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ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMjQ4ODQwLW92ZXJ2aWV3\nDrugs & Diseases > Neurosurgery\nEpidural Hematomas\nAuthor: Jamie S Ullman, MD, FACS; Chief Editor: Brian H Kopell, MD more...\nSections Epidural Hematomas\nRelevant Anatomy\nSurgical Therapy\nPreoperative Details\nIntraoperative Details\nPostoperative Details\nOutcome and Prognosis\nFuture and Controversies\nEpidural hematoma (EDH) is an easily treated form of head injury that is often associated with a good prognosis. In rare instances, such hemorrhages can be spontaneous. Advances in contemporary CT imaging have made confirmation of an EDH diagnosis rapid and accurate. Although epidural hematomas are relatively uncommon (approximately 2% of all patients with head injuries and < 10% of those who are comatose), they should always be considered in evaluation of a serious head injury. Patients with epidural hematomas who meet surgical criteria and receive prompt surgical intervention can have an excellent prognosis if there is limited underlying primary brain damage from the traumatic event. [1]\nEDH occurs in the potential space between the dura and the cranium. Epi is Greek for over or upon. An EDH can also be referred to as extradural (outside of the dura).\nEDH results from interruption of dural vessels, including branches of the middle meningeal arteries, veins, dural venous sinuses, and skull vessels. Continued bleeding and growth can result in intracranial hypertension.\nAn image depicting epidural hemorrhage can be seen below.\nCT scan of an acute left-sided epidural hematoma. Note the typical convex or lens-shaped appearance. The hematoma takes this shape as the dura strips from the undersurface of the cranium, limited by the suture lines. A midline shift of the ventricular system is present. This hemorrhage requires immediate surgical evacuation.\nAs many as 2% of all head-injured patients and 15% of those with fatal head injuries are estimated to have EDH, the incidence of which is proportionate to age in the pediatric population. Approximately 17% of previously conscious patients who deteriorate into coma following a trauma have EDH. [31]\nUsing the Nationwide Inpatient Sample (NIS), a retrospective analysis was performed of all cases of EDH in the United States. A total of 5189 admissions were identified, and in-hospital mortality and complication rate were determined to be 3.5% and 2.9%, respectively. [2]\nTrauma is the typical cause of EDH. The trauma frequently is a blunt impact to the head from an assault, fall, or other accident. Dystocia, forceps delivery, and excessive skull moulding through the birth canal have been implicated in EDH in newborns. [3]\nUnlike the subdural hematoma, cerebral contusion, or diffuse axonal injury of the brain, EDH is not generated secondary to head motion or acceleration. EDH is mainly caused by structural disruption of the dural and skull vessels commonly associated with calvarial fractures. Laceration of the middle meningeal artery and its accompanying dural sinuses is the most common etiology.\nIn the posterior fossa, disruption of dural venous sinuses (eg, transverse or sigmoid sinus) by fracture may lead to EDH. Disruption of the superior sagittal sinus may cause vertex EDH. Other non-arterial sources of epidural hemorrhage include venous lakes, diploic veins, arachnoid granulations, and the petrosal sinuses. Anterior temporal tip epidural hematomas have been postulated to form due disruption of the sphenoparietal sinus. [4]\nPosterior fossa epidural hemorrhage can mimic a sinus thrombus by compressing and displacing the sinuses. It is important to recognize this possibility, because treatment of a suspected thrombus with anticoagulation can worsen epidural hemorrhage. [5]\nA small number of epidural hematomas have been reported in the absence of trauma. The etiologies include infectious diseases of the skull, vascular malformations of the dura mater, and metastasis to the skull. Spontaneous EDH can also develop in patients with coagulopathies associated with other primary medical problems (eg, end-stage liver disease, chronic alcoholism, other disease states associated with dysfunctional platelets).