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In: Bubaline Theriogenology, Purohit G.N. and Borghese A. (Eds.). International Veterinary Information Service, Ithaca NY (www.ivis.org), Last updated: 10-Jan-2013; A5715.0113

Maternal Dystocia and Uterine Torsion in Buffaloes

G. N. Purohit Department of Veterinary Gynecology and Obstetrics, College of Veterinary and Animal Science, Rajasthan University of Veterinary and Animal Sciences, Bikaner Rajasthan India. Cattle and buffalo are considered the species in which the incidence of dystocia appears to be highest [1]. Parturition appears to be easier in the river buffalo because of a capacious pelvis, a larger area of ileum and the free and easily separable fifth sacral vertebra [2]. Compared to cows, buffaloes have a less conspicuous shorter and narrower cervix, smaller and less tight vagina and elongated and wide apart vulvar lips (Fig. 1) [3]. In spite of a longer gestation period in buffaloes (305 to 320 days for the river and 320 to 340 days for the swamp buffalo [4]), lesser time is required for completion of first and second stages of labor [2,5,6] (70 and 20 minutes in river buffalo) and there is a preponderance for parturition during night hours [7]. The incidence of dystocia is considered to be higher in river than in swamp buffalo (in which it has not been described) [1] and also in primipara than in pleuripara [4], however, a few studies consider higher incidence of dystocia in pleuriparous buffaloes [8]. In a recent analysis, significantly higher proportion of dystocia affected buffaloes were in the first and second parities compared to all other parities [9].

Figure 1. The vulvar lips of a buffalo. To view click on figure

Causes of Dystocia in Buffaloes

The causes of dystocia are generally classified into the maternal and fetal causes. Buffaloes are known to have greater incidence of maternal dystocia [1,10,11], however, in several other studies; a higher incidence of fetal dystocia was recorded [8,12,13]. In the authors experience buffalo generally have fewer problems with the dilation of the birth canal compared to cattle and there is a greater incidence of uterine torsion in buffaloes [9].

Maternal Causes of Dystocia

The maternal causes of dystocia are considered to be arising either because of the constriction/obstruction of the birth canal or due to a deficiency of the maternal expulsive force [1,14]. 1. Constriction/Obstruction of the Birth Canal The constriction/obstruction of the birth canal can result in maternal dystocia and can be due to pelvic abnormalities, vulvar or vaginal stenosis, neoplasm of the vagina and vulva, vaginal cystocoele, incomplete cervical dilation, uterine torsion and ventral displacement of the uterus. An uncommon cause of constriction of birth canal is carcinoma of the urinary bladder [15,16] with metastasis in the cervix.
1.1. Pelvic Abnormalities

Pelvic abnormalities of the mother that can result in dystocia include small size of the pelvis [9], pelvic deformities or exostoses, osteomalacia and hypoplasia of the vagina and vulva [2]. Breeding of heifers at too young an age, breeding of poorly grown heifers, or breeding of heifers and cows that had pelvic fractures, can result in a smaller pelvis of the mother culminating in dystocia at parturition. Breeding of small sized breeds of buffaloes with breeds of larger size can result in fetuses of bigger size getting stuck in the small sized pelvis of the mother, however; this has not been documented for buffaloes. In buffaloes, the symphysis pubis is not fused completely as it is in cows [17], however, a narrow pelvis is a known cause of dystocia in the buffalo [18]. The incidence of narrow pelvis has been recorded to vary between 2.67% [9] and 7.79% [8]. The incidence of pelvic deformities as a cause of dystocia in buffaloes is described to be 1.2% [19]. In cows and buffaloes, the incidence of narrow pelvis is known to be 9.2% [12]. Pelvic fractures can result into a narrow pelvic canal [20].
Clinical Signs

Usually, there is a lack of progress in the second stage of labor. If the fetus is able to enter the pelvis partially, severe non-progressive straining occurs. If the fetus is too large, then there is no progress in delivery subsequent to first stage of labor. Vaginal examination must be done to compare the fetal and pelvic size. Any previous fractures (Fig. 2) can be ascertained by the palpable presence of calluses or gross change in the shape.

Figure 2. A buffalo with pelvic fracture. Note the angulation of the right side of the hip. To view click on figure
Management of Dystocia

On manual palpation, clinicians must assess whether the fetus can pass through the birth canal with assistance. If this seems possible traction must be applied on the fetus after plenty of lubrication. However, excessive traction in a narrow birth canal is not advisable. It is better to opt for a caesarean section if the birth canal is too narrow, or if it is coupled with fetal postural abnormality [1].
1.2. Vulvar or Vaginal Stenosis/Stricture/Rupture

Formation of scar tissue due to injuries sustained during previous calvings in aged animals, improper relaxation during parturition, congenital stenosis of the vagina, vaginal obstruction by fibrous bands [21], perivaginal abscesses or cysts can occlude the genital passage and obstruct the delivery of the fetus. Spontaneous vaginal ruptures during parturition (Fig. 3) with fetal legs or ovaries entering the ruptured vagina have been observed in buffaloes [22,23]. Occasionally herniation of intestines through the rupture has been reported [24,25]. Fetal parts may get stuck in a ruptured vagina and result in dystocia [26], or the gravid horn may sometimes prolapse through the vaginal rupture [27]. Postpartum vaginal ruptures can sometimes result in prolapse of abdominal organs [24]. Vaginal cysts have been seen in buffalo [28] but they seldom occur at parturition.

Figure 3. A postpartum buffalo with vaginal rupture. To view click on figure

Clinical Signs

Improper vulvar relaxation may be confirmed clinically and there may be difficulty in inserting a lubricated hand into the birth canal. Improper vaginal relaxation is evident on internal examination of the vagina. Perivaginal abscesses or hematomas may be palpable as

soft or firm fluctuating masses pressing the vaginal walls inwardly [1]. Vaginal ruptures can be located by careful palpation. Fluid accumulations can be seen lateral to the vulva (Fig. 4) subsequent to vaginal ruptures during parturition.

Figure 4. A postpartum buffalo with vaginal rupture. Fluid accumulation lateral to the vulva is visible. To view click on figure
Management of Dystocia

The suggested management of a constricted vulva is gentle manipulation with or without an episiotomy cut, about one third down the lateral wall of the vulva through the skin mucosa junction. Mucosal folds in the vagina caudal to the cervix obstructing the passage of the fetus can be broken manually. The use of creams containing prostaglandins E2 are common practice in medical obstetrics and can be tried in functional non-dilation, however, in large sized perivaginal abscesses or hematomas; it is a wise decision to opt for a caesarean section rather than to apply undue traction. The fetus must be delivered by traction in the presence of vaginal ruptures which must then be sutured. Likewise, the prolapsed part must be replaced and the vagina sutured.
1.3. Neoplasms of Vagina, Vulva, Uterus

Sub-mucosal vaginal tumors are uncommon in buffaloes, however, squamous cell carcinoma [29], perivaginal granuloma [30], lipoma [31] and fibroma [29], have been reported but seldom seen clinically during dystocia. Tumors of the cervix include fibroma [32], adenoma, fibro-leiomyoma and squamous cell carcinoma. Carcinoma of the cervix has been recorded in the buffalo [15,16]. The tumor masses in cervix and vagina seldom obstruct the birth canal and are usually noticed subsequent to parturition when they prolapse out. Tumors of the uterus are recorded from genitalia usually obtained postslaughter and include adenoma [33], leiomyoma [34] lipoma [33] and fibroma [29,35]. When noticed clinically, they either prevent a pregnancy or culminate in abortion [36]. The incidence of uterine tumors in buffaloes is known to vary from 0.3% to 0.7% [37].
1.4. Vaginal Cystocoele

Vaginal cystocoele has been described to occur in the buffalo [38,39] and can result in dystocia. The condition involves the protrusion of the urinary bladder either through the eversion of the organ through the urethra [40] or prolapse through a rupture on the vaginal floor [24], which is more likely in buffaloes. Since the prolapsed bladder may obstruct the birth canal, it is suggested to identify the organ and replace it back after repelling the protruding parts of the fetus, under epidural anesthesia and ample lubrication. The vaginal rupture must be sutured after replacement of the urinary bladder. The fetus can then be delivered. Vaginal cyst has been recorded in buffalo [41].

1.5. Incomplete Cervical Dilation

The dilation of the cervix at the time of delivery is essential for the easy passage of the fetus. A wide variety of changes in the hormonal milieu [42], enzymatic loosening of fibrous strands by elevated collagenase [43], and the physical forces of the uterine contractions and fetal mass, are all considered to be involved in producing a sufficient dilatation of the cervix during parturition in the buffalo [44,45]. The activation of the inflammatory network is considered to play an important role in the progress of cervical dilation [46]. An increase in inflammatory cytokines during parturition is known to effect dilation [47] as is the interplay of hormones. In buffaloes, however, cervical non-dilation is rare. Only sporadic cases have been reported [48]. Animals with delivery problems associated with the cervix are those that had already delivered many calves [49]. Cervical non-dilation can occur because of the failure of any of the mechanisms responsible for dilation described above or spasm of the cervical muscles [4] or some other poorly understood mechanisms that results in dystocia. Cervical dilation failure is commonly observed in buffaloes subsequent to correction of uterine torsion and is considered a major obstacle in fetal delivery per vaginum [50] especially in the presence of a dead fetus. Histopathological observations on buffaloes affected with uterine torsion revealed progression towards severe inflammation [51]. These inflammatory and necrotic changes in the cervix subsequent to torsion lead to failure of the cervix to dilate [51].
Incidence

The collective incidence of incomplete cervical dilation in buffaloes is described to vary from 1.78% to 5.1% [9,12].
Clinical Signs

When the cervix is fully dilated, it is not palpable as a separate structure and is continuous with the vagina. Incompletely dilated or undilated cervix is palpable through transrectal examination. By examination per vaginum only a finger or two can be inserted in a partially dilated cervix. Parts of the fetus or the water bags can sometimes be palpated at the cervix. It is uncommon for buffaloes to show poor vulvar relaxation along with improper cervical dilation (Fig. 5).

