Pseudo-Pulmonary Embolism as a Sign of Acute Heparin-Induced Thrombocytopenia in Hemodialysis Patients: Safety of Resuming Heparin after Disappearance of HIT Antibodies

Abstract

Heparin-induced thrombocytopenia (HIT) is a syndrome caused by platelet-activating antibodies that recognize complexes of platelet factor 4 (PF4) and heparin. Thrombocytopenia is the most common clinical feature of HIT. HIT can be considered as a hypercoagulable state, with a high risk of thrombosis. Another feature of HIT is an acute systemic reaction that characteristically begins 5–30 min after receiving an intravenous bolus of unfractionated heparin, such as is commonly given for hemodialysis (HD). Here we present 4 patients who developed acute HIT at or near the start of their chronic HD. All patients were anticoagulated with the low-molecular-weight heparin, nadroparin, for HD. Three of our patients underwent surgery approximately 1–2 weeks before developing HIT. All patients presented with an acute systemic reaction during HD. All patients were treated and further dialyzed with lepirudin. Under this treatment we observed a quick recovery of the platelet count, and patients remained symptom-free. Antibodies against the PF4-heparin complex were detected with a combination of a ‘quick test’ and an enzyme-linked immunosorbent assay test. The likelihood of having HIT previous to the detection of antibodies was estimated with the pre-test probability score criteria. The tests for PF4-heparin antibodies remained positive for an average of 165 days. Three patients underwent a rechallenge with nadroparin after disappearance of the HIT antibodies in their serum. All 3 remained symptomless when they were further hemodialyzed on nadroparin. Our observations indicate that nadroparin can be successfully reintroduced for HD anticoagulation once the patient’s HIT antibodies have disappeared.

The temporal profile of the anti-PF4/heparin immune response

“…However, there is increasing evidence that patients who have a history of clinical HIT do not show a typical anamnestic immune response when reexposed to heparin. 8,11,33 On the contrary, other reports 34,35 suggested that there might sometimes be a more rapid formation of heparin antibodies in the case of reexposure. But neither of these studies 34,35 established that their patients had had 2 distinct episodes of HIT.…”

Serological investigation of patients with a previous history of heparin-induced thrombocytopenia who are reexposed to heparin

“…Surprisingly, none of the 10 patients formed anti-PF4/ heparin antibodies, suggesting that the probability of forming repeat antibodies might be even lower than expected, given that approximately 50% of patients form at least a weak anti-PF4/heparin immune response after cardiac surgery, 2,12 and approximately 12% (median of 5 studies [range, 3% to 20% 2,[12][13][14][15] ]) develop a positive platelet activation assay. Two additional studies in hemodialysis patients found no recurrent antibodies or recurrent HIT among 8 patients with previous hemodialysis-associated HIT who, after disappearance of HIT antibodies, resumed anticoagulation either with UFH 16 or with low-molecular-weight heparin (LMWH) 17 for their long-term hemodialysis.…”

Heparin-Induced Thrombocytopenia and Hemodialysis

“…Although hypertension is usually associated with ASR [29], in contrast, acute hypotension often occurs as a sign of cardiovascular collapse during dialysis. When dyspnea as the cardiorespiratory reaction in ASR is prominent, it is considered to be a pseudo-pulmonary embolism [30][31][32]. However, the signs and symptoms are very similar to those in dialyzer reactions, dialytic complications as disequilibrium syndrome, and circuit clotting during the procedure.…”