The levels of evidence (I-IV) supporting the recommendations and levels of recommendation (Level 1-3) are defined at the end of the "Major Recommendations" field.
Immediate attention is warranted at the time of an aneurysmal subarachnoid hemorrhage (aSAH) rupture as a delay in treatment will adversely affect outcome (Level 2; Kowalski et al., 2004; Lorenzi et al., 2003). For signs and symptoms of and diagnostic studies for aSAH, refer to the original guideline document.
Upon admission of the patient to the intensive care unit (ICU), hourly neurologic exam checks (including a complete neurologic exam, National Institutes of Health Stroke Scale, Glasgow Coma Scale, and hemodynamic monitoring) are performed and compared to baseline to detect early deterioration because of aneurysmal rebleed, acute hydrocephalus, ischemia related to inadequate cerebral perfusion (from early cerebral vasospasm or other causes), or other medical complications.
Airway and Oxygenation
Intubation and mechanical ventilation may be indicated for patients with decreased mental status, compromised airways, or acute lung injuries from subarachnoid hemorrhage (SAH; e.g., neurogenic pulmonary edema), aspiration, or a Glasgow Coma Scale motor score of withdrawal. Modes of ventilation vary, especially in patients who have pulmonary complications following SAH. The goal is to maintain adequate oxygenation and ventilation without compromising both intracranial and cerebral perfusion pressures. Positive end expiratory pressure of 5 cm H2O may be used cautiously in the aSAH patient; however, it does decrease blood pressure (BP) and may lead to cerebral ischemia (Level 2; Muench et al., 2005). Pressure-controlled ventilation should be considered if the patient has significant aspiration or early acute respiratory distress syndrome.
Patients recovering from aSAH are critically ill patients at risk for many common secondary injuries such as atelectasis and pneumonia. Hourly monitoring of breath sounds and frequent deep breathing should be encouraged. Coughing is discouraged in the SAH patient before aneurysm securement because of the increased risk of aneurysm rupture with the increased intracranial pressure (ICP) and BP that occurs during coughing.
The exact relationship between aneurysmal rebleed and BP remains to be identified; however, most clinicians agree that to prevent rebleed, BP control is achieved before aneurysm securement. Systolic BP is kept between 90 and 140 mm Hg before aneurysm securement (Level 3; Suarez, Tarr, & Selman, 2006). There are a variety of vasoactive agents used to maintain BP within an acceptable range. Choice of vasoactive agent and BP target range varies depending upon institutional policy (i.e., policy and procedures) and managing clinician preference. Some institutions require clinicians to follow systolic BP, and other institutions follow mean arterial pressure. Typically, BP is maintained within the target range using an initial bolus followed by commencement of an intravenous (IV) drip that is titrated to maintain BP within the target range (Level 2; Kraus, Metzler, & Coplin, 2002). Use of sublingual agents that may cause a rapid drop in BP is not recommended. BP should be lowered in a controlled manner as a sudden drop in BP increases the risk of cerebral ischemia.
Hypotension occurring before aneurysm securement places the patient recovering from aSAH at risk for ischemia. Hypotension should be treated with rapid IV fluid replacement beginning with isotonic saline (0.9%) and colloids as necessary. For persistent hypotension, IV vasopressors should be instituted.
Intracranial Pressure Monitoring
When a patient shows symptoms of increasing ICP, or is at increased risk of increased ICP because of large blood load, an external ventricular catheter or subarachnoid bolt is inserted. This can be done in the operating room (during surgical clipping or as a separate surgical procedure) or emergently at the bedside to decrease ICP. Poor clinical grade on admission, acute neurologic deterioration, or progressive enlargement of ventricles on CT scan are clear indications for the use of an external ventricular device (Level 2; Mayberg et al., 1994; Rordorf et al., 1997; Suzuki et al., 2000). Newer data suggest that external ventricular drainage does not include likelihood of aneurysm rehemorrhage when drainage is performed at moderate pressures (<10 cm H2O) (Level 2; Fountas et al., 2006). Aseptic technique is essential during external ventricular drain or subarachnoid bolt insertion because an infection can occur, especially if the drain is left in for an extended period of time. Cultures are to be routinely performed, and antibiotics are initiated if any signs of infection are present. Some clinicians and institutions use prophylactic antibiotics for aSAH patients with an external ventricular drain, although there is no literature supporting this practice.