Figure 5. On the left, a parturient buffalo with improper vulvar relaxation and cervical dilation. A parturient buffalo with proper vulvar relaxation is shown on the right side. To view click on figure
Management of Dystocia

Attempts can be made to dilate the cervix manually if possible using sponge tents and local anesthetics [2], but because the cervix has many annular rings it is often not possible to dilate the bubaline cervix manually. If the fetus is present in the birth canal, gentle traction over long periods can sometimes dilate the cervix, but excessive traction is not advisable. It sometimes happens that a maldisposed fetus present in a previously dilated birth canal becomes tightly impacted because of continued uterine contractions without fetal delivery. An obstetrician must differentiate such a case from incomplete cervical dilation. If the cervix remains closed, the fetus is alive and its fetal membranes are intact, it is suggested to wait for 30 minutes to allow time for natural dilation. A common confusion for cervical non dilation appears in cases of uterine torsion. Clinicians must differentiate uterine torsion from cervical non dilation by complete vaginal and rectal examination. A deficiency of estrogen is considered to be one important cause of failure of cervical dilation [52], hence, injection of estrogens like estradiol valerate 20-30 mg IM can be helpful, however, estrogen should be given with care in a completely closed cervix because of the dangers of uterine rupture that may follow because of violent contractions. Moreover, the use of estrogens should be extremely judicious as it can result in complete milk cessation, prolapse of genitals and development of ovarian cysts [53]. Likewise, injections of oxytocin 20-40 IU, IV or IM can be given to promote uterine contractions to effect cervical dilation when the cervix is partially dilated. When the legs of a putrefied dead, fetus are present in the birth canal and the fetus cannot come out because of an incompletely dilated cervix, the authors suggest a partial cervicotomy instead of a caesarean. One or two cuts applied on the cervix are usually sufficient to deliver the calf. 2-adrenergic agonist drugs like isoxsuprine at doses of 200-300 mg IV or 0.3 mg clenbuterol IV have been suggested to relax the entire genital tract including the cervix [1] but may not always be helpful because of the complex mechanism that is responsible for cervical dilation which largely remains poorly understood. Moreover, the 2-adrenergic drugs would reduce uterine contractions and hence delay parturition. Thrice hourly massage (15 min each) with 1 liter of sodium carboxymethylcellulose has been suggested [54] to achieve sufficient cervical dilation for fetal delivery when the cervix does not dilate after uterine torsion correction. Prostaglandin injections have also been suggested subsequent to torsion correction when the fetus is alive and the cervix is not sufficiently dilated [55]. Cesarean section is indicated if the cervix is found hard and lobulated subsequent to correction of uterine torsion in buffaloes with a dead fetus [54]. Cesarean section appears to be the best solution when all attempts at cervical dilation have failed. Use of relaxin as a cervical ripening agent and its use for inducing labor in human subjects still remain unclear [56] and hence, its use in animal therapy is out of the question because of the high cost.
1.6. Uterine Torsion

The torsion of the uterus usually occurs in a pregnant uterine horn and is defined as the twisting of the uterus on its longitudinal axis [1]. The pregnant uterus rotates about its long axis, with the point of torsion being the anterior vagina just caudal to the cervix [1] (post cervical torsion). Less commonly, the point of torsion is cranial to the cervix (pre-cervical torsion). Uterine torsion during pregnancy [57,58], at parturition [59-62], or post-partum

[63] is one of the complicated cause of maternal dystocia in buffaloes culminating in death of both the fetus and the dam if not treated early. The degree of torsion is generally 90 to 180 although it can occur up to 360 or even more. Because of the rapidity of fetal death that ensues following torsion and the uterine adhesions with visceral organs that develop, uterine torsion must be considered an emergency. Torsion can result in hemoperitoneum if it is caused by horn butting between animals [64]. A rare case of uterine torsion in a buffalo carrying twin fetuses has been reported [65].
Incidence

The incidence of uterine torsion is considered to be higher in buffaloes although most reported data originate from clinical records and not from actual calvings at organized farms. A retrospective data analysis (2001-2011) of our University farm at Vallabhnagar revealed a zero incidence in 529 calvings of the Surti breed. Data involving clinical cases report that uterine torsion is considered to be the single largest maternal cause of dystocia in buffaloes with incidence as high as 56 to 67% [9,18,60,66] and up to 70% [11]. Uterine torsion cases in buffaloes are 6783% of the dystocia presented at the referral hospitals [14,67-70]. Uterine torsion has been reported mostly in dairy type buffaloes of India, Pakistan [71] and Egypt [72,73], however, reports of its occurrence in the swamp buffalo are not seen. The incidence is known to be higher in pleuriparous buffaloes [18,59,61,74] with maximum frequency during second and third calvings [58,66]. Although a seasonal incidence has been described in buffaloes [18,70], it appears to be because of higher seasonal calvings. The usual age of buffaloes that suffer from uterine torsion is 4-12 years old [74,75].
Etiology

The exact etiology of a higher incidence of uterine torsion in buffalo continues to be poorly understood. The most logistic explanation for rotation of a pregnant uterus on its axis appears to be the instability of the uterus during a single horn pregnancy and inordinate fetal or dam movements [1]. The bubaline amnion is fused at many places to the surrounding allantois, which is attached to the uterine wall [76] and the uterus lies on the abdominal floor during mid and late gestation with no stabilizing attachments hence, rotatory fetal movements during the second stage of labor or late gestation would rotate the uterus. A smaller quantity of fetal fluids and an associated decrease in the size of uterus at the terminal stages of gestation and a lower uterine tone at this time [77], increase the fetal discomfort and this initiates further fetal movements and a greater degree of torsion. A large number of predisposing causes have been described [78,79] for uterine torsion and include anatomical factors, close confinement, hilly tracts, external injury and wallowing habits of the buffaloes and the lowering of front legs by the animal first, when lying down [1]. The higher occurrence of the problem in buffaloes is also hypothesized to be because of a deep capacious and pendulous abdomen of buffalo [69], inherently weaker muscles of the broad ligaments [80-82] and the wallowing habits of the buffalo [69]. However, none of the uterine torsion affected buffaloes presented at a referral hospital, had a history of wallowing or grazing on hills [83] and daily forceful wallowing of pregnant buffaloes failed to induce uterine torsion in one study [84]. The role of broad ligament musculature in the occurrence of uterine torsion is highlighted from the observation that broad ligaments of buffaloes

suffering from uterine torsion are thin and have less muscles compared to their counterparts with other types of dystocia [81]. At least 25% females born to uterine torsion affected dams and 11% non-pregnant buffaloes have poorly developed muscles in broad ligaments [85]. Additionally, broad ligament musculature is better arranged in cattle compared to buffaloes, thus providing better stability to the pregnant uterus of cattle [70,86]. A lack of dorsal attachment of the broad ligament during pregnancy [85] and a lack of support of the broad ligament in the post cervical area predisposes buffaloes to more occurrence of post cervical torsion [87]. A low estradiol and high progesterone during the immediate prepartum period may make the uterus flaccid increasing the risk of uterine torsion [83,88]. Some exciting causes for the occurrence of uterine torsion have been described [9] and include external injury, lack of exercise and irregular movement of animals. Uterus didelphus has been described as one of the causes of uterine torsion in the buffalo [89]. Slight rotations (below 90) are symptomless clinically and may be corrected spontaneously but rotations of higher degree usually do not detorse spontaneously. Among the referred cases of torsion, pregnancy period is generally complete in 8385% of buffaloes [14,70]. Occasionally, uterine torsion can occur between 58th month of pregnancy [90,91]). Torsion of uterus may accompany intestinal obstruction [92], hemoperitoneum [64], uterine rupture [75] and formation of adhesions of uterus with surrounding viscera [93].
Nature of Uterine Torsion

A pregnant uterine horn may rotate at mid to late gestation, at normal parturition time, or sometimes postpartum. The horn may rotate to its right (clock-wise) or left side (anticlockwise) with degree of rotation from 90 to 720. The point of rotation can be caudal to the cervix (post cervical) [94] or just cranial to the cervix (pre-cervical). Uterine torsion generally occurs at late pregnancy and at parturition in buffaloes [95], on the right side of the abdomen at a point just caudal to the cervix and usually rotates to 180 or more from its axis [1,75,95]. Post cervical uterine torsion is common in buffaloes (8799%) [14,59,67,68,70,75,96,97], although in one study pre-cervical torsion was predominant [55]. A preponderance of right side uterine torsion in buffaloes (9598%) [14,55,67,68,70] is postulated to be because of the absence of a muscular fold on the right broad ligament in the buffalo [81,86]. Many other studies also recorded right-sided uterine torsion in buffaloes [1,9,55,58,61,70,81,86,97]. It is probable that pregnancies occurring in the left horn may be rotating towards the left side only when the rumen is partially filled whereas pregnancies in the right uterine horn can rotate easily towards the right side because of non existence of any stabilizing structure on this side.
Clinical Signs

The usual clinical signs are the onset of labor without delivery of fetus and/or fetal membranes and later regression of parturition signs [18,98]. The animal may show signs of mild discomfort. The animal may adopt a rocking horse stance [79] and show mild colic pain and constipation [95]. Partial anorexia, dullness and depression may be evident [59,95]. Restlessness and arching of back and colic may be seen in some buffaloes [58].

