Letter: Estimation of body surface area.
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We evaluated criteria for the diagnosis of ventricular abnormal signal-averaged electrocardiogram (SAE) in 205 healthy children classified by age, body surface area and height. The children were classified by age into 4 groups: under 3 months old, 3 months old or more but less than 1 year old, 1 year old or more but less than 12 year old and 12 year old or more. They were also divided by body surface area into 4 groups: under 0.3 m2, 0.3 m2 or more but less than 0.5 m2, 0.5 m2 or more but less than 1.2 m2, and 1.2 m2 or more. In terms of height, they were classified into 4 groups: under 60 cm, 60 cm or more but less than 80 cm, 80 cm or more but less than 140 cm, and 140 cm or more. The boundary points in these 3 classifications were statistically consistent. Criteria for abnormal SAE in children classified according to age were filtered QRS duration (f-QRSd) > 95 msec, root mean square (RMS) < 30 mu v and duration of low amplitude signal (LAS) > 25 msec in those under 3 months old; f-QRSd > 110 msec, RMS < 25 mu v, LAS > 30 msec in those 3 months or more but less than 1 year old; f-QRSd > 115 msec, RMS < 20 mu v, LAS > 30 msec in those 1 year old or more but less than 12 year old; and f-QRSd > 125 msec, RMS < 20 mu v, LAS > 30 msec in those 12 year old or more. The criteria for evaluating abnormal SAE were similar regardless of whether children were classified by age, body surface area or height. Using these values as criteria, the 205 children were evaluated for the presence of abnormal SAE. All of the children were negative for abnormal SAE using these criteria according to age, body surface area or height. In evaluating abnormal SAE in children, it is useful to classify children by age, body surface area and height and to identify the criteria in each group. In this study, the criteria based on height and age were particularly useful, since these are more convenient than body surface area.
In 179 healthy boys and girls, the relationship between body surface area (S) in dm2 and body weight (bw) in kg was investigated. The body surface was calculated from the DuBois and DuBois formula. For infants below 20 kg, the relationship followed the regression equation S=3.6kg + 9; r=0.996. For infants with bw between 20-40 kg, the regression equation S=2.5.kg + 33; r=0.977 was found. These equations can easily be memorized and may be able to replace nomograms when bedside calculations of the S is required. In addition, formulas for the volume of plasma expander to be used in the prophylaxis and treatment of shock, trauma, and burn injuries are presented.
The body surface area (BSA) of 11 Chacma Baboons has been determined by a coating method using plaster of Paris. The relationship between BSA (Cm2) and mass (g) is adequately described by the simple Meeh formula A = (12.7) M2/3. The inclusion of an additional variable, such as length, is not indicated by the data. The difference in K values between species and individuals is postulated to be determined by variations in body density rather than other factors.
Body surface area (BSA) was introduced into medical oncology in order to derive a safe starting dose for phase I studies of anticancer drugs from preclinical animal toxicology data. It is not clear however, as to why dosing by BSA was extended to the routine dosing of antineoplastic agents. Several formulas exist to estimate BSA, but the formula derived by DuBois and DuBois is the one used in adult medical oncology. This formula was derived based on data from only nine patients; subsequent attempts to validate the formula have found the DuBois formula to either over or underestimate the actual determined BSA. While cardiac output does correlate with BSA, the relationship between BSA and other physiologic measures relevant for drug metabolism and disposition, such as, renal and hepatic function, is weak or nonexistent. Further only epirubicin, etoposide, and carboplatin have been studied to determine if dosing by BSA would reduce interpatient variability, and none of these drugs were found to have significant relationships between their pharmacokinetics and BSA. Future clinical trials of new agents should not presume that dosing based on BSA reduces interpatient variability. Studies should examine the role, if any, BSA has in dosing new chemotherapeutic agents in initial phase I studies.