Although all of these catheters allow monitoring of ICP, the external ventricular catheter permits cerebral spinal fluid (CSF) drainage to control ICP and clear blood from the CSF. The external ventricular catheter is associated with a higher infection rate than other catheters (Level 2; Lozier et al., 2002). Care related to CSF management varies by institution and clinician preference. Continuous drainage of CSF from an external ventricular drain (EVD) at a specified level (above the external auditory meatus or foramen of Monroe as per institutional policy) prevents ICP from rising above that level and allows for continuous clearance of bloody CSF from the ventricles and subarachnoid space (see Guide to the Care of the Patient with Intracranial Pressure Monitoring: AANN Reference Series for Clinical Practice).
In febrile patients (temperature ≥38.3ºC or as per institutional policy), fever reduction should be achieved with administration of acetaminophen every 4–6 hours to achieve normothermia (Level 3; Suarez, Tarr, & Selman, 2006). Surface or intravascular cooling is instituted to maintain temperature <38.3ºC if medications are not effective (Level 3; Suarez, Tarr, & Selman, 2006). It is important to control fever in this population as it is associated with poorer recovery from aSAH (Level 2; Commichau, Scarmeas, & Mayer, 2003; Fernandez et al., 2007). Surveillance cultures may be obtained daily in patients receiving cooling therapy, otherwise cultures should be obtained per Society of Critical Care Medicine guidelines (Level 3; O'Grady et al., 1998). In patients receiving surface cooling, monitor and treat shivering with warm compresses to the hands and sedation or paralytics as needed. Induced hypothermia is not routinely recommended (Level 2; Bederson et al., 2009)
Initial laboratory data provides clinicians with additional baseline data regarding the patient's medical condition and may help in identification of comorbid conditions. Because complications, including cardiac, pulmonary, and fluid and electrolyte imbalances, are known to arise from the moment of aneurysmal rupture, it is imperative to monitor the overall status of the patient.
Initial laboratory data include the following:
- Basic metabolic chemistry and electrolytes
- Cardiac troponin, creatine phosphokinase (CPK) isoenzymes
- Coagulation studies
- Complete blood count
- Type and screen
- Urine toxicology and chemistry
Arterial blood gases are ordered upon admission and as necessary for intubated patients or those in respiratory distress. Admission testing also includes a 12-lead electrocardiogram and a chest x-ray.
The goal is to maintain euvolemia (central venous pressure [CVP] 5–8 mm Hg) in the patient recovering from aSAH (Level 3; Suarez, Tarr, & Selman, 2006). Normal saline may be infused at rates between 80 and 100 cc/hr (2–3 L of 0.9% NaCl per 24 hours; Level 3; Mayer et al., 2005). Avoid fluid restriction for patients with hyponatremia due to cerebral salt wasting because it has been associated with increased cerebral infarction (Level 2; Wijdicks et al., 1985).
Patients should not be given any food, fluid, or medication by mouth until they have passed a bed-side swallow evaluation that includes a water test or have been evaluated by a speech therapist (The Joint Commission, 2010). This includes patients immediately preoperative, stuporous, or comatose. Parenteral nutrition via continuous infusion is started on day 2 after hemorrhage (Level 3; Suarez, Tarr, & Selman, 2006) if the patient is unable to eat or tolerate enteral feedings. If the patient is not preoperative, stuporous, or comatose, advancing the diet as tolerated is ideal (Level 3; Suarez, Tarr, & Selman, 2006). A consult to a speech pathologist to evaluate swallowing capability and aid in diet type selection is recommended for any patient whose ability to swallow is in question.
Although there is significant ongoing research to identify ideal glycemic control in ICU populations, no specific guidelines are routinely applied to the aSAH population. Hyperglycemia has been found to be associated with increased risk of morbidity and mortality following aSAH, therefore, serum glucose should be kept within the range of 80–120 mg/dl with insulin infusion if necessary (Level 3; Suarez, Tarr, & Selman, 2006).
Typically, activity is limited in patients with an unsecured aneurysm. All activities that increase BP (and, therefore, ICP) are limited to prevent rebleed. The patient should be maintained in a quiet environment with limited visitors until after aneurysm securement (Level 3; Suarez, Tarr, & Selman, 2006).
