Mycotic Aneurysms of the Pulmonary Arteries in

Intravenous Drug Addicts

Report of Three Cases and Review of the Literature

CARLOS NAVARRO, M.D.

P. C. TAYLOR DICKINSON, M.D.

PREETHAM KONDLAPOODI, M.D.

JACK W. C. HAGSTROM, M.D.

New York, New York

From the Departments of Pathology and Medicine, Harlem Hospital Center, College of Physicians and Surgeons of Columbia University, New York, New York. Requests for reprints should be addressed to Dr. Carlos Navarro, Department of Pathology, KP 8115, Harlem Hospital Center, 506 Lenox Avenue, New York, New York 10037. Manuscript accepted July 29, 1983.

During the postmortem study of pulmonary lesions in intravenous drug addicts, three patients were found to have bilateral multiple mycotic aneurysms of the peripheral pulmonary arteries in associ- ation with embolic pneumonia. Two of these patients had infective tricuspid endocarditis, and one had hemoptysis. This report draws attention to the occurrence of mycotic aneurysms in this unusual location and suggests that these pulmonary lesions may be more common than currently believed.

Intravenous drug addiction carries a high risk of serious infectious complications, including infective endocarditis [ 11, bacterial pneu- monia [2], and septic pulmonary emboli [3]. Mycotic aneurysms have been reported in this population, but aside from a single instance in- volving the pulmonary arteries [4], all have occurred in the systemic circulation [5-131 (Table I). Mycotic aneurysms of the pulmonary arteries are rare and usually occur in the presence of infective en- docarditis and congenital heart disease [4,14-351 (Tables II and Ill). This report describes three new cases of intrapulmonary mycotic aneurysms in intravenous drug addicts.

Two recent consecutive intravenous drug addicts with pulmonary mycotic aneurysms were seen during the routine review of autopsy cases at the Harlem Hospital Center. A search of the autopsy records from January 1, 198 1, to December 31, 1982, disclosed only one more case with history of intravenous drug addiction and pulmonary mycotic aneurysms, for a total of three of 25 consecutive intravenous drug addicts undergoing autopsy. During this period, there were 38,876 admissions to the institution, of which 1,350 were patients with a history of intravenous drug addiction. In no instance was the diagnosis of mycotic pulmonary aneurysms made clinically.

One other case [4] was recovered from a total of 68 cases of mycotic pulmonary aneurysms collected in the worldwide literature from 1878 to 1982 (Tables II and Ill). Interestingly, a recent necropsy study of pulmonary vascular lesions in 70 intravenous drug addicts did not reveal mycotic aneurysms [36].

CASE REPORTS

Patient 1. Six weeks prior to admission to Harlem Hospital Center, this 34-year-old black woman had delivered a normal full-term child. A month later she was seen in the emergency room complaining of right buttock pain of two weeks’ duration, sore throat of one week’s duration, chills and fever to 38.4% nonproductive cough, and right-sided pleuritic chest pain of one day’s duration. Evaluation at that time revealed egophony, diminished breath sounds, and dullness to percussion at the base of the right lung. Hematocrit was 35 percent, white blood cell count 21,800/mm3, with 80 percent neu-

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trophils, 3 percent band forms, 12 percent lymphocytes, and 5 percent monocy-tes. An infiltrate in the right lower lobe was seen on chest roentgenography. The patient refused ad- mission and was discharged from the emergency room with erythromycin, which she discontinued herself after three days.

Ten days before admission, the patient noted scleral ict- erus and dark urine without changes in the stool. On admis- sion, she complained of a cough of five days’ duration pro- ductive of yellow sputum with flecks of blood and accom- panied by right-sided pleuritic chest pain as well as pain in the right upper abdominal quadrant, left hip, and lumbosacral region.

Past history was significant for two episodes of chole- cystitis with cholelithiasis diagnosed by abdominal ultrasound. There was no history of alcohol abuse, hepatitis, blood transfusion, rheumatic fever, heat-t murmur, or endocarditis. She admitted to long-standing intravenous drug addiction and had been in a methadone maintenance program for the previous 10 years. She denied current illicit drug use.

