Rupture of the heart occurs rarely in animals. It is recorded in cattle where a foreign body penetrating from the reticulum perforates the ventricular wall, and in the left atrium of horses as a consequence of chronic fibrotic myocarditis.1 Rupture of the base of the aorta is not uncommon in horses and has the same effect as cardiac rupture. The pericardial sac immediately fills with blood and the animal dies of acute heart failure due to pericardial tamponade. A similar cardiac tamponade occurs when reticular foreign bodies lacerate a coronary artery or when foals suffer severe laceration of the epicardium during a difficult parturition.
When the aorta ruptures it may do so through its wall just above the aortic valves. The wall may have been weakened previously by verminous arteritis associated with migrating strongyles in horses or onchocerciasis in cattle or by the development of medionecrosis. Another form of rupture occurs through the aortic ring. Death occurs very suddenly; all cases reported by one author affected stallions and coincided with the time of breeding. Cardiac tamponade may occur but the common finding is a dissecting aneurysm into the ventricular myocardium.
Rupture of the aortic arch and the pulmonary artery near the ligamentum arteriosum occurs occasionally in horses. The resultant fistula between the aorta and the pulmonary artery produces a sudden onset of cardiac failure and respiratory distress. Affected horses usually die shortly after the onset of clinical signs but can survive up to 8 days. The rupture is predisposed by abnormalities in the vasa vasorum of the vessels and may have a familial occurrence.2
Aortocardiac fistulas originating at the right aortic sinus are recorded in a series of older horses with sudden onset acute distress and exercise intolerance.3 Five of the seven horses had a characteristic continuous murmur that was loudest at the right fourth intercostal space. Fistulas extended into the right ventricle or atrium in six horses and the left ventricle in one. Five had dissecting tracts in the septal myocardium.
Rupture of the aorta is the usual cause of death in calves with Marfan’s syndrome. Some have dissecting aneurysms of the aorta and pulmonary artery. Calves with Marfan’s syndrome are affected from birth. They have a loud systolic murmur over the base of the heart on the left side in association with enlargement of the aortic root. There are other phenotypic abnormalities, including long thin limbs, joint and tendon laxity, and ocular abnormalities including dorsal displacement of the lens and lens opacity. The nature of the inheritance in cattle is uncertain.4
Cranial mesenteric artery aneurysms have been reported in cattle less than 4 years of age secondary to inherited defects in the wall of the celiac and cranial mesenteric arteries. An autosomal dominant mode of inheritance was suspected.5 An aneurysm of the cranial mesenteric artery was diagnosed in a cow with severe abdominal pain and the presence of a large pulsatile mass at the root of the mesentery.6
Sudden death, or sudden onset of acute heart failure can also result from rupture of components of the heart valves. Rupture of the chordae tendineae of the mitral valve occurs in horses both without apparent predisposing lesions and as a sequel to endocarditis and occurs in adult horses as well as foals.7-9 It is manifested by sudden onset of acute heart failure in horses apparently previously healthy or, when a complication of a pre-existing endocarditis, as a sudden onset complication of the disease or a cause of death. The rupture may involve the chordae of any of the cusps of the valve.7 Rupture of the pulmonary valve producing right heart failure can also occur.10
1 Haaland MA, Davidson JP. Vet Clin North Am. 1983;78:1284.
2 Van der Linde-Sipman JS. Vet Pathol. 1985;22:51.
3 Marr CM, et al. Vet Radiol Ultrasound. 1998;39:22.
4 Potter KA, Besser TE. Vet Pathol. 1994;31:501.
5 Schuiringa-Sybesma AM. Tijdschr Diergeeskd. 1961;86:1192.
6 Angelos JA, et al. J Am Vet Med Assoc. 1995;207:623.
7 Marr CM, et al. Vet Rec. 1990;127:376.
8 Ewart S, et al. J Am Vet Med Assoc. 1992;200:961.
Cor pulmonale is the syndrome of right-sided heart failure resulting from an increase in right heart workload secondary to increased pulmonary vascular resistance and pulmonary hypertension. The most documented cause of pulmonary hypertension in livestock is alveolar hypoxia. Acute alveolar hypoxia (lowered alveolar Po2) is a potent cause of pulmonary hypertension in several species, but cattle are especially reactive and this is the cause of the syndrome of cor pulmonale in cattle at high altitudes, bovine brisket disease, which is described in more detail elsewhere in this text.
An outbreak of cor pulmonale with pulmonary vascular lesions similar to those seen with high mountain disease but occurring in calves not at altitude is recorded; it was postulated but not proved to be the result of the ingestion of feed contaminated with the pyrrolizidine alkaloid monocrotaline.1
Pulmonary hypertension can also result from partial destruction of the pulmonary vascular bed and a reduction in its total cross-sectional area. Pulmonary thromboembolic disease can produce right heart failure by this mechanism. Chronic interstitial pneumonia and emphysema may also induce cor pulmonale by the same mechanism.2
Chronic obstructive pneumonia, where there is airway constriction and accumulation of fluid in distal airways, may induce pulmonary hypertension by a combination of chronic hypoxia and reduction of the pulmonary vascular bed.3 Mean pulmonary artery pressures in calves with respiratory disease was 42 mmHg, compared to 22 mmHg in healthy age-matched calves. Although pulmonary hypertension and right heart hypertrophy may occur in livestock with primary pulmonary disease, clinical cardiac insufficiency is usually minor, and right heart failure rare. Nevertheless it can occur and is a cause of congestive heart failure in cattle.4,5
In goats, cor pulmonale, with right ventricular and right atrial hypertrophy secondary to interstitial pneumonia, may lead to atrial fibrillation,6 and cor pulmonale leading to atrial fibrillation has also been recorded in horses.7
In highly conditioned feedlot cattle, increased intra-abdominal pressure resulting from excessive abdominal fat, forestomach engorgement and recumbency can lead to pulmonary hypoventilation, with decreased alveolar Po2 and subsequent right heart failure, a syndrome analogous to the Pickwickian syndrome in humans.8
Chronic severe elevations in pulmonary venous pressure can lead to constriction and hypertrophy of the vascular smooth muscle of precapillary vessels with resultant pulmonary hypertension. An elevated left ventricular filling pressure is perhaps the more common cause and can set the stage for right heart failure in the left heart failure situations. The toxic principle in poisoning by Pimelea spp. appears to act in part by constricting the pulmonary venules producing pulmonary hypertension, which contributes to the clinical syndrome.
Persistent pulmonary hypertension of the neonate (PPHN) is a common problem in neonatal foals and calves, particularly in calves derived from somatic cell clone technology. Persistent pulmonary hypertension is characterized by persistent postnatal hypoxemia secondary to failure to adapt to extrauterine life. An imbalance between endogenous vasoconstrictors and vasodilators is believed to play a major role in the development and maintenance of PPHN. An increase in plasma concentration of endothelin-1 (a potent vasoconstrictor) has been observed in neonatal calves with PPHN, and the source of endothelin-1 is thought to be the placenta.9 Many cloned calves have abnormal placentation, characterized by a reduction in the number of established cotyledons that are enlarged and edematous. Treatment is symptomatic, focusing on intranasal oxygen administration and maintaining the calf in sternal recumbency.
1 Pringle JK, et al. J Am Vet Med Assoc. 1991;198:857.
2 Panter KE, et al. Vet Hum Toxicol. 1988;30:318.
3 Nuytten J, et al. Zentralbl Vet Med A. 1985;32:81.
4 Angel KL, Tyler JW. J Vet Intern Med. 1992;6:214.
5 Jubb TF, Malmo J. Aust Vet J. 1989;66:257.
6 Gay CC, Richards WPC. Aust Vet J. 1984;60:274.
7 Gelberg HB, et al. J Am Vet Med Assoc. 1991;198:679.
8 Alexander AF. Effects of poisonous plants on livestock. New York: Academic Press, 1978;285.
Etiology Valvular disease is acquired or congenital. Endocarditis is the commonest cause. Some murmurs are functional and not indicative of disease
Epidemiology Functional murmurs are common in the horse and vary with breed and training. Little information is available on the epidemiology of acquired valvular disease
Clinical findings Murmur defined by location, timing, character, intensity and radiation. Possibly precordial thrill, cardiac insufficiency and, in severe cases, congestive heart failure
• Endocarditis. Most common cause – see following section
• Endocardiosis. Common only in pigs
• Rupture of the chordae tendineae, either spontaneous or secondary to endocarditis1
• Laceration, detachment of aortic valve leaflets, either spontaneous or secondary to endocarditis
• Dilatation of the right atrioventricular valve annulus, such as occurs in brisket disease and secondary to some myocardial disease; may result in functional insufficiency of the valves.
• Fenestration of the aortic and pulmonic valves in horses. The cause of the lesions is unknown, although their presence in very young animals, including newborn foals, suggests that some may be congenital defects. The importance of these lesions as causes of valvular insufficiency is doubtful, although they may cause valvular murmurs if they are present close to the attachments of the cusps
• Blood cysts are common on the atrioventricular valves of cattle. They are lined with endothelium, can occur congenitally2 and their incidence and size may increase with age.3 They have no clinical significance. Serous cysts occur occasionally on the mitral valve of cattle.
There is limited information on the epidemiology and the age-specific incidence of valvular disease or murmurs in large animals, although slaughter surveys show a high prevalence of endocardial lesions. Studies at clinical centers indicate that valvular disease is often underdiagnosed in both cattle and horses and that its presence may not be detected in more than 50% of cases.4-6
Auscultatory surveys show a high prevalence of murmurs with breed and horse-use differences. Functional (physiological) murmurs are particularly common in trained, fit racehorses. In a survey of 545 clinically normal horses in England, murmurs were heard in 68%, with a higher prevalence in flat racing and National Hunt horses than in competition and pleasure horses.7 Murmurs with the characteristics of functional ejection murmurs were detected on auscultation over the left hemithorax in approximately 50% of horses and the right side in 8%. Murmurs with the characteristics of early diastolic functional murmurs were detected on the left side in 15% and on the right side in 13%. Murmurs with the characteristics of regurgitation at the mitral, tricuspid and aortic valves were detected in 3.5, 9.2 and 2.2% of horses respectively.
An extensive abattoir survey8 suggests that valvular lesions may be more common in the horse than is clinically appreciated. Approximately 25% of horses had lesions, the majority being nodular or distorting lesions on the valves or chordae tendineae of the left side and, in a significant proportion, murmurs were detected prior to slaughter. Chronic trauma of the valve leaflets was considered an important initiating factor.
In a slaughter survey of pathology in the heart of pigs mitral valve endocardiosis was observed in 63% of pigs and tricuspid endocardiosis in 18% of pigs.9 The prevalence and severity increases with age. These lesions can be associated with prolapse of the mitral valve and jet impact lesions. They have little significance in growing pigs but the significance of endocardiosis to clinical cardiac disease in older sows needs examination.
