acute medicine and surgery Flashcards

Question

Iatrogenic hypoparathyroidism

Answer 1

Clinical signs – muscle tremors, tetany, restlessness and seizures Monitor blood calcium for at least 48hours Emergency calcium therapy – 10mg/kg iv elemental calcium (as 10% calcium gluconate). If signs recur infuse 1mg/kg/hr. Monitor ECG for bradycardia Various vitamin D compounds are available but they vary in speed of onset

Answer 2

Reduced cardiac performance – bradycardia, low contractility, low volume of distribution Lowered thermoregulatory ability Anaemia – reduced tissue oxygen delivery Obesity – low FRC and tidal volumes Lethargy - ?need for premedication? Diminished drug metabolism Muscle wastage Associated conditions – DM, Addison's disease, megoesophagus Goals of anaesthesia Maintain oxygen delivery to tissues Maintain ventilation Maintain cardiac output Maintain normothermia Avoid regurgitation Ideally establish normal thyroid hormone levels with medical management for at least 2 weeks

Answer 3

Mentally depressed animals may require no sedation A positive chronotropic opioid – pethidine at 3-5mg/kg im – is useful Some authors consider ACP unwise – prolonged sedation, vasodilation and hypothermia Anticholinergics (eg atropine 0.02-0.04mg/kg iv) may be useful but may best be reserved for intra-operative bradycardia

Answer 4

Prolonged circulation time and reduced volume of distribution – CARE with doses and WAIT for effect Commonly used agents are suitable Rapid placement of cuffed ET tube essential

Answer 5

Isoflurane or sevoflurane recommended – nitrous oxide inclusion is useful Intermittent positive pressure ventilation should be applied Monitoring should be stringent and performed by dedicated personnel – in particular paying attention to blood pressure and temperature Fluids should be infused as normal In recovery – keep warm and maintain oxygen delivery

Answer 6

May be seen as a result of; Renal failure Addisonian crises Iatrogenic administration ‘Blocked cats’ Urinary tract trauma/bladder rupture Clinical signs; Vomiting/diarrhoea Weakness/lethargy PUPD Bradycardia

Answer 7

Intravenous fluid therapy to restore normal electrolyte levels and treat dehydration or low blood pressure Calcium gluconate 10%- Protects against cardiotoxic effects by stabilising the cardiac membrane potential Insulin and glucose: Shifts potassium from the extracellular to the intracellular compartment Sodium bicarbonate- Corrects metabolic acidosis and shifts potassium from the extracellular to the intracellular compartment Albuterol- Administered via inhalation to shift potassium from the extracellular to the intracellular compartment

Answer 8

treat! Beware of underlying conditions (hypovolaemia, concurrent trauma) STRONGLY recommended to correct BEFORE anaesthesia!

Answer 9

Emergency patients have minimal ‘physiological reserves’ to tolerate the stress of anaesthesia Vital that we fine tune the anaesthetic to minimise effects of the condition But basic principles still apply In fact they become more important Unstable cardiorespiratory system * Altered circulating fluid volume * Metabolic derangements Time pressures and patient status- May limit comprehensive preanaesthetic examination Potentially unknown/limited history Emotional and financial pressures from the owners

Answer 10

Electrolyte imbalances (potassium and calcium) with cardiac arrhythmias- Correct haemodynamically significant arrhythmias before induction if possible Hypovolaemia Respiratory compromise Possible regurgitation and aspiration Pain and distress Metabolic acidosis and increased lactate Most (all) critical patients require some form of pre-operative stabilisation Intravascular access via a patent cannula Rapid administration of anaesthetic, analgesic and emergency drugs Pre- and intraoperative fluids Possibly 2 FL cannulae in GDV cases Fluid stabilisation +/- additives Appropriate drug therapy Shock rates’ of CSL – a bolus of 2x 15ml/kg over 2 x 10 minutes plus potassium infusion (separate line)

Answer 11

Potentially unnecessary if the patient is obtunded Drugs such as the alpha-2 agonists which have major cardiovascular effects should generally be avoided Although the emphasis is usually on correcting the underlying condition quickly it is always necessary to ensure good analgesia in any surgical patient Full mu-agonist opioids are the drugs of choice Pethidine (meperidine) administered intramuscularly is often a good choice- Short acting, excellent analgesia with some sedation, minimal effects on the cardiovascular system Methadone or morphine suitable but may cause a degree of bradycardia and emesis Following premedication monitor the patient for adverse effects

Answer 12

Have emergency drugs (doses calculated) to hand plus syringes/needles Any induction agent can be used Emphasis on minimal effective doses to allow endotracheal intubation For example- Calculate the full dose of an agent such as propofol, but only administer quarter of the dose over 30 seconds = SLOW In most patients this will be sufficient to allow intubation Propofol or alfaxalone +/- a benzodiazepine such as midazolam may allow a reduction in the propofol dose Fentanyl effective with minimal effects on cardiac output but may cause apnoea Etomidate does not alter cardiac output, but causes profound adrenal suppression Ketamine with benzodiazepine potentially useful In the emergency case I prefer to use familiar agents given to effect

Answer 13

Closely monitor cardiorespiratory status Check temperature regularly - Hypothermia common cause of delayed recovery Assess glucose -Particularly in septic patients Analgesia should be given as necessary to ensure patient comfort Appeared very unsettled – causes could be; Pain Dysphoria Nausea Full bladder Anxiety Performed Glasgow Short Form Pain scale example- Pain score = 8 Greater than 5 indicates inadequate analgesia Max received an ‘MLK’ infusion MLK = constant rate infusions of Morphine at 0.1mg/kg/hr Lidocaine at 1mg/kg/hr Ketamine at 0.12mg/kg/hr

Answer 14

Non-Infectious - Water Deprivation/ Salt Poisoning Infectious - Direct - Glasserella parasuis Streptococcus suis Oedema Disease Infectious – Indirect - Congenital Tremor

Answer 15

Water Requirements - Rule of Thumb – 1L per 10Kg of bodyweight i.e. 60Kg pig is drinking approx. 6L water per day!! Direct correlation with feed intakes Excess Dietary Salt- Hopefully unlikely – more a problem when waste products fed Care salt blocks Sudden Water Deprivation - Frozen pipes, Leak, Low Water Pressure Clinical Signs - Gait Abnormalities Recumbency Extension of the Neck ‘Convulsions’ Blind Diagnosis - Assessment of Diet and Water Delivery System Histopathology is Pathognomic – Preserve Brain ‘Meningoenchepahlitis with oedema and eosinophil infiltration’ Epidemiology - Is the problem – in one pen? In Multiple pens? And what water lines feed these? Other ‘tell tail’ signs – is there tailbiting? Treatment / Control - Rehydration may exacerbate the problem! Rehydrate slowly Fix the issue and prevent it from happening again

Answer 16

Gram negative coccobacillus ‘that requires V factor, but not X Factor’ (D.Taylor, Pig Diseases 8th Edition, 2006) Previously known as Haemophilus parasuis Very common globally Mainly affects pigs post weaning when maternal antibodies begin to wane Disease Presentation Part One Acute - Temperature Lameness – Multiple Joints affected Neurological – Head Extension, Recumbency Respiratory – may be associated cough or shallow breathing Mortality Spike Post Mortem - Fibrinous Pleuritis Fibrinous Pericarditis Fibrinous Peritonitis Yellowish-Green Joint Fluid Diagnosis - Clinical Presentation Isolate the bacteria for PCR – Hard

Answer 17

Doxycycline / Penicillin / TMPS / Amoxicillin – Water Soluble and Individual Injection Anti Inflammatories – Water soluble and individual injection Control / Prevention Target Trigger Factors – Draughts, Cold, Concurrent Conditions Vaccination – Sows or Piglets

Answer 18

Many strains worldwide - Zoonotic Cause of joint ill in piglets (not a neurological problem) Most common strain is Type 2 – Septicaemia -> Meningitis Responsible for Neurological signs post weaning Nervous Signs – Tremor, Paddling, Opisthotonus Clinical Presentation: Post Weaning Increased Respiratory Rate Nervous Signs Acute mortality rise Pathology – Bronchopneumonia with Interlobular Oedema Fibrin Strands – Pleural and Peritoneal cavity Vegetative Endocarditis Diagnosis: Clinical Signs, PM findings, Tonsillar Scrapes, Microbiology Treatment: Very Sensitive to Penicillin, Palliative Care (Heat Lamp, Enema, Low light Levels), Fever Control: Target Trigger Factors – Draughts, Cold, Concurrent Conditions, Stocking Vaccination – S.suis Poorly immunogenic and no cross protection from commercial S.suis Type 2 vaccine Autogenous vaccination can be considered

Answer 19

Clinical Presentation- Acute mortality rise Pigs with good Body Condition Score Neurological signs Diet Change No Fever Puffy eyes, Odd Squeal There is often no Diarrhoea! Diagnosis - Ropes – Saliva for PCR Bacterial Isolation – Faecal / Gut Contents Treatment Acute cases – Antibiotics individual injection or water soluble Neomycin, Apramycin Control Vaccination Organism Toxin Zinc Oxide Breeds

Answer 20

Hypomyelinogenesis Cerebellar hypoplasia Limited Mortality Stops when the pig is sleeping Normally seen in Gilt litters Infection in partum

Answer 21

Example: Sows Pre Service – Erysipelas, Parvo Virus & Leptospira  Protect the Pregnancy Pre Farrowing – E.coli and Clostridia  Protect the piglet (colostrum) Example: Piglets At weaning – Mycoplasma hyopneumoniae, PCV2, PRRS(live) Post weaning – Oral Live Attenuated Lawsonia vaccine There is no typical plan: Most commonly farms will vaccinate against Porcine Circo Virus 2 and Erysipelas, Parvo +/- leptospiraDiseases of the Piglet - Infectious Disease

Answer 22

- Clostridium Perfringens Type C - Small Intestinal Haemorrhage - D+, Sudden Death - First 24 hrs Diagnosis Toxin ELISA (on intestinal Contents) Gross and Histological Pathology Beta Toxin Epidemiology/Pathogenesis - Infection from sow at birth - Ingestion of Clostridia - Toxin Release  Necrosis Treatment or Prevention? - - Acute Outbreaks: Mortality of up to 100%, - Colostral Immunity!! Prevention and Control - Management  Colostrum Management, Neonatal Care Environment  Hygiene at Farrowing, Temperature of Farrowing Room (indoor vs Outdoor?) Health  Sow/Gilt Vaccination, Gilt Acclimation Vaccination - Why? Colostral Antibodies  Toxin Who & When? Sow - 3 weeks pre farrowing Gilts – 6 and 3 weeks pre farrowing

Answer 23

- Isospora suis - 4-21 days of age - Preventable if toltrazuril given before day 4 - Combined iron product available (i.e. Baycox Iron / Forcerris)

Answer 24

E.coli - From 24hrs old - Acute - Wasting, Dehydration

Answer 25

Streptococcus suis Glasserella parasuis Clostridum difficile Clostridium perfringens Type A

Answer 26

E.coli - From 24hrs old - Watery/Creamy Yellow D+ - Wasting, Dehydration, Mortality Diagnosis: - E.coli culture - Virulence Factors: Fimbriae  F4, F5, F6 Epidemiology: - At Farrowing (from sow to piglet) - Low Colostrum intakes - Poor Colostrum Quality - Poor hygiene (at farrowing, between litters) Treatment or Prevention? - Acute Outbreaks: Piglets must be treated, Orally - Chronic clinical cases: Prevention Mortality can be up to 70% Fimbriae allow adhesion to the Gut wall Treatment: Oral Apramycin, Paramycin, Injectables – Will they target the pathogens in the gut Prevention and Control Management  Colostrum Management, Neonatal Care Environment  Hygiene at Farrowing, Temperature of Farrowing Room (indoor vs Outdoor?) Health  Sow/Gilt Vaccination, Gilt Acclimation Vaccination Why? Colostral Antibodies Who & When? Sow - 3 weeks pre farrowing Gilts – 6 and 3 weeks pre farrowing Farrowing Room Temperature – 21degrees (ish) Piglets require 28-30degrees, Sow needs to eat and won’t at higher temperatures so always looking at trade offs

Answer 27

- Streptococcus suis (Type I) - 7days to weaning - Swollen Joints, Temperature, Tremors, Sudden Death - Bacteraemia Diagnosis Clinical Cases Bacterial Culture – Brain, Joints, Heart Blood -> serotyping Epidemiology / Pathogenesis - - Sow - Needle Transfer - Carrier Animals (tonsils  Type II Treatment or Prevention? - - Acute Outbreaks: Treat whole litter  Penicillin -Vaccination? Homologous Strain Only  Autogenous Vaccination Be aware we can also see Type II in the farrowing house but hopefully this is something that was covered in the Neurological diseases lecture Prevention and Control Management  Colostrum Management, Neonatal Care Environment  Hygiene at Farrowing, Temperature of Farrowing Room (indoor vs Outdoor?) Health  Sow/Gilt Vaccination, Gilt Acclimation Autogenous vaccination- Herd Specific Pathogen Homologous Strain Cascade Commercially Streptococcus suis Type II vaccines do exist, however there is no cross protection so it is a good candidate for Autogenous vaccination. This must be only be applied under the cascade,

Answer 28

Why? - Outdoor Vs Indoor? Diagnosis- Pale Piglets up to 28 days of age Haemocue: <90g/L – Anaemic 90-110g/L – Sub Clinical >110g/L – Optimal A Treatment that is a prevention… Sow milk is pretty iron deficient by all accounts Reference values provided by CEVA animal health

