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EQUINE VETERINARY JOURNAL Equine iw. J. ( I99 I ) 23 (6) 479-482
Case Reports Diagnosis of pulmonary valve endocarditis in a horse L. NILSFORS, C. W. LOMBARD, D. WECKNER* and C. KVARTt Departments of Clinical Radiology (Box 7029), * Medicine and Surgery and tPhysiology, Swedish University of Agricultural Sciences, S-750-07 Uppsala, Sweden Introduction
Clinical pathology
VALVULAR endocarditis in the horse is a rare condition and affects the left heart more often than the right (Else and Holmes 1972; Deegen, Lieske and Schoon 1980; Fregin 1982; Littlewort 1986; Wagenaar and Kroneman 1986). There are reports of four equine pulmonic endocarditis cases verified at necropsy (Innes, Berger and Francis 1950; Wagenaar, Kroneman and Breukink 1967; Buergelt, Cooley, Hines and Pipers 1985) and one clinically suspected pulmonic endocarditis (von Mill and Hanak 1978) in the literature. Pulmonic valve endocarditis was confirmed at necropsy in one horse in our clinic (S. Persson 1987, personal communication). The purpose of this report is to describe the ante-mortem diagnosis of pulmonic valve endocarditis in a horse.
Blood analysis revealed a high white cell count of 24 x 109/litre with 83 per cent granulocytes, a low Hb of 74 g/litre, a low packed cell volume of 0.28 litres/litre, a normal serum protein, a low albumin/globulin ratio of 0.5 caused by high gamma globulin fractions and a high alkaline phosphatase (ALP) value of 12.2 pkat/litre (normal value for our laboratory is < 8.5 Natjitre). Urea, creatinine, ASAT, CK, GT and bile acids were within normal limits. Pleurocentesis revealed a small amount of pleural fluid with a normal total leucocyte count, but a high proportion of polymorphonuclear cells, 5 15 x 106/litres, to mononuclear cells, 265 x I06/litres (Robinson 1987). Peritoneocentesis had an unremarkable cytology. Bacterial cultures of pleural and peritoneal fluid, urine and blood were negative.
Case history Diagnosric aids
Four months after importation from Poland, a four-year-old Warmblood gelding was referred to the Department of Medicine and Surgery at the Swedish University of Agricultural Sciences. According to the referring veterinary surgeon, the horse had been losing weight for one month without evidence of anorexia or gastrointestinal disturbances. The animal's body temperature had varied between 38.5 and 39.5'C for two weeks prior to presentation, work capacity was limited, a stiff gait was evident in the hind legs and lameness in the left front leg. The horse's history prior to importation is unknown. Clinical findings Phy~icalesamination
The horse weighed 472 kg and had subcutaneous oedema in all four legs, from the hock and carpus and distally. The lameness in the left front leg was localised to the fetlock joint. An old skin wound that had healed by second intention was found on the right chest wall. The horse had engorged jugular veins but no jugular pulse. A palpable thrill was on the left side of the chest in the third intercostal space level with the olecranon. Auscultation of this area revealed a distinct third heart sound and a grade 5/6 holosystolic ejection murmur. On the right side, a grade 4/6 holosystolic murmur could be heard in the third intercostal space level with the humeral joint. Lung auscultation was normal, but the horse reacted with unease to percussion over the right dorsal lung. No line of pleural effusion could be percussed. Over the next three weeks body temperature and respiratory rate varied irregularly between 38 and 39.5"C and 15 to and 20 breathdmin. respectively, and the resting heart rate varied between 40 and 46 beats/min.
