Epidural/Subdural Hematoma Case File

Epidural/Subdural Hematoma Case File

Eugene C. Toy, MD, Ericka Simpson, MD, Pedro Mancias, MD, Erin E. Furr-Stimming, MD

CASE 8

A 17-year-old football player returning a kickoff collided into an opposing player, causing him to lose his helmet, and was subsequently struck on the right side of his head by the defender’s knee. He fell to the ground and was unconscious for 20 to 30 seconds. He was then immediately transported to the closest hospital. Twenty minutes after the accident, he was alert and conscious without neurologic deficit; however, he suffered from amnesia for the event. Physical examination revealed a superficial bruise to the scalp in the right parietal region. Approximately 1 hour after the injury, the patient suffered a generalized tonic-clonic (GTC) seizure. Lorazepam 4 mg intravenous (IV) was administered, and the seizure was aborted. A computed tomography (CT) of the brain was performed approximately an hour and a half after the trauma was unremarkable. He was transferred to a larger hospital shortly thereafter for observation. On admission, neurologic examination showed slight psychomotor slowing and slurred speech, which was thought to be secondary to the previous lorazepam administration due to absence of any focal neurologic deficits. The Glasgow Coma Scale (GCS) score was 15 of 15. Routine laboratory investigations and electrocardiography were normal. After 8 hours of the initial trauma, he complained of a severe headache and had associated nausea and vomiting.

▶ What is the most concerning diagnosis?

▶ What is the next diagnostic step?

▶ What is the next step in therapy?

ANSWERS TO CASE 8:

Epidural/Subdural Hematoma                                        

Summary: This was a case of a 17-year-old athlete with an acute sports-related traumatic brain injury. The injury was associated with a transient loss of consciousness and subsequent GTC seizure. Although his initial examination was nonfocal and screening of CT of the brain was normal, his condition worsened with onset of a severe generalized headache with nausea and vomiting.

• Most concerning diagnosis: An epidural hematoma (EDH).
• Next diagnostic step: Repeat noncontrast CT scan of the brain.
• Next step in therapy: Careful observation and neurologic examination, neurosurgical consultation, and careful evaluation for other signs of trauma.

ANALYSIS

Objectives

1. Understand the mechanism of why an EDH forms and expands.
2. Identify the signs and symptoms associated with an expanding EDH that require urgent neurosurgical intervention.

Considerations

The key feature of this case is that the patient was a healthy individual who had a traumatic closed head injury. He experienced loss of consciousness, followed by a normal lucid period. He then suffered a GTC seizure followed by cognitive slowing after administration of lorazepam. It is not possible to exclude the neurologic symptoms as a result of the original closed head injury. One has to decide whether this suggests an underlying etiology such as migraine headaches, one that is a result of the trauma, or both. A lucid period prior to neurologic deterioration is a classic presentation for an EDH; however, less than one-third of patients with EDHs actually present as such. Other signs and symptoms include headache, nausea, vomiting, and seizure. Other possibilities include a subarachnoid hemorrhage, subdural hematoma, cerebral contusion and diffuse axonal injury, although the transient lucid period would not be typical. A patient with an EDH can rapidly deteriorate due to the expanding intracranial hemorrhage causing mass effect on the brain and brainstem. Moreover, patients with a posterior fossa EDH can have a dramatic deterioration. A patient can be conscious and talking for 1 minute and apneic and comatose the next minute and close to dying from brainstem compression if emergent neurosurgical intervention is not performed.

APPROACH TO:

Epidural Hematoma                                        

EDH is an accumulation of blood between the inner table of the skull and the outer dural membrane. The inciting event is often trauma, frequently with a “blunt instrument.” In 85% to 95% of patients, this type of trauma results in an overlying fracture of the skull. Blood vessels in close proximity to the fracture are the sources of the hemorrhage that lead to an EDH. Because the underlying brain has usually been minimally injured, the prognosis is excellent if treated early and aggressively. Outcome from surgical decompression and repair is related directly to the patient’s preoperative neurologic condition. The incidence of EDHs is about half of that of subdural hematomas. Males outnumber females by 4:1. EDHs usually occur in young adults and are rare in persons younger than 2 years or older than 60 years. This is most likely due to the dura being strongly adhered to the inner table of the skull in elderly patients. Also, the association of hematoma and skull fracture is less common in young children because of the pliability of the calvarium. EDHs may also occur in the spine, namely spinal EDHs. These are also considered a neurosurgical emergency, often times requiring surgical intervention.

EDHs can be divided into acute (58%) from arterial bleeding, subacute (31%), and chronic (11%) from venous bleeding. Two-thirds of the cases of cranial EDH are in the temporal–parietal area and result from a tear of the middle meningeal artery or its dural branches. Frontal and occipital EDHs each constitute approximately 10%, with the latter occasionally extending above and below the tentorium. The rapid bleeding associated with arterial tears is one of the reasons why these lesions require rapid evaluation and intervention. Occasionally, torn venous sinuses can cause an EDH, particularly in the parietal–occipital region or in the posterior fossa. These injuries tend to be smaller and associated with a more benign course. Typically, venous EDHs only form with a depressed skull fracture due to disruption of the dura from the bone and thus create a space for blood to accumulate.