INTRODUCTION: The value of noninvasive markers reflecting repolarization and/or conduction abnormalities in identifying patients with abnormal ECG showing a pattern of atypical right bundle branch block and ST elevation syndrome (Brugada syndrome) at risk for life-threatening arrhythmias is controversial. Because right precordial ST elevation reflects inhomogeneous repolarization, we hypothesized that a correlation between the area of ST elevation, that is, the area of inhomogeneous repolarization, and the inducibility of ventricular tachyarrhythmias (VT) exists. Therefore, the body surface area of ST elevation and the presence of late potentials were compared to the inducibility of VT in patients with the characteristic ECG of Brugada syndrome. METHODS AND RESULTS: A 120-channel body surface potential map was recorded at rest and after administration of a Class I agent (ajmaline, 1 mg/kg) to measure the body surface area of ST elevation (> or = 0.2 mV) in 23 individuals (16 patients had been resuscitated from near sudden cardiac death or had suffered syncope) with an ECG compatible with the diagnosis of Brugada syndrome as well as in 15 healthy controls and in 15 patients with arrhythmogenic right ventricular cardiomyopathy. Late potentials were assessed in 20 of the Brugada patients using signal-averaged ECG. Programmed ventricular stimulation was performed at two ventricular sites with up to three extrastimuli. Mean body surface area of ST elevation (> or = 0.2 mV) of all Brugada syndrome patients was 154 +/- 139 cm2 (control 9 +/- 9 cm2; P < 0.001). In the group of patients with arrhythmogenic right ventricular cardiomyopathy, only one patient was found to have an area of ST elevation (165 cm2). In the presence of ajmaline, area size increased to 330 +/- 223 cm2 in Brugada syndrome patients (P < 0.05). In patients with inducible sustained (n = 15) and nonsustained VT (n = 3), a mean area of 183 +/- 139 cm2 was found, whereas the area was only 52 +/- 58 cm2 in those with no VT induction (P < 0.05). For an area > or = 50 cm2, there were positive and negative predictive values of 92% and 60%, respectively. Positive late potentials were found in 60% of patients and correlated to the inducibility during programmed ventricular stimulation (positive predictive value 100%, negative predictive value 75%; P < 0.001). CONCLUSION: In patients with Brugada syndrome, the body surface area of ST elevation and the presence of late potentials correlate to the inducibility of VT during programmed ventricular stimulation and may be of value as a new noninvasive marker for risk stratification in these patients.
The purpose of this investigation was to determine the relationship among speakers' heights, weights, body surface areas, and speaking fundamental frequencies. The recordings of 30 speakers' readings of a standard prose passage were analyzed by means of the Fundamental Frequency Indicator (FFI) to obtain their speaking fundamental frequency characteristics. The speakers' heights and weights were obtained by means of standard measurement procuedures, and their body surface areas were calculated. Pearson product-moment correlation coefficients, computed separately for men and women, indicated that speakers' heights, weights, and body surface areas were not significantly correlated with their speaking fundamental frequencies; female speakers showed a slight negative correlation while male speakers showed a low, positive trend. Implications of these findings and suggestions for future research are discussed.
Survival after sustaining a 95 per cent body surface area burn is uncommon. We report the successful treatment of a 21-year-old patient who sustained such an extensive burn injury. This report stresses the importance of early aggressive excision of the burn eschar and early coverage with allografts (homografts) and later coverage with autogenous keratinocytes.
The prescribed dose of anticancer agents is most commonly calculated using body surface area as the only independent variable, and it has been shown that this approach still results in large interpatient variability in drug exposure. Here, we retrospectively assessed the pharmacokinetics of 33 investigational agents tested in phase I trials from 1991 through 2001, as a function of body surface area in 1650 adult cancer patients. Twelve of the drugs were administered orally, 19 were administered intravenously, and two were administered by both routes. Body surface area-based dosing was statistically significantly associated with a reduction in interpatient variability in drug clearance for only five of the 33 agents: docosahexaenoic acid (DHA)-paclitaxel, 5-fluorouracil/eniluracil, paclitaxel, temozolomide, and troxacitabine. These results do not support the use of body surface area in dose calculations and suggest that alternate dosing strategies should be evaluated. We conclude that body surface area should not be used to determine starting doses of investigational agents in future phase I studies.
Doses of cytotoxic drugs are routinely adjusted according to body surface area. We have evaluated this practice in 32 women with advanced breast cancer treated with single-agent epirubicin 12.5-120 mg m(-2). Epirubicin and its metabolites were measured by high-performance liquid chromatography (HPLC). Unadjusted plasma clearance was calculated from dose in mg, and adjusted clearance from dose in mg m(-2). Unadjusted clearance did not correlate with surface area, height, weight, per cent ideal body weight or body mass index. There was no difference in the coefficient of variation (CV) of adjusted and unadjusted clearance (39.4% and 37.7% respectively). The AUC that would have resulted from giving an unadjusted dose was calculated. This predicted AUC was accurate, unbiased and had the same CV as the actual AUC. Similarly, in 11 patients an analysis of actual and predicted neutropenia confirmed that unadjusted dosing would have had no significant effect on the pattern of myelosuppression. Normalization of epirubicin dosage according to surface area appears not to reduce either pharmacokinetic or pharmacodynamic variability.
