Biventricular assist for severe acute rheumatic pancarditis

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series. However, patients undergoing CPB accounted for 37% of the reported cases [3]. The patient is more vulnerable to pulmonary artery rupture while on bypass when the heart is empty. Distal catheter migration can occur spontaneously secondary to a reduction in the size of the loop within the right ventricle with repeated inflations or secondary to right ventricular decompression during CPB. Hypothermia may contribute to this higher risk by stiffening the catheter. Although the technique of catheter withdrawal to the right ventricle before institution of CPB popularized by Stone and associates [4] may prevent pulmonary artery rupture, it is not free of potential complications. Reinsertion of the catheter during weaning of CPB can cause ventricular ectopy, perforation of the right ventricular wall or other rare complications. In the present case, the anesthesiologist, without the surgeon's knowledge, had withdrawn the catheter because of a damped tracing during bypass. This manipulation created the circumstances for two complicating factors. First, the excessive distance of catheter withdrawal (to the right atrium) allowed the catheter to coil around the cannula and then migrate into the lumen. This last event was probably the result of manipulation of the catheter while the blood flow was being directed to the VRC. The second complicating factor was the inflation of the balloon in an attempt to refloat the catheter. This maneuver caused immediate obstruction of the venous flow to the oxygenator. Rapid decannulation and removal of the tangled PAC followed by insertion of a new cannula and reinstitution of CPB within 2 minutes prevented serious consequences. In summary, spontaneous distal migration of a PAC is a rare but potentially dangerous event. Although the withdrawal of the catheter may prevent pulmonary artery rupture, consideration should be given to the complications that may arise from a catheter stationed in any of the cardiac chambers. Repositioning of the PAC during CPB should be avoided, and the necessity of constant monitoring of the pulmonary artery tracing cannot be overemphasized. Maintenance of the catheter balloon within 10 cm distal to the pulmonary valve is recommended to prevent permanent wedging and catheter perforation. This may be accomplished by a positionmonitoring PAC described by Robertie and colleagues [5], which permits constant monitoring of the right ventricular waveform through a middle lumen located 10 cm from the catheter tip. However, the best way to prevent the most serious complications is to be aware of their nature and the techniques necessary to avoid them.

References 1. Waller JL, Johnson SP, Kaplan JA. Usefulness of pulmonary artery catheter during aortocoronary bypass surgery. Anesth Analg 1982;61:221-2, 2. Kopman EA. Pressure monitoring during cardiopulmonary bypass. J Thorac Cardiovasc Surg 1984;87:319-20. 3. Shah KB, Rao TLK, Laughlin S, E1-Etr A. A review of pulmonary artery catheterization in 6,245 patients. Anesthesiology 1984;61:271-5. © 1996 by The Society of Thoracic Surgeons Published by Elsevier Science Inc

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4. Stone JG, Khambatta HJ, McDaniel DD. Catheter-induced pulmonary artery trauma. Can it always be averted? J Thorac Cardiovasc Surg 1983;86:146-50. 5. Robertie PG, Johnston WE, Williamson MK, Dudas LM, WaUenhaupt SL, Ganz W. Clinical utility of a positionmonitoring catheter in the pulmonary artery. Anesthesiology 1991;74:440-5.

Biventricular Assist for Severe Acute Rheumatic Pancarditis Bram J. Amsel, MD, Herbert De Raedt, MD, Inez E. Rodrigus, MD, Luc Haenen, MD, Patrick Druw~, MD, Anne Vorlat, MD, Cecile G. Colpaert, MD, and Adrian C. Moulijn, MD, PhD Departments of Cardiac Surgery, Intensive Care, and Pathology, University Hospital of Antwerp, Antwerp-Edegem, Belgium Severe heart failure in acute rheumatic myocarditis is rare. It may be rapidly reversible with treatment, so maximal medical treatment and, if necessary, mechanical support should be given before heart transplantation is considered.

(Ann Thorac Surg 1996;62:267-9) ven in developed countries acute rheumatic fever ~ontinues to appear [1]. There is controversy as to whether valvular or myocardial involvement of carditis is most responsible for heart failure when it occurs [2]. We report here a case of rheumatic pancarditis with such severe myocardial failure that biventricular circulatory assist was necessary to save the patient.

