When Does Bronchial Arterial Embolization Fail To Control Hemoptysis?

turbance. Hyperventilation is a common event during acute panic attacks and there is now the suggestion that at least some patients with panic disorder may have abnormally high sensitivity to inhalation of carbon dioxide. 1 These and other data suggest that at least part of the etiology of panic disorder may be an inherited hypersensitivity of brain stem autonomic nervous system neurons. Administration of anti-panic drugs, such as imipramine, may act to block panic attacks by reducing the threshold for response of these neurons. 2 It is also increasingly clear that panic disorder patients suffer from ingrained cognitive abnormalities by which they misconstrue and catastrophize a host of trivial somatic sensations. Recent advances have been made to develop specific cognitive and behavioral psychotherapies that directly address this problem and that work well in conjunction with pharmacologic treatment. Yellowlees and Kalucy postulate convincingly that asthma may involve the same two problems. Like the patient with panic disorder, at least one set of asthmatic patients undoubtedly inherits an organic respiratory hypersensitivity leading to episodic bronchoconstriction. At the same time, asthmatic patients appear to suffer from anxiety disorder and to exaggerate the significance in some instances of respiratory sensations to the point that they "cognitively" induce an asthma attack. It is intriguing that imipramine appears to have some efficacy in treating asthma. While this may in part be due to an intrinsic bronchodilator effect of the tricyclic drug, Yellowlees and Kalucy suggest that it may also represent the re-regulation of the same autonomic hyperactivity postulated to occur in panic patients. By the same token, it appears worthwhile to consider the possibility that the same kind of cognitive/ behavioral treatments now being tested for panic patients may be efficacious in controlling some aspects ofasthma. Perhaps asthmatic patients should be taught how to systematically control their respiration at the first suggestion of worsening asthma and to avoid the cognitive triggering of unnecessary anxiety and hyperventilation. In recent years we have learned that the central nervous system functions to affect and even control a variety of peripheral systems. We know, for example, that most organs of the immune system are directly innervated by the brain and that stimulation of specific brain centers can routinely induce arrhythmias in experimental animals. Yellowlees and Kalucy add to the growing list of diseases that undoubtedly have central nervous system involvement by pointing to the overlap between anxiety disorder and asthma and the effect of stress on asthmatic symptoms. Their suggestions for future research should be eagerly acted upon.

Jack M. Gorman, M.D.

New York Chief, Division of Clinical Psychobiology, College of Physicians and Surgeons of Columbia University. REFERENCES

1 Connan JM, Fyer MR, Goetz R, Askanazi J, Liebowitz MR, et al. Ventilatory physiology of patients with panic disorder. Arch Gen Psychiatry 1988; 45:31-9 2 Connan JM, Liebowitz MR, Fyer AJ, Stein J. A neuroanatomical hypothesis for panic disorder. Am J Psychiatry 1989; 146:148-61

When Does Bronchial Arterial Embolization Fall To Control Hemoptysis?* Massive and untreated hemoptysis is associated with a mortality of greater than 50 percent. Since the bleeding is from a bronchial arterial source in the vast majority of patients, embolization of the bronchial arteries (BAE) has become an accepted treatment in the management of massive hemoptysis because it achieves immediate control of the bleeding in 75 to 90 percent of the patients. 1·3 Thus, in 10 to 25 percent of the patients hemoptysis is not controlled by this procedure. Moreover, of the patients with initially successful embolization, about 20 percent rebleed, usually within the first six months. Katoh et al, in an article appearing in this issue of Chest, (see page 541) examine the anatomic basis for recurrent hemoptysis following an initially successful BAE. The morphologic changes in the bronchial arterial system that make BAE effective in hemoptysis also seem to defeat its role in some patients. Chronic inflammatory diseases of the lung constitute the most common causes of massive hemoptysis. The alterations in the bronchial arterial system in these inflammatory processes are well documented. 4 •5 There are two kinds of failure associated with BAE; the procedure fails to control bleeding or the patient rebleeds after an initially successful BAE. The mechanisms of each type of failure are different. The important causes of initial failure are the following: (1) extensive and bilateral disease, which is more common in patients who have repeated episodes of massive hemoptysis, probably reflecting the chronicity of the disease; these patients have poor prognosis; in one series, 60 percent of such patients did not respond to any therapy and died; 1 (2) technical failures include inability to catheterize or achieve a secure catheter position in the bronchial artery for a safe BAE; small bronchial arteries, tortuous aorta, and anomalous or aberrant origins of the bronchial arteries are some of the other reasons; and (3) pulmonary artery origin of the bleeding is rather uncommon and CHEST I 97 I 3 I MARCH, 1990

