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Head Injury Treatment & Management


Author: David A Olson, MD; Chief Editor: Stephen A Berman, MD, PhD, MBA more...
Updated: Apr 1, 2013

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.[25]
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 more definitive studies are needed.[81] 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 pressurelowering 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.[82] 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.[83]
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.[84] 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.[85]
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.[86]
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

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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.[87] Furthermore, a current review of
23 randomized, controlled trials concluded that this therapy was of no benefit.[88]
Acute hypothermic treatment has been found to worsen outcomes in patients with diffuse head injuries but to improve
outcomes in patients with surgically-evacuated hematomas. This indicates a potential benefit in this subgroup;
however, further prospective studies are needed.[89]
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.[90]
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.[91] 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.[92] 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.[93]
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.[94] A trial of valproate in early seizure prophylaxis showed a trend toward an
increased mortality rate. Anticonvulsant therapy, if used, should be discontinued after 1-2 weeks unless further
seizures supervene.[95]
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.[96]
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.[97]
Progesterone given intravenously in a phase II, randomized, double-blind, placebo-controlled trial of 100 patients with
moderate and severe head injury showed no adverse effects and reduced 30-day mortality by 57%. Unfortunately,
worse outcomes were seen in the treated group with severe head injuries as measured by the extended Glasgow
Outcome Score, perhaps because of the increased survivorship of sicker patients.[98]
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.[99]
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.[100]
Rosuvastatin given in the acute phase of moderate head injury significantly reduced amnesia in a double-blind
placebo-controlled study of 34 patients.[101]
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.[102] Melatonin is a free radical scavenger, and when injected early in brain-injured
rats, it significantly reduced levels of lipid breakdown products.[103]

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

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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.[104]
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.[105]
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.[106] 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.[107]
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.[108] Other less rigorous
studies have also reported cognitive improvements in donepezil-treated, head-injured patients.[109]
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.[110] Furthermore, levodopa has even produced qualitative
cognitive improvements in a small number of head-injured patients.[111]
Emotional lability and the pathologic laughing and crying associated with pseudobulbar palsy reportedly have
responded rapidly and exquisitely to selective serotonin reuptake inhibitors.[112] Sertraline has shown efficacy in
depression in mild head injury.[113] 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.[114]
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.[115]

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.[116] 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.[117]
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.[118]
Decompressive craniectomies are sometimes advocated for patients with increased intracranial pressure

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refractory to conventional medical treatment. Of 40 patients with severe head injury who underwent this
procedure (some for ICP elevations in isolation and some for ICP elevations with mass lesions), 30% had a
favorable long-term outcome.[119] At least 2 major randomized clinical trials of this intervention are now
underway.
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.

Consultations
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.

Diet
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.

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

Contributor Information and Disclosures


Author
David A Olson, MD Clinical Neurologist, Dekalb Neurology Group, Decatur, Georgia
David A Olson, MD is a member of the following medical societies: American Academy of Neurology
Disclosure: Nothing to disclose.
Specialty Editor Board
Joseph Carcione Jr, DO, MBA Consultant in Neurology and Medical Acupuncture, Medical Management and
Organizational Consulting, Central Westchester Neuromuscular Care, PC; Medical Director, Oxford Health Plans
Joseph Carcione Jr, DO, MBA is a member of the following medical societies: American Academy of Neurology
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College
of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
Florian P Thomas, MD, MA, PhD, Drmed Director, Regional MS Center of Excellence, St Louis Veterans Affairs
Medical Center; Director, National MS Society Multiple Sclerosis Center; Director, Neuropathy Association Center of
Excellence, Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular
Virology, St Louis University School of Medicine
Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of
Neurology, American Neurological Association, American Paraplegia Society, Consortium of Multiple Sclerosis
Centers, National Multiple Sclerosis Society, and Sigma Xi
Disclosure: Nothing to disclose.
Chief Editor
Stephen A Berman, MD, PhD, MBA Professor of Neurology, University of Central Florida College of Medicine
Stephen A Berman, MD, PhD, MBA is a member of the following medical societies: Alpha Omega Alpha, American
Academy of Neurology, and Phi Beta Kappa
Disclosure: Nothing to disclose.

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