One or both lips of the vulva are pulled in (Fig. 6) because of torsion of the birth canal. Vaginal examination reveals twisting of the vaginal mucous membranes and the hand cannot be passed deeper into the anterior vagina which has a conical end in uterine torsion with a degree of 180 or more. In lesser degree torsions, however, the fetus can sometimes be felt. The direction of the vaginal fold twisting is considered the evidence for the direction of the torsion. On trans-rectal examination, the twisted uterine horn can be felt and the broad ligament on the side of torsion is rotated downwards sometimes palpable under the uterus and the ligament on the opposite side is tense and stretched and crossing to the opposite side. The positive diagnosis of uterine torsion should thus, be based on the location of broad ligaments palpated per rectum. Animals at many locations may be presented to the obstetrician after varying times since the first onset of labor; hence, the clinical signs of shock and toxemia may be evident depending upon the severity of the torsion, previous handling, death of fetus and post-torsion complications.

Figure 6. A buffalo with uterine torsion showing twisting of the vulvar lips towards the left side. To view click on figure
Clinical Pathology

The pathophysiological alterations that occur following uterine torsion have been recently reviewed [77]. These alterations have been proposed to be used as prognostic indicators for uterine torsion [75,95,99]. A brief mention is made on a few of the studied parameters. Uterine Changes: Rotation of the uterus compresses the middle uterine vein which results in disturbances in venous circulation and increase in carbon dioxide tension in the fetal blood. Consequently, an uncomfortable fetus makes vigorous movements that may further increase the degree of uterine torsion. With the increase in degree of torsion, there is compression of the middle uterine artery and oxygen going to the fetus is decreased [100,101]. Limited arterial perfusion and venous outflow in the twisted uterus leads to ischemia, hypoxia and cell death causing irreversible damage to the endometrium, myometrium and ultimately death of the fetus. Continued failure of blood supply results in loss of uterine wall elasticity and viability, and hence the uterine wall becomes necrosed, brittle, fragile and prone to rupture [77]. Inflammatory changes can cause adhesions of the uterus with surrounding abdominal tissues [102]. Macroscopically, the color of the uterine wall changes from rose-pink to blue-purple and grey following torsion indicating the progressive metabolic deterioration of uterus [103]. Congestion, edema and hematoma are present in the uterine ligaments, meso-ovarium and ovaries [103]. The damage to uterine tissue and its regenerative potential following the rotation of uterus can be evaluated from

plasma indicators, viz. serum haptoglobin and creatine kinase [77], which increases further following the correction of the torsion by rolling the dam [104]. Blood Components: Uterine-torsion affected buffaloes suffer from normocytic normochromic anemia (decrease in the RBCs, Hb and PCV) due to the accumulation of metabolic waste products or relatively large loss of blood during abnormal parturition [99], although marginal differences were recorded in a few clinical studies [105,106]. The leukogram of torsion affected buffaloes reveal lymphocytopaenia, neutrophilia and monocytosis in association with eosinopenia [99,107-109] which continues till Day 3 postpartum in surgically corrected cases of uterine torsion [105]. Huge decrease in the total plasma proteins and albumin is consistently observed in torsion affected buffaloes [99,106,107,110,111]. This hypoproteinemia is associated with liver malfunction and negative nitrogen balance because of reduced protein intake. Occurrence of torsion of uterus is a highly stressful event as revealed by the huge increase in plasma cortisol which increases further by 1530% following detorsion of uterus through the rolling of the dam [99,112-114]. Hyperglycemia in torsion-affected buffaloes is related to activation of stress axis and increased cortisol release which leads to gluconeogenesis [99,112]. In fact, plasma ketones are elevated in these buffaloes due to improper utilization of glucose [112]. Liver and Renal Functions: Following uterine torsion and after its correction by detorsion or surgical treatment, the activities of aspartate amino transferase (AST), alanine amino transferase (ALT), glutamate dehydrogenase (GLDH), creatine phosphokinase (CK) and gamma glutamyl transferase (GGT) are increased [99,105-108,115] which usually stabilize within 10 days after surgical treatment of uterine torsion [116]. The increase in plasma AST and muscle specific CK is attributed to great muscular exhaustion produced by strong abdominal contractions following uterine torsion [117,118]. At the time of presentation of a uterine torsion case, a substantial increase in plasma urea and creatinine indicates poor prognosis [99,116]. In uterine torsion, ureters lying near the broad uterine ligaments are constricted thus the urine output is reduced and renal functions may be affected [116]. Moreover, the presence of stress-induced decrease in blood flow to kidneys, shock, dehydration and nephropathy resulting from toxic substances liberated by the dead fetus may cause acute or chronic renal insufficiency, leading to decrease in the urea and creatinine elimination [99,119].
Diagnosis:

History and External Signs: Diagnosis is easy when abnormal symptoms appear at the time of parturition. Typical history of a case of uterine torsion will indicate that the animal was about to calve, as shown by milk letdown and relaxation of pelvic ligaments, but adequate time had passed and still there was neither the rupture of fetal membranes nor the appearance of the fetus from vulvar lips [120]. External signs of uterine torsion like displacement of upper commissure of vulva towards inward, left or right, vulvar edema due to compression of the vaginal veins and lymphatic drainage, and a slight depression of lumbo-sacral vertebrae are not the consistent features [77]. Post-cervical torsions can be easily diagnosed by vaginal examination. About 6696% torsions are post-cervical in which the twist of the rotated uterus extends caudal to the

cervix and involves the anterior vagina in rotation. During trans-rectal examination, attention should be paid to the course of broad ligaments to rule out pre-cervical torsion. In normal pregnant animal, the broad ligaments can be palpated on the sides of uterus, whereas in pre-cervical (and post-cervical) torsion, the orientation of the broad ligaments is altered and these can be felt on the crossed and twisted uterus. Accurate determination of the direction of torsion through trans-rectal examination is necessary prior to making attempts at correction, as detorsion in the wrong direction will worsen the problem.
Management of Dystocia

Cases of uterine torsion must be considered an emergency and therapy must be instituted early. It is imperative to precisely evaluate the patients general condition before any handling. The patient must be evaluated for presence of toxemia and shock, since cases presented to the obstetrician after 36 hours, are likely to have one or more of these conditions. The authors suggest the infusion of plenty of fluids along with corticosteroids and antibiotics, whenever necessary, to combat toxemia and shock before handling cases presented after 36 hours delay. It is also usual to assess the type of previous handling or therapies used including previous rolling of the animal. Cases presented after 36-72 hours are likely to have advanced toxemia, fetal death coupled with loss of fluid and uterine inertia. The incidence of uterine rupture is fairly high and therefore a full examination should be made before treatment. It is not common, however, uterine torsion can result in problems like intestinal obstruction [92] and rotation of the urinary bladder in torsion affected buffaloes [121]. Histamine levels are known to be high in buffaloes suffering from uterine torsion [122], hence, antihistaminics should be administered. The technique suggested to detorse the rotated uterus in buffaloes include rotation of the fetus and uterus per vaginum [1,9], rolling of the animal, and laparohysterotomy [1,79]. The choice of the method to be adopted depends on the nature and intensity of the torsion, the viability of the fetus and the time lapse since the onset of dystocia. Rotation of the fetus per vaginum is possible only in mild degrees of torsion where the obstetricians hand can touch the fetus and sufficient fluids are present in the uterus [55,77]. The fetus is grasped by a bony prominence such as elbow, sternum or thigh and swung from side to side before being pushed right over in the opposite direction of torsion. If both fetal limbs are palpable, they can be tied in the cuffs of a caemmerers torsion fork or a Kuenhs crutch and an assistant can rotate them. If the manipulation is successful, the torsion will disappear and the vaginal folds will regain normal shape and the fetus can be delivered with little difficulty. However, sufficient lubrication must be available in the birth canal and uterus before attempts at rotating the fetus are made using instruments. When too much time has passed since the onset of the problem, the uterus will tightly contract around the fetus and detorsion with this method is not possible. Success rate is high if the dam is standing, the cervix is sufficiently dilated to grasp the fetus and the fetus is alive. Rolling the buffalo utilizes the principle of rolling the animal around its uterus while the uterus remains static. It is one of the oldest and simplest methods to relieve uterine torsion in buffaloes. The animal must be rolled preferably on grass with its head lower than the rear quarters [123,124]. Vicious animals must be given a sedative. The animal is laid down in lateral recumbency on the same side to which the torsion is directed. The two hind legs are