Bacterial endocarditis in slaughter pigs has been recorded with a prevalence of 3.1 per 10 000 animals.10
The important clinical indications of valvular disease are audible murmurs and palpable precordial thrills. Murmurs may occur at any phase of the cardiac cycle and are caused by the vibrations of turbulent flow of blood transmitted to the surface of the chest. Vibrations of strong intensity may also result in palpable vibrations at the surface of the chest.
Blood flow is normally laminar and without turbulence. Turbulence in flow may be produced by a sudden change in the diameter of the vessel through which the blood is flowing. Its occurrence is directly related to the velocity of flow and inversely related to blood viscosity.
With murmurs associated with valvular lesions the valve lesion produces a sufficient change in stream bed diameter to result in turbulent flow. The turbulence may occur when the valves do not close properly (regurgitation or insufficiency) and blood is forced through atrioventricular orifices during ventricular systole, or through semilunar orifices during ventricular diastole. Turbulence may also occur when the valves do not open completely (stenosis) and blood is forced through a stenotic semilunar orifice during ventricular systole or enters the ventricle through a narrow atrioventricular orifice during ventricular diastole.
The severity of the turbulence and hence the murmur can be increased with higher flow velocities such as occur with exercise and by factors that decrease blood viscosity such as anemia or hypoproteinemia.
Acquired valvular disease usually results in insufficiency of the affected valve and less commonly both insufficiency and stenosis. Congenital lesions more commonly result in stenosis of the valve.
A change in vessel diameter such as occurs with dilatation of the aorta or pulmonary artery can produce turbulence and a murmur. A reduction in blood viscosity contributes to the frequency of murmurs occurring in anemic and hypoproteinemic states and hemic murmurs are common in anemic cattle, particularly over the pulmonic valve.
Turbulent flow may occur in the absence of a change in stream bed diameter if a certain critical velocity of flow is exceeded. This is believed to be the cause of functional or ejection murmurs that occur commonly in horses and lactating dairy cows during the rapid ejection phase even at rest and especially following exercise.
Stenosis of the outflow valves results in an increased pressure load on the heart and compensatory hypertrophy (concentric hypertrophy). Insufficiency of the semilunar valves or of the aortic or pulmonic valve produces a volume load on the heart and is followed by compensatory dilatation and hypertrophy (eccentric hypertrophy). If the valves on the left side of the heart are affected, especially the aortic valve, the changes in ejection of the blood from the ventricle produce changes in the character of the peripheral pulse. Involvement of the tricuspid valve will produce changes in the jugular pulse.
The presence of valvular lesions and murmurs may mean little except that some degree of cardiac reserve is lost. This may be small in degree, and moderate stenosis or incompetence can be compensated and supported for long periods. The importance of valvular lesions that do not result in cardiac insufficiency rests in their possible contribution to disease in other organs by the liberation of emboli, and the necessity for close examination of the heart when they are present.
The purpose for which the animal is maintained also has some bearing on the significance of a murmur. Valvular lesions are of much greater importance in racing animals than in those kept for breeding purposes. The challenge to the clinician is to determine the significance of a murmur to the health and performance of the horse and to the safety of the rider.
Only the clinical findings referable to valvular disease are discussed here. The clinical findings in chronic (congestive) heart failure, which may coexist, are discussed elsewhere.
Auscultation is the fundamental basis of examination and a knowledge of the optimum areas of auscultation and the significance of the murmurs encountered are essential. When a murmur is detected it should be categorized according to its timing and duration, intensity, location, and character. There is room for improvement in the correct identification of heart murmurs, and specialist clinicians can more accurately identify the likely site of heart murmurs than other clinicians.11
Timing allows a subdivision into systolic, diastolic and continuous murmurs and immediately shortens the list of possible defects present. There is little problem in differentiating systolic from diastolic murmurs at slow heart rates because of the temporal difference between the length of the systolic and diastolic period. However, where there is a murmur present at fast heart rates this distinction is less obvious and it is possible to misclassify the period of the cycle in which the murmur is occurring.
• Murmurs should be timed with reference to the arterial pulse, which occurs in early to mid-systole if a proximal artery is examined
• A convenient artery is on the posteriomedial aspect of the carpus and radius in cattle and horses
• A less satisfactory alternative is timing with the occurrence of the apex beat
• Timing by relation to the heart sounds is unreliable as these are frequently altered in character and at fast heart rates a diastolic murmur may be mistaken for a systolic one
• Systolic murmurs are associated with stenosis of the outflow valves or insufficiency of the atrioventricular valves
• Diastolic murmurs are associated with insufficiency of the outflow valves or stenosis of the atrioventricular valves
• A continuous murmur or one that occurs during both systole and diastole may be associated with both stenosis and insufficiency of the same valve or with multiple valvular lesions but more commonly results from the turbulent flow of blood from a high-pressure to a low-pressure system with no intervening valve, such as occurs with a patent ductus arteriosus.
Duration during systole or diastole is determined by a careful examination of the murmur with relationship to the period between the heart sounds. Systolic murmurs are further classified as early, late, holo- or pansystolic according to their occurrence and duration in the period between the first and the second heart sounds and diastolic murmurs as early (occurring between S2 and S3), holodiastolic or presystolic (occurring between the atrial fourth heart sound and S1). Pansystolic and pandiastolic murmurs, occurring throughout the systole or diastole, have greater significance than murmurs that occur, for example, only in early systole and early diastole.
Intensity or loudness of a murmur provides a guide to its significance. A system of grading the intensity of murmurs that has been found to be of clinical value is as follows:
• Grade I. The faintest audible murmur. Generally only detected after careful auscultation by an experienced clinician
• Grade II. A faint murmur that is clearly heard after only a few seconds auscultation
• Grade III. A murmur that is immediately audible as soon as auscultation begins and is heard over a reasonably large area
• Grade IV. An extremely loud murmur accompanied by a precordial thrill. The murmur becomes inaudible if the stethoscope is held with only light pressure on the chest
• Grade V. An extremely loud murmur accompanied by a precordial thrill. The murmur can still be heard when the stethoscope is held with only light pressure against the chest.
Grade I murmurs are not clinically significant whereas grade IV and V invariably are. The significance of grade II and III murmurs varies according to their cause. A system that grades on a six-grade basis is also used and differs only in a further subcategorization of moderately loud and loud murmurs.
The presence of a precordial thrill is determined by palpation over the point of maximal intensity of the murmur and palpation on the chest over other areas of the heart. A precordial thrill indicates that there is considerable energy generated by the turbulent flow and defines the intensity of the murmur in the top two grades in both grading systems.
Location and radiation of a murmur is related to its areas of generation and transmission. The point of maximum intensity (PMI) is noted with reference to the areas of maximum audibility of the heart valves described earlier under the heading of examination of heart sounds. Low-intensity murmurs are generally restricted to the auscultatory area overlying their area of generation. The auscultatory areas of the heart and of the individual heart sounds have been described earlier in the section on arrhythmias. The vibrations associated with very loud murmurs may be transmitted to other auscultatory areas but generally they are most intense near the area of generation, as is any associated thrill. Murmurs and thrills can be restricted to local areas and it is essential to examine several auscultatory areas over both sides of the heart.
Character is determined by change in intensity during the duration of a murmur and is defined as crescendo, crescendo–decrescendo, decrescendo or plateau. Murmurs may also be described according to their frequency characteristics by terms such as blowing, honking, musical and buzzing, but these interpretations are very subjective and often not repeatable between examiners. Blowing murmurs do not have a major frequency peak of harmonics and therefore do not have an easily identifiable pitch. In contrast, musical, honking and buzzing murmurs have a primary frequency and associated harmonics. Musical murmurs have a higher fundamental frequency (pitch) than honking or buzzing murmurs, whereas honking murmurs are shorter in duration than buzzing murmurs.12
Following this examination the functional defect producing the murmur and the valve involved are determined from the characteristics of timing and duration, location and radiation, and also any secondary effects that may be present in arterial or venous pulse characteristics. The severity of the lesion is judged in part on the intensity of the murmur but also on the degree of cardiac insufficiency that is present. As a rule all pansystolic mitral and tricuspid murmurs, all holodiastolic murmurs, all right-sided murmurs and all murmurs with a palpable precordial thrill should be considered pathological. The cause of the lesion cannot be determined from auscultation but may be determined from the results of general clinical and special pathological examinations and by a knowledge and consideration of the common causes of valvular disease that involve the particular valve affected in the animal species being examined.
Murmurs not associated with cardiac abnormality occur in all large-animal species, but particularly the horse and the lactating dairy cow. Those associated with turbulence produced during periods of high-velocity flow are often called functional murmurs or flow murmurs; those associated with turbulence resulting from decreased viscosity and increased flow are often called physiological murmurs.
Functional systolic ejection murmurs are very common in young, fit horses and occur occasionally in cattle, sheep and pigs. In horses, they are heard best over the base of the heart, usually on the left side over the aortic valve region, in some horses on the right side, but not usually on both sides in the same horse. They are early to mid systolic murmurs of low intensity (grade 1–3), and are crescendo decrescendo or decrescendo in character. In horses they are usually more audible at heart rates slightly elevated above the resting rate. Occasionally in horses, an ejection murmur is audible over the pulmonary valve.
In cattle they are most common at the base of the heart on the left side. A systolic ejection murmur is very common over the left anterior heart base in lactating dairy cattle and this murmur is thought to be due to turbulence at the pulmonic valves. Auscultation of this murmur requires placement of the stethoscope directly over the pulmonic valve; this murmur is usually not auscultable when the heart is auscultated at the fourth to fifth intercostal space. Holosystolic murmurs (grade 1–3) are heard in some calves in the first 2–3 weeks of life. They are possibly associated with minor deformation of the atrioventricular valves by hematocysts at the edge of the valve leaflets, which are common in young calves.
An early diastolic murmur occurs in horses, most commonly in young Thoroughbreds and Standardbreds, and is believed to be due to vibrations associated with the rapid flow of blood into the heart in early diastole. It is a soft (grade 1–2), high-pitched, early diastolic murmur. When heard over the apex area it is probably a variation of the S3 sound.
A presystolic murmur of grade 1–2 intensity and rumbling sound is occasionally heard in horses and is probably a component of the atrial fourth heart sound.
Recumbent cattle commonly have a low intensity (grade 1–3) crescendo–decrescendo systolic murmur that is auscultated over the right side. It will disappear when the animal stands. A similar murmur occurs where there is ruminal distension and bloat.
In newborn calves and foals a systolic murmur is frequently audible over the base of the heart and it is believed to be due to a partial temporary patency of the closing ductus arteriosus. In newborn pigs a continuous murmur may be heard and this is often replaced by an early systolic murmur audible for the first week of life.
