Dystocia Flashcards

1
Q

What does dystocia mean?

A
  • difficulty giving birth
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2
Q

What % of calvings are affected by dystocia?

A

8-10%

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3
Q

Causes of dystocia

A

At conception or early gestation
- foetal sex
- foetal abnormalities
- twins
- sire factors (e.g. breed, calving ease)
- dam factors (e.g. parity, calving history)

At late gestation
- gestation length
- foetal oversize
- dam undersize
- hypocalcaemia
- peri-parturient stress

At parturition
- foeti-maternal disproportion
- uterine torsion
- foetal malpresentation
- uterine inertia
- cervical or vulval stenosis

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4
Q

Most common causes of dystocia

A

Cattle = foeto-maternal disproportion
▪ 50-80%

Sheep = malpresentations
▪ > 50% of cases

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5
Q

Effects of dystocia

A

▪Reduced welfare
▪Reduced production
– Cow = subsequent lactation
– Calf = 1st lactation
▪ Stillbirth
▪Dam death
▪Postpartum problems ▪E.g. RFM, metritis, injuries

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6
Q

Options for management of dystocia

A

▪Manual correction and deliver per vaginum ▪Caesarean section
▪Foetotomy (foetus needs to be dead)
▪Euthanasia of dam +/- foetus

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7
Q

Manual correction and delivery

A

▪ Will only be successful if foeto-maternal disproportion NOT present
– Malpresentations
– Some soft tissue obstructions (e.g. vulval stenosis)
▪ Correct malpresentation
– Epidural can be helpful (if soft tissue obstructions)
– Consider episiotomy

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8
Q

Indications for c-section

A

▪ foeto-maternal disproportion
▪malpresentations that cannot be corrected
▪breech calves
▪elective (e.g. high value calves) (ethical q’s re breeding animals knowing they’ll need a c-section, e.g. Belgian blues)

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9
Q

When are c-sections not suitable?

A
  • if calf decomposing→foetotomy
    – would contaminate the dams abdomen with bacteria -> very likely to get peritonitis
  • Alternative approach needed if C-sec performed
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10
Q

Foetotomy (AKA ‘embryotomy’)

A

▪Foetus will not survive – only suitable if already dead (preferable to C-sec if not fresh) or if euthanasia of foetus required
– but euthanasia of the foetus is very tricky, esp without contamination/damage of the dam as well
▪Epidural recommended→provides analgesia and reduces straining
▪Partial or total
– Partial = removal of part of the foetus only (e.g. head)
– Total = division of the whole foetus into two or more sections
▪ Fetotome prevents soft tissue damage to the dam with the wire

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11
Q

Advantages of foetotomy

A
  • Reduction in foetal size allows easier delivery
  • Can be quick (especially partial)
  • Can be done without assistance (although assistance recommended if possible)
  • Avoids C-sec
    – Especially useful if C-sec contraindicated
    (emphysematous foetus)
    – Better for dam in some circumstances
  • Can be performed with minimal equipment if required
    – Especially sheep
    – Partial and subcutaneous need less equipment
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12
Q

Disadvantages of foetotomy

A
  • Risk of iatrogenic injury
    – Can be severe or even life-threatening
  • Can take a long time (especially total)
    – Exhaustion of dam and vet
  • Requires training and technical competency
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13
Q

Percutaneous foetotomy

A
  • Percutaneous = dissection is made through foetal skin
  • ‘classic’ technique
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14
Q

Subcutaneous foetotomy

A

= limb removal without skin
- An incision made in the skin
- Foetotomy knife introduced under the skin and limb dissected away from body
- Easier, less tiring and less equipment needed

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15
Q

Indications for percutaneous foetotomy

A
  • Foeto-maternal disproportion
  • Pathological foetal oversize
  • Congenital foetal malformations
  • Malpresentations that cannot be corrected

NB: these all only apply where the foetus is already dead

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16
Q

Indications for subcutaneous foetotomy

A
  • Same as for percutaneous except correction must be achievable through limb removal only
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17
Q

Less common causes of dystocia

A
  • Dropsical conditions (placental origin)
  • Congenital abnormalities (foetal origin)
  • Teratogens
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18
Q

What does ‘dropsy’ mean?

A

= accumulation of fluid

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19
Q

What are the 2 dropsical conditions?

