reproductive and endocrine Flashcards

Question

20-year-old horse Presented for a suspected foot abscess on the right fore The mare is non weight bearing on the leg and there is a bounding digital pulse. Her heart rate is 60 bpm and she is sweated up. You successfully pare the foot, and the abscess begins to drain Whilst you are there the owner notes that the mare has lost her top line and has been drinking and urinating more than normal and would like the mare tested for PPID. There are no other clinical abnormalities noted on clinical examination How do you respond?

Answer 1

trh test as horse is stressed and otherwise unwell but more usefull to wait until systemically well and do basal acth this allows better interpritation and less liklyhood for borderline results ppid may be behind the abcess as it causes immunocompromised states

Answer 2

PPID without insulin dysregulation likely keep monitoring managment to take precations against lamainitis incase insulin desensitivity developes

Answer 3

try oral glucose test to see if insulin remains at acceptable level if yes- put to grass if no- continue to controle feed and manage

Answer 4

Change from placental to lung oxygenation Lungs have to inflate for first breath- Requires surfactant on lung surface Stimulus for taking first breath is a build up of CO2- Respiratory acidosis in first few minutes of life sulfactant availability in premies Adaption to the external environment- Takes 24-48hours Cardiopulmonary Gastrointestinal tract Urinary Thermoregulation Neurological Skeletal

Answer 5

Make sure environment is as clean and dry as possible- Contaminated environments are a major risk factor for neonatal disease Move neonate out of harms way and place in front of dam Encourage animal to lie in sternal- lungs have equal opertunity to expand recumbency for dam to clean off- ‘Frog legging’ an animal can help them to stay in this position and allows both lungs expand evenly Do not ‘swing/hang’ an animal by its back legs to clear fluid- Rumen fluid If animal is struggling for breath, percuss the chest and massage fluid out of nose and mouth

Answer 6

Most common cause is relative foetal oversize- Oedema, bruising and fractures can be common (esp, rib fractures) Foetus becomes hypoxic due to reduced oxygen delivery: Compression of umbilical cord Premature placental separation Metabolic acidosis then occurs due to lactic acid production and build up Severe resp acidosis due to poor lung function Net result: Acidaemia + Hypoxaemia in new born Newborn then fails to suck (acidosis greatly reduces suck reflex) Colostrum intakes affected, leading to failure of passive transfer Ruminants are born essentially agammaglobulinaemic and therefore nearly entirely reliant on colostrum for immunity

Answer 7

Blood Gases?- Not practical in the field Labile results asses time to sternal recumbency- Should be within 5 minutes If >9mins risk of death is increased Reduction/absence of suck reflex around the time of birth also sign

Answer 8

ENERGY (high in protein, fats vitamins etc) Immunoglobulins (IgA, IgG, IgM primary immunoglobulins present) Growth factors (IGF-1, IGF-2, Insulin, prolactin, growth hormone, steroids etc) Lots of leukocytes? (enhance lymphocyte response to nonspecific mitogens, increase phagocytosis and bacterial killing ability, and stimulate humoral immune responses (IgG formation) in the calf?? Godden 2008) “Colostrum management is the single most important management factor in determining calf health and survival

Answer 9

Timing!! I.e. When the colostrum was collected from the dam- Decrease in IgG quality with time Breed (Dairy vs beef breeds) Parity- heifers may give less but higher quality Pre-partum nutrition - (adequate dry cow diet, length of diet, BCS of dam) Length of dry period (<30d) Abortion/induction- colostrogenisis may be absent Mastitis

Answer 10

Intake- Inadequate supply Quantity Quality – Dilution effect Poor udder/teat conformation Poor mothering by dam Maternal disease Poor calf/lamb vigour - Reduced sucking ability (acidotic?) Time from birth to sucking- <6 hour timeframe <2hours is gold standard Method of administration Dam/teat/tube feeding Acidosis in calves/lambs reduces the absorption capability Induction of parturition recomendation is 2 liters within first two hors of life then another 2 2hours later

Answer 11

MAJOR RISK FACTOR FOR ALL NEONATAL DISEASE IN RUMINANTS 30-50% calves affected 34% calves failed to suckle in first 6 hours 15% Holstein calves suffer fpt despite receiving 3 litres within first 6 hours Case definition in herd: >20% of calves with TP <55g/L

Answer 12

Measure serum immunoglobulin Refractometer – Total Proteins >55g/L- influenced with dehydration- neonatal diahorea Zinc Sulphate Turbidity (ZST) - >20 Units Sodium Sulphite Turbidity (SST) - Ig > 20g/L Radial Immunodiffusion Nasal Stick test – Measures IgG Lateral flow testing to measure IgG ‘calf-side’? Sample calves from 24hrs-7d old If using TP beware affects of dehydration (false elevation of protein portion of blood) Useful to get a snapshot of current effectiveness of colostrum management- Monitor improvements after giving corrective advice

Answer 13

Adequate pre-partum nutrition Avoid dystocia- Easy calving/lambing sires Tube feed 10% of Bodyweight e.g. 40kg calf gets 4L colostrum ASAP (Within 6 hour window, can split in to 2 feeds)- All dairy calves Beef cows should be closely supervised Keep a store of frozen good quality (>22% Brix) colostrum available Colostrum ‘substitutes’ - £££ and variable efficacy…

Answer 14

Remove calf within 2 hours of birth Collect colostrum ASAP- Check for quality (if poor, then used stored if possible) 10% Bodyweight (between 3-4l) colostrum ASAP (Within 6 hours but preferably within 2!)- Repeat again within 12 hours of birth Feed colostrum for another 3-5 days if possible- Enhance local gut immunity ‘Teflon effect’ Store any excess colostrum Must be of good quality (>22% Brix) Dam must be Johnes negative! Pasteurise? Keep covered and refrigerated if not using straight away

Answer 15

Lambs as for calves- Immunoglobulin from dam via colostrum Zero or inadequate colostrum intake -> inadequate immunity + no energy -> death 50ml/kg in first 6 hours of birth (200ml) 250ml/kg in first 24 hours (1li1tre) Check status in lambs under 7d of age using ZST At risk lambs = triplets, orphans, from thin/hogg/gimmer dam, dystocia, weak lambs Target lambs likely to have problems for supplementary feeding If lamb is hypothermic, give intraperitoneal glucose (20% glucose 10ml/kg) + place in warming box/raise body temp before giving oral colostrum- Hypothermic lambs are prone to regurgitation and therefore inhalation pneumonia/asphyxia

Answer 16

Was the foaling observed or unobserved? The length of the pregnancy and due date – to term? History of the mare Vaccination status of the mare- how? when? tetnus status very important Behaviour of the foal since birth Colostrum intake Placenta passed?

Answer 17

Every foal should be examined within 24 hours of birth General clinical examination Ensure normal behavioural milestones have been met Identify any risk factors for onset of disease or problems that require addressing Establish/administer preventative care where required Behaviour- Normal hyperreactivity, bonding with mare, avoidance of humans Head- Symmetry, signs of trauma Signs of milk staining on forehead or around nose Abnormal mucous membrane colour Eyes- Scleral haemorrhage may be present, slow/sluggish PLR & menace Look for signs of uveitis Thorax- Look for normal respiratory rate and effort. Lung sounds audible Check for Trauma/rib fractures - palpate Holosystolic hear murmur (PDA) expected Abdomen- Relaxed, non distended Umbilicus- Heat pain or swelling Limbs- Angular/flexural limb deformities/joints Extremities- Warmth and peripheral pulses

Answer 18

What to look for- Evidence of hernia or excessive trauma Inflammation Should be pink, diameter <2cm Management- Dipping of the umbilcal stump in iodine (2%) or chlorhexidine (0.5%) Any heat, swelling or abnormal thickening should be taken seriously and evaluated using US

Answer 19

Meconium- Dark brown pellets or paste all passed within 24hrs Urine- Dilute and large volumes first passed by six hours (colts) or ten hours (fillies)

Answer 20

A foal born at a gestational age of < 320days that displays immature physical characteristics

Answer 21

Characteristics low birth weight Short, silky hair coat Floppy ears Domed head Weakness, prolonged time to stand Flexor tendon laxity Incomplete ossification of tarsal and carpal bones SEVERE CASES Multi-organ dysfunction GI Neurological renal endocrine

Answer 22

Health of the dam during gestation Gestational and foaling environment Ease of delivery Foal’s gestational age at birth Placental abnormalities Adequacy of placental transfer of maternal immunglobulin

Answer 23

Foals are immunocompetant at birth – competent specific & non-specific immune system But immunologically naïve autogenous IgG adult levels by 4 months of age Also some components of non-specific immune system may be compromised (neutrophils, complement, & macrophages) Gap in immunoglobulin is filled by colostrum IgG, IgG(T), (IgA, IgM) Other factors: complement, cytokines, lactoferrin, lymphocytes Half life of maternal IgG 20-23 days Decline by 1-2months More rapid if initially poor levels Remember this from 1st year… 3 Qs Quality Quantity Quickly Colostrum specific gravity can be checked pre-suck Brix optical refractometer <45g/L foal should be considered for donor colostrum supplementation

Answer 24

Specialist enterocytes absorb the immunoglobulins by pinocytosis These cells have a lifespan of a maximum 24hours Maximum absorption occurs within 8hours of life Foal MUST ingest 1L colostrum within first 6hrs Often owners will report they haven't seen the foal suckling Empty udder = fed!

Answer 25

Often owners will report they haven't seen the foal suckling Empty udder = fed! Blood sample should ideally be collected for: Assessment of serum IgG concentration Why? Assessment of colostral transfer of immunity to the newborn foal Screening for failure of passive transfer When? 18-24 hours old – limitations?

Answer 26

to monitor passive tranfer of immunoglobulins Options: Foal side snap tests Immunoturbidimetric method Results: Ideal - >8g/l <4g/l suggest failure 4-8g/l suggest partial failure Incidence of failure of passive transfer 2.9-35% Depends on definition Depends on foal management

Answer 27

Loss of colostrum via premature lactation- May be associated with twinning, placentitis or premature placental separation Inadequate colostrum- Severe illness, premature foaling with disruption of normal maturation (colostrum produced last 2-4weeks of pregnancy) Failure to ingest an adequate volume of colostrum- e.g. neonatal weakness, rejection of the foal Failure to absorb colostrum- esp. premature foals and/or foals with concurrent illnesses, endogenous or exogenous glucocorticoids may hasten maturation or the specialised enterocytes

Answer 28

Depends on timing- >12-24 hours need plasma Plasma source?- Mare, geldings, commercial Colostrum source- Mare, banks, commercial

Answer 29

Immediate – septicaemia Risk is highly dependent on other factors: Stress, management and hygiene Later risk- before full IgG production rapid waning of ingested IgG 1-4 months of age e.g. Rotaviral infections respiratory disease Complete haematology and biochemistry Point of care tests Lactate Increased – sepsis, shock, hypovolaemia, ischamia Glucose Decreased – hypoglycaemia = <5mmol/L USG Hydration status

Answer 30

Foals are more likely to survive if: Owners/vets have recognised problems and acted quickly Transportation to an appropriate hospital with appropriate supportive care before and during transport Response by 24 hours into treatment is often a good indicator Referral should be strongly considered in the following scenarios: suspicion of sepsis; significant prematurity (less than 320 days gestation) or dysmaturity; HIE or other conditions where the foal is unable to nurse by four hours of age; moderate to severe dehydration; severe colic or colic signs that fail to respond to initial medical treatment; suspicion of bladder rupture; excessive posturing, straining or lack of normal urination by 18 hours of age *hypoxic ischaemic encephalopathy *

Answer 31

stim acth test- higher sensitivity for pituitary dependant, less so for adrenal dependant. Good specificity- best test to rule IN cushings Low does dex- high sensitivity, ok specificity Urine cortisol to creatinie ratio- sensitive but not specific (can 100% rule it out) Basal cortisol less usefull as produced in stressed animals- more usefull in addisons

Answer 32

The UCCR is a useful screening test for canine hyperadrenocorticism as a low (normal) result makes Cushing's unlikely, with approximately 90% sensitivity. It is useful in those cases where hyperadrenocorticism is unlikely but needs to be definitely excluded sample must be taken first thing in the morning to minimise stress

