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Most commonly these calves have a ventricular septal defect and wry tail buy propranolol 40 mg cheap, as well as unilateral or bilateral mi- crophthalmia cheap propranolol 40mg without a prescription. Tail defects other than wry tail have been observed in some Guernsey and Holstein calves with microphthalmia and/or ventricular septal defect propranolol 80mg sale. In Guernseys purchase propranolol 40mg, these malformations are thought to be caused by a recessive trait, but in Holsteins, the exact mode of inheritance is unknown. Congenital megaglobus results from anterior cleav- age abnormalities or multiple congenital anomalies producing glaucoma in utero. The resulting absence of an anterior chamber causes congenital glaucoma and buphthalmos. Convergent strabismus with or without associated relative exophthalmos has been described as an inher- ited trait in Jersey and Shorthorn cattle. Bilateral relative exophthal- mos ( bug-eyed cows ) is a condition that has been observed in several dairy breeds and probably is a ge- netic trait. Exophthalmos in these cows does not pro- gress to a pathologic state or exposure keratitis because the eyelids still cover the cornea adequately. The calf also had Congenital nystagmus has been observed in several congenital absence of the tail and a ventricular septal breeds and is common in Holsteins. It persists throughout the animal s life and does not seem to interfere signicantly with vision. The temporal bulbar conjunctiva has become pigmented as a result of chronic exposure. Enucleation has been successful in these cases, and the relatively rare incidence rules against inheritance. Microphthalmic globes usually are not treated, but if no other anomalies exist, the owner may elect to raise a calf with unilateral microphthalmos. Chronic conjunctivitis occurs in some microphthalmic patients and, if persistent and severe, may dictate enucleation to stop chronic discharge and y irritation, thereby aiding patient comfort. Acquired Diseases Acquired megaglobus may follow severe intraocular in- ammation of exogenous or endogenous cause. Endophthalmitis and pan- ophthalmitis secondary to septic uveitis or ocular perfo- ration may also cause megaglobus. If megaglobus is se- vere enough to cause exposure keratitis, the affected globe should be enucleated to prevent eventual perfora- tion or panophthalmitis. Neurologic Diseases Unilateral facial nerve palsy causing ptosis and exposure keratitis is common in calves affected with otitis media/ interna and adults affected with listeriosis. Trauma may cause facial nerve injuries resulting in neuroparalytic keratitis in bovine patients of any age. The most com- mon cause of bilateral eyelid paralysis in cattle is stan- chion trauma wherein a cow pulls back against a stan- chion until her head is trapped along the temporal ridge between the ears and orbit. Signs of neuroparalytic keratitis include lacrimation, ptosis, absence of palpebral response, and progressive corneal exposure damage. Treatment requires therapy for primary diseases and protection of the cornea with frequent application of antibiotic ointments or tarsor- rhaphy. Cattle with facial nerve paralysis appear to be much less likely to develop corneal ulcers than in many other species. Treatment of stanchion paralysis requires warm compresses, systemic antiinammatories, and pro- tection of the cornea with ocular lubricants or broad- spectrum antibiotic ointment if indicated. Tetany of the retractor oculi muscles pulls the improvement in appetite and production as a result of resolution of pain and irritation caused by the enlarged globe caudally in the orbit, allowing passive prolapse of globe. Inammatory Diseases Less frequently, megaglobus follows intraocular neo- plasia or granulomatous infections of the uveal tract. The eyelids can perforations, chronic uveal inammation, and severe be severely swollen as a result of hemorrhage or inam- pinkeye complications such as corneal perforation and mation because cattle have abundant eyelid skin with a iris prolapse. However, if chronic conjunctivitis, surgeon a great deal of tissue to work with if surgical or facial dermatitis from discharges, and y irritation affect plastic repair is necessary. Cellulitis of the eyelids and secondary orbital cellulitis are possi- ble in neglected or dirty wounds. Less common causes of lid inammation include Congenital Diseases actinobacillosis granulomas appearing at the site of pre- Ancillary or supernumerary nasolacrimal duct open- vious eyelid injury and demodectic mite infestation. Lacerations of the eyelid may be closed using a two-layer technique with absorbable sutures (2-0) in the lid stroma and nonab- sorbable sutures (2-0 or 3-0) in the skin. Atypical large bropapilloma growing from the upper Actinobacillosis granulomas should be debulked, eyelid of a Holstein heifer. This tu- mor requires aggressive early therapy to prevent pro- gression, or the cow will be lost. In tion of early tumor formation when the mass is less most instances, the tumors are raised, rm masses with than 2. These large tumors also are are mostly white or have nonpigmented lid margins or more likely to invade adjacent adnexal tissue, orbital nictitans are at risk.