On admission, temperature was 36.4% blood pressure 120/78 mm Hg, pulse 100 per minute, and respiratory rate 28 per minute. She had scleral icterus, scattered inspiratory rales in both lungs, a grade II/VI early systolic murmur heard loudest over the lower sternal border, hepatomegaly, and a palpable spleen tip. The rest of the physical examination was unremarkable.

Laboratory results included hemocrit of 31 percent, leu- kocyte count 7,200/mm3, with 77 percent neutrophils, 4 percent band forms, 9 percent lymphocytes, 5 percent mo- nocytes, 1 percent basophils, 2 percent metamyelocytes, and 2 percent myelocytes. Platelets were diminished. Uri- nalysis revealed 4+ bilirubin but no cells or organisms. The prothrombin time was 13.9/l 1.7 seconds, blood urea nitrogen 28 mg/dl, creatinine 10 mg/dl, glucose 76 mg/dl, sodium 131 meq/liter, potassium 44 meq/liter, chloride 102 meq/liter, bicarbonate 21 meq/liter, arterial pH 7.43, pOn 70 mm Hg, pC02 32 mm Hg, and oxygen saturation 93 percent while breathing room air. Roentgenography of the chest revealed bilateral fluffy infiltrates. Staphylococcus aureus grew in four out of four blood culture specimens obtained on the night of admission.

On the morning following admission, her temperature had risen to 38.4’C, and analysis of the arterial blood revealed a pH of 7.36, pOn 46 mm Hg, pCOp 27 mm Hg, and oxygen saturation 79 percent. Subconjunctival hemorrhages were noted. Results of two-dimensional echocardiography were interpreted as consistent with a tricuspid vegetation with prolapse into the right atrium. The patient began receiving oxacillin, 2 g intravenously every four hours, and gentamicin, 80 mg intravenously every eight hours.

Further laboratory results included bilirubin 9 mg/dl, al- kaline phosphatase 297 units/liter, serum glutamic oxalo- acetic transaminase 193 units/ml, serum glutamic pyruvate transaminase 242 units/ml, and lactic dehydrogenase 388 units/ml. Bone marrow aspiration showed hypercellularity, with a myeloid-to-erythroid ratio of 8: 1, normal megakaryo- cytes, 8 percent megakaryocytes, 8 percent plasma cells, and normal maturation and morphology.

The patient’s respiratory status worsened, necessitating

MYCOTIC

TABLE I

ANEURYSMS IN DRUG ADDICTS--NAVARRO ET AL

Published Cases of Mycotic Aneurysms of Systemic Arteries in Intravenous Drug Addiction

Number of Location References Cases (arteries) Microorganisms

151 5 Femoral, Staphylococcus, brachial, Clostridium superior mesenteric

;;I 1 Right subclavian Staphylococcus 4 Common Peptostreptococcus,

femoral, Proteus, brachial Enterobacter,

Staphylococcus, Enterococcus

[8-131 14 Cerebral Staphylococcus, Streptococcus, Pseudomonas, Neisseria, Candida, Herrelia

vaginicola

transfer to the intensive care unit. Blood gas determination at this time revealed a pH of 7.37, ~02 61 mm Hg, pCOn 33 mm Hg, and oxygen saturation 89 percent while breathing 50 percent oxygen by Venturi mask. The patient underwent intubation and received mechanical ventilation; however, her condition continued to deteriorate and she had a cardiopul- monary arrest 36 hours after admission.

