When Auscultating the apical pulse of a client who has atrial fibrillation the nurse would expect to hear rhythm that is characterized by?

The cardiovascular system is assessed by observation of the animal's general state, mucous membrane appearance, and presence of venous distention or pulsation, as well as by examination of arterial pulse quality and rate and auscultation of the heart rate and rhythm.

Inspection of the patient may raise suspicion of cardiac disease if edema is observed in the submandibular space, brisket, ventral abdomen, udder, or lower limbs, or if abdominal contours suggest the presence of ascites. Obviously this requires differentiation from hypoproteinemic states, vasculitis, thrombophlebitis, lymphadenitis, or other less common diseases. Dyspnea, tachypnea, and grossly distended jugular or mammary veins are possible signs of cardiac disease that may be observed during general inspection of the patient. Weakness and exercise intolerance are other signs that require consideration of cardiac disease. In calves, overt abnormalities such as microphthalmos, wry tail, or absence of a tail signal the possibility of an accompanying ventricular septal defect, and ectopia cordis is grossly apparent by inspection of the thoracic inlet or caudal cervical area. However, many cases of congenital heart malformations occur in the absence of other defects.

During physical examination, mucous membranes should be evaluated for pallor, injection, or cyanosis. The visual appearance of the oral mucous membranes can vary with normal pigmentation patterns specific to the breed (e.g., Brown Swiss and Channel Islands cattle) and often appear pale to the inexperienced examiner in variably pigmented breeds such as Holsteins. In general, inspection of conjunctival and vulval mucous membrane appearance and refill time is preferable. Cyanosis is rare in dairy cattle with the exception of animals that are dying of severe pulmonary disease. However, cattle having advanced heart failure, right to left congenital shunts, and combined cardiopulmonary disease may have cyanotic mucous membranes. Capillary refill time often is prolonged in cattle with advanced cardiac disease.

Close inspection of the jugular and mammary veins for relative distention and presence of abnormal pulsation is a very important part of every physical examination. Proficiency and practice at palpation of major veins is essential before an examiner can differentiate an abnormal finding from the normal range of variation found in cattle of various ages and stages of lactation. Normally mammary veins are more sensitive indicators of increased venous pressure than jugular veins and therefore should be palpated routinely during the physical examination. Jugular veins should be observed during the general inspection and again during thoracic auscultation. Jugular veins should not be palpated until the end of the physical examination because many cattle become apprehensive when the neck region is palpated; this apprehension and subsequent excitement could affect baseline parameters or data being collected during the physical examination. This evaluation of the jugular veins, if deemed necessary, should be done at the end of the physical examination during examination of the head.

Mammary veins should be palpated by applying fingertip pressure. First the vein is palpated gently to detect pulsations suggestive of right heart failure; then the vein is compressed against the abdominal wall by gentle fingertip pressure. The amount of pressure necessary to compress the vein against the abdominal wall normally is minimal. When the vein is difficult to compress or, more commonly, seems to roll away from the fingertips, increased venous pressure from right heart failure may be suspected. These evaluations of the mammary veins obviously are subjective techniques but can be helpful adjuncts to other physical examination findings when practiced during every physical examination. Although pulsations in the mammary veins are considered abnormal findings suggestive of right heart failure, an occasional healthy older cow with a large udder and rich mammary vein branching may have slight mammary vein pulsation and distention.

Evaluation of the jugular veins for pulsation and distention requires differentiation of the “notorious” false-jugular pulsation commonly observed in thin-necked dairy cattle from pathologic true jugular pulsation and distention. False or normal jugular pulsation is a product of reverse blood flow from atrial contraction at the end of diastole and expansion of the right atrioventricular (AV) valve during systole. Passive jugular filling during systole also may contribute, as does a “kick,” or referred carotid artery pulsation. False jugular pulsation arises as a wave that winds its way from the thoracic inlet to the mandible when the cow has her head and neck parallel to the ground. When the head and neck are raised, the false jugular pulse may only ascend a portion of the cervical area or may disappear. A true jugular pulse fills the whole jugular vein rapidly when the head and neck are parallel to the ground or slightly raised. This rapid filling is similar to filling a garden hose with the end held off when water to the hose is turned on full force. In addition, distention of the jugular veins is more obvious with true jugular distention as found in right heart failure (Figure 3-1 ). When confusion exists, the jugular vein may be held off near the ramus of the mandible, blood forced distally toward the thoracic inlet, and the vein observed. Emptying the vein in this fashion will eliminate a false jugular pulse, but a true jugular pulse will refill the emptied vein quickly and indicates right heart failure, increased central venous pressure, or right AV valve insufficiency. Some examiners suggest applying light pressure that partially occludes the jugular vein at the thoracic inlet, thereby mildly distending the jugular vein. This is thought to eliminate false (or normal) jugular venous pulsations from a referred carotid arterial impact. In general, the degree of gross distention of the jugular veins in cattle having right heart failure is more impressive than the degree of pulsation (see video clip 1).

Taking the arterial pulse may be helpful in the assessment of cardiac disease. The middle coccygeal artery is the first artery palpated for pulsation during the physical examination. The facial artery is utilized when treating recumbent (hypocalcemic) cattle, and the median artery is the most convenient to palpate when performing simultaneous cardiac auscultation and pulse monitoring. Pulse rate, rhythm, and quality should be assessed. Pulse quality implies considerations of the size, strength, and duration of the pulse wave and distention of the artery. Most cattle with heart failure have decreased pulse strength, unevenness of the pulse, increased pulse rate, or a pulse rate that is different than the heart rate. Abnormalities in pulse rate or rhythm should alert the examiner to the possibility of cardiac arrhythmias.

Proficiency at auscultation of the heart requires some basic knowledge, willingness to auscult both sides of the thorax carefully during every physical examination, and patience. Many cattle object to stethoscope placement over the sites on the chest wall necessary for cardiac auscultation and will adduct the forelimb tightly against the thorax. This is noticed especially on examining the right side, where cardiac auscultation in cattle requires the stethoscope to be placed very cranial in the axillary area around the third intercostal space. Dairy bulls and large or fat cows have thick chest walls that reduce the intensity of heart sounds. Heart sounds are easier to hear on the left side of normal cattle. The pulmonic valve region is best heard in the left third intercostal space at a level between the shoulder and elbow. The aortic valve region near the heart base is best heard in the left fourth intercostal space at approximately shoulder level. The mitral (left AV) valve region coincides with the cardiac apex and is best heard at the left fifth intercostal space just above the elbow. The right AV (tricuspid) valve is heard far forward in the right third intercostal space at a level halfway between elbow and shoulder.

Although clinicians generally discuss two heart sounds in normal cattle, it is possible to hear four heart sounds in some cattle as it is with horses. Although the potential for four heart sounds is somewhat confusing and may be impossible to differentiate in most clinical patients, examiners should be aware of these facts. The first heart sound (S1) heralds the beginning of systole, is associated with the final halting of AV valve motion after closing and is best heard at the apex regions coinciding with AV valves in the cow. A slight splitting of S1 into separate mitral and tricuspid valve components is possible but is rarely audible in normal cattle. S1 tends to be of lower frequency and longer duration than S2.

S2 usually is not as loud as S1 and coincides with aortic and pulmonic valve closure. Current theory suggests that valve closing sounds associated with the generation of S2 result from the sudden halt in valve motion when it closes. Asynchronous closure of the aortic and pulmonic valves results in audible splitting of S2 in many normal cattle, especially during the inspiratory phase of the respiratory cycle.

Although S1 and S2 comprise the major heart sounds for cattle, S3 and S4 have been described. Ventricular vibrations at the end of rapid filling in early diastole are thought to cause S3, a low frequency sound seldom heard in cattle. S4 sometimes is heard late in diastole and is related to atrial contraction. In cattle with tachycardia, it has been suggested that S4 may in fact closely precede S1 and be mistaken for a split S1. The tripling or quadrupling of heart sounds that resembles a horse's cantering gait is commonly referred to as a gallop rhythm and occurs in the higher range of normal heart rates or when tachycardia exists in some cows. Gallops are diastolic sounds related to atrial contraction (S4 gallop), to ventricular filling (S3), or to both (summation gallop). A prominent and persistent gallop rhythm in a cow with tachycardia may be the first indication of heart disease.

The heart rate of normal cattle is 60 to 84 beats/min. Neonatal calves may have normal heart rates as high as 110 to 120 beats/min, but frequently heart rates this high are brought about by the excitement of being handled or in anticipation of being fed. Not everyone agrees on the aforementioned range of normal heart rates for cattle, and several points should be addressed regarding this topic. Oxen and fat, persistently dry cows used only for embryo transfer may have a slower metabolism than lactating dairy cattle. Therefore somewhat like draft horses, these cattle may have heart rates at the low end of the normal range or even less than 60 beats/min. Conversely healthy but excited, nervous, or aggressive cattle may have heart and pulse rates more than 84 beats/min when approached by any examiner. Therefore the range of 60 to 84 beats/min really is an average and must be interpreted in light of the patient, its surroundings, and its intended use. Following the work of McGuirk et al with fasted cattle, a low normal range of 48 beats/min has been proposed. However, fasted healthy cattle seldom are encountered in the world outside of academic settings, and veterinarians are not frequently asked to examine healthy fasted cattle. An exception may be a cow off feed secondary to the classic broken water cup syndrome because she will become anorectic secondary to water deprivation. Sick cattle seldom have a heart rate less than 60 beats/min only because they are anorectic. Sick cattle that do have heart rates less than 60 beats/min usually have a vagal nerve-mediated bradycardia. Therefore 60 to 84 beats/min is still our preferred normal range for heart rate in adult dairy cattle.

Excited or nervous cattle may have an increased intensity or loudness of the heart sounds in addition to an increased heart rate. Other conditions that increase the intensity of heart sounds may be relative or pathologic. Relative factors include thin body condition, younger animals with thin chest walls, and excitement. Pathologic factors include anemia, the “pounding” heart rate sometimes heard in cattle with endocarditis, and displacement of the heart to a position closer to the thoracic wall by a diaphragmatic hernia or an abscess or tumor in the contralateral hemithorax. “Muffling,” or decreased intensity of heart sounds, may occur for relative reasons such as the increased thickness or fat on the chest wall of adult bulls or heavily conditioned cattle. Muffling also results from pathologic conditions such as pericarditis, pneumomediastinum, diaphragmatic hernia, and displacement of the heart toward the opposite hemithorax by an abscess or tumor in the hemithorax being ausculted. Cattle in shock may have either decreased or increased intensity of heart sounds, depending on the duration and severity of the condition. “Shocky” cows that are weak but still ambulatory tend to have increased intensity of heart sounds, whereas those that are recumbent or moribund have decreased intensity.

Auscultation combined with percussion provides the best subjective means to estimate the position and size of the heart. Heart sounds may radiate over a wider area than normal when transmitted by consolidated lung lobes or pleural fluid or when there is cardiac enlargement.

In calves and thin adult cattle, palpation of the apex beat is possible around the left fourth or fifth intercostal spaces at a level halfway between the elbow and shoulder. Palpation of an apex beat on the right side of adult cattle seldom is possible unless profound cardiac disease or displacement of the heart to the right by space-occupying masses has occurred. Deep palpation with the fingertips over the intercostal regions overlying the heart may elicit a painful response in conditions such as endocarditis, pleuritis, traumatic reticuloperitonitis, and rib fractures.

As in other species, bovine heart murmurs are classified based on intensity and timing. Intensity may be ranked subjectively on a 1 to 6 basis, with 1 of 6 being a faint, barely detectable murmur; 2 of 6 as soft but easily discernable; 3 of 6 as low to moderate intensity; 4 of 6 moderate but lacking a thrill; 5 of 6 loud with palpable thrill; and 6 of 6 so loud that it can be heard with the stethoscope off the chest and evincing a palpable thrill. Classification relative to timing of the cardiac cycle further defines murmurs as systolic, diastolic, or continuous. Further division is provided by terms such as “early systolic” or “holosystolic.” In general, systolic murmurs in cattle reflect AV valve insufficiency or, much less commonly, aortic or pulmonic stenosis, whereas diastolic murmurs reflect aortic or pulmonic valve insufficiency or rarely AV valve abnormalities. Benign systolic murmurs occasionally are heard in excited, tachycardiac calves or cows with anemia, hypoproteinemia, or in those being given rapid intravenous (IV) infusions of balanced fluids. Pathologic systolic murmurs most commonly are found in calves with congenital heart abnormalities such as ventricular septal defect or tetralogy of Fallot and in adult cows with endocarditis. Continuous murmurs are rare but may be encountered in calves having a patent ductus arteriosus or in cows with pericarditis. The point of maximal intensity for each cardiac murmur may add subjective data as to the valve involved in the cardiac abnormality.

Arrhythmias may be benign, pathologic, or secondary to metabolic disturbances in cattle. Sinus bradycardia and arrhythmia have been confirmed in cattle held off feed, in hypercalcemic adult cattle, and in hypoglycemic or hyperkalemic young calves. Sinus tachycardia may result from excitement, pain, hypocalcemia, and various systemic states such as endotoxemia and shock. Cattle with severe musculoskeletal pain often have normal heart rates while recumbent but have tachycardia when forced to rise and stand. Persistent tachycardia should be considered abnormal and may reflect cardiac disease unless other systemic conditions coexist.

Hyperkalemia may cause a variety of arrhythmias and is most commonly observed in neonatal calves that develop acute metabolic acidosis associated with secretory diarrhea caused by Escherichia coli or acute diffuse white muscle disease. Atrial standstill and other arrhythmias have been documented in diarrheic calves having metabolic acidosis and hyperkalemia. Extreme hyperkalemia (.7.0 mEq/L) may lead to cardiac arrest and should be corrected immediately, especially in calves that may require general anesthesia. Because severe hyperkalemia may be associated with pathologic bradycardias, even without confirmatory blood work, the experienced clinician should be alert to the therapeutic need for fluids that will specifically address hyperkalemia in severely dehydrated, diarrheic calves with discordantly low heart rates for their systemic state. Calves with white muscle disease also may have direct damage to the myocardium, which may be manifested by arrhythmias, murmurs, or frank cardiac arrest. Hypokalemia and hypochloremia in cattle with metabolic alkalosis may predispose to the most common arrhythmia of adult cattle—atrial fibrillation.

Hypocalcemia may be present or contribute to cattle having abdominal disorders that lead to metabolic alkalosis. Metabolic alkalosis may be a factor that triggers atrial fibrillation in cattle with normal hearts. Atrial fibrillation causes an irregularly irregular rhythm, with a rate that may be normal or increased (88 to 140 beats/min), depending on the presence of heart disease or the underlying predisposing condition. Atrial fibrillation is associated with irregular intensity of heart sounds. A pulse deficit may be present in any cow with a rapid or irregular cardiac rhythm, especially when the rate exceeds 120 beats/min. Atrial premature complexes (APC) may also occur in cows with gastrointestinal disease and electrolyte abnormalities. APC may preceed or immediately follow atrial fibrillation in some cows. Variation in intensity of the first heart sound during auscultation is characteristic of APC.

Other causes of arrhythmia in adult cattle include sporadic cases of lymphosarcoma with significant myocardial infiltration often causing atrial fibrillation, and ventricular or atrial arrhythmias associated with septic or toxic myocarditis. IV administration of calcium solutions is the major drug-related cause of arrhythmias in cattle, but intravenous administration of antibiotics or potassium-rich fluids occasionally prompts transient arrhythmias.

Sounds ausculted in pericarditis patients are variable, often confused with murmurs, and tend to change on a daily basis if affected cattle are available for daily reevaluation. Classic pericardial “friction” rubs occur at different stages of each cardiac cycle unlike murmurs, which tend to occur at a distinct phase of each cardiac cycle. Squeaky sounds, often similar to that made in compression of a wet sponge, may be heard as a result of pericardial disease. Rubs caused by contact between fibrin on the visceral and parietal pericardium also may be heard. The heart sounds tend to be muffled, and either free fluid or fluid-gas interfaces may lead to splashing or tinkling sounds or to complete muffling of all sounds. During the acute phase of traumatic reticulopericarditis, the character of the sounds tends to change each day. In those with subacute or chronic disease, muffling of the heart sounds or distinct tinkling or splashing tends to be consistently present.

Presence of an arrhythmia or murmur alerts the examiner that the heart may be abnormal. However, heart failure may or may not be present. In cattle, right heart failure is more common than left heart failure. The general signs of right heart failure include:

• 1.

