eMedicine Specialties > Neurosurgery > Trauma

Closed Head Trauma: Treatment & Medication

Author: Leonardo Rangel-Castilla, MD, Staff Physician, Division of Neurosurgery, University of Texas Medical Branch School of Medicine
Coauthor(s): Jaime Gasco, MD, Staff Physician, Department of Neurosurgery, University of Texas Medical Branch School of Medicine; Fadi Hanbali, MD, FACS, Associate Professor, Division of Neurosurgery, Department of Surgery, Texas Tech University Health Sciences Center; Associate Professor, Department of Orthopedic Surgery, Texas Tech University Health Sciences Center; Adjunct Professor, Departments of Neurosurgery and Orthopedic Surgery, Division of Neurosurgery, University of Texas Medical Branch; Paul Salinas, MD, Resident Physician, Department of Neurosurgery, University of Texas Medical Branch at Galveston
Contributor Information and Disclosures

Updated: Sep 22, 2009

Treatment

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.49

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.25 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.47 In addition, in most patients, hyperventilation is not necessary to control ICP.50,51,30,52 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.53

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.54,55 Mannitol is also considered a free radical scavenger.56 Administration of this drug in severe traumatic brain injury patients studied both with jugular bulb oxygen saturation57 as well as with multimodal brain monitoring58 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.59 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.42 These drugs often have an associated morbidity and do not significantly change outcome.60,10

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.24,32 Data from the Traumatic Coma Data Bank (TCDB) reveal that hypotension in patients with severe TBI increases the mortality rate from 27% to 50%.25 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.25 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.61,62 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.63 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.64

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.65 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.66,67 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.68

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.10

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.49

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.69 It seems clear that older individuals, particularly those older than 50 years, do less well with elective decompressive craniotomies.70,71

Consultations

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.

Diet

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.72

Activity

The patient should be prescribed bed rest.

Medication

Neurosurgeons have commonly given prophylactic anticonvulsants for individuals with intracranial hemorrhages. The appropriate duration of treatment is not well established. Individuals who have experienced seizure activity can reasonably be treated with anticonvulsants for 6-12 months, after which reevaluation is necessary. Temkin and colleagues suggest that treatment for longer than 8 days after injury does not reduce the frequency of long-term seizure disorders. Anticonvulsants may be used to treat early (<7 d) posttraumatic seizures. According to Greenberg, prophylactic anticonvulsants do not reduce the frequency of late (>7 d) posttraumatic seizures.73

The recommended anticonvulsant medication in adults is phenytoin or fos-phenytoin (18 mg/kg of loading dose), ensuring therapeutic levels of 10-20 mg/dL. Note that a "therapeutic level" does not necessarily have a direct bearing on adequate control of seizures. A relatively common adverse effect of chronic phenytoin use is gingival hyperplasia and hirsutism, which precludes chronic use in children. Phenobarbital is an acceptable alternative in children who require long-term anticonvulsive therapy (10-20 mg/kg loading dose, then 3-5 mg/kg/d divided bid/tid) to achieve a therapeutic level of 10-40 mg/dL.

The new antiepileptic drug levetiracetam is used in the setting of acute brain injury for seizures treatment or prophylaxis; it is a desirable alternative to phenytoin. It is associated with fewer complications when it is used as monotherapy. Checking for therapeutic levels is not needed. The dose is 500 mg bid IV or PO and advance to 1000 mg bid.74

Anticonvulsants

These agents are indicated for short-term (1 wk) or long-term (6- to 12-mo) posttraumatic seizure control for patients who have experienced posttraumatic seizure activity. Phenobarbital may be considered in children for long-term anticonvulsive therapy.


Phenytoin (Dilantin)

Used for acute seizure prophylaxis in individuals with closed head injuries.