Postmortem studies disclosed extensive nodular yellow-red consolidation of the lung parenchyma bilaterally in association with diffuse acute congestion and edema. Each lung weighed slightly over 1,000 g. Bilateral fibrinous pleuritis without effusion was present. The right middle lobe contained a 3 cm abscess. Microscopically, the foci of consolidation corre- sponded to severe, confluent lobular pneumonia with pre- dominant distribution of the alveolar inflammation around small arteries as compared with a much lesser degree of inflammatory infiltration of the lumens of the bronchial air- ways and immediately dependent alveolar spaces. There were also scattered microabscesses in all lobes. Some of the abscesses were in direct continuity with mycotic aneu- rysms arising in small peripheral pulmonary arteries. Eight aneurysms were present in random samples, two in the right upper lobe, one in the right middle lobe, three in the right lower lobe, and two in the left upper lobe. They ranged in greatest diameter from 0.5 to 3 mm, as measured on the stained paraffin sections. Retrospective gross inspection of the fixed lung tissue did not disclose aneurysmal lesions. In all but one of the aneurysms, the vascular walls were ex- tensively necrotic and densely infiltrated by neutrophils. At the sites of necrosis, there was loss of elastic laminae and outward bulging of the vessel wall (Figure 1). The lumens of the aneurysmal vessels were filled with either abundant leukocytes mixed with blood or fresh thromboemboli. The aneurysm of the right middle lobe was different from the other aneurysms, in that the inflammation and necrosis were confined to a small segment of the wall with focal calcifica-

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TABLE III Reported Isolates In Myootlc Pulmonary Artery Aneurysms’ (1878-1982) [4,14-351

Number Microorganisms of Cases

Staphylococcus aureus 10 Staphylococcus aureus and Aspergillus 1 Streptococcus viridans 4 Streptococcus viridans and Klebsiella aerobacter 1 Streptococcus species 9 Proprionibacterium acnes 1 Diphtheroids 1 Actinomyces 1

l By blood culture and/or culture of cardiac vegetation in 28 of 40 cases with cultures.

tion of adjacent areas (Figure 2). f&y other nonaneurysmal arteries had foreign-body granulomas in their adventitia or nearby ihterstitium. Other significant findings consisted of infective endocarditis of the tricuspid valve, pyogenic hep- atitis, meningoencephaiitis, myocarditis, splenitis, myosiiis, and interstitial nephritis. Focal, segmental necrotizing glo- merulonephritis was also present. In addition, there were three chronic gastric ulcers. Patient 2. This 33-year-old homosexual black man was initially admitted to Harlem Hospital Center three months prior to his final admission. At that time, he gave a two-week his- tory of cough productive of red-green sputum, shortness of breath, and high fever. He also gave a seven-year history of intravenous drug addiction for which he had received meth- adone maintenance for four years.

Physical examination revealed a blood pressure of 100/70 mm Hg, pulse rate 120 per minute, respiratory rate 26 per minute and temperature 39.5OC. There were multiple skin ulcers over the upper and lower extremities. He had rales over the right lower and middle lung fields, and a grade II/VI systolic ejection murmur was heard at the left sternal border. The liver was slightly enlarged.

l&oratory values included hemocrit 22 percent, leukocyte count 10,000/mm3, with 79 percent neutrophils, 2 percent band forms, 16 percent lymphocytes, and 1 percent mono- cytes. The platelets were increased in number. The results of urinalysis were normal. The serum creatinine was 1.0 mg/dl, sodium 123 meq/liter, potassium 44 meq/liter, chloride 92 meq/liter, and bicarbonate 25 meq/liter. The bilirubin was 1.6 mg/dl, alkaline phosphatase 313 units/liter, serum glutamic oxaloacetic transaminase 176 units/ml, and prothrombin time 14.5112.3 seconds. Both S. aureus and group A beta-hemolytic Streptococcus grew in three of three blood culture specimens obtained at admission. Roentgen- ography of the chest showed bilateral, multiple, thick-walled abscesses with air-fluid levels. He was given oxacillin, 2 g intravenously every four hours. Serial echocardiography revealed the development of a tricuspid vegetation.

The pulmonary lesions gradually healed over the period of hospitalization. After one month in the hospital, Klebsiella pneumoniae bacteremia developed from a contaminated intravenous catheter, and the patient was given cephalothin,

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Figure 1. Mycotic aneurysm of pulmo- nary artery. The internal elastic lamina (white mows) disappears at the site of bulging of the vessel wall (black arrows) where dense inflammatory exudate thickens the wall. The vessel lumen is filled with a septic thromboembolus (VerhoenL elastic stain; original magni- fication X 35, reduced by 30 percent).

