Disorders of Parturition and the Puerperium in the Gilt and Sow

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Disorders of Parturition and the Puerperium in the Gilt and Sow OLLI AARNO PELTONIEMI, STEFAN BJÖRKMAN AND CLAUDIO OLIVIERO

‘D

ystocia’ or difficult birth is discussed across the species in Chapters 11 and 12, in which obstetrical terminology is defined, whereas the puerperium in all species is discussed in Chapter 7. The emphasis in both these chapters is on monotocous species, such as cattle and horses; the circumstances in polytocous species such as the pig are very different. In the wild pig, which is considered to be the ancestor of present day farmed pig breeds, the duration of farrowing is short (1–1.5 hours), but the litter size is much small than that of the high prolific commercial sow lines used commercially today. In these, farrowing lasting longer than 5 hours is the norm (Björkman et al. 2017), whereas 10 years ago it was the upper limit for a normal successful farrowing (Oliviero et al. 2008).

Overview: Causes and Incidence Rates of Porcine Dystocia It is generally accepted that the shape of the porcine fetus and its small size in relation to the size of the pelvic inlet of the mother make the incidence of dystocia in sows lower than in other farm animals. Reports are: 0.25% (Jones 1966), 1% (Jackson 1972), 3 % (Randall 1972), and 5% (Waldmann 1993). A survey by Jackson (1972) showed that dystocia was of maternal origin in about 63% and of fetal origin in about 37% of the cases. Maternal causes were mainly uterine inertia (37%), obstruction of the birth canal (13%), and downward deviation of the uterus (9.5%). The relative incidence of the different forms of uterine inertia were: primary (20%), secondary (49%), and idiopathic (31%) inertia. Fetal causes were mainly faulty disposition (33.5%) and oversize (4%). Faulty disposition was caused by breech presentation (14%; faulty posture with both hindlimbs extended forward with the fetus in posterior longitudinal presentation), simultaneous presentation (10%), and postural defects in anterior presentation such as downward deviation of the head (3.5%). In another survey (Wehrend 2003) dystocia was 63% of maternal and 37% of fetal origin. Maternal causes were mainly due to uterine inertia (32%), oedema of the birth canal (9.5%), vaginal prolapse (7%), vaginal injuries (5.5%), obstruction of the birth canal (4%), uterine torsion (2.5%), and bladder flexion (1.5%). Fetal causes were mainly due to fetomaternal disproportion (26%) and faulty disposition (11%). Interestingly, a survey in Germany between 1982 and 1988 (Waldmann 1993) identified that dystocia was almost exclusively due to

maternal causes: 78.6% of dystocias were caused by obstruction of the birth canal, 11.4% by prolapsed vagina, 4.2% by primary uterine inertia, 3.9% by uterine torsion, 0.7% by downward deviation of the uterus, and 0.5% by a prolapsed uterus; only 0.4% were caused by piglet oversize. In this survey, secondary uterine inertia was not considered as a cause. Another survey (Schulz & Bostedt 1995) showed that bladder flexion caused 3.1% and vaginal prolapse 6.3% of dystocias. Dystocia may also occur as a result of the use of prostaglandin F2α and oxytocin to induce or control parturition (see Chapter 8).

Dystocia Due to Obstructive Causes Vaginal Prolapse.  Vaginal prolapse (see Chapter 10) was the cause of dystocia in 11.4% of the cases in the study by Waldmann (1993), in 7% by Wehrend (2003), and 6.3% by Schulz and Bostedt (1995). In the latter study, 78.8% of vaginal prolapses occurred within 1 week before parturition and mostly in sows in their third or more pregnancy. In 21.2% of the cases there was concurrent rectal prolapse. The aetiology is not clear, but it is likely that hormonal imbalances, increased abdominal pressure, and/or very relaxed birth canal caused by instability of pelvic ligaments and/or connective tissue of the perineal area play a role. The vagina can be partially or totally prolapsed, which can be temporary or permanent. If the vaginal prolapse does not resolve spontaneously, treatment is indicated. Otherwise, swelling and oedema of the vaginal mucous membranes can stimulate further abdominal straining and therefore increase the risk of rectal prolapse and vaginal injury with subsequent infection. Bladder Flexion.  Jackson (1972) reported that bladder flexion can cause obstruction of the birth canal resulting in dystocia; he identified it in 13% of the cases. In the survey by Schulz and Bostedt (1995), bladder flexion was associated with 3.1% of dystocias and in the study by Wehrend (2003) with 1.5%. Bladder flexion occurs mainly in multiparous sows in their third or higher pregnancy (Schulz & Bostedt 1995, Jackson 2004) and within 1 week before parturition (50% of all bladder flexions in the survey by Schulz and Bostedt (1995)) or during parturition (Jackson 2004). It can be accompanied by rectal prolapsed, as it was the case in 31.2% of dystocia caused by bladder flexion (Schulz & Bostedt 1995). The aetiology of both disorders is similar. Jackson (1995) reported that it occurred in sows with a very relaxed birth canal and surrounding tissue, together with excessive straining. 315

