Intensive Care Med (1994) 20:222-224
Intensive Care
Medicine 9 Springer-Verlag 1994
Infective endocarditis of the pulmonary valve following pulmonary artery catheterisation P,E Soding 1, J.R. Klinck 2, A. Kong z, M. Farrington 3 1Department of Anaesthesia, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK 2john Farman Intensive Care Unit, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK 3 Department of Clinical Microbiology and Public Health Laboratory, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK Received: 22 February 1993/Accepted: 24 June 1993
Abstract. T h e r i s k o f i n f e c t i v e e n d o c a r d i t i s f o l l o w i n g p u l m o n a r y a r t e r y c a t h e t e r i s a t i o n i n p a t i e n t s w i t h sepsis remains unquantified. Although catheter-induced endoc a r d i a l a n d v a l v u l a r i n j u r y a r e well r e c o g n i s e d , v a l v e inf e c t i o n is rare. A c a s e o f m i x e d p u l m o n a r y v a l v e e n d o c a r ditis a s s o c i a t e d w i t h t h e u s e o f a p u l m o n a r y a r t e r y c a t h e ter (PAC) in a patient with multisystem failure following liver t r a u m a is d e s c r i b e d . T h i s i l l u s t r a t e s t h a t d i a g n o s i s o f i n f e c t i v e e n d o c a r d i t i s i n c r i t i c a l l y ill p a t i e n t s c a n b e d i f f i c u l t b e c a u s e c o n c u r r e n t illness a n d t h e r a p y m a y m i m i c o r m a s k t h e u s u a l p r e s e n t i n g signs. T h e v a l u e o f t r a n s o e s o p h a g e a l e c h o c a r d i o g r a p h y i n t h i s c o n t e x t is e m phasised. Key words:
Endocarditis - Candidiasis - Pulmonary artery Catheter - Complication - Transoesophageal endochardiography
Case report A 29-year-old male lorry driver was admitted to the intensive care unit after emergency surgical repair of a lacerated liver and perforated right hemi-diaphragm following a road traffic accident. He continued to bleed despite surgical intervention and received a blood transfusion of 25 litres. Bleeding was eventually controlled by the use of vasopressin and application of a G-suit, a technique previously described in our unit [1]. The patient developed adult respiratory distress syndrome and acute tubular necrosis requiring haemodiafiltration. Cefotaxime, metronidazole and gentamicin were given during the first 48 h in intensive care, but on the eighth postoperative day he developed signs of sepsis. Strep. faeealis sensitive to vancomycin was isolated from blood and abdominal drainage fluids, while Candida albicans and strep, faecalis were cultured from a central venous line tip. C. albieans was also grown from skin swabs. Vancomycin, gentamicin and metronidazole were given and a pulmonary artery catheter inserted. Noradrenaline and dobutamine were given for circulatory support. After 2 weeks he became jaundiced and developed a right pleural effusion and elevated neutrophil count. Abdominal drainage fluid grew Staph. aureus and Strep. faecalis, both sensitive to vancomycin, and C.
Correspondence to: Dr. P. E Soding
albicans sensitive to fluconazole. Blood cultures grew C. albicans and a 2 week course of fluconazole was added to his treatment. However, he remained unwell with a persistent leucocytosis. Staph. epidermidis sensitive to vancomycin was grown from 2 blood cultures during this period. On the 26th day a laparotomy was performed for drainage of a subphrenic abscess and gall bladder empyema, from which Strep. faecalis was cultured. Following this, invasive monitoring and vasopressive therapy were again required. The patient subsequently improved and vasopressor treatment was discontinued on the 44th day. Antibiotic therapy was reduced to vancomycin alone, which was given to cover a residual subphrenic collection, from which Strep. faeealis was again isolated. The patient's renal function began to improve during the sixth week of admission and haemodiafiltration was discontinued. He then developed night sweats and fever with a persistent leucocytosis. A temporary pacing wire was inserted for episodic sinus bradycardia. Blood cultures grew Staph. aureus while pleural fluid and a central venous catheter tip again grew Strep. faecalis. A new pulmonary systolic murmur was heard on the forty-sixth day and two dimensional transthoracic cardiography raised the suspicion of a vegetation on the pulmonary valve (Fig. 1), which was confirmed by the use of a transoesophageal probe (Fig. 2). This showed mild pulmonary regurgitation without dilatation of the right cardiac cavities. Despite combination therapy with intravenous vancomycin, oral fucidin and intravenous amphotericin B he remained unwell and the vegetation continued to enlarge. His pulmonary regurgitation worsened leading to symptomatic right failure. The pulmonary valve and vegetation were surgically removed and an aortic homograft inserted. This was after administration of a total dose of 980mg of amphoterocin. At surgery a white lobulated mass 2.5 x 1.5 cm, associated with ulceration was found attached to the aortic cusp of the pulmonary valve. A Gram stain of the resected valve is shown (Fig. 3). Candida albicans was isolated in pure growth from two cultures of the valve. The patient recovered and was eventually discharged after twelve weeks of anti-fungal therapy and 15 weeks of vancomycin. Twelve months later he successfully completed a 13 km marathon. During most of his stay in intensive care the patient required central venous access for haemodynamic monitoring, inotropic drug therapy and haemodialysis or haemodiafiltration. A PAC was used for a total of 14 days. All intravascular catheters were replaced or resited under full aseptic conditions no less frequently than every 5th day.
