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From the Department of Anesthesia, Queen's University, Kingston, Ontario, Canada.
Address correspondence to: Dr. Andrew Meikle, Department of Anesthesia, Kingston General Hospital, 76 Stuart Street, Kingston, Ontario, K7L 2V7 Canada. Phone: 613-548-7827; Fax: 613-548-1375; E-mail: andy_meikle{at}hotmail.com
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Clinical Features: A previously healthy, 45-yr-old man presented for repair of a class IV thoraco-abdominal aneurysm. The initial stages of the operation were relatively uneventful, with the exception of an estimated blood loss of 5.0 L. At this point the patient's QT interval became markedly prolonged, and subsequently narrowed in response to supplemental calcium and magnesium. A blood sample taken just before QT prolongation revealed an ionized calcium of 0.98 mmol•L–1 and an ionized magnesium of 0.37 mmol•L–1, indicating, that low magnesium may have contributed to the QT interval prolongation.
Conclusion: This case illustrates the importance of following both ionized calcium and magnesium in the setting of a massive transfusion.
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After a joint discussion with the surgeon, CSF drainage but not femoral/femoral bypass or spinal cooling was utilized. Anesthesia was induced with 140 mg propofol, 50 µg sufentanil, and 100 mg succinylcholine iv. Maintenance was achieved with intermittent sufentanil boluses, nitrous oxide/oxygen, isoflurane, and muscle relaxation with doxacurium. The airway was secured using a #41 French left-sided double lumen tube with the aid of a fibreoptic bronchoscope. Intravenous access consisted of two peripheral 14 gauge intravenous catheters, a #7 French double lumen right internal jugular catheter, and a 20 gauge right radial arterial line. Attempts to keep the patient warm included the use of two forced air warmers, a level 1® normothermic intravenous administration set, and a Fenwal® blood warmer. Prior to aortic cross clamp, 35 g mannitol iv were given and an epidural catheter, previously placed in the intrathecal space, was set to drain at 12 cm H2O. The aorta was cross-clamped at 12:30, five hours after induction of anesthesia.
Throughout the morning the surgery provided a steady blood loss, and by 13:30 the estimated blood loss was 5.0 L. Replacement to that point consisted of 2.0 L pentaspan, 6.0 L normal saline, and six units packed red blood cells and the patient's temperature was 36.8°C. In addition, the patient had received 4 g magnesium, and 1 g calcium chloride in response to low ionized values we had received from our point of care testing facility, a Nova Biomedical stat profile M over the course of the morning.
At this time (13:33) the patient's QT interval became markedly prolonged (Figure
). This was treated with 1 g calcium chloride, and 2 g magnesium with prompt effect and the QT interval returned to baseline. The blood sample from 12:52 revealed ionized calcium of 0.98 mmol•L–1 (normal, 1.13-1.32 mmol•L–1), and ionized magnesium of 0.37 mmol•L–1 (normal, 0.41-0.61 mmol•L–1). The blood sample at 13:50 revealed ionized calcium of 1.38 mmol•L–1 and ionized magnesium of 0.35 mmol•L–1.
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The patient remained in the ICU for eight days. The postoperative course was complicated by ongoing bleeding requiring blood products and hypotension requiring inotropic support. On day three, a left hemicolectomy was performed for a gangrenous left hemicolon. By day six, the patient required dialysis secondary to acute renal failure. Care was then withdrawn on day eight after seizure activity, a CT scan of the brain, and EEG consistent with severe cerebral anoxia were observed.
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The Canadian Blood Services state that citrate toxicity is very rare, but potentially serious as "symptoms can range from muscle tremors to cardiac arrhythmia, and even cardiac arrest."3 With respect to monitoring for hypocalcemia the handbook points out that standard serum calcium estimation does not distinguish the ionized from complexed fractions. However, no specific guidelines about the use of ionized calcium measurements in the setting of transfusion exist. Monitoring of the ECG is referred to in that: "ECG monitoring can be helpful in detecting the effect of hypocalcemia."
The presence of hypocalcemia in massive transfusions has been documented in a previous review of the subject.4 In this report, 471 massive transfusions were reviewed and the ionized calcium was less than normal (1.13 – 1.32 mmol•L–1) in 94% of patients and was very low (<0.70 mmol•L–1) in 46% of patients. When dealing intra-operatively with ionized calcium values it becomes important to realize at what level treatment is indicated. The literature5 suggests ionized calcium <0.60 mmol•L–1 may be associated with cardiac arrest and should be treated aggressively. Conversely, an ionized calcium of >0.80 mmol•L–1 that is asymptomatic does not require treatment. However, the authors recognize that the threshold to treat may be higher than 0.8 mmol•L–1 if the patient is under anesthesia as symptoms cannot be assessed.