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• Fig. 17.1  Downward deviation of the uterus. The most caudal piglets (piglets 1. and 2.) create a bend in the uterine horn under the pelvic bone, creating a downward flexion of the horn and thus causing its obstruction. The latter probably caused kinking of the urethra, resulting in urinary obstruction and bladder distention due the accumulation of urine. The distended urinary bladder was then further forced back into the pelvic cavity and thus ventral to the vaginal floor, causing it to be elevated and forming a ‘mound’, thereby obstructing the birth canal. Downward Deviation of the Uterus.  Downward deviation of the uterus occurred in 9.5% of dystocia cases (Jackson 1995) or only in 0.7% as in the study by Waldmann (1993). The incidence seems to be lower than that of both vaginal prolapse and bladder flexion, though it might be greater in modern highly prolific breeds. Affected animals strain vigorously despite an empty vagina, and at a point in front of the pelvic brim, the uterus deviates sharply in a ventral and caudal direction under the pelvic brim (Fig. 17.1). Affected sows are multiparous, with deep bodies and large litters (Jackson 2004). Causes may be primary uterine inertia and atony of the uterine muscle (Waldmann 1993). Uterine Torsion.  In a uterine torsion the uterus rotates on its long axis. No cases of torsion were reported in the study by Jackson (1972), but there were 3.9% and 2.5%, respectively, in the studies of Waldmann (1993) and Wehrend (2003). It appears to develop shortly before parturition (Waldmann 1993) and mainly in multiparous lean sows. The rotation can involve the uterine body, one uterine horn, or part of one uterine horn, thereby trapping a fetus or fetuses distal to the stricture. The torsion can be clockwise or anticlockwise, and the degree of torsion can be of 180 degrees to 360 degrees, although a complete torsion is very rare (Waldmann 1993). The uterine wall may rupture, and a fetus or fetuses may become pseudoectopic. Moreoften the torsion resolves spontaneously during parturition without any adverse effects. Obstruction Due to Other Soft Tissue Abnormalities.  Other obstructive causes are rare and variable. Furthermore, the precise classification is not always clear in published studies. Incomplete dilatation of the cervix during the first stage of labour seems to be uncommon. When it does occur, it may be the result of an antepartum infection of the placentae or the uterus. Incomplete dilatation at the end of the second stage of labour may become relevant in sows with prolonged parturition. Involution of the cervix can start 6 hours after the beginning of the second stage of labour. Although the cervix will be still open, the loss of elasticity, stretchability, and lubrication can lead to complications for the piglets entering and passing through the birth canal. Because

in modern highly prolific sows the duration of parturition is on average 6 hours (Björkman et al. 2017), this cause of dystocia may now be more relevant. Another soft tissue abnormality that may be increasingly relevant is severe swelling and oedema of the birth canal which can occur in prolonged parturitions, after an obstetrical examination, and/or piglet removal, particularly if the procedure is not done gently (Björkman 2017). The birth canal is very delicate, fragile, and susceptible to trauma. In cases in which there are a large number of piglets entering the birth canal simultaneously followed by manual extraction of piglets, the mucous membranes may react with increased swelling. Furthermore, the mucous membranes can be more easily damaged. Thus in sows with large litters and prolonged parturition, there is an increased need for manual interventions, and dystocia caused by swelling and oedema of the birth canal may be more relevant. In addition, there is evidence that sows with a large litter also have higher oestrogen concentrations in the blood (Edgerton et al. 1971, Kensinger et al. 1986), especially before parturition, resulting in severe oedema of the vulva (Waldmann 2009). Obstruction Due to Bony Tissue Abnormalities.  Obstruction caused by bony tissue abnormalities, e.g., pelvic constriction, are very rare and only cause dystocia when they occur in gilts which have been bred at a too young age (< 200 days) and a too low body weight (< 90 kg) (juvenile pelvis); they rarely occur in sows after fractures, in which there has been poor alignment of the pelvic bones. Gilts should be between 220 to 270 days old, and a body weight of 135 to 170 kg, a backfat depth of 12 to 18 mm, and a body condition of about 3, when they are bred for the first time (Rozeboom 2015). If these recommendations are followed, the incidence of dystocia due to a juvenile pelvis should be very low. Obstruction Due to the Piglets.  Jackson (1972) reported that 37.5% of dystocias were due to a fetal cause. These were due mainly to faulty fetal disposition (33.5%) and oversize (4%). In the study by Waldmann (1993) no fetal causes of dystocia was reported. 57% of the piglets were born in anterior longitudinal presentation, whereas 43% were born in posterior longitudinal presentation. Posterior presentation is not itself a cause of dystocia, unless the piglet is oversized. Currently, fetal causes of dystocia are minimal. It may occur in gilts bred at too young an age or with low body weight (see previous mention), or in which the litter is small. Infection, with porcine parvo virus, can cause small litters. In sows with large litters the smaller piglets can be expelled even when their fetal disposition is incorrect and as a result, simultaneous presentation of two piglets may become more frequent. Congenital abnormalities are very rare; they may include: arthrogryposis, hyperostosis, hydrocephalus, conjoined piglets, schistosoma reflexa, syndactyly, polydactyly, and micromelia (see Chapter 9). Arthrogryposis is characterised by ankylosis of various joints, in various degrees of flexion or extension, as well as the vertebral column resulting in lordosis, kyphosis, or scoliosis. Hyperostosis is stiffness of the forelegs, with enlarged elbow joints and cartilaginous thickening of proximal bones of the forelimbs.

Inadequate Expulsive Force Primary Uterine Inertia.  Primary uterine inertia is defined as the absence of or deficient myometrial contractions (see Chapter 13). Primary uterine inertia, which is the absence of or reduced contractility of the myometrium, was present in 7.5% of dystocias (Jackson 1972) and in 4.2% in Waldmann’s study (1993). In toxaemic sows there may be signs of systemic illness before farrowing



CHAPTER 17  Disorders of Parturition and the Puerperium in the Gilt and Sow

with a foul-smelling vaginal discharge, which is sometimes associated with infections such as porcine parvovirus. Nontoxaemic sows are usually healthy, with a dilated cervix and fetuses palpable within the birth canal but with the absence of contractions. It may be caused by hormonal abnormalities, such as an increased progesterone to oestrogen ratio, and/or deficiencies of oxytocin and prostaglandin secretion and/or their receptors, and nutritional factors, for example diets low in fibre and high in energy. Other less common causes, such as calcium deficiency, have been reported (Framstad et al. 1989). The inability of sows to be able to express normal nest-building behaviour may be an important primary cause of uterine inertia. It has been shown that lack of space and absence of available nest-building materials can be an important stressor in sows, thereby decreasing oxytocin secretion, and the resultant reduced uterine contractility will eventually increase the duration of farrowing (Oliviero et al. 2008). Secondary Uterine Inertia.  Secondary uterine inertia is more common than primary inertia, usually occurring as a result of another cause of dystocia, usually obstructive but also associated with a prolonged parturition particularly associated with a large litter.

