Etiology

Uterine dropsy or hydrops is a sporadic condition usually occurring during the last trimester of pregnancy. Hydrops of the amnion results from fetal anomalies that prevent fetal swallowing or intestinal transport of amniotic fluid and is responsible for approximately 10% of the cases of hydrops. Hydrops of the allantois is the more common condition and is usually accompanied by abnormal placentation characterized by reduced numbers of placentomes and adventitious placentation (multiple areas of adhesion between the endometrium and allantochorion, appearing as miniature placentomes). Therefore hydrallantois usually is considered a maternal abnormality of placentation, whereas hydramnios is considered more likely a fetal problem. Hydrallantois tends to cause rapid (days to weeks) abdominal distention that results in a rounded abdominal appearance as the patient is viewed from the rear, whereas hydramnios usually results in a slow progressive enlargement with eventual pear-shaped appearance. Twinning or multiple fetuses are more likely associated with hydrallantois. Fetal anomalies are common with hydramnios. Pregnancies that are the result of modern in vitro reproductive technologies such as those producing cloned or transgenic fetuses are more commonly beset by abnormal placentation and subsequently represent a greater risk for hydrops allantois. It is possible for nutritional deficiencies to cause hydrops allantois. Fetal hydrops may occur due to accumulation of cerebrospinal fluid (hydrocephalus) or from ascites (usually in Ayrshire calves). These calves, if delivered alive, can survive, but should not be used for breeding.

Signs

The major outward sign of hydrops is progressive abdominal distention during the last trimester that worsens to such a degree as to decrease appetite and cause difficulty in moving or rising (Figure 9-1). Although abnormal fetuses causing hydramnios rarely can cause abdominal distention as early as the midtrimester, this is much less common than hydrops that appears during the last 4 to 6 weeks of pregnancy. The distended uterus takes up so much room in the abdomen that affected cows have reduced appetites because of visceral compression. Weakness results both from reduced feed consumption and from the increased weight of uterine fluids. Secondary ketosis and other metabolic conditions are possible complications as a result of decreased feed intake and fetal nutritional needs—especially if twins are present in cows with hydrallantois. Rectal examination may help to differentiate hydramnios and hydrallantois. In hydramnios, the fetus and placentomes are palpable, but the uterine horns are more difficult to palpate. In hydrallantois, the distended uterine horns appear to fill the abdomen, but palpation of the fetus and placentomes may not be possible because the uterus is stretched tightly by the increased fluid content. Rectal or transabdominal ultrasound examination is helpful in making a diagnosis. Unless the conditions are diagnosed promptly, musculoskeletal complications such as exertional myopathy, hip injuries, hip luxations, and femoral fractures can occur because of struggling to rise or slipping brought on by the tremendous abdominal weight. (As much as 200 liters, or 440 pounds, of additional fluid may accumulate in the case of hydrops allantois.) Rupture of the prepubic tendon and ventral hernias also may occur. Because hydrallantois tends to cause more rapid fluid accumulation, musculoskeletal injuries appear to be more common with this condition than in the slowly enlarging hydramnios patients.

Figure 9-1 Hydrops allantois in a Holstein cow that was 8 months pregnant.

If cattle with hydrops calve or abort spontaneously, the thick viscid amniotic fluid present in hydramnios also can help differentiate this condition from the watery transudative excessive fluid discharged from cattle with hydrallantois.

Cattle with hydrops have normal temperatures but will show progressive tachycardia, anxiety, reduced appetite, and dehydration associated with severe abdominal distention. Fetal hydrops may cause dystocia.

Treatment

Treatment decisions must be tempered by the potential immediate and delayed complications anticipated. Prognosis usually is worse for hydrallantois because abnormal maternal placentation may be expected to cause severe and intractable problems with retained placenta and metritis, making future fertility extremely unlikely. If neglected or allowed to “run their course,” most cattle with hydrallantois will progress to recumbency, cardiovascular collapse, and overwhelming myopathy. Hydramnios may have fewer severe immediate complications with retained placenta and metritis, but in these cases survival of the fetus is unlikely. Perhaps the most important consideration is the overall systemic state. Most hydrops cattle are in a negative energy balance, are 4 to 6 weeks from parturition, have slack udders, and may or may not come into lactation—at least to productive lactation levels. Therefore salvage should be considered unless the cow is particularly valuable or is within 2 weeks of term. Cattle that are recumbent and unable to rise or that already have severe musculoskeletal injuries should be euthanized.

When treatment is elected, several options exist. Induction of parturition is preferable if the uterus has not already been stretched beyond physiological limits, which is unfortunately usually the case. If surgery is elected, uterine fluid should be released over a period of 30 minutes to 2 hours, via a Foley catheter, while intravenous fluids are administered rapidly. This prevents the rapid onset of shock, which may result from venous fluid shifting into the splanchnic pool with abdominal decompression. Although some authors have not found hydrops patients to be markedly dehydrated, our experience differs and supports the comments of Roberts that those patients usually are dehydrated. Dehydration further increases the risk of compartmental pressure changes, subsequent splanchnic pooling, and shock for hydrops patients treated by cesarean section.

Dr. Rebhun’s preference was to induce parturition with IM injections of 30 to 40 mg prostaglandin F_2α (PGF_2α) and 20 mg of dexamethasone. Cervical relaxation may also be attempted by the manual application of synthetic prostaglandin E in the external os and cervical canal. Specific human gynecologic preparations of prostaglandin E are very expensive, but I have had success using misoprostol (1000 mg mixed in sterile obstetrical gel applied thrice daily) as an aid to cervical ripening in some cattle. Pregnant women should not handle this product! Most cattle treated with this combination calve within 24 to 48 hours and should be monitored closely. IV fluids—hypertonic saline is especially useful—are administered to cattle showing any degree of dehydration or inappetence. Supportive glucose or calcium may be indicated when ketosis or hypocalcemia is present. Treated cows are kept in well-bedded box stalls with good footing and are monitored closely because they may require assistance in calving. Milking is started as soon as the fetus is delivered, even when little milk is present in the udder. Most fetuses or calves delivered are abnormal, small, or nonviable. If the calf is more valuable than the cow and ultrasound examination indicates a viable fetus, treatment of the cow with dexamethasone and cesarean section 24 hours later would provide the best chance of having a live calf. In the case of an apparently viable calf, colostrum should be provided from another cow because the patient seldom has normal colostrum. Prognosis is better for those cows near term. Metritis and retained fetal membranes (RFM) should be anticipated and prophylactic antibiotic therapy instituted. Clinicians should anticipate that the cow will have a large, potentially enormous, atonic uterus after calving and will experience highly protracted and challenging involution. Although fetal kidney anomalies are more likely to be associated with hydrallantois, Dr. Rebhun once treated a hydramnios cow that subsequently delivered a calf having polycystic kidneys. Cattle with hydrallantois that survive delivery and avoid life-threatening postpartum metritis should not be bred again. If fetal hydrops causes dystocia, the excessive fluid can be drained to allow fetal extraction.

