Mural Endocarditis Associated with Recurrent False Aneurysm of the Left Ventricle

s y n d r o m e other than c e r e b r a l h y p o x i a . T o our k n o w l e d g e , t h e adult respiratory distress synd r o m e has not been r e p o r t e d following suicidal h a n g i n g ; h o w e v e r , c e r e b r a l hypoxia u n d o u b t e d l y o c c u r s

during

suicidal hanging, and it c a n b e h y p o t h e s i z e d t h a t t h e subsequent p u l m o n a r y c o m p l i c a t i o n s result from centrineurogenic

adult

respiratory

distress

syndrome.

This

s y n d r o m e c o u l d readily explain t h e p o o r prognosis a n d postmortem

findings

in

previously

reported

victims.

pericardial friction rub and a changing pansystolic murmur appeared during the third week of hospitalization. The presence of a false aneurysm was once again demonstrated on ventriculographic studies. This was successfully repaired, employing cardiopulmonary bypass. The sequence of events in this patient suggests that bacterial endocarditis at the site of a previous cardiomyotomy might have led to the development of the second pseudoaneurysm.

T h e s e findings suggest t h a t respiratory m a n a g e m e n t dir e c t e d t o w a r d s t h e t r e a t m e n t of t h e adult

respiratory

distress s y n d r o m e m a y i m p r o v e t h e prognosis in t h e s e patients.

T n f e c t i v e e n d o c a r d i t i s is a w e l l - r e c o g n i z e d c o m p l i c a tion of c a r d i a c s u r g e r y .

1

A l t h o u g h t h e infection is

generally r e l a t e d t o a r e c e n t l y inserted p r o s t h e t i c v a l v e ,

2

sterile t h r o m b i of platelets a n d fibrin at t h e site of a previous c a r d i o m y o t o m y m a y facilitate m u r a l infection.

REFERENCES 1 Sen Gupta BK: Studies on 101 cases of death due to hanging. J Indian Med Assoc 4 5 : 1 3 5 - 1 4 0 , 1965 2 El-Guindy MK, Abdul-Haleem: Delayed asphyxia: A cause of death in interrupted hanging and throttling. J Egypt Med Assoc 5 4 : 4 1 0 - 4 1 6 , 1971 3 Statistical Abstract of the United States ( 9 6 t h e d ) . US Bureau of the Census, 1975, p 155 4 Berlyne N, Strachan M: Neuropsychiatry sequelae of attempted hanging. Br J Psychiatry 1 1 4 : 4 1 1 - 4 2 2 , 1968 5 Stromgren E : Mental sequelae of suicidal attempts by hanging. Acta Psychiatr Neurol Scand 2 1 : 7 5 3 - 7 8 0 , 1946 6 Ferstenfeld J E , Schlueter DP, Rytel MW, et al: Becognition and treatment of adult respiratory distress syndrome secondary to viral interstitial pneumonia. Am J Med 5 8 : 7 0 9 - 7 1 7 , 1975 7 Petty T, Ashbaugh D G : The adult respiratory distress syndrome: Clinical features, factors influencing prognosis, and principles of management. Chest 6 0 : 2 3 3 - 2 3 9 , 1971 8 Moss G, Staunton C, Stein AA: The centrineurogenic etiology of the acute respiratory distress syndromes: Universal, species-independent phenomenon. Am J Surg 1 2 6 : 3 7 - 4 1 , 1973 9 Moss G, Staunton C, Stein AA: Cerebral hypoxia as the primary event in the pathogenesis of the shock lung syndrome. Surg Forum 2 2 : 2 1 1 - 2 1 3 , 1971 10 Moss G, Staunton C, Stein AA: Cerebral etiology of the "shock lung syndrome." J Trauma 1 2 : 8 8 5 - 8 9 0 , 1972

M u r a l Endocarditis Associated w i t h Recurrent False A n e u r y s m of t h e Left V e n t r i c l e * Silvio Pitlik, M.D.; Leon Cohen, and Joseph Rosenfeld, M.D.