Septic thromboemboli originating from an ab- In caudal vena caval thrombosis cheap propranolol 80 mg fast delivery, erosion of a liver ab- scess at the hilus of the liver shower the caudal vena scess into the vena cava with formation of a septic venous cava generic 80 mg propranolol free shipping, right heart cheap 40 mg propranolol with mastercard, and pulmonary arterial circulation proven 80 mg propranolol. Those cattle that have inap- may result in massive thromboemboli to the right heart parent seeding of the pulmonary arteries or survive an and pulmonary artery thrombosis, pulmonary infarc- acute respiratory distress episode caused by thrombo- tion, exotoxemia or endotoxemia, and anoxia. Sudden emboli may eventually develop dyspnea, hemoptysis, death may result, and this syndrome represents one of and anemia. Epistaxis is the most common clinical sign the more common causes of acute death in adult dairy observed in those cows with hemoptysis. This sudden death may represent a hypersensitiv- The pathogenesis of caudal vena caval thrombosis ity reaction following a previous clinically inapparent starts in the forestomach or abomasum and involves thromboembolic episode; however, sudden rupture of a inammatory or ulcerative mucosal lesions that allow large hilar abscess into the caudal vena cava or embolic bacterial seeding of the portal circulation with subse- movement of an existing large septic thrombus may quent formation of liver abscesses. Therefore rumenitis, cause enough direct pulmonary infarction to cause ruminal acidosis, abomasal ulcers, and similar disorders death without the need for a previous sensitizing epi- predispose to the condition. The location is much more important than the Acute Respiratory Distress Syndrome number of abscesses, however, because only those at the This syndrome appears in one animal within a group or hilus of the liver or adjacent to the post cava represent herd. Auscultation of the thorax generally reveals reduced airway sounds resulting from pulmonary edema, pulmonary infarction, and bullous emphysema brought on by exertional respiratory efforts. Rales may be ausculted in some instances, but in general, the lungs are quieter than expected given the obviously labored respirations. The key to diagnosis is the fact that only one animal is affected with severe lower airway disease, and to the owner s knowledge, this cow has had no unique stress or previous problems. Septic thromboemboli create pulmonary abscesses at their endpoint in pulmonary arteries, and aneurysms develop proximal to each of the suddenness of death precludes physical examina- these abscesses within the affected pulmonary arteries. Sudden dis- pulmonary edema, pulmonary infarction, and pulmo- charge of purulent material into the airway creates sep- nary arterial thrombosis. This hemor- Distress Syndrome rhage may be sufcient to result in hemoptysis and Sudden onset of respiratory distress in a single cow subsequent epistaxis. Affected cattle are unthrifty and within a herd raises an index of suspicion of acute frequently have been treated for recurrent broncho- caudal vena caval thrombosis. Some affected cattle develop endocarditis caused by the septic thrombus in the caudal vena cava remain- ing as a source of chronic bacteremia through the right heart and pulmonary arteries. Epistaxis associated with coughing and chronic bronchopneumonia in dairy cattle indicates an extremely guarded prognosis because of the irreversible nature of the pathology in caudal vena caval thrombosis. Other signs such as ascites, generalized visceral edema, and diarrhea are possible if the thrombosis occludes the caudal vena cava and results in portal hypertension. Right heart failure and a chronic passive congestion of the liver may also develop in some chronic cases. The site of The diagnosis of caudal vena caval thrombosis requires rupture into the post cava is apparent as a rough-edged careful necropsy when sudden death results. The affected animals have appeared completely healthy be- purulent remnants of the abscess appear to the left of fore death. In eld situations, the affected cow is treated symptom- atically and gradually may improve over 5 to 10 days. The average lag phase between improvement from the acute syndrome and the onset of epistaxis is 3 to 6 weeks. Diagnosis of Classical Caudal Vena Caval Thrombosis with Epistaxis, Hemoptysis, Anemia, and Chronic Bronchopneumonia This form remains the most common clinical syndrome of caudal vena caval thrombosis. If edema is generalized, diarrhea caused by gastro- thrombus may be lodged in the caudal vena cava and intestinal edema is observed. Thoracic radiographs spaces can also be useful to identify liver abscesses and or ultrasonography are helpful in identifying distinct allows visualization of the hilus and abdominal caudal vena cava close to the hilus. Endoscopy will help conrm the origin of hemorrhage in the lower airway and will allow collection of tracheal wash material for cytology and culture. Treatment Therapy for caudal vena caval thrombosis causing acute respiratory distress is symptomatic and includes: Broad-spectrum antibiotics such as oxytetracycline, cephalosporins, or penicillin to control septic thromboemboli. White maintained on long-term penicillin in the hope that the muscle disease caused by selenium/vitamin E deciency septic thromboemboli may be sterilized. Rifampin may may affect the tongue, muscles of mastication, or mus- be added to improve antibiotic penetration, but this cles involved in swallowing and predispose to inhala- represents extra-label drug use and is expensive. Progno- tion of milk or milk replacer as the affected calf tries to sis is poor because a large thrombus tends to persist in drink. Iatrogenic inhalation pneumonia in calves fol- the caudal vena cava, and constant or intermittent em- lows inadvertent intubation of the trachea with stomach bolic showers are likely to continue. Few cattle have tubes or esophageal feeders or, more commonly, from survived long term. Nipple bottles used to feed calves should only drip sic signs of pneumonia, epistaxis, hemoptysis, and ane- milk when the bottle is turned upside down. Prematu- mia seldom is worthwhile because of the extensive pa- rity or dysmaturity may also predispose to inhalation thology that exists. Inhalation pneumonia also may aspirin (240 to 480 grains/450 kg body weight orally, follow pharyngeal trauma by stomach tubes, esophageal twice daily). Crude or neophytic use of long-term use in an effort to discourage further platelet stomach tubes, feeders, and balling guns by laypeople aggregation and thrombosis.