Adult

Loading dose: 15-20 mg/kg PO/IV once
Initial dose: 100 mg (125 mg suspension) IV/PO tid
Maintenance dose: 300-400 mg/d PO/IV divided tid, or qd/bid if using extended release; increase to 600 mg/d (625 mg/d susp) may be necessary; do not exceed 1500 mg/d
Infusion rate must not exceed 50 mg/min in order to avoid hypotension and arrhythmias; alternatively, 1 g loading dose, then 100 mg tid, checking level qd to achieve therapeutic level of 10-20 mg/dL

Pediatric

<6 years: 15-20 mg/kg PO/IV loading dose once or in divided doses; follow by initial 5 mg/kg/d maintenance dose (range, 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; alternatively, loading dose of 10-20 mg/kg IV, then 5 mg/kg administered qd or divided tid

Amiodarone, benzodiazepines, chloramphenicol, cimetidine, fluconazole, isoniazid, metronidazole, miconazole, phenylbutazone, succinimides, sulfonamides, omeprazole, phenacemide, disulfiram, ethanol (acute ingestion), trimethoprim, and valproic acid may increase toxicity; effects may decrease when taken concurrently with barbiturates, diazoxide, ethanol (chronic ingestion), rifampin, antacids, charcoal, carbamazepine, theophylline, or sucralfate; 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

Perform blood cell counts and urinalyses when therapy is begun and at monthly intervals for several months thereafter to monitor for blood dyscrasias; discontinue use if a skin rash appears, and do not resume use if rash is exfoliative, bullous, or purpuric; rapid IV infusion may result in death from cardiac arrest, marked by QRS widening; caution in acute intermittent porphyria and diabetes (may elevate blood sugar levels); discontinue use if hepatic dysfunction occurs


Phenobarbital (Barbita, Luminal, Solfoton)

Used for acute seizure prophylaxis in children with closed head injuries.

Adult

30-120 mg/d PO qd or 2-3 divided doses; not to exceed 400 mg/d; frequency determined by response

Pediatric

1-3 mg/kg IV/IM

May decrease effects of chloramphenicol, digitoxin, corticosteroids, carbamazepine, theophylline, verapamil, metronidazole, and anticoagulants (patients stabilized on anticoagulants may require dosage adjustments if added to or withdrawn from their regimen); coadministration with alcohol may produce additive CNS effects and death; chloramphenicol, valproic acid, and MAOIs may increase phenobarbital toxicity; rifampin may decrease phenobarbital effects; induction of microsomal enzymes may result in decreased effects of oral contraceptives in women (must use additional contraceptive methods to prevent unwanted pregnancy; menstrual irregularities may also occur)

Documented hypersensitivity; severe respiratory disease; marked impairment of liver function; nephritis

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

In prolonged therapy, evaluate hematopoietic, renal, hepatic, and other organ systems; caution in fever, hyperthyroidism, diabetes mellitus, and severe anemia because adverse reactions can occur; caution in myasthenia gravis and myxedema

More on Closed Head Trauma

Overview: Closed Head Trauma
Differential Diagnoses & Workup: Closed Head Trauma
Treatment & Medication: Closed Head Trauma
Follow-up: Closed Head Trauma
Multimedia: Closed Head Trauma
References
Further Reading
[ CLOSE WINDOW ]

References

  1. Klonoff H, Thompson GB. Epidemiology of head injuries in adults: a pilot study. Can Med Assoc J. Feb 1 1969;100(5):235-41. [Medline].

  2. Klauber MR, Marshall LF, Barrett-Connor E, Bowers SA. Prospective study of patients hospitalized with head injury in San Diego County, 1978. Neurosurgery. Sep 1981;9(3):236-41. [Medline].

  3. Annegers JF, Grabow JD, Kurland LT, Laws ER Jr. The incidence, causes, and secular trends of head trauma in Olmsted County, Minnesota, 1935-1974. Neurology. Sep 1980;30(9):912-9. [Medline].

  4. Kalsbeek WD, McLaurin RL, Harris BS 3rd, Miller JD. The National Head and Spinal Cord Injury Survey: major findings. J Neurosurg. Nov 1980;Suppl:S19-31. [Medline].

  5. Kraus JF, Black MA, Hessol N, Ley P, Rokaw W, Sullivan C, et al. The incidence of acute brain injury and serious impairment in a defined population. Am J Epidemiol. Feb 1984;119(2):186-201. [Medline].