Because of the common complications of intractable retention of fetal membranes and associated metritis and infertility, and the poor prognosis for survival of the fetus, culling of the cow with hydrops allantois may represent the most economical option. Survival and subsequent fertility are much more likely in cows with hydrops amnios but they should not be bred again to the same sire.

Etiology

Rupture of the prepubic tendon and ventral abdominal hernias usually occur during the last month of pregnancy. Contributing causes include the weight of a gravid uterus and periparturient edema of the ventrum. Further predisposition occurs in cattle with twin or multiple pregnancies and those with hydrops. Although more common in pluriparous cattle with a pendulous abdomen, the condition may occur in primiparous cattle. Injuries from direct trauma (especially from animals with horns), being cast or trapped on inanimate objects, or slipping on treacherous footing may be contributing or initiating factors. Factors that increase the uterine mass remain the major cause in cattle. Rarely, rupture of the body wall in the flank area with hematoma formation and obvious swelling occurs at parturition.

Clinical Signs and Diagnosis

Rupture of the prepubic tendon causes a bilateral and complete loss of fore udder definition, and the fore udder points ventrally in continuum with the pendulous ventrally directed abdominal wall (Figure 9-2). The cow assumes a sawhorse stance because of exquisite pain in the abdomen and is reluctant to lie down (Figure 9-3). When the cow does lie down, she tries to assume lateral recumbency to avoid putting pressure on the ventrum. Abdominal distention usually is obvious. The owner usually observes overt or atypical extensive abdominal distention before rupture of the tendon, and cows (like mares) may have the rupture preceded by both extreme abdominal distention and a large plaque of ventral edema. These characteristics have been referred to as “impending rupture of the prepubic tendon” and are a grave sign.

Figure 9-2 Rupture of the prepubic tendon in a 6-year-old Holstein cow.

Figure 9-3 Rupture of the prepubic tendon in a first-calf heifer that was confirmed to have twins. The heifer has a sawhorse stance and would not lie down because of severe abdominal pain.

Cattle with ventral hernias have the same predisposing causes as for rupture of the prepubic tendon but may have unilateral abdominal sagging coupled with an abnormal relationship of the fore udder to the affected side of the abdomen. Ventral hernias have been reported to be more common on the right side in cattle but can occur on either side.

Cattle with either condition become acutely painful at the moment that an “impending” situation becomes a hernia. Tachycardia, tachypnea, an anxious expression, reluctance to move or lie down, and a sawhorse stance are typical findings. Prepubic tendon rupture usually results in more overt pain than ventral hernia, but this is far from absolute.

Rectal examination may help to differentiate the conditions as a purely didactic measure. When true rupture of the prepubic tendon has occurred, the cranial brim of the pelvis may be tipped slightly upward, and the hand may be cupped under the brim because of loss of the prepubic tendon. In ventral hernias, the hernia may or may not be palpable, but the prepubic tendon can be palpated in the caudal abdomen as it attaches to the pelvic brim.

Cattle with either condition may require assistance in calving because pain and inability to generate normal abdominal press may lead to dystocia. In addition, twins or hydrops may be apparent and further the chances of dystocia. Cows with rupture of the prepubic tendon should be salvaged or euthanized because they are in extreme pain. Cows with ventral hernias that do not appear to be in severe pain may be kept for the current lactation but should not be bred back. Cattle thought to be showing signs of “impending rupture” or those suspected to have hydrops should be induced to calve immediately or undergo elective cesarean section in an effort to prevent herniation or rupture of the prepubic tendon. Cattle with either condition that are recumbent and unable to stand or those already having secondary musculoskeletal complications should be euthanized.

When parturition is induced in these cases, it should always be attended. Inserting a nasotracheal or orotracheal tube helps prevent abdominal press with further exacerbation of the abdominal wall rupture, while the calf may still be delivered by traction.

Rupture of the prepubic tendon and ventral hernias are specifically diagnosed based on clinical signs alone but should be differentiated from large hematomas or abscesses cranial to or dorsal to the udder, severe preparturient ventral edema, and inflammatory ventral edema or edema secondary to thrombosis of the mammary vein. The anatomic relationship of the udder to the ventral abdomen usually suffices to differentiate these conditions. Ultrasound examination will help in making a more definitive diagnosis. Anemia would be present with large udder hematomas, and fever might be present with abscesses. Ultrasonography could be very useful whenever the diagnosis is in doubt.

Etiology

Bovine practitioners are familiar with uterine torsion as a cause of dystocia in dairy cattle. Although the exact cause of torsion seldom is discovered in an individual case, prolonged confinement, sudden falls or slipping, a pendulous abdomen, strong fetal movements, and poor uterine muscle tone may predispose. Unicornual pregnancy (where the conceptus fails to occupy both uterine horns) and especially unicornual twin pregnancy may cause instability of the uterus and predispose to torsion. Torsion is less common in Bos indicus breeds, where the uterine broad ligament is attached over a greater length of the uterine horns than in Bos taurus cows. Many parturient torsions occur during the latter part of the first stage of labor or early in the second stage. Other partial torsions of 45 degrees or more may be maintained in this position for weeks or months during late gestation but do not result in signs unless further rotation occurs that interferes with fetal or uterine blood supply.

In addition to these parturient problems, however, uterine torsion can result in clinical signs during the second or third trimester well before term. Such cattle have torsions greater than 180 degrees, and colic signs similar to intestinal obstruction may occur. Roberts states that uterine torsions in the cow have been observed as early as 70 days of gestation. Most cases occurring during the mid-trimester of gestation are characterized by colic and abdominal pain.

Clinical Signs and Diagnosis

Although an uncommon cause of colic, uterine torsion should be considered in the differential diagnosis of any cow showing colic and more than 4 months pregnant. The early signs shown by these cows are similar to those observed in the more common term uterine torsions and include restlessness, treading, anxiety, tachycardia, reduced appetite, and swishing of the tail. The cow may be reluctant to lie down or may get up and down frequently or may perhaps act irritable. As the condition progresses, complete anorexia, progressive tachycardia, and true colic with kicking at the abdomen may appear. Because the condition is seldom suspected in cattle in mid-gestation, further delay in diagnosis may occur if the signs are interpreted as intestinal in origin and treated symptomatically. Rectal examination allows definitive diagnosis because a clockwise or counterclockwise torsion will be identified. Most mid-pregnancy torsions are greater than 180 degrees, thereby causing the right broad ligament to be pulled downward under the torsed organ while the left broad ligament is pulled over the top of the reproductive tract (clockwise or right torsion). The opposite arrangement occurs in counterclockwise or left torsions. The viability of the calf should be determined by palpation and/or ultrasound examination. Counterclockwise torsions are slightly more common, since the uterus rolls toward and over the non-gravid horn.

