Reproductive Surgery, Mare + Foal Flashcards

1
Q

Describe the normal placenta of a horse.

A

Chorioallantoic, diffuse placenta
Should weigh 11% of foals BW

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2
Q

Describe the normal gestational length and length of each stage of parturition in a mare.

A

Gestation = 341 days
Stage 1 = can be days to weeks
Stage 2 = 10-20mins, anything over 20 mins is abnormal
Stage 3 = within 3 hours of stage 2

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3
Q

Name the signs that would indicate a mare is going to foal soon, and when do they appear?

A

Bagging up - 2-6 weeks
Waxing up - a few days
Slackening of sacroiliac ligaments and vulva - a few days to the day of
Dripping milk - 24-48 hours, but they might not get to this stage if they foal early
Nesting behaviours - may or may not happen, a few days
Foaling alarms can be used to help - if they are the halter alarms then they go off when mares lay down so it depends on how much the mare likes to lay down and sleep (can be days before they foal or it could be that night - the point is you need to be checking them everytime it goes off), otherwise the vulva ones only go off when there is stretching and dilation of the vulva so at the start of stage 2
Changes in milk electrolytes (strip testing) - within 24 hours

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4
Q

Explain what happens in a normal stage 1,2, 3 of parturition.

A

Stage 1 - colic-like, pacing, pawing at the ground, rolling, laying down and getting up frequently, sighing, flank watching, can be days or longer, often longer in maidens
Stage 2 - rupture of membranes, see a white bag and often feet coming out of the vulva, mare may or may not initially lie down (they usually lie down but some mares are dumb), mean time of 11 mins, should be able to feel 2 front feet slightly offset and a nose, then the foal will come out (yay)
Stage 3 - passing of the placenta, should be within 3 hours of stage 2, check the placenta for colour, texture, weight, if its all there (super important)

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5
Q

What are some differentials for GI or colic like signs seen in mares immediately post-foaling? (hint: there are 9)

A

GI: impaction/obstipation (pain), large colon volvulus, small colon ischaemic necrosis, caecal impaction

Urogenital: RFM, uterine haemorrhage, uterine tear, bladder injury/prolapse, vaginovulval bruising

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6
Q

What’s the 1,2,3 rule?

A

Foal should be standing in 1 hour
Nursing in 2 hours
Placenta passed in 3 hours

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7
Q

How do we know if there are retained foetal membranes and how do we treat them?

A

If the placenta is still hanging out of the vulva after 3 hours, if the placenta came out but there’s a bit missing

Treatment - removal using gentle traction, oxytocin 1-2ml IM/IV q2-4h (alternate the routes), or CRI 1 IU/min, uterine lavage (Burn’s or Dutch technique)
Analgesia, anti-inflammatories +/- antibiotics if they aren’t clinically well, if just local infection then put the AB in flush bag and put it straight into the uterus (large volume flush for dystocia cases, small volume flush for normal parturitions)

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8
Q

Name the clinical signs of periparturient haemorrhage and how do we diagnose it?

A

Painful, tachycardia, pale MM, colicky, tachypnoeic

Diagnosis - abdominal US, per rectum US if contained in broad lig., +/- abdominocentesis (often not needed)

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9
Q

How do we treat periparturient haemorrhage?

A

Close monitoring
Antifibrinolytics - tranexamic acid 5-10mg/kg
Sedate the mare
If giving oxygen is going to stress the mare out then don’t do it - it doesn’t help that much anyway
If you are going to give fluids just make sure its not Hartmans

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10
Q

How do we treat uterine tears?

A

Antibiotics, anti-inflammatories - TS and bute/flunixin probs
If its a small tear and there is localised peritonitis then medical treatment as above +/- a drain
If its a large tear with generalised peritonitis you need to drain and surgically explore as well as AB + AI

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11
Q

What is the maintenance fluid requirement of a foal? What is it for an adult horse?

A

Foal - 100ml/kg/day
Adult - 60ml/kg/day

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12
Q

What is the most common congenital cardiac defect in horses?

A

Ventricular septal defect (VSD)

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13
Q

What are the normal vital parameters in a foal?

A

HR - 60-80bpm after birth; 120-150bpm for the first few hours then evens out to 80-100bpm
RR - 60-80/min after birth; then equilibrates to 20-40/min after a few hours
Cardiovascular - arrhythmias common in the first 15 mins and murmurs in the first few days (PDA should close within 7 days), digital pulses and warm extremities
Respiratory - crackles are common and can be normal
Umbilicus - should be dry within 24 hours

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14
Q

What do you need to include in a neonatal physical exam? What conditions might you find?