The electrocardiogram showed a regular sinus rhythm with normal intervals (Fregin 1982). Elevation of the S-T segment and a high amplitude of the T-wave in lead I, 11, Ill, aVF, CV6LL and CV6LU. measuring 2.4 mV (twice the Ramplitude) in lead 11, were seen (Fig I). At the point of maximal amplitude in the pulmonic valve area, the murmur on the phonocardiogram (Siemens-Elema, Sweden) described a distinct crescendo-decrescendo pattern in both low and high frequency bands (Fig I). On the right side, the murmur had a less distinct crescendo-decrescendo pattern. M-mode echocardiography (ATL 600 B; USA) revealed a normal left heart internal end diastolic diameter (80 to 130 mm) and a normal right ventricular internal diameter (32 to 52 mm) (Lescure and Tamzali, 1984). An exaggerated systolic and diastolic septal motion was seen and the right ventricular free wall was thicker, 23 mm in diastole, than normal (about 15 mm, L. Nilfors, unpublished data) (Fig 2; right ventricular dimensions were measured on a magnified view of the near field). Moreover, the septal wall thickness appeared to be increased and measured 30 mm at end diastole. On real-time echocardiography (Aloca 725; Aloca, Japan) the right atrium appeared to be of normal size, as was the right ventricular outflow tract. The right ventricular wall appeared hypertrophied. Markedly thickened pulmonic valve leaflets consistent with bacterial endocarditis obstructed the pulmonary artery in diastole (Fig 3). Only the first few centimeters of the pulmonary artery could be seen. Contrast echocardiography of the left and right ventricle using C 0 2 microbubbles in blood did not document any shunts or tricuspid or mitral valve regurgitation. Selective venous blood gas analysis (ABL-3; Radiometer, Denmark) of the cranial caval vein, the right
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Fig I : The top tracing is a Lead I1 electrocardiogram (ECG),and the two bottom tracings are phonocardiograms (PCG) recorded in the pulmanic valve area. Paper speed is 25 mmlsec. Note the elevated S-T segment and the tall T-wave on the ECG. The crescendo-decrescendo murmur visible in hoth the low frequency ( L ) (maximum amplitude 50 H:) and the high frequency (H)(maximum amplitude 400 H z ) hands of the PCG is compatihle with an ouflow tract stenosis. A third heart sound (arrow) is also visihle
Fig 2: M-mode echocardiogram,using a 2.0 MH: transducer. shouitig the right ventricular n*all (RVW). the right ventricle (RV). the left ventride (LV). the left iuntricitlar wall (LVW) and the interi~entricrtlarseptum (IVS). In systole, an esaggerated motion of the septrtni tonsard the left ventricle is seen (solid arrou,),ininiediatelyfdlowed hy an e.va.q,qerated motion toneard the right ventricle in early diastole (openarrow)
Fig 3: A real-time echocardiogram (right parasternal short axis lieu. of the heart hase riewedfionr helow). iising a 3.0 MH: transducerv is shown in systole (aho1.e) and in diastole (helow). Note the thick pitlnionary vahe leaflets (open arrows) seen in systole and the alniosr i m p l e t e ohstriiction of the pulnronic, i d v e (solid arron,) in diastole. AO: aorta. RVO: right \-entr.icrrlarortrflou- tract
atrium, the right ventricle and the caudal caval vein (Lombard, Scaratt and Buergelt 1983) did not reveal any abnormal variations. Intracardiac pressure recordings (pressure transducer EMT 033 connected to a Mingograf 804, by way of a pressure amplifier EMT 863) (Siemens-Elema, Sweden) demonstrated a
markedly increased pressure in the right ventricle and atrium, whereas normal pressures were seen in the pulmonary artery (Fregin 1982) (Table 1). Radiographs of the thorax showed a well delineated homogeneous density of about 8 cm in diameter in the caudal lung lobes suggestive of either an abscess, a focal pneumonia
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TABLE 1: Results of blood pressure measurements from the following locations of the heart; right atrium (RA), right ventricle (RV),pulmonary artery (PA), and left ventricle (LV). Normal values (f sd) (Fregin 1982) Blood pressure (mmHg)
Location RA RV PA A0 LV
Systolic
24 (12.1f33) 135 (45.8f 5.6) 37 (42.1It 5.2) 120 (143.9f 2.5) 120 (148.3f 2.6)
Diastolic
5 (-2.2f 3.7) 16 (5.8f 3.5) 20 (18.3f 4.1) 90 (91.8f 2.6) 14 (16.6f 1.6)
or an embolic infarction. No sign of pleural effusion was found.
Differential diagnosis The subcutaneous oedema, the engorged jugular veins, and an increased heart rate and respiratory rate are all signs of right sided congestive heart failure (CHF) (Fregin 1982; Littlewort 1986). The point of maximal intensity of the holosystolic crescendo-decrescendo murmur and the marked pressure gradient across the pulmonic valve were indicative of a pulmonic stenosis. Initially, there was a possibility of the right sided murmur being caused by a ventricular septa1 defect or by insufficient tricuspid valves. This was excluded by intracardiac blood gas measurements. contrast echocardiography and the absence of vwaves on the right atrial pressure tracing. The right sided murmur probably was the left sided stenotic murmur overheard on the right side. The lack of tricuspid insufficiency explained the absence of a jugular pulse, whereas the distension was a result of increased right atrial and right ventricular pressures. The high right ventricular pressure and the hypertrophied right ventricular wall are signs of a pressure overload (Feigenbaum 1986). The fever, high white cell count, elevated gamma-globulin fractions and the anaemia pointed to an active chronic infection. Therefore, the stenosis was likely caused by a vegetative endocarditis of the pulmonic valve leaflets. This was confirmed by the real-time echocardiogram, which also excluded a congenital pulmonic stenosis. The pleural fluid had an increased proportion of polymorphonuclear cells, but was not abnormal enough to indicate a pleuritis (Robinson 1987). It is plausible that the pleural fluid was influenced by a systemic infection.
