The lung is perfused by two distinct circulations that must be considered when determining the source and planned treatment of hemoptysis. The pulmonary circulation delivers blood under low pressure from the right ventricle to the alveolar capillaries for exchange of oxygen and carbon dioxide. The bronchial circulation, which is approximately 1–2% of the cardiac output, arises from the systemic circulation and provides nutrient flow to the lung parenchyma. A detailed review of the anatomy and physiology of the bronchial circulation has been published (3) and is beyond the scope of this chapter. In brief, two or more arteries arise from the aorta or upper intercostal arteries, enter the lung, and eventually form a plexus, which accompanies the branching airways with small, penetrating arteries, forming another plexus that supplies the bronchial mucosa down to the terminal bronchioles. Farther on, they anastomose with both precapillary pulmonary arterioles and pulmonary veins. Bronchial venous return is more complex: Veins from the proximal airways return blood to the right atrium through the azygous, homozygous, or intercostal veins, whereas the intrapulmonary bronchial venous blood returns through the pulmonary veins to the left ventricle. The latter occurs because of anastomoses between bronchial and pulmonary veins and carries the bulk of bronchial venous return. Although the bronchial circulation is nonessential in the normal adult lung, in the setting of chronic inflammation, neoplasm, or repair after lung injury, bronchial blood flow increases because of increases in both the size and number of vessels. Elevations of pulmonary vascular pressure can affect the bronchial circulation because of the many anastomoses between the dual circulations. In general, hemoptysis occurs because of disruption of the high-pressure bronchial vessels, which become abnormally enlarged and exposed within diseased airways.

This discussion concentrates on the malignant causes of hemoptysis, but awareness of other causes is important because many patients have underlying conditions that may become active problems during treatment of a malignant disease. The differential diagnosis for a patient presenting with hemoptysis is extensive (Table 26.1). Some conditions that are more likely to be associated with massive hemoptysis are shown in Table 26.2. In past years, tuberculosis, bronchiectasis, and lung abscess were the most common causes of massive hemoptysis. The incidence of the latter two has declined in industrialized nations, but tuberculosis remains a significant problem worldwide. Experience with tuberculosis has helped us to understand the pathophysiology of massive hemoptysis. Up to 7% of deaths from tuberculosis have been attributed to massive hemoptysis; autopsy examinations have revealed ruptured pulmonary artery aneurysms. Rasmussen has described localized ruptures of aneurysmal portions of pulmonary arteries passing through thick-walled cavities of chronic tuberculosis, the so-called “Rasmussen’s aneurysms.” Rupture occurs secondary to the infection or the associated inflammatory response (4). Healed calcified mediastinal lymph nodes from prior tuberculosis can erode into the bronchial mucosa, also causing significant bleeding. Tuberculosis distorts lung architecture, causing bronchiectasis with resulting hypertrophy and proliferation of bronchial vessels. Infection or inflammation in these diseased portions of the airway can cause rupture of vessels; the result is massive bleeding caused by the high systemic arterial pressure.

The key element of diagnosis in cases of hemoptysis is the localization of bleeding to the lower respiratory tract. Although blood from the stomach usually has a low pH and blood from the respiratory tract a high pH, bleeding from the nasopharynx, larynx, or gastrointestinal tract may be difficult to distinguish clinically from true hemoptysis. Furthermore, bleeding from these sources may result in cough and the appearance of blood, which can be misinterpreted as hemoptysis. When there is doubt, a thorough examination of the nasopharynx, larynx, and upper gastrointestinal tract should be performed.

Once the lung has been identified as the source of bleeding, the next step is to localize the site of bleeding. Physical examination alone is not sensitive enough; a chest x-ray should be performed, and is often helpful in revealing a tumor or abscess. However, it can be misleading, as blood may be coughed into uninvolved portions of the lungs. Bronchoscopy is the surest way to visualize the source (or at least the segment) from which there is active bleeding. Flexible fiberoptic bronchoscopy is usually attempted first because it can be done relatively quickly at the bedside without general anesthesia, and can access more distal airways than the rigid bronchoscope. The latter has the advantages of greater suction capability, removal of clots or foreign bodies, and airway control that allows for patient ventilation, often necessary in cases of massive hemoptysis. Computed tomography (CT) scan has been compared with bronchoscopy in studies in which hemoptysis is the presenting problem. Patients with preexisting cancer constituted a small proportion of those studied. The CT scan is superior in identifying bronchiectasis, lung abscess, aspergilloma, and distal parenchymal abnormalities; however, the bronchoscope can obtain material that allows cytologic, histologic, and microbiologic diagnoses (16, 17). In a recent study, it was suggested that CT may be the more efficient diagnostic tool (18). In patients with established malignancies, a CT scan may offer important information, as it can delineate peribronchial or mediastinal involvement of tumors that cannot be seen with a bronchoscope. Routine use of CT scan is not of proven benefit but should be considered in cases in which the chest radiographic findings are inconclusive, or to provide a more detailed anatomic localization of an abnormality for the bronchoscopist.

The severity of hemoptysis determines the pace at which a workup should proceed. In a review of 10 years’ experience at Duke University Medical Center, the mortality rate was 9% and 58% if blood loss was less than or more than 1000 mL per 24-hour period, respectively (1). A malignant cause for hemoptysis of greater than 1000 mL per 24 hours increased the mortality rate to 80%. Massive hemoptysis requires rapid intervention to guarantee that the patient has an adequate airway while attempting to control bleeding. If blood loss is minimal and sporadic, a more detailed evaluation can occur without immediate attention to resuscitative efforts. Early consultation with a pulmonary physician and thoracic surgeon is recommended.

Initial diagnostic studies should include chest radiograph, hematocrit, platelet count, blood urea nitrogen, serum creatinine, and coagulation panel. Oxygenation should be monitored by arterial blood gas determination or pulse oximetry, and adequate intravenous access established. Typed and cross-matched blood should be available in cases of significant bleeding. Mild sedation and judicious use of a cough suppressant can be employed, but excessive use compromises a patient’s ability to clear the airway.