A

Cardiovascular - auscultation, arrhythmias common in first 15 mins, murmurs common for the first few days, presence of digital pulses + warm extremities; looking for VSD, other congenital conditions, poor perfusion, MM colour and hydration
Respiratory - auscultation is insensitive for pneumonia + infection, crackles can occur commonly due to compliant chest walls, dependency atelectasis, poor surfactant immaturity
Joints - any swelling, can be septic arthritis
Umbilicus - enlarged or painful, patent urachus (dripping urine)
Eyes - ulcers, entropion, scleral haemorrhage from dystocia/sepsis
Hard palate - congenital abnormalities, nasogastric regurgitation is common especially in weak foals
Limbs - looking for angular or flexural limb deformities
Meconium staining - from foetal distress
Maturity - domed head, silk coat, lax tendons, no ear cartilage
Coprophagy - foal heat

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15
Q

What is the most appropriate way to restrain a foal for physical exam?

A

Hold them by the chest and hamstrings
Can grab the tail or an ear if necessary

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16
Q

Describe the normals of foal behaviour.

A

Sleeping 1/3 of the time, during play time the foal should stay quite close to the mare and the mare will be watching closely
Nursing 7x per hour in the first week, 3x per hour at 4 weeks
Urinating within the first 6 hours for colts, first 11 hours for fillies; they should produce 6-7ml/kg/hour (7-8L urine/day)
Defeacation meconium within the first 3-6 hours

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17
Q

What are the 3 most important checks in newborns?

A

IgG - marker of passive transfer
USG - best marker of dehydration/whether or not the foal is nursing
Umbilicus - make sure you dip is judiciously with dilure disinfectants

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18
Q

What value is considered a PASS in terms of adequate protection in an IgG test?

A

> 8g/L

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19
Q

At what time should we check IgG in newborn foals and why? How does our management of failure of passive transfer change after the foal is 1 day old?

A

Around 12 hours is good as we have past the maximum absorption time (<6 hours) but we still have enough time to supplement enteral colostrum if they aren’t adequately protected before the channels close at 24 hours old. After that we would have to use IV plasma

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20
Q

What USG indicates dehydration in foals?

A

USG >1.014

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21
Q

Explain normal foal clinicopathology.

A

Relatively low PCV and TS (TS>60g/L can be used as a surrogate for an IgG test)
Neutrophil:Lymphocyte >1:1
High ALKP
High creatinine in the first 36 hours due to placenta - if it persists longer than 36 hours then the foal might have renal dx or the placenta was not working as it should

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22
Q

Explain the difference between open and closed castration.

A

In an open castration the tunica vaginalis is opened and retained.
In a closed castration the tunica vaginalis is not opened and is resected along with the testis.

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23
Q

Name the complications of castration. Which 3 are the most common?

A

Most Common:
Haemorrhage
Swelling/oedema
Infection

Others - hydrocele, evisceration/herniation, penile complications (priaprism, paraphysmosis, iatrogenic trauma), persistent masculine behaviour

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24
Q

How do we manage haemorrhage as a complication from castration?

A

Locate + clamp/ligate the bleeding stump - can do standing most of the time
Re-emasculate the stump
Pack with gauze sponges (laparotomy sponges or sterile bandages), + close scrotum
GA –> haemostasis

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25
Q

How do we manage swelling/oedema as a complication of castration?

A

Establish drainage by enlarging the incision - can do standing under sedation
AIs +/- ABs (TS or pen)
Aggressive cold hosing x2/day
Exercise - stick them on the walker for 15 mins/day

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26
Q

How do we manage infection as a complication of castration?

A

If localised - drainage, take a swab for culture, and give BSABs and AI in the mean time (usually a 7d course of peniillin or TS and some bute)
If secondary peritonitis - treat as peritonitis
If scirrhous cord - surgery

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27
Q

How do we diagnose cryptorchadism?

A

Clinical signs
Clinical exam + rectal exam +/-US
Hormonal assays - testosterone, hCG stmulation in horses older than 2 and donkeys, serum oestrone sulphate in horses older than 3

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28
Q

Name the most common penile tumour and how it is treated.

A

SCC

Treatment Options: combination scalpel + cryotherapy or cryotherapy + topical chemo
Scalpel (or laser) excision
Cryotherapy
Posthioplasty (reefing) - if there are multiple sites then remove affected tissue and re-anastomose
Amputation - if its invaded into the tunica albuginea
En bloc resection - pelvic urethrotomy for advanced disease
Chemotherapy - topical 5-fluorouracil, generally takes about 3 treatments

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29
Q

What is the difference between priaprism and paraphimosis?

A

Priaprism is persistent erection due to vascular engorgement of the corpus cavernosum penis.
Paraphimosis is an inability to retract the penis, often secondary to trauma, ACP use or cachexia.

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30
Q

How do we treat paraphimosis?

A

Aggressive topical + systemic AI therapy - NSAIDs, corticosteroids, DMSO
Manual massage, emollient application, cold therapy
Reduce and maintain in prepuce
Elastic bandage + sling
Surgery as last result - irrigation of CCP, create a shunt between the cavernosum and spongiosum, or can phallopexy or phallectomy

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31
Q

Describe the importance of passive transfer of immunity.

A

Due to epitheliochoral placenta foals are born immunocompetent and immunonaive and rely on colostrum for transfer of maternal antibodies.
51% of passive transfer occurs at less than 12 hours of age so it is important that colostrum is ingested from the first nursing.

