eMedicine Specialties > Neurology > Neurological Emergencies
Head Injury: Treatment & Medication
Updated: Jun 8, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
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Treatment
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.15
- 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.69 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.)70
- Interestingly, a 2008 study utilizing the National Trauma Data Bank retrospectively uncovered a 45% reduction in survival in patients who underwent intracranial pressure monitoring.71 These results have been called into question, however, because of a dearth of clinical and neuroimaging data.72
- 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.73 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.74
- 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.75
- 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.76
- 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.77
- 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.78
- Phenytoin has demonstrated efficacy in controlling early posttraumatic seizures, but mortality rates, surprisingly, were unaffected by this benefit. In one study, approximately 2.5% of patients treated with phenytoin had an allergic reaction to the drug during the first 2 weeks of therapy.79 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.80
- Finally, as stated previously, neuroprotective agents mostly have failed to improve the outcomes of humans 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.81
- 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.82
- 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.83
- 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.84
- 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.85
- Rosuvastatin given in the acute phase of moderate head injury significantly reduced amnesia in a double-blind placebo-controlled study of 34 patients.86
- 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.87 Melatonin is a free radical scavenger, and when injected early in brain-injured rats, it significantly reduced levels of lipid breakdown products.88
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.89
- 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.90
- Solid data on cognitive enhancing medications for patients with head injury are lacking. Typically, only small numbers of subjects have been use d 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.91 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.92
- 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.93 Other less rigorous studies have also reported cognitive improvements in donepezil-treated, head-injured patients.94
- 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.95 Furthermore, levodopa has even produced qualitative cognitive improvements in a small number of head-injured patients.96
- Emotional lability and the pathologic laughing and crying associated with pseudobulbar palsy reportedly have responded rapidly and exquisitely to selective serotonin reuptake inhibitors.97 Sertraline has shown efficacy in depression in mild head injury.98 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.99
- 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.100
Surgical Care
Two decades ago, the prompt surgical evacuation of subdural hematomas in less than 4 hours was believed to be a major determinant of an optimal outcome. Subsequent studies have found that the extent of the original intracranial injury and the generated intracranial pressures are 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.101
- 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 especially prone to nonoperative failures.
- Decompressive craniectomies are sometimes advocated for patients with increased intracranial pressure 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.102 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.
Medication
Medications commonly are used in the acute setting to control early seizures, reduce intracranial pressure, and correct electrolyte abnormalities. Nimodipine may be neuroprotective in the subset of patients with traumatic subarachnoid hemorrhages.
In the long-term setting, cognitive and motoric augmentation as well as the control of spasticity and emotional incontinence may require pharmacologic interventions.
Osmotic diuretics
These agents may help reduce intracranial pressure.
Mannitol (Osmitrol, Resectisol)
May reduce subarachnoid space pressure by creating osmotic gradient between CSF in arachnoid space and plasma. Not for long-term use. Initially assess for adequate renal function in adults by administering test dose of 200 mg/kg, given IV over 3-5 min; should produce urine flow of at least 30-50 mL/h of urine over 2-3 h. Same test in children should produce urine flow of at least 1 mL/kg/h over 1-3 h.
Adult
1.5-2 g/kg IV as 20% solution (7.5-10 mL/kg) or as 15% solution (10-13 mL/kg) over period as short as 30 min
Pediatric
Initial dose: 0.5-1 g/kg IV
Maintenance dose: 0.25-0.5 g/kg IV q4-6h
None reported
Documented hypersensitivity; anuria; severe pulmonary congestion; progressive renal damage; severe dehydration; active intracranial bleeding; progressive heart failure
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Carefully evaluate cardiovascular status before rapid administration since sudden increase in extracellular fluid may lead to fulminating CHF; add 20 mEq sodium chloride to each liter of mannitol solution when giving blood simultaneously with mannitol (to avoid pseudoagglutination, do not use an aletrolyte-free mannitol solution)
Anticonvulsants
These agents may help prevent early seizures in head injury.
Phenytoin (Dilantin)
May act in motor cortex, where it may inhibit spread of seizure activity; activity of brainstem centers responsible for tonic phase of grand mal seizures also may be inhibited.
Individualize dose. Administer larger dose in evening if dose cannot be divided equally.