  Ventral edema—the edema may be diffuse or limited to specific regions such as the submandibular area, brisket, ventral abdomen, udder or sheath, and the lower limbs (Figure 3-2 )

• 2.

  Jugular and mammary vein distention with or without pulsations

• 3.

  Exercise intolerance with or without dyspnea

• 4.

  Persistent tachycardia

• 5.

  Ascites with or without pleural fluid

In addition to the general signs, specific cardiac signs such as a murmur, arrhythmia, or abnormal intensity of heart sounds usually are present and contribute to the diagnosis. Probably the most difficult set of differential diagnoses involves diseases that result in hypoproteinemia. Hypoproteinemia also causes ventral edema and may cause exercise intolerance and tachycardia. However, hypoproteinemia would not cause jugular and mammary vein distention and pulsation. Therefore venous distention and pulsation coupled with abnormal heart sounds or rhythm are the key signs when diagnosing heart failure in dairy cattle.

Left heart failure causes dyspnea, pulmonary edema, and exercise intolerance and may lead to cyanosis and collapse or syncope. Specific left heart failure seldom occurs in cattle, but left side failure combined with worsening, antecedent right heart failure may develop as the animal progresses into fulminant congestive heart failure.

Electrocardiography

The electrocardiogram (ECG) is essential for definitive categorization of arrhythmias in cattle. Vector analysis of ECG tracings to determine cardiac chamber enlargements and other pathology seldom is used in cattle because ventricular myocardial depolarization tends to be rapid and diffuse rather than organized, as in some other species. ECG is also indicated when cattle have variation in heart sound intensity, require monitoring for anesthesia or treatment of cardiac arrhythmias, or show signs of heart failure. Cardiac ultrasound, however, has superseded the ECG as a diagnostic tool in determining chamber enlargement and other cardiac pathology.

The base-apex lead system is most commonly used in cattle. The base-apex lead system results in an ECG with large wave amplitude and is sufficient for evaluating most arrhythmias. The positive electrode is placed on the skin over the left fifth intercostal space at the level of the elbow; the negative electrode is placed on the skin over the right jugular furrow roughly 30 cm from the thoracic inlet; and the ground electrode is attached to the neck or withers. The resultant ECG recorded through the base-apex lead system has a positive P wave with a single peak, a QRS complex with an initial positive deflection followed by a large negative deflection, and a variable (positive or negative) T wave (Figure 3-3, A to C ).

A, Normal sinus rhythm with a heart rate of 60 beats/min recorded from a 4-year-old Holstein cow. B, Sinus bradycardia with heart rate of 36 beats/min recorded from a 6-year-old Brown Swiss cow sick with abomasal ulcers. C, Sinus tachycardia with heart rate of 108 beats/min recorded from a 2-year-old Holstein with an acute leg injury.

Echocardiography

Two-dimensional echocardiography and Doppler echocardiography have greatly enhanced our ability to assess cardiac function and visualize anatomic variations and pathologic lesions in cattle. Valvular, myocardial, pericardial, congenital, and acquired lesions can be visualized in real time, measured, and monitored. Qualitative and quantitative assessment of the impact of congenital anomalies and monitoring treatment response of endocarditis, pericarditis, or other myocardial lesions are possible with the appropriate equipment and people trained to conduct and interpret a systematic cardiac examination. In short, echocardiography is now an essential component of a cardiology workup. Sector scanners utilizing a 3.5-mHz (or lower) transducer are most useful for adult cattle. A 5.0-mHz transducer may be helpful when evaluating neonatal calves suspected of having congenital anomalies or other cardiac conditions. Although some clinicians may lack the equipment or expertise with echocardiography, current graduates are being trained in the technique, and continued competition among manufacturers may allow more veterinarians to own this equipment. In any event, referral for echocardiography is indicated for valuable cattle whenever cardiac disease is apparent but a specific diagnosis is lacking. In most cattle, a systematic examination can be conducted from the right parasternal window to provide a long axis four-chamber view of the heart, a long axis view of the left ventricular outflow tract, and a short axis view of the left ventricle just ventral to the mitral valve and at the papillary muscle level. From the same window, all four heart valves can be visualized, chamber sizes can be measured, myocardial functional measurements can be made, and abnormalities of the pericardium can be seen. Congenital lesions like ventricular septal defect (VSD) (Figure 3-4 ) and acquired pericarditis (Figure 3-5 ) are easily visualized by echocardiogram.

Myocardial damage from vitamin E and selenium deficiency may occur at any site in the heart and may be focal, multifocal, or diffuse (Figure 3-6 ). Signs may develop at any time from birth to 4 years of age but are more common in calves less than 3 months of age. Specific cardiac signs are variable and include arrhythmias, murmurs, exercise intolerance, cyanosis, dyspnea, congestive heart failure signs, and acute death. Signs may be subtle or dramatic, depending on the magnitude and locations of myocardial damage. Sudden death can occur spontaneously or following exercise or restraint. Other signs of white muscle disease such as stiffness, difficulty in prehension or swallowing, inhalation pneumonia, and myoglobinuria may or may not be present. Dyspnea may be directly related to the cardiac lesions or may be caused by Zenker's degeneration in the diaphragm or intercostal muscles. Tachycardia (.120 beats/min) and arrhythmias are the most common specific cardiac signs, but murmurs may be present as well.

Diagnosis can be confirmed by measuring blood selenium values, urine dipstick testing to look for positive “blood” (myoglobin) and protein, and serum biochemistry to evaluate creatine kinase (CK) and aspartate aminotransferase (AST) enzymes. If the heart is the only muscle involved, serum enzymes may not be greatly elevated; however, the heart seldom is the only area involved.

Treatment should be instituted immediately with vitamin E and selenium injected at the manufacturer's recommended dosage. Although some commercial preparations include label instructions that include IV use, it is suggested that vitamin E/selenium be given intramuscularly (IM) or subcutaneously to avoid the occasional life-threatening anaphylactic-type reaction seen with these products. The calf should be kept in a small box stall, straw bale enclosure, or hutch, so it can move about but not run freely, lest further muscle damage be precipitated. If pulmonary edema is present, furosemide (0.5 to 1.0 mg/kg) may be given once or twice daily. Concurrent aspiration pneumonia would require intense antibiotic therapy. Vitamin E and selenium injections are repeated at 72-hour intervals for three or four total treatments. Herd selenium status and preventive measures to address the problem should be discussed. Calves that survive for 3 days following diagnosis have a good prognosis.

Cardiac arrhythmias or bradycardia associated with hyperkalemia is primarily observed in neonates having severely acute diarrhea. Enterotoxigenic E. coli causing secretory diarrhea, metabolic acidosis, low plasma bicarbonate values, and hyperkalemia appears to be the most common causative organism. Rotavirus or coronavirus also may be involved in calf diarrhea, but they seldom produce as profound a metabolic acidosis as E. coli.

Less common causes of hyperkalemia include severe diffuse white muscle disease involving heavy musculature of the limbs, ruptured bladders, renal failure, urinary obstructions, and nonspecific shock.

Hyperkalemia reduces the resting membrane potential, which initially makes cells more excitable, but gradually (with further elevation in potassium and further reduction in resting membrane potential) the cells become less excitable. Atrial myocytes seem more sensitive to these effects than those within the ventricles. Cardiac conduction is affected, and several characteristic ECG findings evolve in a typical sequence that correlates well with increasing K+ values: ECG changes include peaking of the T wave, shortening and widening of the P wave, prolongation of the PR interval, eventual disappearance of the P wave, widening of the QRS complex, and irregular R-R intervals (Figure 3-7 ). Atrial standstill characterized by bradycardia and absence of P waves may occur and has been documented in association with hyperkalemia in diarrheic calves. Further progression may lead to AV block, escape beats, ventricular fibrillation, asystole, and death.

In neonates, hypoglycemia is the major differential diagnosis when bradycardia is present. Septic myocarditis or white muscle disease also may be considered if an arrhythmia is present.

Calves less than 2 weeks of age that have developed acute diarrhea, are recumbent, dehydrated, and have bradycardia or arrhythmia should be suspected of being hyperkalemic. Obviously only an acid-base and electrolyte analysis of blood and an ECG can confirm this. However, these may not be available in the field. The consequences of underestimating the life-threatening importance of the heart and K+ relationship in these patients are severe.

Calves suspected to be hyperkalemic based on history, physical signs, and arrhythmia or bradycardia should receive alkalinizing fluids and dextrose. Being neonates, hypoglycemia may contribute to bradycardia when this sign is present. One way to treat metabolic acidosis and hyperkalemia is by IV infusions of 5% dextrose solution containing 150 mEq NaHCO3/L. Usually 1 to 3 L is necessary, depending on the magnitude of the metabolic acidosis and bicarbonate deficit. Glucose and bicarbonate help transport K+ back into cells, and the glucose also treats or prevents potential hypoglycemia. Once the acute crisis has been resolved, the calf may be safely treated with balanced electrolyte solutions containing potassium. Calves with diarrhea, despite having plasma hyperkalemia, have total body potassium deficits and require potassium supplementation. This may be true even in the acute phase of disease, but when serum K+ is 5.0 to 8.0 mEq/L there is no time to worry about a “total body potassium deficit.” We have treated hundreds of calves as suggested above, and those with a venous blood pH of 7.0 or greater have a good to excellent prognosis unless they have had failure of passive transfer of immunoglobulins and subsequent septicemia. Specific insulin therapy as an adjunct to bicarbonate and glucose to correct hyperkalemia is not necessary in calves.

Virtually all types of congenital cardiac anomalies occur in cattle. Most congenital anomalies appear to be sporadic, but inheritance may play a part in some of the most common anomalies. The most common congenital anomalies in cattle appear to be VSDs (Figure 3-8 ), tetralogy of Fallot, atrial septal defects, and transpositions of great vessels.

Most congenital cardiac defects cause distinct murmurs. Calves affected with the most common defects such as VSDs, atrial septal defects, tetralogy of Fallot, or aortic or pulmonic stenosis usually have systolic murmurs. Patent ductus arteriosus, which is rare as a single defect in calves, can cause a systolic or continuous murmur.

Most calves with congenital cardiac defects appear normal at birth but eventually are noticed to have dyspnea, poor growth, or both. Many calves with congenital heart defects are eventually examined by a veterinarian because of persistent or recurrent respiratory signs or generalized ill thrift. The respiratory signs may be real in the form of pulmonary edema associated with heart failure and shunts or be caused by opportunistic bacterial pneumonia secondary to pulmonary edema and compromise of lower airway defense mechanisms. The owners may already have treated the calf one or more times for coughing, dyspnea, and fever, only to have the signs recur. Usually only one calf is affected, thus making enzootic pneumonia an unlikely diagnosis. Regardless of whether pulmonary edema or pneumonia plus pulmonary edema are present, veterinary examination usually detects the cardiac murmur that allows diagnosis. Venous pulsation and distention of the jugular veins may be present, but calves seldom show ventral edema as distinctly as adult cattle with heart failure.

Calves with congenital heart defects that do not develop respiratory signs usually show stunting compared with herdmates of matched age. The degree of stunting varies directly with the severity of the congenital lesions in regard to blood oxygenation but usually becomes apparent by 6 months of age and is very dramatic in calves that survive to yearlings. Some cattle with small defects survive and thrive as adults, but this is rare.

VSDs are the most common defects in dairy calves and are found in all breeds. In Guernseys and Holsteins, VSD may be linked to ocular and tail anomalies. Microphthalmos and tail defects, including absence of tail, wry tail, or short tail, frequently signal VSD (Figure 3-9 ). Sometimes ocular, tail, and cardiac defects all are present in the same calf, but it is more common to find tail or ocular pathology plus VSD. Depending on the size of the VSD, affected calves have a variable life span. Prognosis for most is hopeless because of eventual respiratory difficulty and stunting. However, calves do, in rare instances, survive to productive adult states. The genetics of these multiple defects (eye, tail, and heart) have not been investigated in Holsteins but have been assumed to be a simple recessive trait in Guernseys.

Tetralogy of Fallot and other multiple congenital defects that allow right to left shunting of blood provoke marked exercise intolerance, cyanosis, and dyspnea and may lead to polycythemia secondary to hypoxia. Prognosis for long-term survival is grave in these calves. Ectopia cordis in a calf creates a dramatic sight, with the heart beating under the skin in the neck, but is extremely rare.

The heart is one of the common target sites of lymphosarcoma in adult dairy cattle. Many cattle with multicentric lymphosarcoma have cardiac infiltration based on gross or histologic pathology, but fewer of these cattle have clinically detectable cardiac disease. When the heart is a major target site, cardiac abnormalities are more obvious. The heart seldom is the only organ affected with lymphosarcoma. Therefore detection of cardiac abnormalities coupled with other suspicious lesions (e.g., enlarged peripheral lymph nodes, exophthalmos, melena, and paresis) simply helps to make a lymphosarcoma diagnosis more definite.

Depending on the anatomic location and magnitude of the tumors, cattle with cardiac lymphosarcoma may have arrhythmias, murmurs, jugular venous distention, jugular venous pulsations, or muffling caused by diffuse cardiac or pericardial involvement. Muffling and splashing sounds are possible if a pericardial transudate or exudate is present. The most common site of tumor involvement is the right atrium, but nodular or infiltrative tumors can be found anywhere in the myocardium or pericardium (Figure 3-10 ). The color and consistency of the tumors may vary. Mediastinal lymph nodes also are commonly involved. Cattle with signs of heart disease should be thoroughly examined for other lesions consistent with lymphosarcoma. When multiple lesions exist, the diagnosis is easy. However, cattle examined because of vague signs such as hypophagia and decreased milk production that are found to have tachycardia or other cardiac abnormalities can present diagnostic challenges. Although ECG and thoracic radiographs have seldom helped make a definitive diagnosis, ultrasound may be very helpful to image nodular or large masses of lymphosarcoma. Thoracocentesis and pericardiocentesis to obtain fluid for cytologic evaluation are the most helpful ancillary aids when cardiac lymphosarcoma is suspected. A complete blood count (CBC) and assessment of bovine leukemia virus (BLV) antibody status are indicated, but a positive BLV agar gel immunodiffusion (AGID) or radioimmunoassay (RIA) test does not ensure an absolute diagnosis because most positive cattle never develop tumors (see the section on Lymphosarcoma in Chapter 15). Therefore simply assuming a cow with a positive BLV test and heart abnormality detected on physical examination has lymphosarcoma may be an incorrect assumption. A double line-positive BLV-AGID may add further weight to the suspected diagnosis, as would the finding of a persistent lymphocytosis in a set of CBC results. Clinical identification of masses in other locations or cytology from thoracocentesis or pericardiocentesis provides the best means of definitive diagnosis.

Fever usually is absent in cattle with cardiac lymphosarcoma. Occasional cattle with large tumor masses in the thorax or abdomen may have fever because of tumor necrosis or nonspecific pyrogens produced by neoplasms. Secondary bacterial infections of the lungs or other body systems also may lead to fever, which confuses the diagnosis.

Prognosis is hopeless for cattle with cardiac lymphosarcoma, and most cattle with the disease die from cardiac or multisystemic disease within a few weeks to a few months. Successful attempts at chemotherapy have not been reported to our knowledge. One author has successfully prolonged life up to 6 months in a few cattle with cardiac lymphosarcoma that had significant pericardial fluid accumulations by intermittent pericardial drainage. Occasionally valuable cattle may justify such treatment to allow a pregnancy to be completed or to be superovulated. However, as with many catabolic conditions, owners should be cautioned that maintaining the dam with advanced heart disease for more than a few weeks may produce a gestationally dysmature fetus even if the pregnancy is carried to term, or may seriously affect the cow's ability to superovulate or even produce viable oocytes for in vitro fertilization. There is also the risk of vertical transmission of BLV from dam to fetus in utero, which is greater should the dam have clinically apparent tumors. In one late pregnant cow with severe pericardial effusion caused by lymphosarcoma, we were able to maintain the cow for several weeks by surgically opening the pericardial sac into the pleural cavity, which significantly improved venous return to the heart and the overall condition of the cow. The cow was also treated with isoflupredone.

