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intracerebral haemorrhageA generic term for haemorrhage within the cerebral parenchyma which, when superficial, is most commonly caused by contusions and, if deep, more often linked to hypertension and occurs in the putamen, thalamus, internal capsule, cerebellum or pons.
intracerebral hematomaA hematoma which develops in the cerebral parenchyma, most commonly caused by hypertension. See Epidural hematoma, Subdural hematoma.
in·tra·cer·e·bral he·ma·to·ma(in'tră-ser'ĕ-brăl hē'mă-tō'mă)
|Mean LOS:||6.8 days|
|Description:||MEDICAL: Nonspecific Cerebrovascular Disorders With Major CC|
|Mean LOS:||11.5 days|
|Description:||SURGICAL: Craniotomy for Multiple Significant Trauma|
An intracerebral hematoma (ICH) is a well-defined collection of blood within the brain parenchyma (functional tissue). Most ICHs are related to cerebral contusions; ICHs complicate head injury in 2% to 3% of all head-injured patients. Although they are more frequently associated with closed-head injuries, they can also occur as a result of an open or penetrating injury or a depressed skull fracture. Similar to cerebral contusions, ICHs tend to occur most commonly in the frontal and temporal lobes and are uncommon in the cerebellum. They can also occur deep within the hemispheres in the paraventricular, medial, or paracentral areas in association with the shearing strain on small vessels that occurs with diffuse axonal injuries.
The patient can experience deterioration in cerebral functioning at the time of injury or in the first 48 to 72 hours after injury. Late hemorrhage into a contused area is possible as long as 7 to 10 days after injury. ICHs result in a mortality rate between 25% and 72%. Complications include intracranial hypertension, brain herniation, and death.
Traumatic causes of ICH include depressed skull fractures, penetrating missile injuries (gunshot wounds or stab wounds), or a sudden acceleration-deceleration motion. Depressed skull fractures cause penetration of bone into cerebral tissue. A high-velocity penetration (bullet) can produce shock waves that are transmitted throughout the brain in addition to the injury caused by the bullet directly. A low-velocity penetrating injury (knife) may involve only focal damage and no loss of consciousness. Motor vehicle crashes (MVCs) cause rapid acceleration-deceleration injuries. In cases in which there is no apparent cause for spontaneous ICH, hypertension is the most frequently associated disease. Other potential causes of ICH include hemorrhage at the site of a brain tumor and cerebrovascular accidents.
Spontaneous ICH has been seen in familial congenital coagulation disorders such as factor XI deficiency.
Gender, ethnic/racial, and life span considerations
Head injury, the leading cause of all trauma-related deaths, is associated with MVCs. Males ages 15 to 24 are three times more likely than females to be injured in a crash. Whites have a death rate 40% higher from MVC than African Americans ages 15 to 34. Falls are the most common cause of head injury in adults over age 65.
ICH can occur from nontraumatic causes as well. Strokes are the third leading cause of death in Americans. Although a stroke can occur at any age, 72% occur in people over 65 years of age. People of African American ancestry have higher rates of intracerebral hemorrhage due to hypertension. About 20,000 people die from ICH in the United States each year. The peak incidence occurs in childhood (ages 3 to 12) and in older adults (ages 50 to 70).
Global health considerations
While there are few data available about global trends, people who live in Asia have a higher incidence of intracerebral hemorrhage than people living in other regions of the world, as do people with Asian ancestry living in the United States.
Generally, patients suspected of ICH have a history of traumatic injury to the head. If no history of trauma exists, determine if the patient has a history of hypertension or stroke. In trauma patients, if the patient is not able to report a history, question the prehospital care provider, significant others, or witnesses about the situation surrounding the injury. If the patient was in an MVC, determine the speed and type of the vehicle, the patient’s position in the vehicle, whether the patient was restrained, and if the patient was thrown from the vehicle on impact. If the patient was injured in a motorcycle crash, determine whether the patient was wearing a helmet. Determine if the patient experienced momentary loss of reflexes, momentary arrest of respirations, and possible retrograde or antegrade amnesia (loss of memory for events immediately before the injury or loss of memory for events after the injury). Elicit a history of headache, drowsiness, confusion, dizziness, irritability, giddiness, visual disturbances (seeing stars), and gait disturbances. In addition, others may describe symptoms related to increased intracranial pressure (ICP), such as increased drowsiness or irritability and pupillary dilation on the ipsilateral (same as injury) side.
