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Closed Head Injury Workup

  • Author: Leonardo Rangel-Castilla, MD; Chief Editor: Brian H Kopell, MD  more...
Updated: Feb 24, 2016

Laboratory Studies

Lab studies include the following:

  • CBC count including platelet count
  • Blood chemistries
  • Prothrombin time (PT) or international normalized ratio (INR)
  • Activated partial thromboplastin time (aPTT)
  • Anticonvulsant (eg, phenytoin) level - For patients who have been previously loaded or who were previously on anticonvulsant medications to ensure therapeutic levels

Imaging Studies

CT scanning of the head is the criterion standard for patients with acute closed head injuries.[16] A head CT scan is warranted, except for patients with only minor head trauma who are neurologically intact and not intoxicated with drugs or alcohol. Advantages and disadvantages of head CT scan are summarized in the following table. Table 3. Advantages and Disadvantages of CT scanning in the Head Trauma Evaluation

Table. (Open Table in a new window)

Advantages Disadvantages
Noninvasive and rapid Traumatic vascular lesions may be missed.
Very sensitive for acute hemorrhage DAI is likely to be missed.
Defines nature of ICH (ie, SDH, SAH) Motion artifact may limit study.
Defines anatomical location of lesion Posterior fossa lesions are poorly depicted.
Identifies fractures of the cranium Depressed skull fractures at the vertex (or along the plane of an axial scan) are poorly depicted.
Sensitive to detecting intracranial air The scanner has a weight limit, and a patient may be too heavy.
Sensitive in identifying foreign objects A patient may decompensate while in the scanner.
*Intracranial hemorrhage

†Subdural hemorrhage

‡Subarachnoid hemorrhage


CT scans are helpful in assessing the degree of intracranial injury, in predicting outcome, and, if findings are normal, in avoiding unnecessary hospitalization.[47, 48] CT scans are very sensitive to acute hemorrhage or skull fractures. CT scans aid in evaluating (1) intracranial hemorrhage, (2) skull fractures, (3) mass effect and midline shift, (4) obliteration of the basal cisterns, and (5) evidence of herniation (subfalcine, tonsillar, or uncal).

CT scans cannot diagnose a concussion (which is a clinical diagnosis) and are poor for diagnosing DAI. If DAI has occurred, CT scans may show small hemorrhages in the corpus callosum and cerebral peduncles. In this case, an MRI of the brain should be obtained on an elective basis when the patient is clinically stable because no effective treatment of DAI is currently available. MRI is more sensitive for detecting brainstem injuries, posterior fossa lesions, and brain edema. For advantages and disadvantages of CT scanning in patients with closed head injuries, see Table 3.

As a general rule, a repeat head CT scan is recommended within 4-8 hours of the initial scan in patients with intracranial hemorrhages and/or coagulopathies.[49, 50, 51] A repeat head CT scan is recommended sooner in patients who are deteriorating neurologically.

Spinal cord injuries should be considered possible in patients with closed head injuries. Spinal cord injuries are present in up to 10% of these patients.[45] Accordingly, the cervical spine should be evaluated (with 3 views) during the initial evaluation. C1-C2 should be evaluated with a thin-cut CT scan in intubated patients. If any abnormalities are noted on the initial cervical plain radiographs, this area should be further evaluated with a CT scan. An MRI may be necessary to image a spinal cord injury. A rigid cervical collar (Philly) should remain on at all times while the patient is being evaluated.