tied together by a rope [55]. Both forelegs are also tied together using a separate rope. The animal is rolled suddenly to the direction of the torsion of the uterus. The rapidly rotating body of the buffalo overtakes the more slowly rotating gravid uterus. After the animal has been rolled to 180, its body must be brought back to the original position slowly so that it can be rolled once again. After two rolling, the birth canal should be examined to determine whether the torsion is corrected or not. If corrected properly, the spiral folds and stenosis of the birth canal should disappear and if the cervix is dilated, the fetus can be palpated with ease. Plenty of blood stained fluid comes out of the birth canal if the cervix is open, and this is sufficient evidence of torsion correction. If the torsion is not corrected, the rolling procedure should be repeated 3 or 4 times. If after 4 attempts, the torsion is not corrected, then other procedures for correction of torsion must be considered as uterine rupture can result due to violent rolling [96,125]. Although, torsion may be corrected by rolling animals within 36 hours of the torsion, the potential dangers of uterine rupture with continuous rolling must always be kept in mind. If the vaginal folds are increasing after a rolling, the rolling must be done towards the opposite side. Sometimes, after the correction of torsion, it may take 12 hours or more for the cervix to dilate and hence one should not take rapid action of removing the fetus after torsion correction without proper cervical dilation. Prostaglandin injections are suggested subsequent to torsion correction if the cervix is not dilated. Fetuses are delivered 12-24 h later in such cases. Cervical dilation failure is commonly observed in buffaloes subsequent to correction of uterine torsion and is considered a major obstacle in vaginal fetal delivery [50], especially in the presence of a dead fetus. Unrelieved uterine torsion can also culminate in ring womb [126]. Approaches to dilate the cervix include administration of prostaglandins [1], administration of hyaluronidase [127] and the use of sodium carboxymethylcellulose [54]. Thrice hourly massage (15 min each) with 1 liter of sodium carboxymethylcellulose has been suggested [54] to achieve sufficient cervical dilation for fetal delivery. Prostaglandin injections have also been suggested subsequent to torsion correction when the fetus is alive and the cervix is not sufficiently dilated [55]. Cesarean section is indicated if the cervix is found hard and lobulated subsequent to correction of torsion in buffaloes with a dead fetus [54]. Histopathological observations on buffaloes affected with uterine torsion revealed progression towards severe inflammation [51,102]. These inflammatory and necrotic changes in cervix subsequent to torsion lead to failure of the cervix to dilate [51]. A modification of the rolling technique called Schaffers method, has been described by Arthur [128] and recommended widely [78,91,128] for detorsion of uterus in cows and buffaloes. In this method, a slightly flexible wooden plank of 9 to 12 feet long and 8 to 12 inches wide is placed on the recumbent animals flank with the lower end of the plank on the ground (Fig. 7). An assistant stands on the plank while the buffalo is slowly turned over by pulling the ropes (Fig. 8, 9 and 10). A slight modification of this method has been suggested for the buffalo [129]. The advantages of this technique are that the plank fixes the uterus while the animals body is turned and that, because the buffalo is turned slowly less assistance is required and it is easier for the veterinary surgeon to check the correct direction of the rolling by vaginal palpation [79].

Figure 7. The approach for uterine torsion correction in buffalo using the Schaffers method. To view click on figure

Figures 8, 9 & 10. Rolling of a buffalo with uterine torsion using the Schaeffer's method. To view click on figure Usually, the first rolling is successful in the buffalo [60,61,74]. In Egyptian buffaloes, Schaffers method was described as the best method for rolling [130,131]. However, the thick skin of Indian buffaloes causes skidding of the plank at the time of rolling. Moreover, the pendulous abdomen of the Indian buffalo warrants greater pressure for the fixation of the pregnant uterus. Therefore, modifications were made to Schaffers method, and it is now known as Sharmas modified Schaffers method [132]. Because buffaloes have a capacious abdomen, more pressure is required on the free end of the plank that is being modulated by an assistant resulting in better detorsion compared to the Schaffers method [132]. Using this method, the detorsion rate in Indian buffaloes was 90% in comparison to 40% success rate achieved by Schaffers method [14,132]. When torsion is pre-cervical and duration is <36 h, 3672 h or >72 h, the animals successfully detorsed are 82, 100 or 67%, respectively [96]. In buffaloes, detorsion followed by vaginal delivery is easily accomplished when torsion is <180. With an increase in degree of torsion, more rolls are required to detorse the uterus and the likelihood of a vaginal delivery is decreased [99]. It is suggested that if the torsion is not relieved after 3 rolls then failure should be admitted and surgery is indicated [66]. Buffaloes subjected to injudicious rolling (>3 rolls) had a lower survival rate when compared to those animals where rolling was well planned [133]. Depending upon the prior handling of a case of torsion, buffaloes subjected to 13 rolls had 4478% survival rate, whereas those subjected to more than 3 rolls had 3556% survival rate [133]. In another study, survival rate of buffaloes requiring 12 rolls and 34 rolls for complete detorsion of uterus was 85 and 43%, respectively [113]. Excessive adrenal stimulation due to 1 to 2 extra rolls causes slower decline in plasma cortisol during postdetorsion period [113]. In long standing cases of torsion (>72 h), with apparent

reabsorption of milk and tightened pelvic ligaments, attempts to achieve detorsion of the uterus are usually unsuccessful due to the development of adhesions between the uterus and the adjoining abdominal organs [133]. Detorsion of the uterus in these cases is not possible even after detachment of adhesions [59,134]. Both tissue anoxia and serosal injury following the torsion of uterus are important factors in promoting adhesion formation in the abdominal cavity [135]. The average number of turns required in buffaloes are 2.5 [74] and vaginal delivery takes a longer time after detorsion. Buffaloes with a fully dilated cervix at detorsion had maximum survival [61,66] and detorsion failure occurs in 20% of the cases [66]. In the authors experience, detorsion failure is common in cases presented after 36 hours of delay and in animals where a dead emphysematous fetus is present or uterine adhesions have formed or uterine rupture has occurred. Similar views have been expressed by other workers [136,137]. It is known that detorsion is difficult in the presence of a dead fetus [70]. Myometrial degeneration and endometrial damage is increased in cases of uterine torsion that are delayed for treatment [138]. Laparohysterotomy is suggested in cases of uterine torsion that fail to be corrected by rolling or in long standing cases where the fetus is dead and uterine adhesions/rupture are likely. The outcome of a caesarean when the fetus is dead and emphysematous can be grave. It is advisable to check the patient to assess the general condition before deciding to operate. Caesarean is a method of choice in cases presented with a closed cervix or a dead fetus with subsided symptoms of parturition [18]. It is better to administer plenty of fluid therapy, antibiotics and corticosteroids before starting the operation. Different operative sites for a caesarean are suggested including the right [136,139] or left flank, midline (on or parallel to linea alba), horizontal incision above arcus cruralis [136], or appropriate incision in the right [59], left lower flank [58,60,125] or an oblique ventrolateral approach with the animal in right lateral recumbency [79,140]. The author and a few other workers [10,141] consider the left oblique ventrolateral approach with the animal in right lateral recumbency as a better operative site, as it results in minimum postoperative complications. The anesthesia usually required is mild sedation with local infiltration. Although many anesthetic combinations have been suggested for epidural analgesia including xylazine and medetomidine [142], xylazine and ketamine [143] or xylazine and detomidine [144], however, xylazine is used as a sedative during laparohysterotomy. Doses of 0.05 mg/Kg of xylazine produce mild sedation, and 0.01 to 0.015 mg/Kg induces deep sedation in buffaloes [145,146], however, a lower dosage is suggested as this drug induces marked salivation and bradycardia. Alternatively, combining 0.04 mg/Kg IM of atropine followed by 0.04 mg/Kg of xylazine is suggested to minimize the side effects of xylazine [147]. During the laparohysterotomy, the uterus is brought to the site of incision by holding a fetal extremity and an incision is made. The fetus is removed with due care. Because of fetal death and the consequent uterine adhesions that develop in cases operated after 36 hours, it is not always possible to detorse the uterus before the removal of the fetus. It is uncommon for rupture of the uterus to occur when attempting to correct torsion by rolling the animal. Such ruptures must be searched for during the operation and if possible repaired. If the tear is not reachable, the best option is to inject 20-40 IU oxytocin within the uterine wall at 3-4 or more locations to contract the uterus. The abdominal wound is closed routinely.

The major complications that can occur following uterine torsion are fetal and maternal death [66], uterine rupture, vaginal rupture [125,133] and poor fertility following correction of a long standing case of torsion. Sometimes fatal peritonitis or expulsion of the fetus in the abdominal cavity from a uterine rupture is possible. Uterine torsion affected buffaloes are under acute stress as suggested by elevated plasma cortisol and suppressed ruminal, liver and kidney functions [112,113,148]. In addition, the process of detorsion further enhances adrenocortical activity and potentiates the existing stress on the dam. Attempts made to alleviate stress of uterine detorsion by administration of tranquilizers, such as acepromazine, chlorpromazine or diazepam, before subjecting the dam to detorsion process, have failed to achieve desired success as revealed by the regular monitoring of plasma cortisol [149]. However, dexamethasone administration during immediate postpartum period of successfully detorsed animals, decreases stress and thus increases the chances of survival of the dam [150]. Moreover, stress-induced oxidative damage is reduced and post-dystocia convalescence is improved when antioxidants like vitamin E and selenium are administered to uterine torsion affected bovines [151]. As revealed by plasma concentrations of liver enzymes in uterine torsion affected bovines, the first post-operative week should be critically observed and a liver protection therapy should be instituted during this period [81]. Uterine torsion cases suffer from respiratory alkalosis without much metabolic alterations which stabilizes following detorsion [152]. Determination of bloodgas and acid-base parameters followed by appropriate fluid and electrolyte therapy in torsion affected buffaloes shall prognosticate the chances of survival of dam as well as the calf. As a matter of critical care, monitoring blood-gas and acid-base status as well as electrolytes should be a mandatory procedure in torsion affected buffaloes [152]. With the increase in duration of uterine torsion, plasma and blood volume decreases and the animal progresses towards dehydration and toxemia, this suggests the requirement of immediate fluid therapy [153,154]. Torsion cases can be resuscitated successfully using intravenous administration of small amount of hypertonic saline and dextran40 followed by oral administration of large amount of fresh water. This is a quicker, practical, easy and effective method compared to intravenous administration of huge amounts of normal saline [155]. Dextran40 can maintain elevated plasma and blood volume for longer durations and thus decreases the degree of dehydration [156]. In fact, alterations in plasma cortisol, albumin and glucose following administration of hypertonic saline, dextran40 and oral fluids lead to alleviation of stress [155].
1.7. Downward (Ventral) Displacement of the Uterus