Older individuals' ability to maintain core temperature during cold stress is impaired; however, the relative importance of individual characteristics that influence this response are unknown. The purpose of this study was to determine the relative influence of individual characteristics on core temperature and tissue insulation (I(t)) during mild cold stress. Forty-two young (23 +/- 1 yr, range 18-30 yr) and 46 older (71 +/- 1 yr, range 65-89 yr) subjects, varying widely in muscularity, adiposity, and body size, underwent a transient cooling protocol during which esophageal temperature (T(es)) was measured continuously and I(t) was calculated using standard equations. Multiple-regression analyses were performed to determine predictors of T(es) and I(t), and standardized regression coefficients were analyzed to determine the relative influence of each predictor. Candidate predictors included age, sex, weight, body surface area, body surface area-to-mass ratio, sum of skinfolds, percent fat, appendicular skeletal muscle mass, and thyroid hormone concentrations (triiodothyronine, thyronine). The sum of skinfolds explained 67% (P < 0.01) of the T(es) variance in young subjects vs. 2% (P = 0.30) in older subjects. Conversely, appendicular skeletal muscle mass explained a greater portion of the variance in older subjects for both T(es) (older: 28%, P < 0.01; young: 8%, not significant) and I(t) (older: 46%, P < 0.01; young: 17%, P < 0.01). The T(es) residual variance was considerably larger in older subjects (59-72% vs. 14-42% in young subjects), possibly due to varying rates of physiological aging. These results suggest that the relative influence of individual characteristics changes with aging.
Body surface area (BSA) is used in paediatrics to assess fluid requirement, drug doses, cardiac output and glomerular filtration rate. The aim of this study was to examine, in children with liver disease, the relationship between BSA determined by a traditional nomogram and BSA measured by a novel three-dimensional technique--Loughborough Anthropometric Shadow Scanner (LASS). Subjects were 16 children, mean age 8.1 (range 3.6-14.9) years, with a variety of liver diseases. Twenty-eight controls had a mean age of 7.1 (3.1-10.5) years. All had LASS scans performed as well as 21 anthropometric measurements taken by a single observer. There was a significant relationship between BSA (LASS) and BSA nomogram for liver-diseased children (r = 0.99) and controls (r = 0.96). The BSA nomogram values were significantly greater (P < 0.05) than BSA (LASS) for liver-diseased subjects by 10.1% (-0.35 to +20.6; 95% confidence interval), and for controls by 9.6% (4.1-23.2). Best prediction of BSA (LASS) for liver-disease subjects used height, body weight and gluteal furrow circumference [r2 = 0.997; standard estimated error (SEE) = 0.015 m2] and for controls used body weight alone (r2 = 0.907; SEE = 0.048 m2). BSA nomogram has no additional error in children with liver disease, but may overestimate BSA by 10% compared with a novel three-dimensional body surface scanning technique.
In 41 patients about to start PUVA, the dose of 8-methoxypsoralen (8-MOP) was calculated conventionally according to body weight (0.6 mg/kg), or according to body surface area (25 mg/m2) predicted from height and weight measurements. The two different methods of dosing were used on consecutive treatment days and the plasma 8-MOP concentration was measured on each occasion 2 h after ingestion of the crystalline form of 8-MOP, given to the nearest 10 mg. Body weight calculated doses ranged from 30 to 60 mg with a significant difference in the plasma 8-MOP concentration between the dose groups, indicating a systematic variation according to the weight of the patient. When calculated according to body surface area, only two doses were used (40 or 50 mg), and there was no significant difference in plasma 8-MOP concentration between the groups. Calculation of the dose of 8-MOP using body surface area may be performed quickly and simply provided the height and weight of individual patients is known. We provide evidence that this method of dosing will improve the therapeutic effect of PUVA in psoriasis.
