COUGH
ETIOLOGY
Acute cough, which is defined as duration <21 days, is usually related to respiratory infection, aspiration, or inhalation of respiratory irritants. Subacute cough (present for 3–8 weeks) is often related to persistent inflammation from a tracheobronchitis episode. Chronic cough (>8 weeks in duration) can be caused by many pulmonary and cardiac diseases. Chronic bronchitis related to cigarette smoking is a common cause. If the chest radiograph and physical examination are unremarkable, other common causes of chronic cough include cough-variant asthma, gastroesophageal reflux disease (GERD), postnasal drip related to sinus disease, and medications including angiotensin-converting enzyme (ACE) inhibitors. Irritation of tympanic membranes and chronic eosinophilic bronchitis also can cause chronic cough with a normal chest radiograph. Ineffective cough can predispose to serious respiratory infections due to difficulty clearing lower respiratory secretions; abnormal airway secretions (e.g., due to bronchiectasis) or tracheomalacia can contribute. Weakness or pain limiting abdominal and intercostal muscle use also can lead to ineffective cough.
CLINICAL ASSESSMENT
Key historic issues include triggers for onset of cough, determinants of increased or decreased cough, and sputum production. Symptoms of nasopharyngeal disease should be assessed, including postnasal drip, sneezing, and rhinorrhea. GERD may be suggested by heartburn, hoarseness, and frequent eructation. Cough-variant asthma is suggested by noting the relationship of cough onset to asthmatic triggers. Usage of ACE inhibitors, but not angiotensin receptor blockers, can cause cough long after treatment is initiated.
On physical examination, signs of cardiopulmonary diseases should be assessed, including adventitious lung sounds and digital clubbing. Examination of the nasal passages, posterior pharyngeal wall, auditory canals, and tympanic membranes should be performed.
Laboratory evaluation should include chest radiography. Spirometry with bronchodilator testing can assess for reversible airflow obstruction. With normal spirometry, methacholine challenge testing can be used to assess for asthma. Sputum should be sent for routine bacterial and possibly mycobacterial cultures. Sputum cytology can reveal malignant cells in lung cancer and eosinophils in eosinophilic bronchitis. Esophageal pH probes can be used to assess for GERD. Chest CT should be considered in pts with normal chest radiographs who fail to improve with treatment. Evaluation of hemoptysis is discussed below.
TREATMENT Chronic Cough
In pts with chronic cough and a normal chest x-ray, empiric treatment is directed at the most likely cause based on the history and physical examination. If treatment directed at one empiric cause fails, empiric treatment of an alternative etiology can be considered. Postnasal drip treatment may include antihistamines, nasal corticosteroids, and/or antibiotics. GERD can be treated with antacids, type 2 histamine blockers, or proton pump inhibitors. Cough-variant asthma is treated with inhaled glucocorticoids and as-needed inhaled beta agonists. Pts on ACE inhibitors should be given a 1-month trial of discontinuing this medication. Chronic eosinophilic bronchitis often improves with inhaled glucocorticoid treatment. Symptomatic treatment of cough can include narcotics such as codeine; however, somnolence, constipation, and addiction can result. Dextromethorphan and benzonatate have fewer side effects but reduced efficacy.
HEMOPTYSIS
ETIOLOGY
Hemoptysis, expectoration of blood from the respiratory tract, must be differentiated from expectorated blood originating from the nasopharynx and gastrointestinal tract. Acute bronchitis is the most common cause of hemoptysis in the U.S.; tuberculosis is the leading cause worldwide.
Hemoptysis originating from the alveoli is known as diffuse alveolar hemorrhage (DAH). DAH can be caused by inflammatory diseases including Wegener’s granulomatosis, systemic lupus erythematosus, and Goodpasture’s disease. Within the first 100 days after bone marrow transplant, inflammatory DAH can cause severe hypoxemia. Noninflammatory DAH usually results from inhalational injuries from toxic exposures, such as smoke inhalation or cocaine.
Hemoptysis most commonly originates from small- to medium-sized bronchi. Since the bleeding source is usually bronchial arteries, there is potential for rapid blood loss. Airway hemoptysis is often caused by viral or bacterial bronchitis. Pts with bronchiectasis have increased risk of hemoptysis. Pneumonia can cause hemoptysis, especially if cavitation (e.g., tuberculosis) and/or necrotizing pneumonia (e.g., Klebsiella pneumoniae and Staphylococcus aureus) develop. Paragonimiasis, a helminthic infection common in pts from Southeast Asia and China, can cause hemoptysis and must be differentiated from tuberculosis. Although only 10% of lung cancer pts have hemoptysis at diagnosis, cancers developing in central airways (e.g., squamous cell carcinoma, small cell carcinoma, and carcinoid tumors) often cause hemoptysis. Cancers that metastasize to the lungs can cause hemoptysis less commonly.
Pulmonary vascular sources of hemoptysis include congestive heart failure, which usually causes pink, frothy sputum. Pulmonary embolism with infarction and pulmonary arteriovenous malformations are additional pulmonary vascular etiologies to consider.
CLINICAL ASSESSMENT
The approaches to assess and treat hemoptysis are shown in Fig. 41-1. History should determine whether the bleeding source is likely the respiratory tract or an alternative source (e.g., nasopharynx, upper GI tract). The quantity of expectorated blood should be estimated, as it influences the urgency of evaluation and treatment. Massive hemoptysis, variably defined as 200–600 mL within 24 h, requires emergent care. The presence of purulent or frothy secretions should be assessed. History of previous hemoptysis episodes and cigarette smoking should be ascertained. Fever and chills should be assessed as potential indicators of acute infection. Recent inhalation of illicit drugs and other toxins should be determined.
FIGURE 41-1 An algorithm for the evaluation of hemoptysis. CBC, complete blood count; CT, computed tomography; CXR, chest x-ray; UA, urinalysis. (From Kritek P and Fanta C: HPIM-18.)
Physical examination should include assessment of the nares for epistaxis, and evaluation of the heart and lungs. Pedal edema could indicate congestive heart failure if symmetric, and deep-vein thrombosis with pulmonary embolism if asymmetric. Clubbing could indicate lung cancer or bronchiectasis. Assessment of vital signs and oxygen saturation can provide information about hemodynamic stability and respiratory compromise.
Radiographic evaluation with a chest x-ray should be performed. Chest CT may be helpful to assess for bronchiectasis, pneumonia, lung cancer, and pulmonary embolism. Laboratory studies include a complete blood count and coagulation studies; renal function and urinalysis should be assessed, with additional blood tests including ANCA, anti-GBM, and ANA if diffuse alveolar hemorrhage is suspected. Sputum should be sent for Gram’s stain and routine culture as well as AFB smear and culture.
Bronchoscopy is often required to complete the evaluation. In massive hemoptysis, rigid bronchoscopy may be necessary.
TREATMENT Hemoptysis
As shown in Fig. 41-1, massive hemoptysis may require endotracheal intubation and mechanical ventilation to provide airway stabilization. If the source of bleeding can be identified, isolating the bleeding lung with an endobronchial blocker or double-lumen endotracheal tube is optimal. Pts should be positioned with the bleeding side down. If bleeding persists, bronchial arterial embolization by angiography may be beneficial; however, risk of spinal artery embolization is an important potential adverse event. As a last resort, surgical resection can be considered to stop the bleeding. Cough suppression, typically with narcotics, is desirable.
For a more detailed discussion, see Kritek P, Fanta C: Cough and Hemoptysis, Chap. 34, p. 282, in HPIM-18.