Answer 33

if the dog is overproducing cortisol by testing the response of the adrenal glands to stimulation by the hormone ACTH. As is discussed in the 'What is Cushing's page', ACTH is the hormone produced by the pituitary gland, which then stimulates dogs to produce cortisol. Your vet will undertake this test by first measuring the ‘normal’ level of cortisol in your dog’s blood. They will then inject a synthetic version of ACTH and take a further blood sample after 1 hour. As ACTH naturally stimulates the production of cortisol, the cortisol levels after injection will increase beyond ‘normal’ levels in dogs without Cushing’s. However, this response is normally mild – with most healthy dogs producing a 1 hour cortisol of between 300-400 nmol/l . In most dogs with Cushing’s, cortisol production after injection of synthetic ACTH is much increased, and for the majority of cases a 1 hour cortisol value of greater than 550 - 600 nmol/l will be seen. theres no negative feedback loop in cushings dogs, hence this result sensitivity for this test is low- higher incidence of fase negatives- esspecially with adrenal dependant cases there is also overlap between cushings and non cushings dogs in cortisol levels and so can result in false negs iatrogenic cushings cases will not respond to this case and will stay at base line because drugs have overloaded neg feedback loop

Answer 34

the dog will be injected with a drug called dexamethasone. In dogs that do not have Cushing’s, this injection will completely suppress the production of cortisol. Your vet will determine this by first measuring the ‘normal’ level of cortisol in your dog’s blood. They will then take two further blood samples at 3-4 hours post injection of dexamethasone, and 8 hours after injection. In dogs without Cushing’s, the cortisol levels after injection of dexamethasone will be low when compared to ‘normal’ levels – as the injection of dexamethasone has stopped the dog’s adrenal glands from producing any cortisol. In dogs with Cushing’s, the cortisol levels after injection of dexamethasone will remain elevated– as the dexamethasone is unable to suppress the increased amount of cortisol produced by dogs with the condition. quite sensitive in pituitary dependant cases- dexmethasone negativly feedbacks on hypothalamus and pituitary and so DOES reduce production in these cases 100% sensitive in adrenal dependant cases- there will be no chnge at all in cortisol fairly specific but this reduces markedly with concurrent disease does not work at all in iatrogenic cases also not usefull in stressed patients need to tay in the practice for a while can distinguish between pituitary and adrenal cases

Answer 35

tumour cells produce excessive cortisol regardless of the amount of srenocortitropic hormones in adrenal dependant- large breeds are more likley to get adrenal dependant cushings tumour cells produce excessive adrenocorticotropic hormone regardless of feedback, resulting in increased cortisol from the adrenals in pituitary dependant- small breeds are more likley to get pituitary dependant cushings

Answer 36

measure endoginous adth for pituitary ultrasound adrenals for adrenal

Answer 37

Brief overview: Overproduction of thyroid hormone -> increased sympathetic stimulation and associated signs Common in cats, very rare in dogs. Usually due to hyperplasia or functional thyroid adenoma, rarely adenocarcinoma. Co-morbidities common- Congestive heart failure Renal disease Diabetes mellitus (both due to hyperthyroidism and becuse its common in older cats)

Answer 38

Due to prolonged excessive sympathetic stimulations Increases GA risk for surgery and hospitalisation risk for I131, so medication or diet more appropriate.

Answer 39

Often masked due to increased blood pressure -> increased renal blood flow which prevents azotemia developing. Warn owners that renal disease may be unmasked before starting treatment. Increases GA and hospitalisation risks as per cardiac disease.

Answer 40

Hyperthyroidism increases peripheral insulin resistance so could -> development of DM, but this has not been empirically proven. Hyperthyroidism does make DM more difficult to manage.

Answer 41

Treatment options: Thiamazole (methimazole) Carbimazole Diet Surgery Radioactive iodine

Answer 42

Mechanism of action: inhibits the enzyme thyroperoxidase, thereby reducing synthesis of T3 and T4 “Felimazole” - twice daily oral tablet “Thyronorm” - twice daily liquid Methimazole gel - compounded gel medication administered on the pinna Used to stabilise thyroid prior to surgery or for long term management. Pro’s - Lower risk cf surgery/radioactive iodine, safer in cats with concurrent problems Multiple formulations available Con’s - Oral meds can be difficult for owners Gel formulation can be unreliable, plus risk to owner. Costs can mount up over time.

Answer 43

Mechanism of action: Pro-drug which is converted to thiamazole either in the GIT or immediately following absorption. Thiamazole inhibits the enzyme thyroperoxidase, thereby reducing synthesis of T3 and T4 “Vidalta” - once daily oral tablet As thiamazole, used to stabilise thyroid prior to surgery or for long term management. Pro’s- Lower risk cf surgery/radioactive iodine, safer in cats with concurrent problems Once daily dosing only Con’s- Oral meds can be difficult for owners. Costs can mount up over time.

Answer 44

Diet: Hills y/d – iodine restricted diet Pro’s - Easy for owners No risk of side effects Con’s - Very variably effective. House cats only – complete control of diet needed. Not suitable for multicat households (unless all have hyperthyroidism or dietary separation can be guaranteed) May also need to give bottled water only in some areas (e.g. coastal)

Answer 45

Surgery (thyroidectomy): Four techniques are described; Extracapsular, intracapsular, modified extracapsular, modified intracapsular. Main difference is to what extent the parathyroid glands are preserved or sacrificed. Intracapsular technique maintains the most tissue and therefore has the highest risk of leaving abnormal tissue behind. Extracapsular technique removes the most tissue and therefore has the highest risk of iatrogenic hypothyroidism and hypoparathyroidism- commonly done despite side effects Pro’s - Curative - removes the problem tissue so no further treatment should be required. Useful for cats which will not tolerate medication. Relatively cost effective and does not require specialist facilities. Con’s - Recurrence can occur with ectopic thyroid tissue (5% cases), or residual tissue (unilateral or intracapsular technique). Iatrogenic hypothyroidism and hypoparathyroidism can occur. Requires GA (increased risk in cats with comorbidities).

Answer 46

Mechanism of action: Radioactive iodine (I131) is injected subcutaneously and concentrates in the thyroid gland. I131 produces both beta and gamma radiation; Beta radiation penetrates tissue to a depth of no more than 2 mm (average depth is 0.4 mm) and causes the most damage, gamma radiation causes less local damage as it passes through tissues almost unaltered. Normal thyroid follicles are suppressed in the hyperthyroid cat, so do not take up the I131, are not damaged and will gradually recover function once the overproduction of thyroid hormone ceases. Practicalities: Need to assess for concurrent conditions before considering treatment e.g. renal disease, heart disease. Use anti-thyroid medication while assessing if radioactive iodine treatment is appropriate; withdraw 1-2 weeks before treatment (centre specific). One off treatment, but hospitalisation required until radiation levels have dropped to below safe limits (~12 days). Cats remain slightly radioactive for several weeks, so pregnant people and children should avoid getting too close to the cat after treatment for ~1 month. Pro’s - Curative - removes the problem tissue so no further treatment should be required. Useful for cats which will not tolerate medication. Recurrence very rare Parathyroid glands are not affected. Con’s - Iatrogenic hypothyroidism (10-30% cases) can occur. Requires hospital stay with very limited contact (increased risk in cats with comorbidities). Can only be performed in a specialist center, therefore relatively higher cost.

Answer 47

Depends on therapy: Oral medication Diet Surgery Radioactive iodine

Answer 48

Serum T4: 2-3 weeks after starting treatment. Upper end or above reference range = increase dose Below reference range = decrease dose Euthyroid (in the lower half of the reference range) = recheck as below. Serum T4, biochemistry and hematology recommended at week 4, 8 and 12 after euthyroid state achieved, then every 3-6 months thereafter. Urinalysis and blood pressure every 3-6 months

Answer 49

Serum T4 four weeks after starting diet to demonstrate decreasing levels. May take up to six months for thyroid levels to stabilize – check monthly until euthyroid then q3-6 months ongoing Monitor biochemistry, haematology, urinalysis and blood pressure q3-6 months ongoing.

Answer 50

Unilateral: Serum T4, biochemistry and haematology 2 weeks post surgery to demonstrate euthyroidism. Ongoing monitoring at one, three, six and twelve months post-treatment. Bilateral thyroidectomy: Serum ionised calcium for 3 days post surgery. Ongoing monitoring (T4, B&H) at one, three, six and twelve months post-treatment. TSH if symptoms of hypothyroidism develop or T4 is persistently low (>6m).

Answer 51

Serum T4, biochemistry and haematology at one, three, six and twelve months post treatment. TSH if symptoms of hypothyroidism develop or T4 is persistently low (>6m).

Answer 52

Treatment overview: Management: oral medication or diet. Curative: surgery or radioactive iodine therapy Co-morbidities of note: Congestive heart failure Renal disease Diabetes mellitus Potential treatment complications: Iatrogenic hypoparathyroidism (surgery only) Iatrogenic hypothyroidism (surgery and radioactive iodine therapy) Medication side effects

Answer 53

Underproduction of thyroid hormone -> decreased basal metabolism and associated signs. Common in dogs, very rare in cats- can be induced by treating hyperthyroidism Primary, acquired disease most common (>95%) The most common causes of acquired primary hypothyroidism are lymphocytic thyroiditis and idiopathic thyroid atrophy. Primary congenital, secondary and tertiary hypothyroidism all very rare. Treatment overview: Oral medication (levothyroxine) Co-morbidities of note: Cardiac disease Diabetes mellitus Hypoadrenocorticism Potential treatment complications: Thyrotoxicosis Hamsters- Most commonly due to adrenocortical adenoma or adenocarcinoma. Usually diagnosed on clinical signs due to difficulty in collecting sufficient samples and lack of established reference ranges for hamsters. Medical treatment with metyrapone and adrenalectomy have been reported Horses- Different pathophysiology to small animals – increase in circulating POMC-derived peptides rather than glucocorticoids. More in the second block!

Answer 54

Cardiac disease Diabetes mellitus Hypoadrenocorticism Myxoedema coma

Answer 55

Thyroid hormone deficiency can impair cardiac function -. bradycardia, weak apex beat, arrhythmias Unlikely to directly cause cardiac disease but pre-existing cardiac disease likely to be impacted by concurrent hypothyroidism. Thyroid hormones = positive chronotropic and inotropic effects on the heart, stimulate myocardial hypertrophy, and indirectly affect the cardiovascular system by increasing responsiveness to adrenergic stimulation. Thyroid hormone deficiency can therefore impair cardiac function (bradycardia, weak apex beat, arrhythmias). Unlikely to directly cause cardiac disease but pre-existing cardiac disease likely to be impacted by concurrent hypothyroidism.

Answer 56

Immune mediated endocrinopathy; associative rather than causative link. Hypothyroidism -> significant increases in circulating leptin and insulin -> insulin resistance. May make DM treatment more difficult.

Answer 57

Levothyroxine therapy may -> adrenal crisis (associated with increased steroid hormone clearance), so hypoadrenocorticism must be controlled prior to starting treatment for hypothyroidism. Dose rates should be started at the low end of the range and titrated up.

Answer 58

Rare but serious. Stuporous or comatose dog with hypothermia, bradycardia, hypotension and hypoventilation. Precipitating disease (e.g. cardiac failure, overwhelming sepsis) common, may or may not be related to the thyroid disease. Treatment = thyroid hormone supplementation + supportive care (respiratory support, fluids, warmth) Prognosis guarded

Answer 59

Levothyroxine Synthetic form of thyroid hormone, works exactly like T4 in the body. Tablet and liquid forms available. Avoid concurrent feeding- decreases absorbtion. also dont give oher meds at same time

Answer 60

Serum total T4 concentrations measured at peak (4-6 hours after meds)- (do in morning) T4 >90 nmol/l: decrease dose or consider once daily dosage if twice daily therapy is being used. T4 = 35-90 nmol/l: no change necessary. T4 <35 nmol/l: increase dose. Monitor for clinical signs of thyrotoxicosis . If T4 is normal but clinical signs persist: Inadequate time for an effect to be seen (takes months). Intermittent poor owner compliance (measure cTSH – should be high in these cases). Comorbidity e.g. cardiac disease, skin disease etc.

Answer 61

Overproduction of glucocorticoids from the adrenal glands. Common in dogs, very rare in cats. In dogs pituitary dependant = ~85% cases, majority of the rest are adrenal dependant. Pituitary dependant = micro- or macroadenomas- big tumour so can cause other signs Adrenal dependant = hyperplasia, adenoma or carcinoma. Treatment overview: Trilostane Surgery (rarely performed in dogs, more commonly in cats) Radiotherapy (rarely performed) Hypophysectoy (rarely performed) Potential complications: Macroadenoma induced neurological signs (dogs) Diabetes mellitus Cardiac disease (more common in cats than dogs)

Answer 62

75% Pituitary dependant, 25% adrenal gland dependant. Usually presents as DM which may be insulin resistant, or acutely with cardiomyopathy and/or thromboembolism. Treatment options are generally less successful in cats than in dogs. Adrenalectomy appears to be the treatment of choice, but many considerations: Morbidity and mortality not uncommon Technically difficult, specialist facilities required. Ongoing corticosteroid supplementation highly likely to be needed long term. Radiotherapy, hypophysectomy, and medical treatment also reported.