Deep Vein Thrombosis (DVT) Prophylaxis
Because of limited mobility, patients with an unsecured aneurysm are at risk for DVT. In these patients, thigh-high stockings and pneumatic (sequential) compression devices should be implemented as soon as possible (Level 3; Suarez, Tarr, & Selman, 2006). Anticoagulants (e.g., heparin) should be avoided until after aneurysm securement (Level 3; Suarez, Tarr, & Selman, 2006).
The administration of prophylactic anticonvulsants may be considered in the immediate post-hemorrhagic period (Level 2). The routine long-term use of anticonvulsants is not recommended (Level 2) but may be considered for patients with risk factors such as prior seizure, parenchymal hematoma, infarct, or middle cerebral artery aneurysms (Level 2; Bederson et al., 2009).
Controversy exists on the need for and length of anticonvulsant therapy in patients without a history of seizures because some anticonvulsants have been associated with poor outcomes, and the percentage of aSAH patients developing seizures is small (Level 2; Naidech et al., 2005). If using anticonvulsants, use those that do not change the level of consciousness.
Stool softeners are initiated. The patient with an unsecured aneurysm should not strain to have a bowel movement, and stool softeners maintain soft stool so straining is not required (Level 3). For patients able to take oral nutrition, a high-fiber diet is instituted. For patients on parenteral nutrition, a high-fiber feeding is instituted.
Headache pain is usually intense after aSAH. Analgesics are administered as needed for pain. Pain causes increased BP, heart rate, and anxiety. All of these can increase risk for aneurismal rebleed and, therefore, must be treated (Level 3). Use short-acting and reversible medications when possible.
Agitation can lead to increases in activity, dislodging of catheters, and aneurysmal rebleed. Sedation is administered as needed to patients who are agitated. A short-acting sedative should be used to facilitate frequent neurologic exams free of sedatives. It is not always possible to obtain a neurologic exam free of sedatives, but use of short-acting sedatives increases this likelihood.
Prevention and treatment of nausea and vomiting are also important for the aSAH patient, both before and after aneurysm securement, especially during the first 24 hours. Vomiting increases ICP and can cause aneurysmal rebleed. Patients with nausea should receive an antiemetic routinely.
Gastrointestinal Hemorrhage Prophylaxis
Histamine-receptor antagonists or proton pump inhibitors are instituted to prevent ulcer formation and gastrointestinal hemorrhage.
Alleviate anxiety by explaining procedures and ICU routine to patients and families. Incorporate a multidisciplinary approach, including pastoral care and social work, to address the patients' needs.
aSAH Patient in the ICU
After the aneurysm has been secured, many of the previous care guidelines are maintained; however, some adjustments should be made.
Typically, monitoring of neurologic exam and vital signs are performed every hour after surgery or embolization. If the patient remains stable, exam and vital-sign assessment are decreased to every 2 hours and as necessary. Serial complete neurological assessment, including level of consciousness, cranial nerve assessment, and motor exam performed at the bedside, detects subtle changes from the patient's baseline status. Any changes in neurologic exam are reported to the attending physician, resident, or nurse practitioner immediately. Initial assessment will identify changes related to surgery or possible rebleeding of the aneurysm, cerebral edema, or increasing ICP. Continued assessment is vital to optimize outcomes in this population because cerebral vasospasm is a common secondary sequelae to aSAH and develops very suddenly. Prompt identification of changes in neurologic exam initiates further testing to determine cause of the change and intervention, thereby preventing long-term damage to the brain.
Airway and Oxygenation
For patients who do not require intubation and mechanical ventilation, frequent assessment of airway patency and oxygenation continue. Along with hourly vital-sign assessment, breath sounds are auscultated. Any changes in breath sounds should be reported to the attending physician, resident, or nurse practitioner immediately. Proper oxygenation is necessary to prevent hypoxia and cerebral ischemia. Suctioning may be performed as needed for short intervals with appropriate hyperoxygenation provided prior to suctioning in a patient recovering from aSAH after the aneurysm has been secured.
When the aneurysm is secure, an increase in BP is permitted. Maintaining the systolic pressure at less than 200 mm Hg has been recommended (Level 3; Suarez, Tarr, & Selman, 2006). The target range for ideal BP after aneurysm securement has not been thoroughly defined; however, the goal of BP management is to maintain perfusion of brain tissue and prevent ischemia.
