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15 COUGH AND HEMOPTYSIS

15 COUGH AND HEMOPTYSIS
Harrison’s Manual of Medicine

15

COUGH AND HEMOPTYSIS

Cough
Hemoptysis
Bibliography

COUGH
Produced by inflammatory, mechanical, chemical, and thermal stimulation of cough receptors.
ETIOLOGY

Inflammatory—edema and hyperemia of airways and alveoli due to laryngitis, tracheitis, bronchitis, bronchiolitis, pneumonitis, lung abscess.

Mechanical—inhalation of particulates (dust) or compression of airways (pulmonary neoplasms, foreign bodies, granulomas, bronchospasm).

Chemical—inhalation of irritant fumes, including cigarette smoke.

Thermal—inhalation of cold or very hot air.

Approach to the Patient

Diagnosis (Fig. 15-1)   History should consider: (1) duration—acute or chronic; (2) presence of fever or wheezing; (3) sputum quantity and character; (4) temporal or seasonal pattern; (5) risk factors for underlying disease; and (6) past medical history. Short duration with associated fever suggests acute viral or bacterial infection. Persistent cough after viral illness suggests postinflammatory cough. Postnasal drip is a common cause of chronic cough. Nocturnal cough may indicate chronic sinus drainage or esophageal reflux. Change in sputum character, color, or volume in a smoker with “smoker’s cough” necessitates investigation. Seasonal cough may indicate “cough asthma.” Environmental exposures may suggest occupational asthma orinterstitial lung disease. Past history of recurrent pneumonias may indicate bronchiectasis, particularly if associated with purulent or copious sputum production. A change in the character of chronic cigarette cough raises suspicion of bronchogenic carcinoma.

FIGURE 15-1. An algorithm for the evaluation of chronic cough.

Physical exam should assess upper and lower airways and lung parenchyma. Stridor suggests upper airway obstruction; wheezing suggests bronchospasm as the cause of cough. Midinspiratory crackles indicate airways disease (e.g., chronic bronchitis); fine end-inspiratory crackles occur in interstitial fibrosis and heart failure. CXR may show neoplasm, infection, interstitial disease, or the hilar adenopathy of sarcoidosis. PFTs may reveal obstruction or restriction. Sputum exam can indicate malignancy or infection.

COMPLICATIONS   (1) Syncope, due to transient decrease in venous return; (2) rupture of anemphysematous bleb with pneumothorax; (3) rib fractures—may occur in otherwise normal individuals.

TREATMENT
When possible, therapy of cough is that of underlying disease. If no cause can be found, a trial of an inhaled b agonist (e.g., albuterol) or an inhaled steroid (e.g., triamcinelone) can be attempted. Inhaled steroids may take 7– 10 days to be effective when used for an irritative cough. When symptoms from an irritative cough are severe (syncope, sleep disruption, rib fracture) the cough may be suppressed with a narcotic antitussive agent such as codeine, 15–30 mg up to qid, or a nonnarcotic such as dextromethorphan (15 mg qid). Cough productive of significant volumes of sputum should generally not be suppressed. Sputum clearance can be facilitated with adequate hydration, expectorants, and mechanical devices. Iodinated glycerol (30 mg qid) may be useful in asthma or chronic bronchitis.

HEMOPTYSIS
Includes both streaked sputum and coughing up of gross blood.
ETIOLOGY (Table 15-1)   Bronchitis and bronchiectasis are most common causes. Neoplasm may be cause, particularly in smokers and when hemoptysis is persistent. Hemoptysis rare in metastatic neoplasm to lung. Pulmonary thromboembolism, infection, CHF are other causes. Diffuse hemoptysis may occur with vasculitis involving the lung. Five to 15% of cases with hemoptysis remain undiagnosed.

Table 15-1 Causes of Hemoptysis

Approach to the Patient

Diagnosis (Fig. 15-2)   Essential to determine that blood is coming from respiratory tract. Often frothy, may be preceded by a desire to cough. History may suggest diagnosis: chronic hemoptysis in otherwise asymptomatic young woman suggests bronchial adenoma; recurrent hemoptysis in pts with chronic copious sputum production suggests bronchiectasis; hemoptysis, weight loss, and anorexia in a smoker suggest carcinoma; hemoptysis with acute pleuritic pain suggests infarction.

FIGURE 15-2. Diagnostic approach to hemoptysis.

Physical exam may also suggest diagnosis: pleural friction rub raises possibility of pulmonary embolism or some other pleural-based lesion (lung abscess, coccidioidomycosis cavity, vasculitis); diastolic rumble suggests mitral stenosis; localized wheeze suggests bronchogenic carcinoma. Initial evaluation includes CXR. A normal CXR does not exclude tumor or bronchiectasis as a source of bleeding. The CXR may show an air-fluid level suggesting an abscess or atelectasis distal to an obstructing carcinoma.
Most pts should then have chest CT scan followed by bronchoscopy. While rigid bronchoscopy is particularly helpful when bleeding is massive or from proximal airway lesion and when endotracheal intubation is contemplated, most pts should be assessed by fiberoptic bronchoscopy.

TREATMENT
In addition to treatment of the underlying condition, mainstays of treatment are bed rest and cough suppression with an opiate (codeine, 15–30 mg, or hydrocodone, 5 mg q4–6h). Pts with massive hemoptysis (>600 mL/d) and pts with respiratory compromise due to aspiration of blood should be intensively monitored with suction and intubation equipment close by so that selective intubation to isolate the bleeding lung can be accomplished. In massive hemoptysis, choice of medical or surgical therapy relates often to the anatomic site of hemorrhage and the pt’s baseline pulmonary function. Localized peripheral bleeding sites may be tamponaded by bronchoscopic placement of a balloon catheter in a lobar or segmental airway. Central bleeding sites may be managed with laser coagulation. Pts with severely compromised pulmonary function may be candidates for bronchial artery catherization and embolization.

Bibliography

For a more detailed discussion, see Weinberger SE, Braunwald E: Cough and Hemoptysis, Chap. 33, p. 203, in HPIM-15.

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