Anesth Analg 2001;92:1609-1610
© 2001 International Anesthesia Research Society
CASE REPORTS
Increased Carboxyhemoglobin from Hemolysis Mistaken as Intraoperative Desflurane Breakdown
Eric R. Wohlfeil, MD, PhD*,
Harvey J. Woehlck, MD*,
Jerome L. Gottschall, MD
, and
William Poole, CRNA
Departments of *Anesthesiology and Pathology, Medical College of Wisconsin; and Department of Anesthesiology, Froedtert Memorial Lutheran Hospital, Milwaukee, Wisconsin
Address correspondence and reprint requests to Harvey J. Woehlck, MD, Froedtert Memorial Lutheran Hospital, 9200 West Wisconsin Ave., Milwaukee, WI 53226. Address e-mail to hwoehlck{at}mcw.edu or rkost@fmlh.edu.
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Introduction
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In the current practice of anesthesiology, it is common to use newer anesthetics, such as desflurane and low-flow anesthesia, to conserve the anesthetic agent. Greater awareness of intraoperative anesthetic breakdown may result in the attribution of increased carboxyhemoglobin (COHb) concentrations to this cause on circumstantial evidence. We present a case in which such information initially led to an erroneous conclusion about the source of increased COHb.
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Case Report
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A nonsmoking 39-yr-old woman, height 168 cm, weight 115 kg, had a severe hemolytic episode 5 yr before the current surgery attributed to a cefotetan dependent antibody. The patient was now scheduled for drainage of a pelvic abscess. During the course of the present illness, the patient had received ampicillin/sulbactam, and another severe episode of hemolysis developed. A total of 16 U of packed red cells were transfused in the week preceding surgery, 5 of which were administered within 18 h of surgery. The patient demonstrated the serologic presence of a warm autoantibody, an ampicillin/sulbactam dependent antibody with a titer of 8 in the indirect antiglobulin test (1), and a cefotetan dependent antibody with a titer >131,000. The preoperative hematocrit was 18%.
The patient was scheduled for surgery as the first case on a Friday morning. General anesthesia was induced with thiopental and rapacuronium, and maintained with fentanyl, cisatracurium, and desflurane (5.4% end-tidal) using Baralyme as the absorbent. Fresh gas flows were 1 L/min of oxygen and 1 L/min of air. Ventilation was measured at 10.3 L/min (12 breaths/min, 850-mL tidal volume). Intraoperative pulse oximetry revealed SpO2 = 99%. Because of the small hematocrit and continuing hemolysis, intraoperative laboratory studies were obtained 20 min after induction of anesthesia which revealed a COHb concentration of 7.3%. Intraoperative gas monitoring revealed desflurane as the only anesthetic using the SAM monitor (Smart Anesthesia Multi-Gas monitor; GE/Marquette Medical Systems, Milwaukee, WI).
Because desflurane breakdown via reaction with desiccated absorbent was entertained as a possible source of carbon monoxide (CO), the absorbent was changed to fresh, unused, normally hydrated absorbent, which is incapable of generating CO. However, subsequent analysis of the initial batch of absorbent revealed that it was wet, indicating that it was neither desiccated nor the source of CO production. A respiratory gas analysis confirmed that desflurane breakdown was not responsible because no trifluoromethane was found. Expiratory CO concentrations were near equilibrium with COHb concentrations. After 8 h of postoperative mechanical ventilation (800-mL tidal volume, respiratory rate = 16 breaths/min, FIO2 = 0.40), the COHb had decreased to 4.1%.
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Discussion
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An unexpectedly increased COHb noted in the first general anesthetic of the day (2), especially during desflurane anesthesia with Baralyme as the absorbent (3), should provoke suspicion of anesthetic breakdown. COHb also results from preoperative exposures such as smoking, or from endogenous production. It is well established that metabolism of heme via heme oxidase results in the production of one molecule of CO for each molecule of heme destroyed (4). Measurement of expired CO in patients with hemolytic disease has been used successfully to measure the rate of hemolysis (5–7). Because each heme moiety binds one oxygen molecule, this allows the simple calculation that the production of CO in milliliters is equal to the oxygen binding capacity of the blood that was destroyed. Over the 48 h preceding surgery, hemolysis reduced the hematocrit to 10%. Five units of blood was administered during the 18 h before surgery, yet the hematocrit only increased to 18%. By using an estimated blood volume of 6900 mL, only 552 mL of red cells at constant blood volume would increase the red cell mass to a hematocrit of 18% (1242 mL of red cells) from 10% (690 mL of red cells). The transfusions supplied 975 mL of red cells, suggesting that 423 mL of these red cells was destroyed, resulting in an estimated CO production of 257 mL per 24 h. The normal endogenous CO production is approximately 10 mL per day. A mathematical model of CO uptake (8–10) predicts a COHb concentration between 5.6% and 7.3% using this rate of hemolysis and estimated ventilatory variables. If this patient had received an anesthetic through a closed breathing circuit, the oxygen binding capacity of hemoglobin of 566 mL could become an additional 23% saturated with CO during a 6-h procedure because none of the endogenously produced CO would be removed. Exogenous CO sources were highly unlikely in this patient because she did not smoke before surgery (11). Intraoperative exposure was eliminated by the absence of trifluoromethane (12), another product of desflurane breakdown (13).
This case highlights that, although hemolysis is not usually a clinically significant event in the routine delivery of anesthesia, it has the potential to result in significant CO exposure. This exposure mimics CO production from anesthetic breakdown. Also, low-flow or closed-circuit anesthesia during an episode of hemolysis may dangerously increase COHb concentrations through rebreathing, which decreases the elimination of CO. Anesthesiologists should be aware of all sources of CO in the perioperative period.
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Acknowledgments
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Supported by departmental funds of the Medical College of Wisconsin.
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Accepted for publication January 26, 2001.
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Introduction
Case Report
