HEMOPTYSIS

Hemoptysis is the expectoration of blood that originates below the vocal cords. It is commonly classified as trivial, mild, or massive, the last defined as more than 200–600 mL in 24 hours. The dividing lines are arbitrary, since the amount of blood is rarely quantified with precision. Massive hemoptysis can be usefully defined as any amount that is hemodynamically significant or threatens ventilation, in which case the initial management goal is not diagnostic but therapeutic.
The lungs are supplied with a dual circulation. The pulmonary arteries arise from the right ventricle to supply the pulmonary parenchyma in a low-pressure circuit. The bronchial arteries arise from the aorta or intercostal arteries and carry blood under systemic pressure to the airways, blood vessels, hila, and visceral pleura. The bronchial arterial circulation represents only 1–2% of total pulmonary blood flow but is frequently the source of hemoptysis: It is a high-pressure circuit; it provides the blood supply to the airways and lesions within those airways; and flow can increase dramatically under conditions of chronic inflammation—eg, chronic bronchiectasis.
The causes of hemoptysis can be classified anatomically. Blood may arise from the airways in chronic bronchitis, bronchiectasis, and bronchogenic carcinoma; from the pulmonary vasculature in left ventricular failure, mitral stenosis, pulmonary emboli, and arteriovenous malformations; or from the pulmonary parenchyma in pneumonia, inhalation of crack cocaine, or autoimmune diseases such as Goodpasture's disease or Wegener's granulomatosis. Iatrogenic hemorrhage may follow transbronchial lung biopsies, anticoagulation, or pulmonary artery rupture due to distal placement of a balloon-tipped catheter.

Clinical Findings
Blood-tinged sputum in the setting of acute bronchitis in an otherwise healthy nonsmoker does not warrant an extensive diagnostic evaluation if the hemoptysis subsides with resolution of the infection. However, hemoptysis is frequently a sign of serious disease, especially in patients with a high prior probability of underlying pulmonary pathology. The goal of the history is to identify patients at risk for one of the disorders listed above. Pertinent features are tobacco use, duration of symptoms, and the presence of respiratory infection. Nonpulmonary sources of hemorrhage—from the nose or the gastrointestinal tract—should be ruled out.
Laboratory evaluation should include a chest radiograph and complete blood count, including platelet count. Renal function tests, urinalysis, and coagulation studies are appropriate in specific circumstances. Flexible bronchoscopy reveals endobronchial cancer in 3–6% of patients with hemoptysis who have a normal (nonlateralizing) chest radiograph. Nearly all of these patients are smokers over the age of 40, and most will have had symptoms for more than a week. Bronchoscopy is indicated in such patients. High-resolution CT of the chest is complementary to bronchoscopy. It can diagnose unsuspected bronchiectasis and arteriovenous malformations and will show central endobronchial lesions in many cases. It is the test of choice for suspected small peripheral malignancies.

Treatment
The management of mild hemoptysis consists of identifying and treating the specific cause. Massive hemoptysis is life-threatening. The airway must be protected, ventilation ensured, and effective circulation maintained. If the location of the bleeding site is known, the patient should be placed in the decubitus position with the involved lung dependent. Uncontrollable hemorrhage warrants rigid bronchoscopy and surgical consultation. In stable patients, flexible bronchoscopy may localize the site of bleeding, and angiography can embolize the involved bronchial arteries. Embolization is effective initially in 85% of cases, though rebleeding may occur in up to 20% of patients over the following year. The anterior spinal artery arises from the bronchial artery in up to 5% of people, and paraplegia may result if it is inadvertently cannulated.