The reported rate of mortality ranges from 5% to 43%. Higher rates are generally seen at both ends of the age spectrum (ie, <5 years and >55 years). Mortality is also higher in patients with signs of more extensive anatomic (intradural lesions, increased hematoma volume) or clinical (rapid clinical progression, pupillary abnormalities, increased intracranial pressure [ICP], lower GCS) involvement, in addition to those with EDH in a temporal location. Mortality rates are essentially nil for patients not in coma preoperatively, approximately 10% for obtunded patients, and 20% for patients in deep coma.

EVALUATION

History and Physical Examination

Symptoms of EDH include the following:

• Headache.
• Nausea and/or vomiting.
• Seizures.
• Focal neurologic deficits (eg, visual field cuts, aphasia, weakness, numbness).
• Spinal EDHs typically cause severe localized back pain with delayed radiating pain which can mimic radicular pain seen in disc herniation. Associated symptoms can include weakness, numbness, urinary incontinence, and fecal incontinence.

The physical examination is focused to determine the localization of the deficit and identify signs of increasing ICP and/or herniation.

Physical signs of expanding intracranial mass include the following:

• Cushing response (caused by increased ICP) (triad of hypertension, bradycardia, and irregular respirations)
• Decreased or fluctuating levels of consciousness/GCS
• Dilated, sluggish, or fixed pupil(s), bilateral or ipsilateral to injury
• Coma
• Decerebrate posturing
• Hemiplegia contralateral to injury
• Other focal neurologic deficits (eg, aphasia, visual field deficits, numbness, ataxia)

In addition, the physical examination should include a thorough evaluation for evidence of traumatic sequelae:

• Skull fractures, hematomas, or lacerations
• Contusion, laceration, or bony step-off in the area of injury
• Cerebrospinal fluid (CSF) otorrhea or rhinorrhea resulting from skull fracture with disruption of the dura
• Hemotympanum
• Instability of the vertebral column

DIAGNOSTIC STUDIES

Laboratory Studies

• Complete blood count (CBC) with platelets to monitor for infection and assess hematocrit and platelets for further hemorrhagic risk, including underlying predisposing disorders.
• Prothrombin time (PT)/activated partial thromboplastin time (aPTT) to identify bleeding diathesis.
• Fibrin split products and d-dimers are markers of coagulation abnormalities such as disseminated intravascular coagulation (DIC). With severe head injury, breakdown of the blood–brain barrier with exposed brain tissue is a potent cause of DIC.
• Serum chemistries, including electrolytes, blood urea nitrogen (BUN), creatinine, and glucose to characterize metabolic derangements that can complicate the clinical course.
• Toxicology screen and serum alcohol level to identify associated causes of head trauma and establish whether there is a need for surveillance with regard to withdrawal symptoms.
• Type and cross an appropriate amount of blood to prepare for necessary transfusions due to blood loss or anemia.

Imaging Studies

Immediate noncontrast CT scan of the brain is the imaging of choice acutely for diagnosis. The CT scan shows the location, volume, effect, and other potential intracranial injuries. Cervical spine evaluation is usually necessary because of the risk of neck injury associated with an EDH. Clinical deterioration should prompt repeat imaging with a noncontrast CT of the brain.

Figure 8–1 illustrates the typical findings on brain CT of an EDH:

• Mass that displaces the brain away from the skull.
• Extra-axial.
• Smooth margins.
• Lenticular or biconvex homogenous density.
• Most of these masses are high density on the CT scan.
• Focal isodense or hypodense zones within EDH indicate active bleeding.
• Rarely crosses the suture line because the dura is attached more firmly to the skull at sutures.
• Air in the setting of an acute EDH suggests fracture of sinuses or mastoid air cells.

Figure 8–1. Acute epidural hematoma. The tightly attached dura is stripped from the inner table of the skull, producing a characteristic lenticular-shaped hemorrhage on noncontrast CT scan. Epidural hematomas are usually caused by tearing of the middle meningeal artery following fracture of the temporal bone. (Reproduced, with permission, from Fauci AS, et al. Harrison’s Principles of Internal Medicine. 17th ed. New York, NY: McGraw-Hill; 2008:2599.)

TREATMENT

Prior to definitive treatment with surgery, the most important considerations are to stabilize acute life-threatening conditions, initiate supportive therapy, and try to reduce ICP. Airway control and blood pressure support are vital, as is careful observation. A discussion of the exact procedures is beyond the scope of this chapter. However, elevation of the head of the bed to 30 degrees after the spine is cleared, or reverse Trendelenburg position will reduce ICP and increase venous drainage. 

