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From the Department of Anesthesia and Critical Care, Massachusetts General Hospital, Boston, Massachusetts.
Address correspondence and reprint requests to Loreta Grecu, MD, Department of Anesthesia and Critical Care, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, Boston, MA 02114. Address e-mail to lgrecu{at}partners.org.
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Abstract |
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Introduction |
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A 58-yr-old woman with osteoarthritis was admitted at our institution in June 2005 for a left total hip replacement under spinal anesthesia. She had a right endoscopic carpal tunnel release in 2003 under a Bier block without any complications. The patient’s medical history was significant for hypertension, well controlled with amlodipine, and migraine headaches controlled by rizatriptan. She had no history of coronary artery or lung disease but had a family history of coronary artery disease. She had two miscarriages. She had never received a blood transfusion. She denied any history of tobacco, alcohol, and illicit drug use. She had no known allergies. Nine days before the scheduled surgery, the patient donated 1 unit of autologous blood.
Her preoperative vital signs were within normal limits, physical examination was unremarkable, and there were no findings to suggest cardiac or pulmonary dysfunction. Preoperative laboratory examination revealed no significant abnormalities other than a hematocrit of 32.1%.
On the morning of surgery, the patient was given 2 mg of midazolam. Spinal anesthesia was administered using 4 mL of 0.5% bupivacaine, injected at L4-5. Propofol, 25–30 µg·kg–1·min–1, was infused throughout the case. One gram of cefazolin was administered at the beginning of the case. The intraoperative course was uneventful. Total operative time was 2 h 43 min, during which she received 1 mg of hydromorphone and 1850 mL of lactated Ringer’s solution. She had 200 mL of urine output and 150 mL of blood loss.
The postoperative hematocrit in the recovery room was 28%. The orthopedic surgeon elected to transfuse the unit of autologous blood. Before transfusion her blood pressure was 119/63 mm Hg, heart rate 72 bpm and regular, and tympanic temperature 98.0°F. The transfusion was initiated using a blood filter (Large Standard Blood filter 170–260 µ filter; Baxter, Deerfield, IL). After approximately 80 mL was administered, the patient developed acute stridor with arterial oxygen saturation decreasing to the low 80s. Her blood pressure increased to 163/75 mm Hg, her heart rate increased to 90 bpm, and her temperature increased to 99.3°F. The patient did not receive any other medications during this period. On auscultation, stridor was heard, decreased breath sounds were heard bilaterally, without wheezing, and a diagnosis of laryngospasm was made. The transfusion was stopped, and ventilation was assisted with a bag and mask. The patient’s oxygen saturation gradually returned to baseline, although she continued to complain of dyspnea. Treatment with nebulized racemic epinephrine did not improve her symptoms. She remained conscious throughout the episode. A stat chest radiograph showed no evidence of pulmonary edema, infiltrates, or other pathology.
The decision was made to restart the blood transfusion, considering that a reaction to autologous blood was quite unlikely. Approximately 2 min after restarting the transfusion, the patient experienced another episode of dyspnea accompanied by stridor but without oxygen desaturation. Auscultation again revealed stridor and decreased breath sounds bilaterally, without wheezing. There was no rash. The transfusion was stopped, and assisted ventilation again relieved her symptoms.
The patient remained in the postanesthesia recovery area overnight for observation. She had an uneventful recovery and remained afebrile and hemodynamically stable.
Because laryngospasm developed twice shortly after blood transfusion was started and resolved each time when it was stopped, we concluded that the transfusion was responsible for the laryngospasm.
The Transfusion Medicine Service was consulted and a transfusion reaction report was initiated. There was no evidence of clerical error, hemolytic transfusion reaction, or other serologic incompatibility. The possibility of bacterial contamination was not investigated. The blood filter was considered an unlikely cause and thus was not pursued. We concluded that the patient had a febrile nonhemolytic transfusion reaction (FNHTR), and recommended that in the future she should be exposed only to leukoreduced blood products.
