The focus of treatment following surgical clipping or endovascular obliteration of an aSAH includes prevention of: rebleeding, vasospasm, delayed cerebral ischemia, hydrocephalus, and other complications.
The risk of rebleeding is maximal in the first 2 to 12 hours (after rupture), with reported rates of rebleeding between 4% and 13.6% within the first 24 hours (Connolly, 2012). Naidech et al. report a the rebleeding rate among patients who underwent aneurysm repair was 5% (22/444); this rate was higher among patients with clipped rather than coiled aneurysms (5.7% vs 2.4% (Naidech et al., 2005).
Factors associated with rebleeding include:
- Delayed aneurysm obliteration
- Poor neurologic status on admission
- LOC at the time of the initial bleed
- Previous warning headaches
- Large aneurysm
- Hypertension >160 mm Hg (Naidech et al., 2005; Connolly et al., 2012).
The most important strategy to reduce the risk of rebleeding includes early aneurysm obliteration and blood pressure management. "The magnitude of blood pressure control to reduce the risk of rebleeding has not been established, but a decrease in systolic blood pressure to <160 mm Hg is reasonable" (Connolly et al. 2012).
Signs and symptoms of rebleed include sudden severe headache, severe nausea or vomiting, changes in LOC, and new onset neurological deficits. Therefore, nursing priorities center on blood pressure control, astute serial neurological assessments, reducing patient anxiety and optimizing patient comfort.
Antihypertensives medication must be titrated carefully to avoid lowering cerebral perfusion pressure that could lead to cerebral ischemia. Titratable medications used to lower BP include nicardipine, and in some instances labetalol or sodium nitroprusside. Clevidipine, a very short-acting calcium channel blocker may be used to control acute hypertension (Connolly et al., 2012; McNett & Koren, 2016).
Oral nimodipine is a Class I; Level of Evidence A, American Heart Association/American Stroke Association recommendation for all patients with aSAH. "It should be noted that this agent has been shown to improve neurological outcomes but not cerebral vasospasm. The value of other calcium antagonists, whether administered orally or intravenously, remains uncertain (Connolly et al., 2012)."
Sedation and Analgesia for acute brain injury (Oddo, 2016):
- Cerebral blood flow (CBF) - sedatives and analgesics can decrease cerebral perfusion pressure (CPP) by reducing mean arterial blood pressure (MAP) and also by inducing myocardial depression and peripheral vasodilatation. These dose dependent side effects increase the risk of cerebral vasospasm. The risk is managed with careful titration of CPP and normovolemia.
- ICP - Sedatives and analgesics can reduce ICP by decreasing MAP and cerebral blood volume. In intubated patients, sedatives and analgesics can reduce ICP by lowering intrathoracic pressure caused by agitation and coughing. Lower intrathoracic pressure increases jugular venous outflow thereby lowering ICP.
- Seizure suppression - seizures produce a mismatch between cerebral metabolism and oxygen availability. Anti-epileptics, barbiturates, benzodiazepines, propofol, ketamine and other drugs are being used to reduce the risk of secondary seizures.
Antifibrinolytic (Connolly et al., 2012)
Antifibrinolytic, therapy with tranexamic acid or aminocaproic acid is reasonable to reduce the short-term (<72 hours) risk of early aneurysm rebleeding if there are no thromboembolic contraindications and if the aneurysm ablation must be delayed. Patients should be screen for contraindications and DVT risk. Antifibrolytics should be discontinuation 2 hours prior to planned endovascular aneurysm ablation. (Neither aminocaproic acid nor tranexamic acid are FDA aapproved for prevention of aneurysm rebleeding.)
Cerebral vasospasm (CV) refers to the prolonged progressive narrowing of cerebral arteries and arterioles. Cerebral vasospasm after aSAH results in decreased cerebral perfusion and is associated with increased morbidity and mortality.
Management of CV and DCI Recommendations
- Oral nimodipine should be administered to all patients with aSAH
- Maintenance of euvolemia and normal circulating blood volume is recommended to prevent DCI
- Prophylactic hypervolemia or balloon angioplasty before the development of angiographic spasm is not recommended
- Transcranial Doppler is reasonable to monitor for the development of arterial vasospasm
- Perfusion imaging with CT or magnetic resonance can be useful to identify regions of potential brain ischemia
- Induction of hypertension is recommended for patients with DCI unless blood pressure is elevated at baseline or cardiac status precludes it
- Cerebral angioplasty and/or selective intra-arterial vasodilator therapy is reasonable in patients with symptomatic cerebral vasospasm, particularly those who are not rapidly responding to hypertensive therapy
Connolly et al., 2012
CV typically begins on day 3 following hemorrhage, peaking at day 7, and resolving by day 21 (Diringer et al., 2011; Lucke-Wold et al., 2016). The presence of vasospasm can be confirmed on radiographic or sonographic images (Diringer et al., 2011). Routine transcranial Doppler screening may be ordered for patients after aneurysm rupture/repair, as velocities may indicate onset of vasospasm and therapies may be augmented based on parameters (Connolly et al., 2012). Perfusion CT or MRI may also be used to identify areas of cerebral ischemia caused by vasospasm (Connolly et al., 2012).