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COUGH

Cough is an important physiologic mechanism that defends against respiratory pathogens and helps to clear the tracheobronchial tree of mucus, foreign particles, and noxious aerosols. Excessive cough is one of the most common symptoms for which patients seek medical care and may represent up to one-third of a pulmonologist's outpatient practice referrals. Persistent severe cough, seen in interstitial lung disease or bronchiectasis, may impair respiration as well as disrupt sleep and social functioning. Bronchospasm (brought on by repetitive forced exhalation), syncope, rib fractures, and urinary incontinence are all potential complications. A reduced or absent cough, seen in some postoperative patients or those with neuromuscular disease, will reduce clearance of secretions and may impair oxygenation.
Cough may be voluntary or involuntary. Involuntary cough is stimulated by vagal afferent receptors in the trachea, especially at the carina, and the larynx but also from others throughout the head and neck. Stimulation of cough receptors may be mechanical, as in cases of aspiration, or irritative.

Clinical Findings
It is important to distinguish acute (< 3 weeks) from chronic cough. Acute cough most commonly follows viral or bacterial upper respiratory tract infection. Within 2 days after onset of the common cold, 85% of untreated patients cough; 26% are still coughing 14 days later; in a few, cough will persist for 6–8 weeks. Many patients with persistent cough following upper respiratory tract infection have underlying asthma. Other causes of acute cough include aspiration, pneumonia, pulmonary embolism, and pulmonary edema.
The most common cause of chronic cough is a low-grade chronic bronchitis secondary to exposure to tobacco smoke, though smokers do not commonly seek medical attention for this problem. Over 90% of nonsmokers presenting for evaluation of chronic cough suffer from postnasal drip, gastroesophageal reflux disease, or asthma (even without other symptoms). Angiotensin-converting enzyme (ACE) inhibitors have become another common cause. In primary care settings, single causes predominate.
The character and timing of chronic cough and the presence or absence of sputum production do not permit an etiologic diagnosis and should not be used as the sole basis for empirical therapy. The history and physical examination should attempt to identify anatomic locations of the afferent limb of the cough reflex in light of the common causes listed above. A nasal discharge, frequent need to clear the throat, and mucoid or mucopurulent secretions in the posterior pharynx suggest postnasal drip. Sinus radiographs may be diagnostic of acute or chronic sinusitis. Wheezing on chest auscultation or airflow obstruction on pulmonary function tests suggest asthma. In cough-variant asthma, methacholine bronchoprovocation testing may be positive in the absence of clinical findings of asthma. Gastroesophageal reflux disease is an important cause of chronic cough but is associated with the fewest clinical clues. Patients may complain of heartburn or regurgitation, but cough may be the only symptom. Barium swallow is specific but insensitive, and esophageal pH monitoring may be necessary. Chest radiographs are best reserved for cough in smokers and patients with hemoptysis or constitutional symptoms such as fever and weight loss.

Treatment
The first step is to eliminate irritant exposures such as tobacco smoke (primary or secondary) and occupational agents and to discontinue medications such as ACE inhibitors or beta-blockers, including eyedrops. Cough due to ACE inhibitors should subside within 1–4 days after discontinuing the medication, though it may take weeks to months. Postnasal drip syndrome due to allergic rhinitis that does not respond to antihistamines should be treated with intranasal steroids. Chronic sinusitis may require prolonged antibiotics directed against Haemophilus influenzae. Cough caused by asthma that does not respond after 2 weeks of bronchodilators and corticosteroids suggests another contributing condition. Cough due to gastroesophageal reflux disease is difficult to treat, since H2 blockers may not be adequate. Most practitioners now initiate antitussive therapy for gastroesophageal reflux disease with proton pump inhibitors. Patients whose cough began after an upper respiratory tract infection usually respond to treatment with an antihistamine-decongestant combination or treatment for asthma.