Management Inappropriate Use of Exogenous Oxytocin.  Oxytocin is widely used to augment normal uterine contractions. Its uterotonic has been demonstrated by Mota-Rojas et al. (2005a), who showed that exogenous oxytocin increases the number, intensity, and duration of myometrial contractions. However, its use has been shown to have negative effects on the outcome of farrowing, for example increased incidence of intrapartum asphyxia and stillbirths (Mota-Rojas et al. 2002, Alonso-Spilsbury et al. 2004, Mota-Rojas et al. 2005b) and the duration of piglet expulsion. Several studies (Welp et al. 1984, Chantaraprateep et al. 1986, Dial et al. 1987, Alonso-Spilsbury et al. 2004) have shown that oxytocin can increase the frequency of dystocia and therefore the need for subsequent obstetrical assistance. However, most of the adverse effects have been associated with its use when not truly indicated, e.g., at the beginning of fetal expulsion when oxytocin concentrations and oxytocin binding sites in the endometrium and myometrium are high (Lundin-Schiller et al. 1996, Phaneuf et al. 2000). The time of administration is appropriate when the expulsion of the last piglet was at least 30 minutes ago, and if the obstetrical examination showed that piglets are still present within the uterus but none are within the birth canal. Furthermore, the birth canal should be fully dilated and unobstructed. Body Condition.  There is a negative correlation between the amounts of backfat and farrowing duration (Oliviero et al. 2010). The fatter the sow, the longer the duration of farrowing. The reason may be that increased backfat reflects the level of fatty infiltration of the tissues of the birth canal, resulting in a reduction in the diameter of the birth canal, as well as predisposing to secondary uterine inertia. Another reason may be that a higher level of fat is known to affect lipid-soluble steroids and may affect the progesterone to oestrogen ratio, a consequence of which is that it affects oxytocin receptor activation. Abnormalities due to oxytocin receptor activation may weaken the expulsive phase of parturition. This hypothesis is supported by the observation of Oliviero et al. (2008), who observed that fat sows had a delayed decline in peripheral progesterone concentrations beyond day 1 after parturition. Furthermore, Björkman et al. (2017) observed a negative correlation between backfat and the depth of the uterine wall antepartum, which could be the result of a delayed decline in

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progesterone or a higher progesterone to oestrogen ratio, which could impair the degree of myometrial hypertrophy during pregnancy and hence before parturition. Constipation.  There is a negative correlation between constipation and farrowing duration (Oliviero et al. 2010). The more constipated the sow, the longer the duration of parturition. The reason may be that constipation results in an accumulation of faeces in the rectum that causes a physical obstruction to the passage of the piglets, resulting in secondary uterine inertia. Another reason may be that constipation may result in impaired uterine contractions due to the effects of lipopolysaccharides. Lipopolysaccharides are endotoxins produced by Gram-negative bacteria that increase around the time of parturition and are associated with constipation. Endotoxins can be absorbed from the gut and influence the normal endocrine changes associated with farrowing, resulting in primary uterine inertia. A third explanation may be that the discomfort and pain associated with constipation may also influence the hormonal changes associated with parturition. Studies have found that opioids inhibit oxytocin during parturition (Bicknell & Leng 1982, Douglas et al. 1995. Brown et al. 1999). Therefore pain due to prolonged constipation could promote the release of opioids and, consequently, impair oxytocin secretion, thus reducing myometrial contractions.

Dystocia: Examination History of the Sow.  Before examining an individual sow with suspected dystocia, it is important to obtain details of her previous farrowing history, if appropriate, by examining her records for breeding and obstetrical history; these may be manually or electronically recorded. Details include general health, number of litters and their sizes, and duration of previous gestations. Duration of Farrowing.  The timescale before intervening in the process of parturition is critical. Knowing the normal physiology and behaviour of the particular sow and her immediate cohorts is important. Previous studies (Oliviero et al. 2008) have reported the average values for the duration of farrowing were 200 to 300 minutes, which were considerably longer than those reported earlier. However recent data suggests that with ever increasing litter numbers, there is a concomitant increase in the duration of farrowing. Björkman et al. (2017) have recently reported that in highly productive sow lines, the average duration of farrowing was 400 minutes, which was influenced by parity and number of stillborn piglets. Thus classifying a sow as suffering from dystocia according to the 5-hour principle as occurred 10 years ago is not applicable now. By providing the sow with an open farrowing pen and adequate amounts of suitable nest-building material, and dispensing with farrowing crates, reduces the duration of farrowing by approximately 90 minutes (Oliviero et al. 2008). Inter Piglet Interval.  The decision on when it is appropriate to intervene will depend on a number of factors, e.g., if the interpiglet interval is prolonged at the beginning and end of the second stage of parturition, if the piglet fetus is large, especially some males, and if it is dead. General Examination.  Frequent observations of the sow before farrowing should enable the signs of impending farrowing to be detected. General examination may include measuring body temperature; it normally increases above 39°C 24 to 48 hours before the birth of the first piglet and heart rate peaks before and during parturition. Nesting behaviour is greatest 6 to 12 hours before the first piglet is born. Palpation of the mammary gland for the composition and presence of colostrum, which normally runs

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freely during parturition, appearing first in the cranial pair of the mammary glands some hours before beginning of parturition. After the onset of the second stage of labour and as it progresses, the number of piglets born, as well as their vitality and uniformity, should be assessed (Oliviero 2010). A lack of uniformity in the weight of new born piglets may be an indicator for a large litter; low piglet vitality may indicate a prolonged inter piglet interval. Large litters may result in uterine inertia, and prolonged interpiglet intervals may be indicative of endocrine imbalances or obstructive dystocia. Continuous straining by the sow without piglet expulsion, bleeding, or an abnormal vaginal discharge, including meconium staining of the piglet as well as loss of movement immediately after birth (see piglet vitality scoring later in this chapter) are indicative of disturbances of farrowing. Intervention Criteria.  As discussed previously, if the inter piglet interval is longer than 2 hours or the overall duration of farrowing is longer than 5 hours, it is indicative of dystocia. Although the criteria for intervention may have changed in recent years, intervention should always be based on the history and health of the sow and the piglets that have been born.