Ventral displacement of the uterus is an uncommon cause of dystocia in buffaloes [97]. It is seen in animals with a ventral hernia or rupture of the prepubic tendon where the pregnant uterus passes downward into the point of the hernia.
Clinical Signs

If the herniation is large enough, a herniated uterus can be recognized externally with ease. The uterus may herniate on the left or the right side of the abdomen. Affected animals have difficulty in lying down and getting up. Large left side herniation of the uterus may be associated with mild degree torsion of the uterus and would displace the rumen cranially

with resultant rumen function disorders. Herniation of a lesser degree results in a first stage labor without fetal delivery. The birth canal may sometimes be occluded.
Management of Dystocia

In mid-gestation herniations, support must be given to the abdominal floor by tying strong canvas around the abdomen. Such pregnancies would continue to term with support except, when the herniations are large sized. In herniations at or around parturition, it is better to restrain the animal in dorsal or lateral recumbency to assist the delivery of the fetus because the fetus may be beyond reach in a standing animal. An alternative is to raise the abdominal floor using a wooden plank or a strong canvas held and lifted by two assistants. If vaginal delivery is not possible, then a caesarean section must be performed. Further breeding from such animals should be discouraged.
1.8. Carcinoma of Urinary Bladder

Carcinoma of the urinary bladder is extremely rare in the bubaline species. The transitional type cell carcinoma [15] seldom causes dystocia but results in dysuria, however, squamous cell carcinoma is associated with extensive fibrosis with metastasis in the wall of cervix, vagina and perivaginal adipose tissue resulting in marked constriction of the birth canal and dystocia. Clinically hard polyploidy growths are palpable over many places in the birth canal. The affected animals show dysuria and futile efforts to deliver the fetus [16]. Attempts to dilate the birth canal and deliver the fetuses by injecting estrogens and oxytocin usually fail and the fetus should be delivered by caesarean section [16]. The dysuria continues even after fetal delivery and animals usually die or must be euthanized. 2. Failure of the Expulsive Forces The failure of expulsive forces can be due to either abdominal or uterine causes. The condition where the uterine expulsive forces fail to deliver a fetus is known as uterine inertia. The uterus quietens and the progression of the fetus out of the birth canal does not follow because of the lack of contractions in the uterus. Uterine inertia is classified conventionally into primary and secondary uterine inertia [91].
2.1. Primary Uterine Inertia

In this condition, although cervical dilation occurs and the fetus is in normal presentation, position and posture, it is not delivered due to the lack of uterine contractions. The process of birth begins but does not continue into the second stage of labor. The most common cause of primary uterine inertia in buffaloes is considered to be hypocalcaemia [157], with the animal showing signs of milk fever as calving is about to begin. Over distension of the uterus because of dropsical fetal conditions, general debility and environmental disturbances are other causes. A few of the less common causes described [91] include inherited weakness of uterine muscle, toxic infections, myometrial degeneration, senility and nervousness. The incidence of uterine inertia is known to vary between 1.78 and 5.9% [8,9]. Therapy for dystocia management includes intravenous therapy with calcium borogluconate and 15-20 IU of oxytocin IM or IV. When the cause is calcium deficiency,

animals will respond favorably and parturition process will begin. The fetus can be delivered after some time spontaneously or with a little assistance. An injection of oxytocin must be given after removal of the fetus to aid in uterine involution and placental expulsion.
2.2. Secondary Uterine Inertia

Secondary uterine inertia occurs due to exhaustion as a result of dystocia [128]. When the uterine musculature becomes exhausted subsequent to failure of delivery of a maldisposed or oversized fetus or due to obstruction in the birth canal, then the condition is known as secondary uterine inertia. The contractions in the uterus then stop or become weak and transient. The animal shows no progress in parturition after the second stage of labor. The fetal membranes are ruptured and the cervix dilated. If dystocia is prolonged without fetal delivery, the fetal fluids are expelled out and the uterus contracts tightly around the fetus. It is necessary to correct the primary cause of dystocia and deliver the fetus. Doses of oxytocin must be given after fetal delivery to regain uterine contractility. Secondary uterine inertia invariably results in retention of the placenta.
2.3. Uterine Rupture

Rupture of the uterine wall in buffaloes can occur as a result of accidental traumatic injuries, the presence of some weak points [91], or subsequent to severe uterine torsion [18,158,159]. Uterine rupture is considered the result rather than the cause of dystocia [160], the predisposing causes being uterine torsion, breech presentation and abnormal fetal movement. Small tears are insignificant and the fetus may be delivered without much difficulty. Large tears can result in the passage of the fetus into the peritoneal cavity [158]. The resulting severe hemorrhage can result in maternal death. Loops of intestines (Fig. 11) or other visceral organs can prolapse through the vulva if the tear occurs at a time when the birth canal is sufficiently dilated. The general condition of the patient in such cases is extremely poor. Such patients must be managed early with fluid therapy and laparotomy must be performed immediately. The fetus, whether it is present in the abdomen or in the uterus, must be removed and the uterine tear repaired. Parts of the fetus may sometimes project into the peritoneum through the tear and the fetus develops normally for some time, but such cases are rare. Examinations of such patients reveal the extra uterine presence of the fetus [161] and such animals may experience colic or other clinical signs. The vaginal delivery of such fetus is extremely difficult and unrewarding and hence a laparotomy is suggested.

Figure 11. A buffalo with prolapse of intestines subsequent to uterine rupture at parturition. To view click on figure
2.4. Failure of Abdominal Expulsive Forces

The abdominal musculature plays an important part in the second stage of labor to expel the fetus. Failure of abdominal expulsive forces can occur due to painful conditions, tears in the muscles, or weak muscles as are seen in old and weak animals. Conditions like traumatic reticulitis/pericarditis [162,163], painful conditions of diaphragm like hernia [164-168], may cause voluntary inhibition of attempts to strain. The birth fails to occur in such causes despite the presence of normal preparatory signs and first stage labor. In cases of abdominal distension, the fetus must be delivered with assistance with the patient in recumbent position. In conditions, like traumatic pericarditis a caesarean is suggested.
References

1. Purohit GN, Barolia Y, Shekher C, et al. Maternal Dystocia in cows and buffaloes: A review. Open J Anim Sci 2011; 1:41-53. 2. Kodagali SB. Notes on Applied Bovine Reproduction. Part II. Bovine Obstetrics. ISSAR, Gujarat Chapter, Anand, Gujarat, India 2003. 3. Agarwal SK, Tomer OS. Eds Reproductive technologies in buffalo. Indian Vet Res Institute, Izatnagar, UP, India. 1998; 10. 4. Jainudeen MR. Reproduction in the water buffalo. In: Current therapy in Theriogenology. Morrow DA, Ed. WB Saunders Company, Philadelphia 1986; 443449. - Available from amazon.com 5. Mody M, Chauhan RAS, Shukla SP. Process of parturition in buffaloes. Indian J Anim Reprod 2002; 23:141-143. 6. Ramasamy M, Singh M. A comparative study on normal and abnormal parturition in Karan Fries Cattle and Murrah buffaloes. In: Proceedings of the National Symposium Reproductive Technologies for Augmentation of Fertility in Livestock. Nov. 14-16, IVRI, India. Compendium of Abstracts. 2002; 148-149. 7. Kaushish SK, Mathur BK, Mathur AC. Factors affecting parturition in buffaloes. In: Proceedings of the XIX Annual Convention of ISSAR and National Symposium. 22-24 August, Kolkata. India. Compendium of Abstracts 2003; 38. 8. Phogat JB, Bugalia NS, Gupta SL. Incidence and treatment of various forms of dystocia in buffaloes. Indian J Anim Reprod 1992; 13:69-70. 9. Purohit GN, Kumar P, Solanki K, et al. Perspectives of fetal dystocia in cattle and buffaloes. Vet Sci Dev 2012; 2:31-42. 10. Saxena OP, Varshney AC, Jadon NS, et al. Surgical management of dystocia in bovine: A clinical study. Indian Vet J 1989; 66:562-566. 11. Nanda AS, Brar PS, Prabhakar S. Enhancing reproductive performance in dairy buffalo: major constraints and achievements. Reprod Suppl 2003; 61:27-36. PubMed 12. Sharma RD, Dhaliwal GS, Prabhakar S, et al. Percutaenous Fetotomy in management of dystocia in bovines Indian Vet J 1992; 69:443-445. 13. Singla VK, Sharma RD. Analysis of 188 cases of dystocia in buffaloes. Indian Vet J 1992; 69:563-564.

