A 34-year-old black woman presents to your office with symptoms of cough, dyspnea, and fatigue. Physical examination shows cervical adenopathy and hepatomegaly. Spleen tip is palpable. Her chest radiograph is shown below. Which of the following is the best approach in establishing a diagnosis?
Sarcoidosis is a systemic illness of unknown etiology. There is a higher prevalence in female patients and in the African American population. Most patients have respiratory symptoms, including cough and dyspnea. Hilar and peripheral lymphadenopathy is common, and 20% to 30% of patients have hepatosplenomegaly. The chest x-ray shows symmetrical hilar lymphadenopathy. The diagnostic method of choice is fiberoptic bronchoscopy with transbronchial biopsy, which will show a mononuclear cell granulomatous inflammatory process. While liver and mediastinal lymph node biopsies are often positive, bronchoscopy is a safer and less invasive procedure. ACE levels are elevated in two-thirds of patients; since an elevated ACE value is common in other granulomatous diseases, it is not specific enough to exclude alternative diagnoses. Open-lung biopsy is more invasive and would only be considered if fiberoptic bronchoscopy failed to yield a diagnosis.
A 64-year-old woman is found to have a right-sided pleural effusion on chest x-ray. Analysis of the pleural fluid reveals pleural fluid to serum protein ratio of 0.38, a lactate dehydrogenase (LDH) level of 110 IU (normal 100-190), and pleural fluid to serum LDH ratio of 0.46. Which of the following disorders is most likely in this patient?
Classifying a pleural effusion as either a transudate or an exudate is useful in identifying the underlying disorder. Pleural fluid is exudative if it has any one of the following three properties: a ratio of concentration of total protein in pleural fluid to serum greater than 0.5, an absolute LDH greater than 2/3 the upper normal in serum, or a ratio of LDH concentration in pleural fluid to serum greater than 0.6 (the “Light criteria”). Causes of exudative effusions include malignancy, pulmonary embolism, pneumonia, tuberculosis, abdominal disease, collagen vascular diseases, sarcoidosis, uremia, Dressler syndrome, and chylothorax. Exudative effusions may also be drug induced. If none of the aforementioned properties are met, the effusion is a transudate. Differential diagnosis for a transudative effusion includes congestive heart failure, nephrotic syndrome, cirrhosis, Meigs syndrome (benign ovarian neoplasm with effusion), and hydronephrosis. Exudative effusions are the result of an inflammatory process causing proteins to leak across the capillary membrane. Transudative effusions are caused by alterations in hydrostatic or oncotic pressures with normal capillary permeability.
. A 25-year-old man presents to the clinic for evaluation of infertility. He has a life-long history of a productive cough and recurrent pulmonary infections. On his review of symptoms he has indicated chronic problems with abdominal pain, diarrhea, and difficulty gaining weight. He also has diabetes mellitus. His chest x-ray suggests bronchiectasis. Which is the most likely diagnosis?
Patients with cystic fibrosis are now surviving into adulthood. The median survival is approximately age 41. Most cases are diagnosed in childhood; however, because of variable penetration of the genetic defect, approximately 7% are not found until the patient is an adult. Most male patients (> 95%) are azoospermic. Chronic pulmonary infections occur, and bronchiectasis frequently develops. Diabetes mellitus and gastrointestinal problems indicate pancreatic insufficiency. This patient should have sweat chloride measurement; if abnormal (sweat Cl above 70 mEq/L), cystic fibrosis transmembrane conductance regulator (CFTR) mutation analysis should be ordered. COPD or emphysema at this age would be unusual unless the patient were deficient in alpha-1 antitrypsin. Immunoglobulin deficiencies can cause recurrent sinopulmonary infections but would not cause malabsorption or infertility. Whipple disease causes malabsorption but not the pulmonary manifestations or infertility; it would be vanishingly rare in a young patient. Asthma would not cause the abdominal symptoms, diabetes, or changes of bronchiectasis.
A 62-year-old automobile worker presents with gradually worsening exertional dyspnea over the preceding several months. Recently, he has noticed right pleuritic chest pain. He has hypertension, well controlled on amlodipine 5 mg a day. He takes no other medications. He has never noticed cough or wheezing while at work. He worked for 15 years in construction and demolition and for 20 years thereafter in the service department of an automotive dealership. He denies fever, chills, or night sweats. On physical examination, he is in no respiratory distress but has right basilar dullness. His finger oximetry reads 96% on room air. Chest x-ray reveals a moderate right pleural effusion and lateral pleural thickening on both sides. Thoracentesis shows reddish fluid, which on formal analysis, is an exudate with 45,000 RBCs/hpf. Cytology is negative. What is the most likely explanation for this patient’s symptoms?