Answer 29

7-11days old (Lindsey et al., 2012) - Yellow Pasty D+ Diagnosis - Clinical Signs Detcetion of Oocysts in piglet Faeces Treatment- Toltrazuril / Combined Treatment or Prevention?- Toltrazuril 24-72hrs of age Hygiene Where are the Oocysts coming from?- Sow/Gilt is a reservoir for infection

Answer 30

Legislation exists, there are many other additions depending on the scheme, one example is Red Tractor which 95% of the pigs in the UK are sold under Why do we do it? – Born with 8x very sharp outward facing teeth, needle teeth Veterinary Derrogation required Why? Facial Necrosis -Extremely Painful -Welfare Issue Teat Damage -Welfare Issue

Answer 31

Why? Tail Bites are a Welfare Issue - Painful - Open Wound - Hard to Heal - Lead to Secondary Infections (Public health concerns) Not all farms tail dock and as an industry we are trying to move away from this practice. However, whilst enrichment helps tail biting will occur in any system. When it is epidemic it is very hard to treat and animals suffer. There are many risk factors and it is not black and white

Answer 32

Castration GP mycosis Lacerations Umbilical loss in foals Easy to recognise Not always easy to quantify, especially in a moving animal

Answer 33

Uterine artery rupture Mesenteric artery rupture (strongyle migration) Tumours - haemangiosarcoma, splenic disease Thoracic large vessels rupture in racehorses Renal haemorrhage Rib fracture (esp. foals) Much harder to detect Absence of visible blood loss Can also be difficult to quantify Abdomen/ Thorax Broad ligament/ uterus Intestinal lumen – Increased BUN/ normal creatinine Coagulopathy is a rare cause of haemorrhage in the horse but can be an issue after haemorrhage (consumptive coagulopathy)

Answer 34

Tachycardia Tachypnoea Cold extremities Anxiety or depression (obtunded) Pale mucous membranes/ prolonged CRT Weak arterial pulse Flow murmur (dec. blood viscosity) Sweating Colic / abdominal distension (intra-abdominal haemorrhage) Decreased CVP / arterial pulse pressure/MAP

Answer 35

Hyperlactataemia (impaired tissue oxygenation) most sensitive indicator in acute blood loss Hypoproteinaemia Anaemia PCV and TP may be normal in acute blood loss- Not very sensitive in early stages Splenic contraction can maintain PCV in acute stages PCV and TP remain normal until fluid redistributes from the interstitial spaces (takes up to 12 hours) Serial monitoring required TP changes first ( 4-6 hours post insult) Treat based on clinical signs not PCV!

Answer 36

Blood volume is estimated as 8% of body weight 500kg horse = 0.08 x 500 = 40 L In horses' general guidance acute loss of > 30% (> 12 L in a 500kg horse) of blood volume. Signs of hypovolaemic shock -> Blood transfusion

Answer 37

normal heart rate normal resp rate normal capillary refil time normal blood pressure other physical exam findings- possible mild anxiety

Answer 38

increased heart rate increased resp rate mildly prolonged capillary refill time normal blood pressure other physical exam findings- mild anxiety

Answer 39

moderatly to severly increased heart rate increased resp rate prolonged capillary refill time decreased blood pressure other physical exam findings- anxious or depressed; cool extremities

Answer 40

severly increased heart rate increased resp rate Very pale mucous membranes sever hypotension other physical exam findings- obtunded; cool extremities

Answer 41

Control blood loss if possible Administer appropriate fluid therapy Prepare for blood transfusion if estimate greater than 30% blood loss (Do not drain haemothorax/abdomen unless respiratory distress (thorax)) Internal haemorrhage there is recycling of up to 2/3 RBC's and most of protein

Answer 42

Surgical ligation / pressure- Pressure bandage / tourniquet (distal limb) Manual pressure Ligation of testicular artery Packing of sinuses Not always possible- Intraabdominal haemorrhage Guttural pouch Pro-coagulants- Topical: Chitosan (e.g. ‘Celox’ gauze/granules/’Hemcon’) Kaolin based gauzes (e.g. ‘QuikClot’) Smectite (‘Woundstat’) Absorbable for smaller areas: Gelatin (‘Gelfoam’) (mechanical) Fibrin sealants (‘Surgiflo’) ( biologic) Are they superior to standard packing/ pressure? Side effects? (embolisation) Stabilise clots: Antithrombolytic Drugs- Inhibit fibrinolysis and stabilise clot Two options Aminocaproic acid Tranexamic acid - Better evidence to support use (mainly in humans – little data in horses) 8 X more potent than aminocaproic acid Therapeutic doses in horses have been shown to be much lower in horses than humans Reasonably cost effective

Answer 43

Chitosan (e.g. ‘Celox’ gauze/granules/’Hemcon’) Kaolin based gauzes (e.g. ‘QuikClot’) Smectite (‘Woundstat’)

Answer 44

for smaller areas: Gelatin (‘Gelfoam’) (mechanical) Fibrin sealants (‘Surgiflo’) ( biologic)

Answer 45

No evidence to support use

Answer 46

Is the haemorrhage controlled or uncontrolled? What are the practicalities to consider for “in the field” use? Don’t forget coagulation factor replacement Is there a suitable donor available if required? Commercial haemoglobin-based fluids – availability? Expense? Uncontrolled bleeding- Persistent hypotension is very dangerous. Aim of treatment should be to support the circulating blood volume to the minimum required for adequate tissue perfusion until haemorrhage is controlled. ballaence between adiquate perfusion and potential to worsen bleeding The use of crystalloids / synthetic colloids in the face of uncontrolled haemorrhage can: Dilute RBC/clotting factors Increase blood pressure – destabilise clot, increase bleeding? Additionally synthetic colloids have been shown to cause: hypocoagulation in humans/horses But if no blood products are immediately available crystalloids are indicated in the face of severe haemorrhage as a salvage procedure

Answer 47

Has the haemorrhage stopped? No/Unsure: ‘Permissive hypotension’: “Provide enough perfusion pressure to vital organs such that function is maintained while keeping blood pressure below the normal range in the hope that clot formation will not be disrupted” Aim to maintain MAP ~ 60mmHg, SAP<90mmHg Give maintenance isotonic crystalloids – 2-3ml/kg/hr. Hypertonic saline generally contraindicated in uncontrolled haemorrhage Consider blood transfusion: for any ‘transfusion triggers’: These are guidelines. They need to be balanced against the clinical picture, practical limitations and what fluids are available to you

Answer 48

Definitive haemostasis (e.g. clamping of an external bleeding vessel) - Fine to expand volume using crystalloids, hypertonic saline, blood as dictated by the clinical picture. If crystalloids are used, volume administered should be at least as great as the estimated blood loss. Can give initial bolus ( 10ml/kg rapidly) Clinical signs, PCV, and laboratory evidence of tissue hypoxia can then be used to determine the need for transfusion. Unstable control e.g Clot / uterine artery/ haemothorax- Cautious replacement of circulating volume – Blood ideal as not diluting Rbc’s. You would be more concerned about rapid volume expansion in these cases. Care not to displace clot / cause haemorrhage via increased blood pressure

Answer 49

Acepromazine- Controversial Theory: systemic vasodilation effect – lower blood pressure - reduce haemorrhage. But if blood loss persists it will worsen the hypotension. Only use if stable cardiovascular function Probably not recommended in acute haemorrhage

Answer 50

Transfusion triggers >25% - 30 % blood volume lost Signs of hypovolaemic shock PCV <20% / Hb<7g/dL (in acute bleed) ( < 12% in chronic anaemia) Lactate >4mmol/L These are guidelines and should be used in combination with the clinical picture

Answer 51

Large healthy gelding > 500kg. Good temperament. Minimum PCV of 35%, and a total protein 6.0 g/dL (60 g/L). No universal donor as 8 equine blood groups and > 30 different factors Ideally be negative for the Aa and Qa alloantigens (most antigenic) Avoid mares that have had foals or horses who have themselves previously received a transfusion Donkeys and Mules have RBC antigen “donkey factor”. Can not act as donors and can only receive horse blood if free from anti donkey factor Ab May not be necessary in emergency situations when the recipient has had no prior exposure to blood products Routine crossmatching evaluates haemagglutination Haemolytic reactions are not detected unless rabbit complement is added Major crossmatch- Donor’s RBCs and the recipient’s serum Minor crossmatch - Recipient’s RBCs and the donor’s serum Up to 20% of the donor horse’s blood volume can be collected at one time. For a 500kg horse who has 40 L of blood this = 8L Often, we are using client owned horses so typically we collect less than 20% Crystalloid fluids can be given to replace blood volume, and are recommended when greater than 15% blood volume is collected

Answer 52

Calculating the deficit- Equation may only be used if the horse’s PCV accurately reflects the blood loss ((normal PCV- animal PCV)/normal PCV) x Blood volume Blood volume = 0.08 x body weight example- 500 kg TB racehorse – normal PCV = 35% Presents with a PCV of 10 following an episode of acute haemorrhage ((35-10) ⁄ 35) x (0.08 x 500) = ? (25/35) x 40 = 28.6 L Aim to deliver 30 – 50% of the deficit as volume has already increased through mobilization of interstitial fluid, voluntary intake of water, and administration of intravenous fluids (0.3 – 0.5) x 28.6 = 8 – 14 L The volume to be transfused may be limited by the volume of blood that can be safely removed from the donor horse Warm to room temperature Filter giving set Pre-transfusion examination ( HR/RR/ Temp) SLOW (<0.5ml/kg/hr for 10-15 mins) Monitor for reaction reactions- Usually in first 15 minutes More common after multiple transfusions Agitation, tremors, urticaria, pruritis, piloerection, colic, nasal oedema, pulmonary oedema, weakness, collapse, tachycardia, tachypnoea, dyspnoea, pyrexia, death STOP Consider use of corticosteroid or antihistamine Or in severe cases adrenaline Decide necessity to try to cautiously continue If re-starting, do so SLOWLY If reaction recurs, STOP and find another donor….

Answer 53

Classification of Colic- “Medical Colic” “Surgical Colic” Inconclusive- Schedule Re-examination Avoid Flunixin Call the Referral Centre Persistent pain despite analgesia Progressive abdominal distension Tachycardia (>60bpm) Signs of hypovolaemia Absence of borborygmi Abnormal rectal findings Gastric reflux (>4L)

Answer 54

Decompress stomach- NG tube in situ? Analgesia Report of treatment administered Directions for owner Rug and bandage limbs

Answer 55

Observation- Pain assessment- colon torsions post foaling are particulary painfull Establish a baseline Watch loose External examination “Safety First”- prepeare sedation- xylozine- controls situation Belly Tap- Blood Work- Stomach Tube- Ultrasonography- Rectal Exam- Cardiovascular Assessment- TPR – Remember the T!- pyrexia big diagnostic- often not surgical Heart Rate (N.B. Buscopan suppresses parasympathetic innervation causing tachycardia- don mistake for diagnostic) Pulse Quality Peripheral Skin Temperature Mucous Membranes (inc. CRT) Skin Turgor “Stableside PCV” History- Signalment Immediate colic history Previous colic history Management or feeding changes Recent travel or exercise Dentistry Worming history Concurrent illness “Windsucking” Pregnancy Gastrointestinal Auscultation- Appreciation of “Normal” Hypermotility Hypomotility Caecal contractility (“The Flush”) Tympany Sand

Answer 56

Accurate assessment in patients with abdominal pain Particular value: Small patients Lack of adequate restraint Excessive straining Rectal tears Advanced pregnancy Alcohol saturation without clipping- Cotton wool and container Spray bottle Clipping- Draft breeds Ponies Donkeys Individual horse-to-horse variation Low frequency (2-5MHz) curvilinear transducer- Ideal 30cm depth Rectal transducer- 10-12cm depth Distended SI often dependent Peritoneal fluid assesment Machine Settings- Image optimization- Frequency Time-gain compensation controls Depth settings Overall gain Key principles- Scan with the highest frequency that will allow adequate penetration Depth settings should be adjusted frequently – dependent on structure of interest Larger horse will require a lower frequency than foal or fit TB Limited Technique- Ventral abdomen Left caudal ICS (renosplenic window) FLASH Technique- Fast Localised Abdominal Sonography of the Horse Full Examination Paralumbar fossa/flank region Tuber coxae to stifle ICS (5-17th) Ventral lung margin to costochondral junction Ventrum Sternum to inguinum Costochondral junctions to midline

Answer 57

Fast Localised Abdominal Sonography of the Horse Seven Topographical Locations: Ventral abdomen Gastric window- 10-15th ICS, Ventral to the lung, Gastric contents not normally visible , Splenic vein useful landmark, Occasionally SI loops in this region- Gastric Distension Splenorenal window- Predominant feature of the LHS Can extend to the right of midline Left kidney deep to spleen- (Paralumbar fossa- 15-17th ICS) Homogenous echogenicity- Hyperechoic relative to liver and kidney Nephrosplenic Entrapment (LDDLC) Left middle third of abdomen Duodenal window- Right kidney 14-17th ICS, Descending duodenum -Ventral to the right kidney, Deep to right liver lobe in 11-17th ICS Right middle third of the abdomen Thoracic window

Answer 58

“Safety First” Spasmolytic Lubrication Sedative Twitch Stocks Appreciation of “Normal” Examination of the faeces- Consistency Sand Mucus Parasites Systematic Examination Quadrant System Clockwise starting Left Dorsal

Answer 59

Spleen – caudal edge Nephrosplenic ligament Nephrosplenic space Left kidney – caudal pole Aorta Root of mesentery – smaller horses

Answer 60

Duodenum - Rarely palpable Distension Caecum- Ventral and medial taenia Dorsocaudal-ventrocranial Inguinal Ring- especially in stallions