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Arrhythmias are less common in frequency than structural heart disease as a cardiac cause of syncope buy propranolol 80mg visa. In general the common etiological pathway of cardiac origin of syncope is diminished cardiac output and subsequent decreased cerebral perfusion propranolol 40mg with visa. The classic features are syncope occurring on exertion or in the recumbent position cheap 40mg propranolol with visa. The Romano Ward syndrome is inherited in an autosomal dominant fashion whereas Jervell and Lange Nielsen syndrome is inher- ited in an autosomal recessive fashion and is associated with sensorineural deafness purchase 40mg propranolol with amex. Syncope occurs in approximately two-thirds of gene carriers, with sudden death in ~15% of untreated cases. Clinical presentation includes syncope, seizures, palpitations, and unfortunately sudden death. The delayed recov- ery predisposes to the development of early after-depolarizations and subsequent torsades de pointes arrhythmias. T wave morphology is important in making the diagnosis and is characteristic for each genotype (Fig. Acute treatment include intravenous magnesium and potassium administration, and temporary cardiac pacing. Removal of any aggravating fac- tors, correction of electrolyte imbalance, and intravenous isoproterenol adminis- tration are also additional forms of therapy. In both children and adults the risk for sudden death is highest in sleep or at rest. Wolff Parkinson White Syndrome It is the most common form of pre-excitation in children. It occurs as a result of an accessory pathway between the atrium and the ventricles the bundle of Kent. Other Arrhythmias There are other less common types of arrhythmias which may lead to syncope and sudden cardiac death. Catecholaminergic polymorphic ven- tricular tachycardia is an infrequent cause of syncope in children and adolescent. Arrhythmogenic right ventricular dysplasia is a genetic condition marked by ventricular arrhythmias and right ventricular abnor- malities. T wave inversion over the right precordial leads is seen when patients are in sinus rhythm. It results in left ventricular hypertrophy, involving the interventricular septum. Hypertrophy may be present in infants, but typically develops during childhood and adolescence. The underlying pathophysiology is decreased cardiac output secondary to left ventricular outflow tract obstruction and arrhythmias. Medical therapy with beta-adrenoceptor antagonists (beta-blockers), or verapamil is the first treat- ment option in all symptomatic patients. The absence of non sustained ventricular tachycardia during Holter monitoring has a high nega- tive predictive value in adults but this has not been proven in children or adoles- cents. Patients should be restricted from vigorous exercise since most cases of sudden death occurs shortly after exertion. Aortic Stenosis Aortic Valvar Stenosis is due to decreased valvar size resulting from thickening of the valve leaflets. If severe enough it will result in obstruction of left ventricular outflow and decreased cardiac output. The pathophysiology of aortic stenosis results in obstruction of left ventricular outflow and compensatory increase ventricular wall size. The subendocardium and the papillary muscles are hence most susceptible to ischemia. At rest the compensa- tory coronary artery vasodilation is near maximal, hence with exertion there is very little coronary reserve. Exercise creates an inbalance in oxygen supply and demand which results in ischemia and infarction. The clinical features of severe aortic valve stenosis are easy fatiguability, syn- cope with exertion and sometimes angina type symptoms. On examination there is a an ejection systolic murmur heard best at the aortic region (upper right sternal edge). The management of severe aortic valve stenosis includes exercise restriction and subsequent balloon valvuloplasty. Aortic valve replacement is required in patients who develop recurrent stenosis after valvuloplasty or who have significant regurgi- tation after valvuloplasty. Coronary Artery Anomalies Congenital anomalies of the coronary artery may result in syncope and sudden cardiac death in the adolescents. The origin of the left coronary artery from the right main coronary artery is the most common coronary anomaly. When the anomalous branch passes between the aorta and the right ventricular infundibulum the associa- tion with sudden death is increased. Bell-Cheddar and Ra-id Abdulla Patients present with recurrent syncopal attacks or chest pain with exercise or exertion.