Treatment

Unlike treatment methods available for term uterine torsions (e.g., manual detorsion, mechanical detorsion, “plank in the flank,” and rolling), mid-trimester uterine torsions are best managed by manual correction following laparotomy. Attempts to roll the cow or use the plank-in-the-flank technique are usually unsuccessful because of lack of fetal mass and tend to further damage the already compromised uterus while risking hemorrhage or further transudative or exudative peritoneal effusion. When rolling was attempted in some early cases, the technique failed and subsequent laparotomy revealed severe serosanguineous peritoneal effusion and some frank hemorrhage. When diagnosed early and corrected by laparotomy, cattle with mid-trimester uterine torsions have a better chance of delivering a live calf. Fetal death and eventual abortion are likely following correction in neglected cases, severe torsions, or those with obvious vascular compromise. Prolonged cases can have uterine necrosis and die from septic shock.

Etiology

Uterine rupture is an unfortunate consequence of dystocia in cattle. Although the condition rarely is observed following unassisted delivery, most cases occur following forced traction, uterine torsions, fetotomy, or delivery of emphysematous fetuses. Iatrogenic ruptures can also result from frustrated manipulations as the veterinarian becomes exhausted following prolonged attempts to relieve dystocia. Prolonged dystocias, emphysematous fetuses, and failure to lubricate sufficiently during extraction can increase the resistance and “drag” between fetus and maternal reproductive tract and predispose to rupture of the uterus. Abdominal pressure of the uterus against the pelvic brim can cause pressure necrosis and spontaneous uterine rupture.

Clinical Signs

When a veterinarian is present for the dystocia, manual examination of the cervix and uterus through the vagina should be performed following delivery of the calf. Full-thickness uterine tears usually can be diagnosed at this time unless the injury occurs in the uterine horns distal to the reach of the veterinarian.

When the condition is undetected initially or a veterinarian has not been present for the dystocia, clinical signs usually appear within 1 to 5 days postpartum. Depression, inappetence, fever, tachycardia, rumen stasis, and abdominal guarding because of peritonitis appear as the major signs. Some cattle progress rapidly to a condition of septic shock because of massive peritoneal contamination. This is especially common when prolonged dystocia, RFM, or a dead or emphysematous fetus allows bacterial inoculation of the uterus that quickly spreads to the abdomen. The fetal membranes may enter the abdominal cavity through the uterine tear and cause severe, potentially fatal peritonitis. Cattle with large uterine tears and tenesmus associated with dystocia may prolapse intestine through the reproductive tract and have these organs appear at the vulva. Spontaneous rupture caused by unattended dystocia occasionally has resulted in the calf or fetus being extrauterine in the abdomen. Signs of overt peritonitis greatly worsen the prognosis because fibrinous adhesions spread quickly through the abdomen and lessen the chances for uterine repair. When the condition is suspected, a manual vaginal examination following careful preparation of the perineum and vulva is indicated. If the cow is fresh less than 48 hours, a hand may enter the uterus easily, but it may be difficult for the hand to pass through the cervix in cows greater than 48 hours postpartum. A speculum may be helpful, but manual palpation of the tear remains the best means of absolute diagnosis. Most tears are dorsal and just cranial to the cervix. When uterine rupture is detected immediately following delivery, options should be discussed with the owner. Salvage is the best option for cows of average value. Conservative treatment may be attempted when the uterine tear is dorsal and small. Broad-spectrum systemic antibiotics and repeated administration of oxytocin have been used for conservative therapy. The success of conservative therapy is often poor because of the primary problems of dystocia allowing heavy bacterial contamination of the uterus and abdomen. Cows that experience small dorsal uterine tears following manipulation/delivery of a live calf and in which fetal membranes do not contaminate the abdomen have the best prognosis.

When the cow is judged to be extremely valuable direct aggressive therapy including repair of the uterine tear may be necessary.

Treatment

Specific therapy includes surgical correction of the laceration, intensive antibiotic therapy to treat or prevent peritonitis, and supportive measures that may vary in each case. Surgical repair has been accomplished through the birth canal, but obviously this is difficult, is often done blindly, and is frequently unsuccessful. Epidural anesthesia and special extra-long surgical instruments facilitate this technique, but it remains, at best, difficult. This technique is possible only when the condition is recognized immediately and the cervix is wide open to allow two-handed manipulation.

Surgical repair following laparotomy is a better choice but also has inherent difficulties because the site of the tear often is dorsal and close to the cervix—consequently it is difficult to reach and to suture effectively from a flank approach once uterine involution has commenced. Incisions for this type of repair need to be made as far caudal in the paralumbar fossa as possible to facilitate visualization and repair of the rupture. It may be helpful to have an assistant direct the reproductive tract toward the operator by placing an arm through the birth canal. Flank laparotomy also is necessary for those rare cases having the fetus or fetal membranes free in the abdomen.

Recently we have attempted repair of uterine tears in dairy cattle after medical prolapse of the uterus by inversion through the caudal birth canal. This technique requires pharmacologic relaxation of the organ to allow manual prolapse. A slow IV infusion of 10 ml of 1:1000 epinephrine is administered by an assistant while the veterinarian holds the uterus after passing a gloved arm through the cervix. As uterine relaxation occurs, the uterus is retracted through the vagina and a surgical repair of the uterine tear completed. The uterus then is returned to normal position similar to replacing a spontaneous uterine prolapse. Despite the epinephrine-induced relaxation of the organ, retraction still may be difficult. In addition, the cardiovascular consequences of IV epinephrine constitute a risk to the patient but may be the lesser of two evils when contrasted with the disadvantages of other repair methods.

Bactericidal antibiotics are indicated preoperatively and for at least 2 weeks postoperatively if repair has been successful. Intraperitoneal lavage with saline and antibiotics or very dilute Betadine is indicated and facilitated when the uterine tear is repaired through a flank approach. Further supportive therapy such as IV fluids, NSAIDs, or short-acting corticosteroids for cattle showing early signs of shock may be indicated. Prognosis is poor to guarded for cattle with uterine rupture.

Etiology

Prolapse of the uterus is a condition well-known to bovine practitioners. In dairy cattle, the condition is not thought to be inherited and seldom recurs in subsequent parturitions. Although the exact cause for an individual patient may be difficult to determine, predisposing causes include dystocia, tenesmus, and hypocalcemia. Primiparous cows can be affected, but pluriparous ones are probably at greater risk. Prolapse of the uterus also is fostered by confinement, lack of exercise, and gravitational effects when cattle are allowed to calve with their hindquarters lower than their forequarters, as happens when confined cows calve into the drop of conventional barns. Uterine atony is the common inciting cause and is frequently associated with hypocalcemia in multiparous dairy cattle.