  6. Kraus JF. Epidemiology of head injury. In: Cooper PR, ed. Head Injury. 2nd ed. Baltimore: Lippincott Williams & Wilkins; 1987:1.

  7. US Census Bureau, Population Division. Data as of July 2003. Available at: http://www.census.gov/cgi-bin/popclock. [Full Text].

  8. Feliciano DV, Moore EE, Mattox KL. Trauma. 3rd ed. McGraw-Hill: 1996:267-1065.

  9. Kraus JF. Epidemiology of head injury. In: Cooper PR, ed. Head Injury. 3rd ed. Baltimore: Lippincott Williams & Wilkins; 1993:1-25.

  10. Schwartz SI, Shires GT. Principles of Surgery. 7th ed. New York: McGraw-Hill; 1999:1880-1881.

  11. Frankowski RF, Annegers JF, Whitman S. Epidemiological and descriptive studies, Part 1. The descriptive epidemiology of head trauma in the United States. In: Becker DP, Povlishock JT. Central Nervous System Trauma Status Report. William Byrd Press: Richmond, Va; 1985:33.

  12. Foulkes MA, Eisenberg HM, Jane JA, Marmarou A, Marshall LF. The Traumatic Coma Data Bank: design, methods, and baseline characteristics. J Neurosurg. November 1991;75:S8-S13.

  13. Valadka AB, Robertson CS. Surgery of cerebral trauma and associated critical care. Neurosurgery. supplement 2007;61(1):203-21.

  14. National Academy Press. Injury in America: A Continuaing Public Health Problem. Washington, DC: National Academy Press; 1985:1.

  15. Valadka AB, Ward JD, Smoker WR. Brain Imaging in Neurologic Emergencies. Anaheim, Calif:. Society of Critical Care Medicine;1993:1.

  16. Thurman D, Guerrero J. Trends in hospitalization associated with traumatic brain injury. JAMA. Sep 8 1999;282(10):954-7. [Medline].

  17. De Beaumont L, Lassonde M, Leclerc S, Théoret H. Long-term and cumulative effects of sports concussion on motor cortex inhibition. Neurosurgery. Aug 2007;61(2):329-36; discussion 336-7. [Medline].

  18. Viano DC, Casson IR, Pellman EJ. Concussion in professional football: biomechanics of the struck player--part 14. Neurosurgery. Aug 2007;61(2):313-27; discussion 327-8. [Medline].

  19. Chang EF, Meeker M, Holland MC. Acute traumatic intraparenchymal hemorrhage: risk factors for progression in the early post-injury period. Neurosurgery. Apr 2006;58(4):647-56; discussion 647-56. [Medline].

  20. Cairns CJ, Andrews PJ. Management of hyperthermia in traumatic brain injury. Curr Opin Crit Care. Apr 2002;8(2):106-10. [Medline].

  21. Miller JD. Surgical management of acute and chronic subdural hematoma. In: Schmidek HH, Sweet WH, eds. Operative Neurosurgical Techniques: Indications, Methods, Results. 2nd ed. Philadelpia: WB Saunders Co; 1998:33.

  22. Maxeiner H, Wolff M. Pure subdural hematomas: a postmortem analysis of their form and bleeding points. Neurosurgery. Mar 2002;50(3):503-8; discussion 508-9. [Medline].

  23. Jenkins A, Teasdale G, Hadley MD, Macpherson P, Rowan JO. Brain lesions detected by magnetic resonance imaging in mild and severe head injuries. Lancet. Aug 23 1986;2(8504):445-6. [Medline].

  24. Miller JD, Sweet RC, Narayan R, Becker DP. Early insults to the injured brain. JAMA. Aug 4 1978;240(5):439-42. [Medline].

  25. Wilkins RH, Rengachary SS. Neurosurgery. 2nd ed. New York:. McGraw Hill;1996:2603-2720.

  26. [Best Evidence] Christensen J, Pedersen MG, Pedersen CB, Sidenius P, Olsen J, Vestergaard M. Long-term risk of epilepsy after traumatic brain injury in children and young adults: a population-based cohort study. Lancet. Mar 28 2009;373(9669):1105-10. [Medline].