Answer 63

Less common in dogs cf cats Diabetes mellitus- Doesn’t tend to be causative in dogs, but makes treatment more difficult where concurrent. Causative in cats; two pathways: Peripheral insulin resistance -> increased insulin production initially -> subsequent beta-cell exhaustion and cell death -> diabetes mellitus. Alternatively, glucose toxicity -> decreased insulin secretion -> diabetes mellitus. Cardiomyopathy- More common in cats Excess circulating glucocorticoid -> cardiomyopathy and thromboembolism

Answer 64

Treatment options: Trilostane Other oral medications (mitotane and selegilene) are not licensed for use in the UK. Adrenalectomy (adrenal dependant only) Radiotherapy (macroadenomas only) Hypophysectomy (pituitary dependant only)

Answer 65

Mechanism of action: Reversibly inhibits 3-beta hydroxysteroid dehydrogenase enzyme system, thereby decreasing synthesis of cortisol and aldosterone. Used for both pituitary and adrenal dependant disease Once daily dosing. Capsules may not be split – compounded formulation can be ordered from specialist pharmacies- EXPENSIVE!

Answer 66

ACTH stimulation test pre-treatment and then at 10 days, 4 weeks, 12 weeks, and thereafter every 3 months. ACTH stim needs to be performed 4-6 hours post-dosing. Dose can be adjusted after 10 days if cortisol is too low, or after 4 weeks – Idexx flow chart helpful: give meds in morning to facilitate easy testing

Answer 67

Technically difficult procedure with procedure-related mortality estimated at 30-60% even in referral settings. Pre-operative stabilisation recommended Need to establish full extent of tumour prior to surgery (ultrasound, CT or MRI) Unilateral for adrenal tumour. Bilateral adrenalectomy for PDH is not recommended in the dog and carries risk of post-operative Addisonian crisis.

Answer 68

Used for pituitary macroadenomas which are causing neurological symptoms. Rarely performed referral procedure. Treats neurological signs due to physical decrease in tumour size, but effect of ACTH release is less predictable; medical therapy likely to still be necessary

Answer 69

Surgical removal of the pituitary gland. Rarely performed referral procedure. 50% of treated dogs will develop (possibly transient) diabetes insipidus post-surgery so intensive care facilities required.

Answer 70

Underproduction of glucocorticoids and mineralocorticoids from the adrenal gland. Uncommon in dogs, very rare in cats. Atypical form with only glucocorticoid deficiency reported but much rarer. Immune mediated destruction of the adrenal gland thought to be the most common cause. Iatrogenic (rapid glucocortisoid withdrawal) also occurs Treatment overview: Glucocorticoid therapy Mineralocorticoid therapy (Zycortal) Potential complications: Hypothyroidism Addisonian crisis

Answer 71

Hypothyroidism- Poorly defined link, but can be seen as a polyendocrinopathy. Treatment for hypothyroidism can predispose to Addisonian crisis. Addisonian crisis- Acute presentation of Addison’s disease

Answer 72

Chronic disease: Vague, waxing-waning signs. Weight loss, PU/PD, vomiting and lethargy often reported. Electrolyte changes often, but not always present on bloods. Easy to miss. Addisonian crisis: Hypovolemic shock (weak pulses, prolonged capillary refill time) Bradycardia or tachycardia Collapse Depression Hypothermia Rapidly progressive and life threatening.

Answer 73

Hypovolaemic shock: Rapid infusion of 0.9% saline using shock rates, then decrease once BP stablised. Continue IV fluids until electrolytes stabilized and animal eating again Intravenous glucocorticoids (IV bolus or CRI); move to oral once eating and stable.- dexamethasone often of choice Hypoglycaemia: Glucose CRI Hyperkalemia: Dilution with fluid therapy usually sufficient. If symptomatic e.g. ECG changes, insulin/glucose CRI or calcium gluconate.

Answer 74

Glucocorticoid treatment: Prednisolone most common. Daily administration, titrated to lowest effective dose. Increase at times of stress (risk of Addisonian crisis) Mineralocorticoid treatment: Desoxycortone pivalate (zycortal) Very complicated!

Answer 75

Electrolytes and clinical signs are checked at day 10 and day 25 after the initial zycortal dose. These are used to make dose adjustments to glucocorticoid and/or zycortal according to the flow chart. Electrolytes are checked at day 10 and day 25 after each dose change. If the dose is staying the same, the electrolytes can just be checked at day 25 (provided clinically stable) Once the dog is controlled, routine monitoring of electrolytes is recommended every 3-6 months at day 25 (or the day zycortal is administered if different dosing intervals are being used)

Answer 76

Brief overview: Type 1: destruction of beta cells -> complete and permanent loss of insulin secretory ability. Most common in dogs. Type 2: Peripheral resistance to insulin -> hyperglycaemia. Most common type in cats. Other types exist but are rarer e.g. induced DM due to concurrent endocrinopathy. Type 2 and induced DM can progress to type 1 over time if not controlled. Treatment overview: Diet Oral hypoglycaemics Insulin therapy Ovariohysterectomy (bitches) Co-morbidities of note: Obesity Acromegaly Hyperadrenocorticism Hyperthyroidism Hypothyroidism Pancreatitis Complications- Diabetic neuropathy Ocular disease Urinary tract infection Diabetic ketoacidosis

Answer 77

Hypothyroidism Associative rather than causative link Can increase insulin resistance and make DM more difficult to manage Conditions which can induce peripheral insulin resistance -> DM: Obesity Acromegaly – see block 2 Hyperadrenocorticism Hyperthyroidism? Pancreatitis – chronic inflammation of the pancreas -> destruction of pancreatic tissue including beta cells. Other inflammatory disorders e.g. gingivitis, stomatitis, etc.

Answer 78

Diabetic neuropathy Ocular disease Urinary tract infection Diabetic ketoacidosis

Answer 79

Due to glucose build up in nerves (which do not require insulin to take up glucose) -> toxicity and nerve damage. Presenting signs include hindlimb weakness and muscle wasting. Signs can improve with better control of DM.

Answer 80

Cataracts (dogs) – due to osmotic disruption of the lens due to an accumulation of sorbitol (a metabolic product of excess glucose)- looks like cataract split into three sections Retinal neuropathy (cats and dogs) – pathophysiology unclear.

Answer 81

Presence of glucose in the urine predisposes to the development of infections. Can ascend and cause pyelonephritis if left untreated.

Answer 82

Life threatening metabolic crisis; occurs with uncontrolled DM Presentation: Signs of PU/PD, vomiting, lethargy and anorexia likely to have been present, may have decompensated by time of presentation to severe depression or even coma. Clinical exam: Tachypnea or slow deep breathing (Kussmaul respiration) + acetone smell on breath, profound dehydration, hypothermia, slow CRT. Investigations: Urinalysis – glucosuria +/- ketonuria Increased serum ketones + hyperglycaemia Metabolic acidosis (pH <7.3)

Answer 83

Correct dehydration: If hypovolaemic shock is present, give a bolus (20ml/kg for dogs or 15ml/kg for cats, over 15 minutes) Otherwise, calculate fluid deficit and replace over 12 hours. Maintenance fluid requirements may be high due to polyuria 2o to hyperglycaemia Address electrolyte and acid/base disorders: Hypokalaemia – address by adding potassium into IV fluids. Must be done prior to insulin therapy- insulin drives potassium into cells so will make any deficit worse Phosphate – will decrease 12-24hr after starting therapy so supplement proactively. Calcium and magnesium – only tx if symptomatic. Acidosis – bicarbonate correction only required in severe cases (pH <7.1 or bicarbonate concentration <10 mmol/l) provided renal function is normal Halt ketosis and address hyperglycemia: IV or IM rapid acting regular (soluble) insulin given initially. CRI preferred - BG must be checked every 2 hours for at least the first 36 hours and adjust CRI and/or provide supplemental dextrose as necessary. Continue regular insulin until animal clinically stable and eating. Identify and address underlying or precipitating factor: >70% cases in dogs and the majority of cases in cats involve a concurrent disorder Pancreatitis, UTI, Cushing’s disease, CKD and infection = most common concurrent conditions in dogs. Hepatic lipidosis, cholangiohepatitis, pancreatitis, CKD and infection = most common concurrent conditions in cats.

Answer 84

Diet Oral hypoglycaemics Insulin therapy Ovariohysterectomy (bitches)

Answer 85

Aims of a diabetic diet: Weight loss (obese animals)/maintain ideal body condition. Minimise post-prandial blood glucose increases (calorie content from protein and fat rather than carbohydrate; high fibre content). Be palatable to encourage regular, predictable intake Useful in all uncomplicated diabetic patients to help control disease. Cats can go into diabetic remission with diet alone in some cases. Not suitable for patients with concurrent renal disease (high protein content) or pancreatitis (relatively high fat content).

Answer 86

Not used in dogs. In cats, used in cases where owners feel unable to give injections. Glipizide Velagliflozin – brand new! Glipizide: Previously the only drug suitable for use as a sole agent in cats. Mechanism of action: Stimulates insulin secretion from the pancreas. Effective in approx. 40% patients; may stop working over time. Velagliflozin: Released last week Mechanism of action: Sodium glucose co-transporter 2 inhibitor; stops reuptake of glucose from the urine after it has been filtered out. Diarrhoea = common side effect Risk of UTI due to glucosuria Risk of euglycaemic ketoacidosis as no mechanism to move glucose into cells.

Answer 87

diatbetes treatment Released last week Mechanism of action: Sodium glucose co-transporter 2 inhibitor; stops reuptake of glucose from the urine after it has been filtered out.- controlls hypoglycemia and hence controlles clinical signs Diarrhoea = common side effect Risk of UTI due to glucosuria Risk of euglycaemic ketoacidosis as no mechanism to move glucose into cells.- drug just pushes glucose out of bosy Only for use in newly diagnosed diabetics (no previous insulin therapy) Do not use in dehydrated animals Screen and monitor for ketonuria Any patient receiving velaglifozin who becomes unwell should have ketones checked using a ketometer (urine sticks = poor sensitivity)

Answer 88

Caninsulin (porcine insulin) Intermediate duration of action Can be given via u-40 syringes or using vetpen with cartridges. Once daily dosing suitable for most dogs, cats require at least twice daily dosing. Given via s/c injection

Answer 89

Prozinc (protamine zinc insulin human) Longer acting form of insulin, more suitable for cats. Once daily dosing suitable for most dogs, twice daily for cats. Given via s/c injection Care with vial – prozinc insulin is delicate and can become inactivated with shaking. very sensitive to temp change- store IN fridge, not in fridge door

Answer 90

Adjunct to insulin therapy. High concentrations of progesterone and growth hormone in diestrus antagonize insulin. Once DM is stabilised, entire bitches should be sterilised to aid long term management.

Answer 91

Owner should keep a diary containing the following: Insulin dose, and time of administration. Daily food intake (time offered, amount offered, amount consumed) Daily water intake (amount offered, amount consumed) Demeanor Weekly weight and body condition Presence of urine glucose and/or ketones (daily if possible) Blood glucose curves Best performed at home if possible as reduces the effect of stress on blood glucose levels Values are then sent to the vet to be interpreted. Other monitoring options: Continuous glucose monitoring is now starting to be offered for veterinary patients. Fructosamine- Serial measurements to evaluate trends in glycaemic control most useful. May be useful for Velagliflozin HBA1C- Monitoring test of choice in humans. Further studies needed in veterinary species.

Answer 92

First curve is done 2-3 weeks after starting insulin therapy. Must use a veterinary glucometer e.g. AlphaTrak Method: Capillary blood samples collect from the pinna. 1st blood sample in the morning before the animal has had food or insulin. Then sample every 2 hours for 12 hours. Interpretation: maximum ideally below 14mmol/L, nadir ideally between 5-8mmol/L accounts for somogyi overswing- aka rebound hyperglycaemia Response to an overdose of insulin As hypoglycaemia begins to develop, release of glucose from hepatic glycogen stores is triggered -> rebound hyperglycaemia +/- glucosuria CARE: risk this could be interpreted as a need for increased insulin if single glucose measurements are used, when a dose decrease is actually required. if signle blood glucose taken wrong interpritation more likley

Answer 93

the presence of viable bacteria in the bloodstream

Answer 94

the clinical syndrome defined by the presence of both infection and a systemic inflammatory response

Answer 95

defined by certain abnormalities of vital signs and laboratory results. SIRS is frequently defined as presence of at least 2 of the following criteria: hyper- or hypothermia; tachycardia; tachypnoea; and an abnormal white blood cell count or increase in band neutrophils

Answer 96

An exaggerated, systemic inflammatory response to infection” Leading cause mortality foals in first week Much of the pathophysiology and clinical signs reflect the immune response to infection, rather than direct actions of the infective organism on the body. Common sequela of Failure of Passive Transfer and, in addition to development of SIRS, presentation may be characterised by bacteraemia, pneumonia, enterocolitis, omphalophlebitis, meningoencephalitis or arthritis. Important comorbidity of other neonatal diseases, such as prematurity, neonatal encephalopathy, neonatal isoerythrolysis, ruptured bladder clinical signs- Lethargy and depression (can be severe leading to neurological signs) Unwillingness to suckle. Temperature – can be elevated, normal or subnormal. Heart rate frequently elevated to 120 bpm but may have inappropriate bradycardia Tachypnoea. Petechiation of pinnae or mucous membranes. Recumbency. Dehydration /Hypoperfusion ( weak pulse/ cold extremities/ dec. urine output) Mucous membranes – congested, muddy, pale. Scleral congestion. Localising signs of infection (pneumonia, enterocolitis, omphalophlebitis, meningoencephalitis or arthritis) *** Don’t be deceived by TPR, look at the whole foal prognosis- Improving over time Use of serial lactate levels can assess response to therapy. Survival rates in the literature from 44-71% Prognosis for athletic performance? Septic arthritis may decrease prognosis depending on severity. Early detection is vital Don’t delay treatment whilst waiting for lab results Administer broad-spectrum antibiotics as soon as possible (take samples for blood culture first if possible) Fluid bolus therapy to predefined clinical goals (improved mentation/ urination). Reassess between each bolus. Plasma therapy (Can be given as part of fluid bolus) Hospitalisation is often required – refer for intensive treatment.