Tricuspid valve insufficiency resulting from endocarditis is the most common acquired valvular lesion in cattle, pigs and sheep. Insufficiency may also result from dilatation of the valve annulus in chronic anemia and with cor pulmonale in conditions such as high altitude disease in cattle. Tricuspid regurgitation can also occur with general heart failure that follows left-sided failure. Because of the association with bacterial endocarditis, tricuspid insufficiency in cattle, pigs and sheep is usually indicative of significant cardiac disease or the presence of marked pulmonary hypertension. However, in horses, the murmur of tricuspid insufficiency may be present with little evidence of impaired performance.7
There is a harsh holosystolic or pansystolic plateau-type murmur most audible over the tricuspid valve area. Loud murmurs project dorsally and to the cranial part of the thoracic cavity on both right and left sides. The murmur is usually accompanied by an exaggeration of the systolic component of the jugular pulse. Congestive heart failure, if it occurs, will be manifest in the greater circulation.
This is the second most common acquired valvular disease in horses, cattle and pigs. The insufficiency may result from endocarditis or rupture of the mitral valve chordae.13-15 There is a loud harsh holosystolic or pansystolic murmur that is most intense in the mitral area. The murmur transmits dorsally and in severe cases may also be heard on the right side. There is frequently marked accentuation of the occurrence of the third heart sound, which may be mistaken for the second sound. A late systolic crescendo murmur has also been associated with mitral insufficiency.16
The pulse characters are unchanged until the stage of cardiac failure. Cases of mitral insufficiency may compensate at rest and may be only evidenced by decreased work tolerance. Failure, if it occurs, will be initially associated with left ventricular volume overload; however, in some cases the retrograde flow of blood through the mitral valve may lead to pulmonary hypertension and the additional occurrence of right-sided heart failure.
Acute-onset heart failure is usually associated with rupture of the valve chordae.17 In the horse, mitral insufficiency may predispose to atrial fibrillation.18
This is the most common acquired valvular defect in horses. There is a loud holodiastolic murmur, frequently accompanied by a thrill caused by the reflux of blood from the aorta into the left ventricle during diastole. The murmur is generally audible over the left cardiac area and is most intense at the aortic valve area and radiates to the apex. It may modify the second heart sound or start immediately following. The murmur may be noisy or musical and the relative intensity varies from horse to horse. Frequently it is decrescendo in character but other variations in its intensity occur. Valvular insufficiency of a sufficient degree to have functional significance is accompanied by an arterial pulse of very large amplitude and high systolic and low diastolic blood pressures (water-hammer pulse). The pulse wave may be great enough to cause a visible pulse in small vessels and even in capillaries. Rarely this lesion is accompanied by a diastolic jugular pulse due to transmission of the impact of the reflex wave across the ventricular septum to the right side of the heart.
There is a harsh systolic murmur, most audible high up over the base of the heart on the left side and posteriorly. The murmur replaces or modifies the first heart sound and is often crescendo– decrescendo in character. A systolic thrill may be palpable over the base of the heart and the cardiac impulse is increased as a result of ventricular hypertrophy. The stenosis has most functional significance when the pulse is abnormal, with a small amplitude rising slowly to a delayed peak reflecting the diminished left ventricular output. There may be signs of left-sided heart failure and this lesion may also be associated with syncope.
Acquired lesions of this valve are rare in large animals. The auscultatory characteristics are similar to those produced by aortic valve lesions but there are no abnormalities of the arterial pulse. Pulmonary stenosis produces a distinct murmur at the third intercostal space on the left side of the chest19 but some cases of pulmonary stenosis in the horse have no murmur.15 Murmurs may also be audible anterior to the aortic valve area on the left side of the chest. Heart failure, if it occurs, is right-sided.
Stenosis of either atrioventricular valve is uncommon. There is a diastolic murmur caused by passage of blood through a stenosed valve during diastolic filling and audible over the base of the heart on the relevant side. The severity of the lesion will govern the duration of the murmur but there is likely to be a presystolic accentuation due to atrial contraction. Right atrioventricular valve stenosis may be accompanied by accentuation of the atrial component of the jugular pulse. Some degree of mitral stenosis may occur in acquired lesions that manifest primarily as an insufficiency.
Clinicopathological findings will reflect the changes caused by the primary disease and are significant only when there is endocarditis. Two-dimensional echocardiography, Doppler echocardiography and color flow Doppler echocardiography are the most valuable noninvasive methods for the examination of valvular disease and allow a detection of the defect, its nature and its severity.20-24 Echocardiography may detect regurgitant flow and flow through stenotic valves that is not detected by auscultation.
Care is needed when the heart is opened to ensure that the valves can be viewed properly from both upper and lower aspects. Lesions of endocarditis may be visible or there may be perforations, distortion or thickening of the valves or breakage of the chordae tendineae. Endocardiosis in pigs is characterized by accumulation of glycosaminoglycans and hyaluronan and myofibroblast differentiation of fibroblasts.25
Fregin GF. Medical evaluation of the cardiovascular system. Vet Clin North Am Equine Pract. 1992;8:329-346.
Patteson MW, Cripps PJ. A survey of cardiac auscultatory findings in the horse. Equine Vet J. 1993;25:409-415.
Patteson M, Blissitt K. Evaluation of cardiac murmurs in horses 1. Clinical examination. In Pract. 1996;18:367-373.
Blissitt K, Patterson M. Evaluation of cardiac murmurs in horses 2. Echocardiography. In Pract. 1996;18:416-426.
Reef VB. Heart murmurs in horses: determining their significance with echocardiography. Equine Vet J Suppl. 1996;19:71-80.
1 Ewart S, et al. J Am Vet Med Assoc. 1992;200:961.
2 Kemler AG, Martin JE. Am J Vet Res. 1972;32:249.
3 Marcato PS, et al. Vet Pathol. 1996;33:14.
4 Roussel AJ, Kasari TR. Compend Contin Educ Pract Vet. 1989;11:769.
5 Power HT, Rebhun WC. J Am Vet Med Assoc. 1983;182:806.
6 Ball MA, Weldon AD. Cornell Vet. 1992;82:301.
7 Patterson MW, Cripps PJ. J Equine Vet. 1993;25:409.
8 Else RW, Holmes JR. Equine Vet J. 1972;4:57.
9 Guarda F, Negro M. Dtsch Tierarztl Wochenschr. 1989;96:377.
10 Ichikawa T, et al. J Jpn Vet Med Assoc. 1991;44:153.
11 Naylor JM, et al. J Vet Intern Med. 2001;15:507.
12 Naylor JM, et al. J Vet Intern Med. 2003;17:332.
13 Holmes JR, Miller PJ. Equine Vet J. 1984;16:125.
14 Miller PJ, Holmes JR. Equine Vet J. 1985;17:181.
15 Maxton AD, Reef VB. Equine Vet J. 1997;29:394.
16 Patteson M, Blissitt K. In Pract. 1996;18:367.
17 Brown CM, et al. J Am Vet Med Assoc. 1983;182:281.
18 Reef VB, et al. Equine Vet J. 1998;30:18.
19 Nilsford L, et al. Equine Vet J. 1991;23:479.
20 McGladdery AJ, Marr CM. Equine Vet Educ. 1990;2:11.
21 Reef VB. Compend Contin Educ Pract Vet. 1990;12:1312.
22 Reef VB. Vet Clin North Am Equine Pract. 1991;7:435.
23 Blissitt K, Patterson M. In Pract. 1996;18:416.
24 Blissitt KJ, Bonagura JD. Equine Vet J Suppl. 1995;19:82.
Etiology Bacterial, occasionally parasitic infection
Epidemiology History of ill-thrift, chronic illness, periodic milk drop, shifting lameness
Clinical findings Type of murmur depends on valves of species predilection. Embolic nephritis, arthritis, tenosynovitis or myocarditis
Clinical pathology Blood culture
Necropsy findings Valvular lesions, often vegetative, maybe rupture of chordae tendineae. Embolic lesions in other organs
Diagnostic confirmation Murmur or persistent tachycardia with evidence of bacteremia, a positive blood culture. Can be confirmed by echocardiography
Treatment Antimicrobial agents based on culturing causative agent. Prolonged therapy required. Case fatality uniformly high in cases that have heart failure
Most cases of endocarditis in farm animals are caused by bacterial infection but whether the infection gains entrance by direct adhesion to undamaged endothelium, or through minor discontinuities of the valvular surfaces, or by hematogenous spread through the capillaries at the base of the valve, is uncertain. A number of different organisms have been associated with this disease. The common infectious causes of endocarditis in animals are listed below.
There is limited information on the epidemiology of the endocarditis. (See Epidemiology, valvular disease.)
Chronic bacteremia predisposes to endocarditis. There may be a history of an ongoing septic process such as mastitis, metritis, foot abscess or traumatic reticular peritonitis, or of a procedure, such as the use of an indwelling intravenous catheter, that might lead to bacteremia. Commonly there is a history suggestive of low-grade infection. In cattle, ill-thrift with periodic, dramatic but temporary fall in milk production is a common history. The animals often have a lower body condition than expected for their stage of production and there is frequently a history of intermittent lameness.4 Horses may present with similar suggestive histories, including shifting leg lameness, intermittent joint distension, coughing, seizures, jugular vein thrombosis, colic, diarrhea, poor growth and umbilical infection.6 In sows it is common for agalactia to develop in the first 2–3 weeks after farrowing, followed by a loss of weight, intolerance to exercise and dyspnea at rest.
Endocarditis may arise from implantation of bacteria onto the endocardium from the bloodstream or by bacterial embolism of the valve capillaries. Endocarditis is predisposed by trauma to the endothelial surface exposing collagen and leading to binding of platelets, activation of the extrinsic coagulation cascade with deposition of fibrin and the formation of sterile platelet–fibrin deposits.
Endothelial damage may occur along the lines of closure of valves in association with turbulent flow and also can occur for the same reason on areas of the mural endocardium. These areas are subsequently colonized by circulating bacteria and the organisms grow in these areas enmeshed in a tight, avascular network of fibrin and platelets with further serial deposition of platelets and fibrin.10 This is the mechanism of endocarditis that occurs secondary to turbulent flow in congenital heart disease and of that produced by trauma such as cardiac catheterization. Myocardial disease may lead to edema of the valves, which may also predispose to endothelial damage.
Endocarditis in large animals occurs most commonly secondary to a chronic infection at some distant site and a persistent bacteremia without predisposing lesions in the heart. Certain organisms have the ability to directly adhere to endothelium and it is probable that this is the major pathogenic factor.
