Massive Hemoptysis

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Chapter 26 Massive Hemoptysis

Hemoptysis is the coughing up of blood or bloodstained sputum. Massive hemoptysis is variably defined as 200 to 1000 ml of blood expectorated in 24 hours; 600 ml is a widely accepted figure.1,2 Blood loss is rarely measured and is difficult to quantify. A more practical definition of massive hemoptysis is that which is acutely life-threatening. Although massive hemoptysis is uncommon, it is potentially lethal and has a mortality rate of between 9% and 59%.1 The management of patients with massive hemoptysis requires a team approach, with involvement from specialists in intensive care, pulmonology, interventional radiology, and thoracic surgery.

ETIOLOGY

The causes of massive hemoptysis are listed in Table 26-1. Tuberculosis is the most common cause worldwide, but in developed countries chronic inflammatory lung diseases (e.g., bronchiectasis) and lung cancer are the most common causes.

Table 26-1 Causes of Massive Hemoptysis

Neoplastic Bronchial carcinoma
  Metastatic lung cancer
  Leukemia
Infectious Bronchiectasis
  Bronchitis
  Tuberculosis
  Fungal infections
  Paragonimiasis (parasitic lung fluke)
  Hydatid cyst
Vascular Pulmonary infarction or embolism
  Mitral stenosis
  Bronchoarterial fistula
  Rupture of a thoracic aortic aneurysm
  Arteriovenous malformation
Vasculitic Wegener granulomatosis
  Behçet disease
  Goodpasture syndrome
  Systemic lupus erythematosus
Miscellaneous Anticoagulant therapy
  Coagulopathy
  Trauma
  Lymphangioleiomyomatosis
Iatrogenic Pulmonary artery rupture secondary to a pulmonary artery catheter
  Malposition of a chest drain
  Tracheoarterial fistula

Adapted from Jean-Baptiste E: Clinical assessment and management of massive hemoptysis. Crit Care Med 28:1642-1647, 2000.

In the majority of cases massive hemoptysis is caused by bleeding from branches of the bronchial arteries. Bleeding from branches of the pulmonary artery accounts for less than 10% of cases. Occasionally, microvascular (alveolar) bleeding occurs secondary to an immune-mediated vasculitis.

There are normally three bronchial arteries, one on the right and two on the left. The right-sided artery usually arises from the third posterior intercostal artery, whereas the two left-sided arteries usually arise directly from the aorta. The bronchial circulation normally receives less than 1% of the cardiac output, but with chronic inflammatory lung disease, the bronchial vessels undergo marked proliferation and this percentage increases. Because the bronchial arteries are part of the systemic circulation, bleeding from these arteries tends to be more dramatic than that from the lower pressure pulmonary arterial system. Bronchial arterial bleeding is almost always the source of bleeding in patients with chronic inflammatory lung disease. It may be controlled by bronchial arterial embolization and vasoactive drugs.

Pulmonary arterial bleeding tends to occur because of ulceration of the vascular wall due to a locally destructive process, such as necrotizing lung cancer, necrotizing pneumonia, or a cavitating aspergilloma, and it is less amenable to control by vasoactive substances or embolization. However, these conditions more commonly cause bronchial artery bleeding. Evidence of pulmonary arterial bleeding may be obtained from the circumstances (e.g., following manipulation of a pulmonary arterial catheter) or from a negative bronchial arteriogram. Hemoptysis that occurs following lung transplantation is due to pulmonary arterial bleeding because the bronchial arteries are not reimplanted at the time of surgery.

DIAGNOSIS AND TREATMENT

As in all situations in which a patient develops an acute critical illness, diagnosis and treatment must proceed in parallel. An algorithm for the diagnosis and management of massive hemoptysis is provided in Figure 26-1.

Immediate Resuscitation and Lung Isolation

As little as a few hundred milliliters of blood within the alveolar space can cause impaired gas exchange. Thus, massive hemoptysis will cause death by asphyxia well before hypovolemic shock develops. The primary goal during resuscitation is to achieve adequate oxygenation.

All patients should be admitted to the intensive care unit, receive high-flow face-mask oxygen, and be monitored by pulse oximetry, an electrocardiogram, and an intraarterial catheter. Large-bore intravenous cannulas should be inserted, and blood loss should be replaced with crystalloid solution or blood transfusion as appropriate. A chest radiograph should be sought urgently and blood samples obtained for arterial blood gas analysis, complete blood count, cross-match, coagulation studies, electrolytes, and renal- and liver-function tests. Coagulopathy should be corrected by blood component therapy and, if appropriate, vitamin K.

If it is known which lung is bleeding, the patient should be positioned on his or her side, with the bleeding lung dependent so as to minimize soiling of the nonbleeding lung. Other maneuvers that can be tried include antifibrinolytic therapy (see Chapter 30), nebulized epinephrine (5 mg in 5 ml doses repeated every 15 minutes), and intravenous vasopressin. The recommended dose of vasopressin in this situation (20 units over 15 min followed by an infusion of 0.2 units/min.3) is very high and must be used with caution in patients with cardiac disease or hypovolemia.