  27. Bouma GJ, Muizelaar JP, Stringer WA, Choi SC, Fatouros P, Young HF. Ultra-early evaluation of regional cerebral blood flow in severely head-injured patients using xenon-enhanced computerized tomography. J Neurosurg. Sep 1992;77(3):360-8. [Medline].

  28. Bouma GJ, Muizelaar JP, Bandoh K, Marmarou A. Blood pressure and intracranial pressure-volume dynamics in severe head injury: relationship with cerebral blood flow. J Neurosurg. Jul 1992;77(1):15-9. [Medline].

  29. Aggarwal S. Time course of cerebral flow and metabolic changes following severe head injury. Presented at: The 61st Annual Meeting of the American Association of Neurological Surgeons. Boston, Mass:. April 1993.

  30. Marion D, Obrist WD, Penrod LE, et al. Treatment of cerebral ischemia improves outcome following severe traumatic brain injury. Presented at: The American Association of Neurological Surgeons. Boston, Mass:. April 26 1993.

  31. Obrist WD, Marion DW, Aggarwal S. Time course of cerebral blood flow and metabolic changes following severe head injury. Presented at: The 61st Annual Meeting of the American Association of Neurological Surgeons. Boston Mass: April 1993.

  32. Chesnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma. Feb 1993;34(2):216-22. [Medline].

  33. Gopinath SP, Robertson CS, Contant CF, Hayes C, Feldman Z, Narayan RK, et al. Jugular venous desaturation and outcome after head injury. J Neurol Neurosurg Psychiatry. Jun 1994;57(6):717-23. [Medline].

  34. Marmarou A, Signoretti S, Fatouros PP, Portella G, Aygok GA, Bullock MR. Predominance of cellular edema in traumatic brain swelling in patients with severe head injuries. J Neurosurg. May 2006;104(5):720-30. [Medline].

  35. Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet. Jul 13 1974;2(7872):81-4. [Medline].

  36. Jagger J, Fife D, Vernberg K. Effect of alcohol intoxication on the diagnosis and apparent severity of brain injury. Neurosurgery. Sep 1984;15(3):303-6. [Medline].

  37. Pal J, Brown R, Fleiszer D. The value of the Glasgow Coma Scale and Injury Severity Score: predicting outcome in multiple trauma patients with head injury. J Trauma. Jun 1989;29(6):746-8. [Medline].

  38. Waxman K, Sundine MJ, Young RF. Is early prediction of outcome in severe head injury possible?. Arch Surg. Oct 1991;126(10):1237-41; discussion 1242. [Medline].

  39. Vollmer DG. Prognosis and outcome of severe injury. In: Cooper PR, ed. Head Injury. 3rd ed. Baltimore:. Lippincott Williams & Wilkins;1993:533-581.

  40. Salcman M, Schepp RS, Ducker TB. Calculated recovery rates in severe head trauma. Neurosurgery. Mar 1981;8(3):301-8. [Medline].

  41. Born JD, Albert A, Hans P, Bonnal J. Relative prognostic value of best motor response and brain stem reflexes in patients with severe head injury. Neurosurgery. May 1985;16(5):595-601. [Medline].

  42. Townsend CM, Sabiston DC, Beauchamp RD, et al. The Biological Basis of Modern Surgical Practice. 16th ed. WB Saunders Co: Sabiston Textbook of Surgery:; 1994:317-376.

  43. Langfitt TW, Gennarelli TA. Can the out come from head injury be improved?. J Neurosurg. Jan 1982;56(1):19-25. [Medline].

  44. Livingston DH, Loder PA, Koziol J, Hunt CD. The use of CT scanning to triage patients requiring admission following minimal head injury. J Trauma. Apr 1991;31(4):483-7; discussion 487-9. [Medline].

