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 post parturant paresis(hypocalcemia)

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post parturant paresis(hypocalcemia) Empty
مُساهمةموضوع: post parturant paresis(hypocalcemia)   post parturant paresis(hypocalcemia) Icon_minitimeالإثنين 13 ديسمبر 2010 - 19:11

Parturient paresis is an acute to peracute, afebrile, flaccid paralysis of mature dairy cows that occurs most commonly at or soon after parturition. It is manifest by changes in mentation, generalized paresis, and circulatory collapse.
etiology
At or near the time of parturition, the onset of lactation results in the sudden loss of calcium into milk. Serum calcium levels decline from a normal of 10-12 mg/dL to 2-7 mg/dL. Commonly, serum magnesium is increased, serum phosphorus is decreased, and cows are hyperglycemic. The disease may be seen in cows of any age but is most common in high-producing dairy cows >5 yr old. Incidence is higher in the Jersey breed.
clinical finding &diagnosis
Parturient paresis usually occurs within 72 hr of parturition. The disease can contribute to dystocia, uterine prolapse, retained fetal membranes, metritis, abomasal displacement, and mastitis.
There are 3 discernible stages of parturient paresis. During stage 1, animals are ambulatory but show signs of hypersensitivity and excitability. Cows may be mildly ataxic, have fine tremors over the flanks and triceps, and display ear twitching and head bobbing. Cows may appear restless, shuffling their rear feet and bellowing. If calcium therapy is not instituted, cows will likely progress to the second, more severe stage.
Cows in stage 2 are unable to stand but can maintain sternal recumbency. Cows are obtunded, anorectic, and have a dry muzzle, subnormal body temperature, and cold extremities. Auscultation reveals tachycardia and decreased intensity of heart sounds. Peripheral pulses are weak. Smooth muscle paralysis leads to GI stasis, which can be manifest as bloat, failure to defecate, and loss of anal sphincter tone. An inability to urinate may be manifest as a distended bladder on rectal examination. Cows often tuck their heads into their flanks, or if the head is extended, an S-shaped curve to the neck may be noted.
In stage 3, cows lose consciousness progressively to the point of coma. They are unable to maintain sternal recumbency, have compete muscle flaccidity, are unresponsive to stimuli, and can suffer severe bloat. As cardiac output worsens, heart rate can approach 120 bpm, and peripheral pulses may be undetectable. If untreated, cows in stage 3 may survive only a few hours.
Differential diagnoses include toxic mastitis, toxic metritis, other systemic toxic conditions, traumatic injury (eg, stifle injury, coxofemoral luxation, fractured pelvis, spinal compression), calving paralysis syndrome (damage to the L6 lumbar roots of sciatic and obturator nerves), or compartment syndrome. Some of these diseases, in addition to aspiration pneumonia, may also occur concurrently with parturient paresis or as complications
treatment
Treatment is directed toward restoring normal serum calcium levels as soon as possible to avoid muscular and nervous damage and recumbency. Recommended treatment is IV injection of a calcium gluconate salt, although SC and IP routes are also used. A general rule for dosing is 1 g calcium/45 kg (100 lb) body wt. Most solutions are available in single-dose, 500 mL bottles that contain 8-11 g calcium. In large, heavily lactating cows, a second bottle given SC may be helpful because it is thought to provide a prolonged release of calcium into the circulation. SC calcium treatment alone may not be adequately absorbed due to poor peripheral perfusion and should not be the sole route of therapy. No matter what route is used, strict asepsis should be employed to lessen the chance of infection at the injection site. Solutions containing formaldehyde or >25 g dextrose/500 mL are irritating if given SC. Many solutions contain phosphorus and magnesium in addition to calcium. Although administration of phosphorus and magnesium is not usually necessary in uncomplicated parturient paresis, detrimental effects of their use have not been reported. Magnesium may protect against myocardial irritation caused by the administration of calcium. Most products available to veterinarians contain phosphite salts as the source of phosphorus. However, phosphorus found in blood and tissues of cattle is primarily in the form of the phosphate anion. Because no pathway exists for the conversion of phosphite to the usable phosphate form, it is unlikely that these solutions are of any benefit in addressing hypophosphatemia.
Calcium is cardiotoxic; therefore, calcium-containing solutions should be administered slowly (10-20 min) while cardiac auscultation is performed. If severe dysrhythmias or bradycardia develop, administration should be stopped until the heart rhythm has returned to normal. Endotoxic animals are especially prone to dysrhythmias caused by IV calcium therapy.
Administration of oral calcium avoids the risks of cardiotoxic side effects and may be useful in mild cases of parturient paresis. Calcium propionate in propylene glycol gel or powdered calcium propionate (0.5 kg dissolved in 8-16 L water administered as a drench) is effective and avoids the potential for metabolic acidosis caused by calcium chloride. Oral administration of 50 g of soluble calcium results in ~4 g calcium being absorbed into the circulation.
