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Blood pressure and outcome after aneurysmal subarachnoid hemorrhage

All adult patients treated for aSAH between January 2003 and June 2016 at our neurovascular center were eligible for this study. The exclusion criteria were: (a) hospital admission later than 48 h after ictus; (b) hospital stay at our clinic for less than 72 h; (c) no aneurysm treatment; (d) mycotic aneurysm as a bleeding source; (e) no data on MAP values.

The approval of the institutional ethics committee (Ethik-Kommission, Medizinische Fakultät der Universität Duisburg-Essen, Registration number: 15-6331-BO) for this study was obtained and has been performed in accordance with the ethical standards laid down in the 1964 Declaration of Helsinki and its later amendments. The study was registered in the German clinical trial registry (DRKS, Unique identifier: DRKS00008749). All patients or their relatives gave written informed consent within the treatment contract before inclusion into the database.

aSAH treatment: general aspects

All patients with a suspected aSAH received radiographic imaging (digital subtraction angiography (DSA) or computed tomography (CT) angiography of the head) for identification of the bleeding source. Commonly, aneurysm treatment was performed within 24 h after hospital admission by endovascular coiling or microsurgical clipping. Acute hydrocephalus was treated by insertion of an external ventricular drain allowing the measurement of the intracranial pressure (ICP). Raised ICP (> 20 mmHg) was treated conservatively by drainage of cerebrospinal fluid, head elevation, osmotherapy, deep sedation, and relaxation. Patients with increased ICP refractory to conservative management were referred to decompressive craniectomy. Cerebral perfusion pressure (CPP) was maintained over 60 mmHg. Posthemorrhagic hydrocephalus was treated with ventriculoperitoneal shunt placement. Follow-up CT scans of the head were performed in the first 24 h after aneurysm treatment, and if clinically indicated (i.e. failed weak up attempt, increased ICP, clinical deterioration).

aSAH treatment: cerebral vasospasm and blood pressure management

All patients were administered nimodipine orally for 21 days after ictus. Fluid management included the maintenance of euvolemia. In addition, transcranial doppler (TCD) ultrasound was performed at least once a day for the first 14 days after ictus. Patients showing clinical signs of vasospasm in form of (a) TCD velocities higher than 120 m/s and compromised consciousness; (b) new neurological deficits or a decline in the Glasgow coma scale over 2 points not related to other reasons (like rebleeding or hydrocephalus) were scheduled for immediate DSA for the verification and invasive endovascular treatment. As first line therapy, pharmacologic angioplasty was performed using intraarterial nimodipine. Mechanical angioplasty (transluminal balloon angioplasty) was performed only as a rescue option in large proximal intracranial arteries. In case of recurrence of new deficits or increased TCD values, endovascular therapy was repeated up to twice daily until the resolution of vasospasm signs. Post angiographic TCD and/or clinical recovery was reevaluated to determine the success of treatment.

Until obliteration of the aneurysm, systolic blood pressure was kept < 150 mmHg using antihypertensive drugs, if needed. After aneurysm treatment, MAP was retained at ≥ 70 mmHg for the first 14 days after ictus in all aSAH individuals. In patients with confirmed clinical and angiographic vasospasm, the MAP was raised to ≥ 90 mmHg using norepinephrine administration via a central line, if necessary. In cases where the designated MAP target could not be reached with norepinephrine alone, the intensive care physician used additional vasopressors depending on the individual patient’s situation. MAP target was kept for the duration of VS. In patients with an unvoluntary systolic blood pressure (SBP) over 220 mmHg, blood pressure was lowered up using antihypertensive medication without compromising the designated MAP. Blood pressure was monitored continuously via arterial line and was documented every 2 h in the patients’ chart.

Data management

The variables of interest, including radiographic, clinical, laboratory and demographic characteristics of the patients, were collected from the electronic patients’ records and the institutional prospective aneurysm database. The radiographic data were separately reviewed by the senior author (RJ) blinded at this time for any clinical information.

