Epidemiologic Notes and Reports Elevated Intraoperative Blood Carboxyhemoglobin Levels in Surgical Patients -- Georgia, Illinois, and North Carolina

In October 1990, three hospitals, one each in Georgia, Illinois, and North Carolina, reported 26 episodes of elevated blood carboxyhemoglobin (COHb) levels (normal: less than 3% in a nonsmoker, less than 10% in a smoker) during surgery in patients with no known carbon monoxide (CO) exposure. All three hospitals are large, medical-school-affiliated, training institutions. Hospital A (Georgia) reported 15 episodes from January 1987 through September 1989; hospital B (North Carolina), eight episodes from January through October 1990; and hospital C (Illinois), three episodes from January through September 1990. All of the episodes were detected during routine blood gas analyses that included COHb measurements (co-oximetry). In eight episodes, peak COHb levels were greater than 20%. Usually, when an elevated COHb level was detected intraoperatively, 100% oxygen was administered, an alternate gas source was instituted, and COHb levels returned to normal. No deaths or serious complications were reported.

To determine the extent and potential source of the problem and to identify risk factors for developing an elevated intraoperative COHb level, hospitals B and C conducted independent investigations and reported the findings to CDC. In Georgia, the Fulton County Health Department, the Georgia Department of Human Resources, and CDC conducted an epidemiologic investigation at hospital A. For this investigation, a case was defined as an isolated intraoperative COHb level greater than or equal to 8% (nonsmoker) or greater than or equal to 20% (smoker) in any patient undergoing general anesthesia from January 1987 through October 1990. Of approximately 16,000 surgical patients for whom intraoperative COHb levels were recorded, 15 (0.1%) met the case definition.

Potential risk factors were evaluated by a case-control study. Each case-patient was compared with two randomly selected control-patients (i.e., any surgical patient with an intraoperative COHb level less than 3% who underwent general anesthesia the same year as the case-patient). Case- and control-patients were similar in sex, mean age, smoking history, mean duration of anesthesia, and severity of illness as measured by American Society of Anesthesia class. Case-patients were more likely than control-patients to have had their operations performed on a Monday or Tuesday (odds ratio (OR)=6.6, 95% confidence interval (CI)=1.4-33.2), in a particular operating room that was routinely inactive during weekends (OR=5.7, 95% CI=1.1-32.2), or after the anesthesia equipment had not been used for greater than or equal to 24 hours (OR=79.8, 95% CI=6.8-2240.6).

Although routine sampling of the anesthesia circuits was not performed at hos pital A while cases were occurring, intermittent measurements in the 16 months following the last case have not detected elevated CO in the anesthesia circuits. At hospital B, elevated levels of CO greater than 1000 parts per million (ppm) were detected in some anesthesia circuits while cases were occurring. Reported by: CT Ingram, MD, Dept of Anesthesiology, Emory Univ School of Medicine, Atlanta; WR Elsea, MD, RJ Finton, MPH, Fulton County Health Dept; JD Smith, Epidemiology Office, JA Wilber, MD, State Epidemiologist, Georgia Dept of Human Resources. EA Brunner, MD, Anesthesiology Dept, Northwestern Univ Medical Center, Chicago; BJ Francis, MD, State Epidemiologist, Illinois Dept of Public Health. RE Moon, MD, Dept of Anesthesiology, Duke Univ Medical Center, Durham; JN MacCormack, MD, State Epidemiologist, North Carolina Dept of Environment, Health, and Natural Resources. Center for Devices and Radiologic Health, Food and Drug Administration. Div of Field Svcs, Epidemiology Program Office; Epidemiology Br, Hospital Infections Program, Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note:

Elevated COHb levels can be detected in persons with CO poisoning from exposure to smoke or automobile exhaust (1). CO toxicity occurs when CO binds to hemoglobin and causes subsequent tissue hypoxia. CO levels as low as 0.05% (500 ppm) in inhaled air can result in COHb levels as high as 20% (2). Signs and symptoms of CO toxicity are directly related to the duration and magnitude of exposure to CO and may occur at levels as low as 10%; levels greater than 60% are often fatal (1-3). Although most case-patients at hospital A had peak COHb levels greater than 10%, and some greater than 30%, none were considered to be symptomatic when emerging from anesthesia.

Although the mechanism of CO production in the cases presented in this report is unknown, at least two possible explanations exist: 1) contamination of the anesthetic gases or 2) a chemical interaction between the anesthetic gases and the CO2 absorbent. At hospital A, even though cases were clustered in one operating room, evidence did not support a tainted gas supply; the same gas source and distribution system served all operating rooms and chemical evaluation of the gas for contaminants was negative. Potential chemical interaction of the anesthetic gases and the CO2 absorbent was supported by the association of cases with exposure to anesthesia machines that had not been used for greater than or equal to 24 hours. Previous reports have documented an interaction between certain anesthetic gases (e.g., trichloroethylene--a gas no longer used) and the CO2 absorbent to produce CO; there may be a potential for such a reaction associated with new agents currently in use (4,5).

Until the exact mechanism of CO production is identified, the three hospitals have initiated the following actions to minimize the risk of intraoperative anesthesia-associated CO exposure: 1) flushing CO2 canisters with high-flow (about 30 L per minute) oxygen for at least 60 seconds before each anesthetic procedure; 2) replacing CO2 absorbent canisters that have not been used within 24 hours; and 3) using high, fresh gas flows (greater than or equal to 5 L per minute) during anesthesia. Since implementation of these measures, no further cases have been detected.

Since co-oximetry is not routinely performed at all institutions, and neither routine arterial blood gas analysis nor pulse oximetry reliably detect COHb, the extent of this problem is unknown (6). To further characterize this problem, physicians are requested to report episodes of unexplained intraoperative COHb level elevations among surgical patients through state health departments to the Epidemiology Branch, Hospital Infections Program, Center for Infectious Diseases, Mailstop C-10, CDC, 1600 Clifton Road, NE, Atlanta, GA 30333; telephone (404) 639-3407.

References

1. Landry A. Carbon monoxide poisoning: sources, manifestations, treatment. Respiratory Therapy 1985;5:23-5.

2. Freidman PA. Poisoning and its management. In: Braunwald E, ed. Harrison's principles of internal medicine. New York: McGraw Hill, 1987:843.

3. Thom SR, Keim LW. Carbon monoxide poisoning: a review. J Toxicol Clin Toxicol 1989;27:141-56.

4. Petty C. Carbon dioxide absorption. In: Petty C, ed. The anesthesia machine. New York: Churchill Livingston, 1987:71.

5. Firth JB, Stuckey RE. Decomposition of trichloroethylene in closed circuit anesthesia. Lancet 1945;1:814-6.

6. Barker SJ, Tremper KK. The effect of carbon monoxide inhalation on pulse oximetry and transcutaneous pO2. Anesthesiology 1987;66:677-9.

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