The results of one study found that computed tomographic angiography (CTA) findings used in addition to other screening criteria may help identify injuries not captured using conventional screening guidelines alone.[52]

In a systematic review of the clinical utility of single photon emission CT (SPECT) for TBI, SPECT was shown to have some advantages over CT and MRI in the detection of mild TBI and to have excellent negative predictive value. The authors suggest it may be an important second test in settings where CT or MRI are negative after a closed head injury with post-injury neurologic or psychiatric symptoms. The most commonly abnormal regions revealed by SPECT in cross-sectional studies were frontal (94%) and temporal (77%) lobes. SPECT was found to outperform both CT and MRI in both acute and chronic imaging of TBI, particularly mild TBI. It was also found to have a near 100% negative predictive value.[53]

The findings of one study strongly suggest that diffusion tensor imaging (DTI), but not "classic" MRI sequences, is a more precise and accurate measurement to assess a degree of brain injury after blunt trauma. DTI is a valuable research tool to further the understanding of pathophysiological mechanism(s) evoked by blast injury and may become a prognostic tool.[54]

Henninger et al found that in 136 patients 50 years or older who were admitted to a neurologic/trauma ICU, preexisting leukoaraiosis (white matter hyperintensities) was significantly associated with a poor outcome at 3 and 12 months. According to the study findings, the independent association between leukoaraiosis and poor outcome remained when the analysis was restricted to patients who survived up to 3 months, had moderate-to-severe TBI [enrollment Glasgow Coma Scale (GCS) ≤12; P = 0.001], or had mild TBI (GCS 13-15; P = 0.002), respectively.[55]

According to one study, meningeal enhancement on contrast-enhanced fluid-attenuated inversion recovery (FLAIR) images can help detect traumatic brain lesions and other abnormalities that are not identified on routine unenhanced MRI in symptomatic patients with mild traumatic brain injury. The authors therefore recommended contrast-enhanced FLAIR MR imaging when a contrast MR study is indicated in patients with symptomatic prior closed mild head injury. In a study of 25 patients, 3 additional cases of brain abnormality were detected with the contrast-enhanced FLAIR images. Meningeal enhancement was identified on contrast-enhanced FLAIR images in 9 cases, while the other routine image sequences showed no findings of traumatic brain injury. Overall, the additional contrast-enhanced FLAIR images revealed more extensive abnormalities than routine imaging in 37 cases.[56]

Patients who arrive with a decreased GCS and normal findings on head CT scans may have another condition that needs to be considered. These include the following:

  • Acute ischemic stroke (within 24 h) that is not seen on head CT scan
  • Postictal state
  • Spinal cord injury
  • Intoxication or effects of illicit drug use
  • Prior medical conditions (Speaking with family members may help in differentiating acute from chronic conditions.)

Other Tests

Order serum sodium, urine specific gravity, urine osmolarity, and serum osmolarity tests for individuals with urine output of 250 mL/h or more for 3 or more consecutive hours (pediatric patients, >3 mL/kg/h) and for patients who are thought to have diabetes insipidus. Large doses of mannitol can mask diabetes insipidus by producing a high urine output.



Patients with a severe brain injury (GCS score < 8), those who have labile blood pressure, those who require intensive care monitoring, and those who need surgical intervention are likely to require the placement of an indwelling urinary catheter (Foley), placement of a central venous access catheter, and invasive blood pressure monitoring via an arterial line.

ICP monitoring in patients with closed head injuries is a matter of controversy; however, most authors agree that invasive ICP monitoring is warranted in patients with a GCS score of 8 or less and an abnormal CT scan finding, in patients with suspected severe brain edema, or in any situation in which the ICP is suspected to be significantly elevated. The ICP offers data that supplement a reliable neurological examination and can be crucial in patients whose examination findings are affected by sedatives, paralytics, and other factors.

