Special Feature

Critical Care Management of the Patient with Subarachnoid Hemorrhage

By Andrew M. Luks, MD, Pulmonary and Critical Care Medicine, University of Washington, Seattle, is Associate Editor for Critical Care Alert.

Dr. Luks reports no financial relationship to this field of study.

Spontaneous subarachnoid hemorrhage (SAH) is associated with high morbidity and mortality. Although a significant proportion of the deaths occur at the time of or shortly following the initial hemorrhage—10% of patients die before hospitalization while 25% die within the first 48 hours1—getting through this initial period of illness does not ensure good patient outcomes: Patients remain at risk for complications and severe neurologic insults for up to two weeks following the initial bleeding event. As a result, the ultimate outcome of those who survive the initial hemorrhage depends to a large extent on the quality of critical care they receive following admission.

Management of SAH patients has traditionally fallen within the purview of the neurosurgeons and neuro-intensive care specialists, but with increasing efforts to assure intensivist involvement in the management of all ICU patients, it is expected that more general intensivists will be caring for these patients. The purpose of this special feature is to review the critical care management of patients with SAH from the general intensivist's perspective. The review will begin by examining those issues that arise before the aneurysm has been secured and then consider issues that arise later in the course of illness when the risk of non-bleeding complications remains high.

Critical Care Issues Prior to Securing the Aneurysm

Once a patient presents with spontaneous SAH, nothing can be done to reverse the damage of the initial bleeding event. It is imperative, however, to prevent further bleeding episodes, which are a major source of morbidity and mortality.1 Toward this end, the majority of patients undergo a definitive procedure to "secure" the aneurysm. A full discussion of the optimal method (surgical vs endovascular) for this procedure is beyond the scope of this review, but it is important that intensivists at facilities lacking neurosurgical services arrange early transport to neurosurgical centers in order that the definitive procedure can occur with the now-preferred 72-hour window.

Until the aneurysm is secured, the rebleeding risk can be reduced through adequate blood pressure control. Although data are lacking to support particular blood pressure targets, efforts should be made to bring systolic blood pressures below 140 mm Hg. Nicardipine drips are commonly used for this purpose and recent evidence suggests that use of this agent is associated with less blood pressure variability and fewer dose adjustments when compared to intravenous labetalol in patients with various forms of stroke including SAH.2 In the course of lowering blood pressure, however, care must be taken to avoid provoking hypotension, as cerebrovascular autoregulation is lost following SAH and any hypotensive episodes could provoke cerebral ischemia.

Rebleeding risk can also be reduced by reversing any preexisting coagulopathy, although the routine use of antifibrinolytic therapy (e.g., aminocaproic acid) should be avoided because the positive effect on rebleeding rates is offset by an increased incidence of cerebral ischemia.3

During this early period of SAH, patients are also at risk for acute hydrocephalus and its resultant complications. As a result, ventriculostomy is indicated in those patients with intraventricular blood, poor aneurysm grade, or in intubated patients in whom neurologic exam is not possible. Concern has been raised that external ventricular drains increase the rebleeding risk but methodological issues limit the data underlying these claims4 and a more recent study suggests they may have no impact on rebleeding.5 Because external ventricular drains increase the risk of meningitis and/or ventriculitis, strict infection control practices should be implemented when these devices are used.6

Once the Aneurysm Has Been Secured

The risk of rebleeding declines dramatically once the aneurysm has been secured, but patients remain at risk for a variety of other complications that adversely affect outcomes and, in some cases, lead to severe neurologic deterioration.

Vasospasm

In addition to rebleeding and acute hydrocephalus, cerebral vasospasm is another leading cause of morbidity and mortality in those who survive the initial hemorrhage, and extensive effort should be directed toward identifying and treating this complication, which may occur anywhere from 3 to 14 days following the initial hemorrhage. Although angiography remains the gold standard for the detection of cerebral vasospasm, the cost and invasiveness of the procedure limit its widespread application in vasospasm monitoring. Instead, clinicians must rely on a combination of the clinical exam—the onset of vasospasm is often heralded by a change in the patient's level of consciousness—and a variety of imaging modalities including serial transcranial Doppler ultrasonography and SPECT scanning to identify when more invasive testing (angiography) or therapeutic intervention is necessary.

All patients should be placed on prophylaxis with nimodipine (60 mg every 4 hours for 21 days), the lone strategy in vasospasm management that has Level 1 evidence demonstrating a beneficial effect on patient outcomes.7 Many institutions also rely on "Triple-H" therapy (hypertension, hypervolemia, hemodilution) to prevent and treat vasospasm, but a meta-analysis of the four prospective trials that investigated this strategy revealed no evidence of benefit in this regard8; the strategy may also cause further complications such as pulmonary edema from volume overload. While some data suggest that the hypertension component of Triple-H therapy may be of benefit when used alone,9 at a minimum, efforts should be made to avoid volume depletion and hypotension in the two weeks following SAH. To this end, diuretic use should be avoided.