Neurofibroma, although uncommon, frequently causes arrhythmia and variable intensity of heart sound in affected cattle and bulls. Further the cardiac arrhythmia may coexist with paresis or paralysis caused by neurofibroma masses in the spinal canal. Because lymphosarcoma more commonly causes paresis coupled with cardiac disease, this combination of signs is most suggestive that lymphosarcoma is present. Although perhaps a moot point because both diseases are fatal, further medical workup of neurofibroma patients fails to provide confirmation of lymphosarcoma. To date, postmortem examination has been the only means of definitive diagnosis for cardiac neurofibroma. Examiners talented in ultrasound may be able to diagnose these lesions based on the typically gnarled, raised cords of tumor involving the cardiac nerves.

Infections

Septic Myocarditis.

Neonatal septicemia caused by gram-negative bacterial organisms, acute infection with Histophilus somni, and chronic infections in any age of cattle resulting from Arcanobacterium pyogenes are the most common cause of septic myocardial lesions in cattle. Septicemic calves, calves suspected of having H. somni infection, or calves with chronic infections should be suspected of having septic myocarditis if an arrhythmia or other signs of abnormal cardiac function develop during their illness. White muscle disease, hyperkalemia, and hypoglycemia should be considered. Septicemic calves have a guarded prognosis, and septic myocarditis worsens it. Septic myocarditis foci in adult cattle with chronic, active infection or abscesses associated with mastitis, localized peritonitis, foot lesions, or chronic pneumonia are more commonly identified by pathologists than clinicians. Although tachycardia is likely to be present, this finding often is assumed to result from the primary illness rather than from myocarditis. As with calves, adult cattle with septic myocarditis may have paroxysmal cardiac arrhythmias that alert the clinician to the diagnosis. Definitive diagnosis has been difficult in the living patient because test for cardiac muscle enzymes may lack specificity for cardiac muscles. Increased concentration of troponin I may be used to help diagnose myocardial disease. An ECG showing atrial or ventricular premature depolarizations in a calf or cow with evidence of sepsis or a walled-off infection can be used to lend credence to the diagnosis.

Treatment of the primary disease remains the most important part of managing septic myocarditis. If the primary problem and myocardial lesion can be sterilized, the heart may return to normal function.

Septic myocardial disease of adult cattle, as in calves, usually follows septicemia or chronic infections. Septicemic spread of infectious organisms, thrombi, or mediators of inflammation may be involved in the pathophysiology of myocardial injury that occurs in septic cattle. Although relatively uncommon, development of persistent tachycardia with or without an arrhythmia in a patient with infectious disease may suggest myocarditis. Tachycardia is so nonspecific that most examiners attribute the tachycardia to the primary disease rather than secondary myocarditis. Only when the myocardial damage causes signs of heart failure does a diagnosis of myocarditis become easier. Acute death is possible. Arrhythmia, if present, must be assessed using ECG and blood electrolytes and acid-base status to rule out atrial fibrillation associated with metabolic abnormalities. Dairy cattle are most at risk for myocarditis with acute septic diseases such as severe mastitis, metritis, pneumonia, and infection caused by H. somni. Occasional cases also occur secondary to chronic localized infections such as digital abscesses that predispose to bacteremia. Depending on the size and location of the myocardial lesion, clinical signs range from subclinical to overt heart failure. ECG evidence of ventricular arrhythmias would suggest myocardial damage, but supraventricular arrhythmias are possible as well. Unfortunately definitive premortem diagnosis is impossible without advanced echocardiographic or invasive cardiac technique. Treatment must be directed at the primary disease. Minor myocardial lesions away from nodal and conduction tissue may heal or fibrose asymptomatically, whereas large or multifocal lesions may lead to heart failure, persistent tachyarrhythmia, or sudden death.

Toxins

Ionophores such as monensin and lasolocid are capable of damaging myocardial and skeletal muscle when ingested in toxic amounts. Improper mixing of ionophores into rations is the most common error that may lead to toxicity, but accidental exposure to concentrated products also is possible. Obviously this is a potential concern for calves and heifers being fed milk replacer or feeds containing ionophores. Fortunately cattle are much more resistant to the toxic effects of ionophores than are horses, but there is a narrow margin of safety, especially in young calves.

Many poisonous plants are theoretically capable of myocardial injury, but in reality few are likely because of increased confinement of heifers and adult cattle. Eupatorium rugosum (white snakeroot), Vicia villosa (hairy vetch), Cassia occidentalis (coffee senna), Phalaris sp., and others are capable of toxic myocardial damage. Gossypol also is capable of causing myocardial damage when fed in toxic amounts. This fact is of special concern given the increased incidence of feeding cottonseed to dairy cattle. Copper deficiency, especially when chronic, occasionally has been linked to acute myocardial lesions, resulting in death (“Falling disease” in Australia). Many other organic and inorganic toxins have the potential for causing myocardial damage but create more obvious pathology in other body systems and thus will not be discussed here.

No specific treatment is available for toxic myocarditis. Common sense dictates identification and removal of the toxin from the environment, alongside immediate administration of laxatives, cathartics, and/or protectants to decrease absorption and accelerate intestinal transit. Vitamin E and selenium administration and specific supportive treatment for cardiac disease should be instituted, but the prognosis for animals already with congestive heart failure is grave.

Parasitic and Protozoan Infections

Cysticerca bovis may cause myocardial lesions, but these appear rarely in dairy cattle in the northeastern United States. This is the larval form of Taenia saginata, the common human tapeworm. Contamination by human sewage of feedstuffs, pastures, or fields puts cows at risk for this disease.

Although Toxoplasma gondii is capable of infecting cattle, the clinical disease appears rare because cattle rapidly eliminate parasites from tissue. Cattle are exposed to and infected by T. gondii via ingestion of feedstuffs contaminated by cat feces.

Sarcocystis sp. is a common cause of myocardial disease in cattle. Although most infestations are asymptomatic, clinical illness characterized by hemolysis, myopathy, myocarditis, weight loss, rattail, and other signs is possible. Sarcocystis sp. requires two hosts, and carnivores or humans usually are the hosts that shed sporocysts in fecal material that subsequently contaminates cattle feed (see Chapter 15). Cattle then become the intermediate host as intermediate stages of the parasite invade endothelial cells and later stages encyst in muscle—including the myocardium. Subsequent ingestion by carnivores of beef containing cysts continues the cycle.

Histopathologic identification of sarcocystis cysts in myocardium of cattle is very common but seldom deemed significant. Certainly, however, heavy exposure to the organism could provoke significant myocardial damage.

Parasitic or protozoan myocarditis usually requires histopathology or serology for diagnosis. Treatment would be best provided by preventive measures to avoid contamination of cattle feeds by carnivore or human feces.

Inherited Myocardial Disease

A dilated cardiomyopathy has been described in Canadian Holstein-Friesians. This condition appears in Canadian black and white Holsteins and expresses itself as heart disease between 19 and 78 months of age. Although most cattle develop clinical signs within 4 years of birth, some have lived for 6 to 7 years.

Most cases are presented because of signs referable to heart failure such as ventral edema, exercise intolerance, inappetence, dyspnea, tachycardia, muffled heart sounds, and jugular and mammary vein distention and pulsation. Although tachycardia is fairly consistent, other auscultation findings such as arrhythmias, murmurs, or varying intensity of the heart sounds vary in each case. Hepatomegaly consistent with chronic passive congestion of the liver secondary to right heart failure also was present in some patients.

Echocardiography and ECG recordings are required for diagnosis. Ultrasound is the best aid to confirm dilated cardiomyopathy.

Long-term prognosis is hopeless, but affected cattle may be helped in the short term by management with cardioglycosides, and furosemide is indicated if pulmonary edema exists. McGuirk suggests digoxin at 0.86 mg/kg/hr as an IV infusion. This obviously requires diligence, IV catheterization, and hospitalization, or else a very attentive owner. Alternatively, 3.4 mg/kg IV every 4 hours may be utilized but creates greater variation in blood levels and increases the risk of digoxin toxicity. Furosemide is used at 0.5 to 1.0 mg/kg twice daily if pulmonary edema is present. Inappetent cattle may benefit from 50 to 100 g KCl orally each day to maintain potassium levels when being treated with digoxin. Ideally daily or every other day blood acid-base and electrolyte status should be assessed.

Etiology

Bacterial endocarditis is the most common valvular disease or endocardial disease in adult dairy cattle. It also is one of the few treatable heart conditions of cattle. Therefore early suspicion, diagnosis, and appropriate treatment improve the prognosis.

Cattle with chronic infections such as septic musculoskeletal conditions, hardware disease, abscesses, lactic acid indigestion, chronic pneumonia, metritis or mastitis, and thrombophlebitis are at risk for bacterial endocarditis. In addition, cattle with long-term IV catheters have increased risk of endocardial infections. Bacteremia appears essential to the pathophysiology of bacterial endocarditis in cattle.

A. pyogenes is the most common organism isolated from the blood and endocardial lesions of cattle affected with endocarditis, but Streptococcus sp., Staphylococcus sp., and gram-negative organisms may also cause the disease. The right AV valve (tricuspid) is the most commonly infected valve with the left AV (mitral) being the second most common (Figure 3-11 ). Other valves or the endocardium adjacent to valves may also occasionally be the site of infection (Figure 3-12 ). Owner complaints regarding affected cattle include recurrent fever, weight loss, anorexia, poor production, and sometimes lameness.

Signs

Persistent or intermittent fever, tachycardia, and a systolic heart murmur are the most common signs found in cattle having endocarditis. A “pounding” heart or increased intensity of heart sounds also is common, although the heart sounds may vary in intensity or even be reduced in some patients. Vegetative endocarditis may also occur in the absence of an auscultable murmur.

Some cattle with endocarditis appear painful when digital pressure is exerted on the chest wall over the heart region. Fever usually is present, has been present historically, or develops intermittently following initial examination. Some cattle with endocarditis never have fever recorded but do show other signs of illness and a systolic heart murmur or other cardiac signs.

Signs of heart failure may develop along with increased distention and pulsations of the jugular and mammary veins. Tachycardia is a consistent finding, and dyspnea may develop, especially after bacterial showering of the lungs. Arrhythmias are unusual and paroxysmal but may be observed in approximately 10% of patients.

Lameness, often shifting, and stiffness may be observed. Synovitis and joint tenderness sometimes are obvious, but in other patients exact localization of the lameness is difficult. Bacteremia to joints or epiphyses and immune-mediated synovitis have been suggested as origins of this lameness in endocarditis patients.

Laboratory Data

Nonregenerative anemia commonly results from chronicity of the primary infection, the endocardial infection, or both. Neutrophilia is common and was found in 24 of 31 cases in one report, whereas absolute leukocytosis was found in 14 of 31. In this same report, serum globulin values were greater than 5.0 g/dl in 19 of 23 endocarditis patients that had globulin measured. Elevated globulin was believed to be consistent with the chronicity of infection.

Blood cultures are an important diagnostic test, but echocardiography provides the definitive diagnosis. A patient suspected of having endocarditis should have a series of blood cultures submitted rather than a single time-point sample. Although blood cultures in adult cattle may be negative in as many as 50% of endocarditis patients tested, isolating the causative organism from the bloodstream provides the best opportunity for appropriate and successful treatment with a specific antibiotic. Venous blood cultures should be collected after the jugular vein has been clipped and prepared aseptically. The cow should have been held off systemic antibiotics for 24 to 48 hours before culture attempts, if possible. Although one blood culture attempt is better than none, it is preferable to obtain a series of three to four cultures when economics allow. The interval between collections of multiple samples has been debated by clinicians for decades. Some clinicians culture only during a fever spike, some at 3- to 30-minute intervals, some at 6- to 8-hour intervals, and some once daily. We prefer to obtain three cultures at 30-minute intervals in febrile patients and intervals of several hours in nonfebrile patients suspected of having endocarditis.

Diagnosis

Early signs of reduced appetite and production, fever, and tachycardia certainly are not specific for endocarditis. A pounding heart or systolic murmur should suggest the diagnosis and dictate further workup. Diagnosis may be overlooked because of more obvious primary problems such as abscesses, infected digit or other musculoskeletal infection, suspected hardware disease, or thrombophlebitis because these conditions may also cause fever and nonspecific signs of illness. Therefore heart murmurs, a pounding heart, or early signs of heart failure in addition to tachycardia merit consideration of a diagnosis of endocarditis. Lameness and stiffness may be difficult to differentiate from primary musculoskeletal disease or painful stance caused by peritonitis but can be important clinical signs that aid diagnosis. Because of fever, tachycardia, and sometimes polypnea, cattle having endocarditis often are misdiagnosed with pneumonia or traumatic reticuloperitonitis.

Diagnosis of endocarditis usually is based on the patient's history and clinical signs. However, a positive blood culture and echocardiography allow definitive diagnosis. Blood cultures, as mentioned previously, may or may not be successful; however, when positive, they allow appropriate selection of antibiotics. Definitive diagnosis based on two-dimensional echocardiography has proven to be one of the most impressive uses of ultrasound since its widespread use in diagnostics began 10 years ago. Veterinarians trained in echocardiography now have a tool to confirm bacterial endocarditis in most patients (Figure 3-13 ).

Treatment

Long-term antibiotic therapy is required to cure bacterial endocarditis in cattle. Thus cattle selected for treatment must be deemed valuable enough to justify the cost of antibiotics and discarded milk that will be incurred. A successful blood culture allows selection of an appropriate antibiotic based on sensitivity or mean inhibitory concentration (MIC) values. Because endocarditis in cattle usually is caused by A. pyogenes or Streptococcus sp., some clinicians assume penicillin will work and do not bother to do blood cultures. This assumption would be a worthwhile gamble if economics dictate that laboratory costs be minimized.

Therefore penicillin and ampicillin are the drugs of choice for bacterial endocarditis in cattle caused by A. pyogenes and most Streptococcus sp. Although ceftiofur currently has the advantage of “no withdrawal,” it is more expensive and has been overused and abused by clinicians who hope the drug will cure all infections of dairy cattle. Penicillin (22,000 to 33,000 IU/kg twice daily) or ampicillin (10 to 20 mg/kg twice daily) is administered for a minimum of 3 weeks. If gram-negative organisms or penicillin-resistant gram-positive organisms are isolated from blood cultures, an appropriate bactericidal antibiotic should be selected based on MIC or antibiotic sensitivity testing.

Based on work by Dr. Ray Sweeney and others at the University of Pennsylvania, rifampin (rifamycin) has been shown to establish therapeutic blood levels after oral administration to ruminants. Unfortunately there is significant variability in blood levels between treated cattle, which may limit its treatment potential. Rifampin is a unique antibiotic that gains access to intracellular organisms or walled-off infections by concentrating in macrophages. Rifampin always should be used in conjunction with another antibiotic because bacterial resistance may develop quickly when the drug is used alone. The dosage is 5 mg/kg orally, twice daily for cattle. Although some maintain this dosage is too low, it has seemed effective clinically when used in conjunction with penicillin not only for chronic A. pyogenes endocarditis but also for pulmonary abscesses. Therefore if economics allow, oral rifampin has been reported to improve treatment success in cattle with bacterial endocarditis.

Occasionally cattle will become significantly anorectic while receiving rifampin (more so than was noted in association with the primary disease), but in many cases this apparent intolerance to the drug is overcome if administration is discontinued for several days and then reinstituted at the same or lesser dose.

In addition to antibiotic therapy, those cattle showing venous distention, ventral edema, or pulmonary edema require judicious dosages of furosemide. Because many endocarditis patients have reduced or poor appetites, overuse of furosemide may lead to electrolyte depletion (K+, Ca++) and dehydration. Therefore when furosemide is used, the drug should be administered on an “as-needed” basis, and 0.5 mg/kg once or twice daily usually is sufficient.

Because cattle with endocarditis often appear painful or stiff and may have either primary musculoskeletal disorders or secondary shifting lameness, aspirin is administered at 240 to 480 grains orally twice daily. Unfortunately aspirin does not appear to minimize platelet aggregation and is unlikely to prevent further enlargement of vegetative lesions. Free access to salt should be denied of cattle showing signs of congestive heart failure.

Treatment continues for a minimum of 3 weeks. Positive signs of improvement include increasing appetite and production, as well as absence of fever. The heart murmur persists and may vary as treatment progresses. Resolution of the heart murmur and tachycardia coupled with echocardiographic evidence of resolution of the endocarditis lesions are excellent prognostic signs. Many cows that survive are, however, left with persistent subtle or obvious heart murmurs caused by valvular damage. This should not be a concern as long as other signs indicate resolution of infection and heart failure is not present. Cattle with venous distention, ventral edema, or other signs of right heart failure have a worse prognosis than cattle diagnosed before signs of heart failure. However, mild to moderate signs of heart failure should not be interpreted to mean a hopeless prognosis because supportive treatment may alleviate these signs while antibiotic therapy treats the primary condition.