Treatmen t Antibiotic treatment was initiated by the referring veterinary surgeon before culture samples were taken. We continued the treatment with a combination of penicillin G 16,000 iu kg and dihydrostreptomycin 20 mg/kg bwt intramuscularly (im) daily based on the idea of using an antibiotic with broad spectrum coverage. The horse did not improve over a three-week period and was destroyed.
Pathology On gross pathology (Fig 4). a markedly hypertrophied right ventricular wall, a slightly hypertrophied interventricular septum and a normal left ventricle were seen. The main pulmonary artery was enlarged markedly in the valvular area and a distinct mass could be felt. Opening up the pulmonic
Fi,q 4: A large endricarditic niass that extendsfram the right ventricular ougon trai't to the niuin pulmonary artery (open arrow), covering the l arrow). (Part pulnionic w h e . Note the thick right ventricular u ~ l(solid of the right rentriiular u d l is removed). RV: right \ventricle
artery allowed visualisation of a large mass occluding the orifice, leaving only a small passage at the side close to the aorta. The mass had an irregular, verucous structure, originating from all pulmonic valve leaflets and completely obliterating the pulmonic valve structure. No other vegetative lesions were found. Pleural or abdominal effusion was not present. In the right caudal lung lobe, a thromboemolism of the lobar artery producing infarction involving a volume of about 1.000 cm3 of lung tissue was found. Bacterial cultures and histochemistry of the endocarditic mass and the lung infarct did not reveal microorganisms. Microscopic examination of the vegetative lesion showed that it consisted of fibrin, platelets and leucocytes. At the base of the vegetation, organisation had started and granulation tissue had proliferated into the thrombus. Focal parietal endocardial thickening with fibrinous adhesions were seen on the right ventricular wall and on the apical part of the left ventricle.
Discussion The horse's history of weight loss, decreased work tolerance, stiff gait, increased pulse rate and temperature are all
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compatible with valvular endocarditis (Wagenaar and Kroneman 1986). Streptococcus equi, Streptococcus zooepidemicus, Streptococcus SQ., Actinohacillus equuli, Erysipelotrix rhusiopathiae, Escherichia coli. Pseudomonas aeruginosa. Candida parapsilosis, Pasteurella sp. (Buergelt, Cooley, Hines and Pipers 1985, McCormick, Peet and Downes 1985; Robey and Reef 1986; Wagenaar and Kroneman 1986; Dedrick, Reef, Sweeney and Morris 1988) and Mycohacterium tuberculosis ( S . Person 1987, personal communication) have been isolated from endocarditis in the horse. It is plausible that the bacterial cultures in the reported case were negative because of antibiotic treatment. In man, differences between subacute and acute endocarditis in aetiology and pathogenesis are noted. Thus, in subacute endocarditis the inducing bacteraemia often originates from the normal flora in traumatised areas, eg, teeth removal. A valvular defect combined with a jet effect caused by blood flowing from a high to a low pressure area are important predisposing factors. However, degenerative fibrosis or fenestrations, common in the aortic valves, are infrequent in the pulmonic valves (Else and Holmes 1972). In acute endocarditis a skin or lung infection is the most common pre-existing foci of infection and previously normal valves are often found. The causative agents in these cases are highly invasive and adhere directly to the valve (Weinstein 1988). This mechanism may be likely in this case, although the only visible source of infection was the skin wound on the chest wall. A fungal infection cannot be excluded because these produce relatively large vegetations (Weinstein 1988). The parietal endocardial thickening found at necropsy was probably caused by the catheterisation. A right sided endocarditis is likely to produce pulmonary thrombo-embolism (Kasper et a1 1986). This would explain the horse's painful reaction to percussion of the right lung and the radiographic findings. Although it appears that the antimicrobial agents used did cure the infection, the prognosis of the valvular endocarditis described was poor because of a late clinical diagnosis with large vegetations developing. This caused a pulmonic stenosis, which resulted in a right sided congestive heart failure from cor pulmonale. If treatment is attempted at an early stage, long term administration of bactericidal drugs given to maintain high therapeutic levels in the plasma would be indicated (Weinstein 1988). The echocardiographic diagnosis of valvular endocarditis was first reported in man by Dillon eta1 (1973) and in the horse six years later (Pipers, Hamlin and Reef 1979). In the horse in this report, the endocarditis masses on the pulmonic valves were imaged easily with two-dimensional real-time echocardiography. The septal motion pattern seen is usually a result of left ventricular volume overload (Feigenbaum 1986). However, left ventricular wall motion appeared hypokinetic and no other signs of left ventricular volume overload were found. As pulmonary flow is restricted, one would expect a decreased pre-load on the left ventricle and a lower stroke volume. No signs of a reduced left ventricular dimension at end diastole was found and heart rate was only slightly increased. Insufficient tissue oxygenation due to reduced blood flow could have caused a myocardial hypoxia (Hall 1971) which might explain the high T-waves on the ECG (Fregin 1982). However, the myocardium did not show any signs of insufficient oxygenation histologically. The increased respiratory rate was probably due to the infarcated part of the
lung causing pain and a reduced volume of normally ventilated lung tissue. The valvular lesion appeared to obstruct the pulmonic valve completely in diastole and, therefore, a diastolic insufficiency murmur may not have been produced.