14. Srinivas M, Sreenu M, Lakshmi Rani N, et al. Studies on dystocia in graded Murrah buffaloes: a retrospective study. Buffalo Bull 2007; 26:4045. 15. Gupta PP, Kumar N. Dystocia in buffaloes due to carcinoma of urinary bladder. Indian Vet J 1986; 63:508-510. 16. Gupta PP. Infiltrative transitional-cell carcinoma of urinary bladder in a buffalo. Indian Vet J 1983; 60:934. 17. Hadi MA, Sane CR. Critical observations on certain anatomical features encountered during study of female Murrah buffalo pelvis. Indian Vet J 1965; 42:327-330. 18. Singh J, Prasad B, Rathore SS. Torsio uteri in buffaloes (Bubalus bubalis). An anlaysis of 65 cases. Indian Vet J 1978; 55:161-165. 19. Deshmukh MJ. Clinical studies on problems of parturition and post parturient reproductive disorders in buffaloes. M.V.Sc. Thesis, Punjabrao Krishi Vidyapeeth, Akola. 1975. 20. Dubay MB. Dystocia due to stenosis of pelvic outlet in a buffalo. Indian J Anim Reprod 1987; 8:156-157. 21. Azawi OI, Ali AJ, Lazim EH. Pathological abnormalities affecting buffalo cows reproductive tracts in Mosul. Iraqi J Vet Sci 2008; 22:59-67. 22. Ghuman SPS, Singh J, Honparkhe M. Protrusion of an ovary through a vaginal tear subsequent to replacement of a post partum uterine prolapsed in a buffalo. Buffalo Bull 2010; 29:308-310. 23. Dubay MB. Spontaneous vaginal rupture at parturition in a buffalo. Indian J Anim Reprod 1984; 5:115-116. 24. Dhaliwal GS, Prabhakar S, Sharma RD. Spontaneous rupture of vagina in buffalo heifers. Indian J Anim Reprod 1991; 12:98-101. 25. Rao KB, Veeraiah G. Vaginal rupture associated with herniation of intestines in a pregnant buffalo: A case report. Indian J Anim Reprod 1998; 19:170. 26. Balasubramanian S, Jeyakumar S, Pattabiraman SR. Reconstructive surgery of vulvo-vaginal tear in a buffalo heifer: a case report. Indian Vet J 2003; 80:683-684. 27. Siddiquee GM. Protrusion of gravid uterus through ruptured vaginal wall in a buffalo: A case report. Indian Vet J 1992; 69:255-256. 28. Ghuman SPS, Singh TP, Prabhakar S. Prolapse due to vaginal cyst in a buffalo. Indian J Anim Reprod 1998; 19:169. 29. Rama Rao P, Rajya BS. A note on the neoplasms of the female genital system of buffaloes. Indian Vet J 1976; 53:323-324. 30. Dhoble RL, Singh M, Gupta VK, et al. Perivaginal granuloma in a buffalo. Indian Vet J 1992; 69:845-846. 31. Dixit SN, Maira DS. Lipoma in a buffalo-cow. Punjab Vet 1970; 9:2. 32. Sharma GP, Reddy VM, Hafeezuddin M, et al. A note on fibroma of cervix in a buffalo cow. Indian Vet J 1977; 54:763. 33. Kumar N, Singh B. Some neoplasms involving female genitalia of buffaloes. Indian Vet J 1984; 61:185-187. 34. Azawi OI, Al-Sadi HI. Uterine leiomyoma in a buffalo: A case report. Buffalo Bull 2010; 29:80-82. 35. Saxena G, Rani S, Danodia H, et al. Pathological conditions in genital tract of female buffaloes (Bubalus bubalis). Pak Vet J 2006; 26:91-93.

36. Purohit G N, Kumar D, Garg N, et al. Successful removal of a fibroma from the uterus of a cow. Acta Vet Hung 2004; 52:47-50. - PubMed 37. Samad HA, Ali CS, Ahmad KMZ, et al. Reproductive disease of the water buffalo. In: Proceedings of the 10th Int Congr Anim Reprod and AI, Urbana. Vol IV 1994; 14-25. 38. Purohit GN. Etiology, antenatal diagnosis and therapy of fetal complications of gestation in large and small domestic ruminants. Theriogenology Insight 2011; 1:43-62. 39. Nanda AS. Recent Advances in Animal Reproduction and Gynaecology. USG Publishers and Distributors, Ludhiana, India. 1995. 40. Singh P, Bugalia NS, Jakhar KK, et al. Retention of urine due to eversion of urinary bladder in buffaloes. Haryana Vet 2009; 48:112-113. 41. Venkata Naidu G, Murugan M, Srinivas M, et al. Management of a cervical cyst in agraded Murrah buffalo. Buffalo Bull 2009; 28:214. 42. Kindahl H. Endocrine changes in late bovine pregnancy with special emphasis on fetal well being. Dom Anim Endocrinol 2000; 23:321-328. - PubMed 43. Rajabi MR, Dean DD, Beydoun SN, et al. Elevated tissue levels of collagenase during dilation of uterine cervix in human parturition. Am J Obst Gynaecol 1988; 159:971-976. - PubMed 44. Mannari MN. Cervical non-dilation in buffaloes. Gujarat Vet 1969; 3:37-38. 45. Deshmukh ML, Kaikini AS. Studies on problems of parturition in buffaloes-I. Maternal dystocia. Indian Vet J 1976; 53:212-213. 46. Maul H, Nagel S, Welsch G, et al. Messenger ribonucleic acid levels of interleukin-1 beta interleukin-6 and interleukin8 in the lower uterine segment increased significantly at final cervical dilation during terminal parturition, while those of tumour necrosis factor remained unchanged. European J Obst Gynaecol Reprod Biol 2002; 102:143-147. - PubMed 47. Kemp B, Menon R, Fortunato SJ, et al. Quantitation and localization of inflammatory cytokines, interleukin6 and interleukin-8 in the lower uterine segment during cervical dilation. J Assisted Reprod Genetics 2002; 19:215-219. PubMed 48. Das GK, Ravinder K, Deori S, et al. Incomplete cervical dialation causing dystocia in a buffalo. Indian J Vet Res 2008; 17:51. 49. Wehrend A, Bostedt H. The incidence of cervical dystocia and disorders of cervical involution in the post partum cow. Dtsch Tierarztl Wochenschr 2003; 110:483-486. - PubMed 50. Prabhakar S, Matharu SS, Gandotra VK, et al. Corpus luteum does not contribute to higher progesterone concentration around parturition in buffaloes with uterine torsion. Indian J Anim Sci 2007; 77:956959. 51. Singh AK, Prabhakar S, Banga HS, et al. Histopathological observations in cervix of dystocia affected vis - a - vis normally claved buffaloes. Indian J Anim Sci 2010; 80:842-846. 52. Zhang WC, Nakao T, Moriyoshi M, et al. Relationship of maternal plasma progesterone and estrone sulfate to dystocia in Holstein Friesian heifers and cows. J Vet Med Sci 1999; 61:909-913. - PubMed 53. Purohit GN. Analysis of medicaments for therapy of gynecologic problems in buffaloes in rural areas. Annual Report Raj Agric Univ 2009.

54. Honparkhe M, Ghuman SPS, Ajeet Kumar, et al. Cervical massage with sodium carboxy methyl cellulose for achieving complete cervical dilatation in successfully detorted uterine torsion affected buffaloes. Indian J Anim Sci 2009; 79:2629. 55. Purohit GN, Barolia Y, Shekher C, et al. Diagnosis and correction of uterine torsion in cattle and buffaloes. Raksha Technical Rev 2011; 1:11-17. 56. Kelly AJ, Kavanagh J, Thomas J. Relaxin for cervical ripening and induction of labour. Cochrane Database of Systematic Reviews, 2001; 2: CD 003103. 57. Hazzaa A, Nasr MT, Abdel Rahim A, et al. Field observations on the uterine torsion in cows and buffaloes. Alex J Vet Sci 1987; 3:249-263. 58. Murty KK, Prasad V, Murty PR. Clinical observations on uterine torsion in buffaloes. Indian Vet J 1999; 76:643645. 59. Swelum Abdel-Aziz A, Amin SE, Hazzaa MA. Prognosis prediction of uterine torsion mechanical treatment (rolling) after estimation of calcium and creatinine level in the serum of buffaloes (Bubalus bubalis). Theriogenology 2012; 78:10481055. - PubMed 60. Prasad S, Rohit K, Maurya SN. Efficacy of laparohysterotomy and rolling of dam to treat uterine torsion in buffaloes. Indian Vet J 2000; 77:784-786. 61. Matharu SS, Prabhakar S. Clinical observations and success of treatment of uterine torsion in buffaloes. Indian J Anim Reprod 2001; 22:4548. 62. Das GK, Firdous AK, Deori S, et al. Dystocia due to uterine torsion in a buffalo. Buffalo Bull 2010; 29:69-70. 63. Manju T S, Verma SK, Gupta RC, et al. Profiles of some plasma biochemical constituents associated with uterine torsion and following its correction by laprohysterotomy in buffaloes. Indian J Anim Reprod 1985; 6:5761. 64. Jadhao PT. Markandeya NM, Rautmare SS. Uterine torsion along with haemoperitoneum in a buffalo. Indian J Anim Reprod 1993; 14:59. 65. Siddiquee GM, Mehta BM. Uterine torsion in a buffalo with viable twins. Indian Vet J 1992; 69:257-258. 66. Nanda AS, Sharma RD, Nowshahari MA. The clinical outcome of different regimes of treatment of uterine torsion in buffaloes. Indian J Anim Reprod 1991; 12:197-200. 67. Vasishta NK. Torsion of uterus in buffaloes in relation to incidence, etiology and treatment. M.V.Sc. Thesis, Punjab Agriculture University, Ludhiana, India 1983. 68. Malhotra P. Some studies on the cervical changes in the uterine torsion cases with special reference to cervical filtration in buffaloes. M.V.Sc. Thesis, Punjab Agriculture University, Ludhiana, India 1990. 69. Singh P. Recent observations on etiology and treatment of uterine torsion in buffaloes. In: Recent Advances in Animal Reproduction and Gynaeoclogy. Ed A.S. Nanda, USG Publishers and Distributors, Ludhiana, India. 1995; 137-141. 70. Prabhakar S, Singh P, Nanda AS, et al. Clinico obstetrical observations on uterine torsion in bovines. Indian Vet J 1994; 71:822-824. 71. Ahmed M, Choudhary RA, Khan IH. Torsion of uterus as a cause of dystocia in the buffalo. Pak Vet J 1980; 1:22-24. 72. Foud K, El-Sawaf S. Some observations on torsio-uteri in buffaloes with special reference to its etiological factors. Vet Med J Giza 1964; 9:173-177.