A
  • hydrallantois
  • hydramnion
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20
Q

What is hydrallantois?

A

▪ Excess fluid accumulation in the allantois
▪ 85-90% of bovine cases
▪ Placental origin
▪ Foetus normal
▪Sporadic occurrence
▪Up to 10x expected volume of allantoic fluid
– Normal = 8-15 L
▪Fluid accumulates after mid-gestation
▪ Failure in mechanisms of production and absorption
– Excessive production, little-to-no absorption
▪Reduced number of placentomes
▪ Permanent alteration of endometrium

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21
Q

What is hydramnion?

A

▪ Excess fluid accumulation in the amnion
▪ ~10% of bovine cases
▪ Foetal origin
▪ Foetal abnormalities present
▪Related to foetal abnormalities
– Failure of swallowing or digestion of foetal fluids
– Future breeding prognosis of dam is reasonable
▪Progressive abdominal enlargement in 3rd trimester
– Slower development than hydrallantois
– Uterus and abdomen accommodates extra fluid better
– Less sick cow
– Placentomes still palpable
▪May go undiagnosed until parturition
– Large volume of thick, syrupy fluid
– Foetal abnormalities

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22
Q

Can hydrallantois and hydramnion occur together?

A
  • yes occasionally
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23
Q

Hydrallantois prognosis

A
  • guarded to poor
  • if survives, cull of cow recommended
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24
Q

Hydrallantois CS

A

▪Bilateral abdominal distention
– Symmetrical
▪Uncomfortable
▪ Inappetant
▪Reduced/absent rumen function
– Due to compression
▪Recumbency
▪Tight uterine wall palpable per rectum
– Could potentially rupture from rectal

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25
Q

Tx of dropsical conditions

A

▪ Induce/terminate pregnancy
– Prostaglandin / steroids
– Need to provide replacement fluids to cow
-> Prevent hypovolaemia
-> Correct electrolyte disturbances

▪ Euthanasia
– Salvage slaughter if fit to travel

▪ Trochar and drain fluid
– Pass trochar into cervix
– Useful if very close to calving, otherwise would have to repeat frequently
– Rapidly re-accumulation of fluid occurs in hydrallantois
– Need to provide replacement fluids to cow?
-> ongoing debate re whether need to replace fluids
-> risk of hypovolaemic shock BUT it’s extra fluid that shouldn’t be there, so removal may not be an issue
-> IV fluids unlikely to cause harm

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26
Q

Congenital abnormalities

A
  • arthrogryposis
  • schistous réflexes
  • congenital chondrodysplasia
  • hydrocephalus
  • large offspring syndrome
  • cranial defects
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27
Q

Arthrogryposis

A

▪ Relatively common malformation
▪ Limb ankylosis (fusion of the joints in unusual directions)
▪ Usually combined with other congenital malformations (e.g. cleft palate)
▪ Liveborn neonates unable to stand → euthanasia
▪ Foetotomy or C-sec usually needed

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28
Q

Causes of arthrogryposis

A

Genetic
- Autosomasal recessive in Charolais breed
-> Arthrogryposis, cleft palate, scoliosis (spinal twist), kyphosis (spinal rounding)

Viral infection in utero
- Schmallenberg virus
-> Arthrogryposis affecting multiple neonates in same year
->Sheep, goats and cattle all affected.
- Bluetongue virus
-> Ruminants and camelids affected.
->Abortion is more common.
- Akabane virus
-> Not reported in UK
- Viruses are the most common cause, esp if multiple animals affected

Teratogenic plants
- Lupines (not all species)
-> Contain anagyrine.
-> Congenital deformities occur in cattle if ingested between d 40 and 70 of gestation
-> USA.

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29
Q

Schistosomus reflexus

A

▪‘Inside out’ foetuses ▪Rare, fatal malformation
– Likely genetic
▪Foetotomy or C-sec
▪Be careful not to confuse with uterine rupture
▪ Good CE and vaginal exam will differentiate between this and uterine rupture

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30
Q

Congenital chondrodysplasia

A

▪‘Bulldog’ calves
– Short legs
– Domed head
– Brachygnathia inferior (undershot jaw)
▪Dexters, Holstein, Jerseys – Likely genetic
– Other breeds reported
▪Does not always = dystocia