Acknowledgments The authors thank Dr. R. Svanholm for referring the case and Dr. L. Jonsson, for evaluating the autopsy.
References Buergelt. C. D., Cooley, A. J.. Hines. S. A. and Pippers, F. S. (1985) Endocarditis in six horses. Vet. Path. 22.333-337. Dedrick. P.. Reef. V. B.. Sweeney. R. W. and Morris, D. D. (1988) Treatment of bacterial endocarditis in a horse. J. Am. w t . wed. Ass. 193, 339-342. Deegen. E., Lieske. R. and Schoon. H. (1980) Klinische und kardiologische Untersuchungnsbefunde bei 3 Deckhengsten mit Aortenklappeninsuffizienz. Tierur:t/. pras. 8 , 2 I 1-222. Dillon, J. C.. Feigenbaum, H., Konecke, L. L. (1973) Echocardiographic manifestations of valvular vegetations. Am. Heart J. 86,698 Else, R. W. and Holmes. 3. R. (1972) Cardiac pathology in the horse ( I ) Gross pathology. Equirre wt. J. 4, 1-8. Feigenbaum. H. (1986) Echocardiography. 4th edn, Lea & Febiger, Philadelphia. pp 162-I67,3 10-319. Fregin. G . F. ( 1982) The cardiovascular system. In: Eqrririe Medicine arid S i q e r y vol 2. Eds: R. A. Mansmann. E. S . McAllister. P. W. Pratt, American Veterinary Publications, Santa Barbara. pp 645,684-685. Hall, L. W. (1971) Disturbances of cardiopulmonary function in anaesthetised horses. Eqtrirre Vet. J. 3,95-98. Innes, J. M.. Berger. J. and Francis, J. (1950) Subacute bacterial endocarditis with pulmonary embolism in a horse. Brit. Vet. J. 106. 245-250. Kasper. W., Meinenz. T.. Henkel. 8.. Eissner Dagmar, Hahn, K., Hofmann. T.. Zeiher, A. and Hanjorg, J. (1986) Echocardiographic findings in patients with proved pulmonary embolism. Am. Heart. J. 112. 1284-1290. Lescure. F. and Tamzali. Y. ( 1984) Valeurs de reference en echocardiographie T M chez le cheval de sport. Rewe Mdd. Vdt. 135.405-418. Littlewon. M. C. G . (1986) The equine heart in health and disease. In: Ey~rine Siqery and Medicine: vol 2. Academic Press. London pp 76-80. Lombard. C. W., Scaratt, W. K. and Buergelt, C. D. (1983) Ventricular septal defects in the horse. J. Am. vet. nred. Ass. 183,562-56s. McCormick. B. S.. Peet. R. L. and Downes. K. (1985) Erysepe/otri.r rhrtsiopathioe vegetative endocarditis in a horse. Ausr. Vet. .I. 62, 392. Pipers, F. S., Hamlin, R. L. and Reef, V. (1979) Echocardiographic detection of cardiovascular lesions in the horse. J. Med. Swg. 3, 68-77. Robinson, N. E. (1987) Cvrrent Therap! in Veterinary Medicine. 2nd edn. p 729. W. B. Saunders Company, Philadelphia. Roby. K. A. and Reef, V. B. (1986) ECG of the month. J. Anr. i'et. nied. Ass. 188. 570571. von Mill, J. and Hanak, J. (1978) Abnorme Herzbefunde bei Vollblutrennpferden. Mnnatsheftefrrr Veterirtaerniedidi.ir133, 508-5 I I . Wadsworth. A. 8. (1919) A study of the endocardial lesions developing during pi?erinto('occtrsinfection in horses. J. Med. Res. 34. 279. Wagenaar. G. and Kroneman, J. (1986) Cardiovascular disease. In: Eyrtirre diseases. Ed: H. J. Wintzer Verlag Paul Parey. Berlin and Hamburg. pp 4748. Wagenaar. G . . Kroneman. J. and Breukink. H. ( 1967) Endokarditis beim Pferd. Die Blarteri He& 34,38-45. Weinstein. L. (1988) Infective endocarditis. In: Heart Disease: A PxtbooL I J / Cardiovascrtlar Medicine. Vol 2. Ed: E. Braumwald W. B. Saunders Co. Philadelphia. pp 1093-1134.