Answer 61

Pelvic Flexure Left dorsal colon- No palpable taenia or haustra Small colon- Faecal balls Inguinal ring Bladder Reproductive tract

Answer 62

Distended Small Intestine Displaced Intestine Tympany Taut Mesenteric Bands Impaction- Large or Small Colon Caecum

Answer 63

Emergency Often a definitive diagnosis is not possible (or necessary) Exploratory Laparotomy = Diagnostic +/- Therapeutic Better to operate and comprehensively examine the abdomen than to miss a surgical lesion. Pain Response to Analgesia Clinical Examination Diagnostic and Procedural Findings

Answer 64

Pain- Uncontrollable and/or severe Poor/transient response to flunixin meglumine or detomidine Requires further analgesia Gastric reflux- >4L yellow fluid Rectal Findings- Distended small intestine Distended and displaced large colon Distension that cannot be relieved medically Palpable foreign body or mass Auscultation- Absent intestinal sounds Peritoneal Fluid- Increased total protein Presence of red blood cells and degenerate neutrophils N.B. Indicators of hydration or perfusion are not specific for diseases requiring surgery Heart rate Mucous membrane colour CRT PCV Plasma protein concentration

Answer 65

Pain- Depression or lack of pain Temperature - >39.2°C Complete Blood Count- Neutrophilia or neutropenia Auscultation- Progressive intestinal sounds

Answer 66

Strangulated Pedunculated Lipoma Epiploic Foramen Entrapment Large Intestinal Displacement Intussusception Neoplasia

Answer 67

a surgical connection between two structures. It usually means a connection that is created between tubular structures, such as blood vessels or loops of intestine. For example, when part of an intestine is surgically removed, the two remaining ends are sewn or stapled togethe

Answer 68

Within 48 hours of surgery: Incisional/surgical pain Persistent ischemic bowel, for example, ileal stump Continued ischemia/reperfusion injury of bowel Leakage at an enterotomy or anastomosis site Postoperative ileus Recurrent displacement Within 2-7 days of surgery: Obstruction at an anastomosis (e.g., haematoma, impacted ingesta) Delayed adaptation at the anastomosis Peritonitis/anastomotic leakage Postoperative ileus Large colon impaction Gastric ulcers Greater than 7 days after surgery: Adhesions Recurrence of previous problem, e.g. colon displacement Incisional Infection- Culture and sensitivity Drainage and lavage Broad spectrum antimicrobials Abdominal bandage or hernia belt Incisional Herniation- Significance dependent on size of hernia and intended use of horse Hernia belt or abdominal bandage Box rest Herniorrhaphy- 3-6 months post colic surgery Thrombophlebitis- Catheter Removal Culture and Sensitivity Antimicrobial therapy Topical treatment- DMSO? Diclofenac? US Monitoring

Answer 69

NSAID Incisional management +/- suture removal Rehabilitation- 6w box rest 6w small paddock rest Postoperative complications?

Answer 70

Located in the cranial region of the abdomen caudal to the liver. Ingesta enter the stomach via the cardia and exits though the pylorus. The stomach is a dilation of the alimentary canal involved in initial stages of digestion. Cellular lining of the stomach produces various substances involved in digestion. It is entirely glandular in the dog. many blood vessels that feed the spleen are assosiated ith the stomac so torsion can inflame the spleen

Answer 71

Located in between the stomach and large intestines. Made up of the duodenum, jejunum and ileum. Adapted for digestion and absorption of nutrients. Duodenum- Begins cranially in the RHS of the abdomen and runs caudally, then turns left (caudally to the mesenteric artery) and the courses cranially on the left of the midline. Bile and pancreatic ducts empty into the cranial portion. Jejunum- Longest portion of the SI. Sits within the mesojejunum therefore allowing the jejunum to reside throughout the abdomen. Ileum- Shortest position of the SI. It can be difficult to tell it apart from the jejunum. One way of identifying the ileum is identifying the artery running along the boarder of the ileum. This is located 180 degree from the ileum’s attachment to its mesentery. the further along the small intestine the harder it is to operrate

Answer 72

Terminal portion of the intestinal tract connecting the SI to the anus. Compromised of the caecum, colon, rectum and anal canal. Caecum- A diverticulum in the initial portion of the colon involved in absorbing water. Colon- Comprised of the ascending, transverse and descending colon. Involved in nutrient and water absorption. Located in the dorsal abdomen starting on the RHS coursing cranially then passing to the LHS and courses caudally to the left side of the abdomen into the pelvic vanity. opening of the large intestine is not a small practice procedure- large risk of septic peritonitis foreign bodies may be able to be milked to the anus

Answer 73

Initial goals are to assess for shock (hypovolaemic and distributive most common) and localise the problem. Assessing for shock: Heart rate Pulses MM colour or CRT time changes Temperature Respiratory rate and effort If shock is identified, this needs to be addressed asap. See previous lectures: Approach to triage Fluid therapy Diagnosis of shock Localising the problem – many disease processes can present with gastrointestinal signs: Cardiac disease -> vomiting, abdominal distension Hepatic and pancreatic disease -> vomiting, diarrhoea, and/or abdominal pain and distension Urogenital disease -> vomiting, abdominal pain Splenic disease -> abdominal pain and/or distension Endocrine disease e.g. DKA -> vomiting, diarrhoea Musculoskeletal disease, e.g. IVDD spinal pain can present as abdominal pain. Full history and clinical examination is always indicated

Answer 74

Radiography - Plain Contrast Abdominal ultrasound- Abdominal focussed assessment with sonography for trauma (A-FAST) Survey abdominal ultrasound Peritoneal fluid tap Haematology and biochemistry

Answer 75

First choice for suspected obstructive disorders e.g. foreign body, GDV Plain radiographs often enough for diagnosis. Oesophageal foreign body- Poorly defined opacity in the dorsocaudal lungfield. DV radiographs would show this on the midline, increasing suspicion that it resides within the oesophagus rather than a lung. First choice for suspected obstructive disorders e.g. foreign body, GDV Plain radiographs often enough for diagnosis. GDV- Dilation without volvulus – no compartmentalisation of the stomach Dilation and volvulus – gas is compartmentalised by a band of soft tissue. Intestinal foreign body- Gas distension of the intestines - white arrows Foreign body (corn cob)- red arrow No gas beyond the foreign body Intestinal linear foreign body- Plication of the small intestine due to a linear foreign body (white arrow heads) Contrast studies are used less often in emergency presentations, but may help identify strictures, partial obstructions, or intussusceptions in less urgent cases. Intestinal stricture due to neoplasia: Loops of small intestine of normal diameter. Dilated loop of small intestine. Abrupt termination after the most dilated loops of intestine. Feces present in colon More useful than radiographs when effusion is present.

Answer 76

More useful than radiographs when effusion is present. Can pick up more subtle changes e.g. intestinal stricture due to neoplasia, intussusception etc. A-FAST used to detect free fluid for sampling or where a bleed is suspected.

Answer 77

Usually ultrasound guided to avoid accidental organ perforation. Used to distinguish type of free fluid present within the abdomen. Peritoneal lavage reported as a diagnostic tool where fluid is present in volumes too small to sample/ultrasound is not available – rarely done now.

Answer 78

Primarily used to rule out other causes of GI signs, and to assess for any abnormalities which need to be corrected prior to further investigations or surgery. Primarily used to rule out other causes of GI signs, and to assess for any abnormalities which need to be corrected prior to further investigations or surgery. Changes with GI disease: Dehydration -> ↑HCT and TP, azotemia Upper GI obstruction -> metabolic alkalosis due to loss of H+, K+, and Cl- in the vomit. Infectious disease -> WBC changes. See previous clinical pathology lectures, in particular: Electrolytes and Acid Base Proteins, liver and pancreas Haematology

Answer 79

See previous lectures: Approach to triage Fluid therapy Diagnosis of shock Used primarily to correct dehydration. Try and take ongoing losses into account (v+ and d+) Important to correct shock, and electrolyte abnormalities prior to general anaesthesia in surgical cases.

Answer 80

Antiemetics: Primarily used in medical cases e.g. dietary indiscretion or infection. Use of antiemetics contraindicated where obstructive disorders are suspected as they may hide signs of ongoing nausea. Maropitant: Neurokinin 1 (NK1) receptor antagonist; centrally mediated anti-emetic. Some evidence may be better for vomiting than nausea e.g. in CKD cats. Exception = motion sickness Effective against emetogens (drugs which induce vomiting) Ondansetron: Serotonin receptor antagonist; central and peripherally acting antiemetic. Developed to treat chemotherapy induced nausea; effective for both vomiting and nausea. Human drug, use in animals is off license. Metoclopramide: Dopamine receptor antagonist, plus serotonin receptor antagonist at higher doses; centrally acting antiemetic. More effective in dogs than cats Prokinetic in the proximal GI tract – contraindicated with suspected obstructive disease.

Answer 81

H2 receptor antagonists (ranitidine, famotidine): Decrease gastric acid production Increase GI motility Proton pump inhibitors (omeprazole): Decrease gastric acid production – more effective than H2 antagonists Sucralfate: Binds to ulcer sites, creating a barrier and preventing further erosion. Stimulates bicarbonate and PGE production (mucosal defense) and binding of epidermal growth factor (mucosal repair). Works best in acidic environments.

Answer 82

Not indicated in mild cases of vomiting or diarrhoea. Amoxicllin/clavulanate: Indicated perioperatively when entering the GI tract, but use post-surgery should only be continued if there is a therapeutic indication. First choice for haemorrhagic diarrhoea where there is a risk of sepsis (including parvovirus infection). Metronidazole: Commonly used for haemorrhagic diarrhoea as it has secondary GI anti-inflammatory effects. Studies have not been able to demonstrate a significant benefit to using metronidazole in these cases. May be indicated where there is a known Giradia or Clostridia spp. infection

Answer 83

Common foreign bodies: Bones and corn cobs Chew toys and rubber balls Rawhide String Sharp metal objects e.g. sewing needles and kebab skewers. Common sites: Thoracic inlet Heart base Where the oesophagus passes through the diaphragm. Presenting signs Choking/gagging Increased salivation Regurgitation Lethargy, dyspnoea and coughing 2o to aspiration pneumonia Possibly sequale: Aspiration pneumonia Oesophageal perforation/necrosis (see image) Mediastinitis, pleuritis, and pyothorax Radiographs - preferred Radiolucent FB may require contrast (sterile, water-soluble iodinated agent) Allows assessment of lung fields for evidence of aspiration pneumonia etc. Oesophagoscopy- Direct visualisation of the foreign body

Answer 84

Treatment = removal under GA with a cuffed ET tube. Endoscopic removal: Requires air insufflation – care re:oesophageal perforation. Flexible or rigid (easier) endoscope + blunt forceps to remove per os. Otherwise, gentle pressure can be applied to try and move the FB into the stomach then -> gastrotomy. Surgical removal: Gastrotomy (if FB can be moved into the stomach) - less risky than thoracotomy. Thoracotomy – usually requires referral End-to-end anastomosis – may need to be performed where there is severe damage to the oesophagus. Medical treatment post-removal: Sucralfate Anti-inflammatories H2 antagonists/proton pump inhibitors +/- antimicrobials Feed a soft diet Feeding tube Where damage is severe. Needs to enter the GIT beyond the point of damage.

Answer 85

The phone call: “My dog is trying to vomit, but nothing is coming up.” Common signalment: Large breed, deep chested dogs (but also reported in smaller breeds and cat less commonly) Guinea pigs Serious condition – mortality 10%-45% in treated animals. Presenting signs Non-productive retching (dogs) Abdominal distension Lethargy and collapse in later stages Clinical examination: Dyspnea and/or tachypnoea Tympanic anterior abdomen Tachycardia, +/- dysrhythmia Weak pulses Pale mucous membranes and prolonged capillary refill time (CRT) Possible sequale: Cardiac arrythmias (ventricular premature complexes and ventricular tachycardia) Endotoxaemia Gastric necrosis -> peritonitis and/or septic shock Electrolyte and acid base disruptions. Disseminated intravascular coagulation. Diagnosis Radiographs (see prev) Orogastric intubation

Answer 86

Initial treatment Gastric decompression (orogastric tube or percutaneous) +/- lavage Treatment/management of shock Manage dysrhythmias See previous lectures: Fluid therapy Anaesthetic management of emergency patients Anaesthetic dysrhythmias Anaesthetic considerations – see Ian’s lecture Aims of surgery: 1. Identify and remove damaged or necrotic areas of the stomach and/or spleen.- Partial resection of necrotic stomach Complete or partial resection of necrotic spleen. 2. Correct stomach position- Clockwise rotation = most common, but always check 3. Adhere the stomach to the body wall to prevent recurrence0 Incisional and belt loop gastropexy = most common Post surgical care: Continue monitoring electrolytes, acid base, and ECG for 24-48 hours post-surgery. Fluid therapy until oral intake is sufficient to prevent dehydration. Analgesia – opioids Small, soft, low fat meal should be offered 12-24 hours after surgery Anti-emetic (maropitant) if needed. Proton pump inhibitors if ulceration present. Prokinetics? Antibiotics? Prevention- Feed more, smaller meals Avoid stress during feeding Do not use an elevated feed bowl. Avoid breeding from dogs which have suffered from, or have immediate relatives which have suffered from, GDV. Restrict exercise before and after meals?- no studies but often said Prophylactic gastropexy?- recomended by some surgeons

Answer 87

The phone call: “My dog/cat is vomiting everything up, even water.” Gastric foreign bodies only tend to present as an emergency if causing an outflow obstruction or perforation. Intestinal foreign bodies almost always present as an emergency. Linear foreign bodies can be both. Common signalment: Younger animal, known scavenger Clinical examination Dehydration Signs of shock (tachycardia, poor pulses, poor perfusion) Abdominal pain Palpable abdominal mass Pyrexia Possible sequale: Perforation ->peritonitis +/- septic shock Sepsis +/- DIC without perforation Diagnosis- Clinical exam – palpate abdomen and check under the tongue (linear) for evidence of FB. Radiographs (plain or contrast) Ultrasonography Gastroduodenoscopy (may also be therapeutic if FB can be retrieved) Haematology and biochemistry – used to assess systemic state rather than as a diagnostic test.