In many patients recovering from aSAH, ICP monitoring will continue after securement of the aneurysm. Any patient at risk for increased ICP should have continued ICP monitoring. Prolonged elevations in ICP are associated with decreased cerebral perfusion pressure and increase the risk of cerebral ischemia and poor outcome (Level 2; Mayberg et al., 1994; Rordorf et al., 1997; Suzuki et al., 2000).
In febrile patients (temperature ≥38.3ºC or as per institutional policy), fever reduction is achieved with administration of acetaminophen every 4–6 hours to achieve normothermia (Level 3; Suarez, Tarr, & Selman, 2006). Surface or intravascular cooling is instituted to maintain temperature <38.3ºC if medications are not effective (Level 2; Badjatia et al., 2004). It is important to control fever in this population because it is associated with poorer recovery from aSAH (Level 2; Commichau, Scarmeas, & Mayer, 2003; Fernandez et al., 2007). Surveillance cultures are obtained daily in patients receiving cooling therapy, otherwise cultures should be obtained per Society of Critical Care Medicine guidelines (Level 3; O'Grady et al., 1998). In patients receiving surface cooling, monitor and treat shivering with warm compresses, circulating warm air, sedation, or paralytics as needed (Level 2; Badjatia et al., 2004).
The following laboratory values should be obtained daily after the aneurysm has been secured:
- Electrolytes (including magnesium)
- Troponin, CPK isoenzymes (for the first 5 days after hemorrhage)
Also consider arterial blood gases, chest x-ray, and anticonvulsant levels as needed.
IV fluids are maintained to assure adequate hydration. In patients with symptomatic vasospasm, triple H therapy (hypervolemia, hypertension, and hemodilution) remains a frequently used regimen in the prevention of cerebral vasospasm after aSAH. Triple H therapy prevents ischemic deficits in patients with mild to moderate symptomatic cerebral vasospasm by augmenting circulating blood flow and perfusion pressures, increasing cardiac output, improving rheology of blood flow, and increasing collateral circulation (Awad et al., 1987; Kassell et al., 1982; Muizelaar & Becker, 1986). The most common symptoms of symptomatic vasospasm are focal ischemic deficits, reflecting the region experiencing ischemia; focal ischemic deficits are often referred to as delayed ischemic deficits because of the temporal establishment. These patients require more aggressive volume expansion and hypertension. The goal of triple H therapy is to achieve CVP 8–12 mm Hg, hematocrit <30, systolic BP ≥180 mm Hg, and urine output ≥250 ml/hr. These goals can be achieved by infusing large amounts of colloid or crystalloid or through pharmacologic interventions (Level 2; Awad et al., 1987; Janjua & Mayer, 2003; Kassell et al., 1982; Muizelaar & Becker, 1986). Vigilant monitoring of patients is warranted because triple H therapy includes complications such as myocardial injury, pulmonary edema, hyponatremia, cerebral edema, and bleeding of unsecured aneurysm (Awad et al., 1987; Janjua & Mayer, 2003; Mocco et al., 2006; Muizelaar & Becker, 1986; Solomon, Fink, & Lennihan, 1988; Treggiari-Venzi, Suter, & Romand, 2001). Although not yet used as a standard of care in all facilities, invasive monitoring, such as a pulmonary artery catheter, is warranted in patients with cardiac dysfunction to adequately monitor and treat the patient recovering from an aSAH (Level 3; Mayer et al., 2005; Suarez, Tarr, & Selman, 2006). See Figure 7 in the original guideline document for an angiogram showing cerebral vasospasm before and after treatment (see the original guideline document for treatment of the patient with cerebral vasospasm).
Patients recovering from aSAH must be screened for ability to swallow prior to receiving any food, fluid, or medication by mouth. A validated bedside screen that includes a water test should be used. A formal swallow evaluation from a speech therapist should be obtained if there are any questions about the patient's ability to safely swallow. After it has been determined that swallowing is normal, the patient's usual diet with increased fiber may be followed. Patients with impaired swallowing should have a diet prescribed by the speech therapist to prevent aspiration.
After the aneurysm has been secured, patients gradually increase activity. Physical and occupational therapists are consulted postoperatively when patients are stable.
