Patients were treated in accordance with our standardized ICP- and CPP-oriented treatment protocol to avoid secondary insults [4 (link)]. The treatment protocol remained unchanged throughout the study period. Treatment goals were ICP ≤ 20 mm Hg, CPP ≥ 60 mm Hg, systolic blood pressure > 100 mm Hg, central venous pressure (CVP) 0–5 mm Hg before the aneurysm was occluded and 5–10 mm Hg afterward, pO2 > 12 kPa, arterial glucose 5–10 mmol/L (mM), electrolytes within normal ranges, normovolemia and body temperature < 38 °C.
Patients who were unconscious (GCS M < 6) were intubated and mechanically normoventilated. Those patients were sedated with propofol and received morphine as analgesia. Wake-up tests were repeatedly performed. The patients were treated with early aneurysm occlusion, including endovascular embolization or surgical clipping, and all patients received nimodipine (first as infusion of 2 mg/h and later as tablets 60 mg × 6 for 3 weeks in total). The dosage of infusion was reduced temporarily in case of hypotension to avoid negative hemodynamic effects. In unconscious (GCS M < 6) patients, an external ventricular drain (EVD) was inserted to monitor and to drain cerebrospinal fluid (CSF) in case of high ICP. The EVD was initially kept closed to measure ICP and assess the need for CSF drainage. If ICP was above 20 mm Hg the EVD was opened at 15 mm Hg. In severe cases when basal ICP treatment was insufficient, thiopental coma treatment and/or decompressive craniectomy (DC) were last-tier treatments. Arterial blood pressure was maintained with fluids. Inotropes (dobutamine or in second hand norepinephrine) were only used if CPP was below 60 mm Hg and the patient did not respond to intravenous fluid treatment.
DCI was defined as new neurological deficits and/or decreased level of consciousness when other causes, e.g., hydrocephalus and hematomas, were excluded. If a manifest cerebral infarction was excluded, triple-H therapy (hypertension, hypervolemia, and hemodilution) including 500 ml dextran-40 solution (100 mg/ml, Meda AB) and 200 ml albumin (200 mg/ml) were administered for 5 days. Cerebral intra-arterial nimodipine was given in case of refractory vasospasm and angioplasty was performed in case of refractory large-vessel vasospasm. The main target for triple-H therapy was elevation of blood pressure but only to moderately elevated levels in relation to baseline, i.e., in general CPP to around 70–80 mm Hg and systolic blood pressure to around 140–160 mm Hg. Secondary targets were erythrocyte volume fraction (EVF) 32% and CVP 8–14 mm Hg, although these goals were in general met automatically by the fluid therapy given. The targeted levels were increased stepwise if clinical improvement was not seen.
Patients who were unconscious (GCS M < 6) were intubated and mechanically normoventilated. Those patients were sedated with propofol and received morphine as analgesia. Wake-up tests were repeatedly performed. The patients were treated with early aneurysm occlusion, including endovascular embolization or surgical clipping, and all patients received nimodipine (first as infusion of 2 mg/h and later as tablets 60 mg × 6 for 3 weeks in total). The dosage of infusion was reduced temporarily in case of hypotension to avoid negative hemodynamic effects. In unconscious (GCS M < 6) patients, an external ventricular drain (EVD) was inserted to monitor and to drain cerebrospinal fluid (CSF) in case of high ICP. The EVD was initially kept closed to measure ICP and assess the need for CSF drainage. If ICP was above 20 mm Hg the EVD was opened at 15 mm Hg. In severe cases when basal ICP treatment was insufficient, thiopental coma treatment and/or decompressive craniectomy (DC) were last-tier treatments. Arterial blood pressure was maintained with fluids. Inotropes (dobutamine or in second hand norepinephrine) were only used if CPP was below 60 mm Hg and the patient did not respond to intravenous fluid treatment.
DCI was defined as new neurological deficits and/or decreased level of consciousness when other causes, e.g., hydrocephalus and hematomas, were excluded. If a manifest cerebral infarction was excluded, triple-H therapy (hypertension, hypervolemia, and hemodilution) including 500 ml dextran-40 solution (100 mg/ml, Meda AB) and 200 ml albumin (200 mg/ml) were administered for 5 days. Cerebral intra-arterial nimodipine was given in case of refractory vasospasm and angioplasty was performed in case of refractory large-vessel vasospasm. The main target for triple-H therapy was elevation of blood pressure but only to moderately elevated levels in relation to baseline, i.e., in general CPP to around 70–80 mm Hg and systolic blood pressure to around 140–160 mm Hg. Secondary targets were erythrocyte volume fraction (EVF) 32% and CVP 8–14 mm Hg, although these goals were in general met automatically by the fluid therapy given. The targeted levels were increased stepwise if clinical improvement was not seen.
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