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32
Q

How does colostrum differ in composition from milk? What 3 immunoglobulins make up the majority population in colostrum?

A

Colostrum has higher protein + fat and lower lactose than milk
Immunoglobulins - IgGa, IgGb, IgG(T) > IgM, IgA, IgE

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33
Q

What factors decrease colostral quality?

A

Age of the mare >15 yo
Breed - Arab, TB > STB
Stressed or ill mare
PPID
Amount of time post-partum

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34
Q

What is the ideal intake of colostrum?

A

60-90g of IgG in the first 6 hours after birth, approx. 1-1.5L of good quality colostrum (>60g/L) should result in a PASS on IgG testing

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35
Q

What is the easy, in field way to test colostrum quality?

A

Brix refractometer - anything above 30% is brilliant and should correlate to an IgG >8g/L, but anything above 15% is of fair quality still.

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36
Q

What is sepsis?

A

Infection + systemic inflammatory response syndrome (inflammatory dysregulation)

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37
Q

What 4 routes of infection lead to neonatal sepsis? Which is the most common?

A
  1. Oral - most common
  2. Umbilicus
  3. Respiratory
  4. Pre-partum/in utero infection
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38
Q

List the most common organisms causing neonatal sepsis?

A

E. coli!!!!!
Klebsiella, enterococcus, salmonella, streptococcus, staphylococcus, actinobacillus, pasteurella, clostridium, bacteroides

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39
Q

What are the predisposing factors for neonatal sepsis?

A

Maternal illness
Failure of passive transfer
Placental infection or insufficiency - placentitis
Short or long gestational periods - premature or post-mature
Inadequate attention to umbilical stump
Poor hygiene - preparation of mare pre-foaling (clean her up, bandage her tail, clean foaling box), foal examination (no gloves), keep the mare in the foaling environment for 1 month prior so they produce antibodies to the relevant bugs

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40
Q

What are the clinical signs of neonatal sepsis?

A

QAR/obtunded/stuperous/comatose
Reduced appetite
Inc. HR
RR increased but can be dec. if particularly sick
Hypothermia - due to poor peripheral perfusion (shock)
Initially bright red MM with rapid CRT but eventually MM become dark with prolonged CRT
Haemorrhage of MM including episcleral in advanced sepsis, make sure you check the inner pinnae, can advance to DIC
Reduced jugular fill
Weak peripheral pulses + cool extremities
Reduced urine output
Other signs of dehydration - sunken in eyes, inc. USG
Diarrhoea
+/- joint effusion if synovial
Wet and soft umbilicus
Uveitis
Distal limb necrosis - if there are septic thrombi
Neurological signs - if meningitis component
Dermatitis, skin sloughing

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41
Q

Do you need a bacterial culture to confirm a diagnosis of neonatal sepsis?

A

No

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42
Q

What clinicopathological changes are associated with neonatal sepsis?

A

Usually an inadequate IgG
Neutropaenia with bands and toxic changes
Hypoglycaemia
Hyperlactataemia
Metabolic acidosis

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43
Q

Discuss the resuscitative care for a foal with neonatal sepsis.

A

Early antimicrobials - no enterals (reduced gut perfusion due to shock), pen-gent is a good firstline, can use ceftiofur 5-10mg/kg IV/IM q6-12h, gentamicin 12mg/kg q36h, penicillin (w/out procaine) 22,000-50,000IU/kg QID IV
Can do cephalosporins and penicillin as CRIs
ANYTHING GIVEN INTRAMUSCULARLY SHOULD BE IN THE BUTT NOT IN THE NECK
Put the antibiotics in the fluid bag.

Early fluid therapy - 1L at a time, heat it up for 1 minute in a 1000W microwave and give it a good shake so there’s no hot spots (don’t want venous necrosis), can use anything just not hypertonic saline.
Give the first 20ml/kg (about 1L in a 50kg foal) and then assess perfusion, CRT, digital pulses, MM colour, extremity temperature, jugular fill, mentation, urination volume, USG.
If there is an insufficient response give another 20ml/kg, can give up to 3 boluses of 20ml/kg (about 3L of fluid).

If they are still hypovolaemic/hypotensive after 3L of fluid then give them pressors/inotropes or some other drug and send them to a referral institution

Supportive care - glucose (20mL 50% per 1L), parenteral nutrition, don’t bother with oxygen if they are getting more stressed and hyperventilating, no active warming, take care of any wounds, take samples!!
If you can’t easily take samples then give them the ABs and send them anyway, it will reduce sensitivity but it could save their life.

REFER THEM EARLY ON FOR THE BEST PROGNOSIS

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44
Q

You’ve provided resuscitative care for a foal with neonatal sepsis and its stabilised. Well done! Describe the ongoing care for that foal.

