subarachnoid hemorrhage(redirected from Traumatic subarachnoid haemorrhage)
Also found in: Encyclopedia.
Causes and symptoms
subarachnoid hemorrhage (SaH, SAH)
subarachnoid hemorrhageNeurology A severe intracerebral hemorrhage in the subarachnoid space, often due to a ruptured intracranial aneurysm Clinical Abrupt severe headache, loss of consciousness, vomiting Etiology Ruptured cerebral aneurysm, AV malformation, idiopathic Risk factors Aneurysms, polycystic kidney disease; fibromuscular dysplasia, HTN Management Ventilation, oxgenation, fluid, tissue dehydration–eg, mannitol; surgical evacuation; bed rest, sedation, analgesia, anti-seizures. See Warning leak. Cf Intracerebral hemorrhage.
sub·a·rach·noid hem·or·rhage(sŭb'ă-rak'noyd hem'ŏr-ăj)
|Mean LOS:||6.8 days|
|Description:||SURGICAL: Craniotomy and Endovascular Intracranial Procedures With CC|
|Mean LOS:||6.8 days|
|Description:||MEDICAL: Nonspecific Cerebrovascular Disorders With Major CC|
Subarachnoid hemorrhage (SAH) is the direct hemorrhage of arterial blood into the subarachnoid space. Immediately after rupture, intracranial pressure (ICP) rises, resulting in a fall in cerebral perfusion pressure (CPP = mean arterial pressure − ICP). The expanding hematoma acts as a space-occupying lesion as it compresses or displaces brain tissue. Blood in the subarachnoid space may impede the flow and reabsorption of cerebrospinal fluid (CSF), resulting in hydrocephalus. The bleeding ceases with the formation of a fibrin-platelet plug at the point of the rupture and by tissue compression. As the clot, which forms initially to seal the rupture site, undergoes normal lysis or dissolution, the risk of rebleeding increases. More than 30,000 people in the United States have a ruptured intracranial aneurysm each year, although the annual incidence is probably underestimated because death is attributed to other reasons.
Cerebral vasospasm, or narrowing of the vessel lumen, is another common complication of SAH; it occurs in 35% to 49% of individuals. The pathophysiology of vasospasms is not clearly understood, but it is believed that they are precipitated by certain vasoactive substances (e.g., prostaglandins, serotonin, and catecholamines), which are released by the blood into the subarachnoid space. When vasospasm develops, it may last for several days or even several weeks. By decreasing cerebral blood flow, a vasospasm produces further neurological deterioration, cerebral ischemia, and cerebral infarction.
SAH typically results from cerebral aneurysm rupture (70%), which occurs when the blood vessel wall becomes so thin that it can no longer withstand the surrounding arterial pressure. Because aneurysm-forming vessels usually lie in the space between the arachnoid and the brain, hemorrhage from an aneurysm usually occurs in the subarachnoid space. Another less common cause of SAH is arteriovenous malformation.
SAH appears to cluster in families independent of environmental factors, as does the propensity to have vasospasm following surgery. One case study of 1,150 SAH patients reported a 10% incidence of familial SAH among all cases. Risk-associated regions have been mapped to 7q11 and 5q31, although no gene has been definitively identified. Patients with the APOE-e4 allele have demonstrated poorer outcomes after aneurysmal SAH than those with other variants of this gene even though an association between APOE and incidence of SAH has not been well documented. The autosomal dominantly transmitted disorder, polycystic kidney disease (ADPKD), has also been associated with an increased incidence of SAH.
Gender, ethnic/racial, and life span considerations
The peak incidence of aneurysm rupture is between ages 40 and 65. Under age 40, SAH occurs more commonly in men, but after age 50, it is more common in women. Few aneurysms rupture in persons younger than 20. Pregnancy creates a significant risk of SAH, which is higher in the third trimester of pregnancy and a leading cause of maternal mortality. The peak incidence of SAH from arteriovenous malformation is between ages 30 and 40. In the United States, people with African American ancestry have a greater risk for SAH than people with white/European ancestry.
Global health considerations
SAH occurs around the world, with reported rates varying widely between 5 to 30 cases per 100,000 individuals. The Middle East, China, and India have low reported rates, which may partly be due to the low rates of cardiovascular disease for people living in these regions.