The most common symptoms are alterations in level of consciousness, headache, nausea, and vomiting. Seizures and focal neurological deficits may occur. When you examine the patient, note that, just as in cerebral contusions, small frontal lesions may be asymptomatic, whereas larger bilateral lesions may result in a frontal lobe syndrome of inappropriate behavior and cognitive deficits. Dominant hemispheric lesions are often associated with speech and motor deficits. Because many of the symptoms of alcohol intoxication mimic those of head injury, never assume that a decreased level of consciousness is caused by alcohol intoxication alone (even if you can smell the alcohol on the patient’s breath or clothing) rather than a head injury.
First evaluate and stabilize the patient’s airway, breathing, and circulation with particular attention to the intactness of the patient’s cervical spine (do not flex or extend the neck until you know the patient has no cervical spine injury). Next, perform a neurological assessment, watching for early signs of increased ICP: decreased level of consciousness, decreased strength and motion of extremities, reduced visual acuity, headache, and pupillary changes.
During the complete head-to-toe assessment, be sure to evaluate the patient’s head for external signs of injury. Check carefully for scalp lacerations. Check the patient for cerebrospinal fluid (CSF) leakage from the nose (rhinorrhea) or ear (otorrhea), which is a sign of a basilar skull fracture (a linear fracture at the base of the brain). Other signs of basilar skull fracture include raccoon’s eyes (periorbital ecchymosis or bruising around the eyes) and Battle’s sign (bleeding and swelling behind the ear).
Be sure to evaluate the patient’s pupillary light reflexes. An abnormal pupil reflex may result from increasing cerebral edema, which may indicate a life-threatening increase in ICP. Pupil size is normally 1.5 to 6 mm. Several signs to look for include ipsilateral miosis (Horner’s syndrome), in which one pupil is smaller than the other with a drooping eyelid; bilateral miosis, in which both pupils are pinpoint in size; ipsilateral mydriasis (Hutchinson’s pupil), in which one of the pupils is much larger than the other and is unreactive to light; bilateral midposition, in which both pupils are 4 to 5 mm and remain dilated and nonreactive to light; and bilateral mydriasis, in which both pupils are larger than 6 mm and nonreactive to light. Note the shape of the pupil as well because an oval pupil may indicate increased ICP and possible brain herniation. In more seriously injured patients, invasive ICP monitoring with an intraventricular catheter may be initiated for serial assessment of the ICP. Normally, ICP is 4 to 10 mm Hg, with an upper limit of 15 mm Hg. ICP is considered moderately elevated at levels of 15 to 30 mm Hg and severely elevated at levels above 30 mm Hg.
Assess the patient’s and family’s ability to cope with a sudden illness and the change in roles that a sudden illness demands. Expect parents of children who are injured to be anxious, fearful, and sometimes guilt-ridden. Note if the injury was related to alcohol (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.
Note that during the patient’s recovery, subtle neurological deficits (such as subtle personality changes or inability to perform mathematical calculations) may exist long after hospital discharge and may interfere with the resumption of parenting, spousal, or occupational roles.
|Test||Normal Result||Abnormality With Condition||Explanation|
|Computed tomography (CT) scan||Intact cerebral anatomy||Identification of size and location of site of injury or bleeding||Shows anterior to posterior slices of the brain to highlight abnormalities|
Other Tests: Skull x-rays, magnetic resonance imaging, cervical spine x-rays, complete blood count, coagulation studies, glucose test of any drainage suspected to be CSF using a reagent strip
Primary nursing diagnosis
DiagnosisAltered thought process related to cerebral tissue injury and swelling
OutcomesCognitive ability; cognitive orientation; Concentration; decision making; Identity; Information processing; Memory; Neurological status: Consciousness
InterventionsCerebral perfusion promotion; Environmental management; Surveillance; Cerebral edema management; Family support; Medication management
Planning and implementation
If a lesion identified by CT scan is causing a shift of intracranial contents or increased ICP, immediate surgical intervention is necessary. A craniotomy is performed to evacuate the ICH and ischemic tissue if the site is operable or to release ICP if viable tissue will be preserved.