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A 19-year-old Ashkenazi Jewish man who had been studying in Israel returned home to Belgium with a 2-week history of a sore throat and bronchitis. One month earlier he had been hospitalized with diarrhea and dehydration, from which he recovered rapidly but with significant weight loss. Two days after arrival he was hospitalized elsewhere with fever and cardiac tamponade. Pericardiocentesis yielded 1,700 mL of hemorrhagic but nondiagnostic fluid, but echocardiography demonstrated very poor cardiac function. The anti-streptolysine O titer was 647 IU/L. Viral serologic screening was negative. Because of rapidly worsening cardiogenic shock, the patient was transferred to the University Hospital of Antwerp. Echocardiography showed enddiastolic and end-systolic left ventricular internal dimensions of 60 and 53 mm, respectively, and an estimated left ventricular ejection fraction of 0.26 with very poor right ventricular function (Fig 1). The atria were also dilated Accepted for publicationJan 16, 1996. Address reprint requests to Dr Amsel, Department of Cardiac Surgery, University Hospital of Antwerp, Wilrijkstraat 10, B-2650 AntwerpEdegem, Belgium. 0003-4975/96/$15.00 PII S0003-4975(96)00095-1

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A

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balance. Biopsy specimens of the left ventricle (Fig 2A), right atrium, and right atrial appendage (Fig 2B) taken during the operation showed a myocardial, pericardial, and subendocardial inflammatory infiltrate consisting of lymphocytes, histiocytes, and polymorphonuclear leukocytes with interstitial edema, most pronounced in the atrium. There were no Aschoff's nodules. The patient was treated with penicillin, but antiinflammatory treatment was withheld until day 3, at which time cardiac function had not improved. Acetylsalicylic acid (100 m g - kg -1 • day -1) was then given, but administration was stopped because of increased bleeding, and methylprednisolone (10 rag. kg - 1 . day -1) was given. Three repeat sternotomies were performed for bleeding during the first 9 days. From day 5, ie, 2 days after the start of antiinflammatory treatment, progressively improving echocardiographic myocardial function and left ventricular ejection component to the arterial blood pressure curve were noted, and on day 9 the assist devices were successfully explanted without any need for inotro-

B

Fig 1. End-diastolic (A) and end-systolic (B) transesophageal echocardiographic frames demonstrating biventricular dilatation and poor contractile function.

and did not contribute to ventricular filling. Color-coded Doppler echocardiography showed grade II aortic and grade III tricuspid regurgitation and grade I mitral regurgitation. The electrocardiogram demonstrated sinus tachycardia, first degree atrioventricular block, low voltages, right-sided conduction delay with a QRS-duration of 0.11 seconds, and broad Q waves in leads II, III, aVF, V 1, and V 2. After administration of norepinephrine (13 ~g • kg -1 • min -1, dopamine (36/zg • kg -1 • rain-l), and dobutamine (13/~g. kg -1 • min -1) and sufficient volume loading, systolic blood pressure was 80 m m Hg and cardiac output 1.9 L/min. Plasma creatinine and lactate levels were 1.6 and 6.6 mg/L, respectively. Levels of aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase were 510, 330, and 2,204 U/L, respectively (normal values = 17, 22, and 241 U/L). Biventricular assist using ABIOMED (Danvers, MA) BVS 5000 p u m p s was started, immediately yielding good systemic and pulmonary blood flow and diuresis and normalization of hepatic enzyme levels and acid-base

A

B

Fig 2. (A) Light microscopy of left ventricular endomyocardial biopsy specimen showing focal interstitial edema and a sparse to moderately dense inflammatory infiltrate in myocardium and endocardium (right). (B) More pronounced interstitial edema in the right atrial appendage. (Hematoxylin and eosin; ×250 before 35% reduc!ion.)

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pic drugs. A d m i n i s t r a t i o n of acetylsalicylic acid (100 m g • kg -1 • d a y -1) was restarted, a n d m e t h y l p r e d n i s o l o n e administration continued. The patient s u s t a i n e d the following complications: atelectasis of the left lower lobe i m p r o v i n g over 6 weeks, a m i l d sacral p r e s s u r e ulcer, a g r a n d mal epileptic fit c o n s i d e r e d u n r e l a t e d to salicylate treament, salt-losing nephritis, a n d late cytomegaloviral hepatitis. A g a t e d b l o o d pool scan s h o w e d a left ventricular ejection fraction of 0.60 with only septal hypokinesis. Echocardiographic end-diastolic a n d end-systolic internal left ventricular diameters h a d d e c r e a s e d to 49 a n d 32 mm, respectively. Right ventricular function was normal. There was grade II aortic a n d grade I mitral regurgitation a n d a n o r m a l tricuspid valve at color-coded D o p p l e r e x a m i n a t i o n . The e l e c t r o c a r d i o g r a m s h o w e d n o r m a l atrioventricular conduction, a Q R S - d u r a t i o n of 0.08 seconds, absence of Q waves, a n d generalized i n v e r t e d T waves. At 3 - m o n t h follow-up the patient is doing fine a n d has taken up s o m e of his former activities.