Ask if the patient has had a sudden brief loss of consciousness followed by a severe headache; this sign has been reported by 45% of patients who survive SAH. Many also report a severe headache associated with exertion but no loss of consciousness. Establish any recent history of vomiting, stiff neck, photophobia, seizure, or partial paralysis. Establish any history of cerebral aneurysms.
The most common symptoms are neck pain, neck stiffness, loss of consciousness, severe headache, and limited neck flexion. Observe the patient for signs and symptoms of cranial nerve deficits, especially cranial nerves III, IV, and VI. Meningeal irritation may lead to nausea, vomiting, stiff neck, pain in the neck and back, and possible blurred vision or photophobia. Examine for symptoms of stroke syndrome, such as hemiparesis, hemiplegia, aphasia, and cognitive deficits. Cerebral edema, increased ICP, and seizures may also occur. Assess the vital signs for bradycardia, hypertension, and a widened pulse pressure. Other symptoms may result from pituitary dysfunction, caused by irritation or edema, leading to diabetes insipidus (excessive urinary output, hypernatremia) or hyponatremia.
SAHs are graded as follows:
- Grade I: Mild headache with or without meningeal irritation
- Grade II: Severe headache and a nonfocal examination, with or without mydriasis
- Grade III: Mild alteration in neurological examination, including mental status
- Grade IV: Obviously depressed level of consciousness or focal deficit
- Grade V: Patient either posturing or comatose
Provide emotional support for the patient and family. Encourage the patient to verbalize his or her fears of death, disability, dependency, and becoming a burden. Answer the patient’s and family’s questions and involve both the patient and the family or the significant others in all aspects of planning care. If necessary, make home health referrals before the patient’s discharge.
|Test||Normal Result||Abnormality With Condition||Explanation|
|Computed tomography scan without contract (urgent)||Normal brain and supporting structures||Blood collection in subarachnoid space often in the cisterns or sylvian fissure||Identifies areas of bleeding|
Other Tests: Lumbar puncture, complete blood count, coagulation studies, cerebral angiogram, arterial blood gases, serum electrolytes, magnetic resonance imaging if no lesion is found on angiogram
Primary nursing diagnosis
DiagnosisAlteration in tissue perfusion (cerebral) related to interruption in cerebral blood flow or increased ICP
OutcomesCirculation status; Cognitive ability; Neurological status; Tissue perfusion: Peripheral; Communication: Expressive ability; Communication: Receptive ability
InterventionsCerebral perfusion promotion; Circulatory care; ICP monitoring; Neurological monitoring; Peripheral sensation management; Circulatory precautions; Hypovolemia management; Vital signs monitoring; Emergency care; Medication management
Planning and implementation
Surgery is the treatment of choice for a cerebral aneurysm that has ruptured into the subarachnoid space. Until a decision about surgery is made, however, the management of the patient is focused on preventing secondary injury and relieving symptoms.
Monitor ICP to detect brain swelling and hydrocephalus. Maintain fluid volume within a normal range because dehydration increases hemoconcentration, which may increase the incidence of vasospasm. If cerebral edema is present, maintain moderate fluid restriction and administer prescribed steroids; dexamethasone (Decadron) and methylprednisolone (Solu-Medrol) are the drugs of choice. Steroid therapy is continued for at least 1 week postoperatively. Pharmacologic management is also used to control hypertension to prevent rebleeding. The goal of therapy is to maintain the systolic blood pressure at 150 mm Hg. Hypotension must be avoided at all costs because it worsens ischemic deficits. Assess the intravascular volume status with either a central venous access monitor or pulmonary artery catheter, depending on the patient’s condition.