Thigh-high stockings and pneumatic (sequential) compression devices are maintained postaneurysm securement (Level 3; Suarez, Tarr, & Selman, 2006). When the aneurysm has been secured, heparin therapy for prevention of DVT may be considered. Additional factors, such as future need for surgery or angiography, are weighed into the decision to institute heparin therapy.
- Anticonvulsants—If seizures have occurred or the patient is at higher risk for seizure development, prophylaxis is maintained. If using anticonvulsants, use those that do not change the level of consciousness.
- Stool softeners—Stool softeners should be continued because narcotics, other medications, and decreased physical mobility and bowel motility may cause constipation.
- Sedation—Sedation may be warranted particularly in patients who are intubated, have ICP monitors and central lines, or both.
- Antiemetics—Use of antiemetics may be continued as needed.
- Cerebral edema treatment—In patients with cerebral edema, 2% or 3% hypertonic saline may be administered at a rate of 75–150 cc/hr unless contraindicated (Level 2; Suarez et al., 1999). Frequent electrolyte monitoring is indicated at least every 6 hours. Monitor and replace potassium to maintain normal levels. Monitor serum sodium to a goal of 145–155 meq/L and serum osmolarity 300–320 mOsm/L levels. Notify the provider on call if the serum sodium is >155 meq/L. Hypertonic saline therapy can be tapered slowly if no longer indicated (i.e., improving mental status or cerebral edema or the serum sodium rises to dangerous levels >155 meq/L; Level 2; Suarez et al., 1999).
- BP treatment—A variety of pharmacological agents may be used to maintain BP within the target range. See section on "BP Management" above for treatment of BP.
- Calcium channel blockers—Nimodipine (Nimotop), a calcium channel blocker, is the only drug currently approved by the Food and Drug Administration for the prevention and treatment of vasospasm following aSAH. Nimodipine crosses the blood–brain barrier and inhibits calcium entry into cells, subsequently reducing the contractile state of the vascular smooth muscle. It is indicated to reduce the incidence and severity of delayed ischemic deficits from vasospasm following aSAH and has been shown to improve outcomes following aSAH despite a lack of evidence of arteriographic efficacy (Level 1; Allen et al., 1983; Neil-Dwyer et al., 1987; Petruk et al., 1988; Philippon et al., 1986; Pickard et al., 1989). Solomon and colleagues (1988) proposed that the improved outcome with nimodipine was related to it inhibiting calcium entry into ischemic neurons, thereby increasing viability of these cells. Oral or enteral administration of 60 mg of nimodipine every 4 hours is instituted within 96 hours after hemorrhage and continued for up to 21 days.
Other Tests and Treatments
Several tests are used to monitor for presence of cerebral vasospasm. Transcranial Doppler (TCD) ultrasonography uses ultrasound waves projected through a thin spot in the skull to the cerebral blood vessels. The ultrasound waves bounce off of the red blood cells (RBCs) as they flow through the cerebral blood vessel. A decrease in the internal lumen of the blood vessel requires the blood (and hence, the RBCs) to move at a higher velocity. Although TCD ultrasonography is not sensitive or specific enough to use to diagnose cerebral vasospasm, it is a noninvasive diagnostic tool that can be used in conjunction with neurologic exam and other diagnostic tests to manage the aSAH patient. TCD ultrasonography has several limitations. It is only as good as the technologist performing the exam, so a neurophysiologist should be consulted whenever available. There are multiple physiologic states that will increase blood flow, thereby increasing blood velocity. Independent of neurologic exam, TCD can consistently measure middle cerebral artery (MCA) mean velocities and can detect increasing mean MCA velocities. MCA flow velocities <120 cm/sec and >200 cm/sec respectively have a strong negative and positive predictive power for determining which patients will develop ischemic deficits (Level 3; Aaslid, Huber, & Nornes, 1984). Some clinicians and institutions prefer to monitor patients using the Lindegaard index. The Lindegaard index was developed to predict cerebral vasospasm using TCD. It is calculated as mean MCA velocity/mean internal carotid artery (ICA) velocity. A Lindegaard index ≥3 is indicative of MCA vasospasm and ≥6 as severe vasospasm (Level 2; Aaslid, Huber, & Nornes, 1984; Lee et al., 1997; Lindegaard et al., 1988). TCD velocity associated with a decrease in neurological function, or independently in comatose patients, can be used as a preliminary screening method to identify patients requiring further intervention (i.e., CT scan or cerebral angiogram).