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DYSPNEA

Dyspnea is a common symptom. It is analogous to pain in that sensory input from multiple sites in the respiratory system is integrated in the cerebral cortex. In general, dyspnea increases with the level of functional impairment as measured by spirometry. However, there is only a weak correlation between airflow limitation or exercise tolerance and the severity of dyspnea.
Several pathophysiologic processes contribute to dyspnea. The most important is the increased respiratory effort that accompanies many different diseases: airflow obstruction (asthma; chronic obstructive pulmonary disease [COPD]), changes in pulmonary compliance (interstitial fibrosis, congestive heart failure) or chest wall compliance (obesity, pleural disease), intrinsic respiratory muscle weakness (inanition, neuromuscular disease, chronic respiratory failure), or the weakness conveyed by the mechanical disadvantage of hyperinflation (asthma or emphysema). Dyspnea is magnified by increased respiratory drive. Acute hypercapnia is therefore a potent stimulus to dyspnea, hypoxemia a weak one. In mechanically ventilated patients, failure to provide adequate inspiratory flow rates to patients with heightened respiratory drive commonly results in dyspnea that may present as agitation. Stimulation of irritant receptors in the airways intensifies dyspnea, while stimulation of pulmonary stretch receptors decreases it.

Clinical Findings
The history should focus on onset and timing of symptoms, the patient's position at onset of symptoms, the relationship of symptoms to activity, and any factors that may improve or exacerbate symptoms. The clinician can assess dyspnea and response to treatment with a ten-point numeric rating scale by asking the patient, “On a scale of zero to ten, with zero being no shortness of breath and ten being the worst shortness of breath you can imagine, how short of breath are you?” Exertional dyspnea should be quantified, but the absolute level of exertion that precipitates dyspnea is less important than acute changes in the threshold level of activity. A complete allergic, occupational, and smoking history is essential.
Acute dyspnea has a short list of causes, most of which are readily identified: asthma, pulmonary infection, pulmonary edema, pneumothorax, pulmonary embolus, metabolic acidosis, or acute respiratory distress syndrome (ARDS). Panic attacks may present as a respiratory complaint. Orthopnea (dyspnea on recumbency) and nocturnal dyspnea suggest asthma, gastroesophageal reflux disease (GERD), left ventricular dysfunction, or obstructive sleep apnea. Rapid onset of severe dyspnea when supine suggests phrenic nerve impairment and diaphragmatic paralysis. Platypnea (dyspnea that worsens in the upright position) is a rare complaint associated with arteriovenous malformations at the lung bases, resulting in increased shunting and hypoxemia in the upright position (orthodeoxia).
Chronic dyspnea is invariably progressive. Symptoms often first appear during exertion; patients learn to limit their activity to accommodate their diminished pulmonary reserve until dyspnea occurs with minimal activity or at rest. Episodic dyspnea suggests congestive heart failure, asthma, acute or chronic bronchitis, or recurrent pulmonary emboli. Constant dyspnea is most commonly due to COPD but may indicate interstitial lung disease (eg, pulmonary fibrosis), pulmonary vascular disease, or fixed airflow obstruction from severe asthma.
Dyspnea is increasingly being recognized as a major issue in the care of dying patients, and clinicians typically undertreat this symptom.
Evaluation should include a complete blood count, renal function tests, chest radiograph, spirometry, and noninvasive oximetry. Patients over 40 years of age or with a family history of early coronary disease should have an electrocardiogram. Arterial blood gases, measurement of lung volumes, ventilation/perfusion scanning, echocardiography, and cardiopulmonary exercise testing are reserved for cases that elude diagnosis on initial evaluation.

Treatment
In patients with advanced lung disease, the responsible condition may be easily identified but treatment only partially effective. Oxygen improves survival in those who are hypoxemic and can improve the exercise tolerance of all patients. Its effect on dyspnea is variable. Anxiety can play an important role in the distress caused by dyspnea and may be relieved by judicious use of benzodiazepines such as lorazepam, 0.5–1 mg orally every 4–6 hours. Pulmonary rehabilitation can improve respiratory function and train patients in energy conservation and breathing techniques that help moderate their sense of respiratory effort. Opioids reduce respiratory drive and blunt dyspnea. They can be titrated safely even in patients with advanced lung disease. Finally, fresh air or a fan may offer additional relief. Smokers with progressive exertional dyspnea should know that they can limit future loss of function through smoking cessation.

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