Prognosis for endocarditis patients is guarded. Sporadic case reports tend to highlight successfully managed individual cases, but further case series are necessary to suggest accurate recovery rates. Of 31 cattle affected with endocarditis that were admitted to our hospital between 1977 and 1982, 9 responded to long-term antibiotic (8 penicillin and 1 tetracycline) therapy. Based on these data and the experience of other clinicians, the prognosis is better when the diagnosis is made early in the course of the disease. Repeated echocardiographic examination allows for monitoring and reassessment of the valvular lesions during and after treatment. With experience and the correct software, ultrasound examination also allows for specific evaluation of cardiac function (e.g., atrial diameter, fractional shortening) that may more accurately assess the degree of cardiac dysfunction and provide valuable prognostic information.

Etiology

The most common cause of pericarditis in dairy cattle is puncture of the pericardium by a metallic linear foreign body that originated in the reticulum. It is apparent during laparotomy and rumenotomy in cattle that the heart lays very close to the diaphragmatic region of the reticulum. Therefore traumatic reticuloperitonitis occasionally causes septic pericarditis. Hardware that penetrates the reticulum in a cranial direction may puncture the pericardium or impale the myocardium. It can also infect the mediastinum or puncture a lung lobe. Both the foreign body and the tract of its migration can “wick” bacterial contaminants into the pericardial fluid, resulting in fibrinopurulent pericarditis.

Fibrinous pericarditis can also occur in septicemic calves or cattle having severe bacterial bronchopneumonia. This form of pericarditis rarely causes clinically detectable fluid accumulation and seldom leads to overt signs of heart failure as are typical in traumatic pericarditis. Idiopathic hemorrhagic pericardial effusion may also occur in adult cows, causing signs of right heart failure.

Signs

Signs of traumatic pericarditis include venous distention and pulsation, ventral edema, tachycardia, and muffled heart sounds bilaterally (Figure 3-14 ). Fever is usually, but not always, present. Tachypnea and dyspnea may be present in pericarditis patients with advanced heart failure. Cattle having traumatic pericarditis are often reluctant to move, appear painful, and have abducted elbows.

Direct pressure or percussion in the ventral chest or xiphoid area elicits a painful response by the cow with traumatic pericarditis. Dyspnea is caused by a combination of lung compression by the enlarged pericardial mass, pulmonary edema, and reduced cardiac output. Auscultation of the heart reveals bilateral decreased intensity of the heart sounds. This muffling of heart sounds usually coexists with squeaky, rubbing sounds and splashing or tinkling sounds, but these sounds are not present in all cases. A fluid gas interface created by gas forming bacterial organisms in the pericardium creates the most obvious splashing sounds. Lung sounds may not be heard in the ventral third of either hemithorax because of the greatly enlarged pericardial sac's displacement of the lungs dorsally. In addition to these signs, there are two very important clinical facts associated with traumatic pericarditis in dairy cattle:

• 1.

  Most cows with traumatic pericarditis were observed by the owner to be ill 7 to 14 days earlier and may or may not have been diagnosed with traumatic reticuloperitonitis at that time. Frequently the signs of illness were vague and nonspecific, and veterinary attention may or may not have been requested. Typically these cattle improve or appear recovered from this previous illness only to become ill once again and have signs of cardiac disease. Certainly not all cattle have this two-phased clinical course, and some have peracute pericarditis or traumatic myocarditis and die within hours or days. When the history supports a two-phased clinical disease, it is assumed the cow transiently “felt better” after the foreign body left the reticulodiaphragmatic area and entered the chest, thereby alleviating the peritoneal pain and inflammation. Subsequent, worsening sepsis in the pericardial sac and eventual heart failure causes the second phase of disease that generally moves the owner to seek veterinary consultation.

• 2.

  During the acute and subacute phases of traumatic pericarditis, heart sounds may change on a daily basis. Muffling, tinkling, splashing, rubs, murmurs, and other sounds all may be present on one day, absent the next, and present again later. Pathology is dynamic as the relative amounts of fibrin, purulent fluid, and gas in the pericardium change. Chronic cases, on the other hand, tend to have bilateral muffling of heart sounds and a “far away” tinkling as fluid pus is jostled by heartbeats.

Laboratory Data

If the disease is subacute or chronic, neutrophilia is usually present. Cattle afflicted for greater than 10 to 14 days usually have decreased serum albumin and increased serum globulin; therefore total protein values are at least high normal and usually elevated. Hyperfibrinogenemia is typically present at all stages of the disease. Thoracic radiographs, although largely unavailable in the field, often dramatically demonstrate a greatly enlarged pericardium, fluid line, and gas cap above the fluid line. The causative metallic foreign body also may be apparent unless obscured by radiopaque pericardial fluid, fibrin and the cardiac shadow. Cows with idiopathic pericardial effusion generally have normal fibrinogen and globulin cencentrations. Serum liver enzymes may be elevated with serum pericardial effusion regardless of the cause.

Diagnosis

Although the clinical signs of traumatic pericarditis usually are sufficient for diagnosis, definitive diagnosis in the field can be accomplished by two-dimensional echocardiography, pericardiocentesis, or both procedures. Thoracic radiographs, if available, also may be definitive.

Fluid and fibrin in the pericardial sac are easily visualized with two-dimensional echocardiography. Heavy accumulation of fibrin coats the epicardium and visceral pericardium (Figure 3-15 ). This fibrin frequently has the appearance of “scrambled eggs” when seen on postmortem examination (Figure 3-16 ).

Traumatic pericarditis patient's heart and pericardium at necropsy. Purulent fluid has been rinsed away, but the severity of fibrin deposition is apparent as the epicardial surface of the heart is completely covered. The pericardium is greatly thickened and coated with fibrin.

(Photo courtesy Dr. John M. King.)

Pericardiocentesis can be performed with an 18-gauge, 8.75-cm spinal needle or chest trochar of similar length. Following clipping and standard prep of the left thorax, a skin puncture is performed with a scalpel in the fifth intercostal space just dorsal to the elbow. If continuous drainage is desired, a 20-French chest trochar and catheter may be introduced into the pericardium to effect further drainage. The fluid obtained is purulent and fetid. Fibrin clots frequently obstruct flow of the fluid through finer gauge needles or catheters. The purulent fluid greatly exceeds normal values for pericardial fluid (normal 5 protein, 2.5 g/dl, white blood cell [WBC]#5000/ml), and neutrophils are the major cellular component rather than the mononuclear cells normally found in pericardial fluid. Bacteria are easily detected in the gram-stained smears of this fluid.

The major reason for pericardiocentesis is diagnostic differentiation of traumatic pericarditis from diseases that may create similar signs. Lymphosarcoma with pericardial involvement and fluid accumulation is the major differential diagnosis. Occasional cases of idiopathic, nonseptic pericarditis have been documented, in which the clinical signs are very similar to those documented with septic pericarditis, but the fluid tends to be a sterile hemorrhagic transudate with low to moderate numbers of macrophages, neutrophils, and lymphocytes (see video clip 2). Cytology of pericardial fluid would clearly differentiate between these diseases. The prognosis for cattle with the idiopathic hemorrhagic form appears to be better following drainage and antiinflammatory therapy than for pericarditis associated with sepsis or neoplasia. The presence of flocculent, mixed echogenicity fluid with gas shadowing within the pericardium on ultrasound is also characteristic for septic pericarditis.

Pericardiocentesis is not without risk. Potential complications include pneumothorax, fatal arrhythmia, cardiac puncture leading to hemorrhage or death, and leakage of pericardial material into the thorax, resulting in pleuritis. Some, but not all, of these complications can be mitigated by performing the procedure using ultrasound guidance. Leakage into the pleural space is possible because most pericarditis patients do not have attachment of the fibrous pericardium to the parietal pleura. Pericardiocentesis performed on one of the author's patients yielded only gas from the needle and was associated with immediate anxiety, dyspnea, and death within 5 minutes. Postmortem examination confirmed that neither hemorrhage nor cardiac injury had occurred. The gas pocket and fluid distending the pericardium had been under positive pressure and may have become somewhat constrictive or altered compensatory mechanisms when suddenly relieved.

Given the hopeless prognosis usually associated with pericarditis, pericardiocentesis is a worthwhile risk to confirm the diagnosis before salvaging a cow suspected to have the disease.

Treatment

Treatment of traumatic pericarditis in dairy cattle usually is hopeless. Medical therapy with systemic antibiotics and drainage of the pericardial sac rarely, if ever, permanently cures affected cattle. Therefore most therapeutic efforts have been surgical. Thoracotomy and pericardiectomy or pericardiotomy have been performed in many fashions in an effort to provide drainage, search for the foreign body, and prevent fluid or later constrictive damage to the heart. Sporadic case reports and third-hand stories attest to the occasional success of pericardiectomy and fifth rib resections, but success is not common. Authors recommending rib-splitting thoracotomy and pericardiectomy reported that five of nine clinical patients recovered. Results from our clinic, as reported by Ducharme and co-workers, are much more pessimistic with only one of seven surviving thoracic surgery. Pericardiocentesis followed by fluid drainage may result in clinical improvement with prolongation of life to reach a short-term goal like calving. Despite a poor prognosis, surgery remains the treatment of choice for valuable cattle.

To improve a patient's chances of survival, surgery should be performed as early in the course of the disease as possible. Cattle with severe ventral edema and obvious heart failure are not good candidates for surgery. Removal of the causative wire during the thoracotomy may be difficult but obviously is desirable. Usually the wire is mostly or completely in the thorax and would be difficult or impossible to remove through rumenotomy. However, we have observed patients with acute reticuloperitonitis and acute traumatic pericarditis from a single metallic foreign body that was still lodged in the reticulum and was removed through rumenotomy. These patients had clinically detectable pericardial effusions and radiographic evidence of foreign body penetration of the pericardium. Rumenotomy and intensive bactericidal systemic antibiotics are sometimes sufficient treatment of peracute or acute pericarditis in such cases. If pericarditis worsens despite systemic antibiotics and rumenotomy to retrieve the foreign body, thoracotomy may then be considered. Rumenotomy probably is most indicated in acute cases for which it is hoped that some portion of the metallic foreign object remains in the reticulum. Unfortunately it is difficult to know this without the benefit of radiographs, and although indicated in the field, an unsuccessful rumenotomy may further compromise the patient.

It is very disturbing that these “valuable cows” unfortunate enough to develop traumatic pericarditis were not administered a magnet prophylactically at some time in their lives by their owner. The routine administration of a magnet to heifers of breeding age and bulls before 2 years of age should be part of routine disease prophylaxis in dairy cattle.

Treatment of nonseptic pericarditis includes drainage of the pericardial fluid, systemic antimicrobial therapy, and administration of 5 mg of dexamethasone with or without 100,000 units of sodium penicillin into the pericardial space.

Etiology

Conditions of right heart dilatation, hypertrophy, and subsequent failure caused by pulmonary hypertension and increased pulmonary vascular resistance often is referred to collectively as cor pulmonale. This condition is uncommon and sporadic in dairy cattle. Most cases of cor pulmonale occur in cows known to have chronic pneumonia, bronchiectasis, and pulmonary abscesses secondary to bacterial bronchopneumonia, consolidated anteroventral lung lobes from previous pneumonia, or chronic lungworms. Severe chronic interstitial pulmonary disease, although rare, may also result in cor pulmonale in mature cattle with diffuse pulmonary fibrosis. In these instances, pulmonary hypertension initially may result from alveolar hypoxia and subsequent precapillary vasoconstriction. Chronic hypoxia and pulmonary hypertension in cattle may provoke hypertrophy of medial smooth musculature within pulmonary arteries and arterioles, causing further work for the right ventricle. We have treated one adult Holstein cow that had primary pulmonary hypertension.

The most common example of cor pulmonale is “brisket edema” or “mountain sickness” of beef cattle. This disease can occur in dairy cattle, and in fact Holsteins have been reported to be particularly sensitive. However, on a practical basis, to our knowledge, few dairy cattle in the United States are at risk because of a lack of exposure to high altitudes. Brisket disease may be seen at elevations of 1600 m (5249 ft) above sea level and tends to have increasing incidence at elevations above 1600 m. Definite genetic resistance or susceptibility is documented, and affected cattle must be returned to low altitudes early in the course of the disease to survive. Concurrent ingestion of certain plants such as Astragalus sp. and Oxytropis sp. (locoweed) is known to accentuate and accelerate brisket disease in animals at high elevations.

Pulmonary hypertension secondary to pulmonary and bronchial arteritis recently was observed as an endemic problem in a group of dairy calves. Periarteriolar sclerosis and vasculitis were identified pathologically and explained signs of right heart failure observed in the calves. Although unconfirmed, monocrotaline, a pyrrolizidine alkaloid, was suspected as the cause by the authors.

Signs

Dyspnea, tachycardia, ventral edema, and venous distention and pulsation characterize cor pulmonale. Therefore the signs are not unlike those found in other common heart diseases of cattle and require differentiation from cardiomyopathy, endocarditis, lymphosarcoma, pericarditis, and myocarditis.

Murmurs or a gallop rhythm may be ausculted, depending on valvular function, the degree of myocardial hypertrophy, or cardiac chamber dilation. Heart sounds have normal or increased intensity. Greatest attention should be directed toward the lungs to determine chronic abnormalities (e.g., consolidation) that may explain the right heart failure. Affected cattle appear more ill as the degree of dyspnea progresses.

Diagnosis

History of chronic pulmonary disease (or exposure to high altitude), ruling out other cardiac diseases, and finding signs consistent with right heart failure provide suggestive evidence of cor pulmonale. Two-dimensional echocardiography may add further evidence if right ventricular hypertrophy and dilatation is proven. Increased pulmonary arterial pressures, confirmed by cardiac catheterization, are diagnostic but limited to research facilities. Tracheal washes, thoracic ultrasound, or thoracic radiography may contribute to an understanding of the pulmonary problem in selected cases—especially cattle with chronic pneumonia, A. pyogenes pneumonia, abscesses, or diffuse pulmonary fibrosis. Measurement of arterial blood gas concentrations may confirm the presence of underlying hypoxemia.

Treatment

In cattle affected with primary chronic pulmonary disease, treatment of the primary lung disease coupled with furosemide therapy may be beneficial. Cattle known to have had pneumonia in the past and mild but persistent chronic respiratory signs thereafter may benefit from a tracheal wash to establish cytologic and cultural aids to antibiotic treatment of the chronic lung problem. Baermann's technique should be performed if chronic lungworm infestation is suspected. Cattle at high altitude suspected to have brisket disease should receive oxygen and be moved to lower altitudes.

Furosemide is administered at 0.5 to 1.0 mg/kg twice daily as a diuretic. Although digoxin may be considered in these cases, those cattle that require digoxin require hospitalization and incur extreme expense. Therefore use of digoxin seldom is practiced. If digoxin is required for a select case, the recommended dosage is 0.86 mg/kg/hr IV.

Etiology

Arrhythmias in adult cattle can be caused by a variety of drugs, myocardial insults, and metabolic abnormalities. In calves, myocarditis, hyperkalemia, hypoglycemia, and white muscle disease have been discussed previously as factors involved in the pathogenesis of arrhythmias.

Myocarditis may be the most difficult of the adult cow causes to diagnose definitively and therefore is suspected when other known causes are eliminated. Toxic myocardial damage from ionophores and plant toxins, as well as septic or inflammatory mediators (myocardial depressant factor, tumor necrosis factor), must be considered when arrhythmias appear in cattle without gastrointestinal, electrolyte, or other typical predisposing factors.

Calcium solutions are well recognized as being capable of causing cardiac arrhythmias or death when administered IV to cattle. Both hypocalcemia and hypercalcemia have been associated with arrhythmias, and arrhythmias associated with hypercalcemia are thought to be mediated by vagal stimulation. In fact arrhythmias associated with hypercalcemia may be abolished by atropine. However, atropine seldom is used for this purpose because of its negative effects on the gastrointestinal tract of cattle. Atrial fibrillation has been associated with hypocalcemia and also has been reported following treatment of cattle with neostigmine that may have provoked increased vagal tone. Hypocalcemia and hypokalemia in cattle with primary gastrointestinal diseases seem to be major risk factors to the development of atrial fibrillation and atrial premature contractions in adult dairy cattle.

