subdural hematoma

Subdural Hematoma

 

Definition

A subdural hematoma is a collection of blood in the space between the outer layer (dura) and middle layers of the covering of the brain (the meninges). It is most often caused by torn, bleeding veins on the inside of the dura as a result of a blow to the head.

Description

Subdural hematomas most often affect people who are prone to falling. Only a slight hit on the head or even a fall to the ground without hitting the head may be enough to tear veins in the brain, often without fracturing the skull. There may be no external evidence of the bruising on the brain's surface.

Small subdural hematomas may not be very serious, and the blood can be slowly absorbed over several weeks. Larger hematomas, however, can gradually enlarge over several weeks, even though the bleeding has stopped. This enlargement can compress the brain itself, possibly leading to death if the blood is not drained.

The time between the injury and the appearance of symptoms can vary from less than 48 hours to several weeks, or more. Symptoms appearing in less than 48 hours are due to an acute subdural hematoma. This type of bleeding is often fatal, and results from tearing of the venous sinus. If more than two weeks have passed before symptoms appear, the condition is called a chronic subdural hematoma, resulting from tearing of the smaller vein. The young and the old are most likely to experience a chronic condition. This chronic form is less risky, as pressure of the veins against the skull lessens the bleeding. Prompt medical care can reduce the probability of permanent brain damage.

Causes and symptoms

A subdural hematoma is caused by an injury to the head that tears blood vessels. In childhood, hematomas are a common complication of falls. A subdural hematoma also may be an indication of child abuse, as evidenced by shaken baby syndrome.

Symptoms tend to fluctuate, and include:

• headache
• episodes of confusion and drowsiness

• one-sided weakness or paralysis
• lethargy
• enlarged or asymmetric pupils
• convulsions or loss of consciousness after head injury
• coma

A doctor should be contacted immediately if symptoms appear. Because these symptoms mimic the signs of a stroke, the patient should tell the doctor about any head injury within the previous few months.

In an infant, symptoms may include increased pressure within the skull, growing head size, bulging fontanelle (one of two soft spots on a infant's skull), vomiting, irritability, lethargy, and seizures. In cases of child abuse, there may be fractures of the skull or other bones.

Diagnosis

A chronic subdural hematoma can be difficult to diagnose, but a slow loss of consciousness after a head injury is assumed to be a hematoma unless proven otherwise. The hematoma can be confirmed with magnetic resonance imaging (MRI), which is the preferred type of scan; a hematoma can be hard to detect on a computed tomography scan (CT scan), depending on how long after the hemorrhage the CT is done.

Treatment

Small hematomas that do not cause symptoms may not need to be treated. Otherwise, the hematoma should be surgically removed. Liquid blood can be drained from burr holes drilled into the skull. The surgeon may have to open a section of skull to remove a large hematoma or to tie off the bleeding vein.

Corticosteroids and diuretics can control brain swelling. After surgery, anticonvulsant drugs (such as phenytoin) may help control or prevent seizures, which can begin as late as two years after the head injury.

Prognosis

If treatment is provided soon enough, recovery is usually complete. Headache, amnesia, attention problems, anxiety, and giddiness may continue for some time after surgery. Most symptoms in adults usually disappear within six months, with further improvement over several years. Children tend to recover much faster.

Prevention

Because a subdural hematoma usually follows a head injury, preventing head injury can prevent a hematoma.

Resources

Organizations

American Academy of Neurology. 1080 Montreal Ave., St. Paul, MN 55116. (612) 695-1940. http://www.aan.com.

Brain Injury Association of America. 105 North Alfred St., Alexandria, VA 22314. (800) 444-6443. http://www.biausa.org.

Head Injury Hotline. P.O. Box 84151, Seattle WA 98124. (206) 621-8558. http://www.headinjury.com.

Head Trauma Support Project, Inc. 2500 Marconi Ave., Ste. 203, Sacramento, CA 95821. (916) 482-5770.

Key terms

Corticosteroids — A group of drugs similar to natural corticosteroid hormones produced by the adrenal glands. The drugs have a wide variety of applications, including use for inflammatory disorders and swelling.