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DISCUSSION |
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The transfusion of autologous blood is not without risks, which is why the incidence of autologous blood donation has decreased since 1992, when one of every 12 units was autologous (4). In addition to the expense, the autologous transfusion may be associated with risks such as bacterial contamination, clerical errors, and intravascular volume overload. The donation may lead to discarding of unused blood and, paradoxically, the resulting perioperative anemia may increase the need for a blood transfusion.
Autologous blood transfusion reactions are rare. Approximately one in 16,000 autologous donations have a severe reaction that requires hospitalization (5). Furthermore, adverse reactions are reported in 0.16% of all autologous blood transfusions. Approximately 25% of autologous transfusion reactions are classified as FNHTR (1). These are usually not life-threatening, although fever, chills, and dyspnea may be confused with the more severe complications of blood transfusions, such as acute hemolytic reactions, sepsis, and transfusion-related acute lung injury (TRALI).
FNHTR is an expensive complication because the blood unit is usually discarded. The diagnosis of FNHTR in our patient was based on the temporal association with the blood transfusion and its resolution on discontinuation of the transfusion. Our Transfusion Medicine Service reached the same conclusion. FNHTR is characterized by fever. Our patient had only a moderate temperature increase, perhaps attributable to the small amount of blood transfused before the reaction was observed and the transfusion stopped.
Blood transfusions are associated with either immunosuppression or immune activation induced by donor white blood cells. The process of immune modulation is identified by the presence of certain markers, such as soluble receptors of tumor necrosis factor 
, soluble receptor of interleukin 2, and neopterin, a macrophage-derived product (6). These markers are increased after transfusion of both autologous and fresh salvaged red blood cells (RBCs). The increase is shorter after autologous transfusions compared with allogeneic RBC administration. The intensity of the reaction may also depend on the duration of blood storage, which may increase the amount of necrotic white cells and cytokine accumulation. White blood cells are implicated as a cause of FNHTR because cytokines, such as interleukin 1, interleukin 6, and tumor necrosis factor-, are synthesized and accumulated by these cells during storage of blood products (7,8). Interleukin 1 can cause fever by inducing the production of prostaglandin E2 in the hypothalamus. We speculate that the presence of cytokines in the autologous blood unit was responsible for inducing FNHTR in our patient. Cytokines may also be released by the interaction of transfused white cells and preformed antibodies in the recipient, although we believe this is unlikely in an autologous transfusion. Leukoreduction appears to be beneficial in reducing the incidence of FNHTR, with some institutions recommending universal leukoreduction to decrease the incidence of these reactions after allogeneic blood transfusions (9–11).
Pulmonary complications after autologous blood transfusions are rare but have been reported in the medical literature. Allogeneic transfusions cause TRALI due to antileukocyte antibodies (12), manifested as fever, dyspnea, hypoxia, hypotension, and noncardiogenic pulmonary edema. Covin et al. (13) reported a case of pulmonary insufficiency after autologous blood transfusion with hypotension and increased oxygen requirement. This may have been a reaction by the patient’s polymorphonuclear cells to lipids accumulated during storage of the packed RBCs.
Our patient had only laryngospasm and did not meet the criteria for TRALI. In addition, our patient did not have hypotension, prolonged oxygen requirement, or any long-standing pulmonary complications.
We conclude that although rare, reactions to autologous blood may occur in clinical practice. The challenge of this case was to associate the patient’s symptoms with the autologous blood transfusion. The diagnosis was unusual but, in retrospect, it was considered the most likely explanation for the occurrence of laryngospasm in a patient who did not receive general anesthesia.
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Footnotes |
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(TNF), interleukin 1, and interleukin 6 (IL-6) levels in the plasma of stored platelet concentrates: relationship between TNF and IL-6 levels and febrile transfusion reactions. Transfusion 1993;33:195–9.[ISI][Medline]
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