Update on the Management of Subarachnoid Hemorrhage
In addition to the direct effects of the initial hemorrhage and secondary neurological complications, SAH also predisposes to medical complications that may have a detrimental impact on outcome and increase the length of stay in the NICU and in the hospital.
Fever (≥38.3°C) is the most common of all medical complications in SAH patients (41–72%). It was found to be associated with an increased risk of symptomatic vasospasm, an increased length of stay in both the NICU and hospital, poor outcome (modified Rankin Scale [mRS]: 4–6), dependence in activities of daily living and cognitive impairment at 3 months. In SAH patients, the temperature should be monitored in short intervals. Normothermia should be the target in every SAH patient (Table 1). In a case–control study of advanced fever control with surface or endovascular cooling devices in 40 SAH patients, advanced fever control resulted in a lower daily fever burden and better outcomes at 12 months (mRS: 4–6 in 21%) compared with conventional fever management of 80 SAH patients (mRS: 4–6 in 46%; p = 0.03). With a new occurrence of fever, infections need to be sought for and treated. Fever control should be attempted with antipyretics as the first-line therapy, followed by surface cooling or intravascular devices along with treatment for shivering.
Hyperglycemia on admission or persistent hyperglycemia throughout the hospital stay was associated with DCI as well as a poor short- and long-term outcome (Glasgow Outcome Scale: 1–3; mRS: 4–6) after SAH in several investigations. Depending on the definition, hyperglycemia occurs in 30–100% of SAH patients.
A small trial of 55 patients with SAH confirmed the feasibility and safety of continuous insulin infusion for glucose values exceeding 7 mmol/l (126 mg/dl) with glucose assessments performed every 2 h. The first randomized trial of intensive glucose control (target glucose 80–120 mg/dl = 4.4–6.7 mmol/l) versus standard insulin therapy (target glucose 80–220 mg/dl = 4.4–12.2 mmol/l) in 78 SAH patients showed a decreased rate of infection from 42 to 27% in the intensive group. Mortality at 6 months and the frequency of vasospasm were comparable in the two groups. Retrospective studies reflecting the changes in clinical practice, such as the introduction of insulin protocols, demonstrated that good glycemic control (mean glucose burden >7.8 mmol/l [140 mg/dl] and <1.1 mmol/l [20 mg/dl]) significantly reduced the likelihood of a poor outcome at 3–6 months. Hypoglycemia (<60 mg/dl = 3.3 mmol/l) was identified as a powerful independent predictor of mortality at discharge. Hypoglycemia resulting from tight glycemic control was linked to an increased risk of DCI and infarction. This may be seen as a decrease of cerebral glucose as well as an increase in the lactate/pyruvate ratio and glycerol as markers for cell stress when utilizing microdialysis. Clinical signs of systemic and cerebral hypoglycemia may not be obvious in poor-grade SAH patients. Therefore, hypoglycemia should be avoided while applying tight glucose control. If microdialysis is used, the serum glucose level can be titrated according to the cerebral glucose measurements.
Anemia treated with blood transfusions is associated with an increased risk of delayed infarction, mortality and poor functional outcome at 3 months after SAH, as well as brain tissue hypoxia (partial brain tissue oxygen pressure ≤15 mmHg) and metabolic distress (lactate/pyruvate ratio ≥40). In a safety study, 44 SAH patients were randomized to hemoglobin targets of 10 g/dl (6.2 mmol/l) or 11.5 g/dl (7.1 mmol/l). Achieving the higher hemoglobin target by transfusion of packed red blood cells was found to be safe and feasible. It remains uncertain whether anemia after SAH reflects general illness severity, impacts outcome directly or whether the treatment for anemia – blood transfusions – contributes to a poor outcome. To minimize the frequency of anemia, the number of blood drawings should be reduced. Maintenance of hemoglobin levels between 8 and 10 g/dl (5.0–6.2 mmol/l) is recommended. The optimal hemoglobin level in SAH patients still needs to be determined.
SAH may be further complicated by cardiac dysfunction and pulmonary edema due to a catecholamine surge, resulting in neurogenic 'stunned myocardium' or 'neurogenic stress cardiomyopathy' and neurogenic pulmonary edema. Cardiac dysfunction is accompanied by transient electrocardiographic abnormalities, troponin leaks, reversible wall motion abnormalities on echocardiogram, hypotension and reduction of cardiac output. Neurogenic pulmonary edema is caused by an increased permeability of the pulmonary vasculature and may occur isolated or in conjunction with neurogenic cardiac injury. Hypotension, reduced cardiac output and impaired oxygenation may impair cerebral perfusion in the setting of increased ICP or DCI. Troponin I elevations are found in approximately 35% of SAH patients and cardiac arrhythmias in 35%. A recent meta-analysis showed that cardiac abnormalities on an ECG, echocardiography and troponin measurements are linked to DCI, poor outcome and mortality after SAH (discharge 6 months follow-up period). Thus, baseline evaluation with serial cardiac enzymes and an ECG is recommended. Patients with evidence of depressed myocardial function and pulmonary edema should receive echocardiography and monitoring of cardiac output. Standard management for heart failure is applied, with particular focus on cerebral perfusion status. In pulmonary edema, lung protective ventilation and euvolemia are the targets of therapy.
