UPPER LIMB DEEP VEIN THROMBOSIS FOLLOWING CALCIUM GLUCONATE INJECTION

Skin necrosis and calcinosis cutis following extravasation of calcium-containing solution, and vein irritation after injection have been reported. However, vascular thrombotic events have not been reported as a complication of the therapy. We describe a case of i.v. calcium gluconateinduced upper limb deep vein thrombosis (DVT) in a haemodialysis patient. A 61-year-old man was a patient of gouty nephropathy who received regular haemodialysis for half a year. He was quickly given one ampoule of calcium gluconate (10%, 10 mL, 4.66 mEq) as a direct i.v. injection for hypocalcemia through a small vein in the dorsum of his right hand. Then, he noticed progressive swelling and tightness from the right hand to upper arm. He denied history of trauma to his right arm or central venous catheter insertion. A thrombophilia screen including protein C, protein S, anticardiolipin antibodies and lupus anticoagulant were all within the normal ranges except a raised homocysteine level of 14 mmol/L. Computed tomography angiography of the right upper extremity showed the thrombus in the right brachial vein. A vein biopsy was taken from the dorsum of the right hand, which was consistent with phlebitis and thrombus. He was managed with anticoagulation therapy of unfractionated heparin, followed by warfarinization. The right arm swelling then rapidly subsided, and was discharged with oral warfarin sodium (2.5 mg/day) use. Upper limb DVT is an infrequent entity, which has a primary (idiopathic, spontaneous due to effort or traumatic) or secondary (e.g. related to malignancy, hypercoagulability) cause. There is growing evidence directly relating upper limb DVT to iatrogenic causes such as using central venous catheter and total parenteral nutrition. This is the first report on upper limb DVT associated with i.v. injection of calcium gluconate in a patient receiving haemodialysis. Although the pathogenesis of thrombosis secondary to i.v. calcium gluconate is not completely understood, several mechanisms are hypothesized. First, we hypothesize subcutaneous tissue swelling caused by the extravasation of calcium gluconate impeding the venous outflow and resulting in the thrombus formation. The brachial vein thrombosis could be originally existing in this case, and aggravated due to venous blood flow impendence. However, the venous pathway of the upper limb is less likely to develop a DVT compared with the lower limbs due to the relatively high blood flow rate, and gravitational effects. Besides, our case had never received central venous catheter or temporary venous catheter for dialysis. Haemodialysis therapy was performed by arteriovenous graft over his left upper arm. Thus, the probability of an originally existing thrombus could be initially excluded. The hypercoagulability state because of uraemia, malnutrition as low serum albumin level (2.7 g/dL) and a normal thrombophilia screen test in this case could not completely explain the clinical course of acute right arm swelling occurring after i.v. calcium gluconate injection. The second hypothesis is microtrauma of venous endothelium by rapid calcium gluconate injection contributing to activating coagulation cascade and subsequent DVT. We performed a vein biopsy from the dorsum of the right hand, and confirmed phlebitis and thrombosis. Thus, the length of the thrombus may occur from the injection site to the upper arm. The clinical course of acute arm swelling occurring after i.v. drug use further supported the hypothesis of endothelial damage trigger coagulation cascade and subsequent DVT. In conclusion, rapid calcium gluconate injection might confer a potential risk for DVT. It is important for physicians and hospital nurses to be careful in giving parenteral calcium gluconate, especially in patients receiving haemodialysis.