M.D.;

Ruth Melamed,

M.D.;

Acute bacterial endocarditis developed in a 65-year-old man two years after surgical resection of a false aneurysm of the left ventricle. The patient had cerebral embolic manifestations, and coagulase-positive Staphylococcus aureus was cultured from each of six blood samples. A " F r o m the Department of Medicine " C " and the Toor Heart Institute, Beilinson Medical Center, Petah Tiqva, Israel, and the Tel Aviv University School of Medicine, Tel Aviv, Israel. Reprint requests: Dr. Rosenfeld, Beilinson Medical Center, Petach Tikva, Israel CHEST, 7 1 : 2 , F E B R U A R Y ,

1977

E x t e n s i o n of t h e infection f r o m t h e e n d o c a r d i u m l e a d t o disruption of t h e s u t u r e line a n d perforation of t h e v e n t r i c u l a r w a l l .

3

may

consequent

O n r a r e occasions,

this a c c i d e n t m a y result in t h e d e v e l o p m e n t of a false a n e u r y s m of t h e h e a r t .

4

T h i s r e p o r t describes t h e unusual association of a c u t e b a c t e r i a l e n d o c a r d i t i s a n d a false a n e u r y s m of t h e left ventricle. T h e p a t i e n t h a d a previous history of m y o c a r dial infarction followed b y t h e d e v e l o p m e n t of a left v e n t r i c u l a r a n e u r y s m , for w h i c h an a n e u r y s m e c t o m y was p e r f o r m e d . O n e y e a r laser, a false a n e u r y s m d e v e l o p e d at t h e site of t h e previous repair. T h i s , t o o , w a s surgically r e p a i r e d , a n d t h e r e a f t e r t h e p a t i e n t r e m a i n e d well for t w o y e a r s until t h e d e v e l o p m e n t of b a c t e r i a l e n d o c a r d i tis. CASE REPORT A 65-year-old man sustained an anterolateral myocardial infarction in April 1970. Following the infarction, he developed congestive heart failure with ventricular premature beats, for which he was treated with digitalis and quinidine. Clinical examination at that time revealed a paradoxical uplift which was apparent over a wide area of the precordium, and on ventricular angiographic studies a true aneurysm of the left ventricle was demonstrated. Aneurysmectomy was performed in July, 1972. Therapy with digitalis and quinidine was discontinued after the operation, and the patient remained well until March, 1973, when he was readmitted to the hospital because of increasing exertional dyspnea and chest pain. A chest roentgenogram showed bulging left ventricle, and ventriculographic studies disclosed a false aneurysm at the site of the previous cardiomyotomy. No evidence of bacterial endocarditis was found at that time. Surgical resection of the pseudoaneurysm was performed, and the patient remained asymptomatic for a further period of two years. During this time, he was under regular surveillance by our cardiac clinic. No cardiac murmurs were audible, and a review of serial x-ray films of his chest taken at six-month intervals showed that, despite a distorted left ventricular contour from die surgical repair, the cardiac silhouette remained unchanged throughout this period. In May, 1975, the patient was readmitted to the hospital because of the sudden onset of fever and the sudden development of facial weakness with aphasia. The physical examination revealed pyrexia of 3 8 ° C ( 1 0 0 . 4 ° F ) , and the neurological examination showed combined sensory and

