Dystocia and neonatal resuscitation Flashcards

1
Q

What is the normal length of gestation (measured from mating) in

a) Dogs
b) Cats

A

a) Dogs: 57 – 72 days

b) Cats: 52 – 74 days

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2
Q

Explain why there is a variability in gestation length in dogs. Measurement of which hormones may be helpful in closer estimation of parturition date?

A

Causes for variation in expected parturition date include the variable time at which a bitch may stand to be mated relative to time of ovulation, prolonged life of the oocyte and the length of time spermatozoa can survive in the reproductive tract of the bitch (sperm can survive up to 7 days in utero).

Parturition typically occurs 65 days after a peak in LH. At the time of ovulation, progesterone concentration typically measures 4–10 ng/mL. Parturition occurs 63 days (+/−1) following the date of ovulation.

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3
Q

Describe hormonal and physiological changes required for induction of parturition

A

The signal for parturition is thought to be fetal.

Maturation of the foetal adrenal cortices results in cortisol release from the fetal adrenal gland.

↑ oestrogen secretion by ovarian tissue through day 45–60 of pregnancy.

Estrogen stimulates the upregulation of genes encoding myometrial contraction-associated proteins, and promotes prostaglandin release from the uteroplacental complex (now thought to be primarily trophoblastic cells).

Prostaglandin E2 (PGE2) produced is luteolytic, resulting in corpus luteum regression and a reduction in circulating progesterone.

As a result of the luteolytic effect of PGE2, progesterone concentration rapidly drops from a range of 4–10 ng/mL to approximately 2 ng/mL over a 12–24-hour period toward the end of pregnancy.

Falling progesterone is believed to cause a rise in circulating prolactin, and subsequently lactation.

Parturition occurs 24–48 hours following the rapid decline in circulating progesterone.

Prostaglandin F2-alpha plays a key role in increasing the sensitivity of the myometrium to oxytocin.

This in turn facilitates smooth muscle contraction, and softening of the cervix.

Oxytocin also plays a role in parturition.

Oxytocin is secreted via the posterior pituitary gland in response to increased pressure placed upon the cervix.

Oxytocin release results in activation of a sensory pathway that ultimately terminates in the proventricular nucleus of the hypothalamus. Neural impulses are then sent to the posterior pituitary resulting in the release of oxytocin.

Oxytocin in turn increases myometrial contractility.

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4
Q

The following graph shows hormonal changes occurring in a bitch. Label the graph with the following:

a) Progesterone
b) Oestrogen
c) Ovulation
d) Follicular stimulating hormone
e) Luteinising hormone

Additionally, label the graph with the following phases of oestrus (draw a horizontal line to indicate the approximate length of each phase):

o Anoestrus

o Proestrus

o Oestrus

A

Anestrus -20 to -10 days: FSH up then down
E2 increases end of anestrus and over proestrus
Estrus LH peak, E2 start decreasing, ovulation mid estrus, progesterone increases

a) Anoestrus considered to be “obligate” lasting a minimum of 7 weeks after progesterone declines below 1–2 ng/ml, and averages 18–20 weeks (2 to >9mths Romangoli)
b) Proestrus average 9 days (up to 4 wks)
c) Oestrus average 9 days (5-10 days Concannon, 4-24 days Romangoli)

Ref. Concannon 2011, Ettinger (chapter by Romangoli) 2017, Wisconsin Uni http://www.ansci.wisc.edu/jjp1/ansci_repro/lec/lec_25_dog_cat/lec25out.htm

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5
Q

Describe physiological, behavioural and hormonal changes occurring during different stages of normal parturition. Indicate approximate length of each stage.

