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Heparin-induced thrombocytopenia in the pediatric intensive care unit population
Jason Frost1, Leila Mureebe, Pierantonio Russo
1Department of Anesthesiology, University of Missouri, Columbia, USA.
Insights
Heparin-induced thrombocytopenia (HIT) is rare in pediatric intensive care unit (ICU) patients but can cause serious complications. Early diagnosis and cessation of heparin are crucial for recovery.
Area of Science:
- Pediatric critical care medicine
- Hematology
- Pharmacology
Background:
- Heparin-induced thrombocytopenia (HIT) is a prothrombotic immune-mediated complication of heparin therapy.
- While well-documented in adults, HIT is infrequently reported in pediatric populations.
Observation:
- Two pediatric intensive care unit (ICU) patients, aged 2 months and 6 months, developed HIT.
- One patient received heparin as a central line flush, the other during cardiopulmonary bypass.
- Both patients had prior neonatal heparin exposure, with thrombocytopenia noted but not attributed to HIT.
Findings:
- Diagnosis was confirmed via heparin-induced platelet aggregation studies.
- Thrombocytopenia resolved upon discontinuation of heparin.
- One patient experienced a deep vein thrombosis associated with a femoral catheter.
Implications:
- HIT should be considered in the differential diagnosis of thrombocytopenia in pediatric ICU patients.
- Prompt recognition and management of HIT can prevent significant morbidity.
- Further research into HIT in pediatric populations is warranted.
Objectives:
To report the occurrence of heparin-induced thrombocytopenia (HIT), discuss its pathophysiology, and outline an approach to management in the pediatric intensive care unit (ICU) patient.
Design:
Retrospective case reports.
Setting:
Pediatric ICU in a tertiary-care center.
Patients And Results:
Two pediatric ICU patients (2 and 6 mos of age) who developed HIT in the pediatric ICU. One was receiving heparin as a flush solution through a central line and the other had full heparinization during cardiopulmonary bypass. Both had received heparin during their neonatal course and developed thrombocytopenia; however, HIT was not considered as a possible diagnosis. HIT was diagnosed using a heparin-induced platelet aggregation study. The thrombocytopenia resolved with the cessation of heparin administration. One of the patients developed a deep vein thrombosis around a femoral venous catheter.
Conclusion:
Although well described in the adult literature, there have been a limited number of reports of HIT in pediatric-aged patients. Given its potential for morbidity, HIT should be considered in the differential diagnosis of thrombocytopenia in the pediatric ICU patient.
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