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Citrate Toxicity During Massive Blood Transfusion

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Citrate Toxicity During Massive Blood Transfusion Citrate Toxicity During Massive Blood Transfusion Walter H. Dzik and Scott A. Kirkley HE USE OF sodium citrate as the blood anti­ ing complexity required rapid transfusion of larger T coagulant for transfusion science dates from volumes of blood. In 1955 several cases of 'citric 1914 to 1915 and the almost simultaneous acid intoxication' following transfusion were publication of the work of four independent reported by Bunker.9 In the years that followed, investigators. Articles from Hustin,l Agote,2 numerous investigations were published and con­ Weil,3 and Lewisohn,4 published between May siderable controversy developed regarding the 1914 and January 1915, each reported the success­ management of citrate toxicity during massive ful use of citrated blood for human transfusion. transfusion. Recognition and therapy ofcitrate tox­ Because citrate was known to be toxic to animals, icity was enhanced by the widespread application Lewisohn carefully titrated the minimum concen­ in the 1970s of ion selective electrodes capable of tration of citrate required to prevent clotting. accurate measurement of the level of ionized Despite the demonstration by Weil that citrated Ca + +. With the development of advanced blood could be stored for several days and still be trauma care, liver transplantation, and prolonged effective,3 and the discovery by Rous and TumerTurnerS5 extensive surgical procedures in pediatrics, there that citrated blood supplemented by dextrose was has been a renewed interest in the role of citrate capable of more prolonged storage, citrated blood toxicity in the setting of ultramassive transfusion. was not quickly accepted by the general medical This review focuses on citrate toxicity during community. Though used with success in limited massive blood replacement in adults. The chemis­ trialstriais on the battlefield in World War 1,6 try of the citrate calcium interaction; the dose, transfusions with citrated blood were often distribution, metabolism,metabolism, and excretion of citrate; associated with chills and fever which were the toxic effects of citrate; and the treatment of incorrectly attributed to the citrate. Febrile citrate induced hypocalcemiahypoca1cemia are discussed. reactions were so common with citrated blood that Occasionally we have offered a personal view during the 1920s most transfusions consisted of the based on our own experience with massive rapid transfers of nonanticoagulated whole blood, transfusion during hepatic transplantation. Citrate and the use of stored citrated blood did not become toxicity is also discussed in most general reviews 10 commonplace until the mid-1930s. 7 of massive transfusion. ,1l While improvements in transfusion technology and the establishment of blood banks made the CHEMISTRY OF CITRATE administration of blood a standard procedure in the operating room, blood usage was generally limited Citric acid (molecular weight 192 daltons) is a to a few units for any given patient. Advances in ubiquitous organic compound with three ionizable knowledge of the biochemistry of citrate and cal­ carboxyl groups. With three pKs (3.14,4.77, and cium led to an improved understanding of their 6.39) all <7.4, the majority of citrate present in interaction as well as the relationship of serum the body has allaU three carboxyl groups ionized (Fig ionized Ca+ + to total serum calcium.ca1cium. The devel­ 1).l). These ionized carboxyl groups are responsible opment of citrate toxicity due to acute hypocalce­hypoca1ce­ for the major pharmacologic action of citrate, the mia was demonstrated in dogs as early as 1944. 8 binding of divalent cations. This binding is After WoddWorld War II surgical techniques of increas- accomplished by having two of the valences occupied by the divalent calcium ion. Because of the third ionized carboxy group, citrate is still From the Blood Bank and Tissue Typing Laboratory, New highly soluble in aqueous media even when bound England Deaconess Hospital, Department ofoj Medicine, Har­ to a divalent cation. Citrate may bind to any of the vard Medical School, Boston. metallicmetaUic divalent cations and subsequently lower Address requests to Walter H. Dzik, MD, Blood Bank and the concentration of the ionized form of that cat­ Tissue Typing Laboratory, 185 Pilgrim Road, Boston, MA 02215. ion. While most reports dealing with the effects of © 1988 by Grune & Stratton, 1nc. citrate deal with its effects on ionized calcium, 0887 7963/88/0202-0004$03.00/0796318810202-0004$03.0010 wellweU documented depressions of magnesium have 76 Transfusion Medicine Reviews, Vol 2, No 2 (June), 1988: pp 76-94 CiTRATECITRATE TOXICITY DURING MURINE TRANSFUSIONTRANSFUSlON 77 nondiffusable. The nondiffusable form was found CH2COO­ to be bound to serum proteins, especially albumin. I By the 1930s most researchers in the field agreed HO-C-COO- that the diffusable portion of calcium existed in two states, bound to diffusable smallsmallligandsligands such I as lactate or citrate, and in the free or ionized CH2COO- state. 