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Anesth Analg 2003;97:289-290 © 2003 International Anesthesia Research Society
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Abstract |
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IMPLICATIONS: Increased levels of carboxyhemoglobin (COHb) are frequently found in units of packed red blood cells. We report a congenital heart surgery where increased levels of COHb were found in the patient after a blood transfusion and hypothesize that this phenomenon could be dangerous in a cyanotic newborn undergoing open heart surgery.
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Introduction |
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TopAbstractIntroductionCase ReportDiscussionReferences |
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Carbon monoxide (CO) is found in the blood stream as a natural product of hemoglobin (Hgb) degradation, but it can also appear in the blood and tissues as a consequence of breathing polluted air. A level more than 1.5% exceeds air quality standards (1), and more than 5% (10% in smokers) is considered grossly abnormal. We report a case of a sudden increase in blood carboxyhemoglobin (COHb) levels during cardiopulmonary bypass (CPB) in a young child because of a high level of contamination in the partial unit of packed red blood cells (PRBCs) used to prime the CPB circuit.
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Case Report |
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TopAbstractIntroductionCase ReportDiscussionReferences |
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A 9.4 kg 14-mo-old girl presented to our hospital for surgical closure of a moderate ventricular septal defect. Her medical history was remarkable for anemia of unknown etiology, a 4-wk history of diarrhea (all infectious studies were negative), and a record of occasional exposure to second-hand smoke.
After an uneventful induction, an arterial line and central venous catheter were placed. Initially, the PaO2 was 628 mm Hg with an oxygen saturation of 99%, a PCO2 of 28, and a hematocrit of 25% at a body temperature of 36°C (all blood gas levels as well as COHb levels were determined on a Chiron 855 Blood Gas Analyzer [Chiron Inc, Emeryville, CA] at 37°C. This analyzer automatically tests for COHb as well as oxyhemoglobin and methemoglobin). A decision was made at this time to add 150 mL of PRBCs (our blood bank split a full unit into two separate units) to the currently asanguinous prime to maintain the hematocrit around 25% while on CPB. The case proceeded smoothly, and bypass was started approximately 44 min after skin incision. Ten minutes into CPB, the body temperature was 34°C, the PaO2 was 394 mm Hg with an oxygen saturation of 96%, a PaCO2 of 44, and a COHb level of 3.7% with a hematocrit of 24%. The inline arterial oxygen saturation monitor (CDI 500) indicated an arterial saturation of 100% at this time. CO contamination of the donor unit was suspected, and the other half unit was sent back to the blood bank where further testing revealed a COHb level of 7.2% in the donor unit (which was then discarded). The Lilliput 1 oxygenator (COBE Cardiovascular, Arvada, CO) was ventilated with 100% oxygen for the duration of the CPB period. The patient’s COHb level continued to remain high (3.5% at 20 min and 3.4% at 50 min after the start of CPB and 2.4% approximately 15 min after the termination of bypass), but by the next morning, the value had decreased to 0.6%. Extubation of the trachea occurred at the end of the case, and the patient received oxygen by face mask at approximately 35%–40% for the next 5.5 h. Of note, the patient did receive an additional 150 mL of PRBCs overnight before the final COHb reading.
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Discussion |
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Hgb has an affinity for CO that is 200–250 times more than that for oxygen. Thus, the oxygen-Hgb dissociation curve is, in effect, shifted to the left, leaving less oxygen available for delivery to the tissues. Although this patient tolerated the increased levels of COHb without apparent detriment, we became quite concerned about what effect we might have seen in a cyanotic child who is far less able to compensate for deficits in oxygen delivery to tissues. For instance, neonates undergoing the Norwood procedure, where the desired immediate post-CPB oxygen saturation is approximately 70%–75%, would presumably be at the highest risk. The combined effects of higher levels of fetal Hgb before surgery (which shifts the oxygen-Hgb curve to the left) mixing on CPB with a unit of PRBCs with a relatively high level of COHb could contribute to a dangerous situation where an already low oxygen saturation after termination of CPB would be compounded by poor oxygen offloading to the tissues, and life-threatening acidosis could rapidly develop.