In situations where vasospasm does occur, blood pressure and central venous pressure should be raised through the use of vasopressors and intravenous fluids, although prospective, randomized trials have not confirmed that this improves outcomes relative to normo-volemia and normotension. Patients with angiographically confirmed vasospasm may also undergo a variety of interventions, such as balloon angioplasty or vasodilator administration; a discussion of these issues is beyond the scope of this review.

Other Critical Care Issues

Blood Transfusions

It has been argued that SAH is the "heart attack of the brain," and that transfusions should be employed as they would be in patients with acute coronary syndrome, to maintain the hematocrit above 30%. While anemia (Hb < 10 g/dL) is, in fact, associated with adverse outcomes in SAH,10 red blood cell transfusion is also associated with adverse outcomes including death and severe disability.11 The link between transfusion and adverse outcomes may be strongest in those who have no evidence of vasospasm, suggesting that we should tailor transfusion practices based on the clinical characteristics of the patients, although such practices have not been tested in a prospective manner. Until the results of such studies are available, care should be taken to avoid unnecessary transfusions, and arbitrary transfusion thresholds should not be rigidly applied to all patients.

Glucose Control

Multiple studies have established that hyperglycemia is associated with adverse outcomes following SAH, including mortality, vasospasm, and poor neurologic status.10,12 Although studies have suggested a benefit from intensive insulin therapy (IIT) in other post-surgical patient populations,13 there are, as yet, no data demonstrating that IIT improves outcomes in SAH patients.14 In light of data suggesting possible harm from IIT in critically ill patients that may be related to insulin itself or an increased incidence of hypoglycemia,15 care should be taken to avoid implementing protocols with overly strict glucose thresholds until further data become available.

Fever

Temperature > 38.3° C occurs in up to 41% of SAH patients, and is associated with both increased risk of vasospasm and poor neurologic outcomes.16 In up to 25% of cases, no infectious source can be identified and the fever is presumed to be central in origin.16 Efforts should be made to identify all reversible infectious and non-infectious causes of fever, including periodic sampling of cerebrospinal fluid in patients with external ventricular drains, limiting the use of invasive catheters when not necessary (e.g., avoidance of central lines in patients not requiring vasopressors or 3% NS), and maintenance of vigorous infection control practices during repeated handling of devices such as external ventricular drains. Given the adverse impact on patient outcomes, it makes sense that treating fevers aggressively would have a beneficial impact. However, while studies have shown that various medicines (acetaminophen, ibuprofen) and cooling systems are capable of reducing fever in SAH patients, large, controlled trials have yet to demonstrate a positive impact on patient outcomes.

Sodium Balance

Hyponatremia occurs in up to 40% of patients with SAH. It is most commonly due to cerebral salt wasting syndrome (CSWS), but in some cases, results from inappropriate secretion of antidiuretic hormone (SIADH). Distinguishing between the two causes is important, as different therapies are required in each case; SIADH is managed with fluid restriction, while CSWS is managed with sodium administration in the form of saline or salt tablets. The disorders share several common laboratory findings including elevated urine osmolality and urine sodium and low serum uric acid concentrations but can be distinguished by the fact that CSWS patients are typically volume-depleted with normal or elevated serum osmolality while SIADH patients are either euvolemic or slightly hypervolemic and have low serum osmolality. Given the increased risk of diabetes insipidus and the fact that many patients also receive 3% normal saline or mannitol during their treatment, patients should also be monitored for hypernatremia, which has been associated with increased risk of cardiac complications and death following SAH.17

Cardiopulmonary Complications

A detailed discussion of this extensive topic is beyond the scope of this review, but the general intensivist should be aware that SAH patients are at increased risk for cardiac complications including the development of reversible myocardial stunning. Electrocardio-grams should be obtained in all patients. Abnormalities such as symmetrical T-wave inversions and ST changes can be seen and should be followed up with serial troponin levels. Those patients with elevated troponins or persistent hypotension should be evaluated with echocardiography. Because left ventricular dysfunction and impaired cardiac output increase the risk of vasospasm and cerebral ischemia, any patients with evidence of cardiac dysfunction may require more intensive monitoring (e.g., arterial line and pulmonary artery catheter) and the administration of dobutamine to ensure adequate cardiac output and maintain cerebral perfusion.

Pulmonary complications such as neurogenic or cardiogenic pulmonary edema, aspiration pneumonia, and volume overload from Triple-H therapy are also common in SAH. In addition, up to 27% of SAH patients develop acute lung injury, an outcome associated with increased mortality and ICU length of stay.18 While patients should receive standard treatment for these problems, a few issues warrant additional attention. Although there is theoretical concern that high levels of positive end-expiratory pressure (PEEP) may decrease cerebral venous return and lead to elevated intracranial pressure, there is evidence to suggest that both PEEP levels of 15 cm H2O and recruitment maneuvers can be applied safely in these patients.19,20 Strong consideration should be given to monitoring with jugular venous oximetry, brain tissue PO2, and/or intracranial pressure in patients with severe hypoxemia requiring higher levels of PEEP. Low tidal volume ventilation in acute lung injury may lead to hypercarbia and subsequent increases in cerebral blood flow, which may exacerbate intracranial pressure problems. At the same time, routine hyperventilation is no longer used in this patient population, as the associated hypocarbia decreases cerebral perfusion and may provoke ischemia.