  45. Shackford SR, Wald SL, Ross SE, Cogbill TH, Hoyt DB, Morris JA, et al. The clinical utility of computed tomographic scanning and neurologic examination in the management of patients with minor head injuries. J Trauma. Sep 1992;33(3):385-94. [Medline].

  46. McBride DQ, Patel AB, Caron M. Early repeat CT scan: importance in detecting surgical lesions after closed head injury. J Neurotrauma. 1993;10:S227,203.

  47. Stein SC, Ross SE. Moderate head injury: a guide to initial management. J Neurosurg. Oct 1992;77(4):562-4. [Medline].

  48. Stein SC, Spettell C, Young G, Ross SE. Delayed and progressive brain injury in closed-head trauma: radiological demonstration. Neurosurgery. Jan 1993;32(1):25-30; discussion 30-1. [Medline].

  49. Rangel-Castillo L, Robertson CS. Management of intracranial hypertension. Crit Care Clin. Oct 2006;22(4):713-32; abstract ix. [Medline].

  50. Rosner MJ, Daughton S. Cerebral perfusion pressure management in head injury. J Trauma. Aug 1990;30(8):933-40; discussion 940-1. [Medline].

  51. Muizelaar JP, Marmarou A, Ward JD, Kontos HA, Choi SC, Becker DP, et al. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. J Neurosurg. Nov 1991;75(5):731-9. [Medline].

  52. von Helden A, Schneider GH, Unterberg A, Lanksch WR. Monitoring of jugular venous oxygen saturation in comatose patients with subarachnoid haemorrhage and intracerebral haematomas. Acta Neurochir Suppl (Wien). 1993;59:102-6. [Medline].

  53. Muizelaar JP, van der Poel HG, Li ZC, Kontos HA, Levasseur JE. Pial arteriolar vessel diameter and CO2 reactivity during prolonged hyperventilation in the rabbit. J Neurosurg. Dec 1988;69(6):923-7. [Medline].

  54. Muizelaar JP, Wei EP, Kontos HA, Becker DP. Mannitol causes compensatory cerebral vasoconstriction and vasodilation in response to blood viscosity changes. J Neurosurg. Nov 1983;59(5):822-8. [Medline].

  55. Muizelaar JP, Lutz HA 3rd, Becker DP. Effect of mannitol on ICP and CBF and correlation with pressure autoregulation in severely head-injured patients. J Neurosurg. Oct 1984;61(4):700-6. [Medline].

  56. Takagi H, Saito T, Kitahara T, et al. The mechanism of the ICP reducing effect of mannitol. Berlin: Springer-Verlag; 1993:729-33.

  57. Cruz J, Miner ME, Allen SJ, Alves WM, Gennarelli TA. Continuous monitoring of cerebral oxygenation in acute brain injury: injection of mannitol during hyperventilation. J Neurosurg. Nov 1990;73(5):725-30. [Medline].

  58. Gasco J, Sendra J, Lim J, Ng I. Linear correlation between stable intracranial pressure decrease and regional cerebral oxygenation improvement following mannitol administration in severe acute head injury patients. Acta Neurochir Suppl. 2005;95:73-7. [Medline].

  59. Chesnut RM, Gautille T, Blunt BA, Klauber MR, Marshall LF. Neurogenic hypotension in patients with severe head injuries. J Trauma. Jun 1998;44(6):958-63; discussion 963-4. [Medline].

  60. Eisenberg HM, Frankowski RF, Contant CF, Marshall LF, Walker MD. High-dose barbiturate control of elevated intracranial pressure in patients with severe head injury. J Neurosurg. Jul 1988;69(1):15-23. [Medline].

  61. Mattox KL, Maningas PA, Moore EE, Mateer JR, Marx JA, Aprahamian C, et al. Prehospital hypertonic saline/dextran infusion for post-traumatic hypotension. The U.S.A. Multicenter Trial. Ann Surg. May 1991;213(5):482-91. [Medline].

  62. Vassar MJ, Perry CA, Gannaway WL, Holcroft JW. 7.5% sodium chloride/dextran for resuscitation of trauma patients undergoing helicopter transport. Arch Surg. Sep 1991;126(9):1065-72. [Medline].