The half-life of COHb in CO-poisoned patients has been found to be approximately 76 ± 25 minutes in patients breathing 100% oxygen (2). We are assuming this half-life would be similar in patients who have received a transfusion containing COHb, although there are no studies to base this on. While on CPB, we would assume that we could duplicate this half-life with the use of high-flow 100% oxygen as long as the patient was kept normothermic. Unfortunately, most cyanotic heart disease surgeries in neonates require hypothermia (and often deep hypothermic circulatory arrest), and this would probably severely decelerate the rate of CO dissociation from Hgb.
In 2000, Takeuchi et al. (3) reported a novel technique to greatly increase the rate of CO elimination from blood through the use of normocapnic hyperoxic hyperpnea. The test subjects were poisoned with CO in air via face mask until their COHb level was between 10% and 12%. The t1/2 of CO elimination decreased to 31 ± 6 minutes in those subjects who increased their spontaneous minute ventilation two to six times while maintaining normocapnia through the use of a 6% carbon dioxide/94% oxygen mixture. This could probably be duplicated while on CPB by the use of carbogen (5% carbon dioxide/95% oxygen) to maintain normocapnia while increasing the sweep rate of the oxygenator to raise the minute ventilation.
The extent to which the United States blood supply may be contaminated with CO is probably not fully appreciated by most health care practitioners. One study by Aronow et al. (1) in 1982–1983 showed COHb levels as large as 12% in units within their blood bank. Of even greater concern, COHb levels >1.5% (i.e., exceeding air quality standards) were found in 49% of 101 randomly selected units of banked blood at the same institution. Other authors (4) had previously shown an alarming median COHb level exceeding 5% percent for smokers within most areas of the US during 1969–1972 (and even larger levels in select cities). No further studies of the extent of COHb contamination of banked blood have been published since 1984, and it would seem prudent to determine what the present levels are in the national blood supply. Stewart et al. (5) found a statistically significant decrease in the COHb levels of nonsmokers in Chicago between 1970 and 1975, presumably as a result of stronger emission control laws, and one would hope that further reductions (especially among nonsmokers) have continued since that time.
There are no national safeguards in place to prevent the use of PRBC units contaminated with CO. We believe that certain patients may be at increased risk after receiving one of these units, especially a cyanotic newborn undergoing congenital heart disease surgery. To prevent a possible situation like this, we now have a policy of checking all donor units for increased levels of COHb before using them in any patient who is at increased risk (i.e., those with cyanotic heart disease, any patient with tenuous oxygenation, and all newborns). Institutions without such a policy should be cognizant of the risks involved, and if a CPB circuit became contaminated with COHb-containing blood, they may need to make use of some method to reduce the level of COHb in the patient’s blood if oxygen delivery to the tissues is compromised.
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References |
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TopAbstractIntroductionCase ReportDiscussionReferences |
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- Aronow WS, O’Donohue WJ, Freygang J, Sketch MH. Carboxyhemoglobin levels in banked blood. Chest 1984; 85: 694–5.
[Abstract/Free Full Text] - Weaver LK, Howe S, Hopkins R, Chan K. Carboxyhemoglobin half-life in carbon monoxide-poisoned patients treated with 100% oxygen at atmospheric pressure. Chest 2000; 117: 801–8.
[Abstract/Free Full Text] - Takeuchi A, Vesely A, Rucker J, et al. A simple "new" method to accelerate clearance of carbon monoxide. Am J Respir Crit Care Med 2000; 161: 1816–9.
[Abstract/Free Full Text] - Stewart RD, Baretta ED, Platte LR, et al. Carboxyhemoglobin levels in American blood donors. JAMA 1974; 229: 1187–95.
[Abstract/Free Full Text] - Stewart RD, Hake CL, Wu A, et al. Carboxyhemoglobin trend in Chicago blood donors, 1970–1974. Arch Environ Health 1976; 31: 280–6.[Medline]
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