A 68-year-old woman with a prior diagnosis of asthma presents to your clinic for a routine clinic visit. She complains of occasional palpitations and tremor. Her dyspnea is well controlled. Her past medical history is remarkable for hospitalization for mild congestive heart failure 2 months ago; she notes occasional postprandial acid reflux. Her medications include lisinopril, digoxin, furosemide, an intermittent short-acting inhaled beta agonist, and theophylline. She uses an over-the-counter pill (whose name she cannot remember) for the reflux symptoms. On examination her heart rate is 112 beats/minute. S1 and S2 are normal; she has a mild tremor of the outstretched hands. What is the best next step in her management?
Theophylline has been used as a bronchodilator for a number of years. It has been less commonly used in recent years owing to its narrow therapeutic window. The drug is metabolized in the liver. A drug or process that interferes with the activity the cytochrome P450 system will slow the metabolism of theophylline and may lead to the accumulation of toxic levels in the blood. The metabolism of theophylline is slowed by age, infection, CHF (resulting from decreased hepatic blood flow), and a number of drugs. Commonly used drugs that impair the metabolism of theophylline include cimetidine, erythromycin, ciprofloxacin, allopurinol, and zafirlukast. This patient has probably been using over-the-counter cimetidine to treat her reflux symptoms. Stopping theophylline until the drug level has returned will relieve her palpitations and tremor. In the absence of dyspnea, wheezing, or clinical signs of CHF, chest film and spirometry would not be helpful. Using a benzodiazepine to treat her tremor would leave a potentially serious theophylline toxicity undetected. Finally beta agonists are more effective bronchodilators in asthma than is ipratropium; the tremulousness associated with beta agonist use is usually short lived.
A 56-year-old woman presents with cough for the past 2 months and streak hemoptysis for the past 3 days. She denies dyspnea on exertion. She has smoked 2 packs of cigarettes a day for the past 35 years. She is otherwise healthy and has not lost weight. Physical examination is normal. Chest x-ray reveals a shaggy 3-cm nodule in the right mid-lung field. Transthoracic needle biopsy shows a squamous cell carcinoma. PET/CT scan confirms the hypermetabolic 3-cm nodule and shows a 1.5-cm ipsilateral hilar lymph node. Mediastinal lymphadenopathy, intraparenchymal metastases, pleural effusion and distant metastases are absent. Spirometry is normal. What is the best management option for this patient?
This patient has stage IIB non-small cell lung cancer (NSCLC) and should be considered for surgical resection with curative intent. As a general rule, patients with stages I and II lung cancer are surgical candidates unless other medical contraindications or severe COPD are present. Adjuvant chemotherapy is sometimes added, but surgery is the curative modality with the best track record. Patients with stage I lung cancer have tumors localized to the lung. Stage II cancers are associated with ipsilateral peribronchial or hilar lymph node involvement. Mediastinal lymph node involvement, pleural effusion, or distant metastases generally preclude curative surgery. These patients, however, may respond to radiation and/or chemotherapy. Although some patients have achieved long-term remission after radiation therapy, it is less effective than surgical resection. Combination chemotherapy can prolong life expectancy in selected patients but is not considered curative. Endobronchial radiation therapy (brachytherapy) can palliate intractable hemoptysis or bronchial obstruction but is not curative; survival in NSCLC after brachytherapy averages 6 months. “Watchful waiting” would be inappropriate in this patient with potentially curable disease.
A 43-year-old woman complains of gradually worsening dyspnea over the past year. She smokes 1 pack of cigarettes a day. She is trying to “cut back,” because her father, also a smoker, died at age 52 of emphysema. She works as an equestrian riding instructor, often with exposure to animals and hay, but has not noticed exacerbation of symptoms while at work. She has 3 healthy children, one of whom has childhood asthma. On examination, she is comfortable at rest. Her O2 saturation is 93%. She has no basilar crackles or wheezing, but her breath sounds are distant. Chest x-ray shows hyperexpansion especially prominent in the lung bases. Spirometry reveals FEV1 of 46% of predicted but near normal forced vital capacity (FVC). The ratio of FEV1 to FVC is 52%. In addition to advice about smoking cessation, what study would be most important to obtain?