Receii*edfwpublication: 185.88 Accepted: 25.7.91
EQUINE VETERINARY JOURNAL Equine iw. J. ( I99 I ) 23 (6) 479-482
Case Reports Diagnosis of pulmonary valve endocarditis in a horse L. NILSFORS, C. W. LOMBARD, D. WECKNER* and C. KVARTt Departments of Clinical Radiology (Box 7029), * Medicine and Surgery and tPhysiology, Swedish University of Agricultural Sciences, S-750-07 Uppsala, Sweden Introduction
Clinical pathology
VALVULAR endocarditis in the horse is a rare condition and affects the left heart more often than the right (Else and Holmes 1972; Deegen, Lieske and Schoon 1980; Fregin 1982; Littlewort 1986; Wagenaar and Kroneman 1986). There are reports of four equine pulmonic endocarditis cases verified at necropsy (Innes, Berger and Francis 1950; Wagenaar, Kroneman and Breukink 1967; Buergelt, Cooley, Hines and Pipers 1985) and one clinically suspected pulmonic endocarditis (von Mill and Hanak 1978) in the literature. Pulmonic valve endocarditis was confirmed at necropsy in one horse in our clinic (S. Persson 1987, personal communication). The purpose of this report is to describe the ante-mortem diagnosis of pulmonic valve endocarditis in a horse.
Blood analysis revealed a high white cell count of 24 x 109/litre with 83 per cent granulocytes, a low Hb of 74 g/litre, a low packed cell volume of 0.28 litres/litre, a normal serum protein, a low albumin/globulin ratio of 0.5 caused by high gamma globulin fractions and a high alkaline phosphatase (ALP) value of 12.2 pkat/litre (normal value for our laboratory is < 8.5 Natjitre). Urea, creatinine, ASAT, CK, GT and bile acids were within normal limits. Pleurocentesis revealed a small amount of pleural fluid with a normal total leucocyte count, but a high proportion of polymorphonuclear cells, 5 15 x 106/litres, to mononuclear cells, 265 x I06/litres (Robinson 1987). Peritoneocentesis had an unremarkable cytology. Bacterial cultures of pleural and peritoneal fluid, urine and blood were negative.
Case history Diagnosric aids
Four months after importation from Poland, a four-year-old Warmblood gelding was referred to the Department of Medicine and Surgery at the Swedish University of Agricultural Sciences. According to the referring veterinary surgeon, the horse had been losing weight for one month without evidence of anorexia or gastrointestinal disturbances. The animal's body temperature had varied between 38.5 and 39.5'C for two weeks prior to presentation, work capacity was limited, a stiff gait was evident in the hind legs and lameness in the left front leg. The horse's history prior to importation is unknown. Clinical findings Phy~icalesamination
The horse weighed 472 kg and had subcutaneous oedema in all four legs, from the hock and carpus and distally. The lameness in the left front leg was localised to the fetlock joint. An old skin wound that had healed by second intention was found on the right chest wall. The horse had engorged jugular veins but no jugular pulse. A palpable thrill was on the left side of the chest in the third intercostal space level with the olecranon. Auscultation of this area revealed a distinct third heart sound and a grade 5/6 holosystolic ejection murmur. On the right side, a grade 4/6 holosystolic murmur could be heard in the third intercostal space level with the humeral joint. Lung auscultation was normal, but the horse reacted with unease to percussion over the right dorsal lung. No line of pleural effusion could be percussed. Over the next three weeks body temperature and respiratory rate varied irregularly between 38 and 39.5"C and 15 to and 20 breathdmin. respectively, and the resting heart rate varied between 40 and 46 beats/min.
