A 68-year-old white man was transferred from a regional hospital in Nova Scotia for further evaluation of severe hypoxia and pulmonary infiltrates. This man's illness started on April 18, 1993, when he woke up at night with pleuritic chest pain in the left inframammary area radiating to the left shoulder and left lateral chest. He was seen the following day by his family physician, who initially prescribed a muscle relaxant and subsequently an antibiotic, with no improvement in his symptoms. On the morning of May 13, his left-sided chest pain worsened and he became markedly short of breath. He had no cough, sputum, or hemoptysis and there were no fever, chills, or rigors. There was no history ofleg swelling or trauma to his legs. He smoked one pack of cigarettes per day for most of his life, but had recently reduced to a few cigarettes daily. His initial investigations revealed a white blood cell count of 11 .300 cells/ilL, hemoglobin 14.9 g/dL, POz 65 mm Hg on room air, and creatine phosphokinase 67 U/L. Chest x-ray film showed linear opacities in the bases bilaterally representing areas of atelectasis with probable superimposed infiltrate, and a ventilation-perfusion (V /Q) scan revealed a large perfusion defect in the anterolateral aspect of the left lung superiorly and a second one in the perihilar region of the same lung, as well as probable multiple smaller mismatched areas interpreted to indicate a high probability for pulmonary embolism. At this stage, the diagnosis of pulmonary embolism was made and he was started on heparin infusion, with the partial thromboplastin time adjusted to over twice the baseline. Subsequently. he developed further episodes of pain, intermittent low-grade fever, and hemoptysis, and the repeat V /Q scan reported slight adverse changes in the left upper lobe. He then underwent a bilateral lower limb radionuclide venogram that was negative for deep vein thrombosis. After a week of treatment with heparin. warfarin was introduced; when the patient's prothrombin time reached the therapeutic level, heparin was discontinued. On May 24, he started complaining of voiding difficulty and discoloration of his urine. Urine cultures were unremarkable, but he was noted to have proteinuria (0.3 gil) and hematuria (>250 red blood cellS/ilL) on urinalysis. On May 27, his chest pain worsened with deterioration of his oxygenation and he was sent to our institution for further evaluation of a pulmonary renal syndrome. At this time, a chest x-ray film revealed patchy peripheral air space opacification bilaterally, which was predominantly peripheral in location, with sparing of the apices and bases; he subsequently underwent a pulmonary angiogram that showed a marked decrease in flow to most of the left upper lobe and to the lateral aspects of the left lower lobe in association with attenuation of peripheral arteries and marked central pruning of some of the segmental branches in these regions. There were also a number of illdefined filling defects associated with these arteries, interpreted as late sequelae of extensive pulmonary emboli. There was mild renal insufficiency with creatinine 1.65 mg/dL; in addition, the above-mentioned urinary abnormalities persisted. Because a vasculitic process involving lungs and kidneys was suspected, the patient was started on pulse methylprednisolone and warfarin was discontinued. A nephrologic consultation was requested subsequently and a renal biopsy was performed on June 1 with no complications. Subsequently, the patient's condition deteriorated and he died on June 9, 1993, of respiratory failure.
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Jan 1, 1996
F Christiansen + 4
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