  • Patients with an abnormal head CT scan finding, a GCS score of less than 8, or both who require emergent surgery on another organ system should also be considered for some form of ICP monitoring before going to the operating room (or perhaps in the operating room) because frequent neurological examinations are not possible in this setting.
  • ICP monitoring can take 1 of 2 forms, either as an intraventricular catheter or an intracranial fiberoptic monitor (Camino).
    • The intraventricular catheter is preferred in closed head injuries when the ventricles are large enough to accommodate a catheter. The advantage of the catheter is the ability to drain CSF if the ICP is elevated (>20 mm Hg), although ventricles compromised by mass effect make draining much CSF difficult. An accurate pressure reading can be lost if the ventricle collapses around the catheter tip during drainage.
    • The advantage of the fiberoptic catheter is that ICP can be monitored in patients who have very small ventricles, in whom ventriculostomy catheters cannot be inserted. The pressure measurements are not prone to fluctuations in ventricular size. Either procedure provides adequate ICP monitoring.
Contributor Information and Disclosures

Leonardo Rangel-Castilla, MD Fellow in Cerebrovascular and Skull Base Neurosurgery, Barrow Neurological Institute

Leonardo Rangel-Castilla, MD is a member of the following medical societies: American Association of Neurological Surgeons, Congress of Neurological Surgeons, Neurocritical Care Society

Disclosure: Nothing to disclose.


Paul Salinas, MD Resident Physician, Department of Neurosurgery, University of Texas Medical Branch at Galveston

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, Congress of Neurological Surgeons

Disclosure: Nothing to disclose.

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, Congress of Neurological Surgeons

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Ryszard M Pluta, MD, PhD Associate Professor, Neurosurgical Department Medical Research Center, Polish Academy of Sciences, Poland; Clinical Staff Scientist, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health (NIH); Fishbein Fellow, JAMA

Ryszard M Pluta, MD, PhD is a member of the following medical societies: Polish Society of Neurosurgeons, Congress of Neurological Surgeons

Disclosure: Nothing to disclose.

Chief Editor

Brian H Kopell, MD Associate Professor, Department of Neurosurgery, Icahn School of Medicine at Mount Sinai

Brian H Kopell, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, International Parkinson and Movement Disorder Society, Congress of Neurological Surgeons, American Society for Stereotactic and Functional Neurosurgery, North American Neuromodulation Society

Disclosure: Received consulting fee from Medtronic for consulting; Received consulting fee from St Jude Neuromodulation for consulting; Received consulting fee from MRI Interventions for consulting.

Additional Contributors

Paul L Penar, MD, FACS Professor, Department of Surgery, Division of Neurosurgery, Director, Functional Neurosurgery and Radiosurgery Programs, University of Vermont College of Medicine

Paul L Penar, MD, FACS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, World Society for Stereotactic and Functional Neurosurgery, Congress of Neurological Surgeons

Disclosure: Nothing to disclose.

  1. Centers for Disease Control and Prevention. Get the Stats on Traumatic Brain Injury in the United States. Centers for Disease Control and Prevention. Available at Accessed: November 25, 2014.

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

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

  4. 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. 1980 Sep. 30(9):912-9. [Medline].

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

  6. 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. 1984 Feb. 119(2):186-201. [Medline].

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

  8. US Census Bureau, Population Division. Data as of July 2003. Available at: [Full Text].

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

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

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

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

  13. 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.

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

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

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

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

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

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

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

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

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

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

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

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

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

  27. Lv LQ, Hou LJ, Yu MK, et al. Risk factors related to dysautonomia after severe traumatic brain injury. J Trauma. 2011 Sep. 71(3):538-42. [Medline].

  28. 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. 2009 Mar 28. 373(9669):1105-10. [Medline].

  29. Shahlaie K, Keachie K, Hutchins IM, et al. Risk factors for posttraumatic vasospasm. J Neurosurg. 2011 Sep. 115(3):602-11. [Medline].

  30. 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. 1992 Sep. 77(3):360-8. [Medline].

  31. 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. 1992 Jul. 77(1):15-9. [Medline].

  32. 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.

  33. 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:. 1993 April 26.

  34. 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.

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

  36. 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. 1994 Jun. 57(6):717-23. [Medline].

  37. 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. 2006 May. 104(5):720-30. [Medline].

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

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

  40. 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. 1989 Jun. 29(6):746-8. [Medline].

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

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

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

  44. 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. 1985 May. 16(5):595-601. [Medline].