Answer 97

Early detection is vital Often based on clinical judgment in the first instance. Don’t delay treatment whilst waiting for lab results Diagnosis History (FPT/slow to suck/premature or dysmature foals/ maternal illness/ placentitis) Clinical signs Clinical pathology Foal sepsis scoring- attributing various clinical signs and test results scores to give a numerical likleyhood of sepsis

Answer 98

Bacteriology: Blood culture / Synovial fluid culture Haematology: Leucopenia/neutropenia (sometimes neutrophilia) may be normal Thrombocytopenia: may precede signs of DIC acute phase protiens- Fibrinogen/ SAA may be elevated (but low levels do not rule out sepsis) Hypoglycaemia common Pre-renal and renal azotaemia may be present Alterations in liver enzymes common in foals in SIRS Lactate is often increased >2 mmol/l ( may be due to sepsis not anaerobic metabolism) High lactate metabolic acidosis Check IgG

Answer 99

The major goals of treatment are to maintain homeostasis and attempt to neutralise the causative organism and exaggerated immune responses Antimicrobials Fluid resuscitation and cardiovascular support Fluid maintenance Respiratory support Treatment of systemic inflammation and coagulopathies Nutritional support Nursing care – often round the clock.- expensive Require hospitalisation

Answer 100

Majority of organisms obtained from blood cultures are enteric Gram-negative bacteria But… Gram-positive isolates are also recorded in the literature. Choosing broad-spectrum antimicrobials with the least likely resistance against suspected pathogens. Frequently used combinations include β-lactams and aminoglycosides or third or fourth generation cephalosporins. Use neonatal doses (higher body water) = Higher doses Adjust abx based on C&S

Answer 101

Correct hypovolaemia Balanced electrolyte solutions given as 10–20 ml/kg bwt boluses over 10–20 min may be used initially. After each bolus reassess for improvement in perfusion Look for improving pulse, CRT, jugular fill, improving mmem colour, warming of extremities, increased urine output, borborygmi and improved mental status. If no improvement after 3-4 boluses will need inotropes and/or vasopressors to maintain adequate perfusion. Foals cannot tolerate maintenance support with high sodium fluids such as lactated ringers.

Answer 102

1-2 L given slowly (Don’t forget to include this in fluid therapy calculations) Measure IgG but this is rarely a deciding factor in terms of plasma use. Sepsis mediated consumption of antibodies leads to low levels. Adaptive component immune system maybe down regulated. Sepsis and fluid therapy are known to decrease the endothelial glycocalyx layer. This layer protects against inflammation, platelet adhesion and microthrombus formation. Albumin from plasma therapy helps to restore this layer

Answer 103

Foals with sepsis may need respiratory support. Septic shock can lead to: Hypoperfusion of tissues leading to inadequate oxygenation Pulmonary hypertension Abnormal vascular control in the lungs. Use of intranasal oxygen can decrease the work of breathing and optimise gas transport. In extreme cases foals may be ventilated. This is not something we can normally provide in the primary care setting.

Answer 104

Controversial NSAIDs should be used with caution in neonatal foals. Have been implicated in gastroduodenal ulceration and renal papillary necrosis. Should we really use them in these cases?? No strong evidence for improved outcomes First rule: Do no harm

Answer 105

Aim to keep blood glucose level 4-10mmol/l Many septic foals require glucose infusions and can be used alone for 24 hours if enteral feeding not possible. 4mg/kg/min. Can double this rate but monitor blood glucose ( for hyperglycaemia) If foal unable to stand or nurse will need indwelling nasogastric feeding tube if it can tolerate enteral feeding.

Answer 106

Vital part of the treatment. Hygiene/biosecurity Catheter care ( i.v. and urinary) High incidence of abcessation/thrombophlebitis. Skin/ pressure sores Eyes Limbs Physio – regular turning.

Answer 107

Neonatal Encephalopathy: Term used to describe a condition where newborn foals develop a variety of non-infectious neurological signs in the immediate postpartum period Hypoxic ischaemic encephalopathy (HIE) Neonatal Encephalopathy Neonatal maladjustment syndrome (NMS)

Answer 108

cerebral hypoxia and ischaemia occur due to adverse peripartum events. This is a component of perinatal asphyxia syndrome (PAS).

Answer 109

persistent elevations of in-utero neuromodulating hormones (neurosteroids) in the postnatal period Consider NME in foals where the risk factors for HIE are lacking Clinical presentations of HIE / NMS can be very similar. “Normal” foals transition from intrauterine “unconsciousness” to extrauterine “consciousness”. In utero, the equine foetus is maintained in a sleep-like state to reduce energy demands and physical activity (neurosteroids such as allopregnanolone, etc.). Why foals don’t gallop in utero. “Successful” transition requires certain factors during parturition Labour-induced 20-minute physical compression experienced during the second stage of labour, which triggers endocrine changes (in neurosteroid production) that promotes postnatal consciousness. Interference with this can lead to the presence of elevated progestogen concentrations observed in foals with NMS. Clinically these foals are normal aside from the behavioural signs but as high risk of FPT, sepsis and hypoglycaemia ( failure to nurse promptly) Risk factors: Rapid birth ??

Answer 110

Wide spectrum of presenting signs may be observed, from mild behavioural abnormalities to severe neurologic abnormalities Differential Diagnosis for NE Metabolic abnormalities: sepsis, kernicterus, electrolyte abnormalities, hypoglycaemia Meningitis Equine herpesvirus 1 Trauma to the skull or spine Birth defects such as lavender foal (Arabs), hydrocephalus, hydranencephaly or other brain anomalies Behavioural changes Loss of affinity for the mare Inappropriate nursing Abnormal vocalisation Altered mentation Depression / Stupor/ Somnolence Difficult to arouse and coma Cranial nerve dysfunction Loss of suckle reflex Weak tongue tone, tongue protrusion Dysphagia CNS dysfunction Hypotonia or hypertonia, Tremors, Proprioceptive deficits Central blindness, Irregular respiratory patterns Opisthotonos and seizures

Answer 111

Multisystem organ dysfunction is common alongside neurological signs (GI and renal system most susceptible but all body systems may be involved: this is then PAS not just HIE) Risk factors: Placental disease Premature placental separation- red bag senariom- foal has no oxygen for a time Maternal illness Dystocia Caesarean section Birth ‘trauma Hypoxia and Ischaemia -> Oxygen and glucose depletion -> Cell swelling and lysis -> Delay of 6-72 hours -> Hyperaemia Cytotoxic oedema (reperfusion injury) Foals are abnormal from birth or shortly after. Delay phase explains why some foals show delayed onset of signs, or initially appear to continue to worsen despite the hypoxia having resolved.

Answer 112

Thorough History including details of parturition Clinical examination including neurological exam Check IgG (if > 12 hours old) Can treatment be performed “in the field” ??? Haematology and biochemistry may be unremarkable unless sepsis or organ dysfunction Check glucose High creatinine has been associated with foetal distress/ placentitis.

Answer 113

Supportive. In people, therapeutic hypothermia

Answer 114

Madigan “foal squeeze” ( Foals <72 hours old) Mimics the “birth canal squeeze” triggering wakefulness. Resets neurosteroid balance. Will not work in HIE Contraindicated in foals with respiratory compromise/ abdominal distension

Answer 115

HIE: Supportive. In people, therapeutic hypothermia NMS: Madigan “foal squeeze” ( Foals <72 hours old) Mimics the “birth canal squeeze” triggering wakefulness. Resets neurosteroid balance. Will not work in HIE Contraindicated in foals with respiratory compromise/ abdominal distension Support hydration/nutrition and electrolyte derangements Enteral feeding may not be appropriate/ tolerated in foals with PAS and GI dysfunction Control seizures Diazepam (0.1mg/kg IV to 0.2mg/kg IV) first line. Prevent sepsis: Broad-spectrum antimicrobial therapy Hyperimmune plasma Prognosis: Appropriate treatment of uncomplicated cases, survival is estimated at 85 % Poorer if there is PAS and additional multi organ dysfunction Neonatal Encephalopathy is a term used to describe non-infectious neurological signs in the immediate postpartum period. Causes include hypoxia (HIE) and failure to adequately transition appropriately to extra uterine life (NMS). Treatment is often supportive, but foal squeezing can be useful in cases of NMS. Mild cases can be managed in the field, but many cases require hospitalisation. Adequate consideration needs to be given to secondary complications such as risk of infection/ sepsis.

Answer 116

NI most common cause of icterus in newborn foals Foal’s RBCs destroyed by maternal anti RBC antibodies (absorbed from colostrum) Pathogenesis Mare generates an antibody response against a foreign RBC antigen found on the foal's RBCs. The antigen is a red blood cell surface molecule which she lacks on her own cells. Blood group incompatibilities between the mare and the foal caused by the foal inheriting a blood group antigen from the sire that the mare lacks EQUINE BLOOD GROUPS There are 8 major blood groups in horses (A, C, D, K, P, Q, T and U) with 32 distinct red blood cell antigens. Most are weakly antigenic. Majority of NI cases involve the antigens Aa and Qa - mares that are Aa and Qa negative are at a higher risk of producing a foal with NI. The prevalence of NI in Thoroughbreds is 1-2%. In order for NI to occur, certain events must have taken place previously: The foal must have inherited a red blood cell antigen from its sire that is not possessed by the mare (i.e. it is ‘foreign’ to the mare). The mare must have been previously exposed to blood containing the foreign antigen - this usually occurs at a previous foaling but may occur due to a blood transfusion or due to placental leakage (antigen will not cross a normal placenta). The mare must then have developed antibodies against the foreign RBC antigen. The foal absorbs these harmful anti RBC antibodies (along with many others that are beneficial) in the colostrum. The antibodies bind to the foal’s RBCs and destroy them. Antibodies cannot cross the placenta, meaning foals will appear normal at birth. Clinical signs normally develop within 2 to 5 days of birth Prognosis Good in mild uncomplicated cases but poor in severe cases or cases with concurrent sepsis, renal disease, liver disease and kernicterus. NI is causes by destruction of foal's RBCs by maternal antibodies Important differential in any newborn foal with jaundice and anaemia. Very rare in primiparous mare. Blood transfusion can be lifesaving in severe cases. Prevention is always better than cure especially in a mares with previous NI foals ( JFA test) Foals can only absorb colostrum for 24 hours. Muzzling the foal or separating the foal and Dam beyond this period is not helpful

Answer 117

Severity varies with the degree of anaemia and the amount and quality of colostrum ingested. Foals may develop a metabolic acidosis due to anaerobic tissue metabolism. mild- Lethargy Weakness Tire rapidly Jaundice or pale mmem Mild anaemia RR + HR + ( HR>120bpm) Pigmenturia+/- (nephrotoxic) moderate- Marked Lethargy Weakness Jaundice Moderate anaemia RR ++ HR ++ Pigmenturia+/- Depression Anorexia Pyrexia severe- Severe anaemia Dyspnoea Pigmenturia+/- Seizures Kernicterus (severe hyperbilirubinemia leading to CNS effects) Multi organ failure May die acutely PCV may be as low as 5%

Answer 118

Tentative diagnosis of NI any young foal with lethargy, jaundice and anaemia (PCV <15%) Differentials include sepsis, intracorporal haemorrhage, liver disease, EHV1. Definitive diagnosis by demonstrating the presence of antibodies in the mare’s colostrum or serum directed against the foal’s red blood cell antigens. Various methods of doing this with variable sensitivity using agglutination or lytic tests The haemolytic crossmatch of mare serum with foal red blood cells using exogenous complement is considered the test of choice. Jaundiced foal agglutination (JFA) test: red blood cells from the foal and colostrum from the mare. Quick but lacks sensitivity

Answer 119

Often recognised too late to prevent any further absorption of colostral antibodies. Peak of colostral antibody absorption occurs within the first 6 hours after foaling and the gut is effectively ‘closed’ by 24 hours. Monitor PCV and clinical signs Mild cases, stop suckling if still producing/absorbing colostrum (<24 hours old) Do not stress/ exert Blood transfusion if PCV 12-15% or less. Blood lactate levels can help assess degree of tissue hypoxia. blood transfusion- Lifesaving in severely affected foals Risks - transfusion reaction, liver injury from iron overload. Use either cross matched donor /or healthy young gelding OR Washed red blood cells from the Dam. Requires specialist equipment. Additional treatments- Antibiotics (for treatment or prevention of sepsis) Hyperimmune plasma administered if necessary if FPT ( obviously not from Dam) Corticosteroids may prolong the life of antibody- coated red blood cells controversial in compromised neonate

Answer 120

Blood typing, Aa and Qa negative mares breed with care (blood typed stallions). JFA test before the foal nurses Muzzle foals of mares with previous NI foals and find alternative source of colostrum Prognosis Good in mild uncomplicated cases but poor in severe cases or cases with concurrent sepsis, renal disease, liver disease and kernicterus.

