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Table of Contents    
Year : 2015  |  Volume : 63  |  Issue : 4  |  Page : 486-488

Importance of anthropometric indices in subarachnoid hemorrhage

Department of Neurosurgery, Paras Hospitals, Gurgaon, Haryana, India

Date of Web Publication4-Aug-2015

Correspondence Address:
Veer Singh Mehta
Department of Neurosurgery, Paras Hospitals, Gurgaon, Haryana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.161983

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How to cite this article:
Srivastava A, Kumar P, Mehta VS. Importance of anthropometric indices in subarachnoid hemorrhage. Neurol India 2015;63:486-8

How to cite this URL:
Srivastava A, Kumar P, Mehta VS. Importance of anthropometric indices in subarachnoid hemorrhage. Neurol India [serial online] 2015 [cited 2023 Dec 10];63:486-8. Available from:

Predicting the occurrence of vasospasm in cases of spontaneous subarachnoid hemorrhage (SAH) is still a challenge even for the most elite neurosurgeons because of its multifactorial pathogenesis. In this league, an attempt by Dhandapani et al., emphasizing the importance of anthropometric indices in SAH is new, and medical literature has a paucity of data on this type of study. Some studies, however, exist investigating the role of anthropometric indices in ischemic stroke and head injury albeit with a variable outcome.

Anthropometric indices such as mid upper arm circumference (MUAC), triceps skinfold thickness (TSF), and mid arm muscle circumference (MAMC) are noninvasive and inexpensive bedside tests. Despite the convenience in assessing it, and its important role in the management of SAH, MUAC measurement requires careful training and supervision in order to prevent wrapping the measuring tape too tightly or too loosely, which results in an erroneous estimate. A study by Dαvalos et al., estimated that the smallest change over time detectable in MUAC was 8-10% when the measurement was taken by different observers. [1] The use of MUAC in adults may be affected by the redistribution of subcutaneous fat toward the central areas of the body during aging. [2],[3] Dhandapani et al., in their study have taken patients of variable ages between 20 and 85 years, without grouping them separately. This considerably increases the chances of a spurious result. In their study, there is only a 4 mm variation in the TSF; this may, however, vary widely with age.

Badjatia et al. have shown that negative nitrogen balance is significantly associated with underfeeding (during the first 2 weeks) and obesity (a high body mass index [BMI]) in patients with a subarachnoid bleed and a subsequent poor outcome at 3 months. [4] Dhandapani et al., in their prospective study of trends in anthropometric nutritional indices in 56 SAH patients found a significant decrease in the median MUAC at 1-week, despite having achieved the target of total nutritional supplementation through enteral nutrition. They also observed a significant fall in the median TSF without any significant fall in the median MAMC at 1-week. This was attributed to the initial mobilization of fat reserves for the requirements of the metabolic response, in preference to the utilization of somatic protein reserves.

Eleven patients were in Hunt and Hess (H and H) grade IV. Out of these, some may have had weakness of the nondominant limb, which was not recorded in the study and taken for anthropometric measurements. These measurements may vary significantly between the normal and paretic arm. This constitutes the major limitation of the study.

Obesity alters adipose tissue metabolism and endocrinal functions and leads to an increased release of fatty acids, hormones, and pro-inflammatory molecules that contributes to obesity-associated complications. [5],[6] Adipose tissue is considered to be highly active as an endocrine organ that liberates several cytokines and chemokines (collectively referred to as adipokines) that can induce an inflammatory phenotype in the distant tissues. [6] This inflammatory mediator-releasing property of adipose tissues appears to account for the higher plasma levels of adipokines detected in clinically obese subjects. [7],[8] Obese mice exhibit more pronounced inflammatory and brain injury responses to ischemia and reperfusion due to an exaggerated increase in circulating levels of monocyte chemoattractant protein-1. [9]

Dhandapani et al. in their study tried to determine the correlation between the impact of adiposity on patients with SAH and their clinical vasospasm. The patients who developed clinical vasospasm had significantly higher median admission TSF as compared to those who did not develop clinical vasospasm. They, therefore, concluded that various factors such as age, H and H grade, Fisher grade, etc., have no correlation with anthropometric indices. But, the former parameters are well-documented factors responsible for vasospasm. Univariate and multivariate analysis of various factors showed the impact on vasospasm, especially of the H and H grade, the Fisher grade, and the median admission TSF. The median admission TSF of 40 mm (with an interquartile range [IQR] of 35-45 mm) had significant correlation with vasospasm in comparison to the median TSF of 35 mm (with an IQR of 30-40 mm). Therefore, at least a separate column of comparison of the median admission TSF of 35-45 mm must be added to show the influence of other baseline factors, as this median admission TSF of 35-45 mm has clearly shown correlation with vasospasm. Second, there is an overlap of 5 mm in between these two median admission values, TSF 35-45 mm and 30-40 mm, which may have resulted in an erroneous result. In [Table 1], the number of patients in different groups must be mentioned; this could have provided a more illustrated view and an understanding of the study.{Table 1}

Dhandapani et al., also mentioned that in three patients, computed tomographic angiography was not done because of the poor clinical condition of the patients. These patients must be excluded from the study; or, the authors must explain why these patients were included in this study and what their final outcome at the end of 3 months was. Dhandapani et al., also stated that four patients were conservatively managed. They, however, did not mention the reasons for treating these patients conservatively; moreover, how can these patients with the possibility of an intact aneurysm be compared with patients with SAH who underwent clipping/coiling and were receiving hypertensive therapy.