Discussion The diagnosis of infective endocarditis in patients with abdominal trauma and multisystem failure may be diffi-
223
Fig. 1. Transthoracic short axis view of aortic valve demonstrating vegetation on pulmonary valve extending into right ventricular outflow tract. (AO, aorta, PV,, pulmonary valve; LA, left atrium; RVOF, right ventricular outflow; MASS, vegetation)
Fig. 2. Transoesophageal-short axis view of pulmonary valve showing vegetation. (AO, aorta; PV, pulmonary valve; RA, right atrium; SVC superior vena cava; MASS, vegetation)
Fig. 3. Gramstain of ground resected pulmonary valve showing round yeast forms with pseudohyphae (•
cult. Clinical findings such as pyrexia, anaemia, leucocytosis and positive blood cultures have many potential causes in this setting, including catheter-related and abdominal sepsis, drug reactions and ventilator associated bronchopneumonia. Conversely, in our patient, heat loss associated with haemofiltration undoubtedly masked a febrile state. Detection of a new heart murmur or demonstration of a valvular vegetation on transthoracic echocardiography typically indicate advanced disease and may signal a worse prognosis [2]. Because of the close approximation between ultrasonic transducer and cardiac structures transoesophageal echocardiography is recognised to be more sensitive than transthoracic for the identification of vegetative lesions, particularly in patients with underlying pulmonary disease and in those receiving mechanical ventilation [3, 4] (Fig. 4). Earlier use of this technique in our patient, from whom organisms commonly associated with infective endocarditis were repeatedly cultured, may have permitted more prompt diagnosis and treatment. Right sided endocardial injury is a recognised feature of PAC use. Post mortem studies have documented both infective and sterile lesions on valve leaflets, as well as intramural thrombosis and haemorrhage [5-7]. However, right sided infective endocarditis, particularly of the pulmonary valve, is rare [8]. Rupture of a pulmonary artery mycotic aneurysm associated with candidal endocarditis of the tricuspid valve has been described following pulmonary artery catheterisation, but to our knowledge isolated candidal infection of the pulmonary valve complicating PAC use has not previously been reported [8, 9]. Though rare, infective endocarditis is life-threatening and should be considered when balancing risks against the perceived benefits of PAC use in patients with the septic syndrome.
Basal Short Axis
Fig. 4. Two basic views used with a standard transoesophageal probe illustrating close approximate B/N probe and cardiac studies. (AO, aorta; LCA, left coronary artery; RCA, right coronary artery; PV, pulmonary valve; R A A , right atrial appendage; SVC superior vena cava; RLPV,, right lower pulmonary vein; LLPV, left lower pulmonary vein; RUPV, right upper pulmonary vein; LUPV left upper pulmonary vein; L A A left atrial appendage. I, II, 111." transoesophageal probe depth)
224
The pathogenesis of infective endocarditis is thought to involve adherence of blood-borne bacteria or fungi to damaged endocardial surfaces. An organism's ability to adhere to the valvular surface appears to determine the risk of infection. Enterococci, Streptococci and Staphylococci adhere well to valvular endothelium, while E. coli and Klebsiella sp. do so poorly [10]. Some strains of C. albicans are also known to adhere to valvular surfaces. Candida endocarditis, known to be associated with drug addiction and prolonged intensive care, is much less common as a cause of hospital acquired endocarditits than Staph. aureus and Staph. epidermidis [11]. The most common source of nosocomial pathogens causing catheter-related infection and septicaemia is the patient's skin and the critically ill patient is particularly susceptible [12]. In these patients bacteraemia and fungaemia are promoted by broad-spectrum antibiotic treatment, multiple and repeated intravascular catheterisation and impaired host defences. Antibacterial and antifungal therapy, though appropriate, failed to control our patient's symptoms and to prevent progressive enlargement of the valve lesion, probably because of failure of these drugs to adequately penetrate the vegetative mass [13]. Valve infection in this