The electrocardiogram showed a regular sinus rhythm with normal intervals (Fregin 1982). Elevation of the S-T segment and a high amplitude of the T-wave in lead I, 11, Ill, aVF, CV6LL and CV6LU. measuring 2.4 mV (twice the Ramplitude) in lead 11, were seen (Fig I). At the point of maximal amplitude in the pulmonic valve area, the murmur on the phonocardiogram (Siemens-Elema, Sweden) described a distinct crescendo-decrescendo pattern in both low and high frequency bands (Fig I). On the right side, the murmur had a less distinct crescendo-decrescendo pattern. M-mode echocardiography (ATL 600 B; USA) revealed a normal left heart internal end diastolic diameter (80 to 130 mm) and a normal right ventricular internal diameter (32 to 52 mm) (Lescure and Tamzali, 1984). An exaggerated systolic and diastolic septal motion was seen and the right ventricular free wall was thicker, 23 mm in diastole, than normal (about 15 mm, L. Nilfors, unpublished data) (Fig 2; right ventricular dimensions were measured on a magnified view of the near field). Moreover, the septal wall thickness appeared to be increased and measured 30 mm at end diastole. On real-time echocardiography (Aloca 725; Aloca, Japan) the right atrium appeared to be of normal size, as was the right ventricular outflow tract. The right ventricular wall appeared hypertrophied. Markedly thickened pulmonic valve leaflets consistent with bacterial endocarditis obstructed the pulmonary artery in diastole (Fig 3). Only the first few centimeters of the pulmonary artery could be seen. Contrast echocardiography of the left and right ventricle using C 0 2 microbubbles in blood did not document any shunts or tricuspid or mitral valve regurgitation. Selective venous blood gas analysis (ABL-3; Radiometer, Denmark) of the cranial caval vein, the right
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Fig I : The top tracing is a Lead I1 electrocardiogram (ECG),and the two bottom tracings are phonocardiograms (PCG) recorded in the pulmanic valve area. Paper speed is 25 mmlsec. Note the elevated S-T segment and the tall T-wave on the ECG. The crescendo-decrescendo murmur visible in hoth the low frequency ( L ) (maximum amplitude 50 H:) and the high frequency (H)(maximum amplitude 400 H z ) hands of the PCG is compatihle with an ouflow tract stenosis. A third heart sound (arrow) is also visihle
Fig 2: M-mode echocardiogram,using a 2.0 MH: transducer. shouitig the right ventricular n*all (RVW). the right ventricle (RV). the left ventride (LV). the left iuntricitlar wall (LVW) and the interi~entricrtlarseptum (IVS). In systole, an esaggerated motion of the septrtni tonsard the left ventricle is seen (solid arrou,),ininiediatelyfdlowed hy an e.va.q,qerated motion toneard the right ventricle in early diastole (openarrow)
Fig 3: A real-time echocardiogram (right parasternal short axis lieu. of the heart hase riewedfionr helow). iising a 3.0 MH: transducerv is shown in systole (aho1.e) and in diastole (helow). Note the thick pitlnionary vahe leaflets (open arrows) seen in systole and the alniosr i m p l e t e ohstriiction of the pulnronic, i d v e (solid arron,) in diastole. AO: aorta. RVO: right \-entr.icrrlarortrflou- tract
atrium, the right ventricle and the caudal caval vein (Lombard, Scaratt and Buergelt 1983) did not reveal any abnormal variations. Intracardiac pressure recordings (pressure transducer EMT 033 connected to a Mingograf 804, by way of a pressure amplifier EMT 863) (Siemens-Elema, Sweden) demonstrated a
markedly increased pressure in the right ventricle and atrium, whereas normal pressures were seen in the pulmonary artery (Fregin 1982) (Table 1). Radiographs of the thorax showed a well delineated homogeneous density of about 8 cm in diameter in the caudal lung lobes suggestive of either an abscess, a focal pneumonia
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TABLE 1: Results of blood pressure measurements from the following locations of the heart; right atrium (RA), right ventricle (RV),pulmonary artery (PA), and left ventricle (LV). Normal values (f sd) (Fregin 1982) Blood pressure (mmHg)
Location RA RV PA A0 LV
Systolic
24 (12.1f33) 135 (45.8f 5.6) 37 (42.1It 5.2) 120 (143.9f 2.5) 120 (148.3f 2.6)
Diastolic
5 (-2.2f 3.7) 16 (5.8f 3.5) 20 (18.3f 4.1) 90 (91.8f 2.6) 14 (16.6f 1.6)
or an embolic infarction. No sign of pleural effusion was found.
Differential diagnosis The subcutaneous oedema, the engorged jugular veins, and an increased heart rate and respiratory rate are all signs of right sided congestive heart failure (CHF) (Fregin 1982; Littlewort 1986). The point of maximal intensity of the holosystolic crescendo-decrescendo murmur and the marked pressure gradient across the pulmonic valve were indicative of a pulmonic stenosis. Initially, there was a possibility of the right sided murmur being caused by a ventricular septa1 defect or by insufficient tricuspid valves. This was excluded by intracardiac blood gas measurements. contrast echocardiography and the absence of vwaves on the right atrial pressure tracing. The right sided murmur probably was the left sided stenotic murmur overheard on the right side. The lack of tricuspid insufficiency explained the absence of a jugular pulse, whereas the distension was a result of increased right atrial and right ventricular pressures. The high right ventricular pressure and the hypertrophied right ventricular wall are signs of a pressure overload (Feigenbaum 1986). The fever, high white cell count, elevated gamma-globulin fractions and the anaemia pointed to an active chronic infection. Therefore, the stenosis was likely caused by a vegetative endocarditis of the pulmonic valve leaflets. This was confirmed by the real-time echocardiogram, which also excluded a congenital pulmonic stenosis. The pleural fluid had an increased proportion of polymorphonuclear cells, but was not abnormal enough to indicate a pleuritis (Robinson 1987). It is plausible that the pleural fluid was influenced by a systemic infection.