Diuretics — A group of drugs that helps remove excess water from the body by increasing the amount lost by urination.

Fontanelle — One of the two soft areas on a baby's scalp; a membrane-covered gap between the bones of the skull.

sub·du·ral hem·or·rhage

extravasation of blood between the dural and arachnoidal membranes; acute and chronic forms occur; chronic hematomas may become encapsulated by neomembranes.

Synonym(s): subdural hematoma

subdural hematoma

an accumulation of blood in the subdural space, usually caused by an injury or fall. It can be acute with rapid bleeding or subacute with accumulation of blood over a longer period of time. Patients may have a chronic subdural hematoma that slowly occurs over an extended period of time, and some persons may have more than one bleed.

subdural hematoma

Neurology Hemorrhage into the subdural space, which occurs when veins located between the meninges leak blood after a head injury; pressure from the “mass” damages brain tissue and causes loss of function which worsens as the hematoma enlarges and ↑ intracranial pressure, leading to cerebral edema, further ↑ of intracranial pressure, ±accompanied by herniation of the uncal gyri Clinical ↓ consciousness; acute SH progresses rapidly–Sx usually appear within 24 hrs of injury, followed by rapid deterioration; subacute SH usually develops Sx 2 to 10 days post injury because of slower leaking of blood Risks factors Head trauma in extremes of age, overuse of aspirin, anticoagulants, alcoholism. See Subdural hematoma. Cf Extradural hemorrhage.

sub·dur·al hem·or·rhage

(sŭb-dūr'ăl hem'ŏr-ăj)

Extravasation of blood between the dural and arachnoidal membranes; acute and chronic forms occur; chronic hematomas may become encapsulated by neomembranes.
Synonym(s): subdural hematoma.

Subdural Hematoma

DRG Category:	70
Mean LOS:	6.8 days
Description:	MEDICAL: Nonspecific Cerebrovascular Disorders With Major CC
DRG Category:	955
Mean LOS:	11.5 days
Description:	SURGICAL: Craniotomy for Multiple Significant Trauma

Subdural hematoma (SDH) is an accumulating mass of blood, usually clotted, or a swelling that is confined to the space between the dura mater and the subarachnoid membrane. SDHs are space-occupying lesions and thus categorized as focal brain injuries, which account for approximately 50% of all head injuries and 60% of the mortality in head-injured patients. Sometimes an SDH is referred to as a mass lesion because it occupies critical space in the cranial vault. Deaths from SDH usually occur because of the expanding mass lesion that leads to excessive brain swelling and herniation, causing brain stem ischemia and hemorrhage.

SDHs are classified as either acute or chronic on the basis of when symptoms appear. Clinical findings in acute SDHs are evident within 24 to 72 hours after the traumatic event. A subacute SDH produces symptoms within 2 to 10 days; symptoms appear in chronic SDH within weeks or months (Table 1). Generally, head trauma involves both a primary injury and a secondary injury. The primary injury results from the initial impact, which causes immediate neurological damage and dysfunction. The secondary injury follows the initial trauma and probably stems from cerebral hypoxia and ischemia that then lead to cerebral edema, increased intracranial pressure (ICP), and brain herniation. A consequence of increased ICP, brain herniation is a life-threatening condition in which brain structures protrude through an opening in the brain cavity.

Types of Subdural Hematomas

Table 1. Types of Subdural Hematomas

TYPE	DESCRIPTION	ONSET OF SYMPTOMS	SYMPTOMS
Acute	Usually results from brain laceration with injury to the small pial veins bridging the subdural space	24–72 hr	Decreased level of consciousness, hemiparesis, unilateral pupil dilation, extraocular eye movement, paralysis, cranial nerve dysfunction
Subacute chronic	Similar to acute	2–10 days	Similar to acute
Chronic	Usually occurs in the elderly or in problem drinkers who experience atrophy of the brain; often associated with falls	2 wk or more	Interval when patient appears to recover and then progressive deterioration occurs; drowsiness, inattention, personality changes, headache; progresses to hemiparesis, pupil changes, decreased mental status

Causes

The mechanisms of injury associated with the development of SDH are a strong, direct-force, high-speed impact to the head or an acceleration–deceleration force. These can occur in motor vehicle crashes (MVCs), auto–pedestrian crashes, falls, and assaults. Chronic SDH is most commonly associated with falls in the elderly, particularly those on anticoagulants, and in problem drinkers.