Cerebral angiography is the gold standard for diagnosing cerebral vasospasm. The procedure is the same as described in the Diagnostic Studies section in the original guideline document for aneurysm identification. The angiogram provides a clear visualization of the cerebral blood vessels, and a decrease in lumen size is indicative of cerebral vasospasm. Variation in the decrease in lumen size also quantifies severity of cerebral vasospasm. A blood vessel with a significant decrease in lumen size requires intervention.
In patients with symptomatic vasospasm, it is often managed with triple H therapy. More severe symptomatic vasospasm requires more aggressive treatment. Endovascular therapies for refractory vasospasm include both intraarterial vasodilators and mechanical dilatation of vessels with balloon angioplasty. The determination of which of these therapies to use is an individual decision and depends upon the patient's general health and severity of vasospasm. Papaverine is a widely used agent (Fandino et al., 1998; Kaku et al., 1992; Polin et al., 1998; Sawada et al., 1997), although, there is preliminary evidence that verapamil (Feng et al., 2002), nicardipine (Kasuya et al., 2005; Kasuya et al., 2002), nimodipine (Biondi et al., 2004; Hui & Lau, 2005; Tanaka et al., 1982), and fasudil hydrochloride (Tachibana et al., 1999; Tanaka et al., 2005) may be of benefit (Level 2). A review of intraarterial treatment of cerebral vasospasm and mechanisms of action of these drugs was provided by Sayama, Liu, and Couldwell (2006).
For patients at risk for or with known cerebral vasospasm, more aggressive treatment should be used. Patients without symptoms but with elevated TCD velocities or CT evidence of diffuse cerebral vasospasm require at least a central venous catheter, repletion with crystalloids, and the above end points for volume resuscitation (CVP ≥8 and urine output ≥250 mL/hr). CVP monitoring is indicated at least every 2 hours. Treatment with fluid or albumin bolus to keep CVP >5 for normovolemia or CVP >8 mm Hg for hypervolemia is indicated (Level 3; Mayer et al., 2005; Suarez, Tarr, & Selman, 2006). Hypervolemia is desirable in patients without underlying cardiac disease to maintain adequate cerebral perfusion pressure (Level 3; Mayer et al., 2005). Antihypertensive and diuretic agents should be avoided (Level 3; Mayer et al., 2005).
For patients with a secured aneurysm and clinical evidence of cerebral vasospasm, more aggressive therapy is instituted. If not yet performed, cerebral angiography may be performed to accurately diagnose and treat cerebral vasospasm (see above for angiographic treatment of cerebral vasospasm). Pulmonary pressure monitoring may be indicated in patients with cardiac dysfunction with the goal of maintaining pulmonary artery wedge pressure >12 mm Hg and cardiac index >4.0 L/min (Mayer et al., 2005). If desired effect is not attained, cerebral angiography for angioplasty or drug infusion may be undertaken if qualified personnel are available (see above and page 12 and 20 in the original guideline document for angiographic treatment).
Patient Monitoring in the ICU
- Frequent neurological assessment is indicated with a minimum of at least every hour or more frequently when patients are actively ischemic.
- For patients with external ventricular drain or subarachnoid bolt, see Guide to the Care of the Patient with Intracranial Pressure Monitoring: AANN Reference Series for Clinical Practice.
- Monitor TCD values including systolic velocities, mean velocities, and Lindegaard ratio and compare them to baseline and previous values. Discuss elevations (mean MCA velocity >120 mm Hg or Lindegaard ratio ≥3) with attending physician, resident, or nurse practitioner promptly.
- Electroencephalography (EEG) is commonly used to monitor for seizure activity in many patients with neurological conditions. Continuous EEG is used to monitor patients with unexplained neurological deterioration to detect nonconvulsive seizures by providing information about global cerebral activity and cortical function (Wartenberg et al., 2006). Electrodes are placed at distinct positions around the skull, and brain activity is monitored. Typical brain activity shows much variation in the brain waves, while seizure activity is evidenced by rhythmic waves indicating neurons firing in unison. In patients with continuous EEG, collaborate with the EEG technician to ensure that leads are in place. Monitor for clinical seizures.