A

Antibiotics and fluid therapy - 100ml/kg/day
Flunixin - 1.5mg/kg q24h
Plasma if their IgG is inadequate
Nutrition - 4-8mg/kg/minute glucose parenteral vs enteral, 50ml milk q2h for trophic feeding
Monitor ins and outs - urine production
Respiratory/ventilation support if they lose drive and become weak
Regular turning, standing, moving, nursing
Eye care
Instrument care - change lines frequently and catheters, bungs, extensions

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45
Q

What is the survival rate for neonatal sepsis?

A

50-70%

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46
Q

What is a caslick procedure?

A

A procedure where the cranial 2/3 of the vulva are sutured together to prevent faecal contamination of the vagina which can lead to ascending endometritis and pyometra, affecting the mares ability to maintain a pregnancy.

It’s done by doing an epidural and/or line blocking the margins of the vulva and then incising along the mucocutaneous junction, then suturing the fresh edges together, leave the sutures in for 10d and then remove.

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47
Q

What are the indications for doing a caslick procedure in a broodmare?

A

Poor vulval conformation - poor vulval apposition, more than 1/3 above the pelvic brim, more than 10 degree cranial tilt.
Pneumovagina
Splachnoptosis = cranial prolapse or forward retraction of the viscera creating a shelf-like appearance of the cranial vulva.

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48
Q

Describe the 3 grades of perineal lacerations and how to manage them.

A

First degree - superficial mucosa and muscles of the labia and vestibule are torn or damaged; manage with local wound care, daily cleansing with saline, antibiotics, and AIs

Second degree - tearing + disruption of the constrictor vulvae muscle and perineal body only; debride and suture superficially, can Caslick them, give tetanus prophy if they didn’t get it before foaling, antibiotics + AIs

Third degree - damage + disruption of perineal body, anal sphincter + rectum; manual daily evacuation of the vagina until the mucosa heals, delay corrective surgery for 6 weeks, ensure soft faeces pre-op by giving a soft laxative diet, mineral oil + Epsom salt drenches, then recreate the shelf between rectum and vagina + restore the perineal body

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49
Q

Discuss the 4 different ways of diagnosing an ovarian tumour and the recommended treatment.

A
  1. History and clinical signs - behavioural abnormalities if GCT
  2. Rectal palpation
  3. Rectal US
  4. Serum hormonal assays - AMH, but can also do testosterone, inhibin
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50
Q

Name the most common ovarian tumour in mares. Name 4 other differentials for ovarian enlargement/mass.

A

Granulosa cell tumour (GCT)

Other DDx - teratoma, melanoma, cystadenoma, cystic ovarian, haematoma, corpus haemorrhagicum, large CL

51
Q

What are the indications for c-section in a mare?

A

Dystocia of a live foal or instead of a fetotomy
Emergency in near term mare with colic
Term or near term mare with uterine compromise

52
Q

List the organ systems affected in neonatal maladjustment syndrome.

A

Neurologic
Renal
Gastrointestinal
+/- endocrine, cardiac

53
Q

How does the type of neonatal maladjustment syndrome affect the outcome?

A

Immediate onset of signs is less common and has a poorer prognosis
Delayed onset type (12-36 hours after birth) is more common and has a better prognsois because if they were able to nurse in their first 12 hours of life they likely have a normal IgG

54
Q

What are the causes of neonatal maladjustment syndrome?

A
  1. Maternal Disease - anaemia, lung disease, cardiac disease, cardiovascular shock/toxaemia
  2. Placental Disease - premature placental separation, placental insufficiency due to twinning or post-maturity, placentitis
  3. Stage II Labour - red bag delivery (placenta previa), uterine inertia, dystocia, oxytocin
55
Q

List the neurological signs of neonatal maladjustment syndrome.

A

Reduced affinity for the mare - wandering
Inability to find the teat/latch/suckle, nursing on inappropriate objects
Dysphagia, pharyngeal collapse
Blindness
Abnormal ventilation
Seizures
Obtundation/coma

56
Q

List the renal signs of neonatal maladjustment syndrome.

A

Delayed creatinine clearance
Tubular dysfunction
Polyuria
Anuria, oedema

57
Q

List the gastrointestinal signs of neonatal maladjustment syndrome.

A

Meconium impaction
Ileus - colic, reflux, abdominal distension, bacterial translocation, sepsis
Intussusception

58
Q

How do we diagnose neonatal maladjustment syndrome?

A

Clinical signs - it’s pretty obvious
No significant clinicopathologic abnormalities if uncomplicated
Rule out other differentials

59
Q

Describe a treatment plan for a foal affected with neonatal maladjustment syndrome.