A neurosurgeon should be consulted immediately for evaluation of EDH evacuation and repair. Consult a trauma surgeon for other life-threatening injuries. Although surgical treatment has been viewed as definitive, under certain conditions, some EDHs can be treated conservatively with careful observation.

Outcome

The most important factors influencing the outcome after evacuation of an EDH are the initial GCS, pupillary response, motor examination, and associated intracranial injuries seen on the CT scan. In noncomatose individuals, a favorable outcome occurs in 90% to 100% of patients and mortality ranges from 0% to 5%. For patients who are comatose, a favorable outcome occurs between 35% and 75% of the time with a mortality rate of 10% to 40%. Of interest, normally reacting pupils prior to surgery result in a favorable outcome in 84% to 100% of patients, while the great majority of individuals with bilateral abnormal pupillary reactions tend to have a poor outcome, including death. Associated intracranial injuries such as cerebral contusions also adversely impact outcome. Rapid diagnosis and timely evacuation of the hematoma are crucial in optimizing the outcome.

COMPREHENSION QUESTIONS

8.1 A 14-year-old adolescent girl was sideswiped by a car while she was riding her bicycle. She was not wearing a helmet and struck the pavement with her head, losing consciousness for about 45 seconds. The patient then was awake and alert, resting at home. The parents noted later that she became drowsy, slurred her words, and after a few minutes had some weakness of the arms. On examination, the patient was lethargic and did not have any evidence of nuchal rigidity. Which of the following is the most likely diagnosis?

A. Acute EDH

B. Chronic subarachnoid hemorrhage

C. Bacterial meningitis

D. Cerebral contusion

8.2 A 34-year-old woman is brought into the emergency department (ED) after a skiing accident. The patient lost control, hit a tree, and suffered trauma to her head. She was not wearing a helmet. A noncontrast CT of the brain was performed. Homogeneous high density signal throughout the ventricular system is noted. Which of the following is the most likely diagnosis?

A. Acute EDH

B. Subarachnoid hemorrhage with intraventricular extension due to a ruptured proximal middle cerebral artery aneurysm

C. Basal ganglia hematoma

D. Ruptured cavernous angioma

8.3 A 22-year-old college student is brought into the ED after suffering a head injury after falling off the railing of the second story balcony of his dorm. His neurologic examination is normal. He is alert and oriented. The CT scan of the brain performed 1 hour after the event is normal. Two hours later, the patient appears drowsy and does not respond to commands. You review the medication records, and no sedating medications have been given. Which of the following is the best next step?

A. Assume illicit opiate use and give naloxone.

B. Prepare the patient for neurosurgical burr holes.

C. Repeat CT scan of the brain.

D. Administer activated charcoal for probable overdose.

ANSWERS

8.1 A. The lucent interval is typical of EDH. The patient had blunt trauma to the head, followed by a lucid interval, and then cranial to caudal deterioration, which are also classic for EDH.

8.2 B. Blood in the subarachnoid space appears hyperdense and usually can be seen as a homogenous high density signal in the ventricular system.

8.3 C. An evolving EDH can occur any time after the immediate injury. Repeat CT imaging of the brain is indicated if there is any change in the neurologic status of the patient. Thus, although the first CT scan was normal, a second one is indicated due to the change in the patient’s neurologic status. Taking the patient to surgery without clear confirmation is not indicated.

    CLINICAL PEARLS    

▶ The historical hallmark of EDH is injury followed by a lucid, relatively asymptomatic period, followed by deterioration. ▶ With suspected EDH, deterioration can be quite rapid, and close observation is necessary. ▶ EDHs require emergent surgical intervention a large percentage of the time, so early neurosurgical consultation is important. ▶ Noncontrast CT scan of the brain is the recommended radiologic study for initial evaluation.

REFERENCES

Bullock MR, Chesnut R, Ghajar J, et al. Surgical Management of Traumatic Brain Injury Author Group. Surgical management of acute epidural hematomas. Neurosurgery. 2006;58(suppl 3):S7-S15; discussion Si-Siv. 

Lee EJ, Hung YC, Wang LC, et al. Factors influencing the functional outcome of patients with acute epidural hematomas: analysis of 200 patients undergoing surgery. J Trauma. 1998;45:946-952. 

Liebeskind DS. Epidural hematoma. http://www.emedicine.com/NEURO/topic574.htm. Accessed April 17, 2006. 

Neely JC 2nd, Jones BV, Crone KR. Spontaneous extracranial decompression of epidural hematoma. Pediatr Radiol. 2008;38:316-318. 

Offner PJ, Pham B, Hawkes A. Nonoperative management of acute epidural hematomas: a “no-brainer.” Am J Surg. 2006;192:801-805. 

Provenzale J. CT and MR imaging of acute cranial trauma. Emerg Radiol. 2007;14(1):1-12.

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