- Repeat CT scans and cerebral angiography are common tests used to monitor the patient recovering from aSAH. CT scans are routinely performed postoperatively and postcoiling and are warranted when the patient's clinical exam changes. Cerebral angiography should be obtained postoperatively, postcoiling (to ensure aneurysm obliteration), and when clinical exam or TCDs suggest cerebral vasospasm.
- Hemodynamic monitoring is obtained at least every hour or more frequently when titrating vasoactive agents. Monitor peripheral pulses and troponin levels during vasopressor infusion.
- CVP monitoring is indicated at least every 2 hours to keep CVP >5 for normovolemia or CVP >8 mm Hg for hypervolemia (Mayer et al., 2005).
- Pulmonary artery pressure monitoring is indicated in patients with cardiac dysfunction, with pulmonary artery diastolic pressure kept >14 mm Hg or a cardiac index >4.0 L/min (Mayer et al., 2005). Some institutions have incorporated pulmonary artery pressure monitoring as a standard of care for all aSAH patients, although the literature is not clear on the efficacy of this practice.
- In patients requiring mechanical ventilation, frequent arterial blood gases, pulse oximetry (SaO2) and end tidal carbon dioxide (ETCO2) are indicated. Arterial blood gases should be obtained daily and with each change in ventilator settings. Continuous SaO2 or ETCO2 monitoring should be incorporated to maintain SaO2 ≥90% or ETCO2 ≥35–37 mm Hg.
- Suctioning should be performed only as necessary to maintain clear lungs and limited to 15 seconds, hyperoxygenating the patient prior to the procedure. Saline lavage prior to suctioning should be avoided.
- Abdominal assessment is indicated at least every shift.
- Nutritional support is obtained via tube feeding if the patient is unable to take orally.
- Urine output is monitored precisely. A urinary catheter is often warranted to assure accurate monitoring.
- Urine electrolytes and specific gravity should be monitored as these patients are at risk for cerebral salt wasting (CSW) and the syndrome of inappropriate antidiuretic hormone secretion (SIADH).
- It is important to be aware that patients receiving triple H therapy often have high urine output.
- In patients on complete bed rest, skin assessment is performed every shift.
- Frequent turning (at least every 2 hours) is performed for patients unable to move themselves.
- Skin-care techniques are performed every shift with the assessment.
Tight glycemic control is to be maintained, using an insulin drip if necessary. Glucose should be monitored at least daily in all patients recovering from aSAH. In patients requiring an insulin drip, glucose should be evaluated hourly until reaching the target blood glucose (100–120 mg/dL) and then every 2–4 hours.
Social workers and pastoral personnel are consulted to assist in alleviating concerns of patients and families. Social workers should also collaborate with the critical care team to identify and facilitate appropriate after-discharge care.
Current Research and Future Therapies
Refer to the original guideline document for a brief overview of current research and future therapies of cerebral vasospasm including intravenous magnesium sulfate, statins, and neuromonitoring techniques.
Care of the aSAH Patient in the Neurological Unit
When the patient has stabilized and risk of cerebral vasospasm is low, the patient recovering from aSAH is transferred to the neurological unit. Vital signs with complete neurologic examination should be performed every 4–8 hours. Medications should be maintained as in the ICU setting; however, patients should no longer require intravenous vasoactive medications to maintain BP; mechanical ventilation; or central venous pressure, pulmonary artery, or arterial BP monitoring. If anticonvulsants are being used, they should be continued in the unit. Antiemetics should be used as needed, although nausea and vomiting are not common in patients stable enough for transfer to the unit. Pain medications should be continued as needed. Nimodipine should be ordered at the same dose of 60 mg orally every 4 hours until 14–21 days after hemorrhage. Activity should be increased as tolerated by the patient. Physical and occupational therapy should be consulted to determine patient functioning and needs for rehabilitation during the remainder of the hospital stay and after discharge.
Care of the aSAH Patient Outside the Hospital
Most patients recovering from an aSAH will be discharged to their homes. A family member or significant other should be present when discharge instructions are given to the patient. If the patient is being discharged less than 21 days after hemorrhage, nimodipine should be continued for 14–21 days. Other medications should be continued after discharge. The patient should be instructed to take all medications as ordered. The patient should also be encouraged to drink lots of water and other nonalcoholic liquids to ensure hydration after discharge. Although activity is not restricted after discharge, patients should be advised to monitor themselves for tiring and exhaustion and to schedule activities accordingly. Referral to outpatient physical therapy is recommended to ensure maximal recovery.
