2) Recognize the risk of pulmonary hypertension during pregnancy. CASE INFORMATION: A 30-year-old G2P1 with a history of sickle cell disease presented to our institution at 26 weeks gestation with the complaint of preterm contractions. She was admitted and placed on magnesium as a tocolytic. She then began to complain of back and leg pain leading to a diagnosis of a sickle crisis. Her medical history was notable for 3 to 4 inpatient admissions for sickle crises a year. She had a port-a-cath placed 11 months prior to the admission. Her gall bladder was removed two years prior to admission. Her evaluation included room air PaO2 of 68 mmHg and pulse oximetry of 93%, and a chest xray revealed bilateral pulmonary infiltrates in an alveolar pattern. Given a normal urinalysis and urine culture, and no other identifiable trigger for the crisis or the preterm contractions, she was treated for pneumonia. Magnesium was discontinued. The improvement in her oxygenation seemed slower than expected prompting the high-risk team to order an echocardiogram. Her left ventricle and valves were normal, but the right-sided chambers were enlarged and her estimated pulmonary artery systolic pressure was 55mmHg. V/Q scan was normal. This is the first time she was diagnosed as having pulmonary hypertension. Review of prior chest x-rays from another institution revealed that the pulmonary infiltrates had been present for at least 18 months. DISCUSSION: A review of the literature revealed many series of sickle cell patients with chronic lung disease. These patients may be asymptomatic, but abnormalities on pulmonary function testing are an early and reliable marker of this complication. Patients with abnormal chest radiography, pulmonary function testing,x or hypoxia during stable periods have an average life expectancy of 2.6 years. They are at risk for sudden death from subendocardial infarction without epicardial arterial disease. We are surprised that more pregnant patients with long standing sickle cell disease do not have routine screening for lung disease by their physicians. This is particularly important during pregnancy because severe pulmonary hypertension (pressures > 80mmg) from any cause has a post-partum mortality rate as high as 50%. The precise risk with less severe elevations is not known. Given the prevalence of sickle cell disease in the general medical population we recommend that all patients with long standing sickle disease have pulmonary function testing and/or echocardiography to evaluate pulmonary arterial pressures. If chronic pulmonary disease is diagnosed in a woman considering pregnancy then consultation with experienced internists, pulmonary specialists, and perinatologists is warranted.`H complaints or symptoms suggestive of cardiopulmonary diseases. On a follow up visit he reported dyspnea on minimal exertion of two months duration. He also reported chest pressure, dizziness and nausea with the dyspnea. He told his doctor that he has dyspnea even after speaking few sentences. His exam revealed BP= 146/90 Pulse 80 regular. Heart auscultation revealed a normal S1, split S2, and I-II/VI systolic murmur. Lungs were clear to auscultation. Abdomen was soft, no hepatosplenomegaly. No pedal edema. EKG was done in the clinic showed left ventricular hypertrophy. Chest X-ray was normal. Stress echocardiogram revealed a small apical wall motion abnormality worsening with stress. A cardiac catheterization revealed normal coronaries, no wall motion abnormality and left ventricular end diastolic pressure of 35 mmHg. The aortic root was bicuspid with severe coarctation of the aorta at the isthmus. DISCUSSION: Coarctation of the aorta is an unusual cause of hypertension in young adults and is often unrecognized by general practitioners. Although the left ventricle is usually hypertrophied because of the hypertension, the heart is usually normal in size or only slightly enlarged until cardiac decompensation occurs late in the course of the disease. Our patient left ventricular end diastolic pressure was 35 mmHg, which might account to his dyspnea. In retrospect knowing the diagnosis of coarctation our patient has the body habitus of a chronic coarctation of the aorta with a large head and upper extremities and is otherwise short. He had diminished leg pulses. His blood pressure was comparable in upper extremities; however, there was a difference of 50 mmHg between upper and lower extremities. Coarctation of the aorta is a potentially lethal condition at all ages. Many patients first come to medical attention because of signs and symptoms related to hypertension. The diagnosis should be considered in patients with hypertension and diminished leg pulses, and we recommend the routine examination of leg pulses in young adults with hypertension.