Answer 121

Forestomach (rumen, reticulum, omasum) before the abomasum Ingested food first undergoes microbial degradation This makes volatile fatty acids (VFAs) and microbial protein available to the host The ruminant feeds the microbes; and the microbes feed the ruminant! Remember regurgitation (‘chewing the cud’) is important in breaking down food Large volumes of saliva produced in ruminants – buffers pH in rumen, role in digestion, nitrogen source for rumen bacteria; lot of gas also produced from fermentation Neonate – only milk – bypasses the fore-stomach straight to the abomasum – oesophageal groove – abomasum develops quickly Slower growth and development of forestomach dependent on introduction of fibre – quantity and quality of food affects microbes present and predominant species

Answer 122

Mobilisation of fat for the synthesis of glucose, and the production of ketones is normal. Problem occurs when fat mobilisation is excessive, resulting in fatty liver, which then can`t synthesize glucose. Or if liver already compromised, e.g. fluke. Problem is that the drain of glucose to the foetus cannot be switched off (unless ewe aborts or lambs), so ewe descends into downward spiral. Cf dairy cow with ketosis, where response is to reduce milk yield.

Answer 123

First trimester (days 1-45) - Implantation of the embryo Second trimester (days 45-90) - Placental development Third trimester (days 90-147) - Foetal growth and development

Answer 124

Poor body condition Colostrum quantity and quality inadequate Low milk yield Low lamb birthweight- longer to fininsh, lower chance of survival Vaginal prolapse Disease conditions (metabolic and infectious) – ovine pregnancy toxaemia, hypocalcaemia, mastitis Consequences for the lamb: increased incidence hypothermia, immune deficiencies - infectious disease, reduced growth rate

Answer 125

Critical stages to assess the flock: - 8 weeks pre-tupping - Mid-pregnancy - 8 weeks pre-lambing - After weaning Remember: it takes 6-8 weeks for ewe to increase 1 BCS on good grazing- expensive! – farmers mustn’t leave it too late to start addressing body condition! Supplementary feeding may be essential boost the ewe’s body condition hill ewes are gennerally excpected to have lower scores than lowland ewes

Answer 126

Sample representative no. of ewes ideally 2-3 weeks before lambing – across the groups – at least 5 in each group e.g. University of Edinburgh metabolic profiling service for sheep (and cattle): This service analyses the blood samples for: Energy: B-OHB (Beta hydroxybutryrate) – produced in liver of ewes in negative energy balance after using body fat as energy source Protein (low levels indicate problem): Albumin (liver damage, blood loss, malnutrition), UreaN (marker of current protein intake) Minerals: Magnesium (body does not store it, so must be continual supply; hypomagnesaemia) Trace Element: Copper (low levels – ‘swayback’ in lambs; high levels = toxicity)- sheep succeptable to copper toxicity

Answer 127

Energy – most important to maintain BCS Metabolisable energy (ME) – MJ/kg – amount of energy available to the animal from a feedstuff can be dividied into- Fermentable Energy (FE) – for rumen microbes Non-Fermentable Energy (NFE) Fermentable Energy (FE) – Sugar Starch Fibre Non-Fermentable Energy (NFE)- Oils - not available to rumen microbes, but absorbed in digestive tract Volatile fatty acids (VFAs) – products of microbial fermentation in silage – also not available to rumen microbes, but absorbed further down the digestive tract Energy requirements increase as approach lambing, but as lambs grow, rumen space decreases – limits intake capacity – need increasing energy density in the ration - better forage or concentrate feed – balancing act - £ and acidosis risk

Answer 128

Essential for ewe maintenance, reproduction, colostrum, milk production, immune response Ewes short of dietary protein are more prone to disease (and their lambs three types- Metabolisable protein (MP) = MCP + DUP- Microbial crude protein (MCP) plus Digestible undegradable protein (DUP) Effective rumen degradable protein (ERDP)- The protein available to the rumen microbes from eating grass, urea, beans, rapeseed meal etc. Digestible undegradable protein (DUP)- Bypasses the rumen and is digested in small intestine. Most often needed by ewes bearing twins/triplets – ERDP would not be enough protein for these ewes is particularly important to provide high quality protein in last 3 weeks of pregnancy – incl. DUP for multiparous ewes

Answer 129

All foods contain dry matter and water – dry matter has various components- Carbohydrate – starch, sugar and fibre Protein Fat Vitamins Minerals

Answer 130

photosensitisation oxalate poisonins nitrite poisoning can be managed with strip grazing- gradually introduce new feed to prevent gorging

Answer 131

Excessive body condition (BCS 4 and above) Sub-clinical hypocalcaemia High fibre diets, esp. containing root crops Multiple lambs in utero Limited exercise - housed ewes Lameness - prolonged periods lying down Steep fields/elevated indoor feeders

Answer 132

Seen last 2-4 wks pregnancy – negative energy balance – metabolic disorder Underfed, thin ewes (BCS 2 or less) and sometimes overfat ewes Usually lowland flocks with multiparous ewes (e.g. 3 or more lambs) Generally, an underfeeding problem – not enough energy to meet the demands of the pregnancy - look at the flock/batch, not just one animal NB – 85% of foetal growth occurs in last 60 days of gestation – big demand for maternally-derived glucose [Gestation length ~147 days] Flock issues – Severe energy shortage – poor forage quality, inadequate concentrate allowance - Has ration been analysed? Any nutritionist involved? Batched after scanning? Precipitating factors: stress on flock - adverse weather event (e.g. snow cover, severe storm), housing, vaccination handling, transport, dog worrying, severe fluke infestation liver Individual ewe issues – severe lameness, obesity, dental disease, bullying at feeding, temporary inappetence (hypocalcaemia, rumen acidosis)

Answer 133

3 weeks before and 3 weeks after calving

Answer 134

increased energy demand- Foetuses need increasingly more glucose for growth and development – increased hepatic gluconeogenesis in dam required Dam needs enough propionate absorbed from rumen for gluconeogenic precursors leading to- hypoglycemia- If absorption inadequate, surplus acetyl CoA is diverted to ketone body synthesis resulting in hyperketonaemia Glucose drain continues and hyoglycaemia develops leading to- fatty liver- Mobilisation of body tissues to try to meet energy demand – free fatty acids (FFA) and glucogenic amino acids mobilise to the liver Lack of available oxaloacetate (OAA) results in fatty infiltration of liver – seen at PM Clinical signs due to hypoglycaemic encephaolopathy

Answer 135

Early sign – disorientation – isolation from flock/batch Occasional bleating – blindness and separation Wander aimlessly – blind – lack of menace response in eyes, but pupillary reflexes normal Appear dull and depressed on observation (but may be hyperaesthetic (extra sensitive) to touch - can spark convulsions) Abnormal behaviours – head pressing, ‘star gazing’, teeth grinding Fine muscle fasiculations muzzle and ears – twitching Can become collapsed, lose abdominal wall musculature Death can result about 7-10 days after first signs

Answer 136

Note - often a poor response to treatment, especially so if late in getting started – prevention is very much better than cure here Sargison (2007) reported a recovery rate of 30% of treated ewes Act as soon as clinical signs seen – e.g. first refusal of food, dull – pen individually – also consider the batch Improve the diet immediately – appetizing, high energy, fresh water Oral propylene glycol or glycerol for several days (e.g. Ketosaid 99.96% w/w Oral Solution (noahcompendium.co.uk)). IV glucose used by some vets. IV calcium borogluconate – about 20% will also have hypocalcaemia Dexamethasone injection to induce parturition if within 5 days of full term – ‘Cascade’ use – licensed in cattle - (e.g. Dexa-ject (Bimeda), Dexafort (MSD), Colvasone (Norbrook)). Or consider a C-section – as above – near term? Viable lambs? Viability of the ewe? Flunixin meglumine (NSAID) – ‘Cascade’ use

Answer 137

Hypocalcaemia- dont get neuro signs Listeriosis- drooping face, head tilt- not stargazing Acidosis from carbohydrate overfeed Copper poisoning Hypomagnesaemia

Answer 138

NUTRITION: Prevent rather than trying to cure – ensure ewes are on an appropriate diet, especially during last 6 weeks of gestation. Check forage access and trough space if indoors. Forage analysis. BCS: Regularly monitor the ewes’ body condition scores – management tool. Metabolic profiling can also be very useful 2-3 wks before lambing. PREGNANCY SCANNING: Can group ewes and feed accordingly CONTROL OTHER DISEASES: liver fluke, lameness etc. MINIMISE STRESS: only necessary handling, transport etc.

Answer 139

Failure of detachment of the microvillous attachments between allantochorion and the endometrium. Most commonly at the tips of the uterine horns, non-gravid most commonly. The aetiology is not fully understood Anything that affects uterine motility, although can occur from what appear normal deliveries. Dystocia Premature delivery Abortion C section Uterine inertia Placentitis

Answer 140

Induced parturition C section Delayed uterine involution Dystocia and obstetric manipulation Abortion, still birth and twinning Retention of membranes at a previous foaling

Answer 141

Nothing -> DEATH! Life threatening conditions such as: - metritis - septic laminitis - septic myocarditis Due to autolysis of the placenta, bacterial infection, inflammation and systemic release of toxins through disrupted endometrium.

Answer 142

EMERGENCY IN HORSES By definition any mare with foetal membranes still visible after 3-6hrs post partum has retention. Must be treated by 6hrs history- Recent foaling or abortion. Failure to complete third stage of labor within 3 h of birth. Dystocia or other abnormalities at foaling. Recent foaling and a sick mare. Placental membranes not examined after third stage of labor, eg due to the mare foaling outside, followed by predation of the membranes before they were examined. Full clinical history is important Ask to see the placenta – is it complete? clinical signs- Retained membranes hanging from the vulva Pyrexia Dull and depresses Reduced appetite Reduced milk production Endotoxaemia Increased DPs Abdominal pain 12-48h pp. Colic and odorous vaginal discharge (metritis) Necrotic foetal membranes within the uterus provide an excellent environment for bacterial growth and endotoxin production and release. Systemic absorption of endotoxin and bacteraemia occurs due to inflammation and already-present normal pre-and postpartum uterine vessels’ dilation. Prognosis- Generally favorable if therapy and removal is done in a timely manner and treatment aggressive. Prognosis for fertility depends on severity of the insult to the uterus Uterus involution is delayed.

Answer 143

principles- Maintain uterine contractility Modulate uterine inflammation Control bacterial proliferation What can you get the client to do? Tie up the amnion and umbilical cord above the hocks to avoid the mare stepping on it. Prevent life threatening complications!!! Initial medical treatment: Oxytocin 20iu IV 20iu IM Note: Mares can often colic after administration. Uterine lavage? Large-volume uterine lavage- can reduce bacterial load and help prevent sepsis- oxytocin alone should work Should I manually remove? The membranes may be removed by manual detachment or by physical of pharmacological promotion of uterine contractility. Manual detachment potentially causes endometrial haemorrhage or pulmonary embolism, uterine inversion, prolapse and infection, and may leave microvilli imbedded in the endometrium. BUT- If done slowly, it doesn’t pose a serious health risk to the mare and her future fertility. once placenta is removed- Start of systemic antibiotic therapy TMPS 30mg/kg PO BID Pencillin 22,000mg/kg BID and gentamicin 6.6mg/kg SID +/- Metronidazole 20mg/kg PO QID NSAID’s 4.4mg/kg Phenylbutazone or 1.1mg/kg Flunixin meglumine Fluids?

