LAUSR

Dear Editor, Heparin-induced thrombocytopenia (HIT) is a clinical syndrome caused by the formation of antibodies against the platelet factor 4 (PF4)-heparin complex associated with heparin therapy [1]. Antibody binding results in platelet activation and elaboration of pro-thrombotic mediators, which underpin the dual clinical manifestation of thrombocytopenia and thrombosis in HIT, classically between 5 and 14 days following heparin exposure [1]. Notably, thrombosis of the adrenal vasculature paradoxically leads to adrenal haemorrhage, which is a rare but classical presentation of HIT [2]. In such circumstances, two important clinical issues arise: firstly, strategies for therapeutic anticoagulation in the face of significant haemorrhage and secondly the risk of ensuing adrenal crisis, which requires urgent hormone replacement therapy [3]. An 83-year-old lady presented with a 24-h history of upper abdominal pain radiating to the back. She had been discharged the day prior after a 7-day inpatient stay for an elective right total hip replacement, complicated by right-sided segmental pulmonary embolism on day-2 post-operation treated with therapeutic lowmolecular weight heparin (1 mg/kg BD) with bridging to warfarin. On examination, she was tachycardic but remained afebrile and normotensive. Whilst initial haemoglobin was 122 g/L on full blood examination, a repeat test taken six hours later demonstrated a significant drop with severe anaemia (84 g/L) accompanied by reticulocytosis (6.8%) and mild thrombocytopenia (135 × 10/L) (Fig. 1a). A haemolysis screen (bilirubin/LDH/ haptoglobin/blood film) returned negative. Apart from mild hyponatremia (133 mmol/L), her biochemistry (electrolytes/lipase/renal/liver profile) were within normal limits. Computed tomography of the abdomen revealed ill-defined hypodensity in the adrenal glands bilaterally (Fig. 1b) suspicious for adrenal haemorrhage. Monitoring revealed worsening thrombocytopenia (nadiring at 44 × 10/L three days after presentation). Her four T score was calculated to be 7 (high) which carries an estimated risk of HIT of 64% [4]. Highspecificity HIT antibody screen (AcuStar-IgG assay) returned positive with a titre of 78 IU/mL [5]. Her anticoagulation was switched to fondaparinux (7.5 mg daily). Two days after her initial presentation, she developed impending adrenal crisis with relative hypotension and hyponatraemia (nadir 126 mmol/L) with a low early morning cortisol (< 11 nmol/L). A dedicated adrena ls magnet ic resonance imaging conf i rmed established bilateral adrenal haemorrhage (Fig. 1c). Glucocorticoid replacement (IV hydrocortisone 50 mg QID) was promptly commenced. Confirmatory 14Serotonin Release assay was positive (88%, range 0– 20%) at therapeutic heparin level (0.1 IU/mL). The patient stabilised on fondaparinux and was discharged 14 days after admission with resolution of thrombocytopenia on oral glucocorticoid and mineralocorticoid replacement and bridged to warfarin therapy (Fig. 1a). HIT is a rare but clinically critical complication of heparin therapy. Unusual paradoxical presentations such as bilateral adrenal gland thrombosis followed by Aditya Tedjaseputra and Matthew Sawyer are joint first authors.