Answer 88

Medical treatment: Induction of vomiting? Feeding fibre/psyllium? Serial radiographs? Fluid therapy and correct electrolyte and acid base abnormalities – see previous lectures Analgesia – opioids Antibiotics –cephalosporins or amoxy/clav. Foreign body retrieval: Gastric and duodenal FB – possibly endoscopic retrieval. Surgical – gastrotomy, enterotomy, or both. Always check the entire GIT when performing an ex-lap, stomach to colon – it is possible to have multiple foreign bodies! Try and milk foreign bodies to an area of healthy tissue before making the incision. Linear FB may require multiple incisions. End-to-end anastomosis required where tissue is non-viable Post operative care: Ongoing fluid therapy. Continue monitoring and correcting electrolyte abnormalities. Start feeding a low fat diet from 12 to 24 hours post-surgery. Antiemetic if needed Proton pump inhibitors if ulceration present.

Answer 89

Vomiting Dehydration Hypovolemic shock

Answer 90

Intermittent vomiting Weight loss Possibly asymptomatic/incidental finding

Answer 91

Vomiting Dehydration Hypovolemic shock

Answer 92

Intermittent vomiting Dehydration Weight loss Anorexia

Answer 93

GSDs and Siamese cats appear predisposed Intussusception = a ‘periscoping’ of the intestines. The phone call: “My puppy/kitten is really quiet and doesn’t want to eat. They’ve vomited a few times too.” Signalment: Young animals, especially common post-parvoviral infection or parasitic enteritis. Older animals, often associated with intestinal masses (esp cats). Presenting signs: Vary with site and severity of the intussusception. Acute(less comon): Scant, bloody diarrhoea, vomiting, abdominal pain, mass on abdominal palpation. Chronic: Intractable, intermittent diarrhoea, depression, anorexia, and emaciation. Diagnosis Radiographs: Plain often unhelpful, contrast more useful in some cases (thin ribbon of material seen at the site of the intussusception) Abdominal ultrasound – most useful. Haematology and biochemistry Faecal analysis

Answer 94

Medical treatment: Treatment of any underlying condtion In acute cases may need to stabilise as per intestinal foreign bodies. Percutaneous correction may be possible in rare cases; high risk of recurrence Common sites: Ileocolic Jejunojejunal Surgical treatment: Manual reduction +/- enteroenteropexy End-to-end anastomosis Manual reduction: Apply gentle pressure on the neck of the intussusception while ‘milking’ the apex out of the intussusceptiens. Avoid excessive traction – push on the intussuscipiens more than pull on the intussusceptum. Enteroenteropexy- Prevents recurrence of intussusception. Place small intestinal in a series of gentle loops from the distal duodenum to the distal ileum. Bends must be gentle to prevent obstruction. Place sutures to secure the loops, engaging the submucosa, muscularis, and serosa, 6 to 10 cm apart. Resection and anastomosis is indicated if: A mass is detected. It is not possible to manually reduce the intussusception. The tissue is no longer vital. Any part of the blood supply is disrupted during reduction. Post operative care: As for foreign bodies

Answer 95

The phone call: “My dog is collapsed. Their stomach is swollen and they are passing blood from their anus. They seemed fine a few hours ago.” Rare, and almost always fatal. Prompt recognition and surgical intervention is vital. Diagnosis = challenging as c/s non-specific and progress rapidly Radiographs may show uniform distension of the majority of the GIT, but by this stage most of the intestines will be necrotic. Partial volvulus may allow time for surgical intervention and correction, but euthanasia often indicated.

Answer 96

The phone call: “My dog/cat is passing bloody diarrhoea!” Differentials: Parvovirus Clostridial endotoxicosis (2o to other infections, dietary indiscretion etc.) Coagulopathy e.g. rodenticide toxicity Intussusception Foreign body  intestinal trauma (uncommon) Signalment: Parvovirus = unvaccinated puppies Other ddx = middle aged, small breed dogs most commonly reported but possible in any dog. Rare in cats Presenting signs: Haemorrhagic diarrhoea Distinguish from melaena and haematochezia, neither of which should present with diarrhoea. Parvovirus: Watery with mixed fresh and digested blood AHDS: raspberry jam consistency +/- vomiting and/or haematemesis Anorexia Lethargy Clinical examination: Dehydration Hypothermia more common than pyrexia Tachycardia (2o to dehydration and hypovolaemia) Canine AHDS index has been devised to assess the clinical significance of disease. Mortier et. Al. 2015 reported AHDS score <2 can be discharged from hospital, Hall 2023 extrapolated this to any score <2 does not require hospitalisation. Ideally need to make a clinical judgement based on the individual case. Image credit: Hall, E., 2023. Dealing with haemorrhagic diarrhoea in dogs. In Practice, 45(9), pp.516-531. is a table for assesing clinical significance of ahds

Answer 97

AHDS is mostly self limiting with supportive care, therefore not essential to get a definitive diagnosis in most cases. Exception = parvovirus. Always test if any clinical suspicion due to highly infectious nature and risk to other dogs Diagnosis – lots of options main- Haematology and biochemistry Faecal analysis SNAP test for parvovirus secondary- Basal cortisol or ACTH stimulation test (hypoadrenocorticism) Coagulation profiles (bleeding disorders/rodenticide toxicity) Pancreatic specific lipase (pancreatitis) Imaging – non-specific, may be useful if neoplasia or pancreatitis present Serum protein C (marker of intestinal inflammation) - not useful for diagnosis but serial monitoring may have a prognostic value Haematology and biochemistry- Highly variable Haemoconcentration due to dehydration, progressing to decreased PCV Inflammatory leukogram (AHDS) or leucopenia (parvovirus) Hypoproteinaemia Hypokalaemia Pre-renal azotemia Faecal parasitology useful but faecal culture not as the bacteria commonly implicated in AHDS are also present in healthy individuals Faecal antigen SNAP test for parvovirus – false negatives sometime occur. Parvovirus PCR also available, serology less useful in practice Most cases will resolve with supportive care: Fluid therapy: Correct dehydration and hypovolaemia, then maintenance. Antibiotics: Only where there is evidence of sepsis (amoxy/clav)- Widespread use of metronidazole in haemorrhagic diarrhoea is not indicated – see earlier. Dietary modification: – traditionally food was withheld, but studies have shown “feeding through” with a low fat, easily digestible diet decreases morbidity and hastens recovery Antiemetics: e.g. maropitant Analgesia: opioids Supplementary treatment options: Protectants and adsorbants e.g kaolin - frequently used, but weak evidence for efficacy Pro-, pre- and postbiotics – limited evidence for use, but unlikely to do harm. Faecal microbiota transplantation – rarely performed. Little information available on safety and efficacy Prevention Parvovirus - vaccination Otherwise difficult due to wide range of factors which could potentially be involved Prognosis Parvovirus – guarded even with treatment AHDS– generally good with treatment, can be fatal if left untreated.

Answer 98

Barrier nursing essential! Supportive treatment: Fluid therapy Antibiotics (amoxicillin, amoxy/clav) – usually neutropenic, antibiorics indicated as high risk of sepsis Antiemetics e.g. maropitant Gastroprotectants (H2 antagonists or proton pump inhibitors) Nutritional support Severe cases: Blood transfusion (anaemia) Antiviral treatment: Virbagen Omega “For the reduction in mortality and clinical signs of parvovirus (enteric form) in dogs from one month of age.” Monoclonal antibody treatment: Recently released by Elanco in the US- no uk release date “Neutralises canine parvovirus in vivo by selectively binding and blocking the virus from entering and destroying enterocytes.”

Answer 99

“Hyperthermia results from increased muscle activity, increased ambient temperature, or an increased metabolic rate.” May be further categorised into: Heat stroke/exhaustion Exercise induced Malignant hyperthermia (medication/anaesthetic induced). Stress induced hyperthermia common in cats

Answer 100

“Pyrexia occurs when the hypothalamus resets the body’s thermoregulation to a higher point than normal, resulting in physiological mechanisms which increase body temperature.” Can be due to infectious, immune-mediated, or neoplastic disease Rectal temperature >39.2oC Pyrexia of unknown origin: Pyrexia with no obvious cause following diagnostic tests and which has shown no response to treatment with e.g. antibacterials, NSAIDs, steroids etc.

Answer 101

Vaccine reaction May be a trigger for immune mediated disease Infectious diseases in non-vaccinated animals e.g. FeLV, cat flu, parvovirus, leptospirosis, kennel cough etc. Environment: Hunting – Toxoplasma gondii, Salmonella spp. Travel history – Leishmaniasis Ectoparasite control: Tick borne disease e.g. Babesia, Erhlichia, Anaplasma Flea-borne disease e.g. Bartonella Exposure to other animals Infectious disease e.g. FIV, FeLV, infectious gastroenteritis, kennel cough, cat flu Injury e.g. abscess or cellulitis following a bite wound Any other clinical signs which could narrow down which body system is involved: Gastrointestinal tract Urinary tract Neurological system Respiratory system Pancreas Cardiac system Musculoskeletal system

Answer 102

Conservative treatment: NSAIDs – only if no dehydration OR correct dehydration first. Fluids – subcutaneous or oral rehydration Antibiotics – especially in cats where a cat bite is suspected but no bite wound can be found NOTE: Cefovecin (Convenia) – long acting third generation cephalosporin which is massively overused in these cases. Not a first line drug! Retrospective study of 106 cats presented with pyrexia: FIP most common diagnosis by far. Infectious disease most common cause, followed by inflammatory, then neoplastic, immune mediated, and misc causes less common Cats: Cat bite abscess Acute viral and uncomplicated bacterial infections e.g. cat flu, gastroenteritis etc.

Answer 103

Conservative treatment: NSAIDs – only if no dehydration OR correct dehydration first. Fluids – Usually oral rehydration Antibiotics Less clear cut than in cats The most common infectious conditions are acute viral or gastrointestinal infections – antibiotics not indicated for either. Retrospective study of 140 juvenile dogs presented with pyrexia: Steroid responsive meningititis-arteritis most common diagnosis, followed by immune mediated polyarthritis. Immune mediated conditions most common, followed by other non-infectious inflammatory conditions, then infectious. Dogs Acute viral and uncomplicated bacterial infections e.g. kennel cough, gastroenteritis etc. Steroid responsive meningitis-arterititis - now being recognised much more frequently in first opinion practice Steroids: May be trialled where clinical signs are suggestive of SRMA and further investigations are not an option. Need to be wary re:infectious causes of pyrexia – could become worse

Answer 104

Retrospective study of 106 cats presented with pyrexia: FIP most common diagnosis by far. Infectious disease most common cause, followed by inflammatory, then neoplastic, immune mediated, and misc causes less common Retrospective study of 140 juvenile dogs presented with pyrexia: Steroid responsive meningititis-arteritis most common diagnosis, followed by immune mediated polyarthritis. Immune mediated conditions most common, followed by other non-infectious inflammatory conditions, then infectious. Where to start? Choose tests which give you the most amount of information first: Haematology and biochemistry (FeLV and FIV SNAP test for cats) Urinalysis Choose tests which give you the most amount of information first: Thoracic and abdominal radiographs Abdominal ultrasound Faecal analysis? If an underlying cause has still not been identified or confirmed, move on to more specific tests. Immune testing- Saline auto-agglutination or Coombs test for IMHA Antinuclear antibody (where evidence of two or more immune mediated disease processes is present) Rheumatoid factor where an erosive polyarthropathy is present. Acetylcholine receptor antibodies if myasthenia gravis is suspected. Cytology- FNA of masses Cerebrospinal fluid tap – where meningitis is suspected Arthrocentesis – where polyarthrtitis is suspected Bone marrow aspiration and biopsy – where bone marrow disease is suspected e.g. where panleukopenia is present on haematology Infectious disease testing Outdoor cats (esp hunters): Toxoplasma gondii IgG and IgM, tick-borne disease PCR panel (Borrelia, Ehrlichia/ Anaplasma etc.), Bartonella PCR Cats with anaemia: Infectious anaemia panel (Haemotrophic Mycoplasma spp.) Dogs with a travel history: Vector borne disease PCR panel (Leishmania, Babesia, Ehrlichia etc.) Most cases will require: Fluid therapy Anti-inflammatories – either NSAIDs, or steroids where immune mediated disease is present Otherwise, treatment will depend on the underlying disease. If a diagnosis has still not been reached, consider referral. Cats: Cat bite abscess Feline Infectious peritonitis Toxplasma gondii Dogs: Heat stroke Steroid responsive meningitis-arteritis Immune mediated polyarthritis

Answer 105

Presentation: Lethargy Anorexia Pyrexia +/- focal swelling or draining abscess (head, neck, rump, legs and paws = common sites) Diagnosis based on history and clinical signs Treatment depends on presentation

Answer 106

Release pus: Open (if not already draining) and flush with sterile saline (20ml syringe and 19g needle) If abscess is extensive or painful, sedation or GA may be necessary Owners should bathe the wound at home (saline or chlorhexidine) to keep it open and encourage further drainage. Analgesia Meloxicam – analgesia and anti-pyretic. Opioids – if dehydrated Fluids Mild dehydration - single s/c bolus Moderate to severe dehydration - IVFT Antibiotics Only if pyrexic and/or systemically unwell Base on inhouse cytology if possible

Answer 107

Immune mediated disease which develops in some, but not all, FCoV infected cats Presentation: Signalment: Cats <3 or >10 years old from a multi-cat environment (e.g. breeding cattery or shelter). Recent stressor also common. General signs: Anorexia, lethargy, pyrexia, weight loss, pale and/or jaundiced mucous membranes. Presentation (cont): Wet form: Effusions - Peritoneal (65%), pleural (10%), or bicavity (25%) Dry form: Varies with organ system affected. Occular and CNS signs most common (60%), remainder involve abdominal organs Diagnosis is challenging, as many cats will be infected with FCoV without developing FIP. Clinical suspicion is raised by: Consistent history, signalment and clinical signs (wet form especially) Haematology: Non-regenerative anaemia, lymphopenia, IMHA. Biochemistry: Hyperglobulinaemia, hyperbilirubinaemia in the absence of significant changes to other liver enzymes FCoV serology and PCR not diagnostic as not all infected cats develop FIP, but high titres may be indicative Gold standard: Immunostaining of FCoV antigen within macrophages in effusion or tissues + histopathological changes consistent with FIP. Prognosis grave – currently no cure.