MURAL ENDOCARDITIS

227

motor asphasia, upper motor neuronal paralysis of the left facial nerve and a positive Babinski reflex on the left side. The patient's pulse rate was 100 beats per minute, and the blood pressure was 1 2 0 / 8 0 mm Hg. There was no evidence of increased jugular venous pressure. A mild paradoxic systolic uplift of the left precordium was noted. The first heart sound was accentuated, and the third and fourth heart sounds were also audible. No cardiac murmurs were heard. An electrocardiogram showed sinus rhythm, right bundlebranch block, left anterior hemiblock, and evidence of an old anterolateral myocardial infarction. The spleen was not palpable. No finger clubbing or skin petechiae were present. Funduscopic examination did not reveal any abnormality. T h e chest x-ray film showed a mild cardiomegaly with an abnormal left ventricular contour. The admission laboratory investigations showed the following values: erythrocyte sedimentation rate, 4 0 m m / h r ( W e s t e r g r e n ) ; white blood cell count, 6 , 7 0 0 / c u mm, with a normal differential count; hemoglobin level, 12.8 g m / 1 0 0 ml; hematocrit reading, 3 9 percent; platelet count, 3 8 5 , 0 0 0 / c u mm; serum protein level, 7.2 g m / 1 0 0 ml; albumin level, 3.1 g m / 1 0 0 ml; and globulin 4 . 1 g m / 1 0 0 ml. The levels of blood urea, glucose, and electrolytes were all within normal limits. Findings from clinical and microscopic urinalysis were normal, and repeated cultures of urine were sterile. The latex fixation and Rose-Waaler tests were negative, and the serum complement level was normal. Lumbar puncture revealed normal pressure and normal composition of the cerebrospinal fluid. Immediately after the patient was readmitted, coagulase-positive hemolytic Staphylococcus aureus was cultivated on six successive cultures. T h e blood samples were drawn at approximately four-hour intervals over a period of 2 4 hours. At this stage the patient had no urinary catheter or intravenous line which could have served as a source of bacteremia.

Si

s

Ss

F I G U R E 1. Phonocardiogram ( 2 0 0 to 4 0 0 cycles per second) showing presystolic, systolic, and early diastolic components of pericardial friction rub (arrows). Note prominent " A " wave on apexcardiogram. Si, So, and Sg, First, second, and third heart sounds, respectively. otomy. The wall of the false aneurysm consisted of dense fibrous tissue and was closely adherent to the medial surface of the left lung and to the left dome of the diaphragm. No

Intravenous administration of methicillin sodium (Celbenin) in a dosage of 8 m / 2 4 hr was then begun. All neurologic signs, including the aphasia, disappeared 2 4 hours after the patient's admission. The fever subsided after four days of antibiotic therapy, and the patient's temperature remained normal thereafter. During the third week of his hospitalization, the patient complained of a sudden severe pain over the precordium and thereafter a friction rub became audible, accompanied by a grade 3 / 6 pansystolic murmur that was intermittently heard. On serial determinations, the levels of transaminase, lactic dehydrogenase, and creatine phosphokinase remained within normal limits and the electrocardiographic signs of fresh myocardial infarction did not appear on serial tracings. T h e chest x-ray film at this stage showed an overall increase in cardiac size, but because of the pre-existing changes in the left ventricle, no definite alteration in left ventricular shape could be determined. On phonoeardiographic studies the presystolic, systolic, and diastolic components of the pericardial friction rub could be identified ( F i g 1 ) . The patient remained afebrile, his chest pain subsided after 48 hours, and at the conclusion of six weeks of intravenous therapy with methicillin, cardiac catheterization was performed. Ventriculographic studies demonstrated a large false aneurysm of die lateral wall of the left ventricle, with the two cavities communicating with each other through a narrow neck. ( F i g 2 ) . No evidence of mitral regurgitation was seen on left ventriculographic studies. At surgery a large pseudoaneurysm of the posterolateral wall of the left ventricle was seen. T h e cavity of the false aneurysm communicated with the left ventricular cavity through a 5-cm opening at the site of the previous cardiomy-

228

PITLIK ET AL

F I C U R E 2 A (top). Large oval-shaped false aneurysm ( 1 ) lateral to left ventricle ( 2 ) . B (bottom). Left ventriculogram showing narrow communicating channel between left ventricle and aneurysm ( a r r o w ) . CHEST, 7 1 : 2 , F E B R U A R Y ,

1977

evidence of valvular endocarditis was apparent on inspection of the mitral valve leaflets, and the opening in the left ventricular wall was closed. After a stormy postoperative course, during which tracheostomy and prolonged respiratory support were necessary, the patient made a satisfactory recovery.