  63. Winter JP, Plummer D, Bottini A, Rockswold GR, Ray D. Early fresh frozen plasma prophylaxis of abnormal coagulation parameters in the severely head-injured patient is not effective. Ann Emerg Med. May 1989;18(5):553-5. [Medline].

  64. Hawryluk GW, Cusimano MD. The role of recombinant activated factor VII in neurosurgery: hope or hype?. J Neurosurg. Dec 2006;105(6):859-68. [Medline].

  65. Clinchot DM, Otis S, Colachis SC 3rd. Incidence of fever in the rehabilitation phase following brain injury. Am J Phys Med Rehabil. Jul-Aug 1997;76(4):323-7. [Medline].

  66. Ginsberg MD, Busto R. Combating hyperthermia in acute stroke: a significant clinical concern. Stroke. Feb 1998;29(2):529-34. [Medline].

  67. Thompson HJ, Tkacs NC, Saatman KE, Raghupathi R, McIntosh TK. Hyperthermia following traumatic brain injury: a critical evaluation. Neurobiol Dis. Apr 2003;12(3):163-73. [Medline].

  68. Bullock R, Chesnut RM, Clifton G, et al. Guidelines for cerebral perfusion pressure. In: Guidelines for the Management of Severe Head Injury. New York Brain Trauma Foundation: 1995:8-1– 8-10.

  69. Taylor A, Butt W, Rosenfeld J, Shann F, Ditchfield M, Lewis E, et al. A randomized trial of very early decompressive craniectomy in children with traumatic brain injury and sustained intracranial hypertension. Childs Nerv Syst. Feb 2001;17(3):154-62. [Medline].

  70. Guerra WK, Gaab MR, Dietz H, Mueller JU, Piek J, Fritsch MJ. Surgical decompression for traumatic brain swelling: indications and results. J Neurosurg. Feb 1999;90(2):187-96. [Medline].

  71. Schneider GH, Bardt T, Lanksch WR, Unterberg A. Decompressive craniectomy following traumatic brain injury: ICP, CPP and neurological outcome. Acta Neurochir Suppl. 2002;81:77-9. [Medline].

  72. Guidelines for the management of severe traumatic brain injury. XII. Nutrition. J. Brain Trauma Foundation; American Association of Neurological Surgeons; Congress of Neurological Surgeons; Joint Section on Neurotrauma and Critical Care, AANS/CNS. Neurotrauma. 2007;24 Suppl 1:S77-82.

  73. Greenberg MS. Handbook of Neurosurgery. 5th ed. Thieme Medical Publishers; 2001:258-259.

  74. Szaflarski JP, Meckler JM, Szaflarski M, Shutter LA, Privitera MD, Yates SL. Levetiracetam use in critically ill patients. Neurocrit Care. 2007;7(2):140-7. [Medline].

  75. Alexandre A, Colombo F, Nertempi P, Benedetti A. Cognitive outcome and early indices of severity of head injury. J Neurosurg. Nov 1983;59(5):751-61. [Medline].

  76. Levin HS, Gary HE Jr, Eisenberg HM, Ruff RM, Barth JT, Kreutzer J, et al. Neurobehavioral outcome 1 year after severe head injury. Experience of the Traumatic Coma Data Bank. J Neurosurg. Nov 1990;73(5):699-709. [Medline].

  77. Vollmer DG, Torner JC, Jane JA, et al. Age and outcome following traumatic coma: Why do older patients fare worse?. J Neurosurg. 1991;75 (suppl):S37-S49.

  78. [Guideline] Sasser SM, Hunt RC, Sullivent EE, Wald MM, Mitchko J, Jurkovich GJ, et al. Guidelines for field triage of injured patients. Recommendations of the National Expert Panel on Field Triage. MMWR Recomm Rep. Jan 23 2009;58:1-35. [Medline].

  79. Bingham H. Electrical burns. Clin Plast Surg. Jan 1986;13(1):75-85. [Medline].

  80. Bouma GJ, Muizelaar JP. Cerebral blood flow, cerebral blood volume, and cerebrovascular reactivity after severe head injury. J Neurotrauma. Mar 1992;9 Suppl 1:S333-48. [Medline].