Hypocalcemic cows typically respond to therapy immediately. Tremors are seen as neuromuscular function returns. Improved cardiac output results in stronger heart sounds and decreased heart rate. Return of smooth muscle function results in eructation, defecation, and urination once the cow rises. Approximately 75% of cows stand within 2 hr of treatment. Animals not responding by 4-8 hr should be reevaluated and re-treated if necessary. Of cows that respond initially, 25-30% relapse within 24-48 hr and require additional therapy. Incomplete milking has been advised to reduce the incidence of relapse. Historically, udder inflation has been used to reduce the secretion of milk and loss of calcium; however, the risk of introducing bacteria into the mammary gland is high.
prevention
Historically, prevention of parturient paresis was approached by feeding low-calcium diets during the dry period to stimulate intestinal absorption and enhance skeletal resorption prior to the sudden demand for calcium at the onset of lactation. While mobilization of calcium is somewhat enhanced, it is now known that feeding low-calcium diets is not as effective as initially believed. Furthermore, it is difficult to formulate diets that are low enough in calcium. Alternative methods for prevention of hypocalcemia include delayed or incomplete milking after calving, which maintains pressure within the udder and decreases milk production. This practice may aggravate latent mammary infections and increase incidence of mastitis. Prophylactic treatment of susceptible cows at calving may help reduce parturient paresis. Cows are administered either SC calcium on the day of calving or oral calcium gels at calving and 12 hr later.
Most recently, the prevention of parturient paresis has been revolutionized by the use of the dietary cation-anion difference (DCAD), which decreases the blood pH of cows during the late prepartum and early postpartum period. This method is more effective and more practical than lowering prepartum calcium in the diet. The DCAD approach provides an excess of anions over cations in the diet by adjusting the components of the diet, adding anionic salts to the ration, or both. Adding excess anions to the diet is believed to enhance calcium resorption from bone and absorption from the GI tract.
An important strategy for decreasing blood pH in periparturient cattle is reducing the potassium content of the diet. Including corn silage as a major portion of the dry cow’s diet is essential as it tends to have the lowest content potassium of available forages. Alfalfa is another forage source that may prove beneficial in maintaining proper blood pH. In the past, including alfalfa in a dry cow ration was not considered ideal due to the high calcium content. However, it has since been determined that calcium has little effect on the alkalinity of cow’s blood. Withholding potassium fertilizers on fields used to grow dry cow forages is another means of decreasing potassium levels in hay fed to dry cows. Alternatively, anionic salts can be added to counteract the effects of high cation levels (potassium and sodium) in the diet. Anionic salts to consider include calcium chloride, magnesium chloride, magnesium sulfate, calcium sulfate, ammonium sulfate, and ammonium chloride. Recent research evaluating the acidifying activity of different anionic salts has resulted in the following equation that describes the ion balance in rations:
Ion balance (mEq/g) = (0.15 Ca2+ + 0.15 Mg2+ + Na+ + K+) − (Cl- + 0.25 S- + 0.5 P-)
This equation suggests the major ions determining blood pH are sodium, potassium, and chloride. The target value for close-up dry cow rations is +200 to +300 mEq/kg. An important drawback to feeding anionic salts is poor palatability, which can be overcome by using a mixture of anionic salts within a moist, palatable ration such as corn silage, brewer’s grain, distiller’s grain, or molasses. While sulfate salts are more palatable than chloride salts, they are less effective in acidifying the blood.
Administration of vitamin D3 and its metabolites is effective in preventing parturient paresis. Large doses of vitamin D (20-30 million U, sid), given in the feed for 5-7 days before parturition, reduces the incidence. However, if administration is stopped more than 4 days before calving, the cow is more susceptible. Dosing for periods longer than those recommended should be avoided due to potential toxicity. A single injection (IV or SC) of 10 million IU of crystalline vitamin D given 8 days before calving is an effective preventive. The dose is repeated if the cow does not calve on the due date. Newer compounds used (where available and approved) in lieu of vitamin D and less likely to cause hypervitaminosis include 25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol, and 1α-hydroxycholecalciferol. After calving, a diet high in calcium is required. Administering large doses of calcium in gel form (PO) is commonly practiced. Doses of 150 g of calcium gel are given 1 day before, the day of, and 1 day after calving.
Use of synthetic bovine parathyroid hormone (PTH) may prove to be superior to administration of vitamin D metabolites. Vitamin D metabolites enhance GI calcium absorption, whereas PTH enhances GI calcium absorption and stimulates bone resorption. PTH is administered either IV 60 hr before parturition, or IM 6 days before parturition. Drawbacks to the use of PTH include increased labor requirements for administration, as well as the availability of such compounds.
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post parturant paresis(hypocalcemia) Empty
مُساهمةموضوع: رد: post parturant paresis(hypocalcemia)   post parturant paresis(hypocalcemia) Icon_minitimeالإثنين 13 ديسمبر 2010 - 20:34

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