2 g intravenously every four hours, and rifampin, 300 mg orally twice a day for the last two weeks of hospitalization. He was discharged five weeks before his final admission. He had received antibiotic therapy for a total of 64 days during this admission.

Two weeks before his final admission, he noted increased swelling of his ankles. One week later, he experienced right-sided pleuritic chest pain, fever, chills, night sweats, and cough productive of white sputum. He did not have hemop- tysis. On physical examination, he was cachectic, with a blood pressure of 90160 mm Hg, pulse rate of 76 per minute and temperature of 36.0°C. Examination of the chest re- vealed dullness to percussion and scattered rales in the right lung base. A grade II/VI systolic murmur, loudest over the xiphoid, could be heard. Both the liver and spleen were pal- pable. Pitting edema was present up to the knees. The he- matocrit was 32 percent, white blood cell count 26,000/mm3, with 72 percent neutrophils, 22 percent band forms, 2 percent lymphocytes, 1 percent atypical lymphocytes, and 3 percent monocytes. Echocardiography again demonstrated a vege- tation on the tricuspid valve. Five of five sets of blood cultures grew S. aureus and diphtharoids. Sensitivity studies indicated that the S. aureus was resistant to oxacillin. Roentgenography of the chest was interpreted as showing consolidation in the right upper lobe, infiltrates in tha right middle and lower lobes and effusion at the base. There were multiple cavitary lesions of varying size bilaterally. Right-sided thoracentesis on the second hospital day produced bloody fluid with a leukocyte count of 6/mm3, of which 50 percent were polymorphonu- clear leukocytes and 50 percent were lymphocytes. Cultures grew S. aureus and diphtheroids. Despite repeated thora- centesis and intravenous vancomycin therapy, empyema progressed. On the ninth hospital day, he was transferred to the intensive care unit for management of deteriorating cardiovascular status. The following morning, he had a res- piratory arrest and died.

At necropsy, the gross and microscopic appearances of the lungs were very similar to those in Patient 1, including the presence of multiple small abscesses bilaterally, measuring up to 0.3 cm in diameter. The same pattern of angiocentric inflammation was present. There were two mycotic aneu- rysms, one in the left upper lobe and one in the right middle lobe, measuring 2 and 1.5 mm in greatest diameter. As in Patient 1, retrospective review of the lung tissue grossly re- vealed no aneurysmal lesions. Numerous gram-positive cocci were present at sites of pneumonia and abscesses. In addi- tion, both lungs contained multiple old recanalized throm- boemboli in peripheral arteries, in addition to small twisted arteries with focal expansions and irregular lumina suggestive of early plexiform lesions. Other significant findings were tricuspid valve endocarditis with the presence of abundant gram-positive cocci within the vegetations, scattered cerebral abscesses, and multiple “punched out” cutaneous ulcers of all extremities suggestive of “skin popping.” Patient 3. A 27-year-old black woman was brought to the emergency room with tachycardia of 134 beats per minute and without detectable blood pressure. Her extremities bore the scars of intravenous drug addiction. The scanty history available indicated one week of dyspnea and precordial chest pain. She had denied fever or chills. She had been in a methadone maintenance program for the previous two years but was currently using cocaine. After initial resuscitative efforts, her blood pressure was 100/60 mm Hg, pulse rate 140 per minute, temperature 36.5OC, and respiratory rate 40 per minute. The lungs were clear to percussion and auscul- tation. No murmurs were heard. There was no neck stiffness nor any focal neurologic signs.

Laboratory values included hematocrit 30 percent, white blood cell count 5,200/mm3, with 60 percent neutrophils, 38 percent lymphocytes, and 2 percent monocytes. The platelet count was normal. The serum creatinine was 2.6 mg/dl, blood urea nitrogen 25 mg/dl, sodium 137 meq/liter, potassium 31

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meq/liter, chloride 101 meq/liter, and bicarbonate 18 meq/liter. Blood cultures grew S. aureus in four of four sets. Roentgenography was not performed. Within an hour of ad- mission, respiratory failure developed, and despite intensive resuscitative efforts, she died 12 hours later.

