Professor of Anesthesia and Pediatrics, Northwestern University Medical School, Vice Chairman, Director of Research, Department of Pediatric Anesthesia, Children's Memorial Hospital, 2300 Childrens Plaza, Chicago, Illinois 60614.To the Editor:--Goertz et al. [1]described the effects of hypertonic saline/6% hetastarch on left ventricular contractility. A number of years ago, we performed a study [2]examining the hemodynamic response to 25% mannitol (a hypertonic solution) in patients before and during cardiac bypass. We found a 23+/-6% (SE) decrease in systemic arterial pressure with a 38+/-7% (SE) reduction in systemic vascular resistance in prebypass patients. During cardiopulmonary bypass, patients experienced a 30+/-5% to a 40+/-3% (SE) decrease in mean systemic pressure depending on dose and rate of mannitol administration. We also found that the patients not on bypass were able to compensate for the decrease in peripheral resistance by increasing cardiac output by approximately 0.8 l/min. These changes, however, were short-lived, and all hemodynamic parameters returned to baseline within a matter of several minutes.We also performed radiolabeled microsphere studies and dose-response studies in rabbits, [2]examining hypertonic glucose and hypertonic mannitol. We found that rate and dose were important factors influencing change in systemic vascular resistance and in systemic arterial pressure, i.e., the faster the rate of administration and the greater the osmotic load, the greater the hemodynamic effect. The vascular bed primarily responsive to this hypertonic load was in muscle tissue. One wonders how long the hypotension lasted in the patients studied by Goertz et al., whether this was an effect that was sustained for more than a transient period (as we observed with 25% mannitol), and whether the phenomena might have been caused by vasodilation of the vascular supply to muscle tissue, resulting in a reflex rather than a direct cardiac effect.Charles J. Cote, M.D., Professor of Anesthesia and Pediatrics, Northwestern University Medical School, Vice Chairman, Director of Research, Department of Pediatric Anesthesia, Children's Memorial Hospital, 2300 Childrens Plaza, Chicago, Illinois 60614.
Summary We report a case of Raynaud’s phenomenon (RP) triggered by transfusion of cold blood to a pediatric burn patient under general anesthesia. The child was febrile so a decision was made to not use a blood warmer. When the blood was rapidly administered the child suddenly developed ‘desaturation’. The child was placed on 100% oxygen, adequate ventilation assured, and the color of his oral mucosa assessed as ‘pink’. Placement of the oximeter on the opposite hand revealed 100% saturation. To our knowledge, this is the first case of apparent RP reported in a pediatric patient triggered by transfusion of cold blood.
To the Editor: Laser therapy is used to treat a wide range of diseases, including superficial skin lesions and port wine stains. For children, this procedure is usually performed under general anesthesia because of the discomfort and the need for the child to remain motionless. Pulse oximetry is used as a standard monitor during general anesthesia. The pulse oximeter reading can be affected by excessive ambient light, IV administered dye, nail polish, and other causes.1–3 However, the effect of laser on pulse oximetry has not been reported. We observed six cases of laser-induced pulse oximetry dysfunction. All children were undergoing laser therapy with an Alexandrite 755 nm laser (Candela Corporation, Wayland, MA) and were monitored with pulse oximetry (Model #: Masimo MS-5 Tram Board; Software version: 42 M). In each case, the oximeter reading disappeared within seconds of initiating laser treatments. The monitor alarm screen indicated “probe is off the patient.” The oximeter reading returned to normal once the laser was stopped. We, at first, thought that covering the oximeter probe with a towel would correct this artifact but discovered that only covering the oximeter probe with a pair of 755 nm laser-proof eye goggles could eliminate the oximeter dysfunction. We also found that shielding the laser generator with lead aprons had no effect on the inference, suggesting that oximeter dysfunction was most likely not caused by electromagnetic radiation from the laser generator. Subsequent testing of oximeter function in the presence of other lasers revealed a lack of interferencefrom a 532 nm potassium titanyl phosphate laser, a 595 nm pulsed dye laser, and a 1064 nm Nd: Yag laser. These observations suggest that a laser may interfere with pulse oximeter function when its wavelength falls within the same wavelength range detected by commonly used pulse oximeters (660–940 nm). We do not know if other brands of pulse oximeters are similarly affected but speculate that they might be susceptible to the same problem. We recommend shielding the oximeter probe with a pair of eye goggles specific for the laser being used to prevent oximeter dysfunction. Li Zhang, MD, PhD Somaletha Bhattacharya, MD Charles J. Coté, MD Richard R. Anderson, MD Massachusetts General Hospital Boston, Massachusetts [email protected]