Treatmen t Antibiotic treatment was initiated by the referring veterinary surgeon before culture samples were taken. We continued the treatment with a combination of penicillin G 16,000 iu kg and dihydrostreptomycin 20 mg/kg bwt intramuscularly (im) daily based on the idea of using an antibiotic with broad spectrum coverage. The horse did not improve over a three-week period and was destroyed.
Pathology On gross pathology (Fig 4). a markedly hypertrophied right ventricular wall, a slightly hypertrophied interventricular septum and a normal left ventricle were seen. The main pulmonary artery was enlarged markedly in the valvular area and a distinct mass could be felt. Opening up the pulmonic
Fi,q 4: A large endricarditic niass that extendsfram the right ventricular ougon trai't to the niuin pulmonary artery (open arrow), covering the l arrow). (Part pulnionic w h e . Note the thick right ventricular u ~ l(solid of the right rentriiular u d l is removed). RV: right \ventricle
artery allowed visualisation of a large mass occluding the orifice, leaving only a small passage at the side close to the aorta. The mass had an irregular, verucous structure, originating from all pulmonic valve leaflets and completely obliterating the pulmonic valve structure. No other vegetative lesions were found. Pleural or abdominal effusion was not present. In the right caudal lung lobe, a thromboemolism of the lobar artery producing infarction involving a volume of about 1.000 cm3 of lung tissue was found. Bacterial cultures and histochemistry of the endocarditic mass and the lung infarct did not reveal microorganisms. Microscopic examination of the vegetative lesion showed that it consisted of fibrin, platelets and leucocytes. At the base of the vegetation, organisation had started and granulation tissue had proliferated into the thrombus. Focal parietal endocardial thickening with fibrinous adhesions were seen on the right ventricular wall and on the apical part of the left ventricle.
Discussion The horse's history of weight loss, decreased work tolerance, stiff gait, increased pulse rate and temperature are all
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compatible with valvular endocarditis (Wagenaar and Kroneman 1986). Streptococcus equi, Streptococcus zooepidemicus, Streptococcus SQ., Actinohacillus equuli, Erysipelotrix rhusiopathiae, Escherichia coli. Pseudomonas aeruginosa. Candida parapsilosis, Pasteurella sp. (Buergelt, Cooley, Hines and Pipers 1985, McCormick, Peet and Downes 1985; Robey and Reef 1986; Wagenaar and Kroneman 1986; Dedrick, Reef, Sweeney and Morris 1988) and Mycohacterium tuberculosis ( S . Person 1987, personal communication) have been isolated from endocarditis in the horse. It is plausible that the bacterial cultures in the reported case were negative because of antibiotic treatment. In man, differences between subacute and acute endocarditis in aetiology and pathogenesis are noted. Thus, in subacute endocarditis the inducing bacteraemia often originates from the normal flora in traumatised areas, eg, teeth removal. A valvular defect combined with a jet effect caused by blood flowing from a high to a low pressure area are important predisposing factors. However, degenerative fibrosis or fenestrations, common in the aortic valves, are infrequent in the pulmonic valves (Else and Holmes 1972). In acute endocarditis a skin or lung infection is the most common pre-existing foci of infection and previously normal valves are often found. The causative agents in these cases are highly invasive and adhere directly to the valve (Weinstein 1988). This mechanism may be likely in this case, although the only visible source of infection was the skin wound on the chest wall. A fungal infection cannot be excluded because these produce relatively large vegetations (Weinstein 1988). The parietal endocardial thickening found at necropsy was probably caused by the catheterisation. A right sided endocarditis is likely to produce pulmonary thrombo-embolism (Kasper et a1 1986). This would explain the horse's painful reaction to percussion of the right lung and the radiographic findings. Although it appears that the antimicrobial agents used did cure the infection, the prognosis of the valvular endocarditis described was poor because of a late clinical diagnosis with large vegetations developing. This caused a pulmonic stenosis, which resulted in a right sided congestive heart failure from cor pulmonale. If treatment is attempted at an early stage, long term administration of bactericidal drugs given to maintain high therapeutic levels in the plasma would be indicated (Weinstein 1988). The echocardiographic diagnosis of valvular endocarditis was first reported in man by Dillon eta1 (1973) and in the horse six years later (Pipers, Hamlin and Reef 1979). In the horse in this report, the endocarditis masses on the pulmonic valves were imaged easily with two-dimensional real-time echocardiography. The septal motion pattern seen is usually a result of left ventricular volume overload (Feigenbaum 1986). However, left ventricular wall motion appeared hypokinetic and no other signs of left ventricular volume overload were found. As pulmonary flow is restricted, one would expect a decreased pre-load on the left ventricle and a lower stroke volume. No signs of a reduced left ventricular dimension at end diastole was found and heart rate was only slightly increased. Insufficient tissue oxygenation due to reduced blood flow could have caused a myocardial hypoxia (Hall 1971) which might explain the high T-waves on the ECG (Fregin 1982). However, the myocardium did not show any signs of insufficient oxygenation histologically. The increased respiratory rate was probably due to the infarcated part of the
lung causing pain and a reduced volume of normally ventilated lung tissue. The valvular lesion appeared to obstruct the pulmonic valve completely in diastole and, therefore, a diastolic insufficiency murmur may not have been produced.