The problem of hypomagnesemia receives less attention than that of calcium homeostasis. Neither the Canadian Blood Services nor the American Association of Blood Banks mention the problem of hypomagnesemia in their respective manuals. However, low ionized magnesium is a problem in the setting of a massive transfusion due to both the administration of magnesium free crystalloid,6 and binding with excess citrate.7 Citrate toxicity leads to hypomagnesemia because citrate has an equal binding affinity for both ionized magnesium and ionized calcium.8 That this leads to clinically relevant hypomagnesemia has been documented in liver transplantation7 and in the setting of massive transfusion.9
The manifestations of hypomagnesemia mimic hypocalcemia and include central nervous system irritability, skeletal muscle spasm, and cardiac dysrhythmias. Specifically, hypomagnesemia as was seen in our case, is known to cause a prolonged QT interval.1 In addition, cardiac arrhythmias seen in association with hypomagnesemia may only respond to magnesium therapy and are often refractory to conventional antiarrythmics and defibrillation.10 Thus, hypomagnesemia does occur in massive transfusions and its clinical and electrocardiographic features may be difficult to distinguish from hypocalcemia.
The normal range for ionized calcium is 1.13 to 1.32 mmol•L–1. In our case, the ionized calcium was 0.98 mmol•L–1 (well above 0.8 mmol•L–1) 30 min before prolongation of the QT interval. The next measurement 20 min after receiving supplemental 1 g CaCl2iv was 1.38 mmol•L–1, indicating that perhaps low ionized calcium was not entirely responsible for our observed QT prolongation. In contrast, the ionized magnesium was 0.37 mmol•L–1 (<0.41 mmol•L–1) a half-hour before the QT prolongation and despite receiving an additional 2 g Mg iv, remained low at 0.35 mmol•L–1 after the QT interval had returned to baseline. It is then difficult to implicate hypomagnesemia alone as being responsible for the observed prolongation of the QT interval. However, an ionized calcium of 0.98 mmol•L–1 would not be expected to prolong the QT interval. Therefore, we believe that low ionized magnesium may have been partly responsible for the QT prolongation we observed. In addition, by the time the case was finished the patient had received 8 g magnesium and still the ionized magnesium remained below normal. Therefore we agree with previous authors9 who state that serum ionized magnesium should be monitored in the setting of massive transfusion.
When magnesium is to be replaced in the setting of massive transfusion the preparation of choice is magnesium chloride as the sulfate ions in magnesium sulfate can bind calcium and aggravate an associated hypocalcemia.11 Magnesium is known to be a vasodilator. Magnesium is associated with a mild and transient decrease in blood pressure due to peripheral vasodilatation and causes a consistent increase in cardiac index.12 However, large doses of magnesium are well tolerated. This is illustrated in a study in which magnesium was given in doses of 60 mg•kg–1 (about 4 g) over one minute iv as part of an induction technique and only a minor decrease in blood pressure was noted.13 Magnesium supplementation can then be administered fairly rapidly. Although prudence may suggest avoidance of a bolus administration in the setting of massive transfusion because these patients may be cardiovascularly unstable.
In summary, both hypocalcemia and hypomagnesemia are recognized complications of massive transfusion and both may give rise to a prolonged QT interval. Therefore, if the QT interval prolongs in association with massive transfusion, both possibilities should be considered.
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References |
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2 Vengel-Tyler V. American Association of Blood Banks Technical manual, 13th ed. Maryland: American Association of Blood Banks, 1999.
3 Canadian Blood Services. Circular of information for the use of human blood and blood components. Health Protection Branch, Health Canada.
4 Wilson RF, Binkley LE, Sabo FM Jr, et al. Electrolyte and acid-base changes with massive blood transfusions. Am Surg 1992; 58: 535–44.[Medline]
5 Kost GJ. The significance of ionized calcium in cardiac and critical care. Availability and critical limits at US medical centers and children's hospitals. Arch Pathol Lab Med 1993; 117: 890–6.[Medline]
6 Sasaki R, Hirota K, Nakamaru K, et al. Influence of fluid replacement on serum magnesium concentration and proper magnesium supplementation during general anesthesia. (Japanese) Masui 1997; 46: 1179–85.
7 Diaz J, Acosta F, Parrilla P, et al. Serum ionized magnesium monitoring during orthotopic liver transplantation. Transplantation 1996; 61: 835–7.[Medline]
8 Killen DA, Grogan EL, Gower RE, Collins HA. Response of canine plasma-ionized calcium and magnesium to the rapid infusion of acid-citrate-dextrose (ACD) solution. Surgery 1971; 70: 736–43.[Medline]
9 McLellan BA, Reid SR, Lane PL. Massive blood transfusion causing hypomagnesemia. Crit Care Med 1984; 12: 146–7.[Medline]
10 Scheinman MM, Sullivan RW, Hyatt KH. Magnesium metabolism in patients undergoing cardiopulmonary bypass. Circulation 1969; 39(Suppl): I-235–41.
11 Eisenbud E, LoBue CC. Hypocalcemia after therapeutic use of magnesium sulfate. Arch Intern Med 1976; 136: 688–91.[Abstract]
12 James MFM, Cork RC, Dennet JE. Cardiovascular effects of magnesium sulfate in the baboon. Magnesium 1987; 6: 314–24.[Medline]
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James MFM, Beer RE, Esser JD. Intravenous magnesium sulfate inhibits catecholamine release associated with tracheal intubation. Anesth Analg 1989; 68: 772–6.
14 Canadian Adverse Drug Reaction Newsletter. Drugs causing prolongation of QT interval and torsades de pointes. CMAJ 1998; 158: 103–4.
15 Stoelting RK, Dierdorf SF. Anesthesia and Co-Exisiting Disease, 3rd. New York: Churchill Livingstone, 1993.f
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