The major clinical abnormalities associated with endocarditis result from the effect of endocarditis on heart function and from the effects of embolic showering of microorganisms, which can lead to infarction or infection at other sites in the body. The valvular lesions may be vegetative in the early stages of the disease or, more often, there may be fibrosis and shrinking, distortion and thickening of the valve cusps. Both interfere with valve function, leading to cardiac insufficiency and possibly cardiac failure. The functional defect produced by valvular endocarditis is usually, but not invariably, valvular insufficiency. Infected emboli most commonly produce pulmonary embolism with miliary pulmonary abscessation, or infection or abscesses in other organs, including myocardium, kidneys and joints.
In cattle, endocarditis occurs most commonly on the right atrioventricular (tricuspid) valve. The left atrioventricular (mitral) valve is the second valve of predilection, and bilateral involvement of the atrioventricular valves is not uncommon.1,4 In the horse the most common site of infection is the aortic valve, with the left and the right atrioventricular valves being the second and the third valve sites of predilection.11 Endocarditis of the pulmonary valve is uncommon, but is recorded.6,12 The atrioventricular valves are the predilection sites in sheep and swine.
The important finding is a murmur on auscultation or a thrill on palpation of the cardiac area. Details of the specific findings for individual valve abnormalities can be found in the preceding section on valvular disease. A major problem with diagnosis based on the presence of murmurs is that they are not always present or detected in cases of endocarditis, particularly with right sided lesions.1,4,13 Persistent tachycardia should be regarded as the most consistent clinical sign in endocarditis.
Chronic bacteremia and embolic showering of microorganisms results in signs referable to infection and infarction at other sites in the body. There is a constant moderate, fluctuating fever and secondary involvement of other organs may cause the appearance of signs of peripheral lymphadenitis, embolic pneumonia, nephritis, arthritis, tenosynovitis or myocarditis. There is usually much loss of condition, pallor of mucosae and an increase in heart rate.
The clinical course in endocarditis may be as long as several weeks or months, or animals may drop dead without premonitory signs. Endocarditis is also a cause of acute heart failure and sudden death in sows.14 Because sows are confined with minimal exercise during much of the production cycle, the presence of cardiac insufficiency from chronic endocarditis can be masked and sows with chronic endocarditis may have acute heart failure and die at times of intense exercise, such as mating or during movement to other housing.
Rupture of the chordae tendineae of the mitral valve in horses may be predisposed by endocarditis15 or may occur spontaneously,16,17 and occurs in both adults16,17 and foals.18 It is manifested by sudden onset of acute heart failure in horses apparently previously healthy or, when a complication of a pre-existing endocarditis, as a sudden onset complication of the disease or a cause of death. There are signs of acute left failure and there is usually a prominent third heart sound.19 The rupture may involve the chordae of any of the cusps of the valve.17 Rupture of the medial cusp of the aortic valve to produce acute left heart failure and rupture of the pulmonary valve producing right heart failure can also occur.20
Electrocardiographic findings suggestive of endocarditis are sinus tachycardia and decreased QRS amplitudes in a base-apex lead;21 ectopic foci may also be present.
Echocardiographic findings suggestive of endocarditis are hypoechoic and echogenic masses, irregular thickening of valves and rupture of the chordae tendinae.6
A nonregenerative anemia, leukocytosis, neutrophilia, hyperfibrinogenemia and hyperglobulinemia are common but not specific for endocarditis. In chronic cases, where the lesions are due largely to scarring of the valves, hematological findings may be normal. Hypergammaglobulinemia is the most common and consistent finding and an indication of chronic bacterial infection. Where there is passive hepatic congestion there may be an increase in serum alkaline phosphatase and gamma-glutamyltransferase activity. Repeated examination of the urine may reveal transient episodes of proteinuria and the shedding of bacteria associated with renal embolization and infarction.
Blood cultures should be attempted. The avoidance of skin contamination is important and the site should be adequately prepared by initial skin cleansing with 70% alcohol followed by 1% povidone-iodine applied in a circular pattern around the intended venepuncture site. A contact time of at least 2 minutes should be allowed before obtaining blood for culturing.10 The ratio of blood to broth culture medium should be 1:10–1:20, and the broth should be incubated at 37°C for 24 hours before being examined for the presence of turbidity and plated on to traditional blood agar plates. Blood culture is frequently negative and it is recommended that three samples be obtained from separate venepuncture sites during a 1-hour period.10 Sampling at the start of a fever is preferred but clearly impossible; however in animals with a more constant bacteremia, repeat culturing without regard to fever is successful.2,11 Determination of the susceptibility of the organism to antimicrobial agents may aid in treatment.
The lesions are termed vegetative when they are large and cauliflower-like and verrucose when they are small and wart-like. The former are present on the valves in most fatal cases. In the later stages the valves are shrunken, distorted and often thickened along the edges. This stage of recovery is rare in farm animals but may be observed in the semilunar valves in horses. Spontaneous healing is rare and in most cases treatment is commenced at too late a stage.
Embolic lesions may be present in any other organ. Culture of the valvular lesions should be undertaken but in many cases no growth is obtained. The examination of direct smears should always be undertaken.
Treatment is not highly successful because of the difficulty in controlling the infection. The thickness of the lesions prevents adequate penetration of antimicrobial agents and unless the susceptibility of the causative organism is known a range of antibacterial drugs may have to be tried. For this reason there should be repeated attempts at blood culture until the causative organism is cultured in order to allow drug selection on the basis of susceptibility testing. The choice of antimicrobial agent should be one that allows high concentrations in serum relative to the minimal bactericidal concentration, that has minimal side effects over a prolonged period of administration and has a prolonged half-life.12
In the absence of a positive culture the types of organism commonly isolated in cattle suggest the use of penicillin, possibly combined with gentamicin or the use of a potentiated sulfonamide.3,13 The variety of causative organisms in horses recommends the use of broad-spectrum antibacterial treatment.
Duration of treatment needs to be prolonged. It is difficult to judge the duration of therapy required. A fall in temperature can be taken as an indication that infection is being brought under control, but treatment needs to be continued if there is to be success in therapy.3,10,14,15 A period of continual treatment for 4 months with periodic treatment continuing for 14 months in a cow has been recorded.2
Relapse is common. Treatment is expensive and in food animals must be extra-label and is probably uneconomic except for particularly valuable animals. Consequently the treatment of endocarditis should be approached with reservation. Case fatality is high if signs of congestive heart failure are present.
The sequel of embolic lesions in other organs and permanent distortion of valves resulting in valvular insufficiency also militate against a satisfactory outcome. The use of parenteral anticoagulants, as used in humans to prevent further deposition of material on vegetative lesions and to limit embolic disease, has questionable value21 and requires monitoring that is not usually available in veterinary practice.
Evans ET. Bacterial endocarditis of cattle. Vet Rec. 1957;69:1190.
Kasari TR, Rousell AJ. Bacterial endocarditis. Part I. Pathophysiologic, diagnostic and therapeutic considerations. Compend Contin Educ Pract Vet. 1989;11:655-671.
Kasari TR, Rousell AJ. Bacterial endocarditis in large animals. Part II. Incidence, causes, clinical signs, and pathologic findings. Compend Contin Educ Pract Vet. 1989;11:769-774.
Fregin GF. Medical evaluation of the cardiovascular system. Vet Clin North Am Equine Pract. 1992;8:329-346.
Dowling PM, Tyler JW. Diagnosis and treatment of bacterial endocarditis in cattle. J Am Vet Med Assoc. 1994;204:1013-1016.
1 Roussel AJ, Kasari TR. Compend Contin Educ Pract Vet. 1989;11:769.
2 Tyler JW, et al. J Am Vet Med Assoc. 1991;198:1410.
3 Brown CM. Vet Clin North Am Equine Pract. 1985;2:371.
4 Evans ET. Vet Rec. 1957;69:1190.
5 Buergellt CD, et al. Vet Pathol. 1985;22:333.
6 Maxson AD, Reef VB. Equine Vet J. 1997;29:394.
7 Travers CW, et al. J S Afr Vet Assoc. 1995;66:172.
8 Ichikawa T, et al. J Jpn Vet Med Assoc. 1991;44:153.
9 Katsumi M, et al. J Jpn Vet Med Assoc. 1998;60:129.
10 Kasari TR, Roussel AJ. Compend Contin Educ Pract Vet. 1989;11:655.
11 Hillyer MH, et al. Equine Vet Educ. 1990;2:5.
12 Nillsford L, et al. Equine Vet J. 1991;23:479.
13 Power HT, Rebhun WC. J Am Vet Med Assoc. 1983;182:806.
14 Drolet R, et al. Can Vet J. 1992;33:325.
15 Ewart S, et al. J Am Vet Med Assoc. 1992;200:961.
16 Brown CM, et al. J Am Vet Med Assoc. 1983;182:281.
17 Marr CM, et al. Vet Rec. 1990;127:376.
18 Reef VB. J Am Vet Med Assoc. 1987;191:329.
19 Holmes JR, Miller PJ. Equine Vet J. 1984;16:125.
Diseases of the pericardium
Etiology Traumatic, extension from other infection, as component of infections causing polyserositis, or idiopathic
Epidemiology Poorly defined other than for traumatic pericarditis in cattle
Clinical findings Friction sound initially, followed by muffling of the heart sounds, venous congestion, decreased pulse pressure and congestive heart failure
Clinical pathology Pericardiocentesis, echocardiography, radiography
Necropsy findings Inflammation, fibrin and fluid, in pericardial sac. Fibrous pericarditis
Diagnostic confirmation Triad of muffling of the heart sounds, venous congestion, decreased pulse pressure. Pericardiocentesis, echocardiography
Treatment Antimicrobials and drainage. Poor prognosis and supportive treatment
Pericarditis is not common but presents in three general forms; effusive, fibrinous and constrictive, although combinations of one or more of the three forms can occur. Effusive pericarditis is characterized by the accumulation of a protein-rich fluid within the pericardial sac. Subsequent fibrin deposition can lead to fibrinous pericarditis, and if fibrin within the pericardial sac matures to fibrous tissue and fibrosis of the pericardium or epicardium then constrictive pericarditis will result.1 Traumatic pericarditis, perforation of the pericardial sac by an infected foreign body, occurs commonly only in cattle. Traumatic pericarditis is also recorded in the horse2 and in a lamb.3 Localization of a blood-borne infection occurs sporadically in many diseases. Direct extension of infection from pleurisy or myocarditis may also occur in all animals but the clinical signs of pericarditis in such cases are usually dominated by those of the primary disease.
