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A Julie Martchenke, RN, MSN, CS, PNP, Mary Frances D. Pate, RN, DSN, Maria Cruz, RN, BSN, and Serena Phromsivarak, RN, BSN, reply:
HIT is a complication of heparin therapy that presents in 2 forms. In the more serious, but less common HIT type II, some patients receiving heparin develop an immune-mediated thrombocytopenia, which leads to thromboembolic complications in 30% to 50% of cases.1 HIT has been diagnosed in adults for 20 years but only recently recognized in children and neonates. Because it is not fully understood or well known, HIT is probably underdiagnosed in children.2 One study found a 1% incidence of HIT type II in the neonatal intensive care unit population.3 A retrospective study in a pediatric intensive care unit population found a 2.3% incidence of HIT type II–associated thrombosis.4 Our center has noted an incidence of 2.5% in pediatric congenital heart surgery patients alone.
The cardinal laboratory finding of early HIT is a platelet drop below 150 x 109/L or a 50% drop from baseline.4 Generally, in HIT type II, this drop occurs around 5 to 10 days after the first exposure to heparin. If the child has had previous heparin exposures, especially within the last 100 days, thrombocytopenia could occur within 10 hours of new exposure.5 If HIT is suspected because of falling platelet counts or thrombosis, a variety of confirmatory tests are done, most commonly, agglutination tests. In these tests, blood bank platelets are mixed with heparin and the patient’s plasma (containing HIT immunoglobulin [IgG] presumably). Clotting indicates a positive result. These agglutination tests are often negative early in the HIT process and should be repeated multiple times if strong suspicion exists.6 An enzyme-linked immunosorbent assay (ELISA) antibody test and a serotonin release assay to detect HIT IgG antibodies are also available at some facilities. Because the diagnosis is rarely certain initially, other laboratory tests may be done to clarify the differential diagnosis. These include blood cultures and complete blood cell counts to rule out sepsis, a D-dimer assay to rule out disseminated intravascular coagulopathy, and a prothrombotic workup including protein C, protein S, antithrombin III activity level, factor VIII, and homocysteine.6
Thrombosis develops in 30% to 50% of children with HIT type II. In spite of low platelet counts, few patients develop bleeding problems. The presenting signs vary in relation to where clots are formed. In the pediatric cardiac patient, these signs could include cyanosis from an occluding Blalock-Taussig shunt, chylothorax from occluding pulmonary veins, upper body vascular congestion from an occluding superior vena cava, and renal failure from renal artery thrombosis. Clots often form at areas of previous trauma; this may include surgical incision or vascular catheter placement sites.2–4,7
Signs of thrombosis are often first noticed in peripheral or central venous catheters, but may not be noted until the child’s hemodynamic situation worsens. Then, after extensive searching utilizing vascular studies, computerized tomograms, or magnetic resonance imaging, clots are found in the venous or arterial system. The prognosis depends on the site of thrombosis. The morbidity and mortality when thrombosis does occur is quite high.2–4
Once diagnosis is made or strongly suspected, all forms of heparin must be stopped, including heparin infusions, flushes, and the use of vascular catheters with bound heparin.8 Receiving any heparin at all, including small amounts of low-molecular-weight heparin, will perpetuate the HIT process. Stopping heparin alone, however, is not sufficient intervention. Because of the high risk of thrombosis, which may have started before diagnosis, these patients will need an alternative form of anticoagulation.9,10 Currently, in the United States, experts recommend direct thrombin inhibitors for anticoagulation in HIT.
The prototype direct thrombin inhibitor is hirudin, which comes from the saliva of the European medicinal leech. The 2 products currently available are lepirudin and argatroban. Lepirudin is a derivative of hirudin and is available for injection, with a half-life of 1.3 hours and a starting dose of 0.4 mg/kg. This agent is renally metabolized and the dosage needs to be decreased in renal failure. Lepirudin dosing is based on activated partial thromboplastin time, with a goal of 1.5 to 2 times normal.11,12 Argatroban is a chemically produced direct thrombin inhibitor, with a half-life of 40 minutes; this drug is also available for injection. Argatroban is metabolized in the liver and, like lepirudin, levels are adjusted to an activated partial thromboplastin time goal of 1.5 to 2 times normal. The initial dose is 2 µg/kg per minute.13,14
The research indicates that as long as heparin-dependent antibodies remain in the blood (3–6 months), reexposure to heparin will result in a rapid recurrence of HIT.5 After disappearance of heparin-dependent antibodies, brief exposure to heparin (eg, during cardiopulmonary bypass) has a low risk of recurrence of HIT.5 The risk of longer exposures to heparin in these patients is unknown. Current recommendations are to limit heparin exposure and use alternative anticoagulants for prophylaxis and therapeutic interventions. Care-givers should mark the patient’s chart prominently; advise the patient to wear a medic alert bracelet; and plan future surgeries, cardiac catheterizations, and other invasive procedures carefully.
References
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