18 These three states exist in equilibrium in the plasma and it is generally agreed that ionized Ca + + is the physiologically active form. In the C6 H5 07 healthy human, approximately 47% of calcium is Fig 1. Chemical structure ofot citrate. in the ionized form, 40% bound to serum proteins (mostly(most1y albumin), and approximately 13% bound also been reported. 12,13 Citrate binds slightly to smaller ligands. 19 These proportions differ with stronger to Mg + + (formation constant 2.9 X changes in pH, protein concentration, ligand con­ 103) than it does to Ca + + (formation constant centration, and total calcium concentration. 1.88 x 103).12,14,15 Citrate is found in all human While measurement of total serum calcium cells and is an intermediary in the Kreb's citric remains useful for gross or chronic disturbances of acid cycle. Because the citric acid cycle takes serum calcium, acute changes in ionized Ca + + place within the mitochondria of a cell, tissues are often missed with these measurements, Most with a high number of mitochondria per cell (such laboratories use dye binding methods such as or­ as liver, skeletal muscle, and kidney) contain thocresolphthalein or arsenazo III dye where the larger amounts of those enzymes responsible for change in absorption by the dye is proportional to 2o20 the production and metabolism of citrate. WhileWbile the total calcium concentration. AtomicAtomie neither a common nor routine laboratory test, absorption spectrophotometryspeetrophotometry is also used and is plasma citrate levels can be measured by several an accurateaeeurate and reproduciblereprodueible method, but is rarely methods. One common method involves automated and requires earefulcareful maintenancemaintenanee and incubation of plasma with bacterial citrate lyase in standardization, While these methods have good the presence of zinc ions, The reaction produces accuracyaceuraey and precision, the difficultydiffieulty is that total oxaloacetate whichwhieh is then acted upon by malate calcium measurements may not accuratelyaeeurately reflectrefleet dehydrogenase resulting in the production of the eoneentrationconcentration of ionizedealcium calcium which is the NADH from NAD. Production of NADH is physiologically activeaetive form. measured spectrophotometrically after the serum Early attempts to determine the ionized Ca + + proteins are precipitated. The normal adult plasma relied on nomograms for estimation of ionized concentration of citrate is from 0.9 mg/dL to 2,5 Ca+ + from measured total ea1cium.calcium. In 1935, mg/dL when measured with the citrate lyase McLeanMeLean and Hastings, in their extensive mono­ method (Table 1).l). Slightly higher levels are found graph on ealciumcalcium in body fluids, developed a in children and in patients with hepatic or renal nomogram for estimating the eoneentrationconcentration of disease. 16,1716,17 ionized Ca + +. The nomogram was based on the total ealciumcalcium and total serum protein eoneentrationconcentration MEASUREMENT OF CALCIUM at a set pH and temperature. 18 With the advent of Early in this century it was realized that calcium the more rapid ion selectiveseleetive electrodeeleetrode measure­ exists in biologicbiologie fluidsfluids in at least two forms, one ment of ionized Ca + +, this nomogram and diffusable across a dialysis membrane, the other derivations of it, have been shown to give poor 21 estimates of the ionized Ca + + levels. ,22,23 The Table 1. NormalNormai Adult Concentrations ofot Citrate and inaccuraciesinaecuracies ofearly nomograms likely result from Ionizedlonized Calcium the assumption that pH and small ligand eoneentrationsconcentrations had little effect on ionized Ca + + Citrate Ionizedlonized Calcium eoncentration.concentration. Another outdated method for mg/dLmg/dl 0.9-2.5 4.5-5.4 determining ionized Ca + + is the method of mEq/LmEq/l 0.14-0.39 2.3-2.7 Soulier whichwhieh estimated the ionized Ca + + by its tnmol/Ltnmol/l 0.047-0.130 1.1-1.4 effe'cteffe'et on the thromboplastin time of decalcifieddeealcified 78 DZIKOZIK AND KIRKLEY p1asma.plasma. This method is poor for ionized Ca + + normal ranges depend on the individuallaboratory.individual laboratory. greater than 1.5 mmo1/Lmmol/L (3 mEq/L) and can not Estimations ofthe normal range of ionized Ca + + measure values <0.5 mmo1/Lmmol/L (l mEq/L).19 are given in Table 1. The modern era of measurement of ionized Ca + + began with the introduction of ion CITRATE DOSAGE, METABOLISM, se1ectiveselective electrodes: Initially, ion se1ectiveselective
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