A

Maintain cerebral perfusion pressure - fluid therapy, keep the head up and try not to occlude jugular veins excessively
Optimise metabolism - can give oxygen but be careful to avoid excess as can lead to free radical production
Block glutamate receptors - magnesium infusion
DMSO or allopurinol for free-radical management
Manage seizures if they occur - 1-2ml diazepam IV immediately, can midazolam CRI if recurrs, consider phenobarbital to reduce cerebral metabolism
If sudden deterioration then reduce cerebral oedema with mannitol
If they aren’t ventilating properly then give oxygen and ventilate for them temporarily
Encourage nursing from the mare
Preferentially bucket feed over bottle feeding to avoid asphyxiation
NG tube if not drinking - give 10% of BW in milk per day divided into q2h, increase to 20-25% per day over several days but stop if they are tolerating and not getting diarrhoea or colic
Parenteral nutrition if they are getting colic, ileus, diarrhoea - start off with glucose, with a separate line for nutrition + fluids
Milk the mare off every 2 hours +/- domperidone
Swap recumbencies q2h to avoid decubital ulcers and pneumonia because the last thing we need is sepsis
Be vigilant with catheter care
Monitor eyes for ulcers and bladder - catheterise if appropriate
Monitor fluid intake and output - can use furosemide if becoming oedematous and not producing urine
Madigan Squeeze Technique - can be done for up to the first 3 days of life

60
Q

What is the Madigan Squeeze technique?

A

A technique to replicate parturition, put a rope around the chest and pull from the back of the foal, put pressure on for 20 minutes (same length as stage 2 parturition)
It induces a somnolense response and may reset the foal if done within the first 3 days of life (may need to be repeated)
Won’t work in a foal with seizures, hypoventilation, hypoxia, or any other major complications

61
Q

At what length of gestation is a foal considered premature if it’s born?

A

<320 days

62
Q

List the clinical signs of prematurity and explain their significance.

A

Domed forehead
Lax tendons, incomplete ossification of cuboidal bones, angular limb deformities + carpal/tarsal bone collapse –> increased cost of management later and possibility of permanent dysfiguration and decreased athletic performance
Surfactant deficiency + muscle weakness –> reduced respiratory drive
Incomplete aural cartilage
Short, silky coat - they have altered thermoregulation and get cold very easily
Small stature
Entropion
Altered glucose homeostasis
Altered cardiovascular status –> hypotension even with pressors

63
Q

Premature foals often have a low neutrophil to lymphocyte ratio. Why?

A

Foals mature in the last 2 weeks of gestation, and the cortisol surge only lasts 48-72 hours. A premature foal hasn’t had the stress response that comes with space restrictions in the uterus which would usually cause cortisol release and in turn increase the neutrophil count in mature term foals.

64
Q

How can you identify a post-term foal?

A

Gestation >356 or 357 days
Erupted incisors
Long hair coat
Fetlock contracture
Higher incidence of dystocia and meconium impaction

65
Q

A day old colt presents with increasing abdominal distension, tachypnoea, stranguria, and is dull and lethargic. What is your top differential? Is this an emergency?

A

Uroperitoneum
Yes - this is a medical emergency

66
Q

How can we diagnose uroperitoneum?

A

Abdominal ultrasound
Abdominocentesis - creatinine >2:1 abdominal:serum
Biochemistry - azotaemia, hyponatraemia, hypochloraemia, hyperkalaemia

67
Q

Describe the medical management of uroperitoneum.

A

Manage potassium (correct hyperkalaemia) - give glucose/insulin to create intracellular shunt, reduce potassium intake with muzzle fold or dilute with low potassium containing fluids, drain the abdomen to reduce whole body potassium
Give calcium - cardioprotective for the hyperkalaemia
Then go to surgery

68
Q

List the clinical signs of neonatal isoerythrolysis.

A

Dullness, lethargy
Pale yellow mucous membranes
Tachycardia, tachypnoea
Cardiac murmur
Dark yellow urine

69
Q

Describe the pathophysiologic bases of neonatal isoerythrolysis.

A

When an Aa+ or Qq+ stallion and an Aa- or Qq- mare procreate the mare develops anti-Aa antibodies through exposure by prior pregnancy, blood transfusion, or transplacental contamination with foetal blood earlier in the current pregnancy.
At birth, the foal ingests colostrum containing the anitbodies against its own red blood cells which enter the blood stream through the gastrointestinal walls. The antibodies bind to the foals erythroctes leading to agglutination, lysis or both.

70
Q

Discuss the diagnosis of neonatal isoerythrolysis.

A

CBC + biochem - progressive, rapid anaemia, hyperbilirubinaemia, hyperhaemoglobulinaemia
Urinalysis - pigmenturia
Haemolytic crossmatches or agglutination testing

71
Q

Discuss the treatment and management of neonatal isoerythrolysis.

A

<24 hours old - muzzle the foal, provide colostrum and nutrition
>24 hours old - muzzling not required
If HCT <15% then blood transfusion - 1-4L of (ideally) packed red cells from washed mare red cells, a horse that was tested negative or a STB gelding, may need to repeat transfusions

In future - blood type mares and stallions, Jaundice Foal Agglutination Test

72
Q

Be able to name 2 other neonatal foal diseases.

A

Tyzzers Disease
Ventricular Septal Defect
Congenital Eye Malformation
HERDA, WFFS, G6P dehydrogenase deficiency, GBED

73
Q

List the differential diagnoses for foal colic.