t h e p a r t i c u l a r c h r o n o l o g i c o r d e r in w h i c h his illness dev e l o p e d ( w i t h a sudden onset of c h e s t pain, tiie a p p e a r a n c e of a friction r u b , a n d a pansystolic m u r m u r t h r e e w e e k s after establishing t h e diagnosis of bacterial endoc a r d i t i s ) suggests t h a t his p s e u d o a n e u r y s m m i g h t h a v e developed

as a result of e n d o c a r d i t i s

DISCUSSION

bleeding into t h e p e r i c a r d i a l c a v i t y w i t h fatal c a r d i a c t a m p o n a d e ; h o w e v e r , d e n s e p e r i c a r d i a l adhesions m a y limit t h e bleeding a n d p r e v e n t t a m p o n a d e , a n d with blood clot, a

false

a n e u r y s m m a y then be f o r m e d . " Pseudoaneurysm

m a y thus o c c u r as an

complication of m y o c a r d i a l infarction previous ventricular m y o t o m y .

6

15

uncommon

or at t h e site of a

In b a c t e r i a l e n d o c a r d i -

tis, particularly of t h e s t a p h l o c o c c a l variety, t h e f o r m a tion of an

abscess in t h e m y o c a r d i a l

wall has

been

r e p o r t e d to lead to p e r f o r a t i o n a n d c o n s e q u e n t p s e u d o aneurysm of t h e h e a r t .

4 - 7

All of t h e t h r e e u n d e r l y i n g

causes of false a n e u r y s m previousy c i t e d

(myocardial

infarction, c a r d i o m y o t o m y , a n d b a c t e r i a l e n d o c a r d i t i s ) w e r e successively present in o u r patient. T h e first p s e u d o a n e u r y s m in our patient a p p e a r e d at t h e site of t h e previous c a r d i o m y o t o m y a n d w a s c l e a r l y related to t h e a n e u r y s m e c t o m y . His s e c o n d false a n e u rysm w a s d e m o n s t r a t e d b y v e n t r i c u l o g r a p h i c studies six weeks after t h e diagnosis of endocarditis. T h e possibility of endocarditis w a s raised b y t h e clinical manifestations of f e v e r a n d b y the o c c u r r e n c e of a c e r e b r a l e m b o l i c a c cident in a patient with preexisting c a r d i a c disease, a n d t h e diagnosis of e n d o c a r d i t i s w a s c o n f i r m e d b y t h e isolation of S aureus

on all of six s u c c e s s i v e blood c u l t u r e s .

T h e a b s e n c e of a n y o t h e r s o u r c e of b a c t e r e m i a , s u c h as a venous c a n n u l a or urinary c a t h e t e r , a n d t h e n a t u r e of t h e particular

organism

involved

(S

would

aureus)

T h e a b s e n c e of raised levels of e n z y m e s a n d of e l e c t r o c a r d i o g r a p h i c c h a n g e s after t h e episode of c h e s t pain makes t h e diagnosis of an a c u t e m y o c a r d i a l infarction unlikely. V e n t r i c u l a r a n g i o g r a m s did not

demonstrate

mitral regurgitation as t h e e x p l a n a t i o n for t h e systolic m u r m u r . A systolic m u r m u r of this p a r t i c u l a r t y p e w a s recently d e s c r i b e d in association with p s e u d o a n e u r y s m a

result

of

the

jet

passing

through

its

narrow

orifice. * T h e question arises of w h e t h e r t h e false a n e u 1

rysm was t h e u n d e r l y i n g p a t h o a n a t o m i c condition l e a d ing to m u r a l e n d o c a r d i t i s or w h e t h e r t h e latter o c c u r r e d first a n d led to formation of an intramural abscess a n d d e h i s c e n c e at the s u t u r e line of t h e previous m y o t o m y . A c u t e bacterial endocarditis has b e e n known t o o c c u r on a previously n o r m a l e n d o c a r d i u m , c a u s e d b y an invasive organism such as S aureus. -" 3

T h e disease m a y

also d e v e l o p in patients with underlying a c q u i r e d e n d o cardial d a m a g e .