When there is severe impairment in gas exchange (Sao2 <90% on high-flow face-mask oxygen) or marked respiratory distress, the patient should be intubated and ventilated with a large (8.5 to 9 mm internal diameter) single-lumen endotracheal tube. Intubation usually improves gas exchange but increases the likelihood of clot obstruction of the trachea and does not prevent soiling of the nonbleeding lung.

Blood clots within the tracheobronchial tree can cause an abrupt deterioration in gas exchange or failure of ventilation. In this situation, hand ventilation with a manual resuscitator and repeated endotracheal lavage with 0.9% saline (5 to 10 ml) followed by suctioning should be repeated until the obstruction is cleared. If this maneuver fails, the endotracheal tube should be replaced.

Following intubation, fiberoptic bronchoscopy should be performed to identify the site of bleeding and, if necessary, to achieve endobronchial control. Endobronchial control involves isolation of the bleeding lung and selective ventilation of the nonbleeding lung. It is required if bleeding remains active despite intubation. Two methods to achieve endobronchial control are (1) selective endobronchial intubation and (2) the use of a bronchial blocker. Endobronchial intubation is achieved by advancing the endotracheal tube into the left or right main bronchus under bronchoscopic guidance. This technique works best when selective intubation of the left main bronchus is required (for bleeding from the right lung) because with intubation of the right main bronchus (for bleeding from the left lung), the cuff of the endotracheal tube is likely to occlude the origin of the right upper lobe bronchus. A number of purpose-designed endobronchial blockers are available for lung isolation. One device, the Arndt endobronchial blocker (Cook Critical Care, Bloomington, IN), features a balloon-tipped catheter with an endoscopic snare (Fig. 26-2). With the bronchoscope placed through the snare, the tip of the catheter can be directed over the bronchoscope into the left or right main bronchus. The balloon is then inflated, and lung isolation is achieved.

image

Figure 26.2 Arndt Endobronchial Blocker (Cook Critical Care, Bloomington, IN.) See text for details.

(From Grocott HP, Scales G, Schinderle D, et al: A new technique for lung isolation in acute thoracic trauma. J Trauma 49:940-942, 2000.)

As an alternative to bronchoscopically guided endobronchial control, insertion of a double-lumen tracheobronchial tube may be considered (see Chapter 40, Fig. 40-6). However, in patients with massive hemoptysis, accurate placement of these tubes can be very difficult, and physicians who are unfamiliar with these devices should not attempt this procedure. These techniques of lung isolation are only temporizing measures to allow adequate gas exchange to be achieved while more definitive diagnosis and treatment are organized.

Diagnosis, Localization, and Control of the Bleeding Site

Computed Tomography Scanning

High-resolution contrast-enhanced CT scans may provide important diagnostic information that is not apparent on a chest radiograph, particularly the presence of bronchiectasis or small lung cancers.4,6 The CT scan may also suggest a diffuse microvascular cause of the bleeding (e.g., vasculitis or pulmonary venous hypertension secondary to mitral stenosis).

Bronchial Artery Angiography and Embolization

Selective bronchial artery angiography using coils, foam, or other materials allows identification of the bleeding vessel and its embolization. Indicators of a likely site of bleeding include extravasation of dye or the finding of aneurysmal or tortuous vessels. Acute control of hemorrhage is possible in more than 90% of cases.7,8 However, on occasion bleeding begins again within the first few days, so repeated embolization is required. Failure of bronchial artery embolization is usually due to the presence of collateral vessels from the phrenic artery, intercostal, mammary, and subclavian arteries. Embolization of the spinal artery causing spinal cord ischemia may occur when the spinal artery arises from a bronchial artery, although this risk is very low (<1%).9

SPECIFIC CONDITIONS

REFERENCES

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2 Jean-Baptiste E. Clinical assessment and management of massive hemoptysis. Crit Care Med. 2000;28:1642-1647.

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7 Cremaschi P, Nascimbene C, Vitulo P, et al. Therapeutic embolization of bronchial artery: a successful treatment in 209 cases of relapse hemoptysis. Angiology. 1993;44:295-299.

8 Tanaka N, Yamakado K, Murashima S, et al. Superselective bronchial artery embolization for hemoptysis with a coaxial microcatheter system. J Vasc Interv Radiol. 1997;8:65-70.

9 Cowling MG, Belli AM. A potential pitfall in bronchial artery embolization. Clin Radiol. 1995;50:105-107.

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11 Thomas R, Siproudhis L, Laurent JF, et al. Massive hemoptysis from iatrogenic balloon catheter rupture of pulmonary artery: successful early management by balloon tamponade. Crit Care Med. 1987;15:272-273.

12 Ray CEJr, Kaufman JA, Geller SC, et al. Embolization of pulmonary catheter-induced pulmonary artery pseudoaneurysms. Chest. 1996;110:1370-1373.

13 Kearney TJ, Shabot MM. Pulmonary artery rupture associated with the Swan-Ganz catheter. Chest. 1995;108:1349-1352.

14 Schwarz MI, Brown KK. Small vessel vasculitis of the lung. Thorax. 2000;55:502-510.

15 Grocott HP, Scales G, Schinderle D, et al. A new technique for lung isolation in acute thoracic trauma. J Trauma. 2000;49:940-942.