Obstetrical Examination Rectal Palpation.  This should be considered before the vagina is examined for number of reasons. Provided it is performed carefully, it is easily performed, using a gloved hand and plentiful lubricant, and safe. By performing the procedure, one of the potential causes of obstruction of the birth canal, namely a hard faecal mass due to constipation can be removed. It also reduces the likelihood of vaginal faecal contamination during subsequent vaginal examination. Rectal palpation has limitations because it is only possible to reach the body of the uterus and caudal parts of the uterine horns. Vaginal Examination.  This should be done carefully and cleanly using a gloved hand/arm and with plentiful amounts of lubricant. Once the hand is in the birth canal, the mucosa of vagina, cervix, and uterine body should be carefully palpated for any signs of possible damage, including swelling of the mucosa, which readily occurs after an obstructive dystocia. Cranial to the uterine body, the caudal parts of the both uterine horns should be palpated to determine the presence of downward, ventral torsion of uterine horns, which is typical in a sow with a large litter. Ultrasonographic Examination.  Real time transabdominal ultrasonography is very useful as part of an obstetrical examination to identify the number of fetuses present within the uterus, as well as detecting their heartbeats, thus indicating the number that are alive.

Dystocia: Treatment Uterine Inertia.  As described previously, this is the commonest cause of dystocia, occurring in over a third of cases. Clinical examination will show that no fetuses can be palpated in the birth canal, and uterine contractions cannot be detected. Initially, if possible, the sow should be encouraged to stand and move around even outside the farrowing pen. The sow should be treated with oxytocin at a dose of 5 to 10 IU i.m for a maximum of 2 to 3 times; the time interval between the successive injections should not be less than 30 minutes. As a last option, manual palpation of the cervix may be tried to stimulate the release of endogenous oxytocin. Use of Oxytocin in Prolonged Farrowing.  In prolonged farrowings, the overuse of oxytocin may expose those fetuses still

within the uterus to hypoxia because oxytocin reduces blood flow through placenta and also increases the risk of a ruptured umbilical cord and thus the severance of blood supply to the fetus. It is well documented that piglets appear vulnerable to asphyxia during parturition, and the increasing litter size appears as a common denominator for this. Downward Deviation/Torsion of the Uterine Horn.  Large litters seem to predispose the sow to downward deviation/torsion of the uterine horn (Figure 17.1). In the sow, in contrast to other larger domestic species, the twisting of the caudal part of the uterine horn is due to the caudal fetuses becoming positioned ventral to the pelvic bone.

Prevention of Dystocia As described previously, dystocia in sows is relatively rare compared with other multiparous species. Dystocia adversely affects piglets’ survival, thus there is an increase number of stillborn piglets as well as those that are considered to be ‘hypovital’ (Alonso-Spilsbury et al. 2007). It also affects the survival of the sow (Sanz et al. 2007), as well as her subsequent fertility (Oliviero et al. 2013). For all these reasons, it is important to attempt to prevent dystocia throughout the course of pregnancy until the start of farrowing. For example, maintaining good body condition and preventing constipation are important. These factors, unlike mechanical and obstructive causes of dystocia, can be influenced to some extent by proper management and feeding strategies.

Endogenous Hormonal Balance at Farrowing Modern housing and production systems have promoted the confinement of sows in crates during farrowing, whereby the sow’s movement is severely restricted, and she is allowed limited bedding. As a consequence, nest-building at the best is limited or does not occur at all. The sow’s innate behaviour of nest-building is induced by the decline in progesterone and the increase in prolactin prepartum (Algers & Uvnäs-Moberg 2007). As well as these endocrine changes, 6 to 12 hours before farrowing oxytocin increases before peaking at parturition to stimulate effective contractions of the uterus and, as a consequence, rapid birth of the piglets (Taverne et al. 1979, Lawrence et al. 1997). There are studies showing an increase in farrowing duration and stillbirth rate when innate behaviours, such as restricting nest-building by the absence or limited availability of the necessary materials, as well as limiting the mobility of sows by confinement and restraint by the use of the farrowing crate (Oliviero et al. 2008 and 2010, Gu et al. 2011). Allowing the sow to move freely before and during farrowing reduces the duration of farrowing by an average of 100 minutes, thereby reducing the risk of stillborn piglets. A combination of a free pen and the provision of abundant nest-building material increased the circulating level of oxytocin and prolactin before farrowing (Oliviero et al. 2008, Yun et al. 2015). Therefore it is recommended that sows are allowed to move freely to perform natural nest-building behaviour and to provide nest-building material such as straw, hay, sawdust, and paper sheets. This will help to ease the parturition process, reducing risks of prolonged farrowing that may have negative consequences for the sow and her offspring.

Feeding in Late Pregnancy During late pregnancy, to ensure that sows receive enough energy to satisfy the demands of forthcoming milk production, sows



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are usually fed with high energy concentrated diets (Einarsson & Rojkittikhun 1993). Such concentrated diets, which have a much more limited amount of fibre than standard pregnancy diets, can promote obesity and constipation. These two conditions are associated with prolonged duration of farrowing and an increased stillbirth rate (Oliviero et al. 2010). Late pregnancy diets should contain up to 7% to 10% of fibre, in order to reduce constipation and excessive fat deposits (Oliviero et al. 2009). The use of high fibre diets appears to be a beneficial strategy to improve the health of the sow around farrowing (Peltoniemi et al. 2016). If the diet cannot be easily modified, a good fibre source can be provided by offering different types of roughage (straw, hay) or adding any other feedstuffs with high levels of fibre, such as sugar beet pulp (Quesnel et al. 2009). Offering roughage may not only be a way to increase fibre intake and alleviate constipation and obesity, but it can also serve as an appropriate material for nest-building. Preventing sows becoming excessively fat in the last part of pregnancy can be achieved by encouraging sows to be more mobile by allowing them more space, with strategic feed distribution and with provision of interactive substrates like straw or hay. A reduction in feed intake by the sow (up to 50%) may be implemented during the last week before farrowing, which also helps to prevent constipation, as well as other physiological and behaviour aberrations around the time of farrowing.