  81. Chan KH, Dearden NM, Miller JD, Andrews PJ, Midgley S. Multimodality monitoring as a guide to treatment of intracranial hypertension after severe brain injury. Neurosurgery. Apr 1993;32(4):547-52; discussion 552-3. [Medline].

  82. Chan KH, Miller JD, Dearden NM, Andrews PJ, Midgley S. The effect of changes in cerebral perfusion pressure upon middle cerebral artery blood flow velocity and jugular bulb venous oxygen saturation after severe brain injury. J Neurosurg. Jul 1992;77(1):55-61. [Medline].

  83. Colohan A, Dacey RG, Alves WM, et al. Neurologic and neurosurgical implication of mild head injury. J Head Trauma Rehab. 1986;10(9):13-21.

  84. Contant CF, Robertson CS, Gopinath SP, et al. Determination of clinically important thresholds in continuously monitored patients with head injury. J Neurotrauma. 1993;10:S57.

  85. Dendooven AM, Lissens M, Bruyninckx F, Vanhecke J. Electrical injuries to peripheral nerves. Acta Belg Med Phys. Oct-Dec 1990;13(4):161-5. [Medline].

  86. Dendooven AM, Lissens M, Bruyninckx F, Vanhecke J. Electrical injuries to peripheral nerves. Acta Belg Med Phys. Oct-Dec 1990;13(4):161-5. [Medline].

  87. Engrav LH, Gottlieb JR, Walkinshaw MD, Heimbach DM, Trumble TE, Grube BJ. Outcome and treatment of electrical injury with immediate median and ulnar nerve palsy at the wrist: a retrospective review and a survey of members of the American Burn Association. Ann Plast Surg. Sep 1990;25(3):166-8. [Medline].

  88. Gallagher JP, Sanders M. Trauma and amyotrophic lateral sclerosis: a report of 78 patients. Acta Neurol Scand. Feb 1987;75(2):145-50. [Medline].

  89. Iob I, Salar G, Ori C, Mattana M, Casadei A, Peserico L. Accidental high voltage electrocution: a rare neurosurgical problem. Acta Neurochir (Wien). 1986;83(3-4):151-3. [Medline].

  90. Marshall LF, Gautille T, Klauber MR, et al. The outcome of severe closed head injury. J Neurosurg. 1991;75:S28-S26.

  91. Narayan RK. Head injury. In: Grossman RG, ed. Principles of Neurosurgery. New York: Raven Press; 1991:257.

  92. Rimel RW, Giordani B, Barth JT, Boll TJ, Jane JA. Disability caused by minor head injury. Neurosurgery. Sep 1981;9(3):221-8. [Medline].

  93. Rimel RW, Giordani B, Barth JT, Jane JA. Moderate head injury: completing the clinical spectrum of brain trauma. Neurosurgery. Sep 1982;11(3):344-51. [Medline].

  94. Rosner MJ. Pathophysiology and management of increased intracranial pressure. In: Andrews BT, ed. Neurosurgical Intensive Care. New York: McGraw-Hill; 1993:57-112.

  95. Stein SC, Young GS, Talucci RC, Greenbaum BH, Ross SE. Delayed brain injury after head trauma: significance of coagulopathy. Neurosurgery. Feb 1992;30(2):160-5. [Medline].

  96. Temkin NR, Dikmen SS, Wilensky AJ, Keihm J, Chabal S, Winn HR. A randomized, double-blind study of phenytoin for the prevention of post-traumatic seizures. N Engl J Med. Aug 23 1990;323(8):497-502. [Medline].

  97. Turner HB, Anderson RL, Ward JD, et al. NINDS Tramatic coma data bank: intracranial pressure monitoring methodology. J Neurosurg. 1991;75:S21.