patient was probably polymicrobial: C. albicans was demonstrated in the resected valve, but coexisting infection with Staph. aureus and Strep. faecalis was likely and treatment implemented accordingly. Nonetheless, the progressive enlargement of the vegetation resulted in significant pulmonary valve incompetence with right heart failure. It also threatened to obstruct the pulmonary outflow tract and embolize. Surgery was undertaken in this young patient in the face of an otherwise normal heart. Simple excision of the pulmonary valve was felt inappropriate since decompensated right heart failure was present. Long term results of pulmonary valve excision in the face of congenital abnormalities suggest that right heart failure is an inevitable consequence even in the conditioned heart. The choice of valve replacement then rest with mechanical, xenograft or homograft valves. Replacement with either a mechanical or xenograft valve poses the risk of recurrent prosthetic endocarditis with similar incidence. Replacement with a homograft confers early protection against re-infection although later rates of valve endocarditis are similar [14]. The final choice of an aortic homograft to replace a pulmonary valve was dictated by the size of the native vessel and the availability of the homografts from the tissue bank. For these reasons a 21 mm aortic homograft was selected. In summary, infective endocarditis may complicate pulmonary artery catheterisation in patients with sepsis,
in whom the diagnosis may be obscured by co-existing infections and treatment. Transoesophageal echocardiography is invaluable in the detection of this complication and in assessing its response to treatment. Early use of this technique in critically ill patients, especially in the presence of recurrent staphylococcal or streptococcal bacteraemia, is recommended. Acknowledgements. We would like to thank Professor Sir R.Y. Calne, Dr. S.W.B. Newsom, Mr. J. Dunning, and also Dr. J. Hall, Helen Muffet und Charles Graham for their invaluable assistance and expertise with echocardiography.
References 1. Shelly MP, Greatorex R, Calne RY, Park OR (1988) The physiological effects of vasopressin when used to control intra-abdominal bleeding. Intensive Care Med 14:526-531 2. Pederson WR, Walker M, Olson JD, Gobel F et al (1991) Value of transoesophageal echoeardiography as an adjunct to transthoracic echocardiography in evaluation of native and prosthetic valve endocarditis. Chest 100:351-356 3. Shapiro SM, Bayer AS (1991) Transoesophageal and Doppler echocardiography in the diagnosis and management of infective endocrditis. Chest 100:1125 - 1130 4. Editorial (1992) Transoesophageal echocardiography. Lancet 339:709-711 5. Rowley KM, Soni Clubb K, Walker-Smith GJ, Cabin HS (1984) Right-sided infective endocarditis as a consequence of flow-directed pulmonary-artery catheterization. N Engl J Med 3 ~1:1152- 1156 6. Lange HW, Galliani CA, Edwards JE (1983) Local complications associated with indwelling Swan-Ganz catheters: autopsy study of 36 cases. Am J Cardiol 52:1108 - 1111 7. Sage MD, Koelmeyer TD; Smeeton WM (1988) Evolution of SwanGanz catheter-related pulmonary valve nonbacterial endocarditis. Am J Forensic Med Pathol 9:112-118 8. Cremieux A, Witchitz S, Malergue M, Wolff Met al (1985) Clinical and echocardiographic observations in pulmonary valve endocarditis. Am J Cardiol 56:610-613 9. Roush K, Scala-Barnett DM, Dona Bedian H, Freimer EH (1988) Rupture of a pulmonary artery mycotic aneurysm associated with candidal endocarditis. Am J Med 84:142-144 10. Newsom SWB (1982) Microbiology of endocarditis. Thorac Cardiovasc Surgeon 30:336-339 11. Terpenning MS, Buggy BP, Kanffman CA (1988) Hospital-acquired infective endocarditis. Arch Intern Med 148:1601-1603 12. Norwood S, Ruby A, Civetta J, Cortes V (t991) Catheter-related infections and associated septicaemia. Chest 99:968-975 I3. Rubenstein E, Noriega ER, Simserkoff MS, Holzman R and Rahal JJ (1975) Fungal endocarditis: analysis of 24 cases and review of the literature. Medicine 54:331-344 14. O'Brian MF, Gregory Stafford E, Gardner AH, Pohlner PG, McGiffin DC (1987) A comparison of aortic valve replacement with viable cryopreserved and fresh allograft valves, with a note on chromosomal studies. J Thorac Cardiovasc Surg 94:812-823