Disturbed Parturition and the Neonatal Piglet Introduction During the last two decades there has been emphasis on the development of highly prolific pig breeds in many countries, resulting in substantial increases in litter size (Bjerre et al. 2010, Paredes et al. 2012). In order to improve the productivity of sows, a better method would be to select breeding stock based upon the number of piglets weaned. However, due to the common practice of crossfostering small piglets at an early age of life, the total number piglets born has been the preferred method of selection (Su et al. 2007). Litters with greater than a total of 16 born piglets have been associated with higher stillbirth rates (1.5 piglets) compared with litters of 11 to 12 total born piglets (0.6 piglet), and piglets in larger litters also have lighter birthweights (Boulot et al. 2008). Comparing similar litter sizes, Canario et al. (2006) found the probability of stillborn piglets in large litters to be almost twice as high as in a reference litter. Large litters are also associated with longer farrowing times, a higher risk of fetal hypoxia during birth (Herpin et al. 2001), and higher within litter weight variation (Milligan et al. 2002). Piglets’ mortality after birth and before weaning have ranged from 11% to 24% in several countries, and the mortality is mostly observed in the first 5 days of life (Pedersen et al. 2011, KilBride et al. 2012). The main causes of death included crushing, low viability, starvation, and diseases. These levels of preweaning mortality represent a challenge to modern pig production and also a concern for animal welfare.

Weak and Stillborn Piglets: Causes and Consequences Different studies have reported that stillbirths rates vary between 3% to 10% of all pigs born (Borges et al. 2005, Cutler et al. 2006, Oliviero et al. 2010, Vanderhaeghe et al. 2010). According to the

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TABLE Number of stillborn piglets according to 17.1  housing type (n = litters)a

Housing

Number of Stillborn

Average Duration of Farrowing (min)

Pen

0.6 ± 0.8

208 ± 58

89

Crate

1.1 ± 1.1

297 ± 130

133

n

a

Summary of three studies (Oliviero et al. 2008, 2010; Gu et al. 2011).

time of death, stillbirths can be classified into: type I, in which fetuses die before the end of gestation (antepartum or prepartum deaths), due to infectious causes; type II, in which piglets die during parturition (intrapartum deaths) due to noninfectious causes, such as intrauterine asphyxia and dystocia (Sprecher et al. 1974). One cause of type II stillbirths is large litter size (> 16 total born piglets) as previously discussed. Another cause is housing. Both housing and stillbirth rate relate to farrowing duration (Table 17.1). Farrowing duration > 300 minutes was associated with a higher stillbirth rate, compared with the duration of farrowings of <200 minutes (Oliviero et al. 2008 and 2010, Gu et al. 2011). According to the review by Vanderhaeghe et al. (2013), large litter size, high parity, excessive thin or fat sow’s body condition, and limited or no farrowing supervision/birth assistance seem to be the most relevant factors in increasing the stillbirth rate. Thermoregulation is challenging for neonate piglets, and this competence is highly correlated with their vitality after birth. They are born wet, covered by fetal fluids that allows for heat loss by evaporation, so it is important that they quickly dry. They have very little pelage to insulate against heat loss, and they lack brown fat that could be metabolised to generate heat and balance their body temperature (Berthon et al. 1994). Thus newborn piglets are very vulnerable to the effects of environmental temperature and can only use metabolic responses to reduce heat loss if their body temperature is >34°C (Lossec et al. 1998). The main metabolic responses are mobilisation of free fatty acids, shivering, and a modest gluconeogenesis using their own liver’s glycogen reserve. The latter is available and metabolised within a maximum of 15 to 20 hours in starving piglets (Svendsen & Bengtsson 1986, Lossec et al. 1998). Pedersen et al. (2011) found that piglets with a rectal temperature of 36.1°C, 2 hours after birth, had greater odds of being crushed by the sow, whereas in those with a rectal temperature of 38.6°C, the odds were reduced. Herpin et al. (1996) demonstrated that piglets that suffered from hypoxia due to rupture of the umbilical cord or detachment of the placenta during parturition were less viable and needed more time to reach the sow’s udder (120 ± 35 vs 25± 3 min). They also showed a reduced ability to maintain the body temperature (36.3 ± 0.9 vs 38.4 ± 0.1°C) during the first 24 hours of life. In contrast to older animals, the early neonatal piglet does not increase its energy intake in response to cold temperature. In fact, colostrum intake decreases by 36.8% during cold exposure (18° – 20°C) compared with piglets at an ambient temperature between 30° to 32°C, thus exacerbating the likelihood of starvation (Lay et al. 2002). Kammersgaard et al. (2011) found that a birth weight >1.1 kg was the most important single factor in successful recovery from postnatal hypothermia. In addition, Milligan et al. (2002) found that birth weight >1.3 kg was positively correlated with higher piglet preweaning survival. It has been shown that the birth process and individual characteristics influence the piglet’s

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thermoregulatory mechanism. However, in the environment of a modern farrowing unit, with different zones at different temperatures, it is heat preservation rather than mere heat production that determines thermoregulatory success and recovery from postnatal hypothermia (Kammersgaard et al. 2011).

Assessment of Neonatal Vitality Piglet vigour postpartum, in addition to birth weight, is crucial if the piglet is to acquire colostrum and preserve homeothermy (Baxter et al. 2008). Piglet vigour appears to be independent of birth weight, suggesting that small, but proportional, piglets that display high vigour can survive the vulnerable perinatal period (Baxter et al. 2008). The same authors propose the use of a categorical scale to visually assess and score the piglets’ vitality immediately after birth (Table 17.2), which can be predictive of the survival rate of the neonate piglets after birth. In large litters, piglets can suffer from intrauterine growth restriction (IUGR) during uterine development. These piglets have a ‘dolphin-like’ head shape compared with ‘normal’ piglets (Fig. 17.2; Hales et al. 2013). Piglets with a ‘dolphin-like’ head shape ingest insufficient amounts of colostrums and hence have lower glucose levels at 24 hours. In addition, they have less glycogen reserves in the liver (Amdi et al. 2013). These factors combined suggest that if piglets are born with a dolphin-like head shape, they have a lower chance of survival. Identifying IUGR piglets on their head shape and evaluating the

vitality score at birth can provide a rapid and simple method of deciding which piglets need extra support to maximise neonatal survival (Amdi et al. 2013, Baxter et al. 2008).