\nMost epidural hematomas are traumatic in origin, often involving a blunt impact to the head. Patients may have external evidence of head injuries such as scalp lacerations, cephalohematoma, or contusions. Systemic injuries may also be present. Depending on the force of impact, patients may present with no loss of consciousness, brief loss of consciousness, or prolonged loss of consciousness.\nThe classic lucid interval occurs in 20-50% of patients with EDH. Initially, the concussive force that caused the head injury results in an alteration of consciousness. After recovering consciousness, the EDH continues to expand until the mass effect of the hemorrhage itself results in increased intracranial pressure, a decreased level of consciousness, and a possible herniation syndrome.\nWith severe intracranial hypertension, a Cushing response may occur. The classic Cushing triad involves systemic hypertension, bradycardia, and respiratory depression. This response usually occurs when cerebral, particularly brainstem, perfusion is compromised by increased intracranial pressure. Antihypertensive therapy during this time may lead to critical cerebral ischemia and cell death. [6] Evacuation of the mass lesion alleviates the Cushing response.\nNeurological assessment is essential. Attention should be paid to the level of consciousness, motor activity, eye opening, verbal output, pupillary reactivity and size, and lateralizing signs such as hemiparesis or plegia. The Glasgow Coma Score (GCS) is essential in assessing the current clinical condition (see the Glasgow Coma Scale calculator). The GCS has been positively correlated with outcome. In awake patients with a mass lesion, the pronator drift phenomenon might help to assess clinical significance. Drifting of the extremity when the patient is asked to hold both arms outstretched with palms facing upward indicates subtle but significant mass effect.\nThe diagnosis and indications for treatment of EDH are discussed in the following sections.\nBelow the skull bone lies the dura mater, which overlies the leptomeningeal structures, the arachnoid, and the pia mater, which, in turn, overlie the brain. The dura mater consists of 2 layers, with the outer layer serving as a periosteal layer for the inner surface of the skull.\nAs a person ages, the dura becomes more adherent to the skull, reducing the frequency of EDH formation. In infancy, the skull is more pliable and less likely to fracture. EDH can form when the dura is stripped from the skull during impact.\nThe dura is most adherent to the sutures, which connect the various bones of the skull. The major sutures are the coronal sutures (frontal and parietal bones), the sagittal sutures (both parietal bones), and the lambdoid sutures (parietal and occipital bones). EDH rarely extends beyond the sutures.\nThe region most commonly involved with EDH is the temporal region (70-80%). In the temporal region, the bone is relatively thin and the middle meningeal artery is close to the inner table of the skull. The incidence of EDH in the temporal region is lower in pediatric patients because the middle meningeal artery has not yet formed a groove within the inner table of the skull. [7] EDH occurs in the frontal, occipital, and posterior fossa regions with approximately equal frequency. EDH occurs less frequently in the vertex or parasagittal areas.\nAccording to a recent anatomical study by Fishpool et al, the middle meningeal artery is accompanied by 2 dural sinuses that are situated along each side of the vessel. [8] Therefore, laceration of this artery is likely to cause a mixture of arterial and venous bleeding.\nEDH, when not treated by careful observation or surgery, may result in eventual cerebral herniation and brainstem compression, with cerebral infarction or death as a consequence. Therefore, recognition of EDH is extremely important.\nMaugeri R, Anderson DG, Graziano F, Meccio F, Visocchi M, Iacopino DG. Conservative vs. Surgical Management of Post-Traumatic Epidural Hematoma: A Case and Review of Literature. Am J Case Rep. 2015 Nov 14. 16:811-7. [Medline].\nBir 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].\nHamlat A, Heckly A, Adn M, Poulain P. Pathophysiology of intracranial epidural haematoma following birth. Med Hypotheses. 2006. 66(2):371-4. [Medline].