Complications during the immediate postoperative period include brain swelling, bleeding at the operative site, fluid and electrolyte disturbances, hydrocephalus, and the onset of cerebral vasospasm. If an intracranial monitoring system is in place, report ICP rises over 15 mm Hg. Calculate the CPP and maintain the CPP greater than 50 mm Hg. Goals of medication management include control of blood pressure, prevention of seizures, treatment of symptoms (pain, nausea), maintenance of cerebral perfusion, and prevention of elevated intracranial pressure and vasospasm.
|Medication or Drug Class||Dosage||Description||Rationale|
|Nimodipine||60 mg PO q 4 hr||Calcium channel blocker||Reduces venospasm and cerebral ischemia|
|Antihypertensives||Varies by drug||Nitroprusside; propranolol; hydralazine; labetalol||Lower blood pressure (BP), but used only with extreme hypertension (when diastolic BP > 130 mm Hg)|
Other Drugs: Mannitol (osmotic diuretic) may be ordered to decrease cerebral edema, stool softeners, sedatives may be used to induce rest, anticonvulsants, analgesics (acetaminophen or codeine) to control headache, antiemetics, anticonvulsants
Accurate, detailed, and serial assessments are essential. Frequently, the first signs of rebleeding and vasospasm are evidenced through subtle changes in the neurological examination. At any time during the course of SAH, maintenance of airway, breathing, and circulation is the top priority. In the postoperative period, unless otherwise indicated, maintain the bed at an elevation of 30 to 40 degrees. Prevent flexion of the head and maintain proper alignment of the head and neck with towel rolls or sandbags. Avoid hip flexion greater than 90 degrees. Suction the patient as needed to keep the airway open. If deep endotracheal suctioning is indicated, hyperventilate and hyperoxygenate the patient before suctioning and limit suctioning to less than 30 seconds.
To prevent complications from postoperative immobility, turn the patient often and provide skin care. Perform active or passive range-of-motion exercises and encourage deep-breathing exercises when the patient is able. Space all nursing care activities to maintain ICP less than 15 mm Hg. Allow ICP to drop between all activities. Encourage other departments to space x-rays, therapies, and interviews to allow adequate rest and to avoid ICP elevations. Avoid conversations at the bedside that might be disturbing to the patient. Explain all procedures even if the patient does not appear to respond. Use soft restraints only when absolutely necessary; fighting restraints raises ICPs and thereby impedes venous outflow from the brain.
After surgery, monitor the dressing for bleeding or CSF leakage. If either occurs, notify the physician and reinforce the dressing. Inspect the surgical site with all dressing changes for redness, drainage, poor wound healing, and swelling.
Evidence-Based Practice and Health Policy
De Marchis, G.M., Lantigua, H., Schmidt, J.M., Lord, A.S., Velander, A.J., Fernandez, A., …Mayer, S.A. (2014). Impact of premorbid hypertension on haemorrhage severity and aneurysm rebleeding risk after subarachnoid haemorrhage. Journal of Neurology, Neurosurgery, and Psychiatry, 85(1), 56–59.
- In a retrospective cohort study among 1,312 patients treated for subarachnoid hemorrhage, 49% of patients had hypertension, which was associated with a 1.58 times increased risk of mortality at 3 months (95% CI, 1.04 to 2.41; p = 0.03). In this study, 23.8% of patients with hypertension died within 3 months of the initial hemorrhage compared to 11.5% of patients without hypertension (p < 0.001).
- Patients with hypertension presented more frequently with Grade 4 or 5 subarachnoid hemorrhage (42.6% versus 28.2%; p < 0.001). Hypertensive patients were also 1.67 times more likely to have an episode of rebleeding (95% CI, 1.02 to 2.74; p = 0.04) and 4.95 times more likely to develop renal failure while hospitalized (95% CI, 2.19 to 11.2; p < 0.001).
- Neurological findings: Level of consciousness; pupillary size, shape, and reaction to light; motor function of extremities; other cranial nerve deficits (blurred vision, extraocular movement deficits, drooping eyelids, facial weakness); speech loss; headache and facial pain; photophobia; and stiff or painful neck; deterioration of neurological status
Discharge and home healthcare guidelines
Prepare the patient and family for the possible need for rehabilitation after the acute care phase of hospitalization. Instruct the patient to report any deterioration in neurological status to the physician. Teach the patient signs and symptoms of deterioration in neurological status. Stress the importance of follow-up visits with the physician. If the patient has had surgery, teach the patient or caregiver to notify the physician for any signs of wound infection or poor incisional healing. Be sure the patient understands all medications, including dosage, route, action, adverse effects, and the need for routine laboratory monitoring for anticonvulsants.
sub·a·rach·noid hem·or·rhage(sŭb'ă-rak'noyd hem'ŏr-ăj)
Synonym(s): subarachnoid haemmorhage.