Answer 144

administer after placenta is removed TMPS 30mg/kg PO BID Pencillin 22,000mg/kg BID and gentamicin 6.6mg/kg SID +/- Metronidazole 20mg/kg PO QID

Answer 145

administer after placenta is removed 4.4mg/kg Phenylbutazone or 1.1mg/kg Flunixin meglumine Fluids?

Answer 146

Treatment cannot be applied regularly Signs of sepsis present History of/signs of laminitis Lack of experience with these cases

Answer 147

The cotyledons and membranes (‘the cleaning’, ‘the cleansing’, ‘the afterbirth’) are usually expelled within 2-8 hrs of parturition – breakdown of matrix that maintains the foetal-maternal epithelium linkage Retention within the uterus beyond 12-24 hrs = RFM – common problem in cattle (dairy herds) RFM is a risk factor for subsequent development of endometritis and metritis Usually visible, hanging from vulva (sometimes internal only) – smelly! May strain. “Why did the cow not clean?”: Risk factors (multifactorial and complex) - Dystocia, uterine torsion, abortion, stillbirth, C-section, twins, immunosuppression, negative energy balance, selenium/Vit E deficiency, clinical or subclinical hypocalcaemia consiquences- Delayed uterine involution Longer time to first service Decreased pregnancy rates (decreased fertility) Increased risk of endometritis, metritis, ketosis, mastitis Decreased milk production Economic losses: incidence rate of up to 30% on some farms development of bovine metritis- truepallela mitrogenis fusobacterium necrophorum

Answer 148

Manual removal – ‘Cleansing the cow’ (but doing more harm than good?) Insertion of antibiotic pessaries into the uterus – withdrawal period 4 days for milk; 10 days for meat)- expensive, also antimicrobial resistance concern Studies suggest that antibiotic administration, preferably systemically, for cows presenting systemic illness as the preferred therapeutic approach, without preventive intrauterine or systemic AB administration or manual placenta removal.’ (Eppe et al., 2021) Ceftiofur is licensed for treatment of bovine metritis, but as a third-generation cephalosporin its use is not recommended now (AMR) – could use penicillin, oxytetracyline, ampicillin if not pyrexic and ill- leave and monitor some studies suggest an increases incidence of meteitis with manual removal Farmers usually feel that membranes should be removed on the first call and they may resent revisits … The practitioner, however, should have the courage of [their] convictions because an attempted removal, when difficult, damages the uterus. This increases the risk of septicemia and retards recovery Systemic antibiotic injection (useful if cow is systemically ill) Prostaglandin PGF2α/Oxytocin (evidence variable for efficacy in RFM) Potential consequences of manual removal- Bolinder et al. (1988) found that manual removal of RFM prolonged the interval from calving to first functional CL by 20 days Also found that uterine infections were more frequent and more severe after manual removal Manual removal produces trauma and damages uterine endometrium and predisposes towards colonization by pathogenic bacteria

Answer 149

Provide cow comfort Reduce stress around parturition Provide adequate and balanced nutrition (especially transition period) Consider previous history – more likely to retain membranes if they have done it before

Answer 150

RFM is rare in sheep RFM more commonly reported in goats, esp. dairy goats (up to 10% incidence rate) RFM also considered rare in pigs - more likely an indicator there are still piglets remaining in utero – but more prolific sows may be more prone – longer parturition Björkman et al. (2017) found an incidence rate of 3-6% of sows in a study of 142 parturitions in Finland

Answer 151

In cows, defined as a failure to conceive from 3 or more regularly spaced services in the absence of detectable abnormalities In mares, there is no strict definition Problem mare is one that fails to conceive, fails to produce a foal FAILURE TO CYCLE FAILURE TO CONCEIVE PREGNANCY FAILURE

Answer 152

oestrus- variable length (3-7 days) Follicular Phase ovulation- marks end of oestrus dioestrus- +/- 15 days Luteal Phase Normal cycle is 21 DAYS marks end of oestrus dominant follicle releases oocyte cavity fills with blood (corpus haemorrhagicum) mares often show behavioural oestrus for 24 - 48 hrs post ovulation breding season is april to october

Answer 153

variable in length 3-7 days mare sexually receptive cervix open - pink/relaxed uterus oedematous under influence of oestrogen, LH and FSH dominant follicle enlarges, softens and ‘points’ towards ovulation fossa

Answer 154

marks end of oestrus dominant follicle releases oocyte cavity fills with blood (corpus haemorrhagicum) mares often show behavioural oestrus for 24 - 48 hrs post ovulation Timing of mating/insemination relative to ovulation is crucial to breeding success Ideally, ovulation occurs as close as possible AFTER breeding Accurate prediction of ovulation is key

Answer 155

Light masks Blue LED light into one eye Mares can live out Artificial photoperiod 16 hours of light 8 hours of darkness for 6-8 weeks hormonal- GnRH agonists - buserelin/deslorelin Dopamine antagonists - domperidone/sulpiride EXPOSURE TO STALLION IMPROVING BODY CONDITION

Answer 156

Normal - foal heat at 7 -12 days post partum then regular 21 day cycles Some mares may exhibit variable periods of anoestrus after foaling until they resume normal cyclic activity. Sometimes called LACTATIONAL ANOESTRUS

Answer 157

CL remains active beyond normal 15d, delaying return to oestrus late dioestrus ovulation (CL <5d, non responsive) chronic endometritis luteinised anovulatory follicle (LAF) May persist 2-3 months PROGESTERONE level > 1.0ng/ml = presence of luteal tissue

Answer 158

OVULATING AGENTS human Chorionic Gonadotrophin (hCG) GnRH agonist (Deslorelin/buserelin)

Answer 159

Cause unknown (?insufficient pituitary GnRH, follicular oestrogen) Incidence higher in older mares May occur in consecutive cycles Difficult to predict, normal cycle May contain blood - Haemorrhagic Anovulatory Follicle (HAF) Majority become luteinized Usually regress spontaneously, although may take several weeks

Answer 160

most common almost always unilateral, slow growing, benign multi cystic (honeycomb), less often solid mass/large cystic structure contralateral ovary usually small & inactive Hormonally active - may evoke behavioural abnormalities (stallion like behaviour most common reported) Diagnosis - Inhibin, AMH, testosterone, ultrasonography Treatment (if indicated) - SURGICAL removal (flank laparotomy) May be huge

Answer 161

rare unilateral, slow growing, benign, hormonally inactive teratomas may contain hair, bone, muscle etc dysgerminomas may be metastatic/malignant

Answer 162

Excessive post ovulation haemorrhage

Answer 163

Most common is gonadal dysgenesis 63XO (one sex chromosome absent, equivalent to Turner’s Syndrome in humans) Affected mares typically are externally normal but have small ovaries with little or no follicular activity, small flaccid uterus and hypo plastic endometrial glands Mosaic/Chimaera also possible DIAGNOSIS by chromosome analysis/karyotyping NO treatment

Answer 164

ENDOMETRITIS UTERINE ABNORMALITIES- Anovulatory Follicles Ovarian Neoplasia Persistent Corpus Luteum OVIDUCT ABNORMALITIES

Answer 165

= inflammation of endometrium (inner epithelial lining of uterus) By far the most common cause of subfertility/infertility in broodmares (Distinct from METRITIS which is a potentially life-threatening infection of the uterus which occurs almost exclusively post foaling)

Answer 166

Normal physiologic inflammatory response seen immediately after mating/insemination Spermatozoa/seminal fluid/bacteria/debris —> inflammatory reaction which resolves within 24-48 hrs mechanical clearance - myometrial contractions remove fluid/debris innate immune response eliminates excess spermatozoa and bacteria Failure to clear breeding induced endometritis by 48hrs post mating is pathological PERSISTENT BREEDING INDUCED ENDOMETRITIS Mares that suffer from this condition are termed SUSCEPTIBLE MARES Generally older, multiparous mares

Answer 167

Failure to clear breeding induced endometritis by 48hrs post mating is pathological PERSISTENT BREEDING INDUCED ENDOMETRITIS Mares that suffer from this condition are termed SUSCEPTIBLE MARES Generally older, multiparous mares

Answer 168

Usually no external signs Occasionally vulval discharge if severe TRANSRECTAL ULTRASOUND- endometrial oedema - reflects inflammation of endometrium Luminal fluid - amount and character may suggest severity of endometritis contains neutrophils +/- bacteria/fungus UTERINE SAMPLING- Aim is to get a representative sample of the endometrium Choice of technique depends on - Available equipment Familiarity with procedure Time Personal preference Cost Plain transport medium OR Amies Charcoal Transport Medium- Some bacteria affected by light BUT may affect interpretation of cytology Limitations - Sample obtained from a very small percentage of the endometrial surface, which may not be representative of the entire uterus. LOW VOLUME FLUSH 100 - 250ml Hartmann’s UTERINE BIOPSY- Biopsy of the endometrium is primarily used in the evaluation of uterine health, detection of uterine disease, and as a prognostic indicator of the ability of a mare to carry a foal to term samples will be submissted for CYTOLOGY & BACTERIOLOGY

Answer 169

Bacteria that are considered to be sexually transmitted, either through natural mating or contained semen Pseudomonas aeruginosa Klebsiella pneumoniae Taylorella equigenitalis (Contagious Equine Metritis Organism)

Answer 170

ECBOLIC AGENTS- OXYTOCIN- Powerful, but short acting effect 10-20iu from 4 hours post breeding i/v, i/m or s/c Can be repeated 4-6 hourly as necessary PGF2⍺ (eg CLOPROSTENOL)- Less powerful, but longer effect (5hrs) 10-20iu from 4 hours post breeding i/m Luteolytic - beware post ovulation use UTERINE LAVAGE- Clearance of fluid, inflammatory debris, microorganisms from uterine lumen 0.9% saline or Hartmanns From 4 hours post breeding 1-3 litres, typically until retrieved fluid is clear anitibiotics/ antifungales OTHER TREATMENTS- ACETYL CYSTEINE CHLORHEXIDINE HYDROGEN PEROXIDE POVIDONE-IODINE DMSO KEROSENE EQUINE PLASMA STEM CELLS COCA-COLA etc…

Answer 171

Powerful, but short acting effect 10-20iu from 4 hours post breeding i/v, i/m or s/c Can be repeated 4-6 hourly as necessary

Answer 172

IF indicated based on culture and sensitivity of uterine sample Effective against organism detected Soluble Non-irritant Cost effective Administered directly into uterus or mixed with lavage fluid Typically water soluble broad spectrum antimicrobial Systemic antimicrobials may be used in concurrently/instead of intrauterine

Answer 173

Less powerful than oxytocin, but longer effect (5hrs) 10-20iu from 4 hours post breeding i/m Luteolytic - beware post ovulation use

Answer 174

0.9% saline or Hartmanns From 4 hours post breeding 1-3 litres, typically until retrieved fluid is clear Clearance of fluid, inflammatory debris, microorganisms from uterine lumen

Answer 175

CONFORMATION Anything that compromises the barrier that prevents contamination of the reproductive tract VULVA - VESTIBULO-VAGINAL FOLD - CERVIX may predispose the mare to endometritis MINIMAL CONTAMINATION AT BREEDING eg fresh semen AI vs natural cover

Answer 176

Common in older mares Lymphatic origin Unilocular/multilocular few mm to several cm in diameter Contain anechoic lymphatic fluid - easily identifiable on ultrasound May interfere with intrauterine mobility of conceptus (which is vital for MRP) implantation of embryo May be misinterpreted as a pregnancy Removal by laser ablation, thermocautery, manual removal

Answer 177

ADHESIONS - transluminal fibrous adhesions Traumatic origin - obstetric or chemical FOREIGN BODY - recurrent, non-reponsive endometritis Placental remnants, swab tip etc NEOPLASIA - leiomyoma/fibroleiomyoma - uncommon, small, benign. Significant if obstructive or haemorrhagic Malignant endometrial adenocarcinoma reported

Answer 178

Older mares that defy explanation for infertility, almost a diagnosis of exclusion Assess utero-tubular junction (UTJ) hysteroscopically - cysts, adhesions, fibrosis, flattening Oviducts may become blocked by intraluminal accumulations of collagen, cellular and non-cellular debris Application of prostaglandin gel (PGE2) directly onto the oviduct via flank laparoscopy Misoprostol applied directly onto the oviductal papillae via hysteroscopy

