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* From Duke University Medical Center, Durham, NC.
Correspondence to: Duane J. Funk, MD, Box 3094, Duke University Medical Center, Department of Anesthesiology, Section of Critical Care Medicine, Durham, NC 27710; e-mail: duane.funk{at}duke.edu
A 29-year-old woman (A-positive blood type) with a history of primary biliary cirrhosis presented to our hospital for a living related donor liver transplant from her brother. Her postoperative course was complicated by delayed graft function and Candida albicans peritonitis that eventually led to graft failure and the need for urgent retransplantation from a cadaveric O-positive donor. She initially did well but was readmitted to our ICU on postoperative day 7 because of a significant decrease in hemoglobin from 11.1 to 4.5 g/dL.
She was initially resuscitated with 6 U of packed RBCs and had an appropriate rise in her hemoglobin from 4.5 to 10.6 g/dL. Because of the concern of bleeding from the vascular anastomotic site, she was taken for an urgent CT scan of the abdomen. This revealed no intra-abdominal bleeding; however, her hemoglobin level continued to decrease and she required numerous blood transfusions. She was transferred to our ICU for further workup and monitoring. Medications at the time of ICU admission included methylprednisolone, tacrolimus, imipenem, vancomycin, mycophenolate, alprostadil by infusion, ranitidine, and subcutaneous insulin.
Physical Examination
Physical examination revealed an alert, jaundiced woman in moderate respiratory distress. Her vital signs were as follows: BP, 113/53 mm Hg; heart rate, 115 beats/min; and respiratory rate, 32 breaths/min. Her oxygen saturation was 99% on 3 L of oxygen by nasal cannula.
Laboratory Findings
Laboratory studies revealed the following: hemoglobin, 10.6 g/dL; WBC count, 4.5 x 109/µL; platelet count, 387 x 109/µL; serum sodium, 134 mmol/L; potassium, 4.9 mmol/L; chloride, 103 mmol/L; bicarbonate, 18 mmol/L; urea, 26 mg/dL; creatinine, 1.3 mg/dL; total bilirubin, 29.1 mg/dL (conjugated 26.3 mg/dL; unconjugated, 0.5 mg/dL); prothrombin time, 34.2 s; international normalized ratio, 1.4; lactate dehydrogenase, 4,225 U/L; and haptoglobin, 11 mg/dL. Her arterial blood gas while breathing 3 L of oxygen by nasal cannula demonstrated pH 7.38; PCO2, 40 mm Hg; PaO2, 75 mm Hg; HCO3-, 24 mmol/L; arterial saturation, 88.1%; and carbon monoxide level by co-oximetry, 8.9%.
What is the cause of the anemia and oxygen desaturation?
Answer: Severe intravascular hemolysis secondary to passenger lymphocyte syndrome
Answer: Elevated carboxyhemoglobin level secondary to massive intravascular hemolysis
Discussion
Carbon monoxide is a colorless, odorless, nonirritating gas formed from the incomplete combustion of hydrocarbons. The concentration in the atmosphere is < 0.001% and is higher in urban than in rural areas. Carboxyhemoglobin (COHb) is present in low amounts (usually < 2%) in all individuals. Tobacco smoke is an important source of COHb and can reach levels of 10% in smokers.
The only endogenous source of carbon monoxide is from the metabolism of free hemoglobin by the enzyme heme-oxygenase. This enzyme converts free heme to biliverdin, with the byproducts being iron and carbon monoxide. The biliverdin is then converted to bilirubin by the enzyme biliverdin reductase.
There have been other reports of increased COHb levels in patients as a result of both reabsorption of a large retroperitoneal hematoma and transfusion of blood containing high levels of COHb. In both of these cases, the COHb level did not exceed 7%.
Carbon monoxide binds to heme-containing proteins including cytochrome oxidase and interferes with cellular oxidative metabolism. It also shifts the oxyhemoglobin dissociation curve to the left and impairs oxygen release at the tissue level. Carbon monoxide elimination is related to the minute ventilation, fraction of inspired oxygen, and the duration of exposure. While breathing room air, the half-life of COHb is 4 to 6 h. This can be reduced to 40 to 80 min when breathing 100% oxygen and 15 to 30 min while receiving hyperbaric treatment. Low COHb levels (< 15 to 20%) are correlated with symptoms such as nausea, vomiting, and dizziness; and high levels (> 60%) are rapidly fatal. Intermediate levels, however, do not correlate well with symptoms and prognosis, and therefore treatment decisions in this group of patients should not be made on COHb levels alone.
In liver transplantation, the mismatching of donor and recipient blood types is possible because of the decreased expression of major histocompatability complex type I antigens on liver cells and the relative resistance of the liver allograft to humoral rejection. This is not possible with other organs. In our patient, the transplantation of an O-positive allograft into an A-positive host also resulted in the transfer of so-called passenger lymphocytes present in the donor liver. This resulted in the production of anti-A antibodies against the recipient’s RBCs. The passenger lymphocyte syndrome is a rare cause of posttransplant hemolysis. It occurs in both solid-organ and bone marrow transplants, and its frequency increases with the amount of lymphoid tissue transplanted. It occurs more frequently (up to 70%) in lung and heart lung transplants than in kidney or liver transplants (9 to 17%). Hemolysis usually has an abrupt onset and ranges from mild to severe and has a prominent intravascular component as seen in our patient. Antibodies typically appear within 5 to 17 days of transplant and are usually undetectable by 3 months. Interestingly, there is a higher incidence of this syndrome in patients receiving tacrolimus or cyclosporine as part of their immunosuppressive regime. This seems to be due to the rapid and unopposed proliferation of B-cells. The hemolysis associated with this syndrome is usually managed with high-dose corticosteroids, transfusion of compatible RBC transfusions, plasmapheresis, and IV Ig.
Our patient received supportive transfusions, an increase in her corticosteroid dose, and five treatments with plasmapheresis followed by IV Ig therapy. Her COHb level returned to normal after 12 h of 100% oxygen therapy. She did not require hyperbaric oxygen treatment and was transferred to the ward in stable condition. She had no kidney damage, and her liver allograft was functioning satisfactorily at the time of discharge from the unit.
Clinical Pearls
Footnotes
Neither author has any financial disclosures or conflicts of interest.
Received for publication March 14, 2006. Accepted for publication March 21, 2006.
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