Management and Supportive Therapy of Neonates Piglets should be quickly dried soon after birth and placed in a suitable environment to minimise their body heat loss. This can TABLE The vitality score of piglets immediately 17.2  after birth

Vitality Score

Description

0

No movement, no breathing after 15 sec

1

No movement after 15 sec, piglet is breathing or attempting to breathe (coughing, spluttering, clearing its lungs)

2

Piglet shows some movement within 15 sec, breathing or attempting to breathe

3

Good movement, good breathing, piglet attempts to stand within 15 sec

Adapted from Baxter et al. 2008.

• Fig. 17.2  Normal compared with IUGR piglet steep, dolphin-like forehead, bulging eyes, and wrinkles perpendicular to the mouth. (From Hales, J. et al, 2013. Individual physical characteristics of neonatal piglets affect preweaning survival of piglets born in a noncrated system. J Anim Sci. 91: 4991–5003.)



CHAPTER 17  Disorders of Parturition and the Puerperium in the Gilt and Sow

be done using insulated nests, floor heating pads, heating lamps, or combinations of these. A second important step is to ensure that the whole litter has sufficient individual colostrum intake (200 – 250 g) within 12 to 16 hours from the beginning of parturition (Devillers et al. 2011). When possible, small and weak piglets should be assisted to suckle, by helping them to attach to the teat, thus ensuring that colostrum is ingested. It is important to remember that small piglets have difficulty in sucking from big teats, therefore the smallest functioning teats should be selected when assisting suckling. This procedure should be repeated 3 to 4 times within the first few hours if these piglets are not seen actively suckling. Additionally, weakly piglets can be hand fed with colostrum collected from their own mother, or other sows, within 6 to 12 hours from the beginning of farrowing. At this stage, milking by hand is relatively easy, due to the almost continuous (every 5–40 min) milk ejections (Algers & Uvnäs-Moberg 2007). Piglets can be hand fed using a feeding bottle with a suitable nipple or using a syringe connected to a soft silicone plastic tube (3–4 mm in diameter) that is inserted in the oesophagus and then stomach, and administering 20 to 25 mL of colostrum. The correct length of the tube can be assessed and subsequently marked, by measuring it against the piglet from the tip of its nose to the last rib. Great care is necessary to avoid intratracheal intubation insertion and injury to the larynx. Assisted suckling and hand feeding is appropriate in small or normal size litters when only one or two piglets require help. In large litters or when more piglets require assistance, a split suckling strategy could be more effective. In order to minimise the sibling competition for colostrum intake, the litter is split into two groups. The heavier and stronger piglets are kept in the creep area or in a separate box, allowing the smaller piglets to suckle for 60 to 90 minutes, and then the groups are switched. When separating the piglets, both groups should always have free access to a warm creep area. This can be easily achieved by using a box with an additional heat lamp for the separated group, which leaves the creep area accessible for the remaining group to suckle. If some small piglets are still unable to successfully suckle, assisted suckling should be combined with split suckling.

Colostrum Uptake Because of the epitheliochorial nature of the porcine placenta (see Chapter 4), neonate piglets lack maternal IgG at birth. They must acquire maternal immunoglobulins from ingested colostrum for passive immune protection before they produce their own immunoglobulins at around 3 to 4 weeks of age (Rooke & Bland 2002). However, colostrum is produced only during the first 16 to 24 hours after the start of parturition, and even after the first 6 hours, the IgG content in colostrum is halved (Le Dividich et al. 2005). Acquiring adequate colostrum at the right time and in the required amount can be a challenge because of sibling competition, protracted farrowing, and reduced piglet viability. All these factors have a major effect in large litters (Devillers et al. 2007). The same authors found that individual colostrum intake ranged from nil to >700 g during the first 19 hours of life (450 g/kg birth weight), indicating that the capacity for colostrum intake can be high when its supply is unrestricted. In large litters, an ad libitum supply of colostrum is rarely available to all piglets, and probably 200 to 250 g intake per piglet provides sufficient protection. Devillers et al. (2011) found that the preweaning mortality rate was 7.1% when piglets ingested >200g of colostrums, and increased to 43.4% when intake was <200 g. Thus it is not the piglets’ intake capacity that is the limiting factor in satisfying the

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passive immunity requirements, but the production of adequate colostrum by the sow. Colostrum yield is highly variable; it averages 3.3 to 3.7 kg, ranging from <1.5 kg to greater than 6.0 kg (Devillers et al. 2007, Quesnel 2011). However, Andersen et al. (2011) found that, without human assistance to piglets (such as drying, placing under a heat lamp, cross fostering, movement to a nurse sow, split- or suckling assistance), it can be difficult for many sows to adequately nurse more than 10 to 11 piglets. Furthermore, Quesnel et al. (2012) suggested that the genetic selection for higher prolificacy is one of the major causes for the increase in low birth weight of piglets and poor vitality. Insufficient colostrum production has been found to be associated with impaired hormonal status of the sow at farrowing. Abnormal high levels of circulating progesterone (< 4 ng/mL) in blood of sows at farrowing have been related to poor colostrum yield (Foisnet et al. 2010, Hasan et al. 2016a).

Evaluation of Colostrum Quality Hasan et al. (2016b) have recently proposed the use of Brix refractometer to evaluate the IgG content of sows’ colostrum content. Based on the study by Quesnel et al. (2015) and in the review by Hurley (2015), the IgG content in sows peaks within 2 hours after the start of farrowing, with a mean concentration of 64 mg/ mL (range: 50–80 mg/mL), whereas it decreases to around 10 mg/ mL at the end of colostrogenesis (24 hours after the start of farrowing). By using a Brix measurement on the farm, it might help to identify sows with an impaired IgG concentration and allow improved management of lactating sows and neonate piglets. This procedure should be done during early colostrogenesis (0–3 hours after start of farrowing), when colostrum is easiest to collect and when peak levels of IgG occur (Hasan et al. 2016). On the contrary, low IgG levels (10 mg/mL) are not expected to be found during early colostrogenesis. Taking the lower range of the peak IgG level as 50 mg/mL, it should be a fairly reliable point to assess that adequate levels of IgG are present at this stage. Table 17.3 shows a suggestion for the evaluation of the Brix refractometer results. Brix values <20% reflect very low levels of IgG, whereas values >25% reflect good or very good concentrations of IgG. Values between 20% and 24%, defined by the authors as borderline, should not be considered as being inadequate for the IgG content, especially if the Brix values are in the highest range (23% – 24%). Conversely, levels in the lowest range (20% – 21%) might be considered more critical. When borderline results are obtained, the authors suggest taking another sample within 1 to 2 hours, to evaluate if the development of the estimated IgG content is stable.