This woman has COPD (chronic symptoms, obstructive defect on spirometry) at age younger than 45. Early-onset symptoms, even in a smoker, coupled with a positive family history, should raise the possibility of alpha-1 antitrypsin (AAT) deficiency, and a serum AAT level should be ordered. If it is low, a phenotype assay will confirm the abnormal gene product. AAT deficiency tends to cause more prominent alveolar destruction in the lower lung zones, as opposed to usual smoker’s emphysema, which has an upper lobe predominance. Diagnosing AAT deficiency would be important for her family members. In addition, infusion of pooled human AAT, although quite expensive, can raise AAT levels and probably slows progression of the disease. Cystic fibrosis, which is diagnosed by the sweat chloride level, can present with lung disease in adulthood. However, this woman’s lack of cough and sputum production, as well as her normal fertility, makes this a less likely diagnosis than AAT deficiency. Diffusing capacity will be low in any cause of emphysema, and CT scanning will confirm bullous changes, but neither is recommended in the routine management of COPD. High-resolution CT scanning is used in the diagnosis of interstitial, not obstructive, lung disease. This woman has a history of exposure to organic compounds known to cause hypersensitivity pneumonitis, but her lack of symptoms during or soon after exposure, as well as the absence of patchy infiltrates on CXR, makes this diagnosis less likely. Many agricultural workers have immunoprecipitins to thermophilic actinomycetes. In the absence of convincing history, these results are nonspecific.
A 69-year-old woman presents with complaint of chronic cough. She is a former smoker, but quit over 20 years ago. She is healthy except for hypertension, for which she takes amlodipine; she is on no other medications. The cough has been present for 6 months. She produces scant clear sputum in the morning and denies hemoptysis or weight loss. The cough is more prominent at night. It is not exacerbated by exercise or cold exposure. There is no exposure history to potential lung toxins. She denies runny nose, nasal allergies, or postnasal drip. She has occasional heartburn, promptly relieved by two tablets of calcium carbonate. Physical examination and PA/lateral chest x-ray are normal. What is the next best step in the evaluation of this patient?
Chronic cough is a common problem encountered in the clinic. Although patients are often worried about serious disease such as lung cancer, emphysema, or tuberculosis, these dire diagnoses are rare in the absence of a compatible history and chest x-ray. The commonest causes are (1) acid reflux (with inflammation of the larynx and trachea); (2) postnasal drip syndrome; (3) cough-variant asthma; and (4) drug-induced cough due to angiotensin-converting enzyme inhibitors (ACEIs). Extensive testing such as CT scanning, bronchoscopy, or esophageal pH monitoring is not recommended. The practitioner should make the best diagnosis on the basis of initial data, and then institute a therapeutic trial, understanding that a response often takes weeks or months. This patient’s nocturnal symptoms and occasional postprandial reflux (patients often do not have severe symptoms of GERD) would direct you toward a trial of PPIs. If she had allergic symptoms or cobblestoning of the posterior pharynx, a trial of nasal steroids/decongestants would be reasonable. Childhood asthma, intermittent wheezing, or exacerbation of symptoms with exercise or cold exposure would direct you toward a therapeutic trial of bronchodilators. Spirometry is usually normal unless the patient is having symptoms at the time of examination; methacholine challenge can be employed in selected patients. Amlodipine does not cause drug-induced cough. If the patient does not respond to high-dose PPIs, other therapeutic trials might be instituted.
A 25-year-old healthy medical student celebrates the end of his third year with a camping and climbing trip to Colorado. He has a mild headache after flying to Denver; the next day he drives to a cabin at 10,000 ft, and the following day climbs to 13,500 ft with friends. During the climb, he becomes unduly short of breath and develops a cough productive of blood tinged sputum. He is evacuated to a clinic, where he is disoriented and in respiratory distress. His room air O2 saturation is 79%. His neck veins are flat and cardiac examination is normal except for tachycardia. He has bilateral crackles. What statement best characterizes this patient’s medical condition?
This young man is suffering from high-altitude pulmonary edema (HAPE), a life-threatening condition. It is the commonest nontraumatic cause of death in high-altitude climbers. Susceptible persons have increased pulmonary vasoconstriction in response to hypoxia; this damages capillary endothelium and leads to exudation of fluid into the alveoli. Patients with HAPE are at significant risk of recurrence. The cornerstone of treatment is oxygen administration and/or descent to lower altitude, where the partial pressure of oxygen is higher. HAPE is a form of noncardiogenic pulmonary edema; left ventricular function is normal. Although nifedipine decreases pulmonary vascular tone and is a useful adjunct, relief of hypoxia is a much more important aspect of treatment. Rapid ascent, sleeping at high altitude, and individual susceptibility are important risk factors; interestingly, youth and physical conditioning are not protective (perhaps because young people have vigorous pulmonary vascular reactivity). Acetazolamide (a carbonic anhydrase inhibitor) is useful in prevention of acute mountain sickness (which causes malaise and headache) but not of HAPE. Nifedipine has some prophylactic value.
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