DRG Category: 26
Mean LOS: 5.5 days
Description: Surgical: Craniotomy and Endovascular Intracranial Procedures With Complication or Comorbidity
DRG Category: 70
Mean LOS: 6.2 days
Description: Medical: Nonspecific Cerebrovascular Disorders With Major Complication or Comorbidity
Subarachnoid hemorrhage (SAH) is the direct hemorrhage of arterial blood into the subarachnoid between the pia mater and arachnoid mater. SAH and intracerebral hemorrhage are the two forms of hemorrhagic stroke. SAH usually occurs from a ruptured cerebral aneurysm or an arteriovenous malformation (AVM). Immediately after the extravasation of blood, 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 a common complication of SAH; it occurs in 35% to 49% of individuals with SAH. 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 complications such as neurological deterioration, cerebral ischemia, and cerebral infarction. Other short-term complications of SAH are hydrocephalus and rebleeding. Long-term complications include speech and language deficits, weakness or paralysis of the extremities, visual derangements, seizures, headaches, problems with attention or concentration, memory loss, and personality changes.
Both genetic and environmental factors are related to SAH. 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. Stress occurs on the arterial walls, particularly where the arteries branch where the blood is most turbulent. Some types of aneurysms form because the adventitia is very thin in intracranial arteries, which makes them prone to aneurysm formation. 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 AVM, an abnormal tangle of vessels that diverts blood from the arteries to the veins without oxygenating tissue. Risks of SAH include smoking, cocaine use, oral contraception use, hypertension, cerebral atherosclerosis, persistent headache, pregnancy, family history of stroke, and long-term analgesic use.
SAH appears to cluster in families independent of environmental factors, as does the propensity to have vasospasm following surgery. First-degree relatives have a three- to sevenfold higher risk of SAH, and 10% of all cases have a family history. There are six known risk-associated loci, although no genes have been definitively identified. Patients with the apolipoprotein E (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. Autosomal dominant polycystic kidney disease has also been associated with an increased incidence of SAH. There are multiple other syndromes that manifest with vascular abnormalities or aneurysms, which greatly increase the risk of intracranial bleeding and SAH. These include Loeys-Dietz syndrome (TGFBR1, TGFBR2, or TGFB2 mutations), Marfan syndrome (FBN1 mutations), vascular Ehlers-Danlos syndrome (COL3A1 mutations), neurofibromatosis type 1 (NF1), and tuberous sclerosis complex (TSC1 or TSC2 mutations).
The peak incidence of aneurysm rupture is between ages 40 and 65 years. In persons under age 40 years, SAH occurs more commonly in men, but after age 50 years, it is more common in women. Few aneurysms rupture in persons younger than 20 years of age. Pregnancy creates a significant risk of SAH, which is higher in the third trimester of pregnancy and a leading cause of parental mortality. The peak incidence of SAH from arteriovenous malformation is between ages 30 and 40 years.
In the United States, Black persons have a greater risk for SAH than White persons. In urban, safety net hospitals that primarily take care of uninsured persons, patients have longer time between SAH and intervention and poorer outcomes than patients cared for in university hospitals or major medical centers. These differences create significant health disparities, which also exist among rural versus urban patients. Prompt diagnosis and treatment is important in SAH. Patients residing in rural locations have almost a threefold increase in time to neurosurgical admission when compared to patients who live near major medical centers within cities (Nichols et al., 2020 [see Evidence-Based Practice and Health Policy]), potentially leading to delays in the management of SAH.
Risk factors such as smoking, hypertension, and atherosclerosis place persons at risk for SAH. Sexual and gender minority persons have higher rates of smoking than the general population (Centers for Disease Control and Prevention, 2021), which may place them at risk for SAH. Transgender is a term used to describe persons whose gender identity is different from their sex assigned at birth. Approximately 1% of the U.S. population identify themselves as transgender. Cisgender is a term used to describe persons who have gender identity and gender expression aligned with their assigned sex listed on their birth certificate. Compared to cisgender women, transgender women reported higher rates of diabetes, ischemic stroke, angina/coronary disease, and myocardial infarction. Gender-nonconforming men and women reported higher odds of myocardial infarction than cisgender women. Transgender women also had higher rates of any cardiovascular disease than cisgender men (Cacerese, Jackman, et al., 2020; Connelly et al., 2019). While large-scale studies are not available, these factors may place some sexual and gender minority persons at risk for SAH.
