ElHassan et al. Journal of Medical Case Reports 2010, 4:284 http://www.jmedicalcasereports.com/content/4/1/284 Page 3 of 5 Figure 3 Three-dimensional view on computed tomography angiography showing a filling defect in the lumen of the left pulmonary artery (LPA) consistent with LPA thrombosis. of a thrombus (Figure 3). In addition, large collateral vessels originated from the distal thoracic aorta and supplied the left lung (Figure 4). A screening evaluation for a possible inherited thrombophilia disorder was completed in this baby. Blood levels for protein C, protein S, antithrombin activity, concentrations of clottable fibrinogen, plasmi- nogen activity, activities of coagulation factors VIIIC and XII, lipoprotein (a) and homocysteine concentra- tion were within normal limits. DNA-based assays (that is, factor V G1691A mutation and factor II G20210A variant) were also normal [10]. The mother did not complete a thrombophilia screening evaluation. By the third day of life, the baby’s oxygenation index was over 40 despite aggressive medical and ventilatory management and he was thus placed on veno-arterial extracorporeal membrane oxygenation (ECMO). Because he had persistent pneumothorax, minimal “rest” ventilator settings were selected. A low positive end-expiratory pressure (0 to 4 cm H2O) was main- tained for 36 hours until the air leak sealed. The chest tube was removed on day 17 of life. His cardiac and pulmonary function gradually improved on ECMO, allowing decannulation on day 23 of life. This neonate was heparinized during his ECMO course. Because the management of arterial thrombosis in the neonatal period is controversial, no further antic- oagulant therapy was administered after ECMO [11]. He was successfully extubated on day 30 of life. Cranial ultrasounds were normal before and after ECMO. Because of persistent poor oral motor feeding skills a gastrostomy tube was eventually placed. He was then discharged home on day 128 of life on nasal cannula at 0.5 L/min and 100% oxygen. At discharge, he was taking 50% of his nutrition by bottle, with the rest supplemen- ted via gastrostomy tube. The gastrostomy tube was removed at 9 months of life. The oxygen supplementa- tion was discontinued at 10 months of life. A follow-up echocardiogram at one year of life showed low-velocity flow through the LPA at 0.5 cm/s and LPA hypoplasia. On that date, chest radiography showed interval improvement in left lung aeration and minimal compen- satory right lung hyperexpansion. By 18 months of life, this infant did not require further hospitalizations after his NICU discharge or have clinical evidence of reactive airway disease. In addi- tion, he exhibited age-appropriate neurodevelopment (by Bayley Scales of Infant Development II) Discussion Neonatal arterial thrombosis is, in most cases, iatrogenic from indwelling arterial catheters or lines and is rarely described at birth [2-4]. Some inherited thrombophilia defects, for instance, prothrombotic polymorphisms, Factor V G1691A, Factor II G2021A and the homozy- gous TT genotype of the methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism, can also increase risk of neonatal arterial thrombosis [10]. Neo- natal arterial thrombosis occurs primarily in the aorta and can mimic cyanotic heart disease [1-3]. Two babies