The postmortem findings were again very similar to those in Patients 1 and 2 both grossly and microscopically, except for the absence of abscesses despite the necrotizing char- acter of the pneumonia. Again, angiocentric predominance of the alveolar inflammation was present. An additional striking finding was the presence of septic thromboemboli in numerous alveolar capillaries, venules, and small arteries, with the presence of numerous gram-positive cocci in many of them. Fresh bland thromboemboli were also present in several small peripheral arteries bilaterally. Four mycotic aneurysms were present in the right upper lobe and one in the left upper lobe, each measuring 0.5 mm in diameter. One pulmonary vein was the site of segmental acute inflammation and necrosis without aneurysmal dilatation. The cardiac valves were grossly normal, although the leaflets of the mitral valve were focally infiltrated by a few neutrophils and con- tained areas of fibrosis with capillarization microscopi- cally.

RESULTS AND REVIEW OF THE LITERATURE

Clinical Features and Pathology. The significant clinical features and pathologic findings in our three patients and the patient of Jaffe and Condon [4] are summarized in Table IV. Table II lists the significant characteristics of 68 reported cases of pulmonary mycotic aneurysms, 67 of which involved patients without history of intravenous drug addiction and one patient with such a history [4] included in Table IV.

The most frequently reported manifestations of an-

Figure 2. Partially healed mycotic an- eurysm. One segment of the vessel wall is thickened by extensive calcification (arrows) and residual inflammation (hematoxylin and eosin stain: original magnification X 25, reduced by 30 per- cent).

eurysms of the pulmonary arteries, regardless of vessel size and location, and whether mycotic or not, are dyspnea, cyanosis, and hemoptysis [5,7,37]. When the aneurysm involves the pulmonary trunk or one of its major mediastinal or hilar branches, there may be a sensation of chest “fullness,” pulsations, thrills, harsh systolic murmur in the second left intercostal space, and hypertrophy of the right heart with right axis deviation on electrocardiography [ 171. The differential diagnosis from aortic aneurysms, idiopathic dilatation of the pulmonary artery, patent ductus at-teriosus, and atrial septal defect [ 171 is difficult since the same clinical features may be present in all these conditions. Although dyspnea, cyanosis, and hemoptysis are also described in patients with aneurysms involving the peripheral pulmonary branches [25], the chest signs of the centrally located aneurysms, however, are usually absent [4].

Cyanosis was not a feature in any of our patients or in that of Jaffe and Condon (Table IV). Cough and dyspnea, however, were frequent complaints. Chest pain and fever were also observed but are so commonly found in association with right-sided endocarditis as to render them too nonspecific to suggest pulmonary mycotic aneurysm.

Hemoptysis was observed in one of our three patients and in Jaffee and Condon’s patient (Table IV), but in no case was it hemodynamically significant. Although hemoptysis has been reported as a complication of intravenous drug addiction [38], it was also present in 17 of the 67 patients without intravenous drug addiction with pulmonary mycotic aneurysms (Table II). In two of

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these 17 patients, a ruptured intrapulmonary mycotic aneurysm was confirmed [ 19,351. In 12 other patients for whom no mention of hemoptysis was made, a rup- tured mycotic aneurysm was nevertheless found at surgery or at autopsy [22,26]. Ruptured aneurysm was, in fact, responsible for the death of 20 of 27 patients for whom the cause of death was recorded. Pulmonary infarction, with or without cavitation, may also account for hemoptysis in patients with tricuspid endocarditis [38]. Multiple recent pulmonary infarcts were present in one of our patients (Table IV); however, no hemop- tysis developed and no tricuspid endocarditis was found.

