单词 | subdural hematoma | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||
释义 | subdural hematomasubdural hematoma[səb′du̇r·əl ‚hē·mə′tō·mə]subdural hematomaSubdural HematomaDefinitionDescriptionCauses and symptoms
DiagnosisTreatmentPrognosisPreventionResourcesOrganizationsKey termssub·du·ral hem·or·rhagesubdural hematomaNeurology 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)Synonym(s): subdural hematoma. Subdural Hematoma
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.
CausesThe 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 considerationsIntracerebral 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 considerationsTraumatic 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 considerationsFalls 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. AssessmentHistoryQuestion 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 examinationThe 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. PsychosocialThe 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
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 diagnosisDiagnosisIneffective airway clearance related to hypoventilation or airway obstructionOutcomesRespiratory status: Gas exchange; Respiratory status: Ventilation; Symptom control behavior; Treatment behavior: Illness or injury; Comfort levelInterventionsAirway management; Anxiety reduction; Oxygen therapy; Airway suctioning; Airway insertion and stabilization; Cough enhancement; Mechanical ventilation; Positioning; Respiratory monitoringPlanning and implementationCollaborativemedical.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
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). IndependentThe 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 PolicySantarius, 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.
Documentation guidelines
Discharge and home healthcare guidelinesReview 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)Synonym(s): subdural hemorrhage. |
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