Occupational lung disease is an important branch of pulmonology, and new inhaled workplace toxins are being described every year. A detailed occupational history and knowledge of potential culprits are, therefore, critical in patients with unexplained lung disease. This patient’s exposure history is suggestive of asbestos related disease; bilateral pleural thickening (often calcified, a finding especially evident on CT scan) indicates prior asbestos exposure. Occasionally, the pleural involvement is associated with a pleural effusion (often with an elevated red cell count) called benign asbestos pleural effusion (BAPE). “Benign” distinguishes this syndrome from malignant effusions due to lung cancer or mesothelioma, both of which occur with increased frequency in asbestosis. Progressive debility from an interstitial lung disease (which worsens even after asbestos exposure has ceased) may occur in asbestosis, but this patient’s physical examination and chest x-ray do not suggest interstitial disease. Medications, especially nitrofurantoin and cancer chemotherapeutic agents, can cause interstitial lung disease, but amlodipine has not been reported to do so. Tuberculosis occurs with increased frequency in silicosis, not in asbestosis. Although TB can cause a bloody pleural effusion, this patient does not have the systemic symptoms that usually accompany TB. Hypersensitivity pneumonitis is an important cause of occupational lung disease, but it is caused by exposure to organic materials such as thermophilic actinomycetes (farmer’s lung). In addition, hypersensitivity pneumonitis usually causes acute symptoms (including fever) at time of exposure. Occupational asthma is an important category, since continued exposure can lead to irreversible changes. Isocyanates in automobile paints are an important cause of occupational asthma, but the symptoms are usually more acute and associated with wheezing on physical examination. Hypersensitivity pneumonitis and occupational asthma do not cause pleural disease.
A 40-year-old man without a significant past medical history comes to the emergency room with a 3-day history of fever and shaking chills, and a 15-minute episode of rigor. He also reports a cough productive of yellow-green sputum, anorexia, and the development of right-sided pleuritic chest pain. Shortness of breath has been present for the past 12 hours. Chest x-ray reveals a consolidated right middle lobe infiltrate, and CBC shows an elevated neutrophil count with many band forms present. Which feature would most strongly support inpatient admission and IV antibiotic treatment for this patient?
Because of the development of effective oral antibiotics (respiratory fluoroquinolones, extended spectrum macrolides), most patients with community-acquired pneumonia (CAP) can be managed as an outpatient as long as compliance and close followup are assured. The CURB-65 score is the most strongly validated instrument for determining if inpatient admission (either observation or full admission) is indicated. Factors predicting increased severity of infection include confusion, urea above 19mg/dL, respiratory rate above 30, BP below 90 systolic (or 60 diastolic), and age above 65. If more than one of these factors is present, hospitalization should be considered. This patient’s presentation (lobar pneumonia, pleuritic pain, purulent sputum) suggests pneumococcal pneumonia. Pneumococci are the commonest organisms isolated from patients with CAP. Fortunately, S pneumoniae is sensitive to oral antibiotics such as clarithromycin/azithromycin and the respiratory quinolones. A Gram stain suggestive of pneumococci would therefore only confirm the clinical diagnosis. Exposure to influenza is an important historical finding. However, without a prodrome of influenzalike illness (upper respiratory symptoms, myalgias, prostrating weakness), this is still garden variety CAP. In the setting of an influenza-like illness, H influenzae (easily treated with standard antibiotics) and S aureus pneumonia (more problematic to treat) must be considered. Acute lobar pneumonia, even in an HIV-positive patient, is due to the pneumococcus and can be treated as an outpatient. Pneumocystis jirovecii pneumonia is usually insidious in onset, causes diffuse parenchymal infiltrates, and does not cause pleurisy or pleural effusion. Physical examination signs of consolidation confirm the CXR finding of a lobar pneumonia (as opposed to a patchy bronchopneumonia) and would simply affirm the importance of coverage for classic bacterial pathogens (ie, pneumococci, H flu). Atypical pneumonias (still often pneumococcal, but sometimes due to Mycoplasma or Chlamydia) are usually patchy and also do not affect the pleura. Currently recommended treatment regimens cover both typical and atypical pathogens.
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