Initial clinical severity of aSAH was classified using the World Federation of Neurological Surgeons (WFNS) scale12 and was dichotomized into good (WFNS 1–3) and poor grade (WFNS 4–5) for statistical analysis. The original Fisher scale was used to assess the radiological severity of bleeding13, with further dichotomization into high (Fisher 3–4) and low (Fisher 1–2) grades. Occurrence of new cerebral infarction(s) was judged upon the follow-up CT imaging up to 6 weeks after aSAH. New hypodensities visualizable within 48 h after early aneurysm occlusion were referred as early infarcts, whereas later infarct events were allocated as DCI associated infarction.

A mean value of MAP and SBP for the first 14 days after ictus were calculated using the daily mean MAP/SBP values collected from the ICU documentation system. For further statistical evaluation, the 14-days mean MAP values were dichotomized according to the institutional standards of blood pressure management after aneurysm treatment: within (MAP < 95 mmHg, standard MAP [SMAP]) and over (MAP ≥ 95 mmHg, increased MAP [IMAP]) the maximal therapeutic target. No patient showed the 14-days mean MAP value < 70 mmHg. The total dosage of used norepinephrine (in milligram [mg]) was extracted for each patient in the cohort.

Depending on the presence of clinical signs and radiographic proof of cerebral vasospasm (basal vessel constriction or perfusion deficit) the patients in the cohort were referred to vasospasm (VS) and no vasospasm (NO VS) groups (see Fig. 1 with the flow-chart). Patients in the VS group were treated with induced hypertension aiming at MAP ≥ 90 mmHg as long as the vasospasm persisted.

Figure 1
figure 1

Overview of the recruitment process of the study. aSAH aneurysmal subarachnoid hemorrhage, MAP mean arterial pressure, (NO) VS (no) vasospasm.

Along with preexisting conditions recorded from the medical charts, the occurrence of following systemic complications during the hospital treatment was also collected:

  1. (a)

    impaired renal function defined as any decrease of the mean glomerular filtration rate under 60 ml/min/1.73 m2);

  2. (b)

    acute coronary syndrome (ACS) based on the changes in the cardiac enzymes and/or electrocardiography (ECG); 12-channel ECG and laboratory work-up was performed if changes in continuous ECG monitoring (i.e., new atrial fibrillation) or clinical symptoms of ACS occurred.

  3. (c)

    Finally, all chest x-rays during the first 14 days were screened to identify new pulmonary congestion not present on the admission X-ray utilizing the Shochat score (cut-off: 2 points)14.

The outcome was assessed at a 6-month follow-up and documented using the modified Ranking scale (mRS)15. An mRS > 2 was defined as poor outcome.

Study endpoints and statistics

The correlation of the 14-days mean MAP values with the functional outcome at 6 months and DCI associated infarction development were set as the primary endpoint. Secondary endpoint included the impact of the 14-days mean MAP values on the occurrence of systemic complications during aSAH.

All statistical analyses were performed using SPSS Version 27 for Mac (IBM Corp). The significance level was set to p < 0.05. Missing data were addressed using multiple imputations.

Univariate analysis was performed to address the correlation of the 14-days mean MAP with the patients’ baseline characteristics and initial severity of aSAH as well as secondary endpoints. Chi-Square test was used for dichotomous/dichotomized variables; for samples with a size smaller than 5, the Fisher exact test was used. Continuous variables were tested with the Students t-test for normally distributed data and the Mann–Whitney-U test for non-normal distributed data. Multivariable binary logistic regression analysis was performed for the primary study endpoints to prove independent correlations. For the primary endpoints, the results were adjusted for initial clinical and radiological aSAH severity, the need for ICP treatment, presence of premorbid arterial hypertension and patients’ age. In addition, the analyses were performed for aSAH individuals in the VS and NO VS groups separately.

Ethics approval

Ethik-Kommission, Medizinische Fakultät der Universität Duisburg-Essen, Registration number: 15-6331-BO.

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