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Further Reading

Clinical guidelines
Davis PC, Brunberg JA, De La Paz RL, Dormont D, Jordan JE, Mukherji SK, Seidenwrum DJ, Turski PA, Wippold FJ II, Zimmerman RD, Sloan MA, Expert Panel on Neurologic Imaging. ACR Appropriateness Criteria® head trauma. [online publication]. Reston (VA): American College of Radiology (ACR); 2008. 13 p.

Work Loss Data Institute. Head (trauma, headaches, etc., not including stress & mental disorders). Corpus Christi (TX): Work Loss Data Institute; 2008. 152 p.

Sasser SM, Hunt RC, Sullivent EE, Wald MM, Mitchko J, Jurkovich GJ, Henry MC, Salomone JP, Wang SC, Galli RL, Cooper A, Brown LH, Sattin RW, National Expert Panel on Field Triage, Centers for Disease Control and Prevention. Guidelines for field triage of injured patients. Recommendations of the National Expert Panel on Field Triage. MMWR Recomm Rep 2009 Jan 23;58(RR-1):1-35. 78

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Keywords

traumatic brain injury, TBI, closed head injury, nonpenetrating head injury, epidural hematoma, subdural hematoma, subarachnoid hemorrhage, SAH, intraventricular hemorrhage, intracranial hemorrhage, intracerebral hemorrhage, ICH, cerebral contusion, coup injury, contrecoup injury, diffuse axonal injury, DAI, generalized brain ischemia, Duret hemorrhage, brain stem injury, brain death, intracranial pressure, ICP, cerebral perfusion pressure, CPP, cerebrospinal fluid, CSF, decompressive craniotomy, motor vehicle collisions, motor vehicle accident, MVCs, contemporary neuromonitoring

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Contributor Information and Disclosures

Author

Leonardo Rangel-Castilla, MD, Staff Physician, Division of Neurosurgery, University of Texas Medical Branch School of Medicine
Leonardo Rangel-Castilla, MD is a member of the following medical societies: American Association of Neurological Surgeons and Congress of Neurological Surgeons
Disclosure: Nothing to disclose.

Coauthor(s)

Jaime Gasco, MD, Staff Physician, Department of Neurosurgery, University of Texas Medical Branch School of Medicine
Jaime Gasco, MD is a member of the following medical societies: American Association of Neurological Surgeons and Congress of Neurological Surgeons
Disclosure: Nothing to disclose.

Fadi Hanbali, MD, FACS, Associate Professor, Division of Neurosurgery, Department of Surgery, Texas Tech University Health Sciences Center; Associate Professor, Department of Orthopedic Surgery, Texas Tech University Health Sciences Center; Adjunct Professor, Departments of Neurosurgery and Orthopedic Surgery, Division of Neurosurgery, University of Texas Medical Branch
Fadi Hanbali, MD, FACS is a member of the following medical societies: American College of Surgeons, American Medical Association, and Congress of Neurological Surgeons
Disclosure: Nothing to disclose.

Paul Salinas, MD, Resident Physician, Department of Neurosurgery, University of Texas Medical Branch at Galveston
Disclosure: Nothing to disclose.

Medical Editor

Paul L Penar, MD, Professor, Department of Surgery, Division of Neurosurgery, University of Vermont School of Medicine
Paul L Penar, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, and Congress of Neurological Surgeons
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Ryszard M Pluta, MD, PhD, Associate Professor, Neurosurgical Department Medical Research Center, Polish Academy of Sciences at Warsaw, Poland; Senior Researcher, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, NIH
Ryszard M Pluta, MD, PhD is a member of the following medical societies: Congress of Neurological Surgeons and Polish Society of Neurosurgeons
Disclosure: Nothing to disclose.

CME Editor

Paolo Zamboni, MD, Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy
Paolo Zamboni, MD is a member of the following medical societies: American Venous Forum and New York Academy of Sciences
Disclosure: Nothing to disclose.

Chief Editor

Allen R Wyler, MD, Former Medical Director, Northstar Neuroscience, Inc
Allen R Wyler, MD is a member of the following medical societies: American Academy of Neurological and Orthopaedic Surgeons, American Association of Neurological Surgeons, and Society of Neurological Surgeons
Disclosure: Nothing to disclose.

 
 
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