Treatment of Medical Complications
In addition to the direct effects of the initial hemorrhage and secondary neurological complications, SAH also predisposes to medical complications that may have a detrimental impact on outcome and increase the length of stay in the NICU and in the hospital.
Fever
Fever (≥38.3°C) is the most common of all medical complications in SAH patients (41–72%). It was found to be associated with an increased risk of symptomatic vasospasm, an increased length of stay in both the NICU and hospital, poor outcome (modified Rankin Scale [mRS]: 4–6), dependence in activities of daily living and cognitive impairment at 3 months. In SAH patients, the temperature should be monitored in short intervals. Normothermia should be the target in every SAH patient (Table 1). In a case–control study of advanced fever control with surface or endovascular cooling devices in 40 SAH patients, advanced fever control resulted in a lower daily fever burden and better outcomes at 12 months (mRS: 4–6 in 21%) compared with conventional fever management of 80 SAH patients (mRS: 4–6 in 46%; p = 0.03). With a new occurrence of fever, infections need to be sought for and treated. Fever control should be attempted with antipyretics as the first-line therapy, followed by surface cooling or intravascular devices along with treatment for shivering.
Hyperglycemia
Hyperglycemia on admission or persistent hyperglycemia throughout the hospital stay was associated with DCI as well as a poor short- and long-term outcome (Glasgow Outcome Scale: 1–3; mRS: 4–6) after SAH in several investigations. Depending on the definition, hyperglycemia occurs in 30–100% of SAH patients.
A small trial of 55 patients with SAH confirmed the feasibility and safety of continuous insulin infusion for glucose values exceeding 7 mmol/l (126 mg/dl) with glucose assessments performed every 2 h. The first randomized trial of intensive glucose control (target glucose 80–120 mg/dl = 4.4–6.7 mmol/l) versus standard insulin therapy (target glucose 80–220 mg/dl = 4.4–12.2 mmol/l) in 78 SAH patients showed a decreased rate of infection from 42 to 27% in the intensive group. Mortality at 6 months and the frequency of vasospasm were comparable in the two groups. Retrospective studies reflecting the changes in clinical practice, such as the introduction of insulin protocols, demonstrated that good glycemic control (mean glucose burden >7.8 mmol/l [140 mg/dl] and <1.1 mmol/l [20 mg/dl]) significantly reduced the likelihood of a poor outcome at 3–6 months. Hypoglycemia (<60 mg/dl = 3.3 mmol/l) was identified as a powerful independent predictor of mortality at discharge. Hypoglycemia resulting from tight glycemic control was linked to an increased risk of DCI and infarction. This may be seen as a decrease of cerebral glucose as well as an increase in the lactate/pyruvate ratio and glycerol as markers for cell stress when utilizing microdialysis. Clinical signs of systemic and cerebral hypoglycemia may not be obvious in poor-grade SAH patients. Therefore, hypoglycemia should be avoided while applying tight glucose control. If microdialysis is used, the serum glucose level can be titrated according to the cerebral glucose measurements.
Anemia
Anemia treated with blood transfusions is associated with an increased risk of delayed infarction, mortality and poor functional outcome at 3 months after SAH, as well as brain tissue hypoxia (partial brain tissue oxygen pressure ≤15 mmHg) and metabolic distress (lactate/pyruvate ratio ≥40). In a safety study, 44 SAH patients were randomized to hemoglobin targets of 10 g/dl (6.2 mmol/l) or 11.5 g/dl (7.1 mmol/l). Achieving the higher hemoglobin target by transfusion of packed red blood cells was found to be safe and feasible. It remains uncertain whether anemia after SAH reflects general illness severity, impacts outcome directly or whether the treatment for anemia – blood transfusions – contributes to a poor outcome. To minimize the frequency of anemia, the number of blood drawings should be reduced. Maintenance of hemoglobin levels between 8 and 10 g/dl (5.0–6.2 mmol/l) is recommended. The optimal hemoglobin level in SAH patients still needs to be determined.
Neurogenic Stunned Myocardium & Pulmonary Edema
SAH may be further complicated by cardiac dysfunction and pulmonary edema due to a catecholamine surge, resulting in neurogenic 'stunned myocardium' or 'neurogenic stress cardiomyopathy' and neurogenic pulmonary edema. Cardiac dysfunction is accompanied by transient electrocardiographic abnormalities, troponin leaks, reversible wall motion abnormalities on echocardiogram, hypotension and reduction of cardiac output. Neurogenic pulmonary edema is caused by an increased permeability of the pulmonary vasculature and may occur isolated or in conjunction with neurogenic cardiac injury. Hypotension, reduced cardiac output and impaired oxygenation may impair cerebral perfusion in the setting of increased ICP or DCI. Troponin I elevations are found in approximately 35% of SAH patients and cardiac arrhythmias in 35%. A recent meta-analysis showed that cardiac abnormalities on an ECG, echocardiography and troponin measurements are linked to DCI, poor outcome and mortality after SAH (discharge 6 months follow-up period). Thus, baseline evaluation with serial cardiac enzymes and an ECG is recommended. Patients with evidence of depressed myocardial function and pulmonary edema should receive echocardiography and monitoring of cardiac output. Standard management for heart failure is applied, with particular focus on cerebral perfusion status. In pulmonary edema, lung protective ventilation and euvolemia are the targets of therapy.
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