Intravenous Immunoglobulin (IVIG) in Severe Heparin-Induced Thrombocytopenia (HIT) in a Traumatic Brain Injury (TBI) Pat
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PRACTICAL PEARL
Intravenous Immunoglobulin (IVIG) in Severe Heparin‑Induced Thrombocytopenia (HIT) in a Traumatic Brain Injury (TBI) Patient with Cerebral Venous Sinus Thrombosis (CVST) Niall A. Buckley1*, Mustafa K. Baskaya1 and Marin E. Darsie1,2 © 2020 Springer Science+Business Media, LLC, part of Springer Nature and Neurocritical Care Society
Introduction There is an absence of literature discussing heparininduced thrombocytopenia (HIT) management in traumatic brain injury (TBI) patients with post-traumatic cerebral venous sinus thrombosis (CVST). Of an estimated 21 to 69 million annual global TBI cases, 29.2% may suffer post-traumatic CVST [1–3]. CVST management includes correcting causes, initiating anticoagulation, treating intracranial hypertension, and anticonvulsant prophylaxis [4]. Unfractionated heparin (UFH) and low molecular weight heparin (LMWH) are first-line anticoagulation in CVST [5]. HIT occurs more frequently in patients receiving therapeutic compared to prophylactic UFH and with prophylactic dosing of UFH compared to LMWH [6–8]. As many as 2.6% of patients receiving prophylactic UFH and 0.2% receiving prophylactic LMWH develop HIT [7, 8]. HIT was also reported in one of 64 TBI patients after the initiation of prophylactic UFH [9]. Management of HIT necessitates discontinuing heparin products and initiating alternative anticoagulation (Table 1) [7]. Occasionally, cases of HIT are severe and treatment-refractory. Several case reports describe treatment of such cases using intravenous immunoglobulin (IVIG), resulting in stabilized platelet counts, reduced platelet activation, and reduced thrombotic complications [10–13]. IVIG is thought to inhibit platelet activation by binding platelet receptors, which would otherwise *Correspondence: [email protected] 1 Department of Neurological Surgery, University of Wisconsin Hospitals and Clinics, 600 Highland Avenue, Madison, WI 53792, USA Full list of author information is available at the end of the article
bind with heparin–platelet factor 4 complexes and HIT antibodies [10]. We present a case of severe HIT in a TBI patient with post-traumatic CVST, which did not improve until after the administration of adjunctive IVIG.
Case Description Initial Stabilization, Surgical Intervention, and Neurocritical Care Management
A 44-year-old male was brought to the University of Wisconsin Emergency Department by emergency medical services after being involved in a motor vehicle collision. A field intubation was performed due to facial trauma and an initial Glasgow Coma Scale (GCS) score of 5 (E1V1M3). En route, hypertension, and hypercapnia were treated with fentanyl, rocuronium, and a 3% hypertonic saline bolus. Neurological exam in the trauma bay, of GCS 3T and minimally reactive pupils, was confounded by neuromuscular blockade. Computed tomography (CT) scans of the head and cervical spine demonstrated a 2.6 cm left temporoparieto-occipital and cerebellar epidural hematoma (EDH) causing 7 mm of rightward midline shift (Fig. 1), traumatic subarachno
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