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was seen in less than 10 percent of the patients;3 the specific conditions causing the pulmonary arterial bleeding in this group are acute and chronic lung abscess and tuberculosis; such patients can be treated by either surgery and/or embolization of the pulmonary arterial branches. 6 Recurrence of hemoptysis following an initially successful BAE is more common. The most important causes are incomplete embolization, progression of the native disease, and recanalization of the embolized vessels. Probably all three factors operate in each patient, to a varying degree. The first two are clearly more important. Incomplete embolization is often due to inadequate evaluation of the non bronchial systemic collateral circulation. 7 These are most extensive in aspergillosis and pleuropulmonary tuberculosis. The contribution of the collateral circulation may be underestimated as the angiographer frequently depends on indirect signs of pulmonary hemorrhage such as hypervascularity and systemic-pulmonary shunt. The extent to which the systemic collateral vessels exhibit these indirect signs is variable and the findings may be less than striking, particularly when the bronchial arteries are the primary source of the bleeding. Complete evaluation of all the collateral circulation can be very lengthy and in many cases has to be performed in stages. Recruitment of new collateral channels is an extremely variable event. I suspect that this is more frequent in the presence of active infection. Botenga8 has shown that in chronic inflammatory diseases, systemic-pulmonary shunts can appear in the presence of acute infection and disappear when the infection is treated. Presence of such shunts would be an additional factor in further collateral formation. The suggestion of combining regional antibiotic infusion with BAE in selected patients may have some merit. 3 The choice of embolic material is also important. Some authors suggest that an absorbable gelatin sponge (Gelfoam) is adequate for long-term BAE. However, a more permanent occlusive material such as a polyvinyl sponge (Ivalon) may be preferable. In BAE it is equally important to occlude the bronchial arterial capillary bed as well as the more proximal segments since bleeding may also result from rupture of thin-walled, precapillary, radicles of the bronchial arteries in the walls of the segmental bronchP Ivalon was thought to result in permanent vascular occlusion.9·10 Katoh et al have shown that arteries embolized with Ivalon and Gelfoam can also recanalize. Two factors may play a role. The commonly used Ivalon particles are between 150 and 250 J,Lm in diameter. The macroscopic anastomoses between the bronchial and pulmonary artery branches can be larger than 200 J.Lm even in normal lungs; these certainly hypertrophy to even larger size in diseased states. So, a variable number of these particles probably end up in 518

the pulmonary circulation rather than in the bronchial capillary bed. Almost all angiographers use Gelfoam pieces to effect proximal occlusion. lvalon plugs may be more permanent. A safe intravascular sclerosing agent, once found, may be more suitable to achieve the desired peripheral and proximal occlusion. Finally, it must be realized, as pointed out by Katoh et al, that BAE is only a palliative procedure and does not cure the underlying disease that caused the hemoptysis in the first place. Though not perfect, BAE still achieves its goals of stopping massive hemoptysis, comparable to any other single treatment choice in this difficult to manage clinical complex. Hrudaya Nath, M.D. Birmingham, Alabama Department of Radiology, Cardiopulmonary Section, The University of Alabama at Birmingham. Reprint requeBts: Dr. Nath, Cardiopulmonary Section/Rtuliology, 619 South 19th Street, Binningham, Alabama 35233 REFERENCES

1 UOacker R, Kaemmerer A, Picon PD, Rizzon CFC, Neves CMC, Oliveira ESB, et al. Bronchial artery embolization in the managment of hemoptysis: technical aspects and long-term results. Radiology 1985; 157:637-44 2 Remy J, Arnaud A, Fardou H, Giraud R, VOisin C. Treatment of hemoptysis by embolization of bronchial arteries. Radiology 1977; 122:33-7 3 Rabkin JE, Astafjev VI, Gothman LN, Grigorjev YC. Transcatheter embolization in the management of pulmonary hemorrhage. Radiology 1987; 163:361-65 4 Cudkowicz L. The blood supply of the lung in pulmonary tuberculosis. Thorax 1952; 7:276-78 5 Marchand P, Gilroy JC, Wtlson VH. An anatomical study of the bronchial vascular system and its variations in disease. Thorax 1950; 5:207-21 6 Remy J, Lemaitre L, Lafitte JJ, Vilain MO, Michel JS, Steenhouwer F. Massive hemoptysis of pulmonary arterial origin: diagnosis and treatment. AJR 1984; 143:963-69 7 Keller FS, ROsch J, Loftin TG, Nath PH, McElvein RB. Nonbronchial systemic collateral arteries: significance in percutaneous embolotherapy ror hemoptysis. Radiology 1987; 164:687-92 8 Botenga ASJ. The role of bronchopulmonary anastamoses in chronic inftammatory processes of the lung. AJR 1968; 104:829-

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9 Tadavarthy SM, Moller JH, Amplatz K. Polyvinyl alcohol (lvalon)-a new embolic material. AJR 1975; 125:609-16 10 White Rl Jr, Strandberg Jv. Gross GS, Barth KH. Therapeutic embolization with long-term occluding agents and their effects on embolized tissues. Radiology 1977; 125:677-87

Needle Aspiration in Lung Cancer Risk of Tumor Implantation Negligible

Is Not

Therecurrence recent unfortunate experience of chest wall of lung cancer at the site of previous

fine needle aspiration biopsy seven months following