A

Non-strangulating obstruction - meconium impaction, large intestine impaction, intussusception
Strangulating obstruction - intestinal volvulus, herniation
Congenital - intestinal atresia, ileocolonic aganglionosis
Other - gastroduodenal ulceration, peritonitis, uroperitoneum, umbilical or abdominal abscess, enterocolitis

74
Q

In terms of the approach to foal colic - what differences between adults and foals are important to recognise?

A

Pain tolerance in foals is much lower as they have never experienced abdominal pain
Rectal palpation is not possible however you can still do digital palpation for meconium impactions
Abdominal radiography +/- contrast can be used, US is also very useful
Paunch/abdominal distension could also be from small intestinal disease as foals have a much more compliant abdomen and smaller overall abdominal space
Refluxing foals can be difficult because they require a smaller tube to achieve nasogastric access but refluxing works best with a wider tube to create a pressure gradient
Abdominocentesis is not routinely performed due to the body wall being much thinner, and risk of omentum coming out the hole made with the teat cannula
PCV and TP is not as good an indicator as for hydration as USG in foals

75
Q

What is your top foal colic differential if the age of onset is 6-24 hours old?

A

Meconium impaction

76
Q

What is your top foal colic differential if the age of onset is 48-72 hours old?

A

Uroperitoneum

77
Q

What is your top foal colic differential if the age of onset is 3-5 weeks old?

A

Small intestinal intussusception

78
Q

What is your top foal colic differential if the age of onset is 8-16 weeks old?

A

Small intestinal volvulus

79
Q

What is a normal USG for a foal?

A

Equal to or less than 1.005

80
Q

What does meconium normally look like and by how long after birth should it have passed by?

A

Black to dark brown + pasty to firm in consistency
Variable amount
Passage should be complete by 48 hours

81
Q

Discuss the management and treatment of meconium impaction.

A

Rehydration +/- glucose - either enteral or IVFT, consider hydration status (give fluids if they are dehydrated - USG >1.020, lactate >2mmol/L)
Control pain - flunixin, meloxicam, ketoprofen, butorphanol, diazepam, xylazine in older foals
Enema/s - 500-1000mL for a 50kg foal, either commercially made or plain non-fragranced pH neutral hand soap diluted with water also works

If unresponsive to firstline therapy then can try retention enema using acetylcysteine (4% concentration) - leave in for 30-45 minutes
+/- enteral paraffin oil via NG tube

82
Q

What is the foal dose for flunixin? How does it differ from adults?

A

1.5 mg/kg IV q24 hours
For adults the dose is 1.1 mg/kg IV q8-12 hours

83
Q

What is the foal dose for meloxicam?

A

0.6 mg/kg IV/PO q12 hours
For adults the dose is q24 hours

84
Q

Which 2 drugs can be used for foal sedation?

A

Diazepam and butorphanol

0.05 mg/kg diazepam IV
0.2-0.5ml butorphanol for a 50-100kg foal

85
Q

There is a sedative drug that should be avoided in foals younger than 6 weeks old - which one is it and why?

A

Xylazine - alpha-2 agonist
They are unable to increase their stroke volume enough to overcome bradycardia effects on cardiac output

86
Q

List 6 causes of foal diarrhoea.

A

Non-infectious:
Foal heat
Nutritional - milk-replacement fed foals, sand ingestion
Perinatal asphyxia-associated diarrhoea
Systemic disease - endotoxaemia, sepsis

Infectious:
Parasitic - Strongyloides westeri, Parascaris equorum, small and large strongyles, cryptosporidium
Virus - rotavirus, coronavirus, adenovirus
Bacteria - Clostridium perfringens biotype A and C, C. difficile, Salmeonella, Bacteroidesfragilis, Rhodococcus equi, Lawsonia intracellularis

87
Q

What are some ways clients can reduce the risk of foal diarrhoea?

A

Good disinfection and hygiene practices
Foaling down in pasture

88
Q

What is the most common viral cause of diarrhoea in foals?

A

Rotavirus

89
Q

Discuss the pathophysiology of rotavirus infection and how it causes diarrhoea.

A

Brush border lactase enzyme deficiency, leading to what is effectively lactose intolerance. Inadequate digestion of milk leads to the formation of osmotic diarrhoea in the colon as more sugar is in the gut drawing water into the lumen.
Compensatory crypt cell proliferation also leads to increased secretions.
Rotavirus produces an enterotoxin that contributes to the diarrhoea formation additionally.

90
Q

Explain preventative measures we can use against rotavirus infection in foals.

A

Maternal vaccination - if first pregnancy then vaccinate in gestational months 8,9,10 and every pregnancy after just a booster in the last month of pregnancy
Environmental management
Biosecurity plan

91
Q

What cause of diarrhoea is the most common in foals under 3 days old?

A

Bacterial diarrhoea

92
Q

List the clinical signs and signalment of clostridial diarrhoea in foals.

A

Signalment - 3-5 days old
Cx - faecal blood, abdominal distension, colic, haemodynamic collapse prior to diarrhoea, reflux (enterocolitis)

93
Q

List the clinical signs of salmonellosis in foals.