  45. 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.

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

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

  48. 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. 1992 Sep. 33(3):385-94. [Medline].

  49. 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.

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

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

  52. Emmett KP, Fabian TC, Dicocco JM, Zarzaur BL, Croce MA. Improving the screening criteria for blunt cerebrovascular injury: the appropriate role for computed tomography angiography. J Trauma. 2011 May. 70(5):1058-65. [Medline].

  53. Raji CA, Tarzwell R, Pavel D, Schneider H, Uszler M, Thornton J, et al. Clinical utility of SPECT neuroimaging in the diagnosis and treatment of traumatic brain injury: a systematic review. PLoS One. 2014. 9(3):e91088. [Medline]. [Full Text].

  54. Mac Donald CL, Johnson AM, Cooper D, et al. Detection of blast-related traumatic brain injury in U.S. military personnel. N Engl J Med. 2011 Jun 2. 364(22):2091-100. [Medline].

  55. Henninger N, Izzy S, Carandang R, Hall W, Muehlschlegel S. Severe leukoaraiosis portends a poor outcome after traumatic brain injury. Neurocrit Care. 2014 Dec. 21(3):483-95. [Medline].

  56. Kim SC, Park SW, Ryoo I, Jung SC, Yun TJ, Choi SH, et al. Contrast-enhanced FLAIR (fluid-attenuated inversion recovery) for evaluating mild traumatic brain injury. PLoS One. 2014. 9(7):e102229. [Medline]. [Full Text].

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

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

  59. 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. 1991 Nov. 75(5):731-9. [Medline].

  60. 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].

  61. 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. 1988 Dec. 69(6):923-7. [Medline].

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

  63. 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. 1984 Oct. 61(4):700-6. [Medline].

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

  65. 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. 1990 Nov. 73(5):725-30. [Medline].

  66. 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].

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

  68. 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. 1988 Jul. 69(1):15-23. [Medline].

  69. 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. 1991 May. 213(5):482-91. [Medline].

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

  71. 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. 1989 May. 18(5):553-5. [Medline].

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

  73. Aledort LM. Off-label use of recombinant activated factor VII--safe or not safe?. N Engl J Med. 2010 Nov 4. 363(19):1853-4. [Medline].

  74. Logan AC, Goodnough LT. Recombinant factor VIIa: an assessment of evidence regarding its efficacy and safety in the off-label setting. Hematology Am Soc Hematol Educ Program. 2010. 2010:153-9. [Medline].

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

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

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

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

  79. 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. 2001 Feb. 17(3):154-62. [Medline].

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

  81. 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].

  82. Huang YH, Lee TC, Chen WF, Wang YM. Safety of the nonabsorbable dural substitute in decompressive craniectomy for severe traumatic brain injury. J Trauma. 2011 Sep. 71(3):533-7. [Medline].

  83. Clifton GL, Coffey CS, Fourwinds S, Zygun D, Valadka A, Smith KR Jr, et al. Early induction of hypothermia for evacuated intracranial hematomas: a post hoc analysis of two clinical trials. J Neurosurg. 2012 Jul 27. [Medline].

  84. Scotter J, Hendrickson S, Marcus HJ, Wilson MH. Prognosis of patients with bilateral fixed dilated pupils secondary to traumatic extradural or subdural haematoma who undergo surgery: a systematic review and meta-analysis. Emerg Med J. 2014 Nov 10. [Medline].

  85. 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.

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

  87. 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].

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

  89. 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. 1990 Nov. 73(5):699-709. [Medline].

  90. Raj R, Mikkonen ED, Kivisaari R, Skrifvars MB, Korja M, Siironen J. Mortality in Elderly Patients Operated for an Acute Subdural Hematoma: A Surgical Case Series. World Neurosurg. 2015 Nov 5. [Medline].