Some patients recovering from an aSAH will be discharged to a rehabilitation center for more intensive physical and occupational therapy. Medications should be continued after discharge. Nimodipine should be continued for 21 days after hemorrhage. In the rehabilitation setting, intake and output should be monitored closely to prevent dehydration.
Patient and Family Education
For the SAH patient, education may not be possible immediately upon admission to the hospital. In many cases, the patient is too ill or has too low of a level of consciousness to benefit from education. However, when the patient is awake enough, education by the health professionals should begin immediately.
Because of the severity of SAH, education usually focuses on the family members. It is normal for the family to be overwhelmed and have many questions. Because of the stress that the family members experience, many times education must be repeated and reinforced until the family members can process this information.
The brain may take 6–15 months to recover to the fullest ability (Haug et al., 2007; Samra et al., 2007). It is quite common for headaches to last up to 6 months or longer. The family also must be educated on the symptoms of another stroke. These symptoms include, but are not limited to, severe headache, sudden speech difficulties, sudden vision change, inability to move one side of the body, and numbness or tingling on one side of the body. The patient should call emergency services if any of these symptoms appear.
Although there is no literature supporting the screening of family members of aSAH patients for aneurysms, some physicians refer first-degree relatives for magnetic resonance imaging (MRI), magnetic resonance angiography, computed tomography (CT) angiography, or angiography for cerebral aneurysms. The family members considered at risk and the technique used for screening are currently based on physician preference.
The American Stroke Association (www.strokeassociation.org ) and the National Stroke Association (www.stroke.org ) have excellent Web sites that can be resources for nurses, patients, and family members. Another resource that is excellent for education of the family is a booklet titled Brain Aneurysm: Understanding Care and Recovery. This booklet is distributed by Krames and may be ordered by calling 800/333-3032. This booklet is also endorsed by the American Association of Neuroscience Nurses.
Key areas of patient, family, and caretaker education in the subarachnoid hemorrhage population are as follows:
- What is a brain aneurysm?
- What is a subarachnoid hemorrhage?
- Signs and symptoms of a ruptured aneurysm
- What is hydrocephalus?
- What is cerebral vasospasm?
- Possible medical procedures that the patient may encounter while in the hospital
- CT scan
- Lumbar puncture
- Transcranial Doppler ultrasonography (TCD) ultrasonography
- Treatment options
- Clipping of aneurysm via craniotomy
- Endovascular procedures (coiling)
- Length of hospital stay
- ICU stay (average 10–14 days)
- Step-down/unit stay (average 5–7 days)
- Common complications are as follows:
- Cerebral vasospasm
- Loss of short-term memory
- Behavior changes
- Skin breakdown
- Urinary/bowel incontinence
- After the hospital
- Inpatient rehabilitation
- Long-term nursing care
- Screening of first-degree relatives
Documentation is similar to the documentation for the ischemic stroke patient. Documentation should include the following:
- Time of onset
- Neurological assessment: level of physical functioning, cognitive level, muscle strength, and cranial nerve findings. (Some providers prefer the nurse to describe "what they saw" versus saying that a certain cranial nerve is not functioning.)
- Vital signs: BP, pulse rate and rhythm, respirations, oxygen saturation, temperature, blood glucose, CVP, ICP (if patient has an EVD), cardiac output (if patient has a Swan-Ganz catheter)
- Input and output
- Swallowing ability
- Mechanism of communication
- Activity level
- Skin integrity
- Psychosocial issues
- Patient and family education
- Discharge planning
Levels of Evidence
Class I: Randomized controlled trial without significant limitations or meta-analysis
Class II: Randomized controlled trial with important limitations (e.g., methodological flaws, inconsistent results), observational study (e.g., cohort, case control)
Class III: Qualitative study, case study, or series
Class IV: Evidence from reports of expert committees and/or expert opinion of the guideline panel, standards of care, and clinical protocols that have been identified
Levels of Recommendation
Level 1: Recommendations are supported by class I evidence.
Level 2: Recommendations are supported by class II evidence.
Level 3: Recommendations are supported by class III and class IV evidence.