A 50-year-old patient with long-standing chronic obstructive lung disease develops the insidious onset of aching in the distal extremities, particularly the wrists bilaterally. There is a 10-lb weight loss. The skin over the wrists is warm and erythematous. There is bilateral clubbing. Plain film of the forearms reveals bilateral periosteal thickening, possible osteomyelitis, but no joint abnormality. Which of the following is the most appropriate management of this patient?
The clinical picture suggests hypertrophic osteoarthropathy. This process, the pathogenesis of which is unknown, is characterized by clubbing of digits, periosteal new bone formation, and arthritis. Hypertrophic osteoarthropathy is associated with intrathoracic malignancy, suppurative lung disease, and congenital heart problems. Treatment is directed at the underlying disease process. While x-rays may suggest osteomyelitis, the process is usually bilateral and easily distinguishable from osteomyelitis. The first step in evaluation of this patient is to obtain a chest x-ray looking for lung infection and carcinoma. The process is periarticular, not articular; so septic arthritis, treated with parenteral antibiotics, would not be a consideration. Although there is warmth over the wrists, the clubbing and periosteal changes would not be seen in rheumatoid arthritis, so wrist aspiration and methotrexate therapy would not address the underlying problem. An elevated sedimentation rate could be seen in neoplasm, infection, and inflammatory arthritis and would therefore be of little diagnostic value.
A 76-year-old woman presents with worsening dyspnea for the past 4 weeks. She has noticed fatigue, 10-lb weight loss, and occasional night sweats. On examination, she is in mild respiratory distress. Her RR is 22, and her BP is 134/76. She has mild generalized lymphadenopathy, with the largest node measuring 1.5 cm. Lung examination reveals bibasilar dullness without rales or wheezes. Her neck veins are not distended. CXR shows moderate left-sided pleural effusion. A thoracentesis is performed, revealing milky fluid. Pleural fluid protein and LDH demonstrate an exudative effusion. The pleural fluid cell count is 4800/mm3 with 14% neutrophils, 12% mesothelial cells, and 74% lymphocytes. Pleural fluid triglyceride is 170 mg/dL. What is the likely cause of this patient’s illness?
Milky pleural fluid associated with high pleural fluid triglyceride level (above 110) indicates chylothorax, usually caused by disruption or compression of the thoracic duct. Hence, most chylous effusions are left-sided. Trauma is the commonest cause, but in this patient, lymphoma should be strongly considered. The lymphocytes in the pleural fluid may be monoclonal in origin. Flow cytometry of these cells or biopsy of one of the accessible peripheral lymph nodes will reveal the diagnosis.
A 40-year-old alcoholic develops cough and fever. Chest x-ray, shown below, shows an air-fluid level in the superior segment of the right lower lobe.
Which of the following is the most likely etiologic agent?
The chest x-ray shows a pulmonary abscess in the right lower lobe with an air-fluid level. This is characteristic of an anaerobic infection. These are usually associated with a period of loss of consciousness and with poor oral hygiene. The location of the infiltrate suggests aspiration, also making anaerobic infection most likely. The superior segment of the right lower lobe is the segment most likely to develop aspiration pneumonia. Lung abscess indicates a necrotizing process, which is uncommon with the “typical” bacterial pathogens pneumococci and H influenzae, and very rare in the usually patchy “atypical” pneumonias caused by Legionella and Mycoplasma.
A 30-year-old man is admitted to the hospital after a motorcycle accident that resulted in a fracture of the right femur. The fracture is managed with traction. Three days later the patient becomes confused and tachypneic. A petechial rash is noted over the chest. Lungs are clear to auscultation. Arterial blood gases show P O2 of 50, PCO2 of 28, and pH of 7.49. Which of the following is the most likely diagnosis?
Because clinical signs of neurologic deterioration and a petechial rash have occurred in the setting of fracture and hypoxia, fat embolism is the most likely diagnosis. This process occurs when neutral fat is introduced into the venous circulation after bone trauma or fracture. The latent period is 12 to 36 hours. A pulmonary embolus usually has a longer latent period. In addition, pulmonary embolus would not cause the petechial rash. Confusion out of proportion to the degree of hypoxemia is also seen with fat emboli. Unilateral pulmonary edema can be seen with aspiration and after rapid expansion of a pneumothorax, but not with fat embolism. Hematoma of the chest wall can occur after trauma, but does not cause hypoxemia and confusion. An early pneumonia would not be associated with a petechial rash.
A 70-year-old patient with chronic obstructive lung disease requires 2 L/minute of nasal O 2 to treat his hypoxia, which is sometimes associated with angina. The patient develops pleuritic chest pain, fever, and purulent sputum. While using his oxygen at an increased flow of 5 L/minute, he becomes stuporous and develops a respiratory acidosis with CO2 retention and worsening hypoxia. What would be the most appropriate next step in the management of this patient?
This patient presents with severe COPD and hypoxemia. Chronic CO2 retention has blunted his hypercarbic drive to breathe; he is dependent on mild hypoxia to stimulate respiration. An inappropriately high oxygen delivery has decreased even that drive, with resulting acute respiratory acidosis and CO2 narcosis. However, stopping the oxygen will result in severe hypoxemia. Of the choices listed, the initiation of mechanical ventilation is the only acceptable choice. If the patient’s mental status were better, noninvasive ventilation (BiPAP) might be considered. Medroxyprogesterone has only a mild stimulatory effect on the respiratory center, and is not appropriate therapy in this case. Antibiotics and inhaled bronchodilators are appropriate treatments for COPD exacerbation but would not manage this patient’s acute hyper-carbic respiratory failure. The patient has declared a deteriorating course. Continuing to monitor his status on the general medicine ward would probably be fatal. This patient has respiratory (not metabolic) acidosis. Bicarbonate plays a minimal role in this acidosis. The correct therapy is to improve the patient’s ventilation.
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