Two of our three patients had florid tricuspid valve endocarditis, whereas the third patient had changes consistent with residual endocarditis in the mitral valve and evidence of sepsis (Table IV). The patient of Jaffe and Condon’s [4] also had septicemia and had ques- tionable tricuspid endocarditis. In comparison, of the 67 patients with pulmonary mycotic aneurysms who did not have a history of intravenous drug addiction, 47 had infective endocarditis, 12 had systemic infection without endocarditis, and data were insufficient to establish either sepsis or endocarditis in the remaining eight (Table II). Of the 70 patients with a history of intravenous drug addiction who did not have evidence of pulmonary mycotic aneurysms [36], none had right-sided endo- carditis or was septic except one patient with left-sided endocarditis.

Embolic pneumonia was a significant finding in all three of our patients and was also recorded in Jaffe and Condon’s patient (Table IV). In our patients, embolic pneumonia was more severe in areas surrounding mycotic aneurysms than in those without aneurysms. More importantly, a striking angiocentric pattern of in- flammation was present whether or not the vessel was aneurysmal or contained septic material, whereas the bronchial airways and peribronchial lung parenchyma were totally free of inflammation or much less affected. This is evidence of the primarily embolic origin of the pneumonia in these patients.

The pulmonary aneurysms in our three patients were all peripherally located, whereas in Jaffe and Condon’s [4] patient, the aneurysm was centrally located. The size of the aneurysms in our patients varied from 0.5 to 3 mm in greatest diameter, and none was grossly identifiable. Forty-two of 77 pulmonary aneurysms found in the 67 patients without a history of intravenous drug addiction (Table II) involved the pulmonary trunk and the main extrapulmonary branches. In the remaining 35 intrapulmonary aneurysms in this population, the di- ameter of the mycotic aneurysm averaged 1.1 cm in cases in which size was specifically mentioned. Roentgenographic Flndings. In aneurysms of the pulmonary trunk, perihilar coin lesions with definite

MYCOTIC ANEURYSMS IN DRUG ADDICTS-NAVARRO ET AL

TABLE IV Significant Clinical and Morphologic Features in Four Patients with intravenous Drug Addiction and Pulmonary Mycotlc Aneurysms

Patient 1 2 3 4’

Cough + + - +

Dyspnea + + + + Chest pain + - + -

Fever - + - + Hemoptysis + - - + Tricuspid endocarditis+ + + - ? Embolic pneumonia t + + + Lung abscess t +r - -

Pulmonary thromboemboli + t -f - Pulmonary intarcts - - t - Pulmonary hypertension - + - - Pulmonary aneurysm, main - - - +

branches Pulmonary aneurysm, peripheral + t + -

branches Pyogenic meningitis t t - - Brain abscess t - -

Chronic persistent hepatitis t t t - Microorganisms +5 +§ +s -**

Outcome Dead Dead Dead Alive

l Jaffe and Condon [ 41. + Vegetative. t Cavitated. * Gram-positive cocci in lung parenchyma and aneurysms at au- topsy. l l Klebsiella aerobacter from aneurysm, Streptococcus viridans in blood culture.

vascular connections or rapid change in the contour of the pulmonary artery can be seen on chest roentgen- ography [4,39]. Other helpful findings are encroach- ment of the aneurysmal shadow on the retrosternal space between the aortic arch and the left atrial shad- ows in the right anterior oblique view and impingement upon the inferior aspect of the aortic window in the left anterior oblique view [ 171.

In peripherally located pulmonary aneurysms, the chest roentgenographic appearance is frequently nondiagnostic and indistinguishable from that of in- flammatory, thromboembolic, or neoplastic conditions [4]. Pulmonary angiography is the definitive diagnostic study [37].

In one of our three patients (Patient l), the initial finding on chest roentgenography was an infiltrate in the right lower lobe that developed into bilateral fluffy in- filtrates. The latter corresponded to areas of embolic pneumonia at autopsy. In Patient 2, chest films showed multiple cavitary lesions that were discovered to be abscesses at autopsy. Chest roentgenography in Jaffe and Condon’s [4] case demonstrated consolidation and a thin-walled cavity. An aneurysm was seen on the pulmonary angiography.