In most cases of pericarditis in horses no causative agent is isolated.1 There is commonly a history of upper or lower respiratory tract disease. Most cases are fibrinous or septic4,5 but an effusive nonseptic form is also described and has been called idiopathic effusive pericarditis.6 Pericarditis in horses occurs predominantly in adults. Idiopathic effusive pericarditis has been diagnosed in two dairy cows.7
In the early stages, inflammation of the pericardium is accompanied by hyperemia and the deposition of fibrinous exudate, which produces a friction sound when the pericardium and epicardium rub together during cardiac movement. As effusion develops the inflamed surfaces are separated, the friction sound is replaced by muffling of the heart sounds, and the accumulated fluid compresses the atria and right ventricle, preventing their complete filling. Congestive heart failure follows. A severe toxemia is usually present in suppurative pericarditis because of the toxins produced by the bacteria in the pericardial sac. Gas will occur along with fluid in the sac if gas-producing bacteria are present. If sufficient gas is present, the classical washing machine sound of fluid splashing with each heart beat will be auscultated. This is not as commonly heard in clinical cases as muffling of the heart sounds.
In the recovery stage of nonsuppurative pericarditis the fluid is reabsorbed and adhesions form between the pericardium and epicardium to cause an adhesive pericarditis, but the adhesions are usually not sufficiently strong to impair cardiac movement.
In suppurative pericarditis the adhesions that form become organized, starting on day 4–6,8 and may cause complete attachment of the pericardium to the epicardium, or this may occur only in patches to leave some loculi which are filled with serous fluid.6 In either case restriction of cardiac movement will probably be followed by the appearance of congestive heart failure.
In the early stages there is pain, avoidance of movement, abduction of the elbows, arching of the back and shallow, abdominal respiration. Pain is evidenced on percussion or firm palpation over the cardiac area of the chest wall, and the animal lies down carefully. A pericardial friction sound is detectable on auscultation of the cardiac area. The temperature is elevated to 39.5–41°C (103–106°F) and the pulse rate is increased. Associated signs of pleuritis, pneumonia and peritonitis may be present.
In most cases of pericarditis caused by traumatic reticuloperitonitis, hematogenous infection or spread from pleuritis, the second stage of effusion is manifested by muffling of the heart sounds, decreased palpability of the apex beat and an increase in the area of cardiac dullness with decreased amplitude of the peripheral pulse. If gas is present in the pericardial sac each cardiac cycle may be accompanied by splashing sounds. Signs of congestive heart failure become evident. Fever is present, the heart rate is markedly increased and toxemia is severe, although this varies with the types of bacteria present. This is the most dangerous period and affected animals usually die of congestive heart failure, or of toxemia, in 1–3 weeks.9-11 Those that survive pass through a long period of chronic ill health during which the toxemia subsides relatively quickly but congestive heart failure diminishes slowly. In this stage of chronic pericarditis additional signs of myocarditis, particularly irregularity, may appear. The heart sounds become less muffled and fluid sounds disappear altogether or persist in restricted areas. Complete recovery is not common.
In the horse, both the idiopathic effusive and the septic forms of pericarditis present with marked muffling of the heart sounds, tachycardia, distension of the jugular veins and subcutaneous edema of the ventral body wall.4,12 A nonseptic pleural effusion is also commonly present in cases of septic pericarditis in the horse9,13 but not in idiopathic effusive pericarditis.14
A marked leukocytosis and neutrophilia, as well as hyperglobulinemia, are usually present in traumatic pericarditis because this has many of the characteristics of a large internal abscess. In the other forms of pericarditis changes in the blood depend upon the other lesions present and on the causative agent. In the stage in which effusion occurs a sample of fluid may be aspirated from the pericardial sac and submitted for bacteriological examination. The technique is not without danger, as infection may be spread to the pleural cavity.
Pericardial fluid can also be examined cytologically but usually the smell (reminiscent of retained placenta and toxic metritis in cattle) is sufficiently diagnostic in cattle with traumatic pericarditis. In septic pericarditis the fluid represents an inflammatory response, whereas in idiopathic effusive pleuritis in horses there are very few cells in the sediment.12,15 Mean right ventricular diastolic and intrapericardial fluid pressures are increased in a corresponding manner in cows with clinical signs of right-sided heart failure.10 Cattle with muffled heart sounds and a large pericardial fluid volume also have a decrease in cardiac output to approximately two-thirds of normal values.10
Electrocardiography can aid in diagnosis. Electrocardiographic changes include sinus tachycardia and, in animals with right-sided heart failure and hydrothorax, diminished amplitude of the QRS complex.10 Contrary to popular belief, hydropericardium in the absence of hydrothorax leads to an increase, and not a decrease, in QRS amplitude. Moreover, removal of large volumes of pericardial fluid does not usually result in an immediate change in QRS amplitude. Also contrary to popular belief, electrical alternans is not commonly present in dogs and humans with pericardial effusion and if present, occurs only within a narrow range of heart rates. The prevalence of electrical alternans is unknown in large animals with pericardial effusion but is suspected to be extremely low because the pericardium and heart are much more fixed in position within the thorax.
Radiography may be of diagnostic value, with six of seven cows having a gas–fluid interface present on standing lateral thoracic radiographs.16 Radiography has the additional benefit of potentially identifying the location of the penetrating wire; this information would assist surgical removal of the wire via a rumenotomy. Radiography may also aid in the clinical differentiation of pericardial effusion from pleural effusion.
Echocardiography is the most valuable diagnostic procedure and will show the presence of fluid in the pericardial sac. Echocardiography usually permits differentiation of effusive and fibrinous pericarditis.5,7,9,14
In the early stages there is hyperemia of the pericardial lining and a deposit of fibrin. When effusion occurs there is an accumulation of turbid fluid and tags of fibrin are present on the greatly thickened epicardium and pericardium. Gas may also be present and the fluid may have a putrid odor. When the pericarditis has reached a chronic stage the pericardium is adherent to the epicardium over a greater or lesser part of the cardiac surface.6 Loculi containing serous fluid often remain. Embolic abscesses may be present in other organs. Lesions typical of the specific causative diseases listed above are described under their specific headings.
• Mediastinal abscess15
• Hydropericardium occurs in congestive heart failure, mulberry heart disease of pigs, herztod of pigs, gossypol poisoning, clostridial intoxications of sheep and lymphomatosis
Antibacterial treatment of the specific infection should be undertaken if possible on the basis of susceptibility on organisms cultured from the pericardial fluid. Where the inciting agent cannot be grown a broad-spectrum antibiotic or a combination to give a broad spectrum is used. A combination of penicillin and gentamicin is common and provides cover of the likely organisms associated with this infection. Pericardiocentesis, copious lavage with warmed 0.9% NaCl solution, and drainage should be conducted as required to relieve the fluid pressure in the pericardial sac, decrease the transmural pressure gradient across the atrial and ventricular walls and caudal and cranial vena cava, and thereby facilitate diastolic filling. Pericardiocentesis should be performed under ultrasonographic guidance and with electrocardiographic monitoring.
The prognosis varies with the etiological agent but it is generally grave in cases of septic pericarditis in horses4,5 mainly because the stage of effusion is followed by one of fibrosis and constrictive pericarditis.17 Success in treatment of a series of six cases of septic pericarditis in the horse is recorded with the use of indwelling pericardial drains to allow twice-daily lavage and drainage and the instillation of antibiotics directly into the pericardial sac. This allows high concentrations of antimicrobial agents and the twice-daily infusion of 1–2 L of fluid may help prevent the development of constrictive pericarditis. In cattle thoracotomy and pericardiotomy are used to establish drainage or to allow marsupialization of the pericardium to the body wall.18 Low treatment success rates are generally reported for the disease in cattle with or without surgical drainage,16,19 and it is likely that cases that responded to fifth rib resection and pericardial marsupialization would have responded to pericardial drainage and intrapericardial lavage and antimicrobial administration.
There is a more favorable prognosis for the treatment of idiopathic effusive pericarditis in horses and cattle with aggressive therapy and the use of pericardiocentesis, pericardial lavage and corticosteroid or NSAIDs is an effective therapy.7,12,14
1 Perkins SL, et al. J Am Vet Med Assoc. 2004;224:1133.
2 Bertone JJ, et al. J Am Vet Med Assoc. 1985;187:742.
3 Abo-Shekada MN, et al. Br Vet J. 1991;147:78.
4 Dill SG, et al. J Am Vet Med Assoc. 1982;180:266.
5 Buergelt CD, et al. Compend Contin Educ Pract Vet. 1990;12:872.
6 Roth L, King JM. J Vet Diagn Invest. 1991;3:52.
7 Jesty SA, et al. J Am Vet Med Assoc. 2005;226:1555.
8 Leak LV, et al. Am J Anat. 1987;180:373.
9 Bernard W, et al. J Am Vet Med Assoc. 1990;196:468.
10 Fisher EW, Pirie HM. Aust Vet J. 1965;121:552.
11 Holmes JR. Vet Rec. 1960;72:355.
12 Freestance JF. Equine Vet J. 1987;19:38.
13 Bennett DG. J Am Vet Med Assoc. 1986;188:814.
14 Worth LT, Reef VB. J Am Vet Med Assoc. 1998;212:248.
15 Smith BP. J Am Vet Med Assoc. 1977;170:208.
16 Ducharme NG, et al. J Am Vet Med Assoc. 1992;200:86.
17 Hardy J, et al. Equine Vet J. 1992;24:151.
18 Rings DM. Vet Clin North Am Food Anim Pract. 1995;11:177.
Etiology Abnormality in heart or vascular structure results in anomalous blood circulation. Cause of congenital defects unknown, some may be heritable
Epidemiology Sporadic occurrence. Usually present with cardiac failure shortly after birth but some defects compatible with life and detected incidentally
Clinical and necropsy findings Specific for individual defects
Clinical pathology Echocardiography most useful diagnostic aid
Diagnostic confirmation Echocardiography and postmortem examination
An increasing number of clinical reports on congential cardiovascular defects are appearing in the veterinary literature. However, their general importance is low.
The cause of congenital cardiac defects is unknown, but it is assumed they result from injury during development or from single recessive genes or polygenic sets that have lesion-specific effects on cardiac development.1 Ventricular septal defects have been observed in twin cattle.2 Heritable ventricular septal defect is recorded in miniature pigs3 and suspected in cattle.4
Congenital cardiac anomalies occur in all species but are not common in any one of them. The prevalence is probably highest in cattle and lowest in horses.3
The relative frequency of individual cardiac defects in 36 calves at postmortem examination in one study5 was:
Ventricular septal defect – 14%
Right ventricular hypoplasia – 13%
Left ventricular hypoplasia – 13%
The animals were neonatal calves and the relative frequencies are biased towards defects that are incompatible with longer life. In general, ventricular septal defect is the most common cardiac defect in cattle.
In a large series of necropsy examinations on lambs,6 1.3% had cardiac anomalies, of which approximately 90% were ventricular septal defects.