Prolapse usually occurs within hours of calving and almost always within 24 hours of calving. Instances of uterine prolapse occurring several days following calving are cited by many practitioners but are extremely rare.

Clinical Signs and Diagnosis

The clinical signs are dramatic and suffice for definitive diagnosis (Figure 9-4). Occasionally neophyte handlers or those privileged to have never seen the condition will confuse uterine prolapse with vaginal prolapse, but the sight of a fully prolapsed uterus is difficult to confuse with other conditions. Conspicuous placentomes on the exposed endometrium make the prolapsed uterus impossible to confuse with any other organ. The cow may appear healthy otherwise; this is often the case in primiparous cattle. Pluriparous cows with uterine prolapse often show varying degrees of hypocalcemia such as weakness, depression, subnormal temperature, anxiety, struggling or prostration, and coma. Tenesmus is common to most cases. Signs of shock should be differentiated from those of hypocalcemia because a small percentage of prolapse patients may develop hypovolemic shock secondary to blood loss (internal or external), laceration of the prolapsed organ, or intestinal incarceration within the prolapsed organ. Extreme pallor, a high heart rate, and prostration are grave signs in such cattle. Rarely the cow is found dead, especially when an unobserved calving has occurred. The prolapsed uterus often is heavily contaminated with bedding, feces, dirt, and placenta. Some bleeding is common from exposure injuries to the placentomes or endometrium. If the affected cow is able to stand and walk, the massive organ hangs near the hocks and can be stretched, traumatized, or lacerated as it flops back and forth against the rear quarters.

Figure 9-4 Uterine prolapse.

Treatment

Uterine prolapse is one of the true emergencies in bovine practice, and rapid owner recognition followed by prompt veterinary treatment greatly improves the prognosis. When notified of the condition, the veterinarian should instruct the owner to keep the cow quiet and to cleanse the exposed organ and keep it moist. Warm water containing dilute (1%) iodine and a clean towel or sheet work well for this purpose. If possible, the owner also may be instructed to elevate the organ to the level of the ischium or higher to relieve vascular compromise and subsequent edema, as well as lessen the chance of injury. When the veterinarian arrives at the scene, overall assessment of the situation is in order before proceeding with specific treatment. The cow’s position, overall physical status, and the environment should be assessed. Specifically:

This overall assessment and a very quick history and cursory physical examination can be completed within minutes and may improve the end results greatly.

Specific treatment is subject to great individual variation as regards when to administer calcium, whether to perform the repair with the patient recumbent or standing, when to give certain drugs, and aftercare. The basic premises are, however, agreed on by most practitioners.

Figure 9-5 Adult cow positioned in sternal recumbency for replacement of uterine prolapse

(Courtesy Dr. Nigel Cook.)

Retention sutures placed in the vulva following replacement of uterine prolapses are also controversial. They are ineffective for prevention of reprolapse and may rarely mask the condition by allowing the uterus to become trapped in the vagina. Since the common predisposition for uterine prolapse is uterine atony, complete restoration of the uterus to its normal position and treatment to enhance uterine tone are sufficient to prevent recurrence of the condition.

Prognosis

The prognosis for uncomplicated uterine prolapse is good, and most cows that respond promptly will breed back following routine monitoring and treatment of their metritis. Furthermore, dairy cows that have had prolapses do not have a higher incidence of the problem at future calvings. Of cows with uterine prolapses, 75% or more should do well.

Of cows that do not do well, a low percentage will reprolapse within 1 to 3 days, some cannot be replaced at all, some die as a result of intestinal incarceration in the prolapse or bleed out, some develop severe peritonitis or perimetritis from uterine tears, and some do irreparable damage to the prolapsed organ. The owner should be made aware that the cow could die at any time during or following replacement when shock is obvious. Reprolapse is an extremely bad sign, and cows that repeatedly prolapse after initial correction seldom do well. It is wise to reexamine all prolapse patients 3 days after repair to assess the overall systemic state and make specific recommendations regarding metritis or uterine injury. Decisions on further antibiotic and other therapy can be discussed with the owner at this time.

Etiology

RFM or retained placenta is a very common condition in dairy cattle. Fetal membranes should be expelled in less than 8 hours following normal parturition; therefore retention for longer than 8 to 12 hours is considered abnormal. Abortion, either infectious or sporadic, occurring during the last half, of pregnancy frequently results in RFM. Hydrops, uterine torsion, twinning, and dystocia in general result in increased incidence of RFM when compared with normal parturitions. Heat stress and periparturient hypocalcemia also predispose to the condition. Cows induced to calve by pharmacologic means such as exogenous corticosteroid administration should be anticipated to have RFM. Nutritional causes such as overconditioning of dry cows and carotene and selenium deficiencies also have been incriminated. Low levels of vitamin A as occur in hyperkeratosis and polybrominated biphenyls toxicity are associated with RFM, metritis, and abortion. In selenium-deficient areas, cattle that have low selenium values may have an increased incidence of RFM, metritis, and cystic ovaries. Vitamin E, which has been shown to enhance neutrophil function, also may be involved. Cattle fed stored feeds from areas that are selenium deficient should be monitored for selenium status and supplemented routinely. Selenium and vitamin E could be related to RFM either as a result of pure deficiency or altered neutrophil function.

Cattle that have RFM following parturition may be at greater risk of the condition in subsequent years. Perhaps more importantly, epidemiologic studies show that cows with RFM have a higher incidence of metabolic diseases, mastitis, metritis, and subsequent abortion. Therefore despite the fact that many cows with RFM remain asymptomatic as regards immediate uterine health, associated diseases are a definite risk. Decreased resistance to uterine and other infections in cattle with RFM is partially explained by proven neutrophil dysfunction associated with the condition in periparturient cows. In addition to reduced neutrophil function, cattle with acute metritis associated with RFM could have a depletion of neutrophils in the peripheral blood as a result of acute recruitment of neutrophils to the infected uterus as evidenced by the degenerative left shift in the leukogram observed in some septic metritis patients. Although septic metritis or chronic endometritis does not occur in most cattle with RFM, the urge to treat RFM is based primarily on the inability to predict which cows will develop clinically significant sequelae.

Recent evidence strengthens the hypothesis that RFM is mediated by impaired neutrophil function beginning in the late dry period. Reduced neutrophil migration toward tissue extracts of placentomes can be detected as long as 2 weeks before calving in cows that go on to develop RFM. Other neutrophil functions, such as oxidative burst (a component of neutrophil bacterial killing action) are also impaired in these cows. Impaired neutrophil function has also been recorded in hypocalcemic cows. Indeed, many of the etiological factors associated with RFM have also been correlated to impairment of neutrophil function, including vitamin and mineral deficiencies, heat stress, or exogenous corticosteroid administration. The poor neutrophil function in affected cows extends into the postpartum period and probably mediates most of the complications usually associated with RFM.