A

Diarrhoea
Pyrexia
+/- colic, reflux, abdominal distension, signs of sepsis

94
Q

Describe the expected clinicopathological findings for a foal with salmonellosis.

A

Initial degenerative neutropaenia and evidence of toxicity
Rebound neutrophilia
Inc. fibrinogen
Hypoproteinaemia
Electrolyte disturbances
Change in IgG

95
Q

A 5 day old foal comes in with a serious case of enterocolitis. It had a normal IgG when checked previously, why do we need to re-check it in these cases?

A

Serious cases of enterocolitis can cause foals to become catabolic and start using up their own proteins for energy and opsonisation of the antigen as they don’t have huge amounts of their own antibodies yet. Thus IgG may start being used, so you need to check and may possibly have to administer more plasma if it’s dropped.

96
Q

How do we diagnose infectious diarrhoea in foals?

A

Clinical signs and clinicopathology (CBC and biochem)
Blood culture - good for Salmonellosis or concurrent sepsis
Faecal culture - good for Salmonellosis but need 5 samples
Faecal PCR - Salmonella, rotavirus, coronavirus, cryptosporidium
Toxin detection, ELISA/PCR - good for clostridial organisms
Faecal antigen testing - good for rotavirus

97
Q

Discuss the appropriate management of a foal with diarrhoea.

A

Maintain hydration with enteral or IVFT - crystalloids and colloids, maintain acid-base and electrolyte balance
Replace bicarbonate as needed
NSAIDs
Nutrition - enteral if possible and the gut is still working but if they are colicky, have abdominal distension, haemorrhagic D+, rotaviral or clostridial infection then want to rest their GIT for 12-24 hours, so need to give parenteral, want to start glucose/dextrose (4-8mg/kg/minute IV) immediately if they are not nursing, add in amino acids and fats 12 hours later

Anti-diarrhoeals - biosponge (PO or via NG tube BID), bismuth subsalicylate (2-4ml/kg per day)
Antimicrobials depending on the causative agent OR if we are assuming sepsis - metronidazole (clostridial disease), maybe gentamicin (salmonella)

98
Q

Describe appropriate parenteral fluid administration in a foal with diarrhoea.

A

10-20ml/kg either 0.9% NaCl or LRS over 30 minutes, repeat until symptoms improve
Then give the rest of the calculated deficit over 6 hours
Calculate the ongoing losses based on body weight changes and estimated amount of diarrhoea (2-3L loss over a 24 hour period in neonates)
Add on maintenance fluid requirements - 100ml/kg/d for neonates, plasmalyte 56 with 5% dextrose or Normasol M fluids are suitable

99
Q

How do we calculate bicarbonate deficit and how can we replace it?

A

= base deficit (mEq/L) x BW(kg) x 0.5(bicarbonate space)

If replacing parenterally then replace half rapidly then the other half over the next 4-6 hours
If replacing enterally then use baking soda

100
Q

What are the 3 types of umbilical hernias?

A
  1. Reducible
  2. Irreducible
  3. Strangulating
101
Q

Which is less likely to cause problems? A 4 finger umbilical hernia or a 2 finger umbilical hernia? Why?

A

4 finger umbilical hernia is less likely to be problematic because its so large that intestines are unlikely to get stuck in them and become strangulated and necrose and be painful

102
Q

Explain the diagnosis of umbilical hernias.

A

Palpation
Clinical signs
Ultrasound of the hernia site

103
Q

Discuss the management of a ventral/body wall hernia.

A

Belly bandage/hernia belt
Confinement
Diet - prevent excessive straining, so keep it soft
Treat underlying cause
If upcoming parturition may need to plan elective caesarean
Surgical if >10 weeks post infection (fibrous ring)

104
Q

What is a valgus deformity? Which joint is it more common in?

A

An angular limb deformity in which the lower part of the leg is bent OUTWARD with reference to the horses body.
More common to see in the carpus and tarsus.

105
Q

What is a varus deformity? Which joint is it more common in?

A

An angular limb deformity in which the lower part of the leg is bent INWARD with reference to the horses body.
More common to see in the fetlocks.

106
Q

At which joints does angular limb deformity usually affect?

A

Fetlock, carpus (knee), tarsus (hock)

107
Q

Name the 3 most common aetiologies of angular limb deformities in foals.

A
  1. Asynchronous longitudinal growth
  2. Joint instability
  3. Delayed endochondral ossification of cuboidal bones
108
Q

What is a windswept foal and what is it usually associated with?

A

A foal with angular limb deformities in more than 1 leg, usually 1 side has a varus deformity and the other a valgus deformity, giving them the appearance that a gust of wind has bent their legs.
It’s frequently associated with uterine malpositioning (leading to asynchronous longitudinal growth)

109
Q

Describe how we use radiography to diagnose angular limb deformities caused by asynchronous longitudinal growth.

