Evaluation of heparin-induced thrombocytopenia (HIT) laboratory testing and the 4Ts scoring system in the intensive care unit.

BACKGROUND: Over-diagnosis of heparin-induced thrombocytopenia (HIT) results in costly and unnecessary laboratory screening and treatment with direct thrombin inhibitors. Our aim was to evaluate the utility of the 4Ts scoring system to predict HIT in multiple ICU settings and to characterize our treatment of these cases. METHODS: Eighty-two patients from multiple ICU settings who underwent laboratory testing for HIT were classified as low-, intermediate-, or high-risk patients based on retrospectively adjudicated 4Ts scores. These results were compared with platelet-factor 4 enzyme-linked immunosorbent assays (PF4 ELISAs), optical density (OD) values, and serotonin-release assays (SRAs) to assess the utility of the 4Ts score to rule out ICU-related HIT and reduce laboratory and drug expenditures. RESULTS: Of the 82 patients reviewed, only 12 (11.4%) were PF4-positive and only 1 (1.2%) was SRA-positive for HIT. Heparin was discontinued in only 63.4% of patients suspected to have HIT. There were no significant differences in mean day of platelet fall, mean platelet nadir, and mean percent fall in platelet count between PF4-positive and negative patients (all p > 0.2). There was, however, a significantly higher proportion of patients with an intermediate to high 4Ts score in the PF4-positive group than in the PF4-negative group (66% vs. 30%, respectively; p = 0.02). The mean PF4 OD value in patients with intermediate to high 4Ts scores was significantly higher than in patients with low 4Ts scores (0.658 vs. 0.258, respectively; p < 0.001). The negative predictive values of the 4Ts score relative to the PF4 and SRA were 92% and 100%, respectively. The estimated laboratory and pharmacologic cost avoidance potential of the scoring system in this cohort was $21,450. CONCLUSION: Our modified 4Ts scoring system appears to be an effective tool for predicting HIT in the ICU and could avoid significant drug and laboratory expenditures if implemented prospectively. The clinical management of patients suspected of HIT is highly variable at our institution. Clinical protocols and education encouraging the proper identification and treatment of suspected HIT need to be established.

Angioedema associated with dihydropyridine calcium-channel blockers in a child with Burkitt lymphoma.

PURPOSE: A case of severe macroglossia and angioedema in a child with Burkitt lymphoma who was treated with two dihydropyridine calcium-channel blockers is reported. SUMMARY: An eight-year-old white boy arrived at the pediatric emergency department with complaints of abdominal pain and distention after an episode of mild abdominal trauma. Physical examination results were significant for diffuse abdominal tenderness and distention, with a large palpable mass in the right quadrants. Computed tomography revealed a large abdominal mass, and a biopsy confirmed a diagnosis of Burkitt lymphoma. Before initiation of chemotherapy, the child developed tumor lysis syndrome, with subsequent renal failure and cardiorespiratory compromise. Once the patient was stabilized and sedated on mechanical ventilation, tumor-directed chemotherapy was initiated, and rapid tumor regression ensued. To control episodes of hypertension, nicardipine was initiated and titrated to achieve the blood pressure goals. Three days after initiation of nicardipine therapy, the child developed facial swelling and significant, protruding macroglossia. Eight days after nicardipine initiation, a tracheotomy was required due to upper airway obstruction; at that time, the patient was converted to amlodipine administered via nasogastric tube for continued blood pressure control. The boy's macroglossia persisted for another 18 days, until a multi-disciplinary drug therapy review resulted in the discontinuation of amlodipine. Within one week of the withdrawal of amlodipine, the child's macroglossia was completely resolved. CONCLUSION: An eight-year-old boy with Burkitt lymphoma developed severe macroglossia and angioedema when treated with nicardipine. The reaction persisted throughout treatment with amlodipine and resolved quickly after amlodipine was withdrawn.