Oxytetracycline in propylene glycol vehicles may cause decreased cardiac output and stroke volume, as well as decreased heart rates and aortic pressures. Systemic hypotension and cardiac asystole also has been observed when these drugs are given IV to awake, healthy calves. It is common knowledge among bovine practitioners that oxytetracycline, especially when prepared in propylene glycol vehicles, should be administered slowly and as a solution diluted with saline or dextrose to avoid hypotension, collapse, or death in both calves and adult cattle.

Atrial fibrillation is the most common arrhythmia occurring in adult dairy cattle (Figure 3-17, A and B ). A report suggests that atrial premature contractions in cattle with gastrointestinal disease may occur as commonly as atrial fibrillation. Atrial premature contractions often were associated with hypocalcemia and sometimes with hypokalemia in this study. Atrial premature contractions probably reflect vagotonia associated with abdominal distention or gastrointestinal diseases and are characterized using ECG by abnormal premature P waves (P’) from depolarization at an atrial site different from the sinus node. Atrial premature contractions usually result in a normal QRS-T on the ECG unless they enter the ventricle when it is partially refractory or if the AV node is refractory to excitement. In any event, it appears that atrial premature contractions may precede or predispose to atrial fibrillation. Sporadic irregularities rather than the irregularly irregular rhythm of atrial fibrillation are ausculted during atrial premature contractions in cattle.

A and B, ECG recording from two different cows showing characteristic changes of atrial fibrillation. Both A and B demonstrate an irregular rhythm with normal QRS complexes but no P waves. In A, the f (fibrillation) waves are coarse and the heart rate is more rapid than in B, which demonstrates relatively fine f waves along with a normal heart rate.

Atrial fibrillation may occur with or without underlying heart disease and fortunately usually is a secondary event unrelated to primary heart disease. There may be a normal or fast heart rate, depending on the severity of the underlying condition, but the rhythm is always irregular with variation in the intensity of heart sounds and pulse deficits when the heart rate is rapid. There is an absence of P waves and presence of f (fibrillation) waves demonstrated by ECG recordings (see Figure 3-17).

Signs

Signs of atrial premature contractions and atrial fibrillation are nonspecific unless underlying primary heart disease is present, whereon general signs of heart failure also may be observed. Close observation of the jugular vein may reveal occasional abnormal pulsations in cows with atrial premature contractions. Signs of heart failure, such as venous distention or ventral edema, usually are not present in cattle with atrial fibrillation, except in advanced cases that have progressed to congestive heart failure. Because most cows with either atrial premature contractions or atrial fibrillation have a primary gastrointestinal or other medical disorder, the signs vary in each case. Without question, cattle with abomasal displacement and other diseases characterized by abdominal distention are most frequently affected by atrial fibrillation. Specific signs of atrial premature contractions or atrial fibrillation are associated with cardiac auscultation. Sporadic arrhythmias and variations in the intensity of S1 typify atrial premature contractions. Although the heart rate varies, perhaps dependent on the primary disease, it often is within the normal range. Atrial fibrillation, on the other hand, leads to more obvious abnormalities in cardiac auscultation. Marked irregularities in rhythm, tachycardia, and dramatic variations in the intensity of heart sounds are obvious. Pulse deficits may be present in cattle with rapid heart rates, and an absence of the S4 has been reported. Although exercise intolerance is possible with atrial fibrillation, cattle seldom show this sign because they are not “raced.”

Atrial fibrillation also may occur as a result of primary heart disease (e.g., lymphosarcoma of the atrium and heart failure). This is a grave prognostic sign in such cases.

Diagnosis

Although cardiac auscultation is highly suggestive, ECG is necessary to make a definitive diagnosis of atrial premature contractions (Figure 3-18 ) or atrial fibrillation in cattle (see Figure 3-17). Key ECG findings in each condition are listed below and shown in the figures:

Atrial premature contractions = abnormal premature P waves (P’) = normal QRS-T unless occurring during refractory period of ventricle or AV node = sporadic

Atrial fibrillation = absence of P waves = F waves may be apparent = “irregularly irregular” rhythm = tachycardia (usually) = pulse deficit

Treatment

Treatment of atrial fibrillation in cattle seldom is necessary because resolution of the patient's primary medical or gastrointestinal problem generally results in return to normal sinus rhythm. Medical or surgical treatment of the primary problem coupled with correction of existing acid-base and electrolyte abnormalities is indicated for cattle whose problems include atrial fibrillation.

Routine administration of oral or subcutaneous calcium solutions as indicated and oral supplementation with 50 to 100 g of KCl orally, twice daily for 3 to 5 days are excellent empiric and supportive treatments for cattle with abomasal displacements or other causes of abdominal distention that also have atrial premature contractions or atrial fibrillation.

Occasionally atrial fibrillation persists several days to several weeks following resolution of the primary problem. Persistent atrial fibrillation raises concerns, lest the long-term condition lead to eventual heart failure. Heart failure has been suspected to result from prolonged (a course of years) atrial fibrillation in horses. Similar suspicions exist in cattle, but we know of no work that confirms this theory pathologically. In addition, cattle with atrial fibrillation that persists more than 1 month following resolution of a gastrointestinal or medical problem may in fact have myocardial disease causing atrial fibrillation or acquire heart disease because the noncontracting atria will develop progressive dilation that eventually results in tricuspid and mitral valve regurgitation, rather than one simply induced by electrolytes. It also is possible that some cows with persistent atrial fibrillation had it before the onset of their medical or gastrointestinal disease. Therefore discussions of appropriate criteria on which to base treatment are subjective. If medical or surgical therapy fails to resolve the primary illness in cattle also having atrial fibrillation, it is difficult to know how much the arrhythmia contributes to ongoing inappetence, depression, and decreased milk production.

If atrial fibrillation persists for 5 days beyond treatment or resolution of the primary problem, it is thought it should be treated with quinidine therapy. This may be premature in cattle that are clinically improved by resolution of their primary problem. Therapeutic intervention in cattle that are improving should be delayed at least 14 days because spontaneous resolution may occur during this time. Failure of cattle to resolve atrial fibrillation spontaneously may result from ongoing medical, gastrointestinal, acid-base, or electrolyte abnormalities. Treatment with quinidine or digoxin followed by quinidine may be expensive and requires careful clinical and ECG monitoring to avoid toxic side effects.

However, if atrial fibrillation persists beyond a reasonable time following resolution of a primary illness or is thought to be partially responsible for vague signs of illness in a patient or is thought to risk eventual heart failure, treatment may be considered. The following treatment protocols have been suggested:

• 1.

  Simple atrial fibrillation that has persisted despite resolution of primary disease:

  • Quinidine 48.0 mg/kg in 4 L of saline or lactated Ringer's solution administered at a rate of 1 L/hr IV. Balanced fluids may be given concurrently via the opposite jugular vein.

• 2.

  Atrial fibrillation that is complicated by extreme tachycardia or that has not responded to previous quinidine therapy:

  • Digoxin 0.86 mg/kg per hour or 11.0 mg/kg thrice daily IV for 4 to 5 days. Following this time, quinidine is administered as in (1) above.

  • Digoxin—loading dose 22.0 mg/kg once followed by 0.86 mg/kg/hr for 2 to 4 days. Following this time, quinidine is administered as in (1) above.

In all treatment protocols, side effects of quinidine such as diarrhea, rumen hypermotility, and tachycardia must be anticipated. Signs of quinidine toxicity may include arrhythmias other than atrial fibrillation, prolonged QRS complexes, or collapse. If signs of toxicity appear, the rate of infusions should be slowed or stopped. IV sodium bicarbonate also may be administered. Some cattle are reported to show blepharospasm and ataxia just before conversion to normal rhythm.

Cattle having atrial fibrillation that persists despite therapy or cattle with ongoing primary illnesses may have myocardial disease or vagotonia that interferes with conversion to normal rhythm. Prognosis remains guarded for these patients and for untreated atrial fibrillation patients that remain in atrial fibrillation for more than 30 days following apparent successful resolution of their primary gastrointestinal or medical disease.

Etiology

Traumatic venipuncture and perivascular reactions to irritating drugs from attempted IV therapy are the major causes of venous thrombosis and thrombophlebitis. Dextrose solutions and calcium solutions that contain dextrose are the greatest offenders because of the tissue reaction that develops around hypertonic dextrose solutions. Tetracycline, phenylbutazone (not to be used in dairy cattle over 20 months of age), and IV sodium iodide also are capable of causing a severe thrombophlebitis when inadvertent perivascular leaking occurs.

Traumatic or repeated venipuncture may result in simple thrombosis, thrombophlebitis, or septic thrombophlebitis. Poor restraint, improper preparation of the vein for venipuncture, inexperience in venipuncture, and inappropriate selection of needles for IV therapy increase the risk of injury to veins. The common use of disposable 14-gauge needles for jugular venipuncture in cattle has increased the incidence of venous injury because these needles are only 3.75 cm (1.5 in) long—too short to be placed properly for adult cattle. Furthermore, these same needles are extremely sharp and can lacerate the intima of the vein if the cow moves at all. Prolonged use of indwelling IV catheters risks both thrombophlebitis and septic thrombophlebitis. Septic thrombophlebitis of any cause creates a major risk of endocarditis or pericarditis in cattle.

Dehydrated cattle and endotoxic cattle are especially prone to thrombosis during attempts at venipuncture. The normally thick bovine skin becomes even more difficult to penetrate when the animal is severely dehydrated. This is especially true in neonatal calves that are severely dehydrated by diarrhea. Repeated venipuncture efforts in those patients may injure the vein and cause thrombosis. Endotoxic patients and septicemic patients that are predisposed to coagulopathies may develop venous thrombosis very easily. Platelet activation and other coagulation factors may contribute to venous thrombosis in such cattle, even when an experienced clinician performed venipuncture. In some endotoxic or septic patients, gelatinous or “Jell-O-like” clots appear at the site of venipuncture within seconds of entering the intima of the vein. Further attempts at venipuncture often result in extension of the thrombus along the length of the vessel.

Although the jugular is the most commonly damaged vein in dairy cattle, mammary and tail veins may suffer damage occasionally. It is contraindicated to perform venipuncture in the mammary vein except in dire emergencies or when both jugular veins have been thrombosed. Injury to the mammary vein not only damages the vein but also causes persistent udder edema of both the forequarters and hindquarters on that side and will negatively impact future production.

Although most thromboses, thrombophlebitis, and septic thrombophlebitis are iatrogenic because of the aforementioned conditions, occasional cases develop spontaneously. Neonatal calves always are at risk for umbilical vein omphalophlebitis and consequential septicemic spread of bacteria to distant sites. In adult cattle, the mammary vein is the most common vein to suffer spontaneous thrombosis, and this usually occurs during the dry period. Trauma by other cows butting the patient or simple pressure thrombosis caused by preparturient udder and ventral edema or excessive abdominal weight when lying on hard surfaces may contribute to this condition. Thrombosis and/or rupture of the perineal vein and caudal udder hematoma formation may occur in the region of the rear udder support and escutcheon (see the section on Udder Hematomas in Chapter 8).

Signs

Signs associated with simple thrombosis include palpable soft or firm clots within the vein. The vein may appear grossly distended by the thrombus or be of normal diameter. When the vein is held off below the thrombus, a fluid wave of blood cannot be ballotted within the vessel. Acute thrombi tend to be soft or “Jell-O-like,” whereas chronic or subacute thrombi may be firm to the touch. Edema may be apparent as a result of poor venous return in areas “downstream” from the thrombus. Therefore facial edema may appear with jugular thrombosis and ipsilateral udder edema with mammary vein thrombosis. Thrombosis may cause the patient mild pain, but it is not as painful as thrombophlebitis. “Needle tracks” or palpable swelling may be apparent in the skin overlying the site of thrombus formation.

Thrombophlebitis causes more obvious swelling in and around the affected vein. A perivascular component to the swelling and pain are more likely than with simple thrombosis (Figure 3-19 ). Palpable warmth to the swelling may be present, and subcutaneous edema usually appears downstream from the lesion. It may be difficult to differentiate a sterile thrombophlebitis from a septic thrombophlebitis. In general, fever and inappetence are more common with septic thrombophlebitis. Both may be painful and warm, and when the jugular vein is involved, the patient may be reluctant to raise or lower its neck or eat. Ipsilateral Horner's syndrome develops in some cattle with jugular thrombophlebitis. Thrombophlebitis of the mammary vein causes marked ventral abdominal pain over the site and severe ipsilateral udder and ventral edema (Figure 3-20 ). Because septic thrombophlebitis predisposes to bacterial endocarditis in cattle, careful auscultation of the heart is indicated in all cases (Figure 3-21 ). Tissue necrosis associated with extremely irritating drugs (e.g., 50% dextrose, 20% sodium iodide, and phenylbutazone) placed perivascularly or resulting in thrombophlebitis eventually will cause sloughing, cellulitis, or sterile abscess formation. Bacterial contamination of such lesions ensures abscess formation and eventual drainage.

Severe thrombophlebitis involving the tail vein may result in sloughing of the entire tail (Figure 3-22 ).

Diagnosis

Clinical signs usually suffice for diagnosis. Two-dimensional ultrasound may be used to confirm the diagnosis, assess the extent of thrombosis, and detect fluid or pus accumulations that may be drained in septic thrombophlebitis.

Treatment

Simple sterile thrombosis requires no treatment other than avoidance of further injury to the vein. In acute cases, cool compresses may be applied to the site overlying the thrombus, but this only minimizes hematoma formation. If simple thrombosis is complicated by perivascular injection that risks thrombophlebitis, subcutaneous tissues around the swelling should be injected with normal saline in an effort to dilute the drug deposited in the perivascular region. In addition, warm compresses should be applied to the area several times daily.

Sterile thrombophlebitis is best managed by warm compresses and oral aspirin therapy (240 to 480 grains orally, twice daily for adult cows). Sterile thrombophlebitis may or may not eventually slough or abscess. Cases caused by irritating drugs are more likely to slough or abscess. Signs of improvement include stabilization or reduction in the degree of swelling, improved appetite and production, and less pain.

Septic thrombophlebitis requires intensive therapy lest further complications such as endocarditis occur. Warm compresses several times daily, systemic bactericidal antibiotics, and oral aspirin therapy are indicated. Unless culture results from a draining abscess or catheter tip indicate otherwise, procaine penicillin 20,000 to 30,000 IU/kg IM or subcutaneously twice daily should be chosen because of its activity against A. pyogenes. When septic thrombophlebitis associated with IV catheters occurs, the catheter tip should be cultured following its removal from the vein. An effort should be made to avoid further IV therapy in all patients having thromboses or phlebitis because injury to one vessel may predispose to multiple thromboses. When IV therapy is essential for patient management, extensive care is essential for future placement of IV catheters or injections. Therapy for septic thrombophlebitis usually is long term (several weeks), and relapses are common if therapy is halted prematurely. Occasional cattle with septic thrombophlebitis may have intermittent fever, depression, and inappetence, as well as swelling and pain at the site of venous injury. Such chronic thrombophlebitis is not as common as in horses but may require similar surgical removal of the affected area of vein. Positive signs for cattle being treated for septic thrombophlebitis include normal temperature; increased appetite and production; reduced pain, swelling, and heat at the site; and decreasing amounts of drainage in those cases suffering sloughing or abscess drainage.

The prognosis for simple thrombosis is fair. If further injury to the vessel is avoided, some veins recannulate with time. The prognosis for thrombophlebitis is guarded, and most affected veins do not recannulate. In addition, subcutaneous edema of the tissue “downstream” to the vein injury is more common and requires a longer time to resolve.

Prevention

Good restraint, proper technique and equipment, and clinician experience are the best ways to avoid iatrogenic vein injuries. Careful preparation of the selected vein and cutdowns through the skin with small scalpel blades are very important aids when injecting or catheterizing a vein in a known high-risk patient such as a severely dehydrated or endotoxic cow (see Chapter 2).

Etiology

Mammary vein lacerations are the most common life-threatening venous laceration in dairy cattle. Sharp objects or barbed wire is the usual cause of injury, and blood loss can be profound unless the animal is attended to quickly.