\nGean AD, Fischbein NJ, Purcell DD, et al. Benign anterior temporal epidural hematoma: indolent lesion with a characteristic CT imaging appearance after blunt head trauma. Radiology. 2010 Oct. 257(1):212-8. [Medline].\nSingh S, Ramakrishnaiah RH, Hegde SV, Glasier CM. Compression of the posterior fossa venous sinuses by epidural hemorrhage simulating venous sinus thrombosis: CT and MR findings. Pediatr Radiol. 2016 Jan. 46 (1):67-72. [Medline].\nUllman JS. Cerebrovascular pathophysiology and monitoring in the neurosurgical intensive care unit. Andrews BT. Intensive Care in Neurosurgery. New York: Thieme; 2003. 29-46.\nMiller DJ, Steinmetz M, McCutcheon IE. Vertex epidural hematoma: surgical versus conservative management: two case reports and review of the literature. Neurosurgery. 1999 Sep. 45(3):621-4; discussion 624-5. [Medline].\nFishpool SJ, Suren N, Roncaroli F, Ellis H. Middle meningeal artery hemorrhage: an incorrect name. Clin Anat. 2007 May. 20(4):371-5. [Medline].\nMayr R, Troyer S, Kastenberger T, et al. The impact of coagulopathy on the outcome of traumatic epidural hematoma. Arch Orthop Trauma Surg. 2012 Jun 8. [Medline].\nAl-Nakshabandi NA. The swirl sign. Radiology. 2001 Feb. 218(2):433. [Medline].\nArrese I, Lobato RD, Gomez PA, Nunez AP. Hyperacute epidural haematoma isodense with the brain on computed tomography. Acta Neurochir (Wien). 146(2):193-194. [Medline].\nPark HK, Joo WI, Chough CK, Cho CB, Lee KJ, Rha HK. The clinical efficacy of repeat brain computed tomography in patients with traumatic intracranial haemorrhage within 24 hours after blunt head injury. Br J Neurosurg. 2009 Dec. 23(6):617-21. [Medline].\nChen TY, Wong CW, Chang CN. The expectant treatment of \"asymptomatic\" supratentorial epidural hematomas. Neurosurgery. 32(2):176-179; discussion 179. [Medline].\nOffner PJ, Pham B, Hawkes A. Nonoperative management of acute epidural hematomas: a \"no-brainer\". Am J Surg. 2006 Dec. 192(6):801-5. [Medline].\nBasamh M, Robert A, Lamoureux J, Saluja RS, Marcoux J. Epidural Hematoma Treated Conservatively: When to Expect the Worst. Can J Neurol Sci. 2016 Jan. 43 (1):74-81. [Medline].\n[Guideline] Bullock MR, Chesnut R, Ghajar J, Gordon D, Hartl R, Newell DW. Surgical management of acute epidural hematomas. Neurosurgery. 2006 Mar. 58(3 Suppl):S7-15; discussion Si-iv. [Medline]. [Full Text].\nSongara A, Patil HG, Nayaran S. Traumatic posterior fossa extradural hematoma: case report and review of literature. Int Surg J. 2016. 3(1):369-71. [Full Text].\nLi S, Zhang H, Jiao QF, Liu Z, Mao BY. A comparative study on therapeutic method of traumatic epidural hematoma. Chin J Traumatol. 2007 Jun. 10(3):166-70. [Medline].\nServadei F, Nanni A, Nasi MT. Evolving brain lesions in the first 12 hours after head injury: analysis of 37 comatose patients. Neurosurgery. 1995. 37(5):899-906; discussion 906-907. [Medline].\nRocchi G, Caroli E, Raco A, Salvati M, Delfini R. Traumatic epidural hematoma in children. J Child Neurol. 2005 Jul. 20(7):569-72. [Medline].\nBerker M, Cataltepe O, Ozcan OE. Traumatic epidural haematoma of the posterior fossa in childhood: 16 new cases and a review of the literature. Br J Neurosurg. 17(3):226-229. [Medline].\nBozbuga M, Izgi N, Polat G. Posterior fossa epidural hematomas: observations on a series of 73 cases. Neurosurg Rev. 1999. 22(1):34-40. [Medline].\nChesnut RM, Servadei F. Surgical treatment of post-traumatic mass lesions. In: Marion DW, ed. Traumatic Brain Injury. 1999:81-99.\nKelly DF, Nikas DL, Becker DP. Diagnosis and treatment of moderate and severe head injuries in adults. In: Youmans JR, ed. Neurological Surgery. 1996. 3:1643-1645.\nLee EJ, Hung YC, Wang LC. Factors influencing the functional outcome of patients with acute epidural hematomas: analysis of 200 patients undergoing surgery. J Trauma. 45(5):946-952. [Medline].\nLiau LM, Bergsneider M, Becker DP. Pathology and pathophysiology of head injury. In: Youmans JR, ed. Neurological Surgery. 4th ed. 1996:1549-1594.\nLiu JT, Tyan YS, Lee YK, Wang JT. Emergency management of epidural haematoma through burr hole evacuation and drainage. A preliminary report. Acta Neurochir (Wien). 2006 Mar. 148(3):313-7; discussion 317. [Medline].\nLobato RD, Rivas JJ, Gomez PA. Head-injured patients who talk and deteriorate into coma. Analysis of 211 cases studied with computerized tomography. J Neurosurg. 75(2):256-261. [Medline].