Answer 108

Treatment options: Immune mediated disease so currently therapy aims at modifying the immune response using steroids. Interferon (virbagen omega) shown to be ineffective for FIP Antiviral drugs targeting FCoV replication now being investigated but not yet available.

Answer 109

Clinically silent in the vast majority of cats, self-limiting intermittent diarrhoea in approx. 20% Rarely, severe acute and chronic forms of disease will develop: Acute: Pyrexia, anorexia, CNS signs, multifocal inflammation. Chronic: Vague, recurrent illness, chorangioretinitis is common. Possible breed disposition -Norwegian forest cat, Birman, ocicat and Persian cats. Clinical suspicion is raised by: History (hunting) and clinical exam findings consistent with multifocal inflammatory disease. High T. gondii IgM and IgG (ideally rising titres taken 2-4 weeks apart) H&B and urinalysis not useful for diagnosis, but may show which organ systems are effected. Definitive diagnosis: Detection of tachyzoites in tissue biopsies or cytology samples. Immunohistochemistry or immunofluorescence on histology samples.

Answer 110

Primary treatment: Clindamycin BID for 4 weeks Supportive treatment: Fluid therapy if dehydrated Appetite stimulants e.g. mirtazapine. Ocular inflammation – topical glucocorticoids Care re:systemic immunosuppressants Elimination of the parasite is very difficult, and recurrence is common.

Answer 111

Almost always due to Exposure to high environmental temperatures (e.g. hot car) Recent physical activity, usually in hot weather. Presenting signs: Continuous panting +/- cyanotic mucous membranes Hypersalivation Stiffness Collapse in severe cases check bloods continuously to moitor renal function

Answer 112

Most common form of canine meningitis. Typical presentation: Young dog Pyrexia Neck pain with no other neurological deficits Less common signs include cranial nerve deficits and, in chronic cases, deficits associated with spinal cord damage. Diagnosis is often made on signalment and clinical examination alone. Haematology: Leucocytosis with left shift Biomarker: C-reactive protein (non-specific for inflammatory disease) CSF cytology: Most important diagnostic test. Acute phase = pleocytosis, non-degenerated neutrophilic granulocytes, increased protein content, and a negative microbiological culture. Chronic phase: Predominant cell type changes to lymphohistiocytic cells (lymphocytes and macrophages) – risk of false negative results. MRI: Useful to rule out other common ddx

Answer 113

Prednisolone = 1st line treatment for moderate to severe cases. NSAID (carprofen) use has been reported for mild cases with CSF cell counts <200 cell/uL. Azathioprine may be used as a second line drug in combination with prednisolone.

Answer 114

Can be primary (idiopathic) or secondary to another inflammatory condition which -> immune complex formation Presenting signs: reluctance to walk, altered gait (stilted, “walking on eggshells”) or lameness, multiple swollen, painful joints. Non-specific presenting signs: pyrexia, lethargy, inappetence, vomiting, diarrhoea. Definitive diagnosis is based on arthroscopy of at least three joints demonstrating: WBC > 3000/uL Neutrophils > 10% TP > 2.5 g/dL Negative culture BUT because IMPA can be 2o, a full suite of baseline tests are recommended to evaluate for underlying inflammatory conditions

Answer 115

Prednisolone = 1st line treatment for IMPA, +/- azathioprine as per SRMA. Major differential for IMPA is septic arthritis, therefore recommended to wait for culture results before starting prednisolone. Opioid analgesia should be started while waiting for results.

Answer 116

when was her last season how much exactly is she drinking are there any other animals in the house? could she have been ated eating? vomiting? dihorea? have you noticed any clinical signs any acess to toxins?

Answer 117

temperature pulse respiritory mucous membranes- colour, crt, moinstness vulvar exam- discharge? cytology? open or closed cervix palpate abdomen mamary gland

Answer 118

pyometra Oestrogen stimulation of the uterus, followed by periods of progesterone influence -> Synthetic progesterones (alazin highly predisposes dogs to pyos, should be spayed) administered over long periods OR Oestrogens given for misaligment Endometrial proliferation, uterine glandular secretions, cervical closure and decreased myometrial contractions Cystic endometrial hyperplasia/endometrial hyperplasia Secondary invasion with bacteria (often E. coli) <- Underlying UTI, renal disease etc. may predispose to infection Neutrophilic inflammation, accumulation of pus within the uterus, +/- septic shock, decreased responsiveness to ADH  polyuria

Answer 119

Open vs closed pyometra- Open: Pus drains out of the cervix Closed: Pus is trapped within the uterus, higher risk of rupture and sepsis. Closed pyometra is almost always an emergency requiring surgery. May consider medical management of open pyometra in certain cases- Mild symptoms Valuable breeding bitches Animals with increased anaesthetic risk (geriatric, underlying health concerns) Note: High risk of recurrent pyometra after the next season when medical management used- should be bred or spayed before next season involvment of- repro system renal system- interfirence with antidiuretic hormone from pyo toxins interfiere with ADH immune system- acumulation of neutorophils in uterus can deprive other areas of the

Answer 120

Haematology and biochemistry Cytology (vaginal discharge) Ultrasound Culture and sensitivity

Answer 121

Haematology and biochemistry- neutropenia, leukocytocis, anemia, azotemia Cytology (vaginal discharge)- degen neutrophils adnf bacteria Ultrasound- fluid filled uterus Culture and sensitivity- +++

Answer 122

sue to her age and her relative stability surgical managemnt would be the most appropriate it is unlikly she would be bred from any more

Answer 123

antibiotics- amox/clav fluid therapy- stabalise protaglandin- colprostenol galastop- cabergoline- medical treatment of closed pyo- dopamine agonist alizin- algiprestone- progesterone receptior antaonist- relaxes cervix to allow puss out licenced for abortion but off licenese use for . three doses at days 1,2 and 7 cloporestol- prostaglandin in combo with alepredistone not licensed in dogs causes luteolusis and uterine contactions

Answer 124

Most commonly affected species. OHE indicated – short oestrus cycle means recurrence almost inevitable. Medical management usually attempted prior to surgery to decrease GA risk. Antibiotic choice = fluorquinolones Fluids – s/c

Answer 125

are the puppies doing ok? when did she start? whe was the last puppies passes? did the straining stop when the last puppie was born or some time fter? how long between each puppies? has there been any stressors? how many placentas has she passed? is there one for each puppie? what diet has she been fed?- puppie food is best has their been any discharge? has the bitch whelped previously? were their issues? is thier known issues in this line

Answer 126

tpr mm whats her consition?- exhasted ect mentation abdominal palpation check vaginal canal can we feel a puppy? fetal heart rate

Answer 127

absence or weakness of fergusons respone increases suspision of hypocalcemia puppies are not in distress- too high heart very uncommon uterine inertia

Answer 128

Maternal factors: Primary uterine inertia – multifactorial, genetic disposition suspected. Secondary uterine inertia – multifactorial, hypocalcaemia/hypoglycaemia play a more prominent role. Birth canal abnormalities (breed conformation, stricture, masses etc.) Foetal factors: Size mismatch (large puppy, small bitch) Malformations Malposition Inertia = most common reason for dystocia across breeds, birth canal conformation/size mismatch more common in brachycephalics

Answer 129

Secondary uterine inertia – multifactorial, hypocalcaemia/hypoglycaemia play a more prominent role.

Answer 130

bloods- check calcium levels- low calcium levels does not rue out hypocalcemia as cellular calcium levels not shown check ketones- hypoglycemia- pregnancy toxemia check how many puppies left

Answer 131

medical managment- calcium- increases strenth of contraction 10% calcum gluconate soluiton as slow IV . can be done sc but potential side efects. oral ineffective give calcium and wit before gic=ving oxytocin- more time if given subcut oxytocin- increases frequency of contrations microdoses more effecteive than higher doses can be given sc, im or iv 30 min for up to 3 soses give both in all cases regardless of bloods glucose if hypoglycemic 3 rounds of medical managment then go for c section bsava maual has step by step process palpation to manilpulat epuppies nto canal but not likley as no puppie in birth canal 4 puppies is about the limit for mediclal intervention as mother will be fatigued labour should not be too prolonged if trying medical managment do not make a dog contract on a suck puppies surgical options- obstructive dysticua non obstructive with greater than 4 puoppies pre operative fluids recomended oxytocin can be given after c section aid uterine involution and milk let down use intradermals to prevent puppies form interfering with sutures use abdominal lavage, pre operative antibiotics- amox- ongoing antiobiotics recomended may recomed dpay at time of c-section- increased surgical time? increased infection risk? decreased mothering behaviour- increase in pain, unkown reasons? previos opinion is not to do spay but more modern retrospective analysis says risk is not as increased as previously feared eventual spay should be recomended as dog is poor breeding candidate- calium suplimentation durign pregnacy not shown to help.

Answer 132

has he been fighting? has he been bred from recently? what other rabbits does he live with? eating? drinking? urinating? faeces?

Answer 133

weight loss gut noises check scrotum, penis na dprepuce check for wounds check teeth check lympnodes chekc temperature

Answer 134

neoplasia- sertoli cell tumour, seminoma, lymphoma, intersticail cell tumour, teratoma tsticular torsion- trauma orchitis/ epidydimitis- p.multiocidia, t.caniculi, myxomatosis- tramatic cause common in rabbits scrotal herniation- via ingunal canal- very wide in rabbits

Answer 135

you suspect orcitis due to p.multiocidia- pyrexia, swolled lympnodes, bilateral presentation

Answer 136

cytology- neitrophils, gram stain (pink gram neg) culture and sentitivity serology-usefull??? pcr- fna of effected testicke haematology and biochem- left shift, stress leukogram, otherwise fairly normal which distingushed it from neoplasia (paraneolatic hypercalcemia). torsion and herniation will not show anything here ultrasound- most usefull for guiding next step- may apear non homogonous

Answer 137

medical managemt- NSAIDs (meloxicam), antibiotics (c+S, BE AWARE OF GUT STASIS, penetrating power important with testicals)- TMPs, cold compress surgical mangment stasis managment acute onset so medical managment as the promary method is recomended- may get absess on stump that can travek into abdoment surgical managment as first line for chronic cases

Answer 138

Caused by a virus of the family Picornaviridae, genus Aphthovirus Virus has 7 immunologically distinct serotypes: A, O, C, SAT1, SAT2, SAT3, and Asia1 – they don’t confer cross immunity No reports of FMD cases due to serotype C since 2004 - this serotype is now considered to be extinct in the field Signs range from mild or inapparent to severe Severity clinical signs varies depending on: strain of virus; exposure dose; age and breed of animal; host species; and degree of host immunity Deaths are uncommon except in young animals, which may die from multifocal myocarditis or starvation Most adults recover in 2–3 weeks, although secondary infections may slow recovery (c.f. developing countries) Morbidity may approach 100% Mortality in general is low in adult animals (1–5%) but higher in young calves, lambs and piglets (20% or higher). Recovery in uncomplicated cases usually takes about 2 weeks vaccination os banned and stamping ou policy used sue to its massive effect on trade- vaccine may be used in future as part of control policy- ring vaccination- animals a certain radiusa wasy from outbreak vaccinated to pen it in

Answer 139

Generally stated as up to 14 days Reported to be 1–12 days in sheep, with most infections appearing in 2–8 days Range of 2–14 days in cattle Usually 2 days or more in pigs (with some experiments reporting clinical signs in as little as 18– 24 hours)

Answer 140

Pyrexia, anorexia, shivering, reduction of milk production for 2–3 days, then: - Smacking of the lips, grinding teeth, drooling saliva, lameness, stamping/kicking the feet - Vesicles seen on oral mucous membranes and/or between the claws and coronary band (not swelling, swelling is blue tonge) , udder/teats - Rupture of vesicles – erosions – can age lesions - Death of calves - myocarditis

Answer 141

Infected sheep may well be asymptomatic or have lesions only at one site Common signs are pyrexia and mild to severe lameness Vesicles occur on the feet, in the coronary band and interdigital spaces - may rupture and be hidden by foot lesions from other causes Oral lesions often not noticeable, or may be severe - generally appear as shallow erosions Agalactia in milking sheep and goats is a feature. Significant numbers of ewes abort in some outbreaks Death of lambs/kids may occur without clinical signs

Answer 142

Pyrexia May develop severe foot lesions and lameness with detachment of the claw horn, particularly when housed on concrete Vesicles often occur at pressure points on the limbs, especially along the carpus Vesicular lesions on the snout and dry lesions on the tongue may occur Young pigs up to 14 weeks of age may die suddenly from heart failure (myocarditis)