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COMMENTS

Aneurysms of any type affecting the pulmonary arteries are extremely uncommon [22]. In a worldwide survey of necropsy data, only eight cases were cited in 109,571 autopsy reports [ 181, and only six instances of pulmonary artery aneurysm were found among 4,126 intrathoracic aneurysms [ 181. Similarly, aneurysms of the pulmonary arteries of mycotic origin are rare enough to be missing from some major reviews of mycotic aneurysms [37,40,41], whereas in other more detailed surveys [ 141, the incidence is very low (5.3 percent) compared with aortic (25 percent), intracranial (12.8 percent), or other major vascular locations.

Reports of mycotic aneurysms of the pulmonary ar- teries in intravenous drug addicts are conspicuously rare in the world literature. We were able to find only one instance [4] among a total of 68 cases of mycotic pulmonary artery aneurysms described in the world literature from 1878 to 1982 (Table II).

The apparent rarity of these lesions in intravenous drug addicts is surprising since the great majority of pulmonary mycotic aneurysms have occurred in the presence of infective endocarditis or septicemia (Table II). Infective endocarditis is a frequent complication of intravenous drug addiction, with more than 50 percent of the cases involving the tricuspid valve [ 11. The rarity, then, of pulmonary mycotic aneurysms in this population is even more surprising, especially considering the significant increase in the incidence of tricuspid en- docarditis from 1.1 percent to 11 percent of all cases of endocarditis during the period from 1938 to 1977 [42,43]. Recurrent thromboembolism has also been mentioned as an important underlying condition in pa- tients with pulmonary mycotic aneurysms [26]. Since endocarditis, septicemia, and pulmonary thromboem- bolism are all commonly seen in intravenous drug ad- dicts [ 11, theoretically, mycotic aneurysms should be frequent in this population. Their absence in a study of pulmonary lesions in 70 intravenous drug addicts [40] probably reflects the fact that none of the patients had right-sided endocarditis, and only one patient had sepsis and left-sided endocarditis.

We believe that mycotic aneurysms of the pulmonary arteries are probably much more frequent in intravenous drug addicts than the recorded literature suggests. The

clinical manifestations of mycotic aneurysms are often nonspecific, particularly when the lesions are located in visceral arteries such as pulmonary [5,7,37]. The characteristic painful tender pulsatile mass of the su- perficially located aneurysm, e.g., femoral artery, is not usually detectable in aneurysms affecting the deep viscera. The suspicion of mycotic aneurysm of the pulmonary artery has to be based, therefore, on indirect evidence.

Embolic pneumonia develops in right-sided endo- carditis probably from the impaction of clumps of bacteria or septic thromboemboli in the pulmonary vasculature [44,45]. In intravenous drug addicts, septic thrombophlebitis of the extremities or subcutaneous abscesses, often seen in these patients, may be another source of septic pulmonary emboli [44] and, potentially, a factor in the development of pulmonary mycotic an- eurysms. The morphologic evidence in our patients also indicates that mycotic aneurysms may serve as one portal of entry into the lung parenchyma in the devel- opment of embolic pneumonia.

Previous authors have emphasized a significant pathogenetic association between pulmonary hyper- tension and the development of mycotic aneurysms in the peripheral pulmonary arteries [26]. In our survey, only one of the four patients with intravenous drug ad- diction (Table IV) and 26 of the 67 patients without in- travenous drug addiction (Table II) had evidence of pulmonary hypertension. Pulmonary hypertension is therefore not essential for the development of mycotic aneurysms in the pulmonary circulation.

This report suggests that mycotic aneurysms of the pulmonary arteries in patients with intravenous drug addiction, particularly those with tricuspid endocarditis, may be more common than currently believed. Their actual incidence and contribution to morbidity and mortality in this patient population will not be known until both clinicians and pathologists actively search for these lesions.

ACKNOWLEDGMENT

Ms. Marilyn E. Lopez assisted in the preparation of this manuscript and Ms. Ella Griffin, Ms. Waveney Rodney, and Ms. Grace Lew provided invaluable technical as- sistance.

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June 1984 The American Journal of Medicine Volume 78 1131