We describe a neonate of 38-week and 6-day gestation born by lower uterine cesarean section for breech presentation, where it was evident on delivery that there was significant edema of the right arm from the deltoid to the distal tips of the fingers. Doppler flow ultrasound revealed extensive arterial thromboembolus. Intravenous heparin was prescribed for three days at a dose of 27.5？U/kg/h, targeting an activated partial thromboplastin time (APTT) of 60–75 seconds, followed by a course of subcutaneous enoxaparin at a dose of 1.8？mg/kg and then 2？mg/kg twice daily, titrated to a factor Xa level of 0.5–1.0？U/mL for another three days. Significant clinical improvement occurred and the child was eventually, discharged on subcutaneous enoxaparin. Magnetic resonance imaging showed multiple intracranial abnormalities. At five months increased upper limb tone, brisk reflexes, and small head circumference were noted. At one year, increased tone and increased paucity of movement on the right side persisted, and some speech delay and visual inattention were noted. Recent follow-up at 16.5 months of age demonstrated a right sided hemiplegia with increased tone and brisk reflexes. We describe the case in detail and review current knowledge regarding the management of arterial thrombosis in the neonate. 1. Introduction Neonatal arterial thrombosis is a serious condition resulting in high rates of morbidity and mortality [1]. The ability to form a blood clot in a controlled manner is essential; however, uncontrolled or excessive clotting may be life-threatening. The normal formation of a fibrin clot in the body is tightly regulated by anticoagulants. Regularly, local thrombin binds with thrombomodulin located on endothelium activating protein C. Activated protein C along with its cofactor protein S then inhibits factors Va and VIIIa by cleavage, preventing random clot formation. Additionally, antithrombin directly inhibits thrombin and factors IXa, Xa, XIa, and XIIa. The major causes of thrombosis in childhood are introduced venous access devices; the presence of phospholipid antibodies; proteins C and S mutations; factor V (Leiden) mutations; antithrombin deficiency, and less commonly: dysfibrinogenemia; anomalies in the molecular architecture of fibrinogen, and hyperhomocysteinemia, which affects both the vascular wall structure and coagulation constituents [2–4]. Although our understanding of the adult hemostatic system is quite sophisticated, several key differences underlie the structure and function of the neonatal system that make direct therapeutic
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