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31
Q

Hydrocephalus

A

▪ Increase in CSF volume → domed head
▪ Calves born alive may have neuro deficits
▪ Teratogenic viruses implicated
– BVDv
– BTV
– Akabane virus (not UK)
▪ May also form part of mixed congenital disorders
▪ Mild cases may calve unassisted
▪ Severe cases = C-sec or partial foetotomy (remove head)

32
Q

Large offspring syndrome

A

▪ Also termed ‘abnormal offspring syndrome’
– Varied congenital abnormalities reported
▪ Associated with assisted reproductive technologies – Embryo transfer
– In vitro techniques
– Cloning
▪ Exact mechanisms unclear
▪ Very large neonates
– May be 2x average size
– Dystocia
– Macroglossia (enlarged tongue)
-> can affect ability to suckle and feed

33
Q

Cranial defects

A
  • Ancephaly
  • Otocephaly
  • Bicephaly
34
Q

What is ancephaly?

A
  • no head
35
Q

What is otocephaly?

A
  • some head structures present but no skull
36
Q

What is bicephaly?

A
  • 2 heads
37
Q

What is a teratogen?

A
  • agents causing foetal abnormalities or death
38
Q

How does the timing of exposure to teratogens influence the outcome?

A

▪Zygote→affected by chromosomal or genetic abnormalities. Often result in embryonic death

▪Embryo→affected by environmental and infectious agents. Most high risk period for developing abnormalities

▪Foetus→more resistant to environmental teratogens but structures that develop late are still susceptible to being affected (e.g. palate)

39
Q

Effects of BVD virus on calves

A
  • Abnormalities of the brain, eyes and neurological development
  • Foetal death
  • PI calves
    – May be small but may appear normal
    – Increased susceptibility to disease
    – May develop mucosal disease
40
Q

Common viral teratogens (& who they affect)

A
  • BVD virus
  • Border disease virus
  • Schmallenberg virus
  • Bluetongue virus
  • Akabane and Aino viruses
41
Q

Effects of border disease virus on lambs & kids

A
  • Abnormalities of skin, skeleton and neurological system
    – ‘hairy little shakers’
  • Foetal death
  • PI lambs
    – Similar to PI calves
42
Q

Effects of Schmallenberg virus

A
  • Arthrogryposis
  • Foetal death
43
Q

Effects of bluetongue virus

A
  • Arthrogryposis and other deformities
  • Foetal death and abortion (more common than malformations)
44
Q

Effects of Akabane and Aino viruses

A
  • Congenital malformations
  • Not currently in UK
  • Midge spread→may be seen in future
45
Q

Examples of environmental teratogens

A
  • Hemlock
  • Nitrates/nitrites (nitrate accumulating plants e.g. sugar beet, alfalfa) (nitrite based fertilisers)
  • Ergotism (mouldy feed)
  • Lead
46
Q

Effects of hemlock

A
  • Skeletal abnormalities if ingested between days 40-70 of gestation
  • Abortion
  • NB. is highly toxic to cattle and often causes death of dam
47
Q

Effects of nitrates/nitrites

A
  • Excess nitrate consumption exceeds rumen capacity for metabolism → nitrate and nitrite absorbed into circulation → interacts with haemoglobin → oxidation to methaemoglobin
  • This process can also occur in the placenta → foetal death, weak calves
48
Q

Effects of ergotism

A
  • reduced size offspring
49
Q

Effects of lead

A
  • Concentrates in CNS of foetus
    – Neurological defects
    – Reduced foetal size
  • Also causes problems in the dam
50
Q

Examples of pharmacological teratogens

A
  • Benzimidazoles
  • Tetracyclines
  • Steroids
  • Prostaglandins
  • Xylazine
51
Q

Effects of benzimidazoles on sheep

A
  • Abnormalities of the foetal skeleton, kidneys and vascular system
52
Q

Effects of tetracyclines on all ruminants

A
  • Dental discolouration
53
Q

Effects of steroids on all ruminants

A
  • Abortifacient
54
Q

Effects of prostaglandins on all ruminants

A
  • Abortifacient
55
Q

Effects of xylazine on all ruminants

A
  • Abortifacient in later stages of pregnancy
  • Causes uterine contraction -> abortion
  • Detomidine also has similar, but less pronounced effects
56
Q

What is puberty in cattle driven by?