Adult
Loading dose: 15-20 mg/kg PO/IV once or divided doses followed by 100-150 mg/dose at 30-min intervals
Initial dose: 100 mg (125 mg susp) PO/IV tid
Maintenance dosage: 300-400 mg/d PO/IV divided tid (qd/bid if using extended release); increase to 600 mg/d (625 mg/d susp) may be necessary; not to exceed 1500 mg/24h
Rate of infusion not to exceed 50 mg/min (to avoid hypotension and arrhythmias)
Adjust dosage on basis of clinical response and toxicity; steady state, trough levels can be helpful with typical therapeutic values ranging between 10 and 20 mg/mL; however, nutritional depletion with low serum albumin levels may result in higher free levels of drug than typically measured protein-bound levels; also, because of nonlinear pharmacokinetics, small changes in dosing can result in large fluctuations in serum levels
Pediatric
Loading dose: 15-20 mg/kg PO/IV once or divided doses
Initial dose: 5 mg/kg/d PO/IV divided bid/tid
Maintenance dose: 4-8 mg/kg PO/IV divided bid/tid
>6 years: May require minimum adult dose (300 mg/d); not to exceed 300 mg/d
Amiodarone, benzodiazepines, chloramphenicol, cimetidine, fluconazole, isoniazid, metronidazole, miconazole, phenylbutazone, succinimides, sulfonamides, omeprazole, phenacemide, disulfiram, ethanol (acute ingestion), trimethoprim, and valproic acid may increase toxicity
Barbiturates, diazoxide, ethanol (chronic ingestion), rifampin, antacids, charcoal, carbamazepine, theophylline, and sucralfate may decrease effects
May decrease effects of acetaminophen, corticosteroids, dicumarol, disopyramide, doxycycline, estrogens, haloperidol, amiodarone, carbamazepine, cardiac glycosides, quinidine, theophylline, methadone, metyrapone, mexiletine, oral contraceptives, and valproic acid
Documented hypersensitivity; sinoatrial block; second- and third-degree AV block; sinus bradycardia; Adams-Stokes syndrome
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Rapid IV infusion may result in death from cardiac arrest, marked by QRS widening
Perform blood counts and urinalyses when therapy is begun and at monthly intervals for several months thereafter to monitor for blood dyscrasias; discontinue use if skin rash appears, and do not resume use if rash is exfoliative, bullous, or purpuric; caution in acute intermittent porphyria and diabetes (may elevate blood glucose); discontinue use if hepatic dysfunction occurs
Electrolytes
Magnesium is given in hypomagnesemic states to ensure that adequate stores are present during acute phase of head injuries.
Magnesium sulfate
Nutritional supplement in hyperalimentation; cofactor in enzyme systems involved in neurochemical transmission and muscular excitability. In adults, 60-180 mEq of potassium, 10-30 mEq of magnesium, and 10-40 mmol of phosphate per day may be necessary for optimum metabolic response.
Adult
1 g IV/IM q6h for 4 doses up to 8-12 g/d in severe hypomagnesemia
Alternatively, 3 g PO q6h for 4 doses prn
Pediatric
25-50 mg/kg/dose IV/IM q4-6h for 3-4 doses
Nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade observed with aminoglycosides and potentiate neuromuscular blockade produced by tubocurarine, vecuronium, and succinylcholine; may worsen myasthenia gravis caused by these agents; may increase CNS effects and toxicity of CNS depressants and betamethasone and cardiotoxicity of ritodrine
Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
May alter cardiac conduction, leading to heart block in digitalized patients; monitor respiratory rate, deep tendon reflexes, and renal function when administered parenterally; use cautiously in renal impairment; caution when administering since may produce significant hypertension or asystole; in overdose, calcium gluconate (10-20 mL IV of 10% solution) can be given as antidote for clinically significant hypermagnesemia
Barbiturates
These agents may help reduce intracranial pressure that is refractory to other conventional measures.
Pentobarbital (Nembutal)
Short-acting barbiturate with sedative, hypnotic, and anticonvulsant properties. Can produce all levels of CNS depression.
Adult
Loading dose: 10 mg/kg IV over 30 min; 5 mg/kg qh X 3
Maintenance dose: 1 mg/kg/h IV or adjusted so that serum level is in range 3-4 mg%
Pediatric
Administer as in adults
Alcohol may produce additive CNS effects and death; chloramphenicol may inhibit pentobarbital metabolism; may enhance chloramphenicol metabolism; MAOIs may enhance sedative effects; valproic acid appears to decrease barbiturate metabolism, increasing toxicity; can decrease effects of anticoagulants (patients may require dosage adjustments if barbiturates added to or withdrawn from regimen); by inducing microsomal enzymes, may decrease effect of contraceptives (alternate form of birth control suggested); may decrease corticosteroid and digitoxin effects through induction of hepatic microsomal enzymes, which increase metabolism; decreases theophylline levels and may decrease effects; may decrease verapamil bioavailability
Documented hypersensitivity; liver failure
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Patient may become tolerant to hypnotic effects; caution in hypovolemic shock, respiratory dysfunction, renal dysfunction, congestive heart failure, previous addiction to sedative hypnotics, and congestive heart failure
Calcium Channel Blocker
Nimodipine has been demonstrated to improve outcomes of patients with traumatic subarachnoid hemorrhages.
