Body Surface Area Calculation standard, continued…
Back to BSA report page 3 of report by Thanh Vu, B.Sc. (pharm),
( click here to go to the Body Surface Area BSA calculator )
Calculating BSA in obese individuals is more controversial, with each center developing its own policy. Robin O’Brien, the drug information pharmacist at the BCCA stated that some oncologists at BCCA use 2.2m2 as the maximum BSA with which to calculate the dose. BC Children’s Hospital uses the Mosteller Equation, substituting actual body weight (ABW) and then ideal body weight (IBW) into the equation and taking the average of the resulting BSA’s.
Recently, the convention of using BSA for dose calculation has been questioned. Some authors point out that drug pharmacokinetics (PK) appear largely unexplained by variability in body surface area. Since individuals have a variable ability to metabolize and eliminate drugs, the same dose of drug will have a different effect among individuals. BSA fails to take into account this interpatient variation in PK for most cytotoxic drugs. Therefore, there is an argument in favor of re-evaluating the routine use of BSA for dose calculation.
Some authors have argued that more efforts should be emphasized on the factors that make a more significant contribution to variability in pharmacokinetics, since these are likely to have greater influence on the variation in clinical effect. These factors include variation in drug absorption, drug metabolism and variability between patients in body composition. Reilly and Workman12 noted that although it is common practice to give a fixed dose based on BSA, and to reduce the dose when unacceptable toxicity is seen, doses will not commonly be adjusted upwards in the absence of toxicity. Therefore, under-treatment will generally remain uncorrected.
Grochow et al13 examined pharmacokinetic data from 306 adults receiving 9 cytotoxic drugs and found no correlation between BSA and pharmacokinetic parameters. Thus, the authors suggested that basing drug dose on body surface area is not very useful, except for drugs in which exposure depends on renal clearance or cardiac output. Many studies that have been conducted showed that PK parameters are a more reliable predictor of toxicity than dose according to BSA.
Other methods of dose determination are being reviewed. Two such methods include therapeutic drug monitoring (TDM) and PMT dosing, which consists of determining a Prime dose, Modifying the prime dose before it is administered, and then adjusting the next dose based on the presence or absence of Toxicity. Slevin et al14 used therapeutic drug monitoring of etoposide to treat patients with small-cell lung cancer, and showed that TDM allowed early dose modification to ensure a predictable plasma concentration of etoposide. However, TDM is in the early stages of development and there are many barriers that limit its use. Gurney noted that one of the main barriers to the acceptance of TDM into routine clinical practice is financial cost and inconvenience. There is a substantial cost for obtaining blood samples, laboratory costs, and cost in terms of labor and time involved in analyzing the results. In addition, the question of whether drug monitoring is required with every treatment cycle or just with the initial cycle remains unanswered. At this point, the universal use of TDM for chemotherapy administration is unlikely to be practical. However, TDM may be suitable for patients with abnormal drug handling abilities.