Acknowledgments The authors thank Dr. R. Svanholm for referring the case and Dr. L. Jonsson, for evaluating the autopsy.
References Buergelt. C. D., Cooley, A. J.. Hines. S. A. and Pippers, F. S. (1985) Endocarditis in six horses. Vet. Path. 22.333-337. Dedrick. P.. Reef. V. B.. Sweeney. R. W. and Morris, D. D. (1988) Treatment of bacterial endocarditis in a horse. J. Am. w t . wed. Ass. 193, 339-342. Deegen. E., Lieske. R. and Schoon. H. (1980) Klinische und kardiologische Untersuchungnsbefunde bei 3 Deckhengsten mit Aortenklappeninsuffizienz. Tierur:t/. pras. 8 , 2 I 1-222. Dillon, J. C.. Feigenbaum, H., Konecke, L. L. (1973) Echocardiographic manifestations of valvular vegetations. Am. Heart J. 86,698 Else, R. W. and Holmes. 3. R. (1972) Cardiac pathology in the horse ( I ) Gross pathology. Equirre wt. J. 4, 1-8. Feigenbaum. H. (1986) Echocardiography. 4th edn, Lea & Febiger, Philadelphia. pp 162-I67,3 10-319. Fregin. G . F. ( 1982) The cardiovascular system. In: Eqrririe Medicine arid S i q e r y vol 2. Eds: R. A. Mansmann. E. S . McAllister. P. W. Pratt, American Veterinary Publications, Santa Barbara. pp 645,684-685. Hall, L. W. (1971) Disturbances of cardiopulmonary function in anaesthetised horses. Eqtrirre Vet. J. 3,95-98. Innes, J. M.. Berger. J. and Francis, J. (1950) Subacute bacterial endocarditis with pulmonary embolism in a horse. Brit. Vet. J. 106. 245-250. Kasper. W., Meinenz. T.. Henkel. 8.. Eissner Dagmar, Hahn, K., Hofmann. T.. Zeiher, A. and Hanjorg, J. (1986) Echocardiographic findings in patients with proved pulmonary embolism. Am. Heart. J. 112. 1284-1290. Lescure. F. and Tamzali. Y. ( 1984) Valeurs de reference en echocardiographie T M chez le cheval de sport. Rewe Mdd. Vdt. 135.405-418. Littlewon. M. C. G . (1986) The equine heart in health and disease. In: Ey~rine Siqery and Medicine: vol 2. Academic Press. London pp 76-80. Lombard. C. W., Scaratt, W. K. and Buergelt, C. D. (1983) Ventricular septal defects in the horse. J. Am. vet. nred. Ass. 183,562-56s. McCormick. B. S.. Peet. R. L. and Downes. K. (1985) Erysepe/otri.r rhrtsiopathioe vegetative endocarditis in a horse. Ausr. Vet. .I. 62, 392. Pipers, F. S., Hamlin, R. L. and Reef, V. (1979) Echocardiographic detection of cardiovascular lesions in the horse. J. Med. Swg. 3, 68-77. Robinson, N. E. (1987) Cvrrent Therap! in Veterinary Medicine. 2nd edn. p 729. W. B. Saunders Company, Philadelphia. Roby. K. A. and Reef, V. B. (1986) ECG of the month. J. Anr. i'et. nied. Ass. 188. 570571. von Mill, J. and Hanak, J. (1978) Abnorme Herzbefunde bei Vollblutrennpferden. Mnnatsheftefrrr Veterirtaerniedidi.ir133, 508-5 I I . Wadsworth. A. 8. (1919) A study of the endocardial lesions developing during pi?erinto('occtrsinfection in horses. J. Med. Res. 34. 279. Wagenaar. G. and Kroneman, J. (1986) Cardiovascular disease. In: Eyrtirre diseases. Ed: H. J. Wintzer Verlag Paul Parey. Berlin and Hamburg. pp 4748. Wagenaar. G . . Kroneman. J. and Breukink. H. ( 1967) Endokarditis beim Pferd. Die Blarteri He& 34,38-45. Weinstein. L. (1988) Infective endocarditis. In: Heart Disease: A PxtbooL I J / Cardiovascrtlar Medicine. Vol 2. Ed: E. Braumwald W. B. Saunders Co. Philadelphia. pp 1093-1134.
Receii*edfwpublication: 185.88 Accepted: 25.7.91