M-mode echocardiography was used to estimate left ventricular wall mass in 136 older normal subjects (Group I: 78 men and 58 women, ages 20 to 97 years) and 105 younger normal subjects (Group II: 52 male and 53 female subjects, ages 1 day to 23 years). Echocardiographic left ventricular mass (in grams) was estimated from the following formula: left ventricular mass = 1.05 ([ left ventricular internal diastolic dimension + ventricular septal thickness (diastole) + posterior wall thickness (diastole)] - [left ventricular internal diastolic dimension]). In both groups, female subjects had a slightly smaller left ventricular mass than male subjects (mean difference 7.2% in Group I, p less than 0.05, and 3.6% in Group II, p = 0.05) for any given age and body surface area. Left ventricular mass varied linearly with body surface area and increased as a function of age. In group I subjects, echocardiographic left ventricular mass (in grams) could be estimated by the general formula: left ventricular mass = 124 (body surface area) + A +/- C, where A is the age-dependent intercept; +/- C encompasses a 95% prediction interval for normal values, which is assumed to be nearly constant (+/- 58 g); and body surface area is expressed in square meters. In the Group II (younger) subjects, with age not considered, left ventricular mass (in grams) could be estimated from the following formula: left ventricular mass = 115 (body surface area) -11 +/- C, where +/- C = +/- 32% and this 95% prediction interval varies as a percentage of the mean.(ABSTRACT TRUNCATED AT 250 WORDS)
Values for body surface area (BSA) are commonly used in medicine, particularly to calculate doses of chemotherapeutic agents and index cardiac output. Various BSA formulas have been developed over the years. The DuBois and DuBois (Arch Intern Med 1916;17:863-71) BSA equation is the most widely used, although derived from only 9 subjects. More recently, Mosteller (N Engl J Med 1987;317:1098) produced a simple formula, [weight (kg) x height (cm)/3600](1/2), which could be easily remembered and evaluated on a pocket calculator, but validation data in adults are rare. The purpose of the present study was to examine the BSA based on Mosteller's formula in normal-weight (body mass index [BMI], 20-24.9 kg/m(2)), overweight (BMI, 25-29.9 kg/m(2)), and obese (BMI, >/=30 kg/m(2)) adults (>18 years old) in comparison with other empirically derived formulas (DuBois and DuBois, Boyd [The growth of the surface area of the human body. Minneapolis: University of Minnesota Press; 1935], Gehan and George [Cancer Chemother Rep 1970;54:225-35], US Environmental Protection Agency [Development of statistical distributions or ranges of standard factors used in exposure assessments Washington, EPA/600/8-85-010. Office of Health and Environmental Assessment; 1985), Haycock et al [J Pediatr 1978;93:62-6], Mattar [Crit Care Med 1989;17:846-7], Livingston and Scott [Am J Physiol Endocrinol Metab 2001;281:E586-91]) and with the new 3-dimensional-derived formula of Yu et al (Appl Ergon. 2003;34:273-8). One thousand eight hundred sixty-eight patients were evaluated (397 normal weight [BMI, 23 +/- 1 kg/m(2); age, 50 +/- 14 years; M/F, 289/108], 714 overweight [BMI, 27 +/- 1 kg/m(2); age, 52 +/- 11 years; M/F, 594/120], and 757 obese [BMI, 36 +/- 6 kg/m(2); age, 53 +/- 11 years; M/F, 543/215]). The overall BSA was 2.04 +/- 0.24 m(2): 1.81 +/- 0.19 m(2) in normal-weight, 1.99 +/- 0.16 m(2) in overweight, and 2.21 +/- 0.22 m(2) in obese subjects. These values were significantly higher in overweight and obese patients compared with the values using the DuBois-DuBois formula (overall, 2.00 +/- 0.22 m(2), P < .01; normal weight, 1.81 +/- 0.19 m(2), P = .93; overweight, 1.97 +/- 0.16 m(2), P < .01; obese, 2.14 +/- 0.21 m(2), P < .001). We could show an excellent correlation between the results obtained from each formula, with all correlations of 0.97 or higher (between 0.971 and 0.999). Body surface area prediction with the commonly used DuBois formula underestimated BSA in obese patients by as much as 3% (male) to 5% (female). Based on the formula of Yu et al, however, BSA is overestimated when these traditional formulas are used. Although Mosteller's formula is recommended based on its simplicity and suitability for laboratory and clinical work in adults, accuracy studies in whites with 3-dimensional one-pass whole-body scanning are needed.
Direct measurement of body surface area (Ab) was made on 20 male adult Nigerians of African descent by coating and planimetry. The results were compared with estimated Ab values obtained using six widely accepted height and weight prediction equations. The results show that existing formulas do not predict surface areas of our subjects accurately. Measured Ab values of our subjects were 6-22% greater than predicted values obtained from non-African nomograms. Using these results, we computed new variables for height and weight formulas that accurately predict the surface area of Africans. The closest fit to measured values is given by the equation Ab(m2) = 0.001315 x Height 1.2139 (cm) x weight 0.2620 (kg) +/- 0.04815 (SEE). The new variables are significantly different from those of existing equations. Our height variable is several times greater than the weight variable and reflects a greater importance of height than weight in determining the surface area of Africans than is the case with Caucasians.
We previously derived a formula for calculating human body surface area (BSA) from V (body volume) and L (reference body length): BSA=(9 pi VL)(0.5). In this paper, we analyse first the effects of body density variation on BSA during growth and the scaling relation of BSA to body mass. Then we utilise the derived formula to calculate BSA of animals and compare the obtained data with the direct measurements on the same animals, including rat, chicken, dog, and cattle, from the literature. It is shown that two problems remain to be solved for applying the derived formula to all mammals and other animals: one is to find out the L for each species of animal by means of direct measurements, and the other is to obtain the variation of body density during growth.