Answer 179

TWINNING EARLY EMBRYONIC LOSS ABORTION PLACENTITIS EMBRYO - Day 1- 40 FOETUS - Day 40 - term

Answer 180

Early Embryonic Loss (EEL) up to 70d gestation Equine conceptus visible via transrectal ultrasound from day 10 post ovulation Pregnancy loss pre 10 days difficult to detect intrinsic factors- Endometrial disease (acute/chronic endometritis, endometrial cysts, periglandular fibrosis) Maternal age (oocyte quality decreases with age) Progesterone deficiency - Primary luteal insufficiency not reported extrinsic factors- SYSTEMIC DISEASE disease (eg enteritis, mastitis) endotoxemia —> elevated PGF2⍺ —> luteolysis NUTRITION - poor body condition results in lower pregnancy rates & higher incidence of EEL TOXINS - endophyte infected fescue, MRLS IATROGENIC - Gamete handling/manipulation in embryo transfer

Answer 181

Rate of twin conception in Thoroughbred mares 10 - 15% Double/multiple ovulations common with better breeding management and effective use of ovulating agents Stallion fertility - twinning more likely in mares bred to highly fertile stallions, more specifically those with extended longevity of viable spermatozoa Very small chance (c.1%) that multiple fetuses will be born alive and survive the neonatal period Vast majority will abort the pregnancies by 7–9 months of gestation, due primarily to placental insufficiency Early identification and management of twins before fixation most effective Options exist for post fixation management of twins, but these methods are generally far less successful

Answer 182

Abortion - pregnancy failure between 70 - 300 days gestation Definitive diagnosis often not found May result from systemic disease in mare Usually categorised into INFECTIOUS and NON-INFECTIOUS causes

Answer 183

Ascending placentitis (bacterial) Equine Herpes Virus type I (EHV 1) infection Equine Viral Arteritis MRLS (eastern tent caterpillar) Leptospirosis Nocardiform placentitis PME of foetus and membranes should be performed where possible to identify cause

Answer 184

Twinning Umbilical cord torsion Congenital abnormalities Maternal disease

Answer 185

In UK almost exclusively ASCENDING PLACENTITIS - infection arising from the caudal pole, extending cranially Mare may show premature udder development/lactation +/- vulval discharge, but often asymptomatic If extensive, may compromise foetus and lead to abortion Diagnosis via transrectal ultrasound - caudal pole of placenta examined - combined thickness of uterus and placenta (CTUP) measured Increased thickness or separation of uterus & placenta are suggestive of placentitis TREATMENT Broad spectrum systemic antimicrobials NSAIDs +/- progesterone supplementation +/- pentoxyfylline Serial ultrasound to monitor effect of treatment

Answer 186

Normal age-related changes to ovarian function, uterine health and perineal conformation may lead to decreased reproductive performance Geriatric mares generally have longer follicular phase, decreased oocyte availability and a higher incidence of EEL/abortion May be Cushings related

Answer 187

Pregnancy loss in cattle is common. Fertilisation rates = 85% but pregnancy rates = 45% Most loss occurs <19 days and losses <40 day often go unnoticed. Later foetal death can lead to mummification or maceration Mummification: foetal death with persistence of CL. Cervix closed, no uterine contractions Maceration: mummified foetus undergoes putrefaction and autolysis. Cervix open and allows bacterial entry

Answer 188

Day 1-19 Genetic defect Poor quality ova Endometritis Lack of Interferon Tau Heat stress Infection LED same + manag,ent stresses

Answer 189

Chlamydia abortus (EAE) Toxoplasma gondii Salmonella sp Campylobacter foetus foetus Brucella abortus Border disease Fungal causes

Answer 190

Brucella abortus *NOTIFIABLE Leptospira spp Trueperella pyogenes Listeria monocytogenes Campylobacter fetus Neospora caninum Salmonella dublin BVDV Fungal causes

Answer 191

Can persist for extended periods outside the body Infection typically by ingestion Venereal transmission possible Infection -> haematogenous spread to uterus ->causes necrotic placentitis and endometritis Infected females usually only abort once Clinical signs: Abortion storm in naïve herd Abortion in late pregnancy RFM common UK is Officially Brucellosis-Free (OBF) infectious cause of abrotion Diagnosis: Based on demonstrating organism in blood, milk or vaginal swabs Organism in cotyledonary smears and tissues from foetuses Management: Parenteral abx to treat any puerperal metritis Control: In UK all abortions and premature births must be reported Lactating dairy cows are routinely screened for antibodies

Answer 192

Serovar hardjo most important in UK Infection arises from contact with infected urine or abortion products Venereal spread also possible from carrier bulls Can be carried and excreted by sheep Infection -> rapid multiplication in udder and uterus -> bacteraemia Clinical signs: Sudden milk drop Variable lethargy, pyrexia, inappetence Abortion occurs 3-12 weeks after infection, with most in last trimester

Answer 193

Microscopic Agglutination Test (MAT) Problems with test related to variations in size and duration of MAT titres Enzyme-linked immunosorbent assay (ELISA) In acute infection paired serum samples will demonstrate seroconversion Fluorescent antibody test (FAT) for antigen in fetal tissues Herd screening by bulk milk ELISA

Answer 194

Treatment: Antibiotic of clinical milk drop cases to reduce shedding Single injection of streptomycin/dihydrostreptomycin Control: Improved management Vaccination

Answer 195

Sporadic abortions in winter Ubiquitous and potentially ZOONOTIC Infection through ingestion of contaminated, poorly-conserved silage Clinical Signs: Transient fever and illness Abortion at time of illness or later (typically late gestation) Foetus commonly autolysed

Answer 196

Isolation of organism from liver or abomasum of foetus, placenta or vaginal discharge Micro abscesses and cotyledonary lesions on foetal post-mortem

Answer 197

Abortion not linked to CNS infection or illness Antibiotics not indicated Avoid feeding poor quality silage

Answer 198

Protozoan parasite Most commonly diagnosed cause of bovine abortion Dogs are only confirmed definitive host Shed oocysts -> faecal-oral infection of susceptible cattle Once infected breeding cattle can become chronically infeted leading to repeat abortions Can also have live, congenitally infected calves Vertical transmission maintains disease in herds Clinical Signs: Abortion at 5-6 months Abortion storms possible Mummification of foetuses common

Answer 199

Serum ELISA positive not diagnostic Defintive diagnosis by PM of foetus

Answer 200

Reduce risk of contamination of feed by dogs Prevent access to calving/abortion products

Answer 201

ZOONOTIC Common cause of abortion in sheep (rare in cattle) Cause of Enzootic Abortion Infection occurs in flock due to introduction of infected ewe When this ewe aborts heavily infected lambing products contaminate environment Bacteria ingested by naïve ewes; early pregnancy = abort, late pregnancy = latent infection and abort following year Ewes not ill at time of abortion and then become immune

Answer 202

Treatment: At risk ewes can be treated with oxytetracycline Will reduce losses but not eliminate infection- difficult and costly Prevention: Vaccination Accreditation schemes identify infected flocks

Answer 203

Protozoan parasite Cats act as definitive host Ingest infected mice/birds -> oocysts in cat faeces -> ewes ingest contaminated feed Outcome of infection depends on stage of pregnancy Non-pregnant = immunity Early pregnancy = EED and barren Mid-late pregnancy = foetal death + mummification/fresh dead lambs/weak lambs Diagnosis by examination of cotyledons = pale pin-head sized spots No treatment Vaccine available for prevention

Answer 204

Sporadic cause of abortion storms Usually occurs in one season as develop strong immunity Infection by introduction or carrier sheep or contamination of troughs/feed Abortions seen ~1 month before lambing Affected ewes not typically ill Aborted lambs are fresh, red inflamed placenta Treatment of ewes yet to lamb with oxytetracycline may reduce losses No vaccine available

Answer 205

Genetic defects Heat stress Management stress Nutrition ie mycotoxins Iatrogenic ie. abortifacient drugs

Answer 206

Genetic factors associated with pregnancy loss include gene mutations, chromosomal abnormalities and polygenic defects These can be amplified by AI and inbreeding. Increased detection of recessive lethal alleles capable of causing abortion in individual Mutant allele carrier frequency is particularly high in mummified foetuses Congenital defects can be visible however in many cases there is a normal phenotype. Abortion traits are now included in national genetic selection programmes

Answer 207

Nutritional Causes: There is limited evidence for nutritional causes of abortion in modern farming though Nutrient imbalances may be more likely in extensively managed pregnant cows Nutritionally-induced abortion has most frequently been attributed to deficiencies of selenium, iodine and vitamin A Abortifacient toxins are found in plants (phytotoxins), e.g. nitrates. Mycotoxins may play a role in abortion though ruminants are considered more resistant to feed-borne mycotoxins than monogastrics. ergot-infested, ryegrass-induced abortion has been reported in suckler cows Mycotoxins are not routinely tested for in abortion case submissions

Answer 208

Hormones may cause abortion via either administration or abnormal endogenous circulating concentrations. Accidental administration of hormonal products, e.g. PGF2a, is an infrequent cause of iatrogenic abortion Abortion can be induced by; PGF2 from day 7 - 150 PGF2 + dexamethasone days 150 – 270 PGF2 or dexamethasone day 275+ Increasing endogenous steroid hormones can increase risk of abortion Stress, pain etc.

Answer 209

Traumatic injury during parturition is most commonly related to foeto-maternal disproportion and mismanagement of dystocia Common injuries may include uterine and vaginal tears. May involve all parts of genital tract. May be superficial -> full thickness; contusion -> severe haemorrhage Severe haemorrhage may be rapidly life threatening to the cow Full thickness uterine tears may be repaired by flank laparotomy or manual prolapse of the uterus First degree lacerations may not require closure Second degree perineal lacerations should be sutured as soon as possible Third degree perineal lacerations and cervical lacerations should be allowed to heal for 6-8 weeks before attempting to repair Superficial lacerations may not require repair; antibiotics indicated and subsequent infections may lead to more serious sequelae including erosion of blood vessels

Answer 210

Post-partum disease: Retained foetal membranes Maturation of the placenta- Any factors leading to premature calving Twinning Elective caesarean Heat stress Exsanguination of foetal side of placenta Uterine contractions-Uterine inertia Hypocalcaemia Others Hereditary predisposition Age/parity Season Selenium deficiency Normal processes; 1. maturation of placenta. 2. exsanguination of foetal side (shrinking of villi and separation from maternal crypts). 3. Uterine contractions (unbuttoning of cotyledons from caruncles) Studies have shown that RFM may be related to oestradiol and progesterone concentrations and ratios however this has not been replicated in the field when looking at affected and non-affected animals. PGF – in vitro studies show decreased PGF2a and increased PGE2 Premature births can be due to; twins, abortion, elective c-section, induction of calving, heat stress, Other factors may include hereditary predisposition, age, parity, season.

Answer 211

Variety of opinions on treatment of RFM Literature discusses; No treatment Treatment for uterine infection (but not directly of RFM) Manual removal (not in small ruminants) Administration of ecbolic agents Oxytocin analogues Prostaglandins Manual removal has been proved to have potential detrimental effects on the cow and subsequent fertility. If undertaken then should be no earlier than 4 days post calving, removal must be gentle and will ideally be limited to withdrawal once they are detached. If not detached then the cow could be left for longer. Reports of up to 15 days for detachment. Excess force should not be used as it may causes tearing of membranes and retention of parts. Response to oxytocin is general poor/non-existent after 24 hours. PGF2a acting directly on placentomes. No treatment only if cow otherwise well.