73. El-Naggar M. Evaluation of field oriented treatment of uterine torsion in buffaloes in Egypt. Indian Vet J 1978; 55:6167. 74. Pattabiraman SR, Singh J, Rathor SS, et al. Non-surgical method of correction of bovine uterine torsiona clinical analysis. Indian Vet J 1979; 56:424428. 75. Amin SM, Amer HA, Hussein AE, et al. Creatine phosphokinase and aspartate aminotransferase profiles and its relation to the severity of uterine torsion in Egyptian buffalo. Anim Reprod Sci 2011; 123:163-168. - PubMed 76. El-Naggar MA, Abdel-Rouf M. The fetal membranes and fluids in the Egyptian buffalo. Zentralbl Veterinarmed A 1971; 18:108-123. 77. Ghuman SPS. Uterine torsion in bovines: a review. Indian J Anim Sci 2010; 80:289-305. 78. Sane CR, Luktuke SN, Deshpande BR, et al. Reproduction in Farm Animals. Varghese Publishing House, Bombay, India 1982. 79. Purohit GN. Maternal causes of dystocia in cows and buffaloes. In, Suresh SH, Tandle MK eds. Veterinary Obstetrics A Practical Guide. Jaypee Brothers Medical Publishers New Delhi 2006; 16-25. 80. Bagi AS, Vyas KN. Structure of broad ligament during non pregnant state and first trimester of pregnancy in the Surti buffalo. Indian Vet J 1983; 60:619-622. 81. Singh P. Studies on broad ligament in relation to uterine torsion in buffaloes. M.V.Sc Thesis; Punjab Agric. University, Ludhiana, India 1991. 82. Singh P, Sharma RD, Saigal RP, et al. Uterine torsion in buffaloes. National symposium on Recent Advances in Clinical Reproduction in Dairy Cattle. Chennai, India. 1992; 45. 83. Nanda AS, Sharma RD. Studies on serum progesterone levels in relation to occurrence of uterine torsion in buffaloes (Bubalus bubalis). Theriogenology 1986; 26:383389. - PubMed 84. Agarwal RG. Some studies on uterine torsion with special reference to its etiology and treatment in buffaloes. Ph.D. Thesis, Punjab Agric. Univ., Ludhiana, India. 1987. 85. Brar PS, Saigal RP, Nanda AS, et al. Role of broad ligament in the causation of uterine torsion in dairy buffaloes. Indian J Anim Sci 2008; 78:940-942. 86. Brar PS, Saigal RP, Sharma RD, et al. Histology and histochemistry of broad ligaments in buffaloes. Indian J Anim Sci 2008; 78:464-467. 87. Brar PS, Saigal RP, Sharma RD, et al. Is weak broad ligament a predisposing factor for uterine torsion in dairy buffaloes? Indian J Anim Sci 2008; 78:943-946. 88. Bugalia NS, Phogat JB, Umed S. Peripheral plasma progesterone and oestradiol17 profiles in buffaloes affected with uterine torsion. Buffalo J 1995; 12:353356. 89. Singh P, Prabhakar S, Kochar HP, et al. Uterus didelphus - A cause of torsion of uterus in a buffalo. Indian Vet J 1995; 72:172-173. 90. Singh J, Nauriyal DC, Pattabiraman SR, et al. Uterine torsion at mid-gestation in a buffalo. Indian Vet J 1979; 56:700. 91. Purohit GN, Maternal dystocia in cattle and buffaloes. In: Purohit GN eds. Domestic Animal Obstetrics. Lambert Academic Publishing Germany. 2012; 310337. - Available from amazon.com 92. Dhaliwal GS, Prabhakar S, Sharma RD. Intestinal obstruction in association with torsion of uterus in a buffalo. Pak Vet J 1992; 12:4243.

93. Siddiquee GM. Studies on the etio-pathology and therapeutics of uterine torsion in buffaloes. Ph.D Thesis. Punjab Agricultural University Ludhiana, Punjab, India. 1988. 94. Deori S, Kumar R, Jaglan P. Post cervical uterine torsion in a buffalo - A case study. Indian J Anim Reprod 2009; 30:85. 95. Ali A, Derar R, Hussein HA, et al. Clinical, haematological and biochemical findings of uterine torsion in buffaloes (Bubalus bubalis). Anim Reprod Sci 2011; 126:168-172. - PubMed 96. Prabhakar S, Dhaliwal GS, Sharma RD, et al. Success of treatment and dam survival in bovines with pre-cervical uterine torsion. Indian J Anim Reprod 1997; 18:21-23. 97. Purohit GN, Mehta JS. Dystocia in cattle and buffaloes: A retrospective analysis of 156 cases. Vet Pract 2006; 7:31-34. 98. Abdel-Ghaffer AE, Abou-El Roos MEA. New trends regarding the diagnosis and treatment of uterine torsion in buffaloes. Assiut Vet Med J 2002; 46:249-256. 99. Amer HA, Hashem MA. Relationship between clinical and biochemical picture of uterine torsion in Egyptian buffaloes (Bubalus bubalis). Internet J Vet Med 2008; 4:1-8. 100. Schulz J, Beuche W, Elze K. Torsio uteri in cattle. Vet Med 1975; 30:659665. 101. Schnfelder A, Richter A, Sobiraj A. Doppler ultrasound studies of the uterine arteries in cows with spontaneous parturition and with uterine torsion intra partum. Wien Tierarztl Monatsschr 2005; 92:7480. 102. Malik JS, Verma SK, Sharma DN. Histopathological studies on uterine torsion in buffaloes. Indian Vet J 1990; 67:603-606. 103. Schnfelder A, Schoon HA, Sobiraj A. Macroscopical and histological findings on the uterus in cattle with surgically treated uterine torsion. Tierarztl Praxis 2007; 35:325-334. 104. Ghuman SPS, Ajeet Kumar, Honparkhe M. A preliminary study on plasma haptoglobin concentrations in buffaloes following spontaneous or assisted delivery. Buffalo Bull 2009; 28:127130. 105. Phogat JB, Bugalia NS, Verma SK, et al. Plasma cholesterol and haemogram in buffaloes affected with uterine torsion. Indian Vet J 1991; 68:10481052. 106. Singla VK, Sharma RD, Gandotora VK, et al. Changes in certain serum biochemical constituents in buffaloes with uterine torsion. Indian Vet J 1992; 69:805807. 107. Pattabiraman SR, Pandit RK. Studies on haematological and biochemical constituents in blood of buffaloes with uterine torsion. Cherion 1980; 9:338340. 108. Kaur T, Singh B, Kaur T, et al. Reproductive disorders in buffaloes: haematobiochemical studies. Indian J Vet Path 1993; 17:118121. 109. Malhotra P, Sharma RD, Singla VK. Haematological studies in periparturient and uterine torsion affected buffaloes. Indian Vet Med J 1993; 17:111114. 110. Manju TS, Varma SK. Dystocia in buffaloes. Indian J Anim Reprod 1985; 6:54-57. 111. Khatri CK, Khar DK, Singh J, et al. Changes in biochemical blood constituents of buffaloes with uterine torsion and the effect of caesarean section and certain postoperative therapeutic measures. Arch Exp Veterinarmed 1986; 40:461468.

