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Parturition Occurs in three stages: Stage one: initiation of myometrial contractions, removal of progesterone block, cervical dilation Stage two: expulsion of the foetus Stage three: expulsion of foetal membranes

Stage one The foetus outgrows the placentas ability to supply nutrients and oxygen  Foetal stress  Increased concentration of fetal ACTH leading to the release of fetal cortisol from the stimulation of the foetal pituitary and foetal adrenal cortex  Progesterone is then converted to oestrogen (high E2 low P4) Foetal cortisol promotes the synthesis of 17a-hydroxylase, 17-20 desmolase and aromatase which convert progesterone to oestradiol Foetal corticoids also cause the placenta to synthesise PGF 2a (which helps to abolish the progesterone block and causes relaxation of the pelvic ligament through relaxin)  Increase in E2 and decrease in P4 removes progesterone block and initiations myometrial contractions and mucous secretion from the vagina and cervix As both oestradiol and prostaglandin become elevated, the myometrium becomes increasingly more active and begins to display noticed contractions Increased pressure in the uterus causes the foetus to move to attain correct foetal orientation. The foetus moves from a dorso-pubic presentation to dorso-sacral

Stage two Increased pressure on the cervix  Cervical dilation  Ferguson’s reflex (foetus stimulates sensory neurones at the cervix, oxytocin is secreted from the posterior pituitary  oxytocin stimulates contractions of the myometrium)  Expulsion of the foetus NB: in stage two the “water breaks” where the chorioallantois releases foetal respiratory fluids and other fluid by products) Stage three Chorionic villi vasoconstrict and become detached from the crypts of the maternal side of the placenta  Expulsion of foetal membranes NB: serious and potentially fatal complications of failure of stage 3 or retained RFM. The clinical implications vary between species but usually there is increased risk of postpartum disease, decreased milk production, reduced reproductive performance and increased cull rates

Hormones involved Oestrogen: increases secretion by female tract, increases myometrial contractions, increases pressure and cervical stimulation, increases oxytocin PGF2a: causes luteolysis leading to myometrial contractions Relaxin: from PGF2a, causes pelvic ligament stretching

Complications of parturition Horse

Cow

Avian

Retained foetal membranes

Dystocia

Chronic egg laying

Occurs when fetal membranes are retained for more than 3 post-partum (failure of stage 3) and must be treated immediately (medical emergency) Lay membranes out membranes to ensure they are in a ‘F’ shape and all have been expelled correctly RFM 3-8 hours post-partum: administer 10IU oxytocin IV RFM 8 hours post-partum: administer a 100IU oxytocin and saline Burn’s technique: infuse up to 20L of saline solution into the allantoic space

Causes: too big foetus, too small birth canal, head to pelvis ratio is disproportionate, mating a large bull to a small cow, mating before the heifer achieves CMW (55-60% mature BW), two calves presenting at ones, foetal malorientation, previous history of dystocia, strong contractions in stage two with no delivery of foetus

Causes: photoperiod is too long, too much sexual stimulation

Increased risk of postpartum disease, reduced milk production, reduced reproductive performance and increased cull rate

Endometritis

Dystocia: the mechanical obstruction of an egg

Endometritis: inflammation of the endometrium alone Cytological endometritis: the percentage of neutrophils exceeding a threshold, usually between 5 and 18 percent of cells in endometrial cytology samples collected ≥21 days PP Clinical endometritis: >50% purulent uterine discharge in the vagina ≥20 days PP, mucopurulent uterine discharge in the vagina ≥26 days PP Subclinical endometritis: purulent vaginal discharge; ≥8% neutrophils between days 21-33 PP; ≥6% neutrophils between 34-47 days; ≥4% after 47 days PP Puerperal metritis: cow has systemic signs within 10 days PP

Multifactorial causes: hypocalcaemia, oviduct or uterine muscle dysfunction, excessive egg production, large misshapen eggs, old hens, obesity, oviduct tumour Can to nerve paralysis and complications urinating and defecation

The foetal membranes should be ~10% BW Red bag foals Rupture of the chorioallantosis, urine like discharge Foal becomes hypoxic as the connection between maternal and foetal oxygen is detached This is an emergency, remove the foal ASAP and give oxygen therapy

At risk breeds: high risk are Belgian Blue, Limousin, Charolais, Simmental, medium risk are Holstein-Frisian, Murray Gray, Angus and Hereford, with low risk breeds being Jersey

Mucous is scored on character and odour Diagnosis: ultrasonography, time PP, WBC count, cytology, palpation, bacteriology

Consequences: egg binging, hernia, Ca deficiency and osteoporosis Treatment: Lupron, GnRH agonist Egg binding/dystocia Failure of egg to pass through the oviduct at a normal rate/weight

Treatment: progesterone, oxytocin and fluid therapy

Dystocia in Dogs Risk factors

Maternal causes (~75%)

Foetal causes (~25%)

Management

Treatment

Breed: designer dogs, Boston terrier, mastiff, clumber spaniel, French bulldog, bulldog, miniature bulldog etc.