Signs

Small lacerations or penetrations lead to blood loss and hematoma formation, whereas complete lacerations lead to massive blood loss and exsanguination. Other than the obvious venous bleeding from the site, clinical signs are those associated with blood loss anemia. Weakness, polypnea, tachycardia, anxiety, and pallor of mucous membranes indicate a life-threatening degree of blood loss. Heart rates greater than 120 beats/min and respiratory rates greater than 60 breaths/min usually are associated with severe blood loss. These parameters, coupled with extreme pallor of the mucous membranes and weakness, dictate a need for whole blood transfusions.

Diagnosis

The diagnosis is self-evident. Because blood loss is peracute, the packed-cell volume (PCV) should not be used as a decisive parameter when assessing the need for a whole blood transfusion. Peracute blood loss does not allow time for physiologic vasodilation, and a cow with peracute severe blood loss may die with a normal PCV. Some clinicians rely on the respiratory rate, heart rate, mucous membrane color, and degree of weakness to judge the severity of the blood loss.

Treatment

Initial treatment includes temporary hemostasis by hemostats, ligatures, clothespins, or nylon ties followed by a complete physical examination to determine the severity of blood loss. If transfusion of whole blood is indicated (heart rate .120 beats/min, respiratory rate .60 breaths/min, and extreme pallor of membranes), at least 4 L of fresh whole blood should be administered. Following transfusion, surgical correction of the laceration with fine sutures or ligation of the vein should be performed. If the physical status of the patient tolerates it, the cow should be placed in dorsal recumbency to allow the wound to be explored, extended, and assessed before repair or ligature placement.

Because phlebitis and septic thrombophlebitis are potential complications, systemic bactericidal antibiotics such as penicillin or ceftiofur at standard dosages should be given and continued for 5 to 7 days. A belly wrap applied with self-adherent tape is useful as a pressure wrap following surgery.

Caudal vena caval thrombosis secondary to rupture of abscesses near the hilus of the liver into the caudal vena cava is the most common clinical consequence of enteric origin liver abscesses in dairy cattle. Thrombi may form at the site of abscess rupture into the caudal vena cava or lodge between the heart and diaphragmatic region of the vessel. Thromboemboli traverse the right heart to lodge in the pulmonary arterial circulation leading to acute death, acute respiratory distress, or the more common caudal vena caval thrombosis syndrome with subsequent epistaxis, hemoptysis, anemia, and pneumonia. Endocarditis of the right heart valves is another common sequela. Further discussion of this syndrome is covered in Chapter 4.

Congenital portosystemic anastomoses have been identified in calves and usually result in poor growth and neurologic signs. They are further discussed in Chapter 12.

Rupture of major arteries is rare in cattle. Occasional uterine artery tears occur in parturient cattle and are of unknown etiology. Trauma to the artery is suspected and may result from the vessel being trapped in the pelvis as extensive traction is placed on the calf during dystocia. The uterine artery also may experience extreme traction in some severe uterine torsions. Occasional cows having uterine prolapse suffer rupture of the uterine artery and exsanguinate (Figure 3-23 ). Copper deficiency has been suggested but seldom is confirmed as a cause of arterial rupture because it causes degeneration of the elastica within arteries. Deficiency of the enzyme lysyl oxidase, which contains copper, may prevent normal cross-linking of collagen and elastin. Although the aorta seems most at risk for rupture in copper deficiency, Drs. Charles Guard and John M. King have investigated several herds in New York that have had multiple cows die acutely from arterial rupture of the mesenteric arteries or aorta. Histopathology of arteries from affected cattle suggests copper deficiency, but copper levels have appeared normal. Therefore copper deficiency, although suspected, has not yet been proven. Major arterial rupture usually is fatal.

One example of aneurysms in adult dairy cattle is presented by pulmonary artery aneurysms that develop proximal to septic thromboemboli in those with caudal vena caval thrombosis syndrome. These aneurysms later contribute to hemorrhage into the airways following dissection by septic thrombi that abscess.

We have observed several adult dairy cattle with persistent or intermittent colic that subsequently were shown to have mesenteric arterial aneurysms. Surgical removal of the aneurysms may be possible in some cases, but these cattle are likely to suffer arterial rupture and exsanguination eventually. If several cows are affected simultaneously, a toxin such as moldy clover or sweet vernal hay, which can prolong clotting times, should be suspected. For isolated cases the reason for the abdominal hemorrhage is generally unproven, although copper deficiency has been proposed as a causative factor.

Hypertrophy of the tunica media of pulmonary arteries and arterioles and subsequent pulmonary hypertension occurs as a response to prolonged hypoxia in “high altitude” disease or brisket edema of cattle. This situation leads to right heart failure and is further discussed under Cor Pulmonale earlier in this chapter.

Although of nonspecific etiology, vasculitis may occur in conjunction with many infectious, parasitic, and immune-mediated diseases. In dairy cattle, malignant catarrhal fever is a cause of classic generalized vasculitis. Bovine virus diarrhea, bluetongue, Salmonella sp., H. somni, and Erysipelothrix rhusiopathiae are other potential causes of vasculitis in cattle.

Erythron

Evaluation of the erythron with CBC, stained blood smears, PCV, hemoglobin, and other parameters is primarily useful to clinicians monitoring anemia in cattle. It should be emphasized that the PCV for healthy lactating dairy cattle is lower than in many other species (see Table 1-2). Anemia usually is suspected based on physical examination findings and may be confirmed, quantified, and differentiated as to type based on evaluation of the erythron and leukon. Although a single CBC often allows classification of anemia into a regenerative or nonregenerative category, serial CBC analyses are required to follow trends in the erythron. Blood loss anemia and hemolytic anemia are “regenerative anemias,” whereas anemias caused by chronic disease are termed “nonregenerative.” Regenerative simply implies bone marrow response to anemia through increased erythropoiesis. Regenerative anemias in cattle frequently result in overt microscopic evidence of increased erythropoiesis such as increased anisocytosis, polychromasia, reticulocytosis, and occasionally even nucleated red blood cells (RBCs). In addition, an increase in mean corpuscular volume (MCV) and decreased mean corpuscular hemoglobin concentration (MCHC) are typical in regenerative anemias.

Physiologic hemoconcentration occurs with dehydration in calves and adult cattle. Because anemia may be counterbalanced by hemoconcentration, interpretations of PCV in sick cattle must always be made with consideration of the hydration status. True polycythemia (persistent elevation of PCV despite normal hydration) is rare but may occur as a result of familial, geographic, and pathologic conditions. Peracute severe blood loss as might occur in mammary vein lacerations or some abomasal bleeding ulcers does not immediately lower the PCV because physiologic vasodilation requires at least 12 to 24 hours. Therefore the degree of acute, obvious blood loss in a patient can be assessed best clinically by evaluating heart rate, respiratory rate, and mucous membrane pallor.

• 1.

  Anisocytosis = variation in size of RBC. Normal to some degree in cattle 5 increases in regenerative anemias

• 2.

  Polychromasia = variable staining (toward blue) in Wright's type stains 5 indicates “young” RBC or reticulocytes still containing DNA

• 3.

  Basophilic stippling = blue granules, again indicative of DNA 5 also may be observed in chronic lead poisoning

• 4.

  Nucleated RBC = not unusual in cattle with severe but responsive anemia

• 5.

  Heinz bodies = precipitated hemoglobin deposits on the edge of RBC, observed in some hemolytic anemias. New methylene blue stain is helpful for detecting Heinz bodies and polychromasia in smears.

• 6.

  Poikilocytosis = uncommon in cattle RBC

• 7.

  MCV=PCV×10RBC count in million/μl

• increase = usually regenerative anemia

• false increase = blood not spun sufficiently for accurate PCV

• 8.

  Mean corpuscular hemoglobin

  (MCH)=Hb(g/dl)×10RBC count in millions/μl

• increase = increased number of reticulocytes

• 9.

• decrease = responding anemia with reticulocytosis 5 hemolysis

• false decrease = blood not spun down sufficiently

Relative polycythemia resulting from hemoconcentration is extremely common. Absolute polycythemia results from an absolute increase in PCV (usually $60%) that is repeatable, not associated with hemoconcentration, and does not lower in response to fluid therapy. Absolute polycythemia (absolute erythrocytosis) may be primary or secondary. Primary polycythemia also known as polycythemia vera is a rare myeloproliferative condition that usually causes excess production of WBCs and platelets, as well as RBCs. Plasma erythropoietin is decreased below normal levels in polycythemia vera.

Regardless of cause, progressive polycythemia eventually interferes with tissue oxygenation because of hyperviscosity and reduced cardiac output.

Secondary polycythemia is more common than primary polycythemia in cattle and implies a physiologic response to increased erythropoietin. Generally increased erythropoietin is a response to chronic tissue hypoxia. Therefore secondary polycythemia tends to occur in animals kept at high altitudes and in calves having congenital cardiac defects with right-to-left shunts. The chronic hypoxia associated with brisket disease or high altitude disease of cattle is capable of inducing polycythemia (see section on Cor Pulmonale). Tetralogy of Fallot and other severe congenital cardiac defects that create or progress to right-to-left shunting of blood also may cause secondary polycythemia.

Congenital polycythemia in Jersey cattle has been described as a recessive defect. These cattle are thought to have increased erythropoietin of unknown origin and have been grouped with secondary polycythemias.

Clinical signs associated with polycythemia are dyspnea, exercise intolerance, tachycardia, tachypnea, and very injected maroon or muddy-red membranes. Calves affected with polycythemia do not grow properly, regardless of whether the cause is cardiac or inherited. Funduscopic examination allows confirmation of hyperviscosity (Figure 3-24 ) in the retinal vessels. Retinal vessels are greatly increased in diameter, and the stars of Winslow (choriocapillaries on end) are very obvious. The hematocrit is consistently elevated over 55% and often greater than 60%.

Treatment is impractical in most polycythemia patients. This is especially true regarding congenital heart defects and inherited forms of the disease. Specific valuable cattle with high altitude hypoxia may benefit from phlebotomy and a return to lower altitudes. The practicality of the matter, however, dictates that extremely dyspneic cattle are most likely to benefit from phlebotomy, and these animals may die if restrained. If phlebotomy is accomplished, the PCV should be decreased below 50%, the animal moved to lower altitude, and symptomatic therapy given. Suspected hereditary polycythemia cases should be investigated genetically, and family members should be culled.

Blood Loss Anemia

In addition to sporadic trauma and surgical procedures that result in severe blood loss, a long list of differential diagnoses exists for blood loss anemia in cattle. However, several common causes deserve comment.

Bleeding abomasal ulcers may cause acute or subacute blood loss in adult cattle. Melena is associated with most abomasal ulcers causing significant blood loss (Figure 3-25 ). Bleeding abomasal ulcers that result in anemia are rare, despite the fact that abomasal ulceration and perforation are common. Abomasal bleeding also may occur in association with chronic abomasal displacement in cattle. This combination of abomasal problems is most common in dry cows, bulls, and heifers that are not observed as closely as lactating cattle. Thus the abomasal displacement may have existed for days to weeks before diagnosis. The displaced abomasum distention, coupled with large volumes of hydrochloric acid, contributes to mucosal injury and subsequent ulceration with bleeding.

Lymphosarcoma of the abomasum may cause abomasal ulceration, hemorrhage, and blood loss anemia. The clinical signs may be difficult to differentiate from bleeding abomasal ulcers unless other signs of lymphosarcoma are detected during the physical examination.

Acute splenic rupture caused by infiltration of the spleen by lymphosarcoma may cause severe acute or peracute hemoperitoneum with resultant signs of blood loss anemia.

Caudal vena caval thrombosis syndrome may cause blood loss anemia after abscesses resulting from septic thromboemboli lodged in pulmonary arterioles erode into airways or lung parenchyma. Subsequent hemorrhage results in hemoptysis and epistaxis. Melena or fecal occult blood may be detected if the affected cow swallows sufficient quantities of blood. Epistaxis and blood loss also may occur as a result of granulomatous rhinitis and skull trauma.

Parasites are another cause of blood loss anemia. Lice are the most common ectoparasite to cause anemia in both calves and adult cattle in the eastern United States. In other geographic areas, fleas (Ctenocephalides felis) and ticks also may cause significant blood loss. Thanks to modern heifer management systems and routine deworming, endoparasites are uncommon but may result in blood loss, especially in pastured heifers. Eimeria bovis may cause life-threatening anemia as a result of intestinal blood loss. Anaplasma marginale infection may cause fever, jaundice, and severe extravascular hemolysis.

Pyelonephritis in cattle may result in anemia by either blood loss (acute and uncommon) or by nonregenerative mechanisms (chronic and common). Cattle having blood loss associated with acute pyelonephritis also may have colic as a result of blood clots obstructing ureters or urethra (see Chapter 10) and usually have fever. Anemia of chronic infection or perhaps that associated with decreased erythropoietin caused by chronic pyelonephritis may be involved in the anemia observed in chronic pyelonephritis patients. Blood loss anemia, sometimes severe, also occurs in association with thrombocytopenia caused by type 2 bovine virus diarrhea virus (BVDV) infection. Affected animals often have obvious petechial and ecchymotic hemorrhages on oral, vulval, and conjunctival membranes (see section on Thrombocytopenia).

Acquired or congenital defects in hemostasis may cause blood loss by a variety of mechanisms. Once hemostatic dysfunction exists, simple bruising, insect bites, injections, and other minor trauma may cause significant blood loss.

Rupture of the uterine artery during parturition or following uterine prolapse and sporadic rupture of other major arteries are other causes of acute blood loss. Self-induced trauma or laceration of a prolapsed uterus with subsequent hemorrhage has been observed in dairy cattle. Manual removal of a corpus luteum through rectal palpation to induce heat has fortunately fallen out of favor with bovine practitioners. This procedure occasionally resulted in severe blood loss or exsanguination.

Winter dysentery rarely causes severe blood loss from the colon in first calf heifers. Affected heifers have fresh clots of whole blood and severe dysentery and may require whole blood transfusions.

Nonregenerative Anemia (Anemia of Chronic Disease)

Chronic infections and neoplasms are most often associated with inadequate erythrocyte production or nonregenerative anemia. Chronic pneumonia with abscessation, chronic pyelonephritis, multiple abscesses secondary to musculoskeletal problems, endocarditis, and visceral abscesses may cause nonregenerative anemia. Chronic bovine virus diarrhea may rarely cause nonregenerative anemia, although BVDV-associated anemia is more commonly associated with acute disease, thrombocytopenia, and blood loss.

Cattle with chronic bilateral pyelonephritis may have depressed erythropoietin resulting from renal impairment to help explain their nonregenerative anemia. Chronic protein-losing nephropathies such as amyloidosis and glomerulonephritis also may cause nonregenerative anemia.

Lymphosarcoma may result in anemia through several mechanisms: nonregenerative anemia simply because of diffuse neoplasia, nonregenerative anemia caused by myelophthisis in sporadic adult cattle or calves with the juvenile form of lymphosarcoma, and blood loss anemia resulting from neoplastic ulceration of the abomasum or splenic rupture.

Bone marrow depression by chronic bracken fern intoxication may result in nonregenerative anemia plus blood loss anemia secondary to thrombocytopenia and subsequent hemorrhage. In regions where enzootic hematuria occurs in cattle pastured in bracken fern, blood loss anemia commonly accompanies the bladder lesions.

Iron deficiency anemia may rarely cause severe weakness in milk-fed calves. This usually occurs when the PCV is less than 15%. The anemia is characterized as a microcytic and hypochromic anemia. Serum iron will be extremely low, and iron binding capacity will be normal or high. Treatment with blood transfusion is usually curative.

Anemia through Hemolysis

Hemolytic anemias are associated with either intravascular or extravascular erythrocyte destruction. Although extravascular erythrocyte destruction is more common in most species, cattle have several forms of hemolytic anemia caused by intravascular destruction of erythrocytes. A very common cause of intravascular hemolysis in calves is water intoxication. Calves watered intermittently that are then given plentiful supplies of water may overdrink to the point that severe vasodilation occurs and RBC lysis follows. Hemoglobinuria and history are diagnostic. Low-grade fever also may be present resulting from RBC destruction, and neurologic signs develop in extreme cases. Similarly IV administration of hypotonic solutions is an occasional complication observed when electrolytes are not added or are added in insufficient quantities to large fluid containers (20 L of sterile water) before administration. Fever, trembling, hair standing on end, and hemoglobinuria are the clinical signs in the patient that identify the therapeutic error.

