Obesity in aneurysmal subarachnoid hemorrhage

As the number of obese people is globally increasing, reports about the putative protective effect of obesity in life-threatening diseases, such as subarachnoid hemorrhage (SAH), are gaining more interest. This theory-the obesity paradox-is challenging to study, and the impact of obesity has remained unclear in the survival of several critical illnesses, including SAH. Thus, we performed a systematic review to clarify the relation between obesity and SAH mortality. Our study protocol included systematic literature search in PubMed, Scopus, and Cochrane library databases, whereas risk-of-bias estimation and quality of each selected study were evaluated by the Critical Appraisal Skills Program and Cochrane Collaboration guidelines. A directional power analysis was performed to estimate a sufficient sample size for significant results. From 176 reviewed studies, six fulfilled our eligibility criteria for qualitative analysis. One study found paradoxical effect (odds ratio, OR = 0.83 (0.74-0.92)) between morbid obesity (body mass index (BMI) > 40) and in-hospital SAH mortality, and another study found the effect between continuously increasing BMI and both short-term (OR = 0.90 (0.82-0.99)) and long-term SAH mortalities (OR = 0.92 (0.85-0.98)). However, according to our quality assessment, methodological shortcomings expose all reviewed studies to a high-risk-of-bias. Even though two studies suggest that obesity may protect SAH patients from death in the acute phase, all reviewed studies suffered from methodological shortcomings that have been typical in the research field of obesity paradox. Therefore, no definite conclusions could be drawn 1).

263 SAH patients were included of which leptin levels were assessed in 24 cases. BMI was recorded along disease severity documented by the Hunt and Hess and modified Fisher scales. The occurrence of clinical or functional DCI (neuromonitoring, CT Perfusion) was assessed. Long-term clinical outcome was documented after 12 months (extended Glasgow outcome scale). A total of 136 (51.7%) patients developed DCI of which 72 (27.4%) developed DCI-related cerebral infarctions. No association between BMI and DCI occurrence (P = .410) or better clinical outcome (P = .643) was identified. Early leptin concentration in serum (P = .258) and CSF (P = .159) showed no predictive value in identifying patients at risk of unfavorable outcomes. However, a significant increase of leptin levels in CSF occurred from 326.0 pg/ml IQR 171.9 prior to DCI development to 579.2 pg/ml IQR 211.9 during ongoing DCI (P = .049). No association between obesity and clinical outcome was detected. After DCI development, leptin levels in CSF increased either by an upsurge of active transport or disruption of the blood-CSF barrier. This trial has been registered at ClinicalTrials.gov (NCT02142166) as part of a larger-scale prospective data collection. BioSAB: https://clinicaltrials.gov/ct2/show/NCT02142166 2).

In a study involving a nationwide administrative database, milder obesity was not significantly associated with increased mortality rates, neurological complications, or poor outcomes after SAH. Morbid obesity, however, was associated with increased odds of venous thromboembolic, renal, and infectious complications, as well as of a nonroutine hospital discharge. Notably, milder obesity was associated with decreased odds of some medical complications, primarily in patients treated with coiling 3).

A total of 305 consecutive SAH patients (2002 to 2011) were retrospectively reviewed to collect demographics, BMI (kg/m(2)), comorbidities, Glascow Coma Scale, World Federation of Neurologic Surgeons Scale, aneurysm treatment, delayed cerebral ischemia, radiographic infarction, and short-term and long-term (> 24 months) morbidity, and mortality. Patients were stratified by BMI into category 1, < 25 kg/m(2); category 2, 25 -< 30 kg/m(2); and category 3, ≥ 30 kg/m(2).

Results: Categories 1, 2, and 3 had 93, 100, and 87 patients with mean BMIs of 22.4 ± 1.8, 27.6 ± 1.4, and 35.7 ± 4.6 (P < 0.05), respectively. By category, 24-month follow-up was available in 92%, 85%, and 85%. Category 3 had more hypertension, diabetes mellitus, and clipping than category 1. Short-term mortality rates were 17%, 12%, and 8%; long-term mortality rates were 34%, 26%, and 19% (P > 0.05 at all points between categories 1 vs. 3, but not 1 vs. 2 or 2 vs. 3). On univariate analysis, BMI was inversely associated with short-term (odds ratio, 0.91; 95% confidence interval 0.84-0.98; P = 0.009) and long-term (odds ratio, 0.92; 95% confidence interval 0.87-0.97; P = 0.001) mortality. On multivariate analysis including age, World Federation of Neurologic Surgeons Scale, delayed cerebral ischemia, and radiographic infarction, BMI remained significant for short-term (odds ratio, 0.91; 95% confidence interval 0.81-0.99; P = 0.047) and long-term (odds ratio, 0.92; 95% confidence interval 0.85-0.98; P = 0.021) mortality. On Kaplan-Meier survival analysis, P > 0.05 for categories 1 versus 2 and 2 versus 3, but P = 0.005 for categories 1 versus 3.

Conclusions: In our SAH population, higher BMI resulted in less short-term and long-term mortality, but no difference in functional outcome 4).

data for 741 SAH patients. A BMI greater than 25 kg/m(2) was considered overweight and greater than 30 kg/m(2) obese. The outcome according to the Glasgow Outcome Scale at discharge and after 6 months was assessed using logistic regression analysis.

Results: According to the BMI, 268 patients (36.2%) were overweight and 113 (15.2%) were obese. A favorable outcome (Glasgow Outcome Scale score >3) was achieved in 53.0% of overweight patients. In contrast, 61.4% of the 360 patients with a normal BMI had a favorable outcome (P = .021). However, in the multivariate analysis, only age (odds ratio [OR]: 1.051, 95% confidence interval [CI]: 1.04-1.07, P < .001), World Federation of Neurological Surgeons grade (OR: 2.095, 95% CI: 1.87-2.35, P < .001), occurrence of vasospasm (OR: 2.90, 95% CI: 1.94-4.34, P < .001), and aneurysm size larger than 12 mm (OR: 2.215, 95% CI: 1.20-4.10, P = .011) were independent predictors of outcome after 6 months. Of the 321 poor grade patients (World Federation of Neurological Surgeons score >3), 171 (53.3%) were overweight. Of these, 21.6% attained a favorable outcome compared with 35.3% of normal-weight patients (P = .006).

Conclusion: Although many physicians anticipate a worse outcome for obese patients, in our study, the BMI was not an independent predictor of outcome. Based on the BMI, obesity seems to be negligible for outcome after SAH compared with the impact of SAH itself, the patient's age, occurrence of vasospasm, or aneurysm size 5).

Systolic and diastolic blood pressure were strong predictors of aneurysmal SAH, and there was a substantially increased risk associated with smoking. However, high body mass was associated with reduced risk of aneurysmal SAH 6).

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Veldeman M, Weiss M, Simon TP, Hoellig A, Clusmann H, Albanna W. Body mass index and leptin levels in serum and cerebrospinal fluid in relation to delayed cerebral ischemia and outcome after aneurysmal subarachnoid hemorrhage. Neurosurg Rev. 2021 Apr 17. doi: 10.1007/s10143-021-01541-1. Epub ahead of print. PMID: 33866464.
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