Nimodipine (Nimotop)
Indicated for improvement of neurological impairments resulting from spasms following subarachnoid hemorrhage caused by ruptured congenital intracranial aneurysm in patients who are in good neurological condition postictus.
While studies show benefit on severity of neurological deficits caused by cerebral vasospasm following subarachnoid hemorrhage, no evidence that drug either prevents or relieves spasms of cerebral arteries. Thus, actual mechanism of action unknown.
Therapy should start within 96 h of subarachnoid hemorrhage. If capsule cannot be swallowed because patient undergoing surgery or unconscious, a hole can be made at both ends of capsule with 18-gauge needle and contents extracted into a syringe. Contents then can be emptied into patients' in situ nasogastric tube and washed down tube with 30 mL isotonic saline.
Adult
60 mg PO q4h for 21 consecutive d
Pediatric
Not established
Although advantageous in some patients, coadministration with beta-blockers may result in increased adverse effects due to depressant effects on myocardial contractility or AV conduction; fentanyl may cause severe hypotension or increased fluid volume requirements; cimetidine may increase levels
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Rare elevations of LDH, alkaline phosphatase, and ALT levels may occur; hypotension can occur, which can worsen cerebral perfusion pressure
Stimulants
These agents may help increase alertness and some aspects of cognitive functioning in patients with brain injury.
Methylphenidate (Ritalin)
Stimulates cerebral cortex and subcortical structures.
Adult
10 mg PO bid/tid; not to exceed 60 mg/d
Pediatric
Begin at 5 mg PO at breakfast and lunch; gradually increase to effect; not to exceed 60 mg/d
Reduces effects of guanethidine and bretylium; may increase toxicity of phenytoin, TCAs, warfarin, primidone, and phenobarbital; MAOIs increase toxicity
Documented hypersensitivity; glaucoma; Tourette syndrome; motor tics; agitation, tension, or anxiety
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in dementia, seizures, and hypertension; may increase confusion
Dopamine agonist
These agents may increase alertness in patients with brain injury; also may help in occasional patients with posttraumatic parkinsonism.
Levodopa (Dopar, Larodopa)
Large neutral amino acid absorbed in proximal small intestine by saturable carrier-mediated transport system. Absorption decreased by meals, which include other large neutral amino acids. Only patients with meaningful motor fluctuations need consider low-protein or protein-redistributed diet. Greater consistency of absorption achieved when levodopa taken 1 h or more after meals. Nausea often reduced if levodopa taken immediately following meals. Some patients with nausea benefit from additional carbidopa in doses up to 200 mg/d. Half-life of levodopa/carbidopa approximately 2 h.
When more carbidopa required, substitute 1 25/100 tab for each 10/100 tab; when more levodopa required, substitute 25/250 tab for 25/100 or 10/100 tab.
Sustained release (SR) formulation of levodopa/carbidopa is absorbed more slowly and provides more sustained levodopa levels than immediate release (IR) dosage form; SR as effective as IR formulation when levodopa initially required and may be more convenient when fewer intakes are desired.
Patients with dissipating motor fluctuations and no dyskinesia often benefit from prolongation of short-duration response when switched from IR to SR; however, patients with meaningful fluctuations and dyskinesia often experience increase in dyskinesia when switched to SR formulation.
Doses and dosing intervals of SR form may be increased or decreased based on response; most patients have been treated adequately with 2-8 tab/d (divided doses) at intervals of 4-8 h while awake; higher doses (>12 tab/d) and intervals <4 h have been used but usually are not recommended; if <4-h interval used or if divided doses are not equal, give smaller doses at end of day. Allow at least a 3-d interval between dosage adjustments. May administer as whole or half tab, which should not be crushed or chewed.
Adult
IR tab: 1 tab 25 mg carbidopa/100 mg levodopa PO tid or 10 mg carbidopa/100 mg levodopa tid/qid; may increase dosage by 1 tab qd or qod prn, not to exceed 8 tab/d
Tab of 2 ratios (eg, 1:4, 25/100 or 1:10, 10/100, and 25/250) may be given separately or combined prn to provide optimum dosage
SR tab: 1 tab PO bid not more often than q6h
Pediatric
Not established
Hydantoins, pyridoxine, phenothiazine, and hypotensive agents may decrease effects; antacids and MAOIs increase toxicity
Documented hypersensitivity; narrow-angle glaucoma; malignant melanoma; undiagnosed skin lesions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Certain adverse CNS effects (eg, dyskinesias) may occur at lower dosages and earlier in therapy with SR form; caution in patients with history of MI, arrhythmias, asthma, or peptic ulcer disease; sudden discontinuation may cause worsening of Parkinson disease; high-protein diets should be distributed throughout day to avoid fluctuations in levodopa absorption; most common acute adverse effects are nausea, hypotension, and hallucinations; long-term adverse effects include motor fluctuations and dyskinesia (ie, chorea); provide at least 70-100 mg/d carbidopa
Selective serotonin reuptake inhibitors
These agents have been of benefit in patients with head injuries and emotional incontinence.