Uterine inertia (primary and secondary)

Oversized foetuses

History

Elective c-section

Malpresentation or malorientation

Complete physical exam (TPR)

Monstrosities

Clinical reproductive exam

Advantages: maximum number of healthy, viable puppies, safety of dam

Age Parity (common in nulliparous bitches >6 years) Litter size Foetal oversize Monstrosities

Primary: uterus may fail to respond to fetal signals, could be due to a single puppy (single puppy syndrome) due to overstretching of the myometrium due to a large litter size, excessive Fetal fluids or oversized foetuses Secondary: due to exhaustion of uterine myometrium caused as a result of obstruction of the birth canal

Inappropriate breeding’s Obstruction of the birth canal Head to pelvis ratio too large Reasons: uterine torsion/rupture/malpresentation, congenital malformations of the uterus, neoplasms, vaginal septa, fibrosis of birth canal, narrow pelvic canal etc.

Intervention (medial or surgical) Ultrasonography or radiograph Digital examination Signs of foetal distress (HR2ng/mL (P4 serum), decrease in temperature, can use radiographs to determine gestational age

Condition

Aetiology

Clinical signs

Diagnosis

Treatment

Failure of milk secretion

Underdeveloped mammary glans, loss of condition in pups, agitation of bitch and pups

Mammary glands look normal on close examination, no milk is visible on evaluation of teat canal

Promote suckling, provide optimum levels of nutrition, treat underlying disease, oxytocin, metoclopramide and phenothiazine tranquilisers

Mammary gland disorders Agalactia

1°: anatomical or physiological abnormalities

Loss of condition in pups

2°: failure of milk ejection Can be due to premature whelping Mastitis

Ascending bacterial infection, trauma, poor hygiene, haematogenous spread

Swollen glands, reddish, hot and painful

Clinical signs, colour of milk, cytology and culture

Broad spectrum antibiotics Anti-inflammatory drugs, intravenous fluids Hot compress over the gland (help drainage) Nursing form the affected gland (if not abscessed or gangrenous) Gangrenous gland should be debrided and drained with 1% betadine Diuretics Mastectomy in severe gangrene/necrosis

Increased SCC in milk

Agents: E. coli, staphylococci, Bhaemolytic streptococci

Uterine disorders Acute postpartum metritis

History of dystocia, often fetal retention or retained fetal membranes

Heavy vaginal discharge 2-3 days postpartum, toxaemia and depression, puppy deaths during the first week

Ultrasound, radiology, CBC, cytology and culture

Fluids, antibiotics, ovariohysterectomy (depending on severity)

Subinvolution of placental sites

Bleeding from implantation sites

Bleeding from implantation sites Normally bitch has no illness Seen 4-15 weeks postpartum

Vaginal cytology may reveal trophoblast cells

Supportive therapy, antibiotics

Haemorrhage

Vaginal/uterine tear, vessel rupture, VWB syndrome, complications during parturition

Bloody discharge

Incompletion of stage three parturition

Thick dark vaginal discharge (severe problem if accompanied by a

Retained placenta

Distinguish from normal PP discharge

Exploratory laparotomy, blood transfusion,

Exploratory laparotomy

Placenta was not expelled during parturition

Oxytocin, antibiotics, extraction by milking of uterine horn or using

retained foetus or infection)

Uterine rupture

forceps

As a result of dystocia or when oxytocin or prostaglandin is used during dystocia; due to injury during late pregnancy

abdominal pain and distension, rapid deterioration of body condition

Signs of foetal distress

Pre or postpartum period due to depletion of Ca in the extracellular compartment

nervousness, elevated body temperature (>40.5°C), dry mouth and sclera, panting, restlessness, whining, muscle tremors, staggering, stiffness and finally collapse, clonic spasms/seizures, laboured breathing, salivation and death

blood calcium level...