SAH occurs around the world, with reported rates varying widely between 5 and 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. High rates occur in the United States, Finland, Japan, and Australia.
PLANNING AND IMPLEMENTATION
Collaborative
Surgery is the treatment of choice for a cerebral aneurysm that has ruptured into the subarachnoid space. Repair of the ruptured aneurysm may be accomplished by surgical clipping or coiling. The timing of surgery is controversial, but most experts recommend that surgery should take place within 72 hours. Until a decision about surgery is made, however, the management of the patient is focused on preventing secondary injury and relieving symptoms.
Endotracheal intubation and mechanical ventilation should be performed for patients who are unresponsive and cannot maintain their own airway. Experts recommend that the mean arterial blood pressure be kept below 130 mm Hg with the use of IV beta blockers that can be adjusted minute by minute. Beta blockers are also used to control hypertension to prevent rebleeding, which occurs most often within the first 24 hours after rupture. The overall mortality rate of rebleeding is as high as 78%, so measures such as sedation and analgesia are important to reduce the risk. Hypotension must be avoided at all costs because it worsens ischemic deficits and can lead to cerebral ischemia. Monitoring ICP to detect brain swelling and hydrocephalus is essential. In patients with elevated ICP, mechanical ventilation is titrated to achieve a Paco2 of 30 to 35 mm Hg. The intravascular volume status is assessed with either a central venous access monitor or pulmonary artery catheter, depending on the patient's condition. Fluid volume is maintained within a normal range because dehydration increases hemoconcentration, which may increase the incidence of vasospasm. If cerebral edema is present, a moderate fluid restriction is employed. The administration of corticosteroids (dexamethasone, methylprednisolone) to manage ICP remains controversial. Vasospasm is managed with calcium channel blockers such as nimodipine, although transluminal balloon angioplasty may be used if other therapy fails.
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, generally ICP rises over 15 mm Hg are reported to the neurosurgeons, and CPP is maintained at more 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 ICP and vasospasm.
| Medication or Drug Class | Dosage | Description | Rationale |
|---|
| Nimodipine | 60 mg PO every 4 hr beginning within 96 hr of event | Calcium channel blocker | Reduces vasospasm and cerebral ischemia |
| Labetalol | 20 mg IV over 2 min, then 40–80 mg IV every 10 min not to exceed 300 mg; may also be given by infusion 1–2 mg/min not to exceed 300 mg | Beta blocker | Lower blood pressure to maintain a range that allows for sufficient cerebral perfusion |
| Fentanyl | 50–100 mcg IV | Opioid analgesic | Ensures comfort and relieves pain, has sedating properties that allow for rest; can be reversed rapidly; has a short half-life |
Other Drugs: Mannitol (osmotic diuretic) may be ordered to decrease cerebral edema, stool softeners, sedatives and opioids may be used to induce rest, anticonvulsants (phenytoin, phenobarbital, fosphenytoin), analgesics (acetaminophen or codeine) to control headache, antiemetics, anticonvulsants, loop diuretics
Independent
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
Nichols, L., Stirling, C., Stankovich, J., & Gall, S. (2020). Time to treatment following an aneurysmal subarachnoid hemorrhage, rural place of residence and inter-hospital transfer. Australasian Emergency Care, 23, 225–232.
- The authors aimed to examine the effect of geographical location, socioeconomic status, and interhospital transfer on time to treatment following an aneurysmal subarachnoid hemorrhage. They initiated a retrospective cohort study using medical records and calculated time intervals from time of the hemorrhage event to treatment.
- The median time to the intervention was 13.78 hours. Socioeconomic disadvantage was associated with a 1.5-fold increase in time to arrival at the hospital and a 1.76-fold increase in time to neurosurgical admission. Residing in an outer regional location was associated with a 2.27-fold increase in time to neurosurgical admission, and interhospital transfer led to a 6.26-fold increase in time to neurosurgical admission. The authors concluded that time to treatment was negatively influenced by socioeconomic disadvantage, geographical distance from hospitals, and interhospital transfer.