Answer 212

Bacterial contamination of uterine lumen is common Does not always imply disease Bacteria involved include; E.coli A.pyogenes F.necrophorum Prevotella spp Risk factors: Twins Calving environment RFM Dystocia Diet 80-100% of animals have bacteria in uterine lumen in first 2 weeks after calving. Up to 40% still infected by 3 weeks. Twins - Calving environment – bacterial loading (seasonal) RFM - Dystocia – leading to more RFM or damage to maternal tissues or increase pathogen load Diet – overfeeding or underfeeding

Answer 213

Animal with abnormally enlarged uterus and fetid brown watery discharge Associated with signs of systemic illness Fever >39.50C Within 21 days post calving

Answer 214

Not all cows are systemically ill but will have abnormally enlarged uterus. Purulent discharge Within 21 days of calving

Answer 215

Presence of purulent (>50% pus) discharge >21 days after calving Or

Answer 216

In absence of clinical endometritis >18% neutrophils in uterine cytology 21-33 days after calving Or >10% neutrophils at 34-47 days

Answer 217

Treatment often based on severity and grading of discharge Variable methods of grading which incorporate colour, consistency and smell endometritis- Grade 0: normal discharges Grade 1: flecks of pus in mucus Grade 2: 50:50 pus:mucus Grade 3: 100% pus metritis- Treatment often based on severity and grading of discharge Variable methods of grading which incorporate colour, consistency and smell Toxic Metritis grad 5- start with nsaids then when down to grade 4 use wash out support with fluids

Answer 218

Occurs during third stage of parturition Result of abdominal straining plus partially attached membranes (plus gravity) Risk factors; Decreased uterine tone (hypocalcaemia, dystocia etc) Manual extraction of calf and membranes Should be replaced as quickly as possible Instruction given to keep as clean as possible and restrict movement of cow Treat potential underlying cause Low incidence in small ruminants Can occur immediately after parturition or within 12-48 hours Causes similar to cattle Prolonged stage 2 with large foetus Excessive straining due to pain or infection Posterior tract swelling following dystocia or assistance

Answer 219

Epidural Position cow/small ruminant Remove placenta, if possible Thoroughly clean ? Glycerol/sugar solution Fully evert ?Buhner suture Administer epidural anaesthesia (with xylazine for prolonged action in SR) Clean protruding tissue and remove any foetal membranes Using lots of lubrication gently raise uterus and massage back through vulva, starting at proximal edge Replacement can be done through a moist towel to reduce risk of perforation Once replaced use hand to fully evert uterus inside the abdomen Oxytocin can be administered to encourage uterine involution The dam should receive NSAIDs and a course of antibiotics xylozine epidural- 2ml 2% lignocaine + 0.2ml 2% xylazine (adult ewe)

Answer 220

Sire Selection Safe/Easy to handle In good health Appropriate body condition EBVs: Maternal traits Terminal traits Remember, lambs/calves that are born easily, grow rapidly and have good conformation

Answer 221

Examine for abnormalities likely to affect the fertility of the bull now, or in the future BCS, eyes, jaws, heart and lungs Assessment of the musculoskeletal system Most bulls culled because of lameness / musculoskeletal injury Reproductive tract Examination Semen evaluation Libido/serving capacity Scrotal circumference directly related to sperm output (minimum > 34 cm @ 2 y) Size IS everything ! Related to fertility of daughters Palpation of testicles Inspection and Palpation of Prepuce/Penis Palpation of accessory sex glands Prostate and seminal vesicles should be palpated

Answer 222

Collection Volume / density Gross Motility Progressive Motility Morphology Handling of sample is critical Gross motility Drop of fresh semen on warm slide Affected by: Temperature Concentration % live progressively motile sperm Progressive motility 3-4mm drop of semen under warmed coverslip Heated stage important May need to dilute dense semen in warm PBS Target >60% Morphology >70% normal morphology to pass Defects include; Bent tails Detached heads Proximal droplets Distal droplets

Answer 223

Libido and ability to serve must be assessed by farmer If done as part of BBSE need teaser female prepared Observation of mating crucial Crucial to ensure bull is serving cows normally This can’t be done from a distance A few things can go wrong Failure of Intromission Spiral deviation: “corkscrew penis”

Answer 224

INFECTIOUS VIRAL - Equine Herpes Virus 1/4, EVA BACTERIAL - Beta Haemolytic Strep, E coli, Pseudomonas spp, Klebsiella spp, Leptospira spp FUNGAL - Aspergillus spp, Candida NON-INFECTIOUS TWINNING PLACENTAL DISEASE - cord, body pregnancy, cervical pole necrosis, neoplasia FOETAL DISEASE - developmental, foetal diarrhoea syndrome, neoplasia MATERNAL DISEASE - pyrexia, malnutrition, stress, uterine abnormalities PREMATURE PLACENTAL SEPARATION NO DIAGNOSIS

Answer 225

IMPORTANT TO ESTABLISH THE CAUSE Ideally intact whole foetus + membranes Otherwise tissue samples & bacty swabs ISOLATION Until infectious cause ruled out TREATMENT If appropriate

Answer 226

ASCENDING Most common. Microorganisms (often environmental contaminants) gain access to cervical portion of placenta through cervix- most common in uk (really the only one seen) DIFFUSE/MULTIFOCAL Haematogenous spread of infectious agent (leptospira, salmonella, candida)  FOCAL MUCOID Nocardiform placentitis (actinomycetes) Typically older multiparous mares Diagnosis often difficult Often no clinical signs until placentitis advanced Vulval discharge mucopurulent or sanguinous Premature udder development +/- lactation

Answer 227

TRANSRECTAL ULTRASOUND- Caudal pole of placenta – assess CTUP (Combined Thickness of Uterus and Placenta Placental separation?

Answer 228

TREATMENT Broad spectrum antibiotic, NSAIDs, Pentoxyfylline Altrenogest, acetylsalicylic acid (aspirin) PREVENTION Predisposed by poor conformation Routine ultrasound monitoring of previous offenders through second half of pregnancy

Answer 229

Cause unknown ?vigorous foal movement/rolling of mare? 7 months + Usually present with mild colic, may be recurrent may ➞ uterine rupture if prolonged or severe torsion Diagnosis by rectal palpation Diagnosis by RECTAL palpation – unlike in cows, torsion usually occurs cranial to the cervix, so vaginal exam unrewarding Important to assess direction of torsion VENTRAL ABDOMINAL SWELLING- from compromised blood flow and vascular swelling

Answer 230

MOST COMMONLY SEEN IN OLDER MARES DRAFT BREEDS NO OBVIOUS UNDERLYING CAUSE Hydrops, Twinning, Trauma PPT and ABDOMINAL WALL ruptures often occur together -> SEVERE OEDEMA PAIN common dx for painfull abdominal swelling in pregnat mare ventral abdome drops, mare developes lordodis mammary secretions often contain blood absominal rupture occurs in inguanal region

Answer 231

Excessive accumulation of fluid in allantoic or amniotic compartments HydrALLANTOIS - chorioallantoic malfunction HydrAMNION (v rare) - associated with foetal abnormality More common in older mares Rapid onset abdominal distension in last trimester ->low grade colic, lethargy, anorexia... dyspnoea Diagnosis by rectal palpation +/- ultrasound Large fluid-filled uterus - up to 100L fluid (8-15L normal) Difficult to palpate fetus Complications - uterine/abdominal wall rupture Some mares may spontaneously abort, otherwise induction is indicated

Answer 232

Common cause of vulval discharge Usually older mares Fresh blood - dark serosanguinous fluid Grape-like structures on roof of vagina Treatment usually not necessary Can be chemically cauterized (formalin) if persistent

Answer 233

Important to differentiate other late pregnancy conditions from colic of non-reproductive tract origin Late pregnant mare more prone to colon displacement +/- torsion Changes in digestion or visceral positioning/ intestinal motility?

Answer 234

Fetal activity can cause mild, intermittent colic Usually responsive to smooth muscle relaxants INVESTIGATE IF PAIN PERSISTS

Answer 235

poliglecaprone glycomer polydioxanone polyglyconate

Answer 236

polyamide (nylon) polypropylene

Answer 237

polygalactin polyglycolic catgut

Answer 238

Short term use – broken down by the body. Useful in intractable patients! Risk of breakdown if healing is slower than loss of tensile strength

Answer 239

Long term use/where sutures are accessible for removal. Can cause foreign body reactions -> sinus formation, encapsulation, extrusion etc.

Answer 240

Smooth surface -> less friction, drag and tissue trauma, less wicking and less contamination. Poorer handling and greater ‘memory’ and stretch -> less knot security.

Answer 241

Strong, soft (good handling) and braided surface -> good knot security. Braided surface -> more friction, drag and tissue trauma, greater wicking and higher risk of contamination.

Answer 242

Superficial wounds/skin. Easiest choice for aural haematoma. Not used with instruments.

Answer 243

Deep wounds/restricted access. Also tend to be easier for skin incisions as can be used with instruments.

Answer 244

Conventional and reverse Used in tissues with a higher collagen content (skin, fascia)

Answer 245

Round bodied; blunt point or taper point Used in more delicate tissue (fat, muscle and viscera)

Answer 246

Brings tissue into correct anatomical alignment -> best healing, especially for skin. Studies show as effective as inverting for creating a fluid-tight seal. Reduces risk of stricture in intestines. Less useful where there is tension. a) Simple continuous b) Intradermal c) Ford interlocking

Answer 247

Turn the edges of the incision inwards so serosal surface are in apposition. Traditionally used to close hollow viscera (GIT, bladder, uterus) BUT may -> slower healing. May -> structure in narrow lumen organs. Suitable in large lumen (bladder, stomach, uterus) hollow organs. Do not use in skin (poor healing). Cushing suture pattern Utrecht pattern

Answer 248

Turn the edges of the incision outwards Avoid in visceral surgery as may increase risk of adhesions. Used in some tension relieving techniques for skin but -> slower healing. Skin suture of choice for reptiles. Blood vessel and heart incisions - achieve endothelium-to-endothelium contact; avoids thrombus formation on exposed collagen.

Answer 249

Pros: One knot failure less likely to result in knot breakdown; tension can be more easily adjusted. Cons: More suture material needed, more knots -> more irritation.

Answer 250

Pros: Faster, less suture material needed, fewer knots -> less irritation, even tension distribution. Cons: Failure of anchoring knot may -> failure of suture line

Answer 251

Square/surgeons knot Slip knot Chinese finger trap Aberdeen Hand tie vs instrument tie

Answer 252

Most common Start with a simple knot with one throw and the direction is reversed during each successive throw. Apply even tension with both strands parallel to the plane of the knot. Surgeon's knot = two throws to start, then a single throw, reversing direction each time, ongoing. Granny knot = throws all in the same direction. AVOID!

Answer 253

A square knot where one strand is held with more upwards pressure - a knot that can slide down to tighten. Useful when tying deep ligatures. Must be converted to a square knot (even the tension) or have square knots thrown over it to secure the initial knot.

Answer 254

Used for tubes (feeding, drains) Pulling on the tube -> tightening to prevent removal. Simple interrupted suture to start, leaving both ends long. Criss-cross along the tube, with a knot placed on each side to indent slightly. Repeat every 0.5–1 cm, five to six times. Finish with a knot containing multiple throws for security .

Answer 255

Used to end continuous suture patterns, especially intradermal. Very quick and allows the resulting knot to be easily buried. Create a loop at the end of your suture line which passes through the skin. Pass a loop derived from the loose end of your suture material through the 1st loop. Draw the first loop tight, maintaining the second loop. Repeat four to four to six times. Finish by pulling the free end of the suture material through the final loop and drawing tight

Answer 256

Most reliable for consistent square knots Can be difficult in deep areas e.g. abdomen of deep chested dogs

Answer 257

More adaptable to deeper areas Can be quicker to tie Allows tension to be maintained Requires more dexterity and more suture material.

Answer 258

Easiest method and uses the least suture material Can be more difficult to assess tension/knot security. Appropriate for most situations, but can be difficult in deep areas.

Answer 259

Needle choice: Cutting or reverse cutting needle. Suture choice: Monofilament, absorbable or non-absorbable Suture pattern: Intradermal continuous Simple interrupted Cruciate Simple continuous Ford interlocking Skin sutures should be kept loose enough to account for post op swelling.

Answer 260

Needle choice: Taper needle Suture choice: Monofilament or multifilament, absorbable Suture pattern: Simple continuous Simple interrupted Tension relieving (walking sutures) Most skin sutures are removed well before skin has regained full strength, so s/c layer is important.

Answer 261

Needle choice: Taper or reverse cutting Suture choice: Monofilament or multifilament, absorbable (occ non-absorbable) Suture pattern: Simple continuous Simple interrupted Tension relieving (walking, horizontal mattress, vertical mattress, near far)

Answer 262

Needle choice: Round bodied, taper or blunt needle Suture choice: Monofilament, absorbable Suture pattern: Simple interrupted Simple continuous Horizontal mattress Near-far, far near Muscles have poor holding power and are difficult to suture.

Answer 263

Needle choice: Cutting needle Suture choice: Monofilament or multifilament, non-absorbable, minimally reactive Suture pattern: Horizontal mattress Specialist tendon suturing patterns (three-loop pulley, Bunnell, locking loop) . Use the largest suture that will pass through the tendon without trauma.

Answer 264

Needle choice: Cutting needle Suture choice: Monofilament, absorbable Suture pattern: Simple continuous Simple interrupted Cushing (bladder) (figure a) Utrecht (uterus) (figure b) Gambee (GIT) (figure c) Leak test hollow organs following closure.

Answer 265

Needle choice: Round bodied, blunt needle Suture choice: Monofilament, absorbable Suture pattern: Mattress suture patterns most common. Oversewing also described – interrupted horizontal mattress suture with a simple continuous suture over the exposed edge of e.g. partial lung or hepatic lobe resections.

Answer 266

Needle choice: N/A (ligation); Taper (repair) Suture choice: Ligation – Monofilament or multifilament, absorbable (occ non-absorbable) Repair – Monofilament, very fine non-absorbable Suture pattern: Ligation – encircling ligature; square knot. Repair – simple interrupted or simple continuous. Polypropylene = least thrombogenic suture material so is preferred for vascular surgery.

Answer 267

Needle choice: Taper Suture choice: Monofilament, absorbable Suture pattern: Simple continuous Simple interrupted Multifilament sutures sometimes used as their perceived ‘softness’ ->decreased irritation, but also much higher risk of infection.