3

Infection o c c u r r i n g at t h e s u t u r e line

of a c a r d i o m y o t o m y has also b e e n r e p o r t e d .

9

In o u r patient, a preexisting p s e u d o a n e u r y s m

could

well h a v e p r o v i d e d a p p r o p r i a t e conditions for b a c t e r i a l growth and t h e d e v e l o p m e n t of e n d o c a r d i t i s ; h o w e v e r . CHEST, 7 1 : 2 , F E B R U A R Y ,

1977

the

1 Geraci J , Dale A, McGoon D P : Bacterial endocarditis and endarteritis following cardiac operations: Addendum. Wis Med J 6 2 : 3 0 2 , 1963 2 Stein P. Harken D, Dexter L : T h e nature and prevention of prosthetic valve endocarditis. Am Heart J 7 1 : 3 9 3 , 1967 3 Weinstein L, Schlesinger J J ; Pathoanatomic, pathophysiologic and clinical correlations in endocarditis. N Engl J Med 2 9 1 : 8 3 2 - 8 3 7 , 1974 4 Chesler E , Korns M E , Porter G E , et al: False aneurysm of the left ventricle secondary to bacterial endocarditis with perforation of the mitral aortic intervalvular fibrosa. Circulation 3 7 : 5 1 8 - 5 2 3 , 1968 5 Van Tassel RA, Edwards J E : Rupture of heart complicating myocardial infarction: Analysis of 4 0 cases including nine examples of left ventricular false aneurysm. Chest 6 1 : 1 0 4 - 1 1 6 , 1972 6 Smith RC, Goldberg H, Bailey C P : Pseudoaneurysm of the left ventricle: Diagnosis by direct cardioangiography. Surgery 4 2 : 4 9 6 - 5 1 0 , 1957 7 Qizilbash AH, Schwartz C : False aneurysm of left ventricle due to perforation of mitral-aortic intervalvular fibrosa with rupture and cardiac tamponade: Rare complication of infective endocarditis. Am J Cardiol 3 2 : 1 1 0 - 1 1 3 , 1973 8 Macneil D J , Vieweg W V R , Oury J H , et al: Pseudomitrai regurgitation due to false aneurysm of left ventricle treated successfully by surgery. Chest 6 6 : 7 2 4 , 1974 9 Kerr VVF, Wilcken D E L , Steiner R E : Incisional aneurysms of the left ventricle. Br Heart J 2 3 : 8 8 , 1961

add

f u r t h e r s u p p o r t t o t h e diagnosis of bacterial e n d o c a r d i t i s .

as

at

REFERENCES

R u p t u r e of t h e h e a r t almost always p r o d u c e s m a s s i v e

organization of t h e c i r c u m s c r i b e d

located

suture line of t h e previous c a r d i o m y o t o m y .

E m p y e m a d u e t o Streptococcus mutans* Fred R. Sattler, M . D . ,

0 8

and Joel Ruskin,

M.D.f

Empyema due to Streptococcus mutans occurred following dental manipulation in two patients with periodontal disease. Isolation of this dental pathogen from pleural fluid localized the site of origin of the empyemas to the oropharynx and precluded the need to search for a remote intra-abdominal source of these pleuropulmonary infections. Although there is controversy regarding the susceptibility of S mutans to penicillin, the isolates from our patients were markedly sensitive to the drug, and both patients were cured with penicillin therapy and surgical drainage. ' F r o m the Infectious Disease Section, Kaiser Permanente Medical Center, Los Angeles. ° "Fellow, Infectious Disease Section. tChief, Infectious Disease Section, and Assistant Clinical Professor of Medicine, University of California, Center for the Health Sciences, Los Angeles. Reprint requests: Dr. Ruskin, Southern California Permanente Medical Center, 4900 Sunset Blvd., Los Angeles 90027

EMPYEMA DUE TO S MUTANS

229