The exact mechanisms of CV have not been fully elucidated. Multiple inflammatory and spasmogenic cascades have been hypothesized.
- Hemolysis of red blood cells within the subarachnoid space releases a number of spasmogenic by products. These "spasminogens increase the influx of calcium into the vascular smooth muscle, altering myocyte function and causing prolonged contraction and vessel constriction. Oxyhaemoglobin also contributes to release of free radicals and peroxidation of lipids. These changes promote the synthesis of vasoactive eicosanoids and endothelin and inhibit endothelium-dependent relaxation of the arterial wall, resulting in arterial spasm (Dash 2017)".
- Another promising model has been identified by Hanafy, et al. They describe an acute inflammatory response mediated by the resident cerebral macrophage (microglia) production and release of proinflammatory reactive oxygen species and cytokines following phagocytosis of the products of hemolysis (Hanafy, 2013). Subsequently, cytokines induce peripheral neutrophil recruitment and an upregulated inflammatory response appears to predict CV coincident with a CSF neutrophil content of >62% around day three following SAH (Provencio, 2010).
Delayed Cerebral Ischemia
Another major concern after aSAH is development of delayed cerebral ischemia (DCI), which can be a major cause of morbidity and mortality. The term DCI is used to reflect any neurological deterioration caused by cerebral ischemia that lasts more than 1 hour and cannot be explained with radiographic, electrophysiologic, or laboratory findings (Diringer et al., 2011). Patients are at highest risk for DCI 4-14 days after the initial hemorrhage (Vergouwen, et al. (2010). Cerebral ischemia after aSAH can occur due to vasospasm or other factors (edema, decreased perfusion, hemorrhage), and results in DCI. As with vasospasm, DCI can be asymptomatic initially, and can go undetected due to ongoing sedation or poor baseline neurological status (Diringer et al., 2011). The primary mechanism to prevent DCI is euvolemic hemodynamic support. Current recommendations indicate euvolemic status and induced hypertension is the optimal approach for DCI prevention (Dankbaar, Slooter, Rinkel & Schaaf, 2010; Connolly et al., 2012; Diringer et al., 2011) .
N.B - Prophylactic Triple H therapy (hemodilution, hypertension, hypervolemia) and routine use of pulmonary artery catheters or central venous pressure lines soley for fluid management are no longer recommended for the prevention of CV or DCI (Connolly et al., 2012; Diringer et al., 2011).
Electrolyte imbalance - aSAH and other intracranial disorders are associated the dysregulation of serum electrolytes. Hyponatremia is the most common such electrolyte imbalance and may occur in nearly half of aSAH cases (Wijdicks et al. 2016).
Two mechanisms known to cause sodium dysregulation after aSAH:
The importance of hyponatremia remains controvertial with some researchers finding an association with vasospasm caused by excessive secretion of natriuretic peptides, resulting in natriuresis (Connolly et al., 2012; Rahman & Friedman, 2009). Other researchers find no association between vasospasm and neither hypernaturemia or hyponatremia (Qureshi 2002).
Hydrocephalus after aSAH occurs when cerebral spinal fluid (CSF) cannot be absorbed normally through the arachnoid villi due to hemorrhage in the subarachnoid space. Hydrocephalus can be acute (within the first 24 hours), subacute (5-7 days after hemorrhage), or chronic (10 days or later). Acute hydrocephalus occurs in 15-87% of aSAH (Hellingman et al., 2007) and chronic hydrocephalus is present in up to 48% of patients (Connolly et al., 2012).
Placement of external ventricular devices (EVDs) is the primary treatment for acute hydrocephalus (Diringer et al., 2011), while chronic hydrocephalus may require long term ventriculoperitoneal shunts. Symptoms of hydrocephalus are often non-specific and can include drowsiness, stupor, and behavioral changes. Thus, judicious use of sedation and serial neurological assessments are critical for early detection of hydrocephalus.
Critically ill patients are at risk for substantial physiological complications, many of which are exacerbated by cerebral injury. After aSAH, patients may experience fever, hyper or hypoglycemia, anemia, cardiac injury and are at increased risk for deep vein thrombosis (DVT).