Answer 143

‘Tiger striping’ of the heart Can cause mortality in young animals

Answer 144

Direct contact between animals, especially by inhalation of infectious aerosols Direct contact with fomites (hands, footwear, clothing, vehicles, etc.) Ingestion (primarily by pigs) of untreated FMDV-contaminated meat products (swill feeding - illegal) Ingestion of FMDV-contaminated milk (by calves) Artificial insemination with FMDV-contaminated semen Long-distance airborne spread (up to 60 km overland and 300 km over water

Answer 145

Swine vesicular disease (last outbreak in GB 1982) Vesicular stomatitis * Vesicular exanthema of swine * Senecavirus A (Seneca Valley virus)

Answer 146

Main sign of the disease is vesicles: at the top of the hooves between the toes occasionally on the snout, tongue and lips Other signs: lameness loss of appetite pyrexia Some infected pigs may not show any signs of the disease

Answer 147

Rinderpest (globally eradicated) * Bovine viral diarrhoea (BVD) and Mucosal disease- PI animals develope mucosal disease * Infectious bovine rhinotracheitis Malignant catarrhal fever * Bluetongue * Epizootic haemorrhagic disease * Bovine mammillitis * Bovine papular stomatitis; Contagious ecthyma * Non-infectious causes e.g trauma or chemical burn

Answer 148

First suspected at ante-mortem inspection in pig slaughterhouse - Essex, England - 19 February 2001 Confirmed 20 February – Type O, PanAsia strain of FMDV At least 57 farms had already been infected by confirmation date > 2,000 premises infected in total Source: pig farm in north-east England feeding untreated waste food from restaurants/catering establishments 19 Feb 2001 - Ante-mortem inspection – 27 lame sows Reported to State Veterinary Service Slaughter stopped 109 pigs left alive – 28 with suspicious clinical signs 20 Feb – oldest lesion - 5 days old 600 premises had supplied pigs in prev. 2 weeks Feb 22 – index farm identified – sent 35 sows to slaughter plant on 16 Feb. Index farm – pigs – Heddon-on-the-Wall, Northumberland (infected 7 Feb) Virus plume travels 5 km to local sheep/cattle farm 16 sheep leave that farm to Hexham Mart., 13 Feb 10 of these sheep move on to Longtown Mart., Cumbria Up to 24,500 sheep exposed between 14-23 Feb. 181 purchasers from Longtown Mart. – spreads to whole of UK Delayed detection on index farm – abattoir then worked backwards Airborne transmission from pigs on index farm to local sheep farm Movement of infected sheep through markets before first detection Time of year (Feb) – climatic conditions favoured viral survival and movement of sheep extensive Often ‘silent’ infections in sheep – general lack of clinical signs – needed serology

Answer 149

The EU lists the following anaesthetic type drugs to be permitted in food producing species: Xylazine, detomidine, romifidine, isofluorane, ketamine (licensed for goats), thiopental sodium, ligno Drugs: 20mg/ml xylazine, detomidine, romifidine, butorphanol Desired effect standing standing but marked muscle relaxation recumbent Deep recumbent sedation Side effects: saliva production, recumbency, risk of abortion, bloat, regurgitation and inhalation, heat stress, TMPS contraindication, pulmonary oedema risk in sheep Dose range : Xylazine 0.05-0.3mg/kg Duration of action: 30-40min Considerations: Provides some analgesia Slows GI mobility, decreases cardiorespiratory function, ruminants are sensitive to xylazine, fasting, co-morbidities, age, quiet time to induce/recover, space, flooring with grip, pregnant? Route for admin: IM-slower onset, longer duration of action, larger dose, IV -faster onset, shorter duration of action, smaller dose epidural

Answer 150

where it is useful-obstetrical, Caesar, prolapse, embryo fertility work, rectal prolapse, episiotomy, castration When-before you start a possibly painful procedure of the hindquarter or one where an absence of abdominal contractions would be helpful What do you need-clippers, surgical spirit, cotton wool, needle, syringe, procaine (+/- adrenaline) How to do it 18g 1.5inch needle with 5ml procaine in a syringe (600kg cow). Lift the tail to bend it slightly, palpate the first or second sacrococcigeal space (Co1-Co2,or S5-Co1) Clip and sterile prep Insert needle 15degrees to the vertical, Put a drop of procaine in the needle hub, advance the needle until the drop disappears. Attached the syringe and insert the local anaesthetic Considerations-size of animal (dose accordingly-cattle max 1ml/100kg, sheep 1ml/50kg), does it look like its going to sit down? . Within 5-10 minutes-no motion of the tail, no sensation around the perineum, no straining too much can result inthe cow becoming weakened in the hindlimbs

Answer 151

What-gas distension of the abdomen (usually rumen) When and how does it occur: Rumen drinking in calves Milk in rumen ferments, inducing acidosis and gas, ruminal atony Left flank distends after a feed. See discomfort, +/- pasty scour Frothy bloat (consuming fermentable legumes)-cant be eructated- Acute rumen tympany, distress, recumbency, death Free gas bloat in adults (oesophageal obstruction/unable to eructate)- Acute rumen tympany, progressive distress, recumbency, death

Answer 152

How to treat- stomach tube, AB, nsaid, antacid, electolytes. Recurrent bloat:+ local anaesthesia+ red devil trochar or rumenotomy What do you need: clippers, surgical prep, scalpel, red devil, nylon suture, AB, NSAIDs, multivit, electrolytes, procaine How to do it-prep skin, incise the skin in the dorsal paralumbar fossa, apply pressure to the Red Devil and screw it into the abdominal muscle and rumen. Withdraw the cap to release the gas. Remove once the animal is better. Considerations-prepare the client for oozing, slow hole closure

Answer 153

When to decide: legs cross, no room around head/legs, precervical torsion, uterine torsion that wont move, foetal monster, uncorrectable dystocia, suspected uterine tear what do you need: Cow restraint Prep surgeon Prep cow Help to remove calf and resuscitate Surgical kit drugs Xylazine has an ecbolic effect , make uterus moire friable and less mauverable. No analgesia provided by the xylazine How: Epidural-to stop contractions and prevent sensation of the perineal area (5ml 2% procaine, 600kg cow) Clenbuterol IV-to aid manoeuvring the uterus NSAID Antibiotic 3-5days duration (common e.g. penicillin, amoxicillin, tetracycline) Sedation? Clip the left paralumbar fossa area Same abdominal local anaesthesia and incision as an LDA Locate the uterus and bring it to the abdominal incision edge Uterine incision on the greater curvature, 10-15cm from the horn tip using scissors/letter opener. Aim to incise over the calf’s distal limb. Have an assistant take the exposed feet and pull the calf out, begin resuscitation, whilst you carry on. Check for twin/uterine tears. Trim placenta hanging outside the uterus. Using absorbable suture material (eg Catgut) close the uterus with an inverting Utrecht pattern. Repeat this step to make a 2 layer closure Check the abdomen and remove clots Close the abdomen as per an LDA surgery. Administer 2-4ml oxytocin IM to counteract the clenbuterol. Ensure the calfs umbilicus is treated with iodine and that it is fed 10% bodyweight in colostrum in the first 6hours. Complications: Wound infections +/- pus, dehiscence, seroma Become recumbent and stay down Co-morbidities eg hypocalcaemia Retained placenta Death Peritonitis Abdominal Adhesions, reduced future reproductive performance Metritis

Answer 154

Why-prevent pregnancies! Reduce male behaviour. Greater sale options. Who- lay people, vet required if calf over 2m old. When: Calves, lambs, kids: rubber ring <7d old, no anaesthetic Calves/goats: any method >2m old, local anaesthetic Lambs: any method >3m old, local anaesthetic Pigs: any method >7d, local anaesthetic Methods Ring- efficient, safe, requires no local anaesthetic. Complications: rig with incorrectly applied ring. burdizzo, <2mo without anaesthetic open –various methods, ideally 1-3m old, suckler calves often done at 6m Considerations-health, housing hygiene, size, handling facilities, analgesia, antibiotics (?) Illegal application of rings to older calves can cause gangrenous ischemia of the scrotum and tetanus. Rigs: cryptorchid calves should not be unilaterally castrated. The remaining testicle may descend subsequently permitting a fertile animal. Cryptorchid calves should be left entire and reared as bulls. Burdizzo clamp is applied to both sides twice to crush the spermatic chord, inducing ischemic necrosis of the testicle. Poor technique can cause partical castrations.

Answer 155

Local infiltration with 3-5ml procaine under the scrotal skin and into the chord. +/- sedation or GA NSAID (eg Meloxicam) Clean the scrotal skin with hibiscrub Hold the neck of the scrotum pushing the testicles into the sac Make a J shaped incision on the lateral aspect of the scrotum down tot the base, through the vaginal tunic Separate the vascular part of the spermatic chord from the non vascular epididymal ligament complex Strip the vaginal tunic up the vascular part of the chord Twist the testicle several times, then give a sharp pull to break the chord Dangling ductus deferens can be snipped off Spray the scrotal incision with antibiotic/aluminium spray Long acting antibiotic? alternativly the " cut across the bottom version can be used Commonly done as a standing surgery. GA (xylazine and ketamine) for mature bulls or complicated cases such as inguinal hernias. Alternatively, deep sedation, inducing recumbency with xylazine at 0.3mg/kg IM, plus local anaesthesia. Complications: Haemorrhage: watch for continuous bleeding Monitor until reduces Pull vessels with forceps and twist +/- ligate Pack the scrotum with cotton wool May subsequently develop scrotal haematoma/abscess ‘gut tie’ Rare complication in older calves. Remnant of the spermatic chord recoils into the abdomen and adheres to the peritoneum/viscera Can cause intestinal obstructions

Answer 156

Uroliths in ruminants are common. They can be found anywhere in the urinary tract but urethroliths are responsible for the most clinical problems. High grain diets with low Ca:Phos ratio develop struvite crystals. (radio lucent!) Graze silica rich soils develop silica uroliths. High calcium diets develop calcium carbonate uroliths. Sugar beet leaves develop calcium oxalate. Obstruction caused by urethroliths causes urine retention, causing bladder distention, abdominal pain, and eventual urethral perforation or bladder rupture-leading to death from uremia or septicaemia. A disease of adolescent fattening and mature breeding animals, especially in winter when water intake may be limited and when eating a high mineral concentrate diet. Goats are masters of the urolith and they are particularly seen in wethers. Males are predisposed due to the anatomy of the sigmoid flexure (all ruminants) and urethral process (small ruminants). Castration of young males predisposes to urethral obstruction by removing hormonal influences necessary for the mature development of the penis and urethra. Texel and Scottish Blackface predisposed (preferentially secrete phos in urine than salive/faeces) hx- Concentrate feeding, imbalanced Ca:P/Mg presentation- Intermittently blocked urethra: off colour, stranguria, blood tinged urine, Blocked: straining to urinate, anuria, inappetant, colic, tail flagging, vocalisation, mineralised deposits where urine dries on hair Ruptured urethra: Down, dull, depressed, urine smell, distended abdomen .. Prevention: Increase urinary chloride excretion Sodium chloride decrease urine pH Anionic dietary supplements (ammonium chloride) provide Ca:P ratio of 2:1 Calcium supplement (unless calcium based uroliths present!)

Answer 157

Palpate: a urolith in vermiform appendage/urethral process, or sigmoid flexure. Rectal palpate an enlarged/disappeared bladder and urethral pulsations. Urethral process may reveal occluding urolith CBC- Incr: urea nitrogen BUN, creatine, potassium, muscle enzymes Decr: sodium, chloride, urine pH acidic Imaging: U/S distended bladder, urethra, confirm rupture- hypoechoic. Rads to see some # stones and size, urinalysis for crystals, contrast to confirm rupture. Abdominocentesis: creatinine in peritoneal fluid is 2+ more than in plasma. Ddx-cystitis, peritonitis, coccidiosis, peritoneal tumous, ruminal tympany, hydrops, GI obstructions.

Answer 158

Aim for patent urethra, correct fluid+electrolyte imbalances. Medical-sedation, analgesia, local anaesthesia, remove urethral process, attempt to pass a foley catheter and flush out stones, antibiotics, ammonium chloride (decreases urine pH and dissolve stones). Depressed uremic animals may need iv fluids Surgical-mainstay- Perineal urethrostomy (82% non recurrence by 12 month) Penile amputation Tube cystotomy Drain urine from abdomen Bladder marsupialisation (67-84% longterm success) Euthanasia Prognosis-good for small number of years Considerations –calacium carbonate stones are bronze and don’t dissolve Prognosis: Fair after medical, often relapse generally good after surgery (<28% euthanasia for relapse/complications). Perineal urethrostomy –salvage procedure, males cant breed. Considerations: Diet must be evaluated, iceberg disease, long time to correct. Complications include: UTI, strictures, bladder mucosal prolapse, scalding.

Answer 159

What-mainly closed limb fractures, rarely have radiographs Small ruminants do well with amputations How: NSAID: to minimise swelling + provide analgesia +/- sedation What do you need: Minimal bandage material, stirrups, padding for cast top Fibreglass How to mend Hooves IN the cast Confinement Cast on 4-6wk, then bivalve the cast and tape it on for further 2wk Considerations- Manage client expectations, especially if joint/growth plate/infection/sequestra involvement is suspected put 2 bones in a room and they will attempt to ossify! Cases over 400kg require specialist care (refer), poorer prognosis Tibia/radial fracture– add Schroeder-Thomas splint Neonates require regular recasting as they grow ( recast q 2wks) Euthanasia often economical option Future use of animal? Functional limbs required?