Intravascular destruction of RBC occurs in babesiosis (piroplasmosis) in cattle. Fever, anemia, depression, icterus, hemoglobinuria, and other signs associated with anemia occur in this disease. Leptospirosis in calves results in fever, intravascular hemolysis of RBC, and hemoglobinuria. Bacillary hemoglobinuria caused by Clostridium novyi type D (Clostridium hemolyticum) is another infectious disease causing intravascular hemolysis in cattle.

Heinz body hemolytic anemia results from a variety of oxidizing agents that denature hemoglobin. Complexes of globin, a protein, are then observed microscopically as Heinz body inclusions in RBC. Although rare in dairy cattle, Heinz body anemia has been observed in selenium deficiency and in cattle grazing on rye grass (Secale cereale), onions, and Brassica sp. Hemoglobinuria generally is observed in those with these diseases.

Postparturient hemoglobinuria may develop when lactating dairy cattle are fed a ration deficient in phosphorus. Intravascular hemolysis and hemoglobinuria associated with hypophosphatemia tend to appear during the first month of lactation. A depletion of adenosine 5‘-triphosphate (ATP), secondary to phosphorus deficiency, may be involved in the RBC lysis in this condition.

Extravascular hemolysis occurs as a result of immune-mediated RBC destruction in anaplasmosis in cattle. Hemoglobinuria does not occur with this form of hemolysis. Autoimmune hemolytic anemia, as described in other species, is rare or has yet to be documented in cattle other than the RBC destruction that occurs with protozoan RBC parasites. Autoimmune RBC destruction has been suspected in some cattle with lymphosarcoma, but definitive documentation has not yet been provided. Neonatal isoerythrolysis does not occur naturally in cattle, but the disorder has been observed when cattle were vaccinated against anaplasmosis and babesiosis with products of cattle origin. Subsequent passive transfer of maternal antibodies against specific blood types to calves from these cattle results in some calves showing isoerythrolysis.

The anemia sometimes present in cattle having the inherited disease erythropoietic porphyria (“pink tooth”) (see also Chapter 7) is thought to be hemolytic in origin, although several other factors may be involved.

Determination of when an anemic patient requires whole blood transfusion must be made primarily based on the physical examination and secondarily based on PCV. In peracute blood loss, the PCV may be misleadingly high despite obvious pallor, tachycardia, polypnea, weakness, and other general signs that would indicate the need for a transfusion. When acute or subacute (24 to 72 hr) blood loss causes anemia, the usual PCV associated with the need for transfusion is in the range of 12% to 14%. Assuming normal hydration, a PCV greater than 14% seldom requires transfusion, and a PCV of less than 14% usually coincides with heart rates greater than 100 beats/min, respiratory rates of greater than 60 breaths/min, obvious mucous membrane pallor, and weakness. Heart rates that are greater than 120 beats/min and pounding, respiratory rates over 60 breaths/min, and obvious pallor all dictate a need for transfusion regardless of the PCV.

Chronic blood loss and nonregenerative anemias seldom require transfusions, and the slow, gradual development of anemia seems to allow physiologic compensation for the reduced numbers of RBCs. Cattle with chronic anemias may have PCV values of 9% to 10% without appearing in an anemic crisis.

Leukon

Cattle are unique in regard to the leukogram and its response to various diseases and stresses. Certain conditions, especially peracute inflammatory or endotoxic diseases, cause consistent changes in the leukogram, whereas other diseases, although infectious in origin, may be associated with normal or variable leukograms that shed little light on which disease the patient has. Despite having requested leukograms on thousands of bovine patients in an academic referral hospital, we find that the majority of these leukograms, regardless of the cause of illness, have been within normal limits. Despite this fact, the leukogram or, better yet, serial leukograms occasionally may aid greatly in the diagnosis and prognosis for a bovine patient.

WBC reference ranges used at the New York State College of Veterinary Medicine for adult cattle are listed in Chapter 1, page 14.

Stress and glucocorticoids reliably alter the leukogram to create neutrophilia, lymphopenia, and eosinopenia. The numbers of monocytes appear variable. Concurrent inflammatory diseases may alter this typical “stress leukogram.” For example, a cow with acute coliform mastitis that has been treated with dexamethasone may have a normal neutrophil count because of glucocorticoid-induced neutrophilia counterbalancing the expected neutropenia normally found in endotoxemia. This same cow could have a left shift with band (immature) neutrophils present and a lymphopenia in the absence of steroid administration. Cattle and their leukograms are exquisitely sensitive to exogenous corticosteroids. A single injection of 20 mg or more dexamethasone usually results in a stress leukogram characterized by neutrophilia, lymphopenia, and eosinopenia within 24 hours. Calves occasionally may have neutrophil counts of 20,000/ml or more following administration of dexamethasone. In addition to altering numbers of neutrophils, corticosteroids alter the function of neutrophils in a negative fashion. Whereas glucocorticoids are well known for their ability to be immunosuppressive, a single ketosis treatment dose of 0.02 mg/kg dexamethasone, however, is not associated with clinically significant immune function impairment. Neutrophil function may be impaired during the periparturient period and in cattle with retained fetal membranes.

A “degenerative left shift” wherein neutropenia coexists with the appearance of band neutrophils is typical of cattle with severe acute inflammation or endotoxemia. This helpful and, for the most part, consistent leukogram result is seen in dairy cattle affected with severe coliform mastitis, acute Mannheimia hemolytica pneumonia, severe Salmonellosis, severe postpartum gram-negative mastitis, and large perforating abomasal ulcers that cause diffuse peritonitis. Simplistic explanation of this phenomenon revolves around the fact that cattle have a limited bone marrow neutrophil pool to draw on in an acute emergency. Although the degenerative left shift remains a negative prognostic indicator and a positive indicator of severe infection or endotoxemia, it is so typical in cattle that it must be tempered by the patient's signs and response to treatment before using it as the sole basis of a prognosis. Cattle that have a degenerative left shift will often have a return to normal neutrophil numbers within 4 to 7 days following successful treatment of their acute infections. This time lapse may simply reflect the time necessary for resolution of a severe infection. If the infection requires more than 1 week for resolution, rebound neutrophilia usually will occur. Chronic infections may cause a neutrophilia, but many cattle with chronic infections such as visceral abscesses, musculoskeletal infections, chronic peritonitis, and other diseases frequently have normal neutrophil numbers despite having obvious infection. Neutrophilia seems more likely in resolving acute or subacute infections than in chronic infection. Certainly some cattle with chronic infections have neutrophilia, but the magnitude of the neutrophilia seldom is dramatic. It is rare to see an adult cow with more than 18,000 to 20,000 neutrophils unless exogenous corticosteroids have been administered to the animal.

Neutropenia also may be found during severe viral infections such as BVDV infection. Acute BVDV infection causes a leukopenia as a result of either a neutropenia, lymphopenia, or both. Because acute BVDV infection also adversely affects neutrophil function in addition to sometimes reducing absolute numbers, naive cattle acutely infected with BVDV have reduced ability to respond to concurrent or secondary infections until they form antibodies to resolve the BVDV infection. The immunosuppressive effect of acute BVDV infection and the potential for greater morbidity and mortality to be associated with concurrent infectious diseases such as Salmonellosis or Pasteurellosis should not be overlooked diagnostically during a herd outbreak of enteric or respiratory disease.

Absolute lymphopenia occurs in conjunction with stress, exogenous corticosteroid administration, some viral diseases such as BVDV, and some acute severe infections or endotoxemias. Frequently it is difficult to know whether the lymphopenia is associated directly with the disease or simply represents stress associated with a disease. Although eosinopenia should accompany lymphopenia when the cause is stress or corticosteroid administration, eosinophil counts have limited value in this regard. Absolute lymphocytosis that is transient is rare in dairy cattle and when present usually is associated with a neutrophilia in patients recovering from acute infection. Lymphocytosis that is persistent and repeatable usually indicates infection with BLV. Persistent lymphocytosis (PL) is a separately inherited condition that develops in association with BLV infection in certain lines of cattle. The Bendixen method of control of BLV was based on elimination of cattle with PL until a more modern understanding of the disease evolved. Cattle that are BLV positive and have PL may have a greater risk of developing lymphosarcoma than those cattle that are BLV positive without PL but this is controversial. In one study, PL was present in approximately one third of cattle infected with BLV. However, these percentages may vary in individual herds because genetic predispositions affect the trait of PL in response to BLV infection. The lymphocytosis in cattle with PL is generally refractory to stress or corticosteroid treatment. True lymphocytic leukemia does occur in a small percentage of cattle that develop lymphosarcoma following infection with BLV. Lymphocyte counts may range from 30,000 to 100,000 in such cases, and immature lymphocytes and lymphoblasts may be observed.

Eosinophils seldom are of diagnostic significance when interpreting the leukon of cattle. Geographic and management variations may alter the “normal numbers” expected as a result of parasite loads and other conditions. Eosinopenia concurrent with lymphopenia is consistent with stress or exogenous corticosteroid administration. Eosinophilia is rare in dairy cattle. Eosinophilia is thought to indicate heavy parasitism, histamine release, or some immune-mediated or allergic diseases. Unfortunately eosinophil numbers seldom convey useful clinical data. The same is true of basophils.

Monocytosis may be of some value in cattle because it generally is associated with chronicity. For example, a cow having chronic peritonitis may have a misleadingly normal neutrophil count with no left shift but also may have a monocytosis. Monocytosis, although not specific, should at least raise the clinician's index of suspicion for chronic infection. Although monocytosis is not a consistent finding in the peripheral blood of ruminants infected with Listeria monocytogenes, as in humans and rodents so infected, some cattle with listeriosis do have a classical monocytosis. (The name L. monocytogenes evolved from the tendency of monogastric animals to have a peripheral monocytosis in response to infection with the organism.)

Etiology

A fatal syndrome consisting of poor growth, chronic or recurrent infections, and persistent extreme neutrophilia has been observed in Holstein calves since the late 1970s. Affected calves had persistent neutrophil counts exceeding 30,000/ml, and some had counts exceeding 100,000/ml. Such calves were initially described subjectively as having a leukemoid blood response that required differentiation from myelogenous leukemia. Despite their neutrophilia, these calves seemed unable to mount normal defense against common pathogens and minor infections. Although the leukemoid calves sometimes survived for several months, most died before 1 year of age. True incidence of the disease was impossible to estimate because many “poor doing” calves eventually die in field situations without ever having a CBC or other diagnostics performed. A genetic immune-deficiency condition trait was suspected based on clinical observation of the condition in full siblings in a litter of embryo transfer offspring.

Reports from the United States and Japan on selected calves with the disorder suggested a granulocytopathy, and comparative studies of a canine granulocytopathy in Irish Setters and a leukocyte adhesion deficiency in humans brought about further suspicion of an inherited disorder in “leukemoid calves.” Subsequently this was confirmed and termed bovine leukocyte adhesion deficiency (BLAD) by Kehrli et al as a genetic disease in Holsteins that represents a severe deficiency of neutrophil Mac-1 (CD11b/CD18). Recessive homozygotes are affected, and heterozygote carriers have intermediate amounts of the Mac-1 b subunit (CD18). Despite more than adequate circulating neutrophils, affected calves cannot effectively fight infections because their neutrophils have deficient b2 integrin expression, preventing adherence to vascular endothelium and subsequent migration into tissue sites of inflammation.

Signs

Affected calves have chronic or persistent infections and poor growth (Figure 3-26 ). Signs may appear early in life, although some calves live for several months. Relative exposure to a variety of routine pathogens may dictate somewhat the apparent age of onset reported by client histories. Diarrhea and pneumonia are typical signs, but persistent ringworm lesions, persistent keratoconjunctivitis, gingival ulcers, loose teeth, tooth abscesses, poorly healing dehorning wounds, and other lesions also are common. Infections thought to be clinically minor respond poorly or not at all to appropriate therapy. Recurrence of signs and multiple problems are typical.

Diagnosis

Persistent leukocytosis caused by neutrophilia without remarkable left shift is a hallmark of the disease. To date most affected calves studied have had greater than 30,000 neutrophils/ml in their peripheral blood. Although myelogenous leukemia is a consideration, neutrophil function tests differentiate these diseases because neutrophils in myelogenous leukemic patients have decreased neutrophil alkaline phosphatase activity. In addition, the leukemoid blood picture is characterized as a regenerative left shift, whereas BLAD calves have primarily a mature neutrophilia. Furthermore ex vivo tests of adhesion-dependent responses such as chemotaxis and phagocytosis can differentiate between BLAD animals and those with severe, chronic neutrophilia without b2 integrin deficits. Affected calves must be differentiated from calves with chronic abscessation of the thorax or abdomen and calves persistently infected with BVDV that show similar poor growth and apparent reduced resistance to routine pathogens.

Failure to confirm persistent infection with BVDV and ruling out visceral abscessation via radiographs, ultrasonography, and serum globulin values support the diagnosis. Definitive diagnosis alongside identification of carriers can be achieved by restriction analysis of polymerase chain reaction (PCR)-amplified DNA from a suspect individual to allow discrimination between normal, carrier (heterozygote), and affected (homozygote) animals.

Currently artificial insemination (AI) sires are being tested and identified as either carriers or noncarriers of BLAD. The routine genetic screening and identification of carriers by AI companies worldwide will eventually lead to the eradication of the disease. It is rare or nonexistent now.

Treatment

Treatment is only palliative, and most affected calves die before 1 year of age. Exact age of onset, progression, and true incidence are unknown because most sick calves never have a CBC performed. Theoretically it is possible that many BLAD calves die early in life and that only those that survive to develop chronic disease associated with poor growth are suspected to have the disease. Because variable expression of the glycoprotein deficiency is possible in homozygote recessives and in heterozygotes, it also is possible that mild forms of disease and prolonged survival occur.

A factor XI deficiency has been described in Holstein cattle and appears to be a recessive trait. Homozygote recessives bleed excessively or repeatedly following injuries or routine surgical procedures such as castration or dehorning. Hematomas commonly occur at venipuncture sites and may lead to venous thrombosis. Routine coagulation profiles may not show in vitro clotting abnormalities in heterozygote carrier cattle, even though such animals have less factor XI than normal.

Thrombocytopenia

Etiology.

Thrombocytopenia is the most common cause of abnormal coagulation in dairy cattle. Cattle normally have between 100,000 and 800,000 platelets/ml of blood. Platelet survival time is thought to be 7 to 10 days, and megakaryocytes in the bone marrow are the precursors of circulating platelets. Thrombocytopenia may result from decreased platelet production, increased platelet destruction, sequestration, or consumption.

Decreased platelet production generally implies a bone marrow insult. Therefore hemorrhage caused by thrombocytopenia may be the first clinically detectable sign of true pancytopenia. This is the situation with chronic bracken fern toxicity in cattle. Thrombocytopenia and leukopenia tend to be profound long before affected animals become anemic because of the longer normal life span of erythrocytes compared with granulocytes and platelets. Similar thrombocytopenia caused by decreased thrombopoiesis has been reported in association with intoxications resulting from ingestion of trichloroethylene-extracted soybean meal, furazolidone (in calves), and suspected mycotoxins in Australian cattle.

Decreased survival of platelets is probably the most common reason for clinical thrombocytopenia. Infectious diseases cause decreased platelet survival via several mechanisms. For example, an immune-mediated thrombocytopenia has been reported in cattle with East Coast fever, and although not specifically immune-mediated, the thrombocytopenia that occurs in association with certain strains of type 2 BVDV results from decreased platelet survival following viral infection. Thrombocytopenia in adult cattle and veal calves suffering natural acute BVDV infection has been observed, and studies confirm a thrombocytopenia beginning 3 to 4 days following experimental infection with type 2 strains of the virus. Platelet numbers in these cattle then decrease progressively over the next 10 to 14 days (Figure 3-27 ). Animals that survive this acute BVDV infection show a return to normal platelet numbers in conjunction with an increase in serum antibody titers against BVDV.

Infectious diseases also may initiate disseminated intravascular coagulation (DIC) with subsequent consumption of platelets. DIC has been suggested as the cause of thrombocytopenia in acute sarcocystosis and observed clinically in a variety of septicemic and endotoxic states in cattle. Septic metritis and septic mastitis are the most common endotoxic diseases to cause thrombocytopenia in adult cattle (Figure 3-28 ). Thrombocytopenia in these cattle may either be caused by DIC or decreased survival for other reasons. In neonatal calves, thrombocytopenia is most commonly observed in association with neonatal calf septicemia.