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Ketones with abomasal displacements will have primary ketosis propranolol 80 mg with visa, may be detected in the breath order propranolol 80mg free shipping, urine order propranolol 80mg amex, or milk buy propranolol 40mg lowest price. Some sensi- which is not surprising because there is a proven associa- tive individuals can easily recognize this odor. Cows Many cows with primary ketosis give a strong purple color with chronic ketosis/fat mobilization and hepatic lipi- on the urine test, although the urine of individuals with dosis lose considerable amounts of weight, have a poor hepatic lipidosis may only cause a lighter purple color- appetite, but continue to produce moderate amounts of ation. The diagno- Urine ketostrip with urine-positive reaction to acetoac- sis is based mostly on history, clinical examination, and etate from a cow with primary ketosis. Affected cows may appear weak, which could be caused by hypoglycemia, muscle weakness from fatty accumu- lation in muscle, and/or hypokalemia. Some cows may die, be sold, or have complications caused by frequent treatment (e. Serum cholesterol generally returns toward normal value as the cow begins to eat better. Their pre- Treatment for ketosis is aimed at restoring energy me- disposition to sepsis with mild to moderate metritis may tabolism to normal for milk production. These treatments may be com- usually occurs with multiple fetuses and is triggered by bined to suit the needs of the case and the abilities of some other illness or external event that restricts access the herdsman. Cows do not become blind as do sheep allow time for the cow to maintain normoglycemia. Niacin (12 g orally daily) will also inhibit lipoly- sis and is frequently administered daily to cows with chronic ketosis. The most important treatment of cows with chronic fat mobilization and hepatic lipidosis is twice-daily forced feeding. If these treat- ments do not appear to be effective after 3 to 5 days, then it may be necessary to reduce the cows milk pro- duction by milking for 1 minute twice daily until the negative energy balance cycle is broken. There was no obvious smell from the rear required for 4 to 7 days before the ketosis is permanently of the cow, and the metritis did not appear to be severe resolved. We have performed this on many cows with enough to make most cows systemically ill. The severe chronic fat mobilization, and it, along with previously hepatic lipidosis most likely predisposed the cow to the mentioned treatments, has been successful in all but one fatal toxemia from a relatively moderate metritis. Additionally, owners have reported the milk pro- duction for the remainder of the lactation was very good. Although cows with chronic fat mobilization have de- help in restoring the cow s appetite. Cows with nervous layed time of estrus and their production is diminished ketosis can be treated with chloral hydrate (40 g orally during the rst 6 weeks of lactation, their prognosis for daily), which serves as both a sedative and as a substrate complete recovery is excellent. The most frequent complication associated with intervention to prevent irreversible hepatic lipidosis and treatment of these cows is thrombophlebitis caused by multiorgan failure. Intensive support Treatment of periparturient overweight cows with ke- of the cow with dextrose and force feeding is necessary. Cows with chronic as described above and have only limited milk removed fat mobilization and ketosis/hepatic lipidosis are often (if there is mastitis in a quarter, it should be stripped and the best cow in the herd and produce a high milk vol- intramammary antibiotics administered). These cows do not get better overnight with any apy can be used as described previously for cows with treatment and in fact may have already been treated with chronic fat mobilization. Reduced neutrophil and he- the above listed traditional therapy for ketosis for 1 to patic macrophage function in these cows may allow 3 weeks before veterinary attention is sought. Treatment septic conditions such as even mild metritis or mastitis should include continual 5% glucose administration in to overwhelm the patient. Although lipotropic medica- declines by up to 20% in late gestation to the day before tions such as choline and methionine are used by some calving. If lipotropic companied by an increasing rate of lipid mobilization medications are used, rumen-protected choline is pre- from body fat stores. Most herd owners random cows can be used to determine whether energy would agree that 20% of fresh cows with ketosis repre- balance in the late dry period may be responsible for a sent a herd problem. Prob- component testing has also been used to monitor en- ably all cows with clinical ketosis have greater than ergy consumption in lactating cows. Attempts to ommended practices of nutrition and feed bunk manage- decrease milk fat production in early lactation could ment. In many herds with a high incidence of ketosis, the have benecial effects in preventing ketosis as long as problems originate with nutritional mistakes during the milk production were not further increased. Obesity or other diseases that restrict feed intake are a simultaneous increase in hormone-sensitive lipase both potential causes. The process is initiated by prolactin and pre- rumen stula of the difference between intake at 3 weeks cedes the onset of lactation. Insulin secretion declines prepartum and voluntary intake until calving reduced in preparation for lactation. The mammary gland of the the increase in liver triglyceride accumulation from 23% dairy cow does not require insulin for glucose uptake, to 16%.

By V. Cruz. Institute of Computer Technology.