TABLE Colostrum IgG content based on two methods 17.3  of evaluation, and categories of estimation Brix %

ELISA IgG 0–3h, mg/mL, average ± SEM

IgG estimation categories

< 20

14.5 ± 1.8

Poor

20–24

43.8 ± 2.3

Borderline

25–29

50.7 ± 2.1

Adequate

≥ 30

78.6 ± 8.4

Very good

From Hasan et al. 2016b.

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Abnormal Parturition and Reproductive Health Effect of an Abnormal Parturition on Health of the Uterus and Mammary Gland Postpartum There is enough evidence which suggests that a prolonged or abnormal farrowing predisposes the sow to poor reproductive health during the puerperium. When parturition is prolonged, placental retention is more likely to occur with consequential metritis (Björkman et al. 2017). It is also known that, if there is dystocia or farrowing is prolonged, there is an increased frequency of constipation and decreased circulating oxytocin concentrations (Oliviero et al. 2008), both of which predispose to disorders such as postpartum dysgalactia syndrome (PDS). Retained Fetal Membranes.  The time interval between the expulsion of the first and last placenta (placental expulsion duration) has been reported in sows as 4 hours and 4.5 hours (Björkman et al. 2017), and 2.5 hours in gilts (van Rens & van der Lende 2004). Van Rens and van der Lende (2004) showed that an increase in the duration of farrowing was significantly associated with an increase in placental expulsion duration. Björkman et al. (2017) showed that the duration of placental expulsion was mainly affected by the use of exogenous oxytocin during parturition. If the latter was used, then the litter size had the main effect on the duration of placental expulsion, probably due directly to the actual number of placentae that need to be expelled, which increases with increasing litter size. If exogenous oxytocin was not used, the farrowing duration was associated with the placental expulsion duration, confirming the observations made by Van Rens and Van der Lende (2004). Nevertheless, this association was observed only in sows with a farrowing duration of < 700 to 800 minutes. If the farrowing duration was longer, placental expulsion was severely compromised, which occurred in about 6% of the sows. Fifty percent of these sows had a partial retention of their placentae due to either a delayed onset of placenta expulsion and/or an early abortion. Another 50% of them expelled no placental parts and therefore had total retention (Fig. 17.3.); in these sows the average duration of farrowing was 1000 minutes. The most likely cause of impaired placenta expulsion in sows with a prolonged farrowing is secondary uterine inertia. This is supported by the findings of Oliviero et al. (2008) and Castrén and

•

Fig. 17.3  Ultrasound image of retained fetal membranes in a sow. A, Uterine Horn; B, Uterine lumen and endometrium; C, Enlarged blood vessels. (From Björkman et al., 2017.)

colleagues. (1993), who showed that increased farrowing duration is associated with decreased oxytocin levels. In addition, it is also supported by the observation that moderate use of oxytocin towards the end of the second phase of the parturition had a significant effect on reducing the duration of placenta expulsion (Björkman et al. 2017). If retained placentae can be expelled later during the puerperium, or are absorbed within the uterus, or expelled at the subsequent oestrus is not known. Delayed Uterine Involution.  Initially, uterine involution is very rapid during the first week postpartum (Fig. 17.4) when the uterine weight is reduced by 65% (Palmer et al. 1965). Thereafter, uterine involution continuous progressively and uniformly and is completed during the third week postpartum (Palmer et al. 1965, Kudlac & Groch, 1979, Schnurrbusch 1998, Busch 2007). During the initial period, uterine weight loss is mainly due to atrophy and resorption of intraluminal fluid, whereas after the initial period, uterine weight loss is mainly due to changes in the myometrium, notably a reduction in cell numbers, cell size, and amounts of connective tissue; this has been described as ‘reorganisation’ (Busch 2007). Björkman (2017) showed that transabdominal B mode ultrasound can be used to assess the course of the initial stages of uterine involution, by assessing uterine size, echotexture, and content (Fig. 17.5). Schnurrbusch (1998) defined a uterine weight of 500 to 700 g as being indicative of the completion of uterine involution, though Kauffold et al. (2005) and Busch (2007) reported a uterine weight of 1.5 kg. However, although uterine weight is an indicator of the successful completion of uterine involution, it is not necessarily a good indicator for subsequent fertility (Kauffold et al. 2005). During the third week postpartum, many authors reported an increase in uterine weight for the length of the uterine horns (Busch 2007). Busch (2007) interpreted the increase in length and weight of the uterus during week three postpartum as tissue proliferation due to increased oestrogen production by developing follicles and considered that it was a sign of completion of uterine involution. Delayed uterine involution may cause subsequent fertility problems if sows are bred after a short lactation of, for example, 3 weeks. Björkman (2017) reported that prolonged parturition, multiple stillborn piglets, obstetrical intervention, and retained placentae can delay uterine involution. On the other hand, exogenous oxytocin

• Fig. 17.4  Decrease in uterine size (involution) as measured by ultrasound during the first week postpartum. (Adapted from Björkman, S., 2017. Parturition and subsequent uterine health and fertility in sows. (PhD thesis, University of Helsinki.)