Authors considered vasospasm only on the clinical basis. It would have been more appropriate if they would have added transcranial Doppler or digital subtraction angiographic studies to confirm vasospasm. Although, the authors have mentioned that other causes of clinical deterioration were excluded, it is important to know how many patients had deteriorated because of other causes; and what the correlation of this deterioration with TSF and MAMC was.

Andersen and Olsen found that obesity was not only associated with reduced mortality but the risk of readmission for recurrent stroke was also lower in obese stroke patients when compared with normal weight stroke patients suggesting the "obesity paradox" in stroke. [10] Barba et al., have also concluded that obesity in those hospitalized for stroke was associated with reduced in-hospital mortality risk but with an early re-admittance rate. [11] The "obesity paradox" is often attributed to fat acting as a buffer to protect individuals who are in a fragile metabolic state. If this was the case, one would assume that the "obesity paradox" would be apparent across all causes of mortality including that occurring following a SAH. But, in a dose-response meta-analysis of the impact of BMI on stroke and the "all-cause" mortality in stroke patients, a "paradox within a paradox" was observed wherein the risk of "all-cause" mortality increased, while the risk of mortality due to stroke declined, with an increase in the BMI. [12]

Although Juvela et al., found that BMI has significant positive association with cerebral infarction following a SAH, [13] Platz et al., concluded after a large retrospective analysis that obesity seems to have a negligible influence on the outcome after a SAH compared with the impact of SAH itself, the patient's age, the occurrence of vasospasm, or the aneurysmal size. [14] Most of the studies on obesity have been done by considering the BMI as an indicator. The universality of triceps skinfold thickness for measurement of obesity has not been established as yet. Further larger studies are needed to establish the influence of skinfold measures of obesity and muscle mass on the outcome in aneurysmal SAH.

 » References Top

Dávalos A, Ricart W, Gonzalez-Huix F, Soler S, Marrugat J, Molins A, et al. Effect of malnutrition after acute stroke on clinical outcome. Stroke 1996;27:1028-32.  Back to cited text no. 1
de Groot LC, Sette S, Zajkás G, Carbajal A, Amorim JA. Nutritional status: Anthropometry. Euronut SENECA investigators. Eur J Clin Nutr 1991;45 Suppl 3:31-42.  Back to cited text no. 2
Duffield A. Anthropometry, Morbidity and Mortality in Rural Savannah. PhD Dissertation, London School of Hygiene and Tropical Medicine; 1998.  Back to cited text no. 3
Badjatia N, Monahan A, Carpenter A, Zimmerman J, Schmidt JM, Claassen J, et al. Inflammation, negative nitrogen balance, and outcome after aneurysmal subarachnoid hemorrhage. Neurology 2015;84:680-7.  Back to cited text no. 4
Weisberg SP, McCann D, Desai M, Rosenbaum M, Leibel RL, Ferrante AW Jr. Obesity is associated with macrophage accumulation in adipose tissue. J Clin Invest 2003;112:1796-808.  Back to cited text no. 5
Trujillo ME, Scherer PE. Adipose tissue-derived factors: Impact on health and disease. Endocr Rev 2006;27:762-78.  Back to cited text no. 6
Arakelyan A, Petrkova J, Hermanova Z, Boyajyan A, Lukl J, Petrek M. Serum levels of the MCP-1 chemokine in patients with ischemic stroke and myocardial infarction. Mediators Inflamm 2005;2005:175-9.  Back to cited text no. 7
Roytblat L, Rachinsky M, Fisher A, Greemberg L, Shapira Y, Douvdevani A, et al. Raised interleukin-6 levels in obese patients. Obes Res 2000;8:673-5.  Back to cited text no. 8
Terao S, Yilmaz G, Stokes KY, Ishikawa M, Kawase T, Granger DN. Inflammatory and injury responses to ischemic stroke in obese mice. Stroke 2008;39:943-50.  Back to cited text no. 9
Andersen KK, Olsen TS. The obesity paradox in stroke: Lower mortality and lower risk of readmission for recurrent stroke in obese stroke patients. Int J Stroke 2015;10:99-104.  Back to cited text no. 10
Barba R, Marco J, Ruiz J, Canora J, Hinojosa J, Plaza S, et al. The obesity paradox in stroke: Impact on mortality and short-term readmission. J Stroke Cerebrovasc Dis 2015;24:766-70.  Back to cited text no. 11
Bagheri M, Speakman JR, Shabbidar S, Kazemi F, Djafarian K. A dose-response meta-analysis of the impact of body mass index on stroke and all-cause mortality in stroke patients: A paradox within a paradox. Obes Rev 2015;16:416-23.  Back to cited text no. 12
Juvela S, Siironen J, Kuhmonen J. Hyperglycemia, excess weight, and history of hypertension as risk factors for poor outcome and cerebral infarction after aneurysmal subarachnoid hemorrhage. J Neurosurg 2005;102:998-1003.  Back to cited text no. 13
Platz J, Güresir E, Schuss P, Konczalla J, Seifert V, Vatter H. The impact of the body mass index on outcome after subarachnoid hemorrhage: Is there an obesity paradox in SAH? A retrospective analysis. Neurosurgery 2013;73:201-8.  Back to cited text no. 14


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