Therefore infectious diseases may result in thrombocytopenia for a variety of reasons. However, those reasons usually affect platelet survival rather than production. Increased destruction, decreased life span resulting from platelet infection, consumption, vasculitis, and unknown factors contribute to thrombocytopenia in association with these infectious diseases. With the exception of BVDV infection and a few other diseases in which thrombocytopenia has been reproduced experimentally, most thrombocytopenia cases are sporadic and associated with a variety of disorders.

Trauma rarely has been associated with thrombocytopenia in cattle and may lower platelet numbers either by consumption or unknown mechanisms. We have confirmed occasional adult cattle with udder hematomas and cattle that are bleeding into a quarter as thrombocytopenic. It is not known whether the thrombocytopenia in these cattle represents cause or effect, but these patients showed no other evidence of systemic disease. Skull and orbital trauma apparently resulted in profound orbital hemorrhage secondary to thrombocytopenia in a calf (Figure 3-29, A and B ) we treated. The calf completely recovered following a whole blood transfusion and replacement of the proptosed globe.

Immune-mediated thrombocytopenia—or thought to be immune mediated—rarely is observed in ruminants. Perhaps “idiopathic” thrombocytopenia is a better term because clinicopathologic confirmation of true immune-mediated thrombocytopenia seldom is possible in ruminants. Although perhaps more common in goats, idiopathic thrombocytopenia has developed in rare calves having no evidence of infectious disease, trauma, bone marrow depression, and so forth. Morris states, “The diagnosis of idiopathic thrombocytopenia must be based on small vessel hemorrhagic diathesis and severe thrombocytopenia in a horse with normal coagulation times and no other evidence of DIC.” Although this statement refers to horses, obviously it also pertains to cattle because, in general, specific reagents to detect platelet-associated immunoglobulin (Ig) G, serum antiplatelet activity, and other confirmatory tests either have not been developed or are unavailable to most veterinarians.

Signs.

Petechial hemorrhages on mucous membranes coupled with other signs of hemorrhage that may occur from small vessels anywhere in the body typify thrombocytopenic bleeding. Ecchymotic hemorrhages may accompany the petechial hemorrhages on mucous membranes such as the conjunctival, nasal, oral, or vulvar mucosa. Bleeding may occur from the skin at sites of injections or insect bites. Venipuncture causes bleeding, hematoma formation, and possible venous thrombosis. Epistaxis is common in cattle with thrombocytopenia and other signs of bleeding frequently accompanying inflammation or injury to specific sites. For example, cattle with thrombocytopenia associated with acute BVDV infection frequently have fresh blood or clots of blood in their feces because of the irritation of diarrhea. Hyphema, scleral hemorrhages, and hematomas may occur secondary to minor trauma, especially in stanchioned cattle. Melena and hematuria also are possible signs.

Clinical bleeding seldom appears until platelet counts drop below 50,000/ml and usually occurs when platelets are less than 20,000/ml. Obviously stress, trauma, and hydration factors may affect the incidence of bleeding at platelet values less than 50,000/ml. Many cattle with confirmed platelet numbers of less than 20,000 show no evidence of or tendency for bleeding. If stressed, however, or subjected to multiple injections, venipuncture, bone marrow aspirates, rectal examinations, and so forth, these same cattle will begin to bleed.

Diagnosis.

Absolute diagnosis of bleeding resulting from thrombocytopenia depends on:

• 1.

  Platelet count (usually less than 50,000/ml)

• 2.

  Ruling out DIC and other coagulopathies

Although this may be difficult in field situations, confirmation of thrombocytopenic purpura necessitates a coagulation panel to confirm normal values for prothrombin time, activated partial thromboplastin time, thrombin time, fibrinogen, and fibrinogen degradation products (FDPs). Bleeding time and clot retraction are abnormal. In essence, DIC is the major differential diagnosis, and the aforementioned tests differentiate primary thrombocytopenia from thrombocytopenia secondary to DIC.

Once the diagnosis of thrombocytopenia is confirmed by laboratory studies, clues to the cause of this disorder should be sought. Septicemia, endotoxemia, and recent trauma may be clinically obvious, whereas ingested toxins or parenteral drugs may require careful historical data and evaluation of the patient's environment. When no predisposing factor or cause can be determined, “idiopathic” or immune-mediated thrombocytopenia is the diagnosis. Fortunately, this latter category is very rare in cattle.

Bone marrow aspirates or biopsy is indicated whenever the etiology of thrombocytopenia remains obscure, granulocytopenia coexists with thrombocytopenia, or thrombocytopenia has been chronic or recurrent.

Treatment.

Thrombocytopenia resulting in clinical bleeding requires therapy with a fresh whole blood transfusion and treatment of any primary condition. Ideally blood donors should be free of BLV and persistent BVDV infection. The volume of transfused blood will be somewhat dependent on the degree of patient blood loss that has occurred. The standard empiric quantities are a minimum of 1 L for a calf and 4 L for an adult cow, but greater volumes may be essential for severely anemic patients. Blood transfusions are “first aid” for thrombocytopenia, and the success of transfusion completely depends on whether platelet loss or lack of production will continue.

Specific and supportive therapy for primary causes such as endotoxemia, septicemia, trauma, and localized infections may allow a single whole blood transfusion to suffice for treatment of thrombocytopenia secondary to these disorders. Similarly calves or cattle with acute BVDV infection that are thrombocytopenic and bleeding usually require only one transfusion. These BVDV patients often have their lowest platelet counts approximately 14 days following infection. Therefore they are near recovery, and humoral antibodies are peaking at this same time. Whole blood transfusion and supportive care can save many of these patients.

Prognosis must be grave for patients having thrombocytopenia and granulocytopenia because pancytopenia should be suspected. Chronic bracken fern toxicity, furazolidone toxicity in calves, and other conditions that depress bone marrow are difficult to correct. Supportive therapy, whole blood tranfusions, and antibiotics to protect against opportunistic infections would be indicated in these patients. Bone marrow aspirates are essential to confirm the diagnosis.

If a primary cause cannot be found, and idiopathic thrombocytopenia is diagnosed, the clinical course is more difficult to predict. Idiosyncratic drug reactions should be ruled out by history, and drugs having the potential to cause thrombocytopenia should be discontinued. The patient must be monitored with daily platelet counts and physical examination to determine whether bleeding is continuing. Fecal occult blood, multistix evaluation of urine, and inspection of mucous membranes are important means of monitoring idiopathic thrombocytopenic patients. Further whole blood transfusions are not indicated unless signs of bleeding appear. Idiopathic thrombocytopenia patients that have persistent or recurrently low platelet counts of less than 25,000 and bleeding should have bone marrow aspirates evaluated. If the bone marrow is normal, low dose corticosteroids may be used in an effort to increase platelet numbers by increasing thrombocytopoiesis and counteracting a variety of immune mechanisms that may contribute to platelet destruction. Dexamethasone is preferable in our experience and may be therapeutic at doses as low as 0.05 mg/kg once daily. Most adult patients can be further reduced to 0.02 mg/kg once daily after 5 days. Most patients requiring corticosteroids for suspected immune-mediated thrombocytopenia can be weaned off medication within 30 days and do not tend to relapse.

Disseminated Intravascular Coagulation

Etiology.

DIC is a complex coagulopathy characterized both by bleeding and excessive intravascular thrombosis. This apparent contradiction leads to a dramatic—and usually fatal—clinical appearance. Cattle suffering septicemia, endotoxemia, exotoxemia from clostridial infections, and other severe localized infections are at greatest risk for DIC. Septic mastitis and septic metritis are probably the two most common infections to cause DIC in dairy cattle. Fortunately DIC is uncommon in cattle.

Clinical signs of bleeding and thrombosis represent overstimulation of coagulation within vessels that eventually depletes coagulation factors to such a degree that bleeding evolves as a major sign. Fibrinolysis is excessive, and localized or regional tissue hypoxia occurs as a result of thrombosis. Subsequent major organ dysfunction (liver, kidney, brain, gut) may ensue. Because a serious primary disease already exists in patients that develop DIC, patients are further predisposed to organ failure and shock.

Products of inflammation (platelet activating factors) or infectious agents (endotoxin, clostridium a toxin) that encourage procoagulant activity or damage vascular endothelium may activate DIC. However, the exact mechanism by which DIC occurs is unknown, and it is impossible to predict patients that will have DIC complicate their already potentially life-threatening primary disease.

Clinical Signs.

Rapid systemic deterioration in conjunction with vascular thrombosis and hemorrhage should cause suspicion of DIC in patients with serious primary inflammatory or gastrointestinal disease. Hemorrhages may be manifest as petechiae, ecchymoses, hematomas, or bleeding from body orifices. Melena or frank blood clots in the feces may appear—especially in cattle with enteritis. Microscopic or macroscopic hematuria may be present. Bleeding from injection sites and rapid venous thrombosis following venipuncture are typical signs. Epistaxis, hyphema, and visceral hematomas occasionally occur.

Major organ failure may be caused by reduced perfusion associated with thromboses. Lesser degrees of ischemia may cause renal (infarcts or tubular nephrosis), gastrointestinal (bleeding), neurologic (bleeding into central nervous system [CNS]), hemarthroses, or other signs.

As the patient's condition further deteriorates, venous thrombosis may frustrate attempts to improve the systemic state.

Diagnosis.

Coagulation profiles and platelet counts are essential tests to confirm clinical suspicions of DIC in a patient. In all instances, a patient already seriously ill from a primary disease becomes “sicker” and has signs of thrombosis and bleeding. Because both may be caused by similar predisposing causes, DIC must be differentiated from simple thrombocytopenia. Other causes of bleeding such as hepatic failure, warfarin toxicosis, and inherited coagulopathies can only be ruled out by laboratory tests.

Textbook confirmation of DIC requires:

• 1.

  Decreased platelets

• 2.

  Prolonged prothrombin time, activated partial thromboplastin time, and thrombin time

• 3.

  Elevated FDPs

• 4.

  Prolonged bleeding time

• 5.

  Decreased antithrombin III (if available)

Realistically it is unusual to have all of these parameters fit the results suggested above in a patient suspected of having DIC. For example, the prothrombin time and activated partial thromboplastin time may or may not be outside the normal reference range for the laboratory and if abnormal may be only slightly prolonged. In addition, FDP results in large animals with DIC usually fall in the intermediate (10 to 40 mg/ml FDP) or suspicious range rather than being obviously elevated. Decreased fibrinogen levels are not typical of DIC in cattle and if identified may suggest liver disease. Therefore clinical cases of DIC may only fulfill two or three parameters for diagnosis. Those patients fitting the textbook parameters usually are in an advanced state and have a grave prognosis. Most DIC patients have thrombocytopenia, intermediate FDP (10 to 40) results, and may have slight prolongation of prothrombin time or activated partial thromboplastin time.

Treatment.

Treatment of DIC is as poorly understood as the disease itself. Without question, intense treatment for the primary condition must continue. IV fluids are essential to counteract hypotension, tissue perfusion, and major organ failure. Nonsteroidal antiinflammatory drugs, especially flunixin meglumine (0.5 mg/kg body weight twice daily), may be helpful to patients having underlying gram-negative infections or enteric disorders. Severe thrombocytopenia or continued bleeding dictates replacement of clotting factors even though this may provide further substrate for ongoing coagulation. Therefore fresh whole plasma or, more likely in the field, fresh whole blood may be indicated.

Other therapy, such as heparin and corticosteroids, has been suggested, but there appears to be no scientific confirmation of their value in treating DIC, and in fact they may have deleterious effects in patients with DIC.

Prognosis for cattle with DIC is guarded to grave. Most patients with confirmed DIC die.

Coumarin Anticoagulants, Dicoumarol Toxicity, and Diffuse Hepatocellular Disease

Etiology.

Rodenticides such as warfarin and brodifacoum that are coumarin derivatives, coumarin-containing sweet clover (Melilotus spp.) forages that have become moldy or sweet vernal grass, and diffuse hepatocellular disease may cause hemorrhage resulting from lack of liver origin clotting factors. Coumarin competes with vitamin Kl, a precursor of clotting factors II, VII, IX, and X. Excessive fungal growth during improper curing of sweet clover forages causes coumarin to be converted to dicoumarol and results in similar decrease in liver production of the aforementioned clotting factors. Diffuse hepatocellular disease also may prevent normal synthesis of these factors, but this is rare and generally seen only in advanced hepatic failure.

Because factor VII has a shorter plasma half-life than II, IX, and X, a prolonged prothrombin time tends to be the earliest laboratory coagulation abnormality found in patients with coumarin or dicoumarol toxicity. Subsequent prolongation of activated partial thromboplastin time and activated clotting time occurs as the disease progresses. Obvious external blood loss, hematomas, or occult internal hemorrhages causing profound anemia may appear in affected cattle.

Accidental ingestion of rodenticides containing coumarin derivatives or ingestion of sweet clover forages that are moldy tend to cause sporadic or endemic coagulopathies, respectively.

Toxicity of a given amount of ingested coumarin may be enhanced by hypoproteinemia, drugs that are highly protein bound (thus freeing more coumarin from protein binding), reduced hepatic function, and insufficient vitamin K in the diet.

Clinical signs tend to occur within 1 week of the ingestion of the toxic agent.

Clinical Signs.

Ecchymotic hemorrhages, hemarthrosis, hematomas—especially over pressure points, epistaxis, melena, hematuria, and prolonged bleeding from injection sites or insect bites (Figure 3-30, A and B ) all are possible signs. Although not common, petechial hemorrhages may be observed in some patients. In addition, moderate to severe anemia may be apparent resulting from internal or external blood loss and is apparent based on mucous membrane pallor, elevated heart rate, and elevated respiratory rate. Hypoproteinemia also is present when blood loss has been severe. Other less common clinical signs simply reflect bleeding into unusual locations as a result of incidental trauma. For example, seizures or neurologic signs may result from skull trauma. Prolonged bleeding may become obvious following minor surgical procedures such as dehorning in subclinical cattle.

Diagnosis.

Clinical signs, history of exposure to sweet clover forages, or potential exposure to a coumarin-type rodenticide coupled with a prolonged prothrombin time and possibly prolonged activated partial thromboplastin time support the diagnosis when no other clotting abnormalities are identified. Platelet counts also should be normal. The absence of biochemical evidence of hepatic failure rules out liver diseases. Analysis of blood, liver, or feedstuffs for dicoumarol may be available at some diagnostic or toxicology laboratories.

Treatment.

All affected animals should receive vitamin Kl (1.0 mg/kg subcutaneously or IM). Treatment should be repeated twice daily and continue for at least 5 days. Affected animals that are severely anemic should receive 2 to 6 L of fresh whole blood in transfusions from healthy donor cattle (see also Chapter 2).

Vitamin K3 is not a substitute for Kl and in fact may be toxic. Most vitamin K3 products (menadione sodium bisulfite) have been taken off the market because of toxicity to domestic animals and humans.

Affected feed should be discarded and remaining feed inspected before allowing cattle access to it. Rodenticides should be managed carefully to avoid accidental ingestion.

Sudden death resulting from exsanguination may result in cattle from a variety of causes. When called to examine or necropsy a previously healthy animal that develops peracute anemia or dies from blood loss, the veterinarian should consider several diseases:

• 1.

  Obvious external blood:

  • Laceration of a major vessel such as occurs with mammary vein laceration

  • Caudal vena caval thrombosis with obvious bleeding from the mouth and nose

  • Bleeding from the abomasum with obvious melena

• 2.

  Occult or internal blood loss:

  • Manual removal of a corpus luteum during rectal palpation

  • Rupture of the spleen secondary to massive enlargement of the organ with lymphosarcoma

  • Rupture of a uterine or mesenteric vessel (consider both reproductive causes and copper deficiency)

  • Peracute abomasal hemorrhage without obvious melena

Arterial and venous thrombosis are generally associated with septic causes, e.g., vena caval and related pulmonary thrombosis; jugular and vena caval thrombosis associated with septic phlebitis; uterine, mammary, or intestinal thrombosis associated with infectious/inflammatory diseases of those organs; and septic splenic thrombosis. Endocarditis may result in thrombosis of renal or pulmonary arteries. Claviceps purpurea, fescue foot, or ergotism may cause thrombosis of limb, ear, and tail arteries. Aortic and iliac artery thrombosis may occur in young calves (,6 months of age), resulting in an acute onset of posterior paralysis. Treatment of most of the above is generally unsuccessful.

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