Answer 160

Rare in dogs, comparatively common in rabbits and Guinea pigs. Predisposing factors: Obese animals Large litter size Risk periods = last two weeks of gestation and first two weeks post-partum. Diagnosis: History, c/s, urinalysis (glucosuria, ketonuria, proteinuria) Prognosis: Poor to grave Treatment: Intravenous or intraosseous isotonic fluids + dextrose Additional oral glucose Syringe feeding with a diet high in carbohydrates e.g. emeraid intensive care herbivore or critical care formula Some sources advocate emergency C-section. Prevention better than cure: Do not breed from obese animals! Monitor foetal size/number Avoid stress in risk periods Increase carbohydrate supply in risk periods Care re:weight gain Encourage gentle exercise during pregnancy

Answer 161

Mostly seen in guinea pigs. Serous vs follicular cysts Serous cysts: Usually an incidental finding unless they have grown large enough to start impinging on other abdominal organs. Not responsive to hormone therapy. Tx via percutaneous drainage or ovariohysterectomy Mostly seen in guinea pigs. Serous vs follicular cysts Follicular cysts: Often occur alongside follicular cysts. Disrupt hormone cycles -> non-pruritic alopecia Hormone responsive – short acting GnRH agonist preferred hCG risk of anaphylaxis Ovariohysterectomy = curative

Answer 162

Uterine adenocarcinoma = most common intra-abdominal tumour in rabbits Wide range of uterine neoplasias reported in hedgehogs Investigation and treatment as per other species. Where there is no metastasis, surgical treatment = curative

Answer 163

Occurs in jills who are not brought out of oestrus (induced ovulators) Prevention: Surgical neutering (HAC risk) Deslorelin (Suprelorin®) implant Proligestone (Delvosterone®) injection Mating (vasectomised hob) See 3rd year lecture “Reproductive management of exotics” for more details Treatment rarely successful. Aims of treatment are to reduce oestrogen levels to stop bone marrow suppression, and supportive care for the pancytopenia. Oestrogen levels reduced by inducing ovulation: Proligestone injection - preferred Buserelin, leuprolide acetate and hCG also reported Supportive care: Blood transfusion (PCV <15%) Anabolic steroids and iron dextran injections could be considered to facilitate RBC production. Antibiotics if 2o infections present

Answer 164

Similar approach to dogs and cats for most species. Rats different: Fibroadenoma of the mammary tissue most common tumour in both sexes. Mammary tissue very extensive! Hormonal influence – prolactin and oestrogen. In mice mammary adenocarcinoma = most common. Tumour often reach a massive size. Eventually -> trauma to surface, ulceration, necrosis, and infection. Surgical excision required, but recurrence common. Cabergoline may help reduce recurrence? Deslorelin implantation does not reduce tumour recurrence.

Answer 165

Very common in entire males housed in groups. Rabbits and rodents most commonly affected. Wide inguinal canal can -> evisceration. Treatment: Surgical repair Analgesia Antibiosis Prevention Castration Appropriate housing

Answer 166

Common presentation – indicates an underlying issue. ID on conscious rad Conservative management: Warmth Fluids (oral) +/- glucose e.g. critical care formula Calcium gluconate (injectable) PGE2 gel Oxytocin not effective in birds If no response to conservative management or if bird is distressed -> GA and manual removal. Dystocia can -> respiratory compromise, may require IPPV. Applying PGE2 gel prior to attempting removal may help access. Tips for removal: Warm water + KY to aid passage. Break down adhesions genty with your finger Ovocentesis and collapsing the egg may be necessary – make sure all shards removed! Post op analgesia +/- antibiosis Need to identify underlying cause of dystocia

Answer 167

Most common in cockatiels Constant egg production -> Calcium and protein depletion. Bone resorption and pathological fractures. Immunosuppression and 2o infections. Dystocia Conservative management and hormonal management possible. Conservative management: Environmental modification (remove nest, decrease day length). Dummy eggs Behavioural modification (inappropriate mate selection i.e. owner) Diet modification (reduce protein and fat levels, encourage foraging behaviour) Hormonal management: Deslorelin implant: GnRH agonist, acts in the same way it does in mammals. Short acting cf mammals (~6m) plus initial stimulation phase may  increased egg laying. Fairly reliable effect Cabergoline: Mechanism of action uncertain - inhibits prolactin (main MOA in mammals) but levels don’t’ always decrease in birds. Studies show variable efficacy between sp, plus daily oral medication administration may be tricky

Answer 168

Inflammation of the oviduct. May be septic of non-septic May cause: Abnormal eggs and “lash eggs” Dystocia Impacted oviduct -> yolk coelomitis as ovulated ova cannot enter the oviduct Clinical signs reproductive (egg drop, abnormal eggs), or non-specific (weight loss, anorexia) Diagnosis: Signalment (ex-battery hens) Mass or fluid on coelomic palpation Ultrasonography Radiography may confirm mass, otherwise less useful Cloacal endoscopy Cytology and culture of cloacal discharge (septic) Treatment: Anti-inflammatory (meloxicam) Antibiotics if septic (amoxy/clav or based on c+s) Supportive care (fluids, nutritional support, warm environment) Deslorelin to prevent further ovulations If no success, salpingohysterectomy indicated

Answer 169

Occurs when an ovum (egg yolk) is released into the coelomic cavity, either at ovulation or due to oviduct rupture. Ovum breaks up and releases yolk which is highly inflammatory to the serosal surfaces -> sterile coelomitis. Mild cases will self-resolve. Cases where multiple ova escape or which become 2o infected can be life threatening. Clinical signs = lethargy, anorexia, ascites, coelomic swelling, respiratory compromise Diagnosis: Signalment (ex-battery hens) Fluid on coelomic palpation Ultrasonography Coelomic tap Cytology and culture of coelomic fluid Treatment: Abdominocentesis – removes fluid to relieve pressure on the air sacs + collects a sample for further analysis Otherwise as per medical salpingitis treatment. Consider giving prophylactic antifungal treatment with broad spectrum antibiotics - nystatin

Answer 170

Sexually mature drakes Medical management: Cleansing Reduction (+/- cloacal stay sutures) Non-steroidal anti-inflammatory drugs (meloxicam) Antibiosis if indicated Surgical management: Amputation where phallus is necrotic

Answer 171

Older female tortoises most commonly affected, but can see in any female kept in substandard husbandry and/or without a male. Often asymptomatic until coelomitis develops. Diagnosis: Bloods Ultrasound Advanced imaging Treatment: Conservative (no symptoms) Medical – alongside surgery, not useful alone Surgical Conservative: Improve husbandry (temperature, UVB, nutrition) Provide an appropriate nesting site Provide a mate? Medical Fluid therapy (epicoelomic or intraosseous preferred) Anti-inflammatory (meloxicam) for coelomitis Analgesia (morphine, methadone and tramadol) Surgical Covered in depth by Sarah – go back and look at her lecture

Answer 172

Tortoises appear most commonly affected but can also occur in snakes and lizards. Often found incidentally – good reason to perform a conscious rad prior to hibernation. Very rarely requires urgent tx cf mammals Most cases are non-obstructive, so treatment usually medical Go straight to surgical treatment where: Obstructive dystocia Non-obstructive dystocia where there has been no response to medical treatment Where retained eggs are causing other issues e.g. pressure necrosis of the cloaca Logical approach to the healthy animal with retained eggs: Assess and correct husbandry Temperature, UVB provision and diet Nesting site (loose, sandy soil in a quiet area) Mate – males may be harassing females and preventing laying, consider removing from the enclosure temporarily Ensure hydration Bathing usually sufficient in otherwise healthy animals Oral calcium supplementation Logical approach to the healthy animal with retained eggs: Oxytocin +/- injectable calcium Injectable calcium ideally given where hypocalcaemia has been demonstrated on bloods. Oxytocin only really useful for tortoises – max three doses given at hour 0, hour 1, and hour 5-7. Make sure a nesting site is available If no response to oxytocin and egg is palpable via the cloaca or on coelomic palp (squamates): Sedation for egg removal Either via digital manipulation or ovocentesis and collapse of the shell (ensure fragments all removed) In snakes may be able to milk the eggs through the oviduct towards the cloaca. If no response and egg is not palpable: Surgical removal – see Sarah’s lecture

Answer 173

Need to differentiate tissue type: Bladder (only some spp.) Colon Reproductive tissue (oviduct, phallus, hemipene) Cloaca Once tissue type identified, this limits your list of underlying causes to investigate Conservative management in uncomplicated cases: Fluid therapy Reduce inflammation - osmotic dressings, NSAIDs (meloxicam) Reduction (care re:intussusception with hollow organs). +/- stay sutures Need to investigate and treat the reason for prolapse Surgical management in complicated cases: Colon – end to end anastomosis Bladder – Resection may be possible Oviduct – Salpingohysterectomy Phallus/hemiene – amputation, as with poultry.

Answer 174

Typically seen in male animals due to smaller urethra and in dogs, the os-penis Possible also behavioural influences with some conditions (FIC) Will present with signs of straining to urinate and a large, taught bladder* Will sometimes be able to pass small drops of urine due to overflow** If presenting as part of a post-renal AKI, much more likely to have hyperkalaemia than other causes of AKI Can be a structural or functional obstruction Urethral crystalline-mucus plugs (cats) Idiopathic urethral obstruction (cats) Urolithiasis (dog) Prostatic disease (Benign prostatic hypertrophy/prostatic neoplasia/prostatitis/prostatic abscess) Neoplasia Strictures UMN bladder Reflex Dysynergia* (range of others)

Answer 175

One of the most common emergency presentations you will see in primary care practice The most common causes are crystalline-mucoid plug and idiopathic (although urolithiasis is also a notable cause). Generally, only seen in male cats and possible/probable link with FIC in some cases* Indoor and overweight/obese cats also of increased risk Wide variation in presenting signs from ‘just’ clinical signs of stranguria to collapse and peri-arrest. Can present as a medical emergency Can cause a post-renal AKI that, over time, becomes and intrinsic AKI Clinical signs typically present <72 hours Repeated episodes of attempting to urinate, stranguria, pollakiuria, dysuria – may be able to pass small amounts of urine Clients will often describe ‘yowling’ whilst urinating Can progress to vomiting, lethargy, and collapse Clinical examination reveals a large, taught bladder* Often painful/tachycardic and can be hypothermic Severe cases will be bradycardic (🚩Hyperkalaemia)

Answer 176

Clinical Suspicion for urethral obstruction Minimum Database and Electrolytes POCUS ± Radiographs IV placement and start fluids ± treat hyperkalaemia Decompressive cystocentesis ± Sedation/anaesthesia Radiographs Unblocking and placement of indwelling urinary catheter Hospitalisation Discharge

Answer 177

PCV/TP Creatinine/Urea Glucose Lactate Electrolytes A proportion of animals with urethral obstruction will have azotaemia and hyperkalaemia on presentation It is CRITICALLY IMPORTANT that you address hyperkalaemia as soon as possible, especially prior to sedation or anaesthesia The azotaemia is typically the result of post-renal AKI but can result in an intrinsic AKI The hyperkalaemia is believed to be principally the result of reduced excretion of potassium Other abnormalities such as increased lactate, metabolic acidosis, ionised hypocalcaemia, or erythrocytosis may be present Phosphate is typically markedly increased

Answer 178

POCUS is an exceptionally useful tool in emergency and critical care Should be utilised in every suspected renal obstruction Large firm bladder (vs. bladder rupture) Small amounts of free fluid are almost inevitable present Look for sediment/uroliths Lateral abdominal radiographs can be performed in collapsed animals – include perineum and try oblique views DO NOT sedate/anaesthetise until hyperkalaemia has been addressed!

Answer 179

Hyperkalaemia is not uncommon in both upper and lower urinary tract obstruction Varying degrees but can prove fatal if not addressed DO NOT use heart rate/ECG to predict potassium concentration- this must be checked! HYPERKALAEMIA MUST BE CORRECTED PRIOR TO SEDATION/ANAESTHESIA! Lots of pot (potassium) means lots of tea (T), and if you have lots of tea, you need a tea-break (bradycardia)” There is an escalating number of treatment options for hyperkalaemia. With more severe increases in serum potassium will need to start at higher levels of intervention Options for treatment include: Fluid therapy – improve GFR and excretion of potassium 5-20% glucose – Causes insulin-mediated potassium translocation Insulin administration- Translocates potassium into the cells 10% Calcium Gluconate – does not affect potassium but reduces risk of arrhythmias Sodium bicarbonate – alkalinising leading to intracellular movement of potassium Terbutaline – Translocates potassium into the cells

Answer 180

Fluid therapy: 2-4ml/kg/hr of Balanced Crystalloid Glucose: 5-20% of dextrose 0.5-1g/kg IV over five minutes (5% dextrose can then be continued at 2ml/kg/hr) Insulin: 0.5U/kg neutral soluble insulin IV/IM (remember to monitor blood glucose concentrations) Calcium Gluconate 10%: 0.5-1.5ml/kg IV SLOWLY OVER 5-10 minutes monitoring for bradycardia on ECG Sodium Bicarbonate: 1-2 meq/kg IV slowly over 15 minutes Terbutaline: 0.01mg/kg IV SLOWLY over at least 5 minutes

Answer 181

One of the fastest ways to restart glomerular filtration is by relieving the pressure in the bladder. This can be performed whilst other stabilisation attempts are on-going and prior to sedation/anaesthesia and catheter placement There has previously been concern over the risk of bladder rupture – however, SOME clinicians will perform this when required. I would be hesitant to do so in a cat that ‘does not tolerate the procedure’- most likely does not require the procedure urgently After clipping and sterile-prepping, my personal preference is to use an IV cannula under ultrasound guidance Once the needle has pierced the bladder wall and you get urine back, remove the stylet and attach the syringe – this reduces risk of ‘tearing’ the bladder What do to with the urine: A dipstick urinalysis should be performed for a ‘baseline’ reference (although abnormalities are expected) A sediment preparation should be looked at immediately for evidence of crystalluria and casts Urine should be sent routinely for culture and sensitivity (boric, plain, ± charcoal swab) Concurrent urinary tract infections are uncommon in feline urethral obstruction but should be screened for regardless* In young cats suffering their first episode, urine culture can be missed if finances are severely limited If unable to acquire urine at this point, do so once the animal is sedated/anaesthetised – do not use catheter-acquired urine!