A review of 82 publications on congenital cardiac defects in horses showed the following prevalence in the total cases:8
Congenital cardiac defects may result in a pressure load or a volume (flow) load in one or more chambers of the heart. In general the left ventricle can tolerate a pressure load better than the right ventricle and the right ventricle can tolerate a volume load better than the left ventricle. The heart may compensate for the increase in load with minor loss in cardiac reserve or the defects may lead to cardiac failure.
The mixing of oxygenated and venous blood due to the presence of an anatomic abnormality that allows a shunt of blood from the pulmonary circulation to the systemic circulation in the face of high pulmonary vascular resistance is an important factor in the pathogenesis of the clinical signs of some congenital cardiac defects. The resulting anoxic anoxia causes severe dyspnea, and cyanosis may be marked if the right-to-left shunt is large. There is a notable absence of fever and toxemia if intercurrent disease does not develop. Cardiac enlargement is usually detectable if the animal survives past the first week of life.
Animals with some congenital cardiac defects can survive to maturity and be productive and perform adequately. Acute heart failure or chronic (congestive) heart failure may occur when the animals are subjected to a physical stress such as the first pregnancy or activity on the range. The primary appearance of signs of cardiac disease when an animal is 2–3 years of age should not eliminate congenital defects from consideration.
A general description of the more common defects is given below. Some of the defects described in this section are actually defects of the vascular system but are described here for convenience. Diagnosis can be confirmed by the detection of a pressure differential across valves, the detection of shunts by dye dilution and serial blood gas analysis, and by angiocardiography. Echocardiography has developed as an important aid to diagnosis.9
An abnormal position of the heart outside the thoracic cavity is most common in cattle, the displacement usually being to the lower cervical region. The heart is easily seen and palpated and there is an accompanying divergence of the first ribs and a ventrodorsal compression of the sternum, giving the appearance of absence of the brisket. Affected animals may survive for periods of years, as they also may with an abdominal displacement, but those with a displacement through a defective sternum or ribs rarely survive for more than a few days.
This defect of the atrial septum is reasonably common in cattle, usually causes no clinical signs if present as an isolated defect and is detected incidentally at necropsy. Ostium secundum defects are also common in cattle.10 Large defects may allow a shunt in both directions. Relative resistance to outflow from the atria is greater in the left than the right and the shunt, if it occurs, is from left to right. This induces a moderate flow load on the right side of the heart, which is well tolerated. Large flows will generally increase pulmonary vascular resistance and result in moderate right ventricular and right atrial hypertrophy. The increase in outflow resistance from the right atrium results in a decreased flow across the shunt and control of the effects of the defect. Atrial septal defects are of much greater significance when they are present with other cardiac defects and it is extremely rare for an atrial septal defect alone to cause clinical signs of circulatory failure. If these result in a severe right ventricular hypertrophy the shunt may reverse from right to left and cyanosis will occur.
These are one of the most common congenital cardiac defects in sheep, cattle and horses. They are almost invariably subaortic defects occurring high in the septum at the pars membranaceae. In the absence of other defects their presence results in the shunting of blood from the left to the right ventricle, producing a volume load on the left ventricle and left atrium.11
On auscultation there is a loud blowing pansystolic murmur audible over both sides of the chest. It is usually audible over a large area on both sides but most intense at the left fourth intercostal and the right third intercostal space and more intense on the right than the left side. The murmur in this defect is one of the loudest and most obvious murmurs encountered. It does not modify the heart sounds, which are usually increased in intensity. A precordial thrill is frequently palpable on both the left and the right side.
The outcome is determined by the magnitude of the shunt and the degree of resistance to flow from the right ventricle as determined by pulmonary vascular resistance. With large defects the shunt of blood can be considerable and the animal may die at birth or show clinical signs at a few weeks to a few months of age. The major presenting signs during this period are of left-sided heart failure with lassitude, failure to grow well and dyspnea with moderate exercise. The shunt may be less severe and allow an apparently normal existence until maturity, when left-sided or right-sided failure can occur, or cause no apparent problem during life and be detected incidentally on necropsy or abattoir examination. Horses with this defect have raced successfully11 and dairy cows have had many productive lactations.
An increase in pulmonary vascular resistance occurs as the result of increased pulmonary blood flow. In cattle, this increase may be sufficient to cause reversal of the shunt, and cyanosis develops. This syndrome, sometimes referred to as an Eisenmenger complex,12,13 develops in young calves but also in mature animals between 1 and 3 years of age and should always be suspected where there is a sudden onset of cyanosis and exercise intolerance in an animal of this age.
The turbulence associated with flow across the defect may produce secondary changes in the valves located close to the defect, which may complicate the clinical picture. Cattle are prone to develop endocarditis in the region of the septal cusp of the right atrioventricular valve. In horses, endocarditis more commonly involves the medial cusp of the aortic valve.
Other complications are prolapse of the cusps into the septal defect due to lack of aortic root support with the development of aortic regurgitation.11,14 Rupture of the valve may occur to produce a severe additional flow load on the left ventricle, with rapid onset of acute left heart failure and death.
Ventricular septal defects may occur in association with other congenital cardiac or vascular defects, and the clinical findings are varied.11,15,16
There is no practical correction for ventricular septal defects in large animals. It should be emphasized that small defects can produce dramatic auscultatory findings and, unless signs of cardiac insufficiency are present, care should be taken in giving an unfavorable prognosis in pleasure or breeding animals. Pleasure animals with this defect should never be ridden but it is possible for them to live a reasonable lifespan and to breed. Food animals can be sent for early slaughter.
There is insufficient information on the advisability of breeding animals that have this defect. An inheritable predisposition has been suspected in Hereford cattle,4 and chromosomal abnormalities have been demonstrated in association with this defect in cattle.1 Ventricular septal defects have high prevalence in calves and lambs with microphthalmia.
This is almost always a lethal defect in farm animals. The tetralogy consists of three primary abnormalities (ventricular septal defect, pulmonary stenosis, and dextral position of the aorta so that it overrides both ventricles) and secondary right ventricular hypertrophy. The marked increase in resistance to outflow into the pulmonary artery results in a shunt of blood from the right to left with the major outflow of blood through the aorta. The condition presents with clinical signs very early in life, frequently results in death at or shortly following birth and has been reported predominantly in foals and calves. Occasionally, affected animals may live for longer periods and cases are recorded in mature animals.17,18
Affected animals show lassitude and dyspnea after minor exertion such as suckling, with the clinical signs resulting primarily from systemic hypoxemia. Cyanosis may or may not be present, depending upon the degree of pulmonary stenosis, but is usually prominent, especially following exercise. On auscultation a murmur and sometimes a thrill is present and most intense in the left third or fourth intercostal space.
Other cardiac defects that result in cyanosis as a prominent sign occur when there is right-to-left shunting of blood through a patent foramen ovale, a patent ductus arteriosis or ventricular or atrial septal defects as a result of tricuspid atresia or pulmonary atresia.19-21 Right-to-left shunting through these defects is rare and, if present, is usually a terminal event.
Tetralogy of Fallot should be differentiated from an even rarer condition, double outlet right ventricle; the latter is characterized by having both the aorta and pulmonary artery arise from a distinct conus originating from the morphologic right ventricle and from which no fibrous continuity with the atrioventricular valves can be demonstrated. Double outlet right ventricle has been diagnosed in three calves and a foal,22 with clinical signs similar to tetralogy of Fallot.
This defect results from a failure of closure of the ductus arteriosus following birth and is probably the second most common defect in horses after ventricular septal defect. There is some controversy over the period of time involved in normal closure in large animals. Clinically, murmurs associated with a patent ductus arteriosus are frequently heard during the first day after birth in normal foals and may persist for periods of up to 5 days. Physiological studies in foals23 suggest that closure occurs before 24 hours after birth. Patent ductus arteriosus is not a common clinical cardiac defect in older animals, but can occur.24 The ductus arteriosus closes within minutes of birth in calves.
Patent ductus arteriosus produces a loud continuous murmur associated with the left-to-right shunting of blood from the aorta to the pulmonary artery. The intensity of the murmur waxes and wanes with each cycle because of the effects of normal pressure changes on blood flow, giving rise to the name of ‘machinery murmur’. The systolic component of the murmur is very loud and usually audible over most of the cardiac auscultatory area, but the diastolic component is much softer and confined to the base of the heart. The pulse is large in amplitude but has a low diastolic pressure. Surgical correction is possible.
Constriction of the aorta at the site of entrance of the ductus arteriosus causes a syndrome similar to that of stenosis of the aortic semilunar valves; there is a systolic murmur and a slow-rising pulse of small amplitude.
Persistence of the right fourth aortic arch causes constriction of the esophagus with dysphagia and regurgitation. The aorta is situated to the right of the esophagus and trachea and the ligamentum arteriosum in its connection to the pulmonary artery encloses the esophagus in a vascular ring and compresses it against the trachea. Clinical signs are usually evident soon after birth and consist primarily of regurgitation of milk from the mouth and nostrils after suckling, but survival until 5 years of age has been recorded in a bull that showed chronic bloat and visible esophageal dilatation. Resistance to the passage of a stomach tube is encountered just behind the first rib and the diagnosis can be confirmed by radiological examination following a barium swallow. Medical treatment is concerned with the control of aspiration pneumonia, but the correction of the defect is surgical.
This defect25,26 and other defects of the outflow vessels, including pulmonary and aortic hypoplasia and congenital absence of the aortic arch, have been recorded in animals but their prevalence is low.
Congenital fibroelastosis has been observed in calves and pigs. The endocardium is converted into a thick fibroelastic coat and, although the wall of the left ventricle is hypertrophied, the capacity of the ventricle is reduced. The aortic valves may be thickened and irregular and obviously stenosed. The syndrome is one of congestive heart failure. The defect may cause no clinical abnormality until the animal is mature.
Stenosis of the aorta at or just below the point of attachment of the aortic semilunar valves has been recorded as a common, possibly heritable, defect in pigs27 but its differentiation from other causes of heart failure is difficult. Clinically affected animals may die suddenly with asphyxia, dyspnea and foaming at the mouth and nostrils, or after a long period of ill-health with recurrent attacks of dyspnea. In the acute form death may occur after exercise or be unassociated with exertion.