A

Stage 1:

  • nesting behaviour
  • relaxation and dilation of cervix
  • foetus adopts birth posture
  • uterine contraction commences
  • chorioallantois enters vagina
  • duration 6-12h (up to 36h)
  • peak prolactin + drop in progesterone 12-24h prior parturition and increase in PGF2α

Stage 2:

  • uterine contraction continues
  • foetus enters birth canal
  • overt abdominal contraction commences
  • amnion enters vagina
  • foetus expelled
  • duration 2-12h (rarely 24h in bitch, but normal for queen to last up to 24h)
  • increase in oxytocin levels

Intervals between pups 30min up to several hours (BSAVA Manual 4h)

Stage 3:

  • placental circulation lost
  • placental dehiscence and separation occurs
  • uterine and abdominal contractions continue
  • placenta is expelled
  • lochia for up to 3 weeks, uterine involution 12-15 weeks
  • endometrium secretes pulses of PGF2α, oxytocin causes uterus to contract to disrupt contact between uterus and foetal membranes
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6
Q

Define dystocia and 4 clinical categories of small animal dystocia

A

Dystocia is defined as an inability to expel the foetus(es) from the uterus or birth canal

Failure to begin stage 2 labor
Cessation of stage 2 labor before completion
Prolonged unproductive stage 2 labor
Apparently normal stage 2 labor with foetal distress

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7
Q

List at least 7 indicators for clinical examination in a bitch/queen in labour

A

● Client concern
● Signs of systemic illness
● Decline in body temperature, followed by return to
normal temperature with no progression into labor
● Stage 1 labor extends beyond 12 hours with no
evidence of progression
● No puppy within 2 hours of entering stage 2 labor (or
no kitten within 1 hour)
● Forceful abdominal contractions and no fetus within a
30-minute period
● Intermittent abdominal contractions with no fetus
delivered within a 2-hour period
● If pregnancy extends beyond 72 days with no
progression into labor
● Stillborn fetuses are passed
● Uteroverdin in vaginal discharge but no puppy or
kitten passed within 2 hours

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8
Q
  1. List at least 3 maternal and 3 foetal factors that might contribute to dystocia
A
Maternal
Physiologic
Primary uterine inertia
Hereditary
Stress/environmental disturbances
Old age
Obesity
Systemic disease
Uterine overdistention (eg, large litter size, fetuses too big)
Uterine underdistention (eg, small litter size, inadequate fetal fluids)
Estrogen/progesterone balance
Calcium/magnesium balance
Inadequate oxytocin secretion
Prematurity
Secondary uterine inertia
Morphologic
Primary (eg, birth canal too small)
Secondary (eg, abnormal influence on or within birth canal)
Pelvic fractures
Uterine torsion
Uterine rupture
Uterine herniation
Uterine prolapse
Mass-like lesions of pelvic canal, uterus, vagina, or vulva (eg, hyperplasia, neoplasia, hematoma, abscess)
Fibrosis of uterus, cervix, or vagina
Vaginal septum
Fetal
Malpresentation
Oversize (eg, single fetus pregnancy)
Fetal death
Fetal malformations
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9
Q

Name and briefly describe 4 neonatal reflexes that help to assess vigor

A

Dorsal stimulation
A neonate is rubbed strongly over the dorsal lumbar area and should move vigorously and/or squeal in response

Righting reflex
The neonate is placed on its back and should then immediately turn itself over into ventral recumbency

Suckling reflex
A finger, bottle or the dam’s nipple is offered to the neonate that should then begin suckling

Rooting reflex Response
The neonate should push its muzzle into a cupped hand or against its mother’s mammaries in search of milk

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10
Q
  1. True or false?
    a) Normal heart rate at birth for neonatal puppies is 160-180bpm and for kittens 200-220bpm.
    b) Doxapram is a central respiratory stimulant which is unlikely to improve hypoxaemia associated with hypoventilation.
    c) Normal body temperature in puppies and kittens is 35.2-37°C at birth and normalises to adult values at 4 weeks of age.
    d) Mean arterial pressure in neonatal puppies is lower at birth (49mmHg) but normalises by 1 month of age (94mmHg).
A
  1. True or false?
    a) Normal heart rate at birth for neonatal puppies is 160-180bpm and for kittens 200-220bpm. False – for both kittens and puppies it’s 200-220bpm.
    b) Doxapram is a central respiratory stimulant which is unlikely to improve hypoxaemia associated with hypoventilation. True
    c) Normal body temperature in puppies and kittens is 35.2-37°C at birth and normalises to adult values at 4 weeks of age. True
    d) Mean arterial pressure in neonatal puppies is lower at birth (49mmHg) but normalises by 1 month of age (94mmHg). False – it remains that low for first several months and normalises at 9mths of age.
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11
Q