Genetic considerations

Intracerebral hematoma owing to aneurysm rupture has been associated with autosomal dominantly inherited polycystic kidney disease. Hereditary coagulation defects can also increase risk of hematoma.

Gender, ethnic/racial, and life span considerations

Traumatic injuries, which are usually preventable, are the leading cause of death in Americans ages 1 to 44 and the fourth leading cause of death for all age groups. Most head injuries are associated with MVCs, which are three times more common in males than in females in the 15- to 24-year-old age group. In the 15- to 34-year-old age group, European Americans have a death rate from MVCs that is 40% higher than the rate for African Americans. The elderly population and chronic abusers of alcohol have cortical atrophy, which places them at risk for SDH. SDH occurs most often in the 50- to 79-year-old age group. Men have a higher incidence of chronic SDH than women.

Global health considerations

Falls and motor vehicle crashes occur around the world and may lead to SDH. Internationally, falls from heights of less than 5 meters are the leading cause of injury overall, and automobile crashes are the next most frequent cause.

Assessment

History

Question the prehospital care provider, significant others, or witnesses about the situation when the injury occurred. If the patient was in an MVC, determine the speed and type of vehicle, whether the patient was restrained, the patient’s position in the vehicle, and if the patient was thrown from the vehicle on impact. If the injury occurred in a motorcycle crash, ask if the patient was wearing a helmet. If the patient fell, determine the point of impact, distance of the fall, and type of landing surface. Ask if the patient experienced momentary loss of reflexes or momentary arrest of respiration, followed by loss of consciousness. If the patient was unconscious at any time, find out for how long. Determine if the patient experienced a headache, nausea, vomiting, dizziness, convulsions, decreased respiratory rate, or progressive insensitivity to pain (obtundity).

Physical examination

The most common symptoms are headache, decreased level of consciousness, drowsiness, inattention, hemiparesis, and unilateral pupil dilation. The initial evaluation or primary survey of the patient with a head injury is centered on assessing the airway, breathing, circulation, and disability (neurological status). Exposure (undressing the patient completely) is incorporated as part of the primary survey. The secondary survey, a head-to-toe assessment including vital signs, is then completed.

The initial neurological assessment of the patient with SDH includes monitoring the vital signs, assessing the level of consciousness, examining pupil size and level of reactivity, and assessing on the Glasgow Coma Scale, which evaluates eye opening, best verbal response, and best motor response. Clinical findings may include a rapidly changing level of consciousness from confusion to coma, ipsilateral pupil dilation, hemiparesis, and abnormal posturing, including flexion and extension. A neurological assessment is repeated at least hourly during the first 24 hours after the injury.

Examine the entire scalp and head for lacerations, abrasions, contusions, and bony abnormalities. Take care to maintain cervical spine immobilization during the examination. Patients with SDH may have associated cervical spine injuries or thoracic, abdominal, or extremity trauma. Examine the patient for signs of basilar skull fractures, such as periorbital ecchymosis (raccoon’s eyes), subscleral hemorrhage, retroauricular ecchymosis (Battle’s sign), hemotympanum (blood behind the eardrum), and leakage of cerebrospinal fluid (CSF) from the ears (otorrhea) or nose (rhinorrhea). Gently palpate the facial bones, including the mandible and maxilla, for bony deformities and step-offs. Examine the oral pharynx for lacerations and check for any loose or fractured teeth.

Psychosocial

The patient may be anxious about her or his condition during intervals of lucidity. Assess the patient’s ability to cope with a sudden illness and the change in roles that a sudden illness demands. Determine the significant others’ responses to the injury. Expect parents of children who are injured to feel anxious, fearful, and sometimes guilty. Note if the injury was related to alcohol consumption (approximately 40% to 60% of head injuries occur when the patient has been drinking) and elicit a drinking history from the patient or significant others. Assess the patient for signs of alcohol withdrawal 2 to 14 days after admission.