Nutrition

Depending on the severity of the SAH, patients may develop catabolic responses marked by the presence of markedly elevated resting energy expenditures and negative nitrogen balance.21 As a result, it is important to begin early enteral nutrition where feasible with careful attention to preventing aspiration in those who may have impaired mental status and swallowing abilities.

Conclusion

In considering the issues described above, it is important to recognize that solid Level 1 evidence is lacking for many of the management strategies used with SAH patients. As a result, there can be a considerable degree of inter-individual and inter-institutional variation in the care of these patients. Although the proper means for dealing with the various complications may not be clear, the complications and their risk factors are well established and careful attention to these details can go a long way toward assuring better outcomes for patients with this potentially devastating disorder.

References

  1. Boderick JP, et al. Initial and recurrent bleeding are the major causes of death following subarachnoid hemorrhage. Stroke 1994;25:1342-1347.
  2. Liu-Deryke X, et al. A comparison of nicardipine and labetalol for acute hypertension management following stroke. Neurocrit Care 2008;9:167-176.
  3. Roos Y, et al. Antifibrinolytic therapy for aneurysmal subarachnoid hemorrhage: A major update of a Cochrane review. Stroke 2003;34:2308-2309.
  4. Fountas KN, et al. Review of the literature regarding the relationship of rebleeding and external ventricular drainage in patients with subarachnoid hemorrhage of aneurysmal origin. Neurosurg Rev 2006;29:14-18.
  5. Hellingman CA, et al. Risk of rebleeding after treatment of acute hydrocephalus in patients with aneurysmal subarachnoid hemorrhage. Stroke 2007;38:96-99.
  6. Frontera JA, et al. Impact of nosocomial infectious complications after subarachnoid hemorrhage. Neurosurgery 2008;62:80-87.
  7. Meyer FB. Calcium antagonists and vasospasm. Neurosurg Clin North Am 1990;1:367-376.
  8. Treggiari MM, et al. Systematic review of the prevention of delayed ischemic neurological deficits with hypertension, hypervolemia, and hemodilution therapy following subarachnoid hemorrhage. J Neurosurg 2003;98:978-984.
  9. Muench E, et al. Effects of hypervolemia and hypertension on regional cerebral blood flow, intracranial pressure, and brain tissue oxygenation after subarachnoid hemorrhage. Crit Care Med 2007;35:1844-1851.
  10. Wartenberg KE, et al. Impact of medical complications on outcome after subarachnoid hemorrhage. Crit Care Med 2006;34:617-623.
  11. Kramer AH, et al. Complications associated with anemia and blood transfusion in patients with aneurysmal subarachnoid hemorrhage. Crit Care Med 2008;36:2070-2075.
  12. Badjatia N, et al. Relationship between hyperglycemia and symptomatic vasospasm after subarachnoid hemorrhage. Crit Care Med 2005;33:1603-1609.
  13. van den Berghe G, et al. Intensive insulin therapy in the critically ill patients. N Engl J Med 2001;345:1359-1367.
  14. Bilotta F, et al. The effect of intensive insulin therapy on infection rate, vasospasm, neurologic outcome, and mortality in neurointensive care unit after intracranial aneurysm clipping in patients with acute subarachnoid hemorrhage: A randomized prospective pilot trial. J Neurosurg Anesthesiol 2007;19:156-160.
  15. Treggiari MM, et al. Intensive insulin therapy and mortality in critically ill patients. Crit Care 2008;12:R29.
  16. Oliveira-Filho J, et al. Fever in subarachnoid hemorrhage: Relationship to vasospasm and outcome. Neurology 2001;56:1299-1304.
  17. Fisher LA, et al. Hypernatremia predicts adverse cardiovascular and neurological outcomes after SAH. Neurocrit Care 2006;5:180-185.
  18. Kahn JM, et al. Acute lung injury in patients with subarachnoid hemorrhage: Incidence, risk factors, and outcome. Crit Care Med 2006;34:196-202.
  19. Wolf S, et al. Open lung ventilation in neurosurgery: An update on brain tissue oxygenation. Acta Neurochir Suppl 2005;95:103-105.
  20. Wolf S, et al. The safety of the open lung approach in neurosurgical patients. Acta Neurochir Suppl 2002;81:99-101.
  21. Kasuya H, et al. Metabolic profiles of patients with subarachnoid hemorrhage treated by early surgery. Neurosurgery 1998;42:1268-1274.