Which of the following laboratory values are expected to be markedly elevated in neonates when compared with adult dogs and cats?

a) HCT
b) USG
c) ALP
d) Bilirubin

A

Which of the following laboratory values are expected to be markedly elevated in neonates when compared with adult dogs and cats?

a) HCT – Incorrect. HCT decreases from 47.5% at birth to 30% by day 28 in puppies
b) USG – Incorrect. Urine is isosthenuric as ability to concentrate or dilute urine is limited
c) ALP – Correct! As high as 3845 IU/l in puppies, 3x fold increase in kittens
d) Bilirubin – Incorrect. Only mild increase observed

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12
Q

Explain how drug absorption differ in neonates when compared with adults.

A

Drug absorption

Oral absorption of drugs in the neonate is often different from that in the adult due to:

  • Slower transit time as a result of delayed/slowed gastric emptying
  • Increased volume of mucus within the stomach
  • Higher stomach pH

PO route of administration should be avoided during first 72h of life because absorption is significantly higher due to increased GI permeability.

Intestinal flora is also very sensitive to disruption by oral antimicrobial agents.

IV and IO route of administration is the most predictable and is preferred over IM or SC administration.

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13
Q

Explain how drug distribution differ in neonates when compared with adults.

A

Drug distribution

The distribution of drugs is quantified by the volume of distribution. For water-soluble drugs, the volume of distribution is increased in the neonate because it has a greater body water content than an adult.

· For lipid-soluble drugs the volume of distribution is decreased owing to the lower body fat content. There is also decreased binding to plasma proteins and a lower concentration of albumin in neonates.

· The blood–brain barrier is not complete in very young neonates; therefore, there is increased permeability to lipid-soluble drugs and higher concentrations of drugs that are normally removed by p-glycoprotein. This may lead to increased effects of anaesthetics and raised concentrations of avermectins and digoxin in the brain (thus, avoid them).

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14
Q

Explain how drug metabolism and excretion differ in neonates when compared with adults.

A

Drug metabolism and excretion

It accounts for most of the differences in neonatal physiology and thus greatly influences drug disposition.

· Renal clearance of drugs is decreased in neonates and renal excretion of many drugs (e.g. diazepam, digoxin) is diminished, which increases the half-life of the drug in circulation.

· Drugs requiring activation via hepatic metabolism will have lower plasma concentrations, and drugs requiring metabolism for excretion will have higher plasma concentrations.

· Antibiotics that are safe in neonates include penicillins and cephalosporins but the dosing interval should be increased to every 12hours rather than q8h. Tetracyclines should be avoided because of enamel hypoplasia and tooth discoloration, and chloramphenicol because of possible bone marrow toxicity. Metronidazole is a preferred drug for giardiasis and anaerobic infections but the dose and/or frequency should be decreased in neonates.

· Dosages of CV drugs (adrenaline, dopamine, dobutamine etc.) can be difficult to determine due to variable maturity of the autonomic nervous system. Response to atropine and lidocaine is decreased in the neonate.

· Phenothiazine tranquillizers should be used with caution because they induce hypothermia and hypotension as a result of vasodilation which, in the neonate, is not compensated for by an increase in heart rate. Midazolam is probably a better choice of drug for this purpose.

· For analgesia, opiates are very safe in neonates when given at the correct dosage but the animal must be monitored closely because of the propensity of these drugs to depress HR and RR.

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15
Q

Name at least 4 risk factors for increased neonatal mortality.

A

Low birth weight (most significant factor).

Obese dams, singleton litters, being the first neonate born in a litter.

Extended or difficult labour.

Poor prepartum condition of the dam, prematurity, congenital malformations, genetic defects, injury, environmental exposure, malnutrition, parasitism, and infectious disease all contribute to neonatal morbidity and mortality.