Comment In spite of effective antibiotic prophylaxis b e i n g available, r h e u m a t i c fever still occurs w o r l d w i d e [1]. It is an expression of an i m m u n o l o g i c sequel to a group A streptococcal u p p e r respiratory tract infection. Carditis is one of its complications, b u t it is clear that h e a r t failure in the acute setting is usually d u e to valvular destruction [2]. The diagnosis is m a d e according to the presence of an elevated anti-streptolysin O titer a n d the revised Jones criteria [3]. The cardiac biopsies in our case s h o w e d pathologic changes consistent with the diagnosis, although, b e c a u s e of the early presentation, no Aschoff's n o d u l e s were f o u n d [4]. O u r patient h a d severe myocarditis a n d d e m o n s t r a b l e valvulitis a n d pericarditis, the first b e i n g so severe as to require mechanical circulatory s u p p o r t to sustain life. Cardiac transplantation, which was c o n s i d e r e d initially a n d which b e c a m e u n n e c e s s a r y b e c a u s e of the r a p i d i m p r o v e m e n t of biventricular function, has b e e n perf o r m e d in acute r h e u m a t i c fever with d e a t h due to acute rejection on the 45th day [5]. This d e a t h was possibly related to an activated i m m u n e state, and, if so, cardiac t r a n s p l a n t a t i o n m a y not b e suitable t r e a t m e n t for active r h e u m a t i c fever. Steimle a n d associates [6] have found significant i m p r o v e m e n t in left ventricular function in 13 of 49 patients with acute c a r d i o m y o p a t h i e s of different causes a n d have cautioned against p r e m a t u r e t r a n s p l a n tation, b u t clearly our case p r e s e n t e d with such severe biventricular myocardial failure that further t r e a t m e n t without circulatory s u p p o r t w o u l d r a p i d l y have l e d to a fatal outcome. In severe m y o c a r d i a l failure d u e to r h e u matic myocarditis, early ventricular mechanical assist s h o u l d be c o n s i d e r e d in addition to antiinflammatory t r e a t m e n t w h e n necessary. A possible role for cardiac transplantation, w h e n i m p r o v e m e n t of ventricular function does not occur, is uncertain at present. © 1996 by The Society of Thoracic Surgeons Published by Elsevier Science Inc

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References 1. Bisno AL. Group A streptococcal infections and acute rheumatic fever. N Engl J Med 1991;325:783--93. 2. Essop MR, Wisenbaugh T, Sareli P. Evidence against a myocardial factor as the cause of left ventricular dilation in active rheumatic carditis. J Am Coil Cardiol 1993;22:826-9. 3. Dajani AS, Ayoub E, Bierman FZ, et al. Guidelines for the diagnosis of rheumatic fever: Jones criteria, updated 1992. Circulation 1993;87:302-7. 4. Ursell PC, Albala A, Fenoglio JJ. Diagnosis of acute rheumatic carditis by endomyocardial biopsy. Hum Pathol 1982;13: 677-.9. 5. Silva LMMF, Mansur AJ, Bocchi EA, Stolf NAG, Bellotti G. Unsuspected rheumatic fever carditis ending in heart transplantation. Thorac Cardiovasc Surg 1994;42:191-3. 6. Steimle AE, Stevenson LW, Fonarow GC, Hamilton MA, Moriguchi JD. Prediction of improvement in recent onset cardiomyopathy after referral for heart transplantation. J Am Coil Cardiol 1994;23:553-9.

Long Tracheobronchial and Esophageal Rupture After Blunt Chest Trauma: Injury by Airway Bursting Jose L. Martin de Nicolas, MD, PhD, Antonio P. G~mez, MD, Felipe Cruz, MD, PhD, Vicente Diaz-HeUln, MD, C a r m e n Marr6n, MD, Jose I. Martinez, MD, Ramiro G~lvez, MD, a n d Jos~ Toledo, MD, PhD Departments of Thoracic Surgery and General Surgery, Doce de Octubre Hospital, Madrid, Spain Tracheobronchial rupture can b e associated w i t h b l u n t thoracic trauma. An important factor in the p h y s i o p a t h o l ogy of these lesions is reflex closure of the glottis, w h i c h can be related to closed chest trauma. We report a case of nonpenetrating thoracic t r a u m a that caused a l o n g membranous tracheal r u p t u r e from the subcricoid area to the m a i n carina, extending to both main bronchi. In addition, a complex e s o p h a g e a l rupture occurred d u e to the great energy liberated by the airway rupture acting as a real tracheal burst. Both lesions were diagnosed by flexible

bronchoscopy. The postoperative period was without serious complications.

(Ann Thorac Surg 1996;62:269-72) njury to the tracheobronchial tree due to b l u n t chest t r a u m a is u n c o m m o n . However, an increasing n u m b e r of these thoracic injuries have b e e n r e p o r t e d d u r i n g recent years; this t r e n d could be a t t r i b u t e d to an increase in h i g h - s p e e d t r a f i c accidents, a n d also to better care of patients suffering trauma. As soon as tracheobronchial

I

Accepted for publication Jan 19, 1996. Address reprint requests to Dr Martin de Nicolas, Department of Thoracic Surgery, Doce de Octubre Hospital, Ctra Andalucia Km 5'400, 28041 Madrid, Spain. 0003-4975/96/$15.00 PII S0003-4975(96)00299-8