologic trials of this dimension of head injury have been conducted.

Nonmedical therapy

Although a full review of nonmedical therapies is beyond the scope of this article, some promising new developments have occurred in both physical and cognitive therapies.

Constraint-induced movement therapy is a form of physical therapy that emphasizes using the paralyzed arm and minimizes reliance on the unaffected extremity (patients commonly wear mittens on their unaffected arm for several hours a day). This form of treatment has resulted in significantly improved function of the paralyzed arm when used in small numbers of brain-injured patients 1-6 years after their injury. [140]

In a randomized trial in 120 military personnel with moderate-to-severe head injuries, in-hospital cognitive rehabilitation proved unsuccessful compared to a limited in-home program, but a subgroup post hoc analysis indicated that patients with unconsciousness lasting 1 hour or more had a greater functional recovery with in-hospital cognitive rehabilitation than those in the control group. [141]


Surgical Care

Traditionally, the prompt surgical evacuation of subdural hematomas in less than 4 hours was believed to be a major determinant of an optimal outcome. Indeed, a recent publication found a delay in surgery for acute subdural hematomas of over 5 hours was associated with increased mortality. [142] Nevertheless, other recent investigations have emphasized that the extent of the original intracranial injury and the generated intracranial pressures may be more important than the timing of surgery.

  • For example, 70% of 83 patients with GCS scores of 11-15 who had subdural hematomas less than 1 cm in width and no cisternal effacement on neuroimaging or focal neurological deficits were successfully managed nonoperatively with only 6% eventually requiring surgery. [143]
  • Another study of 462 patients with head injuries with CT-imaged intracranial hematomas who were treated nonoperatively found that only approximately 10% progressed clinically and eventually required surgery. Frontal parenchymal hematomas were more likely to require eventual surgery. [144]
  • Decompressive craniectomies are sometimes advocated for patients with increased intracranial pressure refractory to conventional medical treatment. Although some studies have shown favorable long-term outcomes with this procedure [145]
  • The operative and nonoperative management of intracranial injuries is an ever-evolving area of study and, at present, more a matter of neurosurgical judgment than hard and fast decision rules.


In the acute setting, a consultation with a neurosurgeon is critical for patients with moderate or severe head injuries, focal neurological findings, or intracranial pathology identified on neuroimaging.



In the acute setting, nasogastric feedings may need to be initiated for patients with significant head injuries and depressed levels of consciousness or dysphagia. Careful attention to protein stores and electrolyte balance is critical during this phase of treatment.



Usually no general limitations are placed on activity. Patient-by-patient recommendations based on the individual's motoric and cognitive recovery are necessary.