This is an extremely rare congenital anomaly defined by the presence of a single papillary muscle that receives all chordae tendineae from the left atrioventricular valve. An 8-month old colt with a loud left-sided holosystolic murmur was diagnosed with this condition using echocardiography.28
Either or both coronary arteries may originate from the pulmonary artery instead of the aorta. The resulting anoxia causes myocardial weakness in the ventricle of the affected side. Congestive heart failure usually follows. Congenital deformities of the coronary arteries have been recorded in cattle and pigs.29
1 Tschudi P. Schweiz Arch Tierheilkd. 1975;117:335.
2 Besser TE, Knowlen GG. J Am Vet Med Assoc. 1992;200:1355.
3 Swindle MM, et al. Lab Anim Sci. 1990;40:155.
4 Penrith ML, et al. J S Afr Vet Assoc. 1994;65:31.
5 Gopal T, et al. Am J Vet Res. 1986;47:1120.
6 Dennis SM, Leipold HW. Am J Vet Res. 1968;29:2337.
7 Hsu FS, Du SJ. Vet Pathol. 1982;19:676.
8 Cotterill CM, Rossdale PD. Equine Vet J. 1992;24:338.
9 Reef VB. Compend Contin Educ Pract Vet. 1991;13:109.
10 Marakami T, et al. J Jpn Vet Med Assoc. 1991;44:696.
11 Reef VB. Equine Vet J Suppl. 1996;19:86.
12 Machida N. Jpn J Vet Sci. 1986;48:1031.
13 McLennan MW, et al. Aust Vet J. 1996;74:22.
14 Reef VB, Spencer P. Am J Vet Res. 1987;48:904.
15 Wilson RB, Hoffner JC. Cornell Vet. 1987;77:187.
16 Ecke P, et al. N Z Vet J. 1991;39:97.
17 Cargile J, et al. Cornell Vet. 1991;81:411.
18 Rahal C, et al. J Equine Vet Sci. 1997;17:604.
19 Young LE, et al. Equine Vet Educ. 1997;9:123.
20 Anderson RH. Equine Vet Educ. 1997;9:128.
21 Meurs KM, et al. Equine Vet J. 1997;29:160.
22 Prosek R, et al. J Vet Intern Med. 2005;19:262.
23 Scott EA, et al. Am J Vet Res. 1975;36:1021.
24 Prescott JRR, et al. Vet Rec. 1997;74:471.
25 Sandusky GE, Smith CW. Vet Rec. 1981;108:163.
26 Reppas GP, et al. Aust Vet J. 1996;73:115.
27 Van Nie CJ, Vincent J. Vet Q. 1980;2:160.
Cardiac neoplasia
Primary neoplasia of the heart is exceedingly rare and cardiac disease secondary to metastatic neoplasms occurs infrequently. Aortic body adenoma, cardiac fibrosarcoma and pericardial mesothelioma are reported.1-3
Lymphosarcoma is probably the most common metastatic tumor in both cattle and horses but cardiac involvement by melanoma, hemangiosarcoma, testicular embryonal carcinoma, squamous cell carcinoma, lipoma and other tumors is also recorded.4 Angiomas, benign vasoformative tumors, can occur in the heart and are recorded as obstructing blood flow and producing heart failure in a young calf.5
Diseases of the blood vessels
Etiology Arteritis leading to thrombus formation causes ischemia of the tissues supplied by the affected artery
Clinical findings Reduced function or ischemic necrosis vary with the site of the obstruction. Aortic–iliac thrombosis manifest with lameness, muscular weakness, decreased pulse amplitude in affected leg
Clinical pathology Leukocytosis, hyperfibrinogenemia, elevated serum concentrations of muscle enzymes in some cases. Ultrasound more sensitive for diagnosis than rectal palpation
Necropsy findings Thrombosis and embolic lesions, muscle ischemia and necrosis
Diagnostic confirmation Ultrasonography for aortic–iliac thrombosis
Treatment Fibrinolytic enzymes. Surgical removal of thrombus
Injury to vascular endothelium, alteration to normal blood flow (turbulence or stasis) and alterations to the coagulability of blood can predispose thrombosis and thromboembolism.
Coagulopathies and disseminated intravascular coagulation are important in the pathogenesis thromboembolism, which occurs in many infectious diseases.1
• Strongylus vulgaris – horses. Migrating larvae cause arteritis of the anterior mesenteric artery, iliac arteries, base of aorta and occasionally cerebral, renal or coronary arteries. This is a major cause of arteritis and associated clinical disease in horses2
• Aortic–iliac thrombosis in horses. There is some controversy over the etiology of this disease. It may result from strongyle-related thromboembolism with organization of thrombi and their incorporation into the arterial wall with centripetal development of progressive thrombosis. Alternatively spontaneous degenerative vascular disease of unknown etiology, but particularly at the aortic quadrifurcation may result in thrombosis in the area and subsequently thromboembolism of more distal vessels
• Onchocerciasis and elaeophoriasis in cattle, sheep, goats, and horses.
• From vegetative endocarditis or emboli from arterial thrombus in various sites
• Hyperlipemia and hyperlipidemia in horses
• Fat emboli following surgery
• Associated with subclinical Salmonella dublin infection in calves
• Rupture of abscesses into blood vessels – pulmonary embolism resulting from caudal vena caval thrombosis or jugular thrombosis
Clinical atherosclerosis occurs rarely in farm animals. It has been recorded in a horse in which sufficient vascular obstruction occurred to cause severe central nervous signs and a fatal outcome. Spontaneous atherosclerosis is a common necropsy finding in swine, cattle, goats, horses and wild animals but is not associated with clinical disease. Arteriosclerosis and calcification are major findings in enzootic calcinosis and occur following overdosing with vitamin D or its analogs in the prevention of milk fever in cattle and in hypomagnesemia in calves.
In parasitic arteritis, inflammation and thickening of the arterial wall result in the formation of thrombi, which may partially or completely occlude the artery. The common site is in the anterior mesenteric artery, obstruction of the vessel causing recurrent colic or fatal ischemic necrosis of a segment of the intestine. Less common sites include the origin of the iliac artery at the abdominal aorta causing iliac thrombosis, the base of the aorta leading to rupture and hemopericardium, and the coronary arteries causing myocardial infarction.
With other causes of arteritis, the clinical syndrome is dependent upon the site of arteritis or embolism. Arteritis associated with bacterial and viral infections is usually widespread and several organ systems are involved. Bacterial emboli have a predilection to lodge in:
• Vascular plexuses in the kidney to produce renal disease
• The synovial membranes to produce arthritis and tenosynovitis
Less commonly, they may lodge in other vascular plexuses such as the rete cerebri. Large emboli that lodge in the pulmonary arteries cause anoxic anoxia. Embolism in the renal artery causes acute cortical necrosis and gross hematuria.
Vasoconstrictive alkaloids produced by Claviceps purpurea infestation of grass seed heads and Acremonium coenophalium, which infests Festuca arundinaceae and Lolium perenne, cause arteriolar constriction and result in ischemic necrosis and gangrene of distal extremities in cattle.
The clinical findings in mesenteric verminous arteritis of horses and renal and myocardial infarction, gangrene associated with C. purpurea or endophyte infestation of grasses and other diseases listed above are described elsewhere under those headings. The clinical signs of aortic–iliac thrombosis and pulmonary embolism are described here.
Aortic–iliac thrombosis3,4 is reported most commonly in racehorses but occurs in other breeds. It is primarily a disease of horses of over 3 years of age. Either one or both hindlegs may be involved. The clinical manifestations vary according to the stage of progression of the disease and are associated with ischemia of the hindlimbs.
Early mild cases are usually detected in racehorses or horses subjected to maximal exertion where the disease may be a cause of poor performance. In early cases there is lameness only on exercise, the animal returning to normal after a short rest. If the horse is forced to work when lameness develops, the signs may increase to resemble those of the acute form. The lameness takes the form of weakness, usually of one hindlimb, which tends to give way, especially when the animal turns on it. Frequent lifting of the foot or cow-kicking may also be shown.
In more severe cases, lameness or refusal to work may be evident after minimal exercise.
The disease is chronic and progressive, but occasionally the onset may be acute.
In the acute form there is great pain and anxiety and the pulse and respiration rates are markedly increased Profuse sweating may be evident, but the affected limb is usually dry and may be cooler than the rest of the body. The pain is often sufficiently severe to cause the animal to go down and refuse to get up.
Suspect animals should be examined following exercise.
• The affected limb is cool from the mid-gaskin distally and there is usually diminished or variable sweating over this area
• The amplitude of the pulse in the common digital artery is less in the affected limb than in the normal limb or the front limbs
• Slow filling of the saphenous vein of the affected limb can usually be detected
• Palpable abnormalities on rectal examination include enlargement and firmness of the aortic quadrifurcation, irregularity and asymmetry of the internal and external iliac arteries and decreased amplitude or absence of an arterial pulse.
Recovery by the development of collateral circulation or shrinkage of the thrombus is unlikely to occur and the disease is usually chronically progressive with a poor prognosis.
Until recently the detection and diagnosis of the occurrence of this abnormality was limited to horses showing clinical signs and horses where abnormality could be palpated on rectal examination. Ultrasonography is a more sensitive method of detection than rectal palpation.5 Its use as a diagnostic technique may lead to a better definition of the occurrence of this disease and ultimately its pathogenesis. Ultrasonographic measurements are available for the common carotid artery of cattle.6
Iliac thrombosis may also be associated with impotence in stallions due to failure to mount or accompanied by testicular atrophy.7 It has also been associated with a syndrome of ejaculatory failure in which the stallion has excellent libido, good coupling and vigorous thrusting but a failure to ejaculate.8 The reason for this manifestation is not known but it is postulated that the enlarged arteries might impinge on the caudal mesenteric plexus and the hypogastric nerve.8
Aortic and iliac artery thrombosis is reported as an occasional disease of unknown etiology in calves less than 6 months of age.9 Affected calves have a rapid onset of ataxia, paresis or paralysis of one or both hind limbs. Within 24 hours of onset the calves do not bear weight on the affected leg and, in calves affected in both hindlimbs, signs initially occur in a single limb. Affected legs are cold to touch, especially distal to the stifle, have poor muscle tone and the withdrawal reflex and deep pain sensation is absent in the distal portions. Subcutaneous swelling and crepitation is present in some. Thrombosis at the terminal part of the aorta and the iliac quadrifurcation is found at postmortem examination. The umbilical arteries arise from the iliac arteries near the iliac quadrifurcation and it is thought that thrombus formation in the iliac arteries may predispose to this disease.
Severe dyspnea develops suddenly and is accompanied by profuse sweating and anxiety. The temperature and pulse rate are elevated but the lungs are normal on auscultation. In horses the signs usually pass off gradually in 12–24 hours but in cattle the hypoxemia may be more severe and cause persistent blindness and imbecility. Infected emboli may lead to more severe pulmonary embolic disease with arteritis and pulmonary abscessation. There is pulmonary hypertension, and cor pulmonale is a possible sequel. Pulmonary arteritis and aneurysm may be followed by rupture and pulmonary hemorrhage and hemoptysis.