  91. Lukasiewicz AM, Grant RA, Basques BA, Webb ML, Samuel AM, Grauer JN. Patient factors associated with 30-day morbidity, mortality, and length of stay after surgery for subdural hematoma: a study of the American College of Surgeons National Surgical Quality Improvement Program. J Neurosurg. 2015 Aug 28. 1-7. [Medline].

  92. Rovlias A, Theodoropoulos S, Papoutsakis D. Chronic subdural hematoma: Surgical management and outcome in 986 cases: A classification and regression tree approach. Surg Neurol Int. 2015. 6:127. [Medline].

  93. Bir SC, Maiti TK, Ambekar S, Nanda A. Incidence, hospital costs and in-hospital mortality rates of epidural hematoma in the United States. Clin Neurol Neurosurg. 2015 Nov. 138:99-103. [Medline].

  94. 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.

  95. Ley EJ, Srour MK, Clond MA, et al. Diabetic patients with traumatic brain injury: insulin deficiency is associated with increased mortality. J Trauma. 2011 May. 70(5):1141-4. [Medline].

  96. [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. 2009 Jan 23. 58:1-35. [Medline].

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

  98. 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. 1993 Apr. 32(4):547-52; discussion 552-3. [Medline].

  99. 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. 1992 Jul. 77(1):55-61. [Medline].

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

  101. 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. 1990 Sep. 25(3):166-8. [Medline].

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

  103. 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].

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

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

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

  107. 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. 1990 Aug 23. 323(8):497-502. [Medline].

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

CT scan of left frontal acute epidural hematoma (black arrow) with midline shift (white arrow). Note the left posterior falx subdural hematoma and left frontoparietal cortical contusion.
CT scan of left frontoparietal acute subdural hematoma (black arrow). Note the moderate amount of midline shift.
CT scan of bilateral acute intraventricular hemorrhages (black arrow). Note the comminuted skull fractures that involve bilateral frontal, temporal, and parietal bones (white arrow). Note the ischemic changes in both frontal lobes, subarachnoid hemorrhages in the intrahemispheric fissure and left frontal lobe, and multiple intraparenchymal hemorrhages in both frontal poles.
MRI of the brain that shows diffuse axonal injury (DAI) and hyperintense signal in the corpus callosum (splenium), septum pellucidum, and right external capsule.
MRI of the brain (sagittal view) that shows a Duret hemorrhage in the splenium of the corpus callosum.
Cerebral blood flow/cerebral perfusion pressure chart.
Table 1. American Academy of Neurology Concussion Grading Scale
Grade 1 Grade 2 Grade 3
Transient confusion Transient confusion ...
No loss of consciousness No loss of consciousness Brief or prolonged loss of consciousness
Concussion symptoms or mental status change resolves in 15 min or less Concussion symptoms or mental status change resolves in more than 15 min  


Table 2. Glasgow Coma Scale
Best Motor Response Obeys commands 6
Localizes 5
Withdraws (abnormal flexion) 4
Flexion (decorticate posturing) 3
Extension (decerebrate posturing) 2
No response 1
Verbal Response Oriented 5
Confused 4
Inappropriate words 3
Incomprehensible sounds 2
No response 1
Eye Opening Spontaneous 4
To command 3
To pain 2
No response 1
Total   3-15
Advantages Disadvantages
Noninvasive and rapid Traumatic vascular lesions may be missed.
Very sensitive for acute hemorrhage DAI is likely to be missed.
Defines nature of ICH (ie, SDH, SAH) Motion artifact may limit study.
Defines anatomical location of lesion Posterior fossa lesions are poorly depicted.
Identifies fractures of the cranium Depressed skull fractures at the vertex (or along the plane of an axial scan) are poorly depicted.
Sensitive to detecting intracranial air The scanner has a weight limit, and a patient may be too heavy.
Sensitive in identifying foreign objects A patient may decompensate while in the scanner.
*Intracranial hemorrhage

†Subdural hemorrhage

‡Subarachnoid hemorrhage

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