Professor of Anesthesia and Pediatrics, University of California, San Francisco, California 94143–0648 (Fisher).Assistant Professor of Anesthesiology (Birmingham); Professor of Anesthesiology and Pediatrics (Cote), Northwestern University Medical School, Children's Memorial Hospital, Chicago, Illinois 60614.In Reply:-Anderson and Holford disagree with the values for Vd/f that we estimated for rectally administered acetaminophen. To support their claim, they cite two values for the relative bio-availability of rectal versus oral acetaminophen:1. They claim that “bioavailability of rectal compared to oral acetaminophen formulations has been reported as 0.52 (range, 0.24–0.98),” referring to a manuscript by Montgomery et al. [1]Unfortunately, those data were not obtained by Montgomery et al. but are reported in those authors' introduction as the results of “an unpublished adult study,” in which a SmithKline Beecham preparation (rather than the Upsher-Smith preparation used in our study) was examined. We question the relevance of a study performed in adults, the citation of “unpublished data,” whose accuracy cannot be verified, and data from a different preparation.2. They cite a rectal-oral bioavailability ratio of 0.3. This is based on a study in which acetaminophen concentrations peaked at 3 h after rectal administration, yet the final (of four) samples was obtained at 4 h. [2]It is likely that those investigators underestimated the area under the plasma concentration versus time curve, thereby underestimating the relative bioavailability of rectally administered acetaminophen.Anderson and Holford simulate plasma acetaminophen concentrations that might occur with a 20 mg/kg rectal dose. We agree that the mean concentrations observed with this dose do not overlie the simulated values. However, figure 2 in our manuscript demonstrates that mean concentrations for the three doses differ and that our 10-mg/kg dose yields a peak concentration of 4.0 micro gram/ml at approximately 200 min and that our 30-mg/kg dose (normalized to a dose of 10 mg/kg) yields a peak concentration of 3.7 micro gram/ml at approximately 220 min. [3]These times-to-peak concentration are consistent with Anderson and Holford's simulations. Doubling these peak concentrations (to predict the peak concentration attained with a 20-mg/kg dose) yields values of 8.0 and 7.4 micro gram/ml, slightly less than the values predicted by Anderson and Holford's simulations. This difference is expected in that concentrations for each patient should peak at different times so that the average concentration at the median peak time should be less than the average of the individual peak concentrations (Figure 1). Note also that Anderson and Holford use only our most discrepant data (the data from the 20-mg/kg dose) to criticize our model.Anderson and Holford agree with our claim that suppository size may affect absorption characteristics but are concerned that there is no consistent pattern in the dissolution times. We agree and note in our manuscript that additional studies are needed to determine “factors influencing differences in dissolution.” Our model was developed because, with the traditional first-order adsorption model, we observed that “the pharmacokinetics of acetaminophen varied as a function of the dose administered as smaller-… versus larger-dose suppositories.” Allowing for a more complex absorption model markedly improved the quality of the fit. Readers are referred to our manuscript for additional detail.In their pharmacokinetic analysis of rectally administered acet-aminophen, Anderson et al. [4]used the traditional first-order absorption model. Unfortunately, their manuscript provides no graphics that demonstrate whether their absorption model fits the early plasma concentration data. In addition, their first sample was obtained 1 h after drug administration (whereas our first sample was obtained at 30 min), limiting their ability to determine whether their absorption model fit the plasma concentrations that occurred during the initial absorption phase. If they do not look, they will never know if their pharmacokinetic model misspecifies the early absorption phase.In summary, we appreciate Anderson and Holford's interest in our analysis. However, we contend that their simulations are compared selectively, rather than with our entire dataset. In addition, their claim about relative bioavailability of rectal versus oral preparations of acetaminophen is based on questionable data.Dennis M. Fisher, M.D.Professor of Anesthesia and Pediatrics; University of California; San Francisco, California 94143–0648Patrick K. Birmingham, M.D.Assistant Professor of AnesthesiologyCharles J. Cote, M.D.Professor of Anesthesiology and Pediatrics; Northwestern University Medical School; Children's Memorial Hospital; Chicago, Illinois 60614(Accepted for publication December 17, 1997.)
Summary Children with myelodysplasia have an increased incidence of latex allergy, which can lead to severe intraoperative allergic reactions. Despite widespread recommendations to avoid intraoperative latex exposure, little evidence exists to support the efficacy of this practice. We examined the incidence of intraoperative allergic reactions in children with myelodysplasia who underwent 1,025 operations in a 36-month period before and after institution of a standardized latex-avoidance protocol. Risk factors for an intraoperative reaction were found to be a history of latex allergy (p = 0.001) and surgery performed before institution of the latex-avoidance protocol (p = 0.01) The estimate of increased risk for allergic reaction was 3.09 times higher in cases performed without latex avoidance. Recognized violation of the protocol after its institution led to severe allergic reactions in three patients. Our experience suggests that a latex-avoidance protocol reduces intraoperative allergic reactions in children with myelodysplasia. Development of severe allergic reactions with violation of the protocol reinforces the importance of vigilance on the part of all operating room personnel in its implementation.