Sertraline (Zoloft)
Selectively inhibits presynaptic serotonin reuptake.
Adult
50 mg/d PO in am with 50-mg/d increments q2-3d to 100 mg/d, if tolerated; not to exceed 200 mg/d
Pediatric
Not established
Increases toxicity of MAOIs, diazepam, tolbutamide, and warfarin
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in preexisting seizure disorders, recent MI, unstable heart disease, and hepatic or renal impairment
Alert: The UK Medicines and Healthcare Products Regulatory Agency (MHRA) and the US Food and Drug Administration (FDA) have issued an advisory to physicians to be appropriately cautious when using selective serotonin reuptake inhibitor (SSRI) antidepressants in the pediatric population. The advisory reports suicidality (both ideation and attempts) in clinical trials of various antidepressant drugs in pediatric patients. Nonetheless, the FDA has asked that additional studies be performed because suicidality occurred in both treated and untreated patients with major depression and, thus, could not be linked to drug treatment.
Antispasticity medications
These agents may reduce painful cramping and detrimental muscle tightening.
Tizanidine hydrochloride (Zanaflex)
Centrally acting muscle relaxant metabolized in liver and excreted in urine and feces.
Adult
4-8 mg PO q8h prn; not to exceed 36 mg/d
Pediatric
Not established
May interact with alcohol (increase somnolence, stupor) and oral contraceptives (which decrease its clearance); can cause increased hypotensive effects when administered concurrently with diuretics
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in renal impairment
Baclofen (Lioresal)
May induce hyperpolarization of afferent terminals and inhibit both monosynaptic and polysynaptic reflexes at spinal level.
Adult
5 mg PO tid for 3 d; 10 mg tid for 3 d; 15 mg tid for 3 d; 20 mg tid for 3 d; thereafter, additional increases may be necessary; not to exceed 80 mg/d PO divided qid
Pediatric
Not established
Opiate analgesics, benzodiazepines, alcohol, TCAs, guanabenz, MAOIs, clindamycin, and hypertensive agents may increase effects
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in patients with history of autonomic dysreflexia and when spasticity used to obtain increased function; autonomic dysreflexia can result from withdrawal of this medication
Dantrolene (Dantrium)
Stimulates muscle relaxation by modulating skeletal muscle contractions at site beyond myoneural junction and acting directly on muscle.
Adult
Begin with 25 mg PO qd; increase to 25 mg bid/qid, then by 25-mg increments to as high as 100 mg bid/qid prn
Most patients respond to 400 mg/d or less
Pediatric
Start with 0.5 mg/kg PO bid; increase to 0.5 mg/kg bid/qid, then by increments of 0.5 mg/kg to 3 mg/kg bid/qid if necessary; not to exceed 100 mg qid
Clofibrate and warfarin may increase toxicity; estrogen may increase hepatotoxicity in women >35 y
Documented hypersensitivity; active hepatic disease (hepatitis and cirrhosis)
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May cause hepatotoxicity (use only for recommended indications); caution in impaired pulmonary function and severe cardiac insufficiency; may cause photosensitivity with exposure to sunlight
Diazepam (Valium)
Depresses all levels of CNS, possibly by increasing activity of GABA. Individualize dosage and increase cautiously to avoid adverse effects.
Adult
2-10 mg PO tid/qid
Pediatric
<6 months: Do not administer
>6 months: 0.1-0.8 mg/kg/d PO divided tid/qid
Phenothiazines, barbiturates, alcohols, and MAOIs increase toxicity
Documented hypersensitivity; narrow-angle glaucoma
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity)
More on Head Injury |
| Overview: Head Injury |
| Differential Diagnoses & Workup: Head Injury |
Treatment & Medication: Head Injury |
| Follow-up: Head Injury |
| Multimedia: Head Injury |
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References
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Further Reading
Keywords
head injury, symptoms, treatment, coma, concussion, head trauma, traumatic brain injury, intracranial bleed, loss of consciousness, neuroprotection, skull fracture, subdural hemorrhage
Treatment & Medication: Head Injury