CHAPTER 17  Disorders of Parturition and the Puerperium in the Gilt and Sow

• Fig. 17.5  Real time ultrasound image of a sow 3 days postpartum. (A) Enlarged uterine horn. (B) Enlarged blood vessels. (From Björkman et al, 2017.)

hastens uterine involution (Björkman 2017). Compared with the uterus, involution of the cervix is very rapid and completed within 1 week (Busch 2007, Kudlac & Groch 1979). Resumption of Ovarian Function.  Weaning sows immediately after parturition (zero-weaned sows) or <3 weeks postpartum results in a higher incidence of anoestrus and a longer weaning-to-oestrus interval, ovulation failure, or a reduced litter size (Peters et al. 1969, Elliot et al. 1980, Varley & Atkinson 1985, Soede et al. 2009). Sows that fail to ovulate either show follicular regression, with a short/intermittent oestrus, or develop ovarian cysts. If sows are weaned >3 weeks, 98% of them show oestrus signs within a normal weaning-to-oestrus interval of less than 7 days, of which 98% ovulate (Knox & Rodriguez Zas 2001). Anoestrus and cystic ovaries in sows weaned at <3 weeks may be due to the lack of a preovulatory LH surge. The lack of the LH surge is believed to be due to high levels of corticosteroids observed in early weaned sows (Ryan & Raeside 1991) or an impaired responsiveness to a positive feedback of estradiol-17β at the hypothalamic–pituitary level (Soede et al. 2011). The impaired responsiveness may be related to depleted LH stores just after farrowing that will progressively restore during lactation (Crighton & Lamming 1969, Bevers et al. 1981). LH concentrations and the number of LH pulses remain low during days 4 to 14 and gradually increase thereafter (Stevenson et al. 1981, Shaw & Foxcroft 1985, De Rensis et al. 1993b). Besides the restoration of LH pulsatilty, follicular development during early lactation is suppressed and characterised by a large population of small-sized follicles (< 3 mm) and a small population of medium-sized follicles (3–4 mm) (Britt 1985). During the second week postpartum the number of small-sized follicles increases, and during the third week the overall number of follicles and the number of medium-sized follicles increases (Busch 2007). Nevertheless, a preovulatory LH surge will not occur before weaning because suckling and piglet proximity stimulates opioid release (De Rensis et al. 1993b). These opioids inhibit the GnRH pulse generator through neuroendocrine reflexes and therefore the LH secretion. If and how uterine involution affects the restoration of LH concentrations and pulsatility, and therefore follicular dynamics at the ovary, is not known. The restoration of LH-pulsatility and the shift in the follicular pool occur around the same time that uterine involution is complete – during the third week postpartum. Thus it is possible that uterine involution plays a role in the restoration of LH pulsatility and therefore follicular activity. Other

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factors that affect the degree of LH suppression are the suckling intensity and the energy balance of the sow (Soede et al. 2011). Postpartum Dysgalactia Syndrome, PDS.  PDS is the major puerperal disease in pigs. It affects both the sow and neonatal piglets during their first 1 to 3 days of life. It is characterised by insufficient colostrum and milk production by the sow and, as consequence, results in reduced intake by the piglets during the first days of their lives. Martineau et al. (1992) listed the symptoms that may be present in the sow and the piglets, resulting in reduced herd productivity. In the sow the common general symptoms include fever (> 40°C), loss of appetite, and lethargy. The local symptoms are observed as inflammation of the mammary glands, dysgalactia, and metritis. In piglets < 1 week old, there is increased mortality, diarrhoea, and increased heterogeneity in the litter, and for those more than 1 week old, there is increased heterogeneity of the litter and low weaning weights. For the herd there is a reduced number of piglets/ sow/year. PDS is considered to be a multifactorial disease involving different pathways. The current hypothesis is that interactions between endotoxin produced by Gram-negative bacteria in the gut, mammary gland and/or uterus, and alterations in the immune and endocrine functions, play a central role in the development of PDS (Maes et al. 2010, Martineau et al. 2012). In the study by Bostedt (1998), 24.4% of gilts suffered from a feverish puerperal illness; 24.4% exclusively showed signs of mastitis; in 29.5% there was a combination of mastitis and an inflammatory infection of the genital tract; 46.1% of the cases had only infection of the reproductive tract. Predominantly E. coli, followed by Staphylococcus spp. and Streptococcus spp., were isolated from the genital tract. The prominent role of E. coli has also been shown in puerperal mastitis, and therefore E. coli is considered the causative pathogen for agalactia in the majority of cases (Gerjets & Kemper 2009). This is supported by a study of Nachreiner and Ginther (1974) that challenged periparturient sows with lipopolysaccharide (LPS) endotoxin of E. coli and in which sows generated symptoms similar to postpartum agalactia. There is actually little information available about if, and how, farrowing affects PDS. There seems to be a connection between a prolonged duration of farrowing and PDS. For example, both have common risk factors. These are: (1) constipation (Peltoniemi & Oliviero 2015, Hermansson et al. 1978, Martineau et al. 1992, Oliviero et al. 2009); (2) increased back fat (Göransson et al. 1989. Oliviero et al. 2009); (3) no farrowing supervision (Papadopoulos et al. 2010, Björkman et al. unpublished); (4) restricted space in farrowing crates (Bäckstrom et al. 1984, Cariolet 1991, Oliviero et al. 2008); and (5) farrowing induction (Papadopoulos et al. 2010, Smith 1982). Furthermore, associations between prolonged farrowing and general signs of PDS (Tummaruk & Sang-Gassanee 2013, Bostedt et al. 1998), such as fever, anorexia, and metritis (Björkman 2017) have been demonstrated. There seems to be an effect of farrowing duration on puerperal diseases. In a study by Tummaruk and Sang-Gassanee (2013), the percentage of sows with fever during the first 24 hours postpartum increased from 40% to 100%, when the farrowing duration increased from <2 to 4 to 8 h. Furthermore, until the third day postpartum, the percentage of sows with reduced appetite was higher than in sows with a farrowing duration 4 to 8 hours than in sows with <4 hours. A study by Bostedt et al. (1998), which examined gilts suffering from a feverish puerperal illness, found that the farrowing duration had a significant effect. Of the sows, 85.9% of sows with consequent puerperal illness had farrowing durations of >6 hours, whereas

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78.8% of control sows completed parturition in <3 hours. Other significant factors affecting the incidence of feverish puerperal illness were the frequency of obstetrical intervention and the stillbirth rate. The frequency of obstetrical intervention measured in the group of sows was 27%, whereas it was 9.5% in the control group. The stillbirth rate was significant higher in the ailing group than in the control group. Björkman et al. (unpublished) have linked exactly the same factors with puerperal metritis. When the birth canal was palpated and/or piglets removed manually, the incidence of puerperal metritis increased. The same association was found with the number of stillborn piglets. Furthermore, retained retention of placentae was shown to increase the incidence of puerperal metritis significantly.

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