Diagnostic highlights

Test	Normal Result	Abnormality With Condition	Explanation
Computed tomography scan	Normal brain and supporting structures	Blood collection on brain surface	Identified mass lesion

Other Tests: Magnetic resonance imaging, cervical spine x-rays to rule out cervical spine injury; transcranial Doppler ultrasound; skull x-rays; complete blood count; arterial blood gases; plasma electrolytes

Primary nursing diagnosis

Diagnosis

Ineffective airway clearance related to hypoventilation or airway obstruction

Outcomes

Respiratory status: Gas exchange; Respiratory status: Ventilation; Symptom control behavior; Treatment behavior: Illness or injury; Comfort level

Interventions

Airway management; Anxiety reduction; Oxygen therapy; Airway suctioning; Airway insertion and stabilization; Cough enhancement; Mechanical ventilation; Positioning; Respiratory monitoring

Planning and implementation

Collaborative

medical.

Endotracheal intubation and mechanical ventilation are critical to ensure oxygenation and ventilation and to decrease the risk of pulmonary aspiration. A Pao2 greater than 100 mm Hg and a Paco2 between 28 and 33 mm Hg may decrease cerebral blood flow and intracranial swelling. The routine use of hyperventilation is controversial, and some physicians are using Sjvo2 (saturation of jugular venous bulb) monitoring to assess the response to changes in Pao2 and Paco2. Generally, the Paco2 is maintained at 35 to 40 mm Hg.

surgical.

Surgical management is the evacuation of the clot, control of the hemorrhage, and resection of nonviable brain tissue. Rapid surgical intervention is essential. If surgical evacuation is delayed for more than 4 hours, these lesions produce a higher mortality rate. The surgeon exposes the area involved, the clot is evacuated, bleeding from surface vascular structures is controlled with bipolar coagulation, and bridging veins are controlled with Gelfoam or muscle tissue. The surgical site may be drained postoperatively by using a Jackson-Pratt drain for 24 to 48 hours. Possible postoperative complications include intracranial hypertension, reaccumulation of the clot, intracerebral hemorrhage, and development of seizures.

Patients with critical head injuries who have a high probability of developing intracranial hypertension may require invasive ICP monitoring with an intraventricular catheter. Some physicians use a Glasgow Coma Scale score of less than 7 as an indicator for monitoring ICP. The goal is to maintain the ICP at less than 10 mm Hg and the cerebral perfusion pressure (CPP) greater than 80 mm Hg. Management of intracranial hypertension may also be done by draining CSF through a ventriculostomy, either intermittently or continuously according to a predetermined ICP measurement.

Pharmacologic highlights

Medication or Drug Class	Dosage	Description	Rationale
Diuretics	Varies by drug	Furosemide, mannitol	Assist in managing intracranial hypertension (although their use remains controversial)
Sedatives	Varies by drug	Short-acting sedatives: midazolam, propofol (Diprivan), fentanyl	Control intermittent increases in intracranial pressure with a resultant decrease in cerebral perfusion pressure; short action of drugs allows for temporarily stopping infusion so that neurological assessment can be performed
Chemical paralysis	Varies by drug	Mivacurium, atracurium (short-acting agents that have few hypotensive effects)	Improves oxygenation and ventilation for some patients with severe head injuries
Anticonvulsants	Prophylactically	Phenytoin (Dilantin)	Controversial in the routine management of subdural hematoma; overall effectiveness has yet to be determined

Other Drugs: Other drugs includes antibiotics and barbiturates (persistently elevated ICP despite routine interventions may be managed with the induction of a barbiturate coma, which reduces the metabolic rate of brain tissue).