Clinical Signs and Diagnosis

Clinical signs are obvious when the fetal membranes protrude from the vulva or hang ventral from the vulva to the escutcheon, rear udder, or hocks (Figure 9-6). The condition is less apparent when the membranes are retained within the uterus or only project into the cervix or vagina and require a vaginal examination to be detected. Other clinical signs are completely dependent on evolution of associated diseases. Metritis is the most common secondary complication, and clinical signs of metritis or endometritis are identical to those discussed in the metritis section. Secondary metabolic conditions may be linked directly to RFM when metritis exists or merely concurrent when the metritis is insignificant. As previously mentioned, mastitis, metabolic diseases, ascending urinary tract infections, and displaced abomasum may be associated with RFM complicated by metritis or, in the case of infections, because of less than optimal neutrophil function.

Figure 9-6 Retained fetal membranes.

Tenesmus may appear in some cattle because of constant tension and irritation of the caudal reproductive tract by the protruding membranes. Eventually a fetid odor emanates from the RFM, especially when metritis develops, and this may be the initial prompt for producers to seek veterinary attention or instigate treatment themselves.

Untreated, most RFMs separate and fall away 3 to 12 days following calving. Unfortunately some cattle with RFM completely confined to the uterus may retain the membranes for a longer time because of cervical closure or antibiotic treatments, and only pass the RFM after the first estrus. These cows may become quite ill because of secondary metritis and retention of fetid fluid but go undetected initially because of a minimum of discharge and odor.

Clinical debate is sparked when the significance of RFM in dairy cattle is discussed. Because only a small percentage of cattle with RFM become ill and because numerous studies show that the subsequent fertility of cattle allowed to discharge RFM spontaneously is largely unaffected, why should veterinarians ever consider treating a cow with RFM? A frequently quoted reference from 1932 that details the subsequent fertility of 44 cows with untreated RFM compared with 44 herdmates without RFM showed no difference in subsequent fertility. Many other studies have since proven that manual removal of RFM is not only unnecessary but may be harmful. Although accepting these data as regards the simple issue of RFM, the studies tend to ignore the effects of the condition on the overall well-being of the cows with RFM. For example, in Palmer’s 1932 article, only 31.8% of cattle with RFM had normal appetites for the 7 weeks following calving and only 29.5% had “good” milk production. It seems that these data support the observations of owners of cattle with RFM who believe that complete therapeutic disregard for cattle with RFM can lead to disaster. This is particularly true for obese cows with RFM. Reduced appetites leading to metabolic diseases or abomasal displacement are a definite problem in many cows with RFM that develop moderate or severe metritis. Even though the primary problem of RFM can clearly resolve itself naturally given time, the potential for associated and secondary problems exists, and “doing nothing” is often perceived as a potential economic gamble by owners of the modern high-producing dairy cow.

Treatment

A fascinating historical summation of treatment for RFM in cattle involving thousands of patients treated over several decades by the Ambulatory Clinic of the New York State Veterinary College is detailed in Roberts’ text. A summary of these data would suggest that less invasive, less manipulative treatments in association with intrauterine or systemic antibiotics (as indicated by the individual patient’s need and degree of metritis) progressively lessened the mortality rate for cattle with RFM. Cattle that resolve RFM and cycle normally should have fertility rates comparable with unaffected herdmates when breeding is begun at 90 days but may require adjunctive therapy in herds that begin breeding at 50 to 60 days as is common today.

Decisions to treat RFM may be based on medical need when metritis or other illnesses coexist or for the purpose of prophylaxis against metritis and associated problems. Some practitioners and owners take a “wait and see” attitude to avoid antibiotic concerns or unnecessary treatment whenever possible. Others who have herds that historically have a high incidence of metritis, ketosis, or abomasal displacement secondary to RFM tend to intervene prophylactically and therapeutically. Cattle that had dystocia, twinning, induced parturition, obesity, hepatic lipidosis, and RFM should be considered at high risk for metritis and probably justify prophylactic therapy. It is likely that the greatest benefits will accrue when measures are taken to improve management of cows in late gestation, rather than focus attention on cows actually suffering from RFM.

Treatment options include:

Etiology

Postparturient metritis is extremely common in dairy cattle and is best thought of as a spectrum of diseases depicted as a biologic bell-shaped curve. The most severe manifestation of metritis, perimetritis, implies full-thickness infection of the uterus with subsequent serosal leakage resulting in pelvic and peritoneal complications. Perimetritis is rare, potentially fatal, and most often follows severe dystocia. Septic metritis (acute puerperal or postpartum metritis, toxic metritis) refers to a severe puerperal uterine infection of the endometrium and deeper layers that results in systemic signs of toxemia. Puerperal metritis usually occurs from 1 to 10 days postpartum. “Metritis” is sometimes used as a general term for postpartum uterine infections of the endometrium or endometrium and deeper layers that may or may not cause systemic signs but may have implications for future reproductive performance. Infectious causes of reproductive failure such as brucellosis, leptospirosis, trichomoniasis, and campylobacteriosis may also cause varying degrees of metritis, but this discussion will be limited to conventional postpartum metritis.

Bacterial contamination of the uterus following parturition is extremely common during the first 2 weeks postpartum. As many as 93% of dairy cattle may have some bacterial contamination during this early postpartum period, but most infections appear to clear spontaneously because the infection rate decreases to 9% by days 46 to 60. Dystocia, RFM, dirty calving facilities, hepatic lipidosis, uterine atony, and iatrogenic vaginal contamination increase the occurrence of metritis.

The most common bacterium involved in early postpartum (,10 days) metritis is Arcanobacterium pyogenes. Fusobacterium necrophorum, Prevotella melaninogenica, and other anaerobes frequently complicate A. pyogenes infection, and these anaerobes act synergistically with A. pyogenes so the collective pathogenicity of each is increased. During the early postpartum period infection with Escherichia coli, hemolytic streptococci, Pseudomonas sp., Proteus sp., and Clostridium sp. may also be found. E. coli infections during the first 2 weeks postpartum seem to predispose to A. pyogenes infection and clinical or subclinical endometritis later in lactation. Persistent A. pyogenes infection after about 3 weeks postpartum is characterized by white or white-yellow purulent discharge. Although mild infections frequently resolve spontaneously, persistent or severe infections cause endometrial pathology and threaten future fertility. In many cases mild endometrial inflammation persists in the absence of frank uterine discharge, in a condition known as subclinical endometritis, which is common in North American dairy cows and has a severely detrimental effect on subsequent fertility. Involution of the uterus, host defense mechanisms, and regular reproductive cycling postpartum aid resolution of infection.

