ТЕСТИ ПО ДОГЛЯДУ ДЛЯ МОДУЛЬНОГО КОНТРОЛЮ

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Carol Donagh, M.B., John Bruzzi, M.D., Briain MacNeill, M.D., Mark DaCosta, M.D., Jeffrey S. Berman, M.D., and Anthony W. O'Regan, M.D.

N Engl J Med 2011; 365:448-453August 4, 2011

In this Journal feature, information about a real patient is presented in stages (boldface type) to an expert clinician, who responds to the information, sharing his or her reasoning with the reader (regular type). The authors' commentary follows.

A 50-year-old woman presented with rapidly progressive shortness of breath. Five months earlier, she had received a diagnosis of invasive breast carcinoma, at a tumor–node–metastasis (TNM) clinical stage of T2N1M0, and had undergone mastectomy. She received four cycles of cyclophosphamide and doxorubicin, followed by one cycle of paclitaxel with prednisolone. Her fifth cycle of chemotherapy was completed 10 days before presentation. She reported no cough, fever, or chest pain.

This immunocompromised patient presents with shortness of breath. The differential diagnosis is broad and includes acute pulmonary embolism, lymphangitic spread of cancer, and complications of therapy such as drug-induced pneumonitis (as may occur with cyclophosphamide or paclitaxel). Infection is also a concern, especially since she is approaching the time when the white-cell count would be expected to be lowest after chemotherapy. Community-acquired infections, including pneumococcal infection and influenza, should be considered, although fever and other systemic symptoms would be expected with such infections. A cardiomyopathy due to doxorubicin is also possible.

The patient's medical history was otherwise notable only for hypertension treated with perindopril. She was taking no other medications and had no known drug allergies. She was a nonsmoker and had never worked outside the home. She had not traveled recently.

On physical examination, the patient was afebrile. The oxygen saturation was 85% while she was breathing ambient air. The heart rate was 102 beats per minute. Auscultation of her chest revealed no abnormal findings. Heart sounds were normal. The jugular venous pressure was not elevated, and there was no peripheral edema. She had an infusion port in the right internal jugular vein. There was no lower-extremity redness or tenderness.

The hemoglobin level was 10.2 g per liter, the platelet count 124×109 per liter, and the white-cell count 1.9×109 per liter, with a neutrophil count of 0.9×109 per liter. The results of renal- and liver-function tests were normal. The C-reactive protein level was 22 mg per liter. Arterial blood gas analysis showed a pH of 7.47, a partial pressure of oxygen of 49 mm Hg, and a partial pressure of carbon dioxide of 31 mm Hg. A chest radiograph showed no focal abnormality. A transthoracic echocardiogram revealed normal biventricular function, normal valves, and an estimated pulmonary-artery pressure of 22 mm Hg.

This degree of hypoxemia in a patient with a clear lung examination and a normal chest radiograph increases my suspicion that she has a pulmonary embolism. Patients with neutropenic pneumonia or an opportunistic infection such as Pneumocystis jiroveci pneumonia may present with a clear chest radiograph; however, these disorders are less likely in this patient because she is afebrile and not severely immunocompromised. Airway obstruction can also cause hypoxemia with no abnormalities on chest radiography, but obstruction is unlikely without wheezing or stridor on examination.

At this point, pulmonary embolism of thrombotic, septic, or cancerous origin is most likely, given the underlying breast cancer, potential hypercoagulability, and presence of an infusion port. Echocardiography is insensitive for the diagnosis of acute pulmonary embolism; D-dimer testing would be of limited value, because the clinical suspicion of pulmonary embolism is moderate rather than low. I would initiate treatment with low-molecular-weight heparin before proceeding to computed tomographic (CT) pulmonary angiography.

CT pulmonary angiography showed no filling defects in the pulmonary artery, and the lung parenchyma appeared normal. The patient was treated with systemic antibiotics; glucocorticoids were added because of concern that the patient's presentation might represent a hypersensitivity reaction to paclitaxel. Low-molecular-weight heparin was discontinued. Cultures of peripheral and central blood remained negative. On the fifth hospital day, after a brief mobilization from her bed to a chair, the oxygen saturation decreased to 78% while the patient was breathing ambient air. A pulmonary consultation was requested.

The negative predictive value of CT pulmonary angiography is highest when the clinical suspicion of pulmonary embolism is low. In this case, I am concerned that the negative test results may be falsely negative. CT pulmonary angiography did not reveal any other findings to explain the hypoxemia. I would still be concerned that the patient has undiagnosed thromboembolism. Tumor microemboli to the lung are possible if she has previously undiagnosed metastatic disease and may be missed on CT pulmonary angiography if the small vasculature is primarily affected. I would request compression Doppler ultrasonography of the upper and lower extremities to rule out occult deep venous thrombosis. Ultimately, repeat CT pulmonary angiography or non-CT pulmonary angiography, perhaps guided by ventilation–perfusion scanning, may be required to rule out pulmonary embolism. In the absence of fever and with no pulmonary infiltrate on CT scanning, bronchoscopy is not indicated.

On review of the CT pulmonary angiographic study, a hypodense mass in the right atrium was noted. The mass was in close proximity to the tip of the central venous catheter Figure 1