Ongoing monitoring and serial assessments are essential. ICP monitoring and sequential CT scanning may be needed in critically ill patients, and serial neurological assessments are needed on all patients to determine if ICP is increasing. Because bleeding and swelling can progress over several days after injury, the patient is monitored for deterioration even up to 10 days after injury. During periods of frequent assessment, the patient should not be sedated for longer than 30 minutes at a time; longer-acting sedation may mask neurological changes and place the patient at risk for lack of detection.
|Medication or Drug Class||Dosage||Description||Rationale|
|Fentanyl (Sublimaze)||0.05 mg IV as needed||Short-acting opioid analgesic||Provides short-term (30 min) pain control and sedation without long-lasting effects that may mask neurological changes|
Other Drugs: Some patients develop seizures as a complication and need anticonvulsants. Drugs to reduce ICP, such as mannitol, may be used.
After making sure the patient has adequate airway, breathing, and circulation, ongoing serial assessments of the patient’s neurological responses are of highest priority. Timely notification of the trauma surgeon or neurosurgeon when a patient’s assessment changes can save a patient’s life. If the patient is intubated, make sure the endotracheal tube is anchored well. If the patient is at risk for self-extubation, maintain him or her in soft restraints. Notify the physician if the patient’s Pao2 drops below 80 mm Hg, if Paco2 exceeds 40 mm Hg, or if severe hypocapnia (Paco2 < 25 mm Hg) occurs. Aspiration pneumonia is a risk and can occur even with endotracheal intubation. Elevate the head of the bed at 30 degrees to help prevent this complication.
Help control the patient’s ICP. Maintain normothermia by avoiding body temperature elevations. 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 by maintaining the patient in a normal body alignment, limiting venous drainage. 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 appropriate. Help the patient cope with long stretches of immobility by providing diversionary activities that are 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.
Help the significant others and family face the fear of death, disability, and dependency; involve the patient and the family in all aspects of care.
Evidence-Based Practice and Health Policy
Anderson, C.S., Huang, Y., Arima, H., Heeley, E., Skulina, C., Parsons, M.W., …Wang, J.D. (2010). Effects of early intensive blood pressure-lowering treatment on the growth of hematoma and perihematomal edema in acute intracerebral hemorrhage: The Intensive Blood Pressure Reduction in Acute Cerebral Haemorrhage Trial (INTERACT). Stroke, 41(2), 307–312.
- Investigators conducted a randomized controlled trial among 296 patients with a cerebral hematoma to determine if intensive treatment to lower blood pressure had an effect on the growth of the hematoma. One hundred and forty-five patients were randomly selected to receive the standard guideline-based blood pressure treatment, and 151 patients were randomly selected to receive the intensive treatment to lower blood pressure. The target systolic blood pressure was 180 mmHg for the standard guideline group and 140 mmHg for the intensive treatment group.
- The intensive treatment group had significantly lower systolic blood pressures than the standard guideline group within 1 hour of treatment initiation (152 mmHg versus 166 mmHg), during the first 24 hours of treatment (145 mmHg versus 157 mmHg), and over the course of 72 hours (144 mmHg versus 155 mmHg). The mean differences during these time periods ranged from 11.1 mmHg to 13.7 mmHg (p < 0.001).
- The treatment group also demonstrated significantly less mean hematoma growth at 72 hours than the standard guideline group (mean difference, 2.45 mL; 95% CI, 0.75 to 4.16 mL; p = 0.005).
- Trauma history, description of the event, time elapsed since the event, whether the patient had a loss of consciousness and, if so, for how long
- Adequacy of airway, breathing, 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
- 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 medications used to control pain and increased ICP
Discharge and home healthcare guidelines
Be sure the patient understands all medications, including the dosage, route, action, adverse effects, and the need for routine laboratory monitoring for convulsants. Teach the patient and caregiver the signs and symptoms that necessitate a return to the hospital. Teach the patient to recognize the symptoms and signs of postinjury syndrome, which may last for several weeks. Explain that mild cognitive changes do not always resolve immediately. Provide the patient and significant others with information about the trauma clinic and the phone number of a clinical nurse specialist in case referrals are needed. Stress the importance of follow-up visits to the physician’s office. If alcohol counseling is needed, provide a phone number and the name of a counselor. Prepare the patient and family for the possible need for rehabilitation after the acute care phase of hospitalization.