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16
Q

This puppy was stillborn via C-section required due to obstructive dystocia. What’s the pathophysiology of the condition the puppy was likely suffering from? Which breed is predisposed to it?
(big swollen puppy, dead, weird shape)

A

Anasarca, a lethal congenital oedema, can occur with or without concurrent cardiovascular abnormalities. Congenital hereditary lymphoedema causes oedema of the extremities and sometimes head, and is associated with morphological lymphatic abnormalities. The genetics are not known; the trait is thought to be inherited as an autosomal dominant trait.

It’s a recognised problem in bulldogs although other breeds can suffer from it as well.

17
Q

What’s the rationale behind administration of omeprazole to dogs with hydrocephalus?

A

Omeprazole decreases CSF movement into the ventricles via proton pump inhibition

Not sure about the evidence though?

First study in dogs used mock CSF with omeprazole in it and used a more invasive ventriculocisternal perfusion technique to measure the effect of omeprazole administration. Result: 26% reduction in CSF production (1997).

Two more recent studies in dogs (same research group) where oral or IV omeprazole were administered didn’t show improvement as measured by albumin quotient or CSF omeprazole concentration (in the IV study 2019).

Does it mean that commonly prescribed oral or IV doses of omeprazole are actually inefficient in reduction of CSF production?

18
Q

What’s the pathophysiology of cleft palate? What management options can be discussed with motivated owners?

A

Pathophysiology

Secondary cleft palate is a congenital oronasal fistula resulting in incomplete closure of the hard and soft palate.

Cleft palate occurs alone or in combination with a primary cleft palate involving the lip and premaxilla.

Cleft palate results from incomplete fusion of the palatine shelves, most critical at 25–28 days gestation.

Palatal defects are attributed to genetic (recessive or incompletely dominant polygenic inheritance), teratogenic (drugs such as steroids, supplements), nutritional (folic acid deficiency) or infectious (viral) factors.

Therapy

Feeding by orogastric tube is indicated until the puppy reaches a size permitting oral surgery, traditionally advised at 8–12 weeks of age. Palatoplasty in such young puppies remains difficult due to patient size and anticipated postoperative orofacial growth, often necessitating multiple operations. Oesophagostomy or gastrostomy tube placement can facilitate feeding over time, but requires significant client commitment and can still result in aspiration. Palatal prostheses are problematic.

Methods to improve survival of pet puppies with cleft palates are sought by motivated clients. Following the postpartum diagnosis of cleft palate, feeding the dam’s colostrum for 24 hours followed by artificial bitch milk replacer by intermittent orogastric tube can be instituted. At 4 weeks of age, transition to a dry (not soft soaked) commercial paediatric dog food should be made, facilitating swallowing without ingesta becoming misplaced into the nasal cavity. Water should be made available through an overhead ballpoint tube cap system. This permits dogs with secondary cleft palate to attain adult size before reconstructive surgery, which may not be necessary due to closure of the defect with maturity.

19
Q

Briefly explain pathophysiology behind neonatal isoerythrolysis in kittens.

A

Feline placenta is of the endotheliochorial type and only allows small and insignificant passage of maternal antibodies. Neonatal isoerythrolysis occurs in kittens after initial colostral ingestion. The disease occurs as a result of the dam’s and kitten’s blood types being different, and the kitten ingesting antibodies against its own blood type during first 12-24h after birth. Type B cats with type A kittens are the most likely to produce this condition, as type B cats carry strong anti-A antibodies.

(Found on VIN but could not find the reference: 24h post partum kitten’s GIT is unable to absorb antibodies from colostrum and the kitten is no longer at risk of isoerythrolysis.)

The most common breeds with high numbers of type B cats include the Cornish rex, Devon rex, and British short-hair.

20
Q

The fading puppy/ kitten syndrome refers to neonatal death secondary to systemic infection. Give examples of in utero or postpartum infections that can contribute to this presentation.

A

Viral: Distemper, parvovirus, canine (CHV-1) and feline herpesvirus, FIP, FIV, panleukopenia, feline leukemia virus.

Bacterial: Brucella canis (canine), Campylobacter, Salmonella, Klebsiella, streptococci and staphylococci, and Leptospira (canine).

Protozoal: Neospora (canine) and Toxoplasma gondii (canine and feline).

Mycotic infection is rare.