A
  • weight, not age
  • puberty occurs at ~2/3 of adult BW
57
Q

Early unwanted pregnancy in heifers

A

▪Well grown heifers unexpectedly conceive to mis- mating
– Uncastrated youngstock
– Bulls running with herd
– Entire males escaping

Can lead to:
▪Poor heifer growth
▪Increased risk of dystocia

58
Q

How can an early pregnancy in a heifer be managed?

A
  • Wait & see
  • Elective c-section
  • Induce parturition
  • Terminate pregnancy
59
Q

How can an early pregnancy in a heifer be managed - wait & see

A
  • C-sec likely needed→can be less optimal outcomes if performed in emergency
  • Can be effective if farmer aware of mis-mating and requests vet assistance as
    soon as parturition starts
  • Only addresses issue of dystocia
60
Q

How can an early pregnancy in a heifer be managed - elective c-section

A
  • Performed at/near end of gestation before parturition starts
  • Need a idea of gestation duration → scan
  • Only addresses dystocia
  • Justified in this case
61
Q

How can an early pregnancy in a heifer be managed - inducing parturition

A
  • Aim to induce near/at term for viable but small foetus
  • May still need C-sec if calf big
  • Requires reliable insemination date → scan
  • Only addresses dystocia
62
Q

How can an early pregnancy in a heifer be managed - terminating pregnancy

A
  • Prostaglandin
  • Glucocorticoid steroids (dexamethasone)
  • Reliability dependent on stage in gestation → scan
  • Early termination can mean limited effects of pregnancy on dam
63
Q

Pregnancy termination using prostaglandins

A

▪Lysis of CL→pregnancy loss
– Progesterone needed to maintain pregnancy
▪ Abortion occurs within 7days if given <100 days gestation
– >100 days gestation timing and reliability of abortion reduced

64
Q

Why is the stage of gestation an important factor when considering the use of prostaglandins for pregnancy termination?

A
  • <100 days gestation = maximal chances (> 90%)
  • 101-150 days gestation = moderate chances (~ 60%)
  • > 150 days gestation = lower chances (≤ 40%)
    – Because placenta also a source of progesterone between days 150-200
  • > 270 days gestation to induce parturition → live calf
65
Q

Pregnancy termination using glucocorticoid steroids

A

▪Reduces placental secretion of progesterone→ pregnancy loss
– Most effective in last month of gestation
– Can also be used after day 270 to induce parturition →
live calf
▪Dexamethasone
– Give 20-30mg (for most products this is 10-15ml)

66
Q

What can you give for pregnancy termination for mid-late gestation (i.e. >150d) or if uncertain?

A
  • both dexamethasone AND prostaglandin
  • both drugs associated with increased likelihood of retained foetal membranes
  • no other adverse effects for the heifers reported
67
Q

Pregnancy induction - drug choices

A
  • Short acting (corticosteroids)
    – 20-30mg dexamethasone
  • Prostaglandins
  • Prostaglandin + corticosteroid combination
  • Longer acting corticosteroids
    – dexamethasone trimethyl acetate)
68
Q

Short acting
corticosteroids to induce parturition - advantages

A
  • High efficacy (80-90%) when given within 2 weeks of expected calving date
  • Calving occurs within 72hrs of injection
69
Q

Short acting
corticosteroids to induce parturition - disadvantages

A
  • High incidence of retained foetal membranes (RFM)
70
Q

Prostaglandins to induce parturition - advantages

A
  • Calving occurs 24-72 (average 45) hours after injection
  • Give within 2 weeks of calving date
71
Q

Prostaglandins to induce parturition - disadvantages

A
  • High incidence of RFM
  • Failure of induction common if
    given > 2weeks before end of gestation
72
Q

Prostaglandin + corticosteroid to induce parturition - advantages

A
  • More reliable than steroids or PGF alone
    – Especially if dates uncertain
  • Calving occurs 24-48hrs after treatment
73
Q

Prostaglandin + corticosteroid to induce parturition - disadvantages

A
  • Retained foetal membranes commonly occur
74
Q

Longer acting corticosteroids to induce parturition - advantages

A
  • Used if timing of calving more important than calf viability
  • Given 1 month before expected calving date
  • Calving occurs 4-26 days after injection
  • Lower incidence of RFM
75
Q

Longer acting corticosteroids to induce parturition - disadvantages

A
  • Higher incidence of calf death (up to 45%)
  • Dexamethasone trimethyl acetate currently not licensed in UK