Mechanical influences such as severe uterine stretching as occurs in hydrops and twinning, physical injury to the reproductive tract resulting from dystocia, and uterine atony caused by hypocalcemia definitely predispose to infection as well. Dirty calving environments created by repeated use of maternity pens, calving in gutters or free stalls, and calving during periods of prolonged confinement act to increase environmental contamination and increase the prevalence of metritis in dairy cattle. Field observations frequently imply an association between increased prevalence of metritis during periods of extreme heat or extreme cold and during the last months of confinement in conventionally housed cattle in northern climates. Management influences, although hard to define scientifically, are intuitively obvious because clinical metritis is rare in some herds and exceedingly common in others.

The consequences of postpartum metritis are not limited to reproductive matters, and many bovine practitioners believe that clinically significant metritis is the most common primary predisposing cause to displacement of the abomasum for cows in many herds. Affected cows are also predisposed to mastitis and clinical or subclinical endometritis.

Bovine practitioners should be familiar with variation in normal uterine involution and lochia. Normal postpartum uterine discharges tend to be mixtures of mucus and blood, with more mucus the better finding. Blood associated with uterine involution will often color uterine discharges red, orange, or “tomato soup.” The consistency and odor of postpartum uterine discharges are important clues to the presence and severity of metritis in dairy cattle. Highly mucoid discharges in the early postpartum period (,10 days) usually indicate healthy uterine involution and minimal, if any, endometritis.

Although normal cattle have the greatest amount of lochia (several liters) within the first 48 hours postpartum, the amount subsequently discharged from the vulva varies from less than 100 ml (primipara) to 1 L or more (pluripara), and some may be absorbed via the uterus. Lochia consists of mucus, sloughing maternal placental tissue, and blood. Discharge of lochia usually begins at 3 days postpartum and continues through day 10. Around day 9 or 10 postpartum, the yellow-brown to red discharge may show increasing amounts of pink, brown, or red blood coinciding with sloughing of the maternal caruncles and their stalks, which leaves a denuded vascular surface. Such bloodstained mucoid discharge may be apparent as late as day 15 to 18. Cows with excellent postpartum health generally have their first postpartum ovulation around day 15, the second around day 32 or 33, and subsequent ones at regular 21-day cycles. Most of the first postpartum ovulations do not result in observable behavioral signs of estrus.

PGF_2α and its metabolites maintain high levels for 1 to 3 weeks postpartum and tend to remain elevated longer in cattle with metritis or delayed involution. In conjunction with elevated PGF_2α levels, progesterone levels remain at baseline until prostaglandin levels decrease. Administration of exogenous PGF_2α in the first weeks postpartum is unlikely to promote clinically relevant uterine motility or tone.

On rectal palpation, early postpartum uteri have good muscular tone and may have palpable longitudinal ridges associated with muscular contraction. Pluriparous cows usually have uteri too large to retract manually or to palpate fully before day 10 to 14. Some primiparous cows may have sufficient involution to allow full definition of the uterus per rectum by days 10 to 14. Rectal palpation may not, however, be the best means to detect abnormalities in uterine involution during the first 14 days following parturition, and veterinarians should not hesitate to perform clean vaginal examinations and a vaginal speculum examination as adjuncts. The onset of estrus causes a remarkable difference in the size of the organ in most cattle, and slightly cloudy or clear mucus may be massaged from the uterus and cervix at this time. Most grossly detectable uterine involution is completed by 25 to 30 days postpartum, although the uterine horns still may feel thicker or more doughy than normal until days 35 to 40. The process of involution is completed more quickly in primiparous cattle than older cattle, in cattle free of metritis, cattle without RFM, cattle without metabolic disease, and cattle that have not had dystocia. Normally during a vaginal examination at 2 days postpartum, a hand cannot be passed through the cervix, and by day 4, only two fingers can be passed into the cervix. Cervical involution may be delayed by dystocia, cervical trauma, or RFM.

Perimetritis is the most severe manifestation of metritis in cattle. Infection progresses through the entire uterine wall to cause serosal inflammation, exudation, and fibrinous adhesions. Almost invariably this condition is a consequence of dystocia because physical compromise and trauma to the uterus and caudal reproductive tract promote dissemination of bacteria from the uterine lumen and endometrium to the deeper layers. Vascular compromise as occurs in severe uterine torsions and subsequent manipulations to deliver the calf also predispose to perimetritis. True perimetritis results in peritonitis because this condition is not limited to retroperitoneal tissues. Extensive peritoneal exudates, fibrin deposition and adhesions to other viscera, and localization of septic exudates are common in perimetritis patients.

Clinical Signs and Diagnosis

Cattle with septic or toxic metritis become ill within the first 10 days—usually the first 7 days—postpartum. Signs of toxemia such as fever (103.0 to 106.5° F/39.5 to 41.39°C), tachycardia, inappetence, decreased production, rumen stasis, depression, dehydration, and diarrhea are common. Note that fever may be absent in a significant number of cows with acute puerperal metritis. Extremely severe infection may cause recumbency secondary to toxemia, weakness, and metabolic disorders, and death may ensue. A fetid watery uterine discharge may be obvious at the vulva, may stain the tail, or may require a vaginal examination to be detected. Such uterine discharges vary in color from brown to amber to gray or red but always are fluid, low in mucus content, purulent, and have an extremely fetid odor that permeates one’s clothes, hair, and arm even when guarded by an obstetrical sleeve. Although most cows with acute puerperal metritis have a history of dystocia, giving birth to twins, or RFM, not all do. Because these patients are very early postpartum, uterine infection and resultant appetite and gastrointestinal consequences predispose to metabolic diseases such as hypocalcemia and ketosis. The general term toxemia is used because (depending on the exact mix of causative organisms) endotoxins, exotoxins, and other mediators may be involved in the pathophysiology of the systemic signs.

Rectal examination usually reveals a hypotonic or atonic uterus with fluid distention. Physometra also may be present and cause the gas-fluid filled uterine horn to be confused with other viscera such as a distended cecum. Although attempts to retract the uterus should not be forced, gentle massage of the uterine body, cervix, and anterior vagina quickly causes fetid uterine discharges to be expelled from the vulva. A vaginal examination following cleaning of the perineal area is imperative to complete the diagnosis because this procedure allows differentiation of necrotic vaginitis or cervicitis and also allows detection of RFM and other pathology. Transabdominal ultrasound examination can be useful in determining size of the uterus, thickness of the wall, and the presence of fetal membranes or intrauterine gas. Cattle with septic metritis are at increased risk of abomasal displacement as a result of toxemia-induced gastrointestinal stasis and secondary metabolic conditions. A complete physical examination should be completed to rule out concurrent abomasal displacement and other conditions such as septic mastitis.