Answer 182

Most animals will require sedation/anaesthesia for placement of urinary catheter More severe/collapsed presentations may not require any sedation/anaesthesia (or just opioid analgesia)* Hyperkalaemia MUST be addressed prior to sedation/anaesthesia! Often these animals will be unstable so sedation/anaesthetic options should be chosen carefully: 0.3mg/kg methadone ± 0.3mg/kg midazolam IV ± Alfaxalone TIVA OR induction and inhalant (see anaesthesia lectures) Coccygeal epidurals are sometimes performed and provide excellent on-going analgesia (above new-graduate scope!)

Answer 183

If radiographs were not performed at an earlier stage due to the animal not allowing positioning with sedation/anaesthesia – now is a time to take radiographs A right lateral and ventro-dorsal abdominal radiographs should be performed including the perineum Assess all areas for evidence of urolithiasis: Kidneys Ureters Bladder Urethra Sometimes, mineralised urethral plugs can be seen on radiographs

Answer 184

The initial step is to relieve any obstruction that may be present This may involve removing a mucus plug or retro-pulsing uroliths into the bladder Following relieving of an obstruction, placement of an indwelling urinary catheter is strongly recommended as this appears to reduce the risk of recurrence Optimum duration of catheterisation is unknown however most clinicians will leave in for 24-72h. Consider basing duration on return of ‘normal’ urine colour There are many ways of doing this – find the way that works best for you! personal preference: Once the animal is sedated/anaesthetised (if necessary) it is placed in lateral recumbency The penis and a large part of the perineum is clipped I apply an amount of 2% lidocaine cream (e.g., EMLA) to the penis The entire area and prepuce is cleaned with very dilute chlorhexidine or iodine and I use sterile surgical gloves The penis is extruded* and a small amount of sterile lubricant applied I use the plastic sheath of a 20-22g (pink/blue) IV cannula attached to a 5ml syringe with sterile saline to dislodge the obstruction Once the cannula is inserted in the urethra, I applied moderate pressure either side of the penis and use intermittent ‘pushes’ to dislodge any obstruction Top tip: The male feline urethra is not a straight line and follows a ‘curved’ trajectory Once the IV cannula is just past the urethral opening, extend the penis upwards and caudally so that it is parallel to the spine (sometimes you will need to use the prepuce to do so) This straightens out the urethra aiding passage of the catheter Sometimes trying different variations of this position is required to allow passage Care: Although a moderate amount of pressure can be required to dislodge obstructions (especially uroliths) too much pressure can damage the urethra Sometimes either emptying or filling the bladder can aid passage DO NOT over-distended the urethra by applying excessive force with flush DO NOT be too-aggressive with catheter advancement as this can tear the urethra Once the obstruction has been relived an indwelling catheter can be placed. The two most common types are the Slipper Sam Tom-Cat Catheter and the Mila Both of these can also be used to relieve the initial obstruction (I just find a cannula sheath easier!) No evidence to support vigorously flushing the bladder, however, may be prudent in cases with a large amount of sediment Catheters sutured in place and attached to a closed urinary system Buster collar to prevent interference Urinary Catheter Care: A closed system is much preferred compared to intermittent drainage as this reduces the risk of infection The catheter must remain below the animal at all times (to prevent reflux of urine) ideally in a clean litter tray The catheter and collection system should be wiped distally at least twice daily It is heavily advised to avoid antimicrobials whilst a urinary catheter is in place Urine cannot be taken from the collection bag for culture and sensitivity

Answer 185

Optimum duration of catheterisation is unknown however most clinicians will leave in for 24-72h. Expect to see a rapid decrease in creatinine, back, or close to the animal’s baseline. Hyperkalaemia is also seen to rapidly resolve but post-obstructive diuresis can lead to hypokalaemia – monitor and treat as necessary! Aim is to get to point where animal can empty bladder on own If cystoliths/urethroliths present, will need cystotomy* to address once electrolyte and acid-base abnormalities have resolved and creatinine is improving. Otherwise follow supportive care guidelines for AKI (see AKI lectures) Care re: post-obstructive diuresis

Answer 186

After relieving urinary obstructions animals can sometimes enter a phase of post-obstructive diuresis Characterised by an inability of the kidneys to concentrate the urine -> varying degrees of PUPD In some cases the PUPD can be extreme As a urinary catheter is present the ‘ins and outs’ approach can be used (see AKI lectures) HOWEVER- A notable proportion of P.O.D. cases have been shown to be the result of excessive fluid therapy rather than true P.O.D. I frequently see people ‘chasing up’ the fluid rate  fluid overload Consequently, every 8-12 hours attempt to decrease the fluid rate by 25% If a decrease in urine volume is noted and the animal does not start to demonstrate signs of dehydration, then it is more likely that you were giving excessive fluids Serially reassess the rate of fluid therapy and frequently attempt to reduce the rate!

Answer 187

When you believe safe to do so (time/appearance of urine/acid-base/electrolytes) remove the urinary catheter and assess for signs of urination It is important that you palpate the animal’s bladder to ensure that this is true urination rather than overflow Once sure that the animal is able to pass urine (and all else has resolved)  discharge from the hospital Be sure to address potential precipitating factors (FIC, urolithiasis etc.) The reoccurrence rate is up to 60% -> discuss signs to look out for and mitigating factors with the clients (see specific causes)

Answer 188

NSAIDS – There is little-no evidence that providing NSAIDs reduces the risk of reoccurrence. HOWEVER, it is prudent to provide analgesia Although NSAIDs provide excellent analgesia, be cautious of their use in animals that have had a significant or on-going AKI. Alternative options may include gabapentin or sublingual buprenorphine Prazosin (Hypovase) – Historically, this has been used almost routinely in blocked cats – very little evidence to support its use* Diazepam – Oral Diazepam can be hepatotoxic in cats – DO NOT USE!

Answer 189

There are a number of reasons why cats may not be improving as expected. My experience is that the most common is detrusor atony However, urethral rupture/granulation tissue and missed uroliths follow closely In cats that have recurrent episodes, a perineal urethrostomy can be offered (see surgery lectures) Perineal urethrostomy reduces the risk of DISTAL obstruction but does NOT treat the underlying cause * Most clinicians will recommend after the third obstructive episode**

Answer 190

Prolonged bladder overdistension -> damage to the myocyte tight-junctions resulting in reduced/absent ability to contract the bladder Not uncommonly seen in ‘blocked cats’ Typically presents as not attempting to urinate after the urinary catheter is removed despite a full bladder Typically, requires a prolonged period of manual expression* or a longer period of urinary catheterisation Would be unusual to persist longer than 1-2 weeks (search for other causes) Bethanecol (1.25-5mg/CAT PO q8-12hr, 2.5-15mg/DOG PO q8-12hr) may help

Answer 191

Another potential causes of failure to improve as expected is urethral rupture/granulation tissue This typically presents as a cat that is straining to urinate but managing to pass little-to-no-urine A full, usually firm, bladder is expected, if small, may present inflammatory/infectious cystitis Often as a result of damage during catheterisation Can be difficult to diagnose and requires a contrast urethrogram

Answer 192

Ureteral obstruction is much less common than urethral obstruction Treatment typically requires referral to specialist surgeons However, you need to be aware of this as a differential diagnosis for obstructive AKI Most commonly seen in cats but can be seen in dogs Most commonly due to ureterolith (CaOx), but less commonly stricture, neoplasia, or dried-solidified blood stone Can also be seen with accidental ureteral ligation Typically present with renal pelvic and ureteral dilation* Usually able to pass urine as often unilateral (can be bilateral) Diagnosis of ureteral obstruction is made by demonstrating renal pelvic/ureteral dilation on ultrasound* Renal pelvic diameter generally >5-7mm, but >13mm highly suggestive YOU DO NOT NEED TO IDENTIFY THE CAUSE OF OBSTRUCTION! Animals will typically present as post-renal AKI cases but can sometimes be detected as CKD cases. May often see ‘big kidney, little kidney’* Renal pelvic/ureteral dilation can also be seen with pyelonephritis – however often secondary to an obstruction

Answer 193

Medical treatment (fluid therapy/mannitol, prazosin, analgesia) IF mild-moderate increase in creatinine, normal potassium, and stable. ± Antimicrobials as may have secondary infection (urine culture does not always correlate) Surgical management indicated if any of: 1- Marked or progressive azotaemia 2- Oliguria/Anuria 3- Hyperkalaemia 4- Progressive renal pelvic dilation N.b., nephroliths without ureteroliths unlikely to be causing obstruction The surgical treatment of choice for cats is a subcutaneous ureteral bypass device (SUB) This is a referral procedure and needs on-going ‘flushing’ at regular periods for months-years post-operatively (clients need to be invested) The surgical treatment of choice for dogs is usually a stent placement, however this differs by centre In cases that meet the criteria for surgery, this is a surgical emergency! (also need to address the underlying cause for the uroliths)

Answer 194

Upper Motor Neuron (UMN) bladder – Will usually have evidence of a notable degree of ataxia* Prostatic disease – BPH and Prostatitis in entire male dogs, prostatic neoplasia in neutered males Detrusor-Urethral Dyssynergia (Reflex Dyssynergia) – Middle-aged, often highly-strung, male, large-breed dogs**

Answer 195

Same principles as adult Main difference is size Limited ability to perform rectal exam but better for imaging Palpate Inguinal rings and umbilical region for hernias. Evaluate for the passage of meconium Evaluate abdominal distension

Answer 196

Enterocolitis (covered previously) Meconium impaction Transient medical colic (unknown aetiology) Ruptured bladder/uroperitoneum SI/LI obstruction ( volvulus/ impaction/ intussusception) Overfeeding/lactose intolerance Gastric/ duodenal ulcers ( will be covered in more detail in pre rotations) Herniation (inguinal, scrotal, or umbilical) Congenital abnormalities (Atresia ani/ atresia coli)

Answer 197

Initial passage of meconium begins in the first few hours after birth. Generally complete at age 24 h, although can take up to 48 h. Meconium impaction ( failure to pass meconium) can lead to clinical signs of colonic obstruction. Abdominal pain can be mild to severe generally in first 12-36 hours after birth Signs may include abdominal pain (colic), tachypnoea and tachycardia, tail “swishing,” restlessness, straining to defecate, and abdominal (gas) distention Retention may be high, in the transverse or right dorsal colon, or low, in the large colon. Diagnosis, careful digital examination, radiography, ultrasonography Foals >340 d gestation and colts predisposed?

Answer 198

Medical therapy works in most cases Enemas Soapy water (½ teaspoon liquid detergent added to 500 mL water) Phosphate (Fleet®) (no more than 2 administrations in 24 hours) Acetylcysteine retention enema -cleave disulfide bonds in the mucoprotein molecules Analgesia Oral fluids/ laxatives IV fluids Surgery?

Answer 199

Most commonly seen in colts (tear/ congenital defect in dorsal bladder wall sustained/exacerbated during birth) but also seen in fillies. Clinical signs typically noted 1-3 days after birth, but bladder rupture can occur after birth especially in compromised recumbent foals leading to later presentation (several days old). Affected foals often still noted to urinate – normal stream does not exclude uroabdomen although often smaller volumes. Uroperitoneum may also be secondary to urachal tears (secondary to septic omphalitis) or very rarely ureteral defects Uroperitoneum: Clinical Presentation Depression and abdominal distension: may be more apparent after 2 days. Dysuria esp. stranguria– Frequent attempts to urinate with only small amounts voided. Abdominal pain / straining. Severe cases may occur acutely as colic. Tachycardia Tachypnoea Cardiovascular collapse Cardiac arrhythmias. Neurologic signs: seizures, hyperesthesia, spasticity.

Answer 200

Ultrasound: free fluid in the abdomen – appearance of the bladder will vary with size of the defect. Fluid : serum creatinine ratios ≥ 2 are diagnostic Serum electrolyte derangements: caused by equilibration between plasma and the urine contained within the abdominal cavity. Hyperkalemia: may induce arrhythmias Hyponatremia Hypochloremia. Serum BUN and creatinine values can be normal but usually are increased. ( Use foal reference ranges as values differ to adults)

Answer 201

Medical emergency not a surgical one Stabilisation of the patient via abdominal drainage and correction of hyperkalaemia and other electrolyte abnormalities is critical. For hyperkalaemia: Administer 0.9% saline with 5% - 10% glucose. Calcium boroglucanate may be protective Foals should not be taken to surgery until potassium concentrations ≤ 5.5 mEq/L are achieved

Answer 202

Inguinal and Umbilical hernias Umbilical hernias are common in foals (0.5-2%) but bowel incarceration much less so Inguinal hernias – check if can be manually reduced – often not the case if they are causing colic. If no distress or gross enlargement of scrotum, best to attempt to reduce on a daily basis. Most reduce spontaneously over several months.

Answer 203

Can result in mild to severe abdominal pain in the foal May also affect the oesophagus and duodenum Classic signs bruxism, ptyalism and dorsal recumbency and diarrhoea (not seen in adults