Has anyone had any experience with HIT type II ? This is when a hemo patient develps antibodies to heparin and develops throbosis if used
We have one - our plan is to do saline flushes during the tx.
but what’s used for the catheter packing? :?:
Thanks in advance for any insight
Found two abstracts:
- Pediatr Nephrol. 2000 Aug;14(8-9):713-6.
Heparin-induced thrombocytopenia type II on hemodialysis: switch to danaparoid.
Neuhaus TJ, Goetschel P, Schmugge M, Leumann E.
Nephrology Unit, University Children’s Hospital, Zurich. Thomas.Neuhaus@kispi.unizh.ch
Abstract
We report two pediatric patients with end-stage renal failure who developed heparin-induced thrombocytopenia type II (HIT II) on hemodialysis (HD). Both developed acute respiratory distress and chest pain within 30 min of initiating the 5th HD session. The platelets dropped during HD from 168 to 38x10(9)/l and from 248 to 109x10(9)/l, respectively. Marked clots were observed in the dialyzers. Substitution of heparin with the low molecular weight heparin dalteparin had no effect. Switching from anticoagulation to the heparinoid danaparoid resulted in immediate disappearance of all adverse effects, and further long-term HD was uneventful. HIT II was diagnosed clinically; heparin-induced platelet activation test (HIPA) and serum IgG, IgA, and IgM to heparin-platelet factor 4 complexes (HPF4) were both negative. We conclude that HIT II may occur in children on HD. HIT II is essentially a clinical diagnosis, as HIPA and antibodies to HPF4 are not always positive. Once HIT II is suspected, heparin (and low-molecular-weight heparins) should be stopped immediately. Long-term anticoagulation with danaparoid is a valuable option for patients on HD.
- Hemodialysis International
Volume 8 Issue 3 Page 295 - July 2004
doi:10.1111/j.1492-7535.2004.01108.x
Heparin-induced thrombocytopenia during renal replacement therapy
Andrew Davenport
Abstract
There is increasing awareness that antibodies to heparin/platelet factor 4 complex can develop in both those with acute renal failure treated with continuous forms of renal replacement therapy and, to a lesser extent, regular hemodialysis patients. Clinical manifestations include premature clotting of the extracorporeal circuit and increased central venous thrombosis with indwelling venous dialysis catheters, associated with thrombocytopenia and increased platelet activation. Nevertheless, a minority of patients who develop heparin/platelet factor 4 antibodies do not have thrombocytopenia or thrombosis. When systemic anticoagulation is also required to treat venous thrombosis, then synthetic heparinoids or the direct thrombin inhibitors argatroban or recombinant hirudins are the agents of choice. Neither the synthetic heparinoids nor hirudin, however, are without their own problems, in that a minority of patients may have cross-reacting antibodies against the currently available heparinoids, and antibodies may similarly develop against recombinant hirudin, in this case leading to a potentiation of anticoagulant activity and increased risk of hemorrhage.
If you look on PubMed (www.ncbi.nlm.nih.gov/entrez) and type in the search “HIT Type II and hemodialysis” you should see 9 studies. The Neuhaus study is there; the Davenport one is not.