Clinical signs usually suffice for definitive diagnosis of septic metritis. Ancillary data support an overwhelming infection as evidenced by a degenerative left shift in the leukogram and elevated fibrinogen values. Acute recruitment of neutrophils to the uterus out of the bloodstream weakens the patient’s cellular defenses against other infections—especially mastitis. A mild metabolic alkalosis is anticipated in cattle with gastrointestinal stasis. Differential diagnosis includes consideration of septic mastitis, peritonitis of any source, and acute pyelonephritis. Cultures of the uterine fluid never are contraindicated but, frankly, seldom are performed in dairy cattle. It is assumed that A. pyogenes, anaerobes such as F. necrophorum and Prevotella melaninogenica, and other organisms are present. Coliforms are common following dystocia or RFM and could cause additional endotoxin production. Clostridial organisms also have been identified in some septic metritis patients, and Clostridium tetani has been identified rarely in the uterine flora from cattle that develop tetanus secondary to septic metritis. If cultures are elected, both aerobic and anaerobic testing should be performed.

Because of the wide spectrum of severity observed in postpartum endometritis-metritis, some recently postpartum (,14 days) cattle are neither toxemic nor perfectly healthy. This intermediate group of cattle has signs of reduced appetite and depression and frequently has metabolic diseases such as ketosis and hypocalcemia. These cows may or may not be febrile and, if febrile, only mildly so (103.5 to 104.5°F/39.72 to 40.28°C). If rectal examination reveals a poorly involuting hypotonic uterus containing excessive fetid fluid, these animals should be treated for puerperal metritis. These patients also are at risk for abomasal displacement caused by decreased fiber intake and intermittent or constant gastrointestinal dysfunction.

Signs of peritonitis predominate and become apparent 1 to 5 days following parturition. Fever, tachycardia, gastrointestinal stasis, depression, anorexia, and dehydration are present. The patient may assume an arched stance, be reluctant to move or rise from recumbency, have a guarded abdomen, and groan during expiration. Tenesmus is present in some patients. Rectal examination reveals the profound consequences of perimetritis—fibrinous adhesions and inflammation of all pelvic viscera are present such that the rectum cannot be moved and the examiner’s arm is locked in a constant position. If the uterine body can be palpated, crepitus caused by extensive fibrin deposition, adhesions, and abscesses may be palpable. Rectal examination findings coupled with the other signs usually suffice for diagnosis. Once the characteristic circumferential inflammation in the pelvis is palpated, however, it is best to discontinue the rectal examination for fear of worsening the situation, rupturing the uterus, causing the patient severe pain, or increasing the risk of severe tenesmus.

Ancillary data also may be helpful when the condition must be differentiated from retroperitoneal inflammation caused by vaginal perforations or extensive pelvic hematoma or inflammation secondary to dystocia. Abdominal paracentesis will indicate peritonitis based on increased protein and white blood cell counts in perimetritis patients but may be normal or have only moderately increased protein in retroperitoneal conditions. A complete blood count usually shows a degenerative left shift when perimetritis is peracute or acute. Neutrophilia is possible in subacute or chronic cases. Serum albumin tends to be decreased because of extensive protein loss into the uterus and peritoneal cavity in severe perimetritis cases (Figure 9-7). Vaginal examination may be indicated to rule out purely vaginal conditions and should be performed very gently following epidural anesthesia to avoid “malignant tenesmus,” which is a constant straining fueled by movement of air into the rectum.

Figure 9-7 Severe facial edema caused by hypoproteinemia secondary to perimetritis.

The prognosis is extremely poor for perimetritis, and most cows with this condition die within 1 to 7 days after diagnosis. If the cow’s value allows intensive treatment, systemic broad-spectrum antibiotics should be started immediately. IV fluid therapy is necessary because the extensive peritonitis usually results in complete anorexia. Penicillin, tetracycline, and ceftiofur are the most common antibiotics used for systemic therapy. Local or intrauterine therapy is contraindicated in most cases because extensive compromise of the uterine wall increases the risk of perforation. Prostaglandins may be used to encourage evacuation of the uterus but probably are of limited value because the uterus adheres to adjacent visceral and parietal peritoneum. Epidural anesthesia may be necessary if tenesmus exists. NSAIDs may be helpful during the first few days of treatment to counteract endotoxemia and provide a degree of analgesia. Dosage and duration of therapy using these drugs must be limited to minimize the potential for abomasal or renal toxicity.

Cattle that survive show slow but continual improvement as evidenced by a gradual return to normal temperature, normal heart rate, and return of appetite. Long-term (3 to 4 weeks) antibiotic therapy is indicated, and attempts to palpate the reproductive tract should be avoided for 3 to 4 weeks so as not to disturb adhesions. Surviving cows will always have extensive adhesions of the reproductive tract in the caudal abdomen and pelvis. It is best to allow complete sexual rest; prostaglandins should be administered at 14-day intervals to encourage uterine evacuation. Evacuation obviously is hampered by uterine adhesions. The cow should be assessed by rectal palpation once monthly. Despite the presence of extensive adhesions, surviving cattle eventually may resolve many of the adhesions over a 5- to 6-month period and conceive. Frequently these cows only “work on one side”—meaning that one uterine horn, uterine tube, or ovary (or all these) continues to be confined by adhesions. Therefore such a cow may conceive only when an ovulation occurs on the healthy or nonadhered ovary. Careful evaluation of the caudal reproductive tract and the presence of mature fibrous adhesions within the pelvic canal are critical before a decision as to breeding the cow back is made. Some cattle with persistent adhesions may be able to conceive and carry a pregnancy to term but should undergo elective cesarean section rather than attempting a natural or assisted vaginal delivery.

Cattle that do not improve following initial intensive therapy may either die as a result of diffuse peritonitis within the first few days following parturition or else linger as chronic peritonitis patients with persistent low-grade fever, partial anorexia, abdominal distention, hypoproteinemia resulting from albumin loss into the peritoneal space, and wasting.

Treatment Options

Review of the literature regarding the treatment of metritis and endometritis in cattle quickly reveals that few treatments have scientific merit. This lack of scientific data seems at odds with the empiric success enjoyed by most practicing bovine practitioners. Do we give too much credit to our treatment of endometritis patients when, in fact, spontaneous cures are responsible for most success? How then does the veterinarian decide intelligently which cows require treatment and what, if any, drugs to use? Is the veterinarian willing to assume the risk of benign neglect? The consequences of unresolved endometritis such as failure to cycle, failure to conceive, and early embryonic death or abortions are well known and accepted. Therefore when and how should we intervene? This decision is easier when cattle with metritis have associated systemic illness. In cattle without systemic signs, endometritis may resolve spontaneously if normal estrus activity, normal phagocytic cell function, and adequate nutrition all exist.