112. Ghuman SPS, Nanda AS, Prabhakar S, et al. Stress related endocrine and metabolic changes in normally calving and torsion affected buffaloes. Indian Vet J 1996; 73:11421146. 113. Ghuman SPS, Sharma RD, Prabhakar S, et al. Plasma cortisol and blood glucose milieu as an index of stress in buffaloes with uterine torsion. Indian J Anim Reprod 1997; 18:8384. 114. Ghuman SPS, Nanda AS, Sharma RD, et al. Osmotic resistance of erythrocytes in uterine torsion affected buffaloes. Indian J Anim Sci 1997; 67:139140. 115. Kuhad KS, Sharma DK, Singh P, et al. Serum transaminases in prolonged cases of uterine torsion in buffaloes. Indian J Vet Surg 1996; 17:115. 116. Schonfelder A, Furll M, Richter A, et al. Enzyme activities and substrate concentrations in blood plasma of bovines with surgically treated uterine torsion intra partum. Tierarztl Praxis 2007; 35:101-110. 117. Kraft W and Drr U. Clinical laboratory diagnostics in veterinary medicine Aufl. Schattauer, Stuttgart, New York. 2005; 6. 118. Hussein H, Abd Ellah MR. Effects of dystocia, fetotomy and caesarean sections on the liver enzymes activities and concentrations of some serum biochemical parameters in dairy cattle. Anim Reprod Sci 2008; 105:384391. PubMed 119. Noakes DE, Parkinson DJ, England GCW. Maternal dystocia In: Arthurs Veterinary Reproduction and Obstetrics, (Ed.) Noakes D E. Saunders Harcourt, India. 2001. 120. Prabhakar S, Dhaliwal GS, Sharma RD, et al. Success of treatment in relation to milk letdown and pelvic relaxation in bovines with torsion of uterus. Indian J Dairy Sci 1995; 48:323325. 121. Kochhar HPS, Prabhakar S, Singh P, et al. Rotation of urinary bladder with torsion of uterus in a buffalo. Indian Vet J 1994; 71:388389. 122. Matharu SS, Prabhakar S. Blood histamine levels in buffaloes after detorsion of uterus and/or caesarean section. Indian Vet J 1999; 76:524-526. 123. Mannari MN, Tadkod DM. Uterine torsion in buffaloes. Indian J Anim Sci 1976; 10:83. 124. Mudasir Q, Shukla SP, Nema SP, et al. Management of uterine torsion in a she buffalo. Buffalo Bull 2010; 29:75-77. 125. Singh J, Dhaliwal GS. A retrospective study on survivability and fertility following cesarean section in bovines. Indian J Anim Reprod 1998; 19:21-23. 126. Mankad MY, Jadav PV, Parikh PV, et al. Unrelieved torsion and ring womb leading to dystocia in local buffalo. Vet Res Commun 2007; 1:30-31. 127. Malhotra P, Sharma RD, Singla VK, et al. Effect of hyaluronidase and PGF2alpha on the dilatation of cervix in buffaloes suffering from uterine torsion. Indian Vet Med J 1994; 18:4647. 128. Arthur GH, Noakes DE, Pearson H, et al. Eds Maternal Dystocia Treatment: In: Veterinary Reproduction and Obstetrics. WB Saunders Philadelphia 1996; 203221. - Available from amazon.com 129. Prakash S, Nanda AS. Treatment of uterine torsion in buffaloes- modification of Schaffers method. Indian J Anim Reprod 1996; 17:33-34. 130. El Naggar M. Uterine torsion in buffaloes. Indian Vet J 1978; 55:61-67.

131. Samad HA, Ali CS, Ahmad KM. Schaffers method for the correction of uterine torsion in the buffalo. Pak Vet J 1981; 1:2527. 132. Singh P, Nanda AS. 1996. Treatment of uterine torsion in buffaloes Modification of Schaffers method. Indian J Anim Reprod 1996; 17:3334. 133. Dhaliwal GS, Prabhakar S, Singh P, et al. Effects of injudicious handling of uterine torsion on survival rate of dam in buffaloes (Bubalis bubalis). Pak Vet J 1991; 11:117119. 134. Luthra RA, Khar SK. Survival rate following different regimes of treatment in cases of uterine torsion in buffaloes. Indian Vet J 1999; 76:399402. 135. Henderson RA. Controlling peritoneal adhesions. Vet Surg 1982; 11:3033. 136. Sharma SP, Agrawal KBP, Singh DP. Torsion of gravid uterus and laparohysterotomy in bovine - A report on 72 clinical cases. Indian Vet J 1995; 72:11801182. 137. Prasad S, Singh OV, Dabas YPS, et al. Clinical management of delayed uterine torsions of more than 360 in buffaloes. Case reports. Indian Vet J 1988; 75:890891. 138. Mandal PK, Luthra RA, Arya SC. Histopathological observations on buffalo uterus affected with uterine torsion. In: Proceedings of the National Symposium on Reproductive Technologies for Augmentation of Fertility in Livestock. Nov. 14 -16, IVRI, India. Compendium of Abstracts. 2002; 146-147. 139. Singh P, Prabhakar S, Kochar S, et al. Uterus didelphus: A cause of torsion of uterus in a buffalo. Indian Vet J 1995: 72:172-173. 140. Purohit GN. Etiology, prepartal diagnosis and management of maternal complications of gestation in the water buffalo. Int J Appl Anim Sci 2012; 1:39-47. 141. Dhindsa SS, Dhaliwal GS, Ghuman SPS. Prevention of uterine adhesion formation following cesarean section in bovines. Indian J Anim Sci 2010; 80:626628. 142. Singh V, Amarpal, Kinjadekar P, et al. Effect of bupivacaine on epidural analgesia produced by xylazine or medetomidine in buffaloes (Bubalus bubalis). Vet Anaesth Analg 2009; 36:77-85. - PubMed 143. Singh P, Pratap K, Amarpal, et al. Xylazine, ketamine and their combination for lumbar epidural analgesia in water buffalo calves (Bubalus bubalis). J Vet Med A 2006; 53:423-431. - PubMed 144. Tiwari SK, Kumar A, Vainio O. Reversal of sedative and clinicopathological effects of epidural xylazine and Detomidine with atipamezole and yohimbine in buffaloes (Bubalus bubalis). Vet Rec 1998; 143:529. - PubMed 145. Peshin PK, Kumar A. Physiologic and sedative effects of xylazine in buffaloes. Indian Vet J 1979; 56:864-871. 146. Alshara M, Somroo H, Kalhoro B. Effects of xylazine on blood glucose levels in young male buffaloes. Pak Vet J 2000; 20:200-202. 147. Khan I, Kumar A, Peshin PK, et al. Evaluation of atropine-xylazine as a sedative in buffalo calves (Bubalus bubalis). Italian J Anim Sci 2007; 6 (Suppl 2):1003-1008. 148. Ghuman SPS, Sharma RD, Nanda AS, et al. Effect of certain clinical procedures and stressors on plasma cortisol milieu in dystocia affected buffaloes. Buffalo J 1998; 1:7179.

149. Ghuman SPS, Nanda AS, Sharma RD, et al. The effect of tranquilizers on stress response in buffaloes affected with uterine torsion. Indian Vet J 1997; 74:10341036. 150. Sathya A, Prabhakar S, Ghuman SPS. Effects of dexamethasone administration on cortisol concentration and biochemical profile in buffaloes suffering from dystocia. Anim Reprod 2005; 2:233239. 151. Sathya A, Prabhakar S, Sangha SPS, et al. Vitamin E and selenium supplementation reduces plasma cortisol and oxidative stress in dystocia-affected buffaloes. Vet Res Commun 2007; 31:809818. - PubMed 152. Ghuman SPS, Sharma RD, Mirakhur KK, et al. Acid base status and blood gas tensions of normally calving and uterine torsion affected buffaloes. Buffalo J 1998; 14:355360. 153. Dhindsa SS, Gandotra VK, Nanda AS, et al. Effect of duration of dystocia on haematobiochemical alterations in buffaloes. Indian J Anim Reprod 2005; 26:117 119. 154. Dhindsa SS, Gandotra VK, Prabhakar S. Plasma and blood volume in dystocia affected buffaloes. Indian J Anim Sci 2007; 77:837839. 155. Kumar A, Ghuman SPS, Ahuja CS, et al. Effect of oral fluid therapy on endocrine and biochemical status of dystocia affected buffaloes. Indian Vet J 2009; 86:10211023. 156. Kumar A, Ghuman SPS, Honparkhe M. Effect of oral fluid therapy in combination with intravenous dextran40 and hypertonic saline solution on plasma and blood volume in dystocia affected buffaloes. Indian J Anim Sci 2009; 79:479 482. 157. Pargaonkar MD, Tandle MK, Goswami JD, et al. Maternal dystocia followed by uterine prolapse in a buffalo. A case report. Indian J Anim Reprod 1993; 14:125. 158. Narsimha Rao AV, Sreeman Narayana O. Full term extra uterine pregnancy in a Murrah buffalo cow. Indian Vet J 1984; 61:809-810. 159. Singh M, Singh M, Kumar V. Rupture of uterus following uterine torsion in a buffalo- a case report Indian J Anim Reprod 1998; 19:71. 160. Pearson H, Denny HR. Spontaneous uterine rupture in cattlea review of 26 cases. Vet Rec 1975; 97:240244. - PubMed 161. Steklenev EP, Babkin VF. A case of extra uterine pregnancy. Veterinaria 1967; 44:88. 162. Misk NA, Semieka MA. The radiographic appearance of reticular diaphragmatic herniation and traumatic pericarditis in buffaloes and cattle. Vet Radiol Ultrasound 2001; 42:426-430. - PubMed 163. Mohamed T. Clinicopathological and ultrasonographic findings in 40 water buffaloes (Bubalus bubalis) with traumatic pericarditis. Vet Rec 2010; 167:819824. - PubMed 164. Naik PV, Mehendade SS. A rare case of diaphragmatic hernia in a buffalo. Indian Vet J 1969; 625-627. 165. Singh J, Prasad B, Kumar R, et al. Treatment of diaphragmatic hernia in buffaloes. Aust Vet J 1977; 53:473-475. - PubMed 166. Singh J, Dhablania DC, Prasad B, et al. On the etiology of diaphragmatic hernia in buffaloes (Bubalus bubalis). Japanese J Vet Sci 1980; 42:88-91.

167. Misk NA, Semieka MA, El-Sebaie AH. Diaphragmatic hernia in buffaloes. In: Proceedings of the 5th World Buff Congress Italy. 1997; 653-657. 168. Mohindroo J, Kumar M, Kumar A, et al. Ultrasonographic diagnosis of reticular diaphragmatic hernia in buffaloes. Vet Rec 2007; 161:757-758.

Click on the author's name to view a list of his/her publications: G. N. Purohit All rights reserved. This document is available on-line at www.ivis.org. Document No. A5715.0113