\nRadulovic D, Janosevic V, Djurovic B, Slavik E. Traumatic delayed epidural hematoma. Zentralbl Neurochir. 2006 May. 67(2):76-80. [Medline].\nSuzuki S, Endo M, Kurata A, et al. Efficacy of endovascular surgery for the treatment of acute epidural hematomas. AJNR Am J Neuroradiol. 2004 Aug. 25(7):1177-80. [Medline].\nGoodman JC. Neuropathology of Traumatic Brain Injury. HR Winn. Youmans and Winn Neurological Surgery, 4-Volume Set. 7th Ed. Elsevier; 30 Nov 2016. 2765-77.\nAxial CT scan that demonstrates a large vertex, bifrontoparietal epidural hemorrhage (EDH). Air bubbles are within the hematoma.\nCT bone window image of same patient in Media file 2 that demonstrates a large midline fracture.\nCoronal CT scan reconstruction that further clarifies the thickness and mass effect associated with this vertex epidural hemorrhage (EDH).\nSagittal CT scan reconstruction that further defines the anterior-posterior extent of the vertex epidural hemorrhage (EDH).\nCT image of a pre-adolescent male with a left posterior fossa epidural hemorrhage (EDH). Such hemorrhages need to be watched carefully, and the surgical team should have a low threshold for surgical intervention because this region has less room to accommodate mass lesions.\nBone window of the same patient as Media file 6 that reveals a diastasis (separation) of the left mastoid suture.\nJamie S Ullman, MD, FACS Professor, Department of Neurosurgery, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell; Director of Neurotrauma, Northwell Institute of Neurology and Neurosurgery, North Shore University Hospital\nJamie S Ullman, MD, FACS is a member of the following medical societies: American Association of Neurological Surgeons, American College of Surgeons, Congress of Neurological Surgeons\nDisclosure: Principal investigator on a clinical experience protocol for: Helius Medical.\nAnthony Sin, MD Clinical Fellow in Neurotrauma, Department of Neurosurgery, Mt Sinai Services, Elmhurst Hospital Center\nRyszard 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\nRyszard M Pluta, MD, PhD is a member of the following medical societies: Polish Society of Neurosurgeons, Congress of Neurological Surgeons\nBrian H Kopell, MD Associate Professor, Department of Neurosurgery, Icahn School of Medicine at Mount Sinai\nBrian H Kopell, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, American Society for Stereotactic and Functional Neurosurgery, Congress of Neurological Surgeons, International Parkinson and Movement Disorder Society, North American Neuromodulation Society\nDisclosure: Received consulting fee from Medtronic for consulting; Received consulting fee from Abbott Neuromodulation for consulting.\nMichael G Nosko, MD, PhD Associate Professor of Surgery, Chief, Division of Neurosurgery, Medical Director, Neuroscience Unit, Medical Director, Neurosurgical Intensive Care Unit, Director, Neurovascular Surgery, Rutgers Robert Wood Johnson Medical School\nMichael G Nosko, MD, PhD is a member of the following medical societies: Academy of Medicine of New Jersey, Congress of Neurological Surgeons, Canadian Neurological Sciences Federation, Alpha Omega Alpha, American Association of Neurological Surgeons, American College of Surgeons, American Heart Association, American Medical Association, New York Academy of Sciences, Society of Critical Care Medicine\nencoded search term (Epidural Hematomas) and Epidural Hematomas\nClassification and Complications of Traumatic Brain Injury\nTraumatic Brain Injury (TBI) - Definition, Epidemiology, Pathophysiology\nNeurocritical Care for Severe Pediatric Traumatic Brain Injury\nTraumatic Brain Injury in a 39-Year-Old Man: Interactive CT Case Study\nPost Head Injury Endocrine Complications\nChronic Traumatic Encephalopathy (CTE)\nPost Head Injury Autonomic Complications\nMajor Financial Impact, Disability Tied to Post-TBI Epilepsy\nNew Head Injury Data Reinforce Restricted Antipsychotic Use in Dementia\nNeurology Clinical Practice Guidelines - 2019 Year in Review\n7 Potentially Devastating Traumatic Brain Injuries\nAccording to Neurologists\nFDA Warns of 'Serious' Respiratory Problems With Gabapentin\nBedtime Dosing of Hypertension Meds Reduces CV Events\nNovel Over-the-Counter Device May Offer Long-Lasting Pain Relief\n'Low Value' Care? 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