Independent

The highest priority in managing patients with SDH is to maintain a patent airway, appropriate ventilation and oxygenation, and adequate circulation. Make sure the patient’s endotracheal tube is anchored well. If the patient is at risk for self-extubation, maintain him or her in soft restraints. Note the lip level of the endotracheal tube to determine if tube movement occurs. Notify the physician if the patient’s Pao2 drops below 80 mm Hg, Paco2 exceeds 40 mm Hg, or if severe hypocapnia (Paco2 < 25 mm Hg) occurs.

Help control the patient’s ICP. Maintain normothermia by avoiding body temperature elevations. Elevate the patient’s bed to 30 degrees and avoid flexing, extending, or rotating the patient’s neck because these maneuvers limit venous drainage of the brain and thus raise ICP. Avoid hip flexion, which limits venous drainage, by maintaining the patient in a normal body alignment. Maintain a quiet, restful environment with minimal stimulation; limit visitors as appropriate. Time nursing care activities carefully to limit prolonged ICP elevations. Use caution when suctioning the patient: Hyperventilate the patient beforehand and suction only as long as necessary. When turning the patient, prevent Valsalva’s maneuver by using a draw sheet to pull the patient up in bed. Instruct the patient not to hold on to the side rails.

Strategies to maximize the coping mechanisms of the patient and family are directed toward providing support and encouragement. Provide simple educational tools about head injuries. Teach the patient and family appropriate rehabilitative exercises, as necessary. Help the patient cope with long stretches of immobility by providing diversionary activities appropriate to the patient’s mental and physical abilities. Head injury support groups may be helpful. Referrals to clinical nurse specialists, pastoral care staff, and social workers are helpful in developing strategies for support and education.

Evidence-Based Practice and Health Policy

Santarius, T., Qureshi, H.U., Sivakumaran, R., Kirkpatrick, P.J., Kirollos, R.W., & Hutchinson, P.J. (2010). The role of external drains and peritoneal conduits in the treatment of recurrent chronic subdural hematoma. World Neurosurgery, 73(6), 747–750.

• A retrospective review of 408 cases of primary chronic subdural hematoma treated with burr hole evacuation revealed a recurrence rate of 15.9%.
• Among patients with hematoma recurrence, patients who underwent postoperative drainage with an external device or subdural-peritoneal catheter were less likely to have another recurrence compared to patients in whom no drainage device was used (11% versus 33%; p = 0.04).
• Among patients with recurrence, 22% were treated with an external drainage, 22% were treated with placement of a subdural-to-peritoneal catheter, and 56% were not treated with a drainage device at all. There was no significant difference in recurrence rates between drainage devices.

Documentation guidelines

• Trauma history, description of the event, time elapsed since the event, whether or not the patient had a loss of consciousness and, if so, for how long
• Adequacy of airway, breathing, and circulation; serial vital signs
• Appearance, bruising or lacerations, drainage from the nose or ears
• Physical findings related to the site of head injury: Neurological assessment, presence of accompanying symptoms, presence of complications (decreased level of consciousness, unequal pupils, loss of strength and movement, confusion or agitation, nausea and vomiting), CPP, ICP
• Signs of complications: Seizure activity, infection (fever, purulent discharge from any wounds), aspiration pneumonia (shortness of breath, pulmonary congestion, fever, productive cough), increased ICP
• Response to surgery and clot evacuation: Mental status changes, incisional healing, presence of complications (infection, hemorrhage)

Discharge and home healthcare guidelines

Review proper care techniques for wounds and lacerations. Discuss the recommended activity level and explain rehabilitative exercises as appropriate. Teach the patient and family to recognize symptoms of infection or a deteriorating level of consciousness. Stress the need to contact the physician on the appearance of such signs or symptoms. Teach the patient the purpose, dosage, schedule, precautions, potential side effects, interactions, and adverse reactions of all prescribed medications. Review with the patient and family all follow-up appointments that have been arranged. If the patient is a problem drinker, refer the patient to a counselor.

sub·du·ral he·ma·to·ma

(sŭb-dūr'ăl hē'mă-tō'mă)

Extravasation of blood between dural and arachnoidal membranes; acute and chronic forms occur; chronic hematomas may become encapsulated by neomembranes.
Synonym(s): subdural hemorrhage.