A

Looking at position of bones above and below the affected joint for the presence of a pivot point on a dorsopalmar radiograph of the limb
Bone morphology - arthritic changes, physeal dysplasia, wedging

110
Q

What is another really important technique to utilise when diagnosing angular limb deformities?

A

Manipulation!
A lot of foals are turned out or in through their whole leg in early life so it may not actually be an ALD
If its a fetlock then you can pick the leg up and look at the direction of the limb when non-weight bearing to see if there is a deviation

111
Q

A client comes to you with 2 foals that you have diagnosed with angular limb deformities - the first foal is affected in its fetlock, the second foal is affected in its carpus. At what ages do you need to have treated before for each of these foals in order to make use of potential growth left in the physes?

A

Foal 1 (fetlock) - need to take action before 3 months old, ideally between 30-60 days old
Foal 2 (carpus) - need to take action before 6 months old, ideally between 6 weeks to 4 months old

112
Q

Describe the conservative management of an angular limb deformity.

A

Rest!!
Hoof trimming - every 2 weeks, successful for mild angulations, if valgus then trim the outside angle of the hoof, if varus then trimming on the inside angle of the hoof
Hoof extensions - usually only successful in the first 6-8 weeks, if valgus extend then inside of the hoof, if varus then extend the outside of the hoof
Diet modification - decrease energy, increase Ca to P ratio, increase copper

113
Q

Describe the options for surgical treatment of angular limb deformity, and name an advantage and disadvantage for each.

A
  1. Periosteal stripping (hermicircumferential periosteal transection + elevation) = incision on the periosteum to stimulate bone production around the physis on the affected side
    Adv: simple, inexpensive, won’t overcorrect, low risk
    Disadv: may not work if angulation is severe, cosmesis
  2. Bone growth retardation = bridging the physis to slow growth down using a screw and wire most commonly
    Adv: very effective
    Disadv: costly, implants need to be removed (so multiple surgeries), can overcorrect), there has to be potential growth left in the physis for this to work
114
Q

If you were going to do a bone growth retardation surgery on a foal with a VALGUS carpal deformity - which side of the limb does the implant go on and why?

A

Implant goes on the medial aspect of the carpus because the aim is to slow down the side that has normal growth to allow the abnormal side to catch up.

The opposite would be true if dealing with a varus deformity - the implant would go on the lateral aspect of the joint.

115
Q

List the clinical signs of hypoplasia of the carpal or tarsal bones in foals, how you would diagnose it and then treat?

A

Cx - lameness, difficult ambulation, marked curve appearance to hock (if tarsus)
Dx - clinical signs, radiographs
Tx - rest and time, treat symptoms, support bandaging or casting may help

116
Q

Describe the angular limb deformity that usually arises from ligament laxity and how you can tell its laxity and not a true limb deformity.

A

Carpal valgus usually
Diagnose by inspection, palpation + MANUAL CORRECTION
If you manipulate the leg and it straightens then angulates again when you release it then its laxity, you would not be able to straighten a leg with a true ALD because its due to a difference in bone lengths on each side of the joint.

117
Q

How do we treat ligament laxity?

A

Stall rest + controlled exercise
Bandaging/splinting for support
Tube casting - allows periarticular ligaments to strengthen and muscles to be loaded normally

118
Q

Differentiate between a type I and type II club foot (contracture of DIP joint).

A

Type I = less than 90 degree angulation of the dorsal hoof wall
Type II = more than 90 degree angulation of the dorsal hoof wall

119
Q

How do we treat contracture of the DIP joint in foals?

A

Trim heels every 2 weeks
Protect the toe
Toe extensions
Judicious pain relief
20-40mg/kg oxytetracycline IV in foals less than 6 months old initiates DDFT elasticity

If conservative treatment doesn’t work then surgery is indicated/or if they present to you later in life:
1. Desmotomy of inferior check ligament for type I
2. Tenotomy of DDFT for type II (salvage)

120
Q

How do we manage flexor tendon laxity in foals?

A

Majority of cases resolve spontaneously with rest
Controlled exercise
Protect heel bulbs with bandaging
Heel extensions

121
Q

Discuss the treatment for carpal contracture.

A

Bandages or splints for 2 weeks to relax the muscle tendon unit and induce laxity
20-40mg/kg oxytetracycline IV
Surgery if severe - transection palmar carpal ligament in palmar joint capsule

122
Q

List the clinical signs or physeal dysplasia.

A

Flaring of distal metaphyses at multiple sites
Warm + painful
Lameness

123
Q

Name the radiographic signs of physeal dysplasia (hint: there are 7).

A
  1. Physeal widening
  2. Irregular physis outline
  3. Sclerosis + lysis
  4. Bone lipping
  5. Asymmetry of the metasphysis
  6. Wedging of the epiphysis
  7. Asymmetrical cortical bone
124
Q

Discuss the treatment of physeal dysplasia.

A

Rest + confinement
Controlled exercise
NSAIDs
Dietary management - decrease energy and protein
Decrease weight gain
Correct any accompanying orthopaedic problems