Extensive thrombus formation is usually associated with a leukocytosis and a shift to the left and there is an increase in serum fibrinogen concentration. In the majority of cases of iliac thrombosis serum aspartate aminotransferase and creatine kinase activities are within the normal range both before and after exercise7 but in severe cases there may be enzymic evidence of myonecrosis with secondary hyperkalemia and uremia.10 Elevated serum creatine kinase and aspartate transaminase activities are present in aortic and iliac thrombosis in calves. Angiography or ultrasonography are used for diagnostic confirmation.
Obstruction of the affected artery is easily seen when it is opened. The thrombus or embolus is adherent to the intima and is usually laminated. Local or diffuse ischemia or infarction may be evident if the embolus has been present for some time and may have progressed to the point of abscess formation.
Treatment with parenteral anticoagulants or enzymes is carried out only rarely. There are several records of good results in iliac thrombosis in horses after the intravenous injection of sodium gluconate or fibrinolytic enzymes,10 and retrograde catheterization of the ventral coccygeal artery can allow the deposition of these materials at high local concentration. Stallions with ejaculatory failure have had some success at service following treatment with phenylbutazone to reduce pain and gonadotropin-releasing hormone to maximize sexual arousal and lower the ejaculatory threshold.8 Ivermectin in combination with phenylbutazone may aid recovery. A gradually increasing exercise program may improve collateral circulation. Surgical treatment is recorded by partial or complete removal of the thrombus with a thrombectomy catheter.4
1 Morris DD. Compend Contin Educ Pract Vet. 1989;11:1386.
2 Baker JR, Ellis CE. Equine Vet J. 1981;13:43. 47
3 Maxie MG, Physick-Sheard PW. Vet Pathol. 1985;2:238.
4 Brama PAJ, et al. Vet Q. 1996;18(Suppl 2):S85.
5 Reef VB, et al. J Am Vet Med Assoc. 1987;190:286.
6 Braun U, Hohn J. Am J Vet Res. 2005;66:962.
7 Azzie MAJ. In: Proceedings of the 18th Annual Convention of the American Association of Equine Practitioners 1972:43.
8 McDonnell SM. J Am Vet Med Assoc. 1992;200:954.
The development of thrombi in veins may result in local obstruction to venous drainage, in liberation of emboli that lodge in the lungs, liver or other organs, and in the development of septicemia or of endocarditis.
Phlebitis is the common origin of thrombi and may be caused by localization of a blood-borne infection, by extension of infection from surrounding diseased tissues, by infection of the umbilical veins in the newborn and by irritant injections into the major veins.
Thrombophlebitis of the jugular vein is a complication of injections or catheterization in some animals and occurs in all species. It can result from damage to the vascular endothelium by cannula or indwelling intravenous catheters, inflammation caused by chemical irritation or bacterial invasion from contamination during insertion of the needle or catheter or migration along the catheter from the skin.1,2 Phlebitis develops and can be detected clinically 24–72 hours after catheter insertion. A retrospective study of 46 cases in horses indicated that ongoing infectious disease was a risk factor for the development of catheter-associated thrombophlebitis3 and thrombophlebitis is especially common in horses with severe gastrointestinal diseases that are accompanied by endotoxemia. Horses are also at higher risk following surgery.4 Severely ill cows are also more likely to develop jugular vein thrombophlebitis than healthy cows.2
Intravenous injections of irritating materials, such as tetracycline, phenylbutazone, 50% dextrose, hypertonic solutions of calcium gluconate, borogluconate and chloride, or hypertonic saline (7.2% NaCl), may cause endothelial damage followed by cicatricial contraction, with or without thrombus formation. Jugular phlebitis with thrombosis is not uncommon in feedlot cattle that have received repeated intravenous antibiotic medication, and may lead to thromboembolic respiratory disease.
Accidental injection of irritating materials around the vein usually cause a marked local swelling, sometimes with necrosis and local sloughing of tissue, which may be followed by cicatricial contraction of local tissues.
Commonly used as an NSAID, its use in horses may be associated with toxicity, which is manifest with oral and gastrointestinal ulceration and renal medullary crest necrosis.5-7 Affected horses show depression, anorexia and neutropenia with ulcers in the mouth, especially on the ventral aspect of the tongue. Ulcers in the fundic and pyloric portion of the stomach also develop but are usually subclinical, although they may be evident on gastroscopic examination or at necropsy. More severe cases show signs of colic and diarrhea in association with intestinal ulceration and duodenitis, and show evidence of renal disease. Toxicity may develop following either intravenous or oral administration of the drug. Intravenous administration is frequently associated with the development of phlebitis and jugular thrombosis at the site of injection.
Phlebitis may also develop in these animals at sites of venepuncture performed for purposes other than phenylbutazone administration. Experimental studies6 suggest that a phlebopathy induced by phenylbutazone is central to the development of all these lesions, including the oral and gastrointestinal ulceration and the renal crest necrosis. The exact pathogenesis of the vein damage in phenylbutazone toxicity has not been elucidated but, experimentally, toxicity can be prevented by the concurrent administration of prostaglandin E2.7 Clinical pathological examination for leukopenia and a fall in serum aspartate aminotransferase may be of value as a monitoring technique for the development of toxicity during phenylbutazone therapy of disease.
Venous thrombi are relatively common in strangles in the horse, and may affect the jugular veins or the caudal vena cava. Thrombosis of the caudal vena cava due to hepatic abscessation and resulting in embolic pneumonia and pulmonary arterial lesions occurs in cows and is described together with cranial vena caval thrombosis in Chapter 10.
Less common examples of venous thrombosis are those occurring in the cerebral sinuses, either by drainage of an infection from the face or those caused by the migration of parasite larvae. Purpling and later sloughing of the ears which occur in many septicemias in pigs are also caused by phlebitis and venous thrombosis. Thrombosis of the tarsal vein is a complication of infections in the claw of cattle8 and intravenous administration of antimicrobial agents as part of the treatment of septic arthritis or the distal interphalangeal joints.
Clinical signs of venous thrombosis are engorgement of the vein, pain on palpation and local edema. In unsupported tissues rupture may occur and lead to fatal internal or external hemorrhage. Ultrasonographic examination assists the diagnosis and the detection of a cavitating area within the thrombus supports a diagnosis of septic thrombophlebitis.2,3,8 Angiography can also assist in diagnosis. Bacteriological culture should be attempted, preferably from the tip of the removed catheter. A variety of different organisms have been isolated from different cases.3 There are no typical findings on clinicopathological examination but there is often an abnormal leukogram and hyperfibrinogenemia. At necropsy the obstructed vessel and thrombus are usually easily located by the situation of the edema and local hemorrhage.
Diagnosis depends on the presence of signs of asymmetric local venous obstruction in the absence of obvious external pressure by tumor, enlarged lymph nodes, hematomas or fibrous tissue constriction. Pressure of a fetus may cause symmetric edema of the perineum, udder and ventral abdominal wall during late pregnancy, and can be easily differentiated from thrombophlebitis by its symmetry and lack of pain. Local edema due to infective processes such as blackleg, malignant edema and peracute staphylococcal mastitis are accompanied by fever, severe toxemia, acute local inflammation and necrosis.
Parenteral treatment with antimicrobial agents and hot fomentations to external veins, or treatment with a topical anti-inflammatory agent such as 50% dimethyl sulfoxide, is usually instituted to remove the obstruction or allay the swelling. If a catheter is being used it should be immediately removed. Heparin and warfarin treatment in horses is not recommended.9 Ultrasonography is useful to monitor recanalization of the thrombosed vein2 and measurements of the external jugular vein are available for cattle.10
1 Bayly WM, Vale BH. Compend Contin Educ Pract Vet. 1982;4:5227.
2 Pusterla N, Braun U. Vet Rec. 1995;137:431.
3 Gardner SY, et al. J Am Vet Med Assoc. 1991;199:370.
4 Gerhards H. Dtsch Tierarztl Wochenschr. 1987;94:173.
5 Tobin T, et al. J Vet Pharmacol Ther. 1986;9:1.
6 Meschter CL, et al. Cornell Vet. 1984;74:282.
7 Collins LG, Tyler DE. Am J Vet Res. 1985;46:1605.
8 Kofler J, et al. Vet Rec. 1996;138:34.
Hemangioma and hemangiosarcoma are rare in large animals but are described and may be associated with hemorrhage related to the site of the tumor.
Hemangiomas in the skin occur most commonly in young animals and may be congenital.1,2 The tumors grow with age; those on the skin may ulcerate and bleed and may necessitate euthanasia because of their eventual size. Similar tumors may occur in the mouth as pedunculated pink granular masses that ulcerate and bleed. Local hemangiomas on the skin and in the mouth may respond to surgical excision, thermocautery or radiation therapy. Widespread disseminated hemangioma is also recorded in young cattle presenting with multiple skin lesions and multiorgan involvement.3,4 Hemangioma has also been reported with moderate prevalence affecting the ovaries of sows.5
Hemangiosarcoma occurs in horses but is not a common tumor. It is more prevalent in middle-aged and older animals. Affected horses may present with a bleeding subcutaneous mass or with signs of disseminated hemangiosarcoma. Disseminated hemangiosarcomas in horses cause anemia due to hemorrhage into the tumor or into body cavities. In addition there is weight loss, but good appetite, and weakness. Metastasis is extensive to lung, myocardium, brain, retroperitoneum and skeletal muscle,5-8 and myocardial lesions can lead to cardiac arrhythmias. Lesions in skeletal muscle cause difficulties in movement and tumors in the nervous system present with signs of ataxia.9 The thoracic cavity is a common site for metastasis6 and can also be a primary site of the neoplasm.10
A common clinical manifestation is pleural effusion and hemorrhage11,12 and a clinical picture which requires differentiation from other causes of thoracic mass with effusion, which in the horse is more commonly mediastinal abscess, lymphosarcoma, squamous cell carcinoma or pleurisy. Hemoperitoneum, detectable by paracentesis, is present with peritoneal tumors. All the tumors are cavitatious and bleed profusely if incised. Early histopathologic diagnosis may permit a cure in animals with localized masses that can be surgically resected. If masses are not interfering with quality of life and the horse is medically stable, observation may be warranted because spontaneous resolution has been reported.8
1 Sartin EA, Hodge TG. Vet Pathol. 1982;19:569.
2 Lopez MJ, et al. Agri Pract. 1994;15:24.
3 Baker JC, et al. J Am Vet Med Assoc. 1982;181:172.
4 Munroe R, et al. Vet Rec. 1994;135:333.
5 Hargis AM, McElwain TF. J Am Vet Med Assoc. 1984;184:1121.
6 Johnson JE, et al. J Am Vet Med Assoc. 1988;193:1429.
7 Delesalle C, et al. J Vet Intern Med. 2002;16:612.
8 Johns I, et al. J Vet Intern Med. 2005;19:564.
9 Newton-Clarke MJ, et al. Vet Rec. 1994;135:182.
10 Freestone JF, et al. Aust Vet J. 1990;67:269.