Perhaps the best decisions regarding therapy are made in light of an accurate diagnosis. Cattle with minimal delays in involution, minimal uterine fluid or discharge, and normal estrus activity are likely to cure themselves. However, cattle with systemic signs resulting from metritis, with large amounts of uterine fluid or discharges, ovarian inactivity or cysts, or failure of estrus should be considered abnormal and treatment should ensue. Most studies of treatment, or lack thereof, for cattle with metritis do not detail the severity of the problem and are subject to some criticism for this fact, as well as their failure to define the time postpartum when the diagnosis was reached and whether control populations were maintained.

Intrauterine Therapy

Intrauterine antibiotics have fallen largely into disfavor despite having been used for decades in the treatment of metritis in cattle. Intrauterine antibiotics also are often absorbed from the uterus to establish blood and milk levels that cause concern for milk residues and discard, resulting in significant economic losses. Absorption is more likely from healthy uteri, at the time of estrus, and following uterine involution. Certain antibiotics may interfere with phagocytic cell function, may be made inactive by beta-lactamase-producing bacteria, may irritate the endometrium, or may not work well in the relative anaerobic state thought to exist in the uterus. Perhaps the greatest impediment to using intrauterine antibiotics lies in the fact that large amounts of uterine fluid may simply overwhelm or inactivate small doses of locally administered antibiotics. Many intrauterine treatments may be compared to a “drop in the ocean” when used in severe metritis cases. Cephapirin, a first-generation cephalosporin, is available in some countries in a formulation designed specifically for intrauterine administration (Metricure, InterVet). It is not available in the United States. In several trials it has been found to be beneficial for treatment of clinical and subclinical endometritis. Its use in acute puerperal metritis has not been reported.

Despite these scientific reservations, intrauterine therapy may be helpful and is frequently used as a component of therapy. Why does it seem to help? Antibiotics may kill a proportion of the total bacterial populace when administered as intrauterine therapy even when pharmacokinetics and pharmacology are imperfect. Much of the referenced “pharmacology” is extrapolated from data collected in other species rather than specifically documented scientifically for cattle. Intrauterine oxytetracycline (5.5 mg/kg) administered to early postpartum cows did establish high luminal, caruncular, and endometrial levels for at least 24 hours. Another study showed that 3 g of oxytetracycline daily for 3 days (intrauterine) was more successful at sterilizing A. pyogenes metritis than either 3 consecutive days of PGF_2α or no treatment. The numbers of cows in this study were small, however. A more recent study demonstrated that 0.5 g of cephapirin (available in Europe) given within 24 hours of calving improved reproductive performance in cows with RMF or a dead calf. Similarly a recent study using intrauterine ceftiofur (1 g) demonstrated a positive effect in cows with either RFM or twins.

As previously mentioned the early postpartum uterus—especially when infected—does not absorb drugs into the deeper uterine wall or systemic circulation as effectively as an involuted, noninfected uterus. This may be beneficial to intrauterine antibiotics in early postpartum cattle because the major drug levels appear in the lumen and superficial endometrial tissue. Penicillin has been used as an intrauterine therapy. Either 10 million units of procaine penicillin or 10 million units of sodium penicillin have been used to establish effective luminal and endometrial concentrations for 24 hours.

In summation, regarding intrauterine antibiotic therapy as a treatment for endometritis, few drugs have been evaluated thoroughly, the magnitude of infection in treated cattle is difficult to evaluate, the dosage and duration of reported therapies vary tremendously, and many pharmacologic reasons exist as to why intrauterine therapy may not work. Based on literature review and common sense, the disadvantages of intrauterine therapy include:

Despite these disadvantages, veterinarians may choose to use intrauterine therapy in certain circumstances. Based on the previous discussion, it means that rational use of intrauterine therapy requires several considerations.

Systemic Antibiotics

Systemic antibiotics have become the “in vogue” treatment for metritis in dairy cattle over the past decade. The use of systemic antibiotics is justified and often required for metritis that causes systemic illness. However, systemic therapy is definitely overused in cattle with metritis or RFM that do not have a fever or are not systemically ill. This overuse results in significant economic loss for owners because of antibiotic costs and loss of income resulting from discarded milk, although ceftiofur can be used without discarding milk. Veterinarians inexperienced with other treatment options do not discriminate or differentiate metritis based on severity, duration, or association with systemic signs and may be too quick to suggest systemic antibiotic therapy.

Systemic antibiotics are indicated when metritis causes systemic illness in recently postpartum cattle. Knowing that most recently (,10 days) postpartum cattle have mixed (A. pyogenes, anaerobes, coliforms, or others) infections and that chronic endometritis patients are more likely to be mainly A. pyogenes influences the choice of antibiotic. For example, penicillin would be effective against A. pyogenes and most opportunistic anaerobes such as F. necrophorum and Bacteroides sp. It is, however, unlikely that penicillin would eliminate concurrent coliform infection. Procaine penicillin (22,000 U/kg once daily) would likely maintain effective concentration in the uterus. Ceftiofur may be more effective against coliforms and was found to have lower mean inhibitory concentration (MIC) against A. pyogenes and anaerobic bacteria cultured from the uterus than did oxytetracycline. Ceftiofur derivatives have been shown to reach concentrations in both uterine tissue and uterine fluid of healthy postpartum cows that exceeds the MICs for E. coli, F. necrophorum, Bacteroides spp., and A. pyogenes. Ceftiofur is currently the most commonly used antibiotic for treating metritis in our hospital. Valuable cows are sometimes treated with ceftiofur at a dosage higher than the label dose of 2.2 mg/kg once daily. Oxytetracycline dosed at 11 mg/kg twice daily may only establish uterine tissue concentrations of 5 mg/kg—a level thought to be less than that required to kill A. pyogenes. This is interesting and somewhat difficult to fathom in light of the apparent widespread success experienced by veterinarians treating septic metritis patients with once-daily systemic oxytetracycline. The apparent contradiction may be explained partially by dosage because many veterinarians administer 13.2 to 15.4 mg/kg oxytetracycline, which can be nephrotoxic. It could also be theorized that oxytetracycline somehow manages to control or reduce populations of organisms other than A. pyogenes that produce endotoxins or exotoxins that result in the majority of systemic signs. A combination of a systemic sulfa drug (sulfadimethoxine) and oxytetracycline also has been used successfully by many practitioners as systemic therapy for metritis associated with illness in recently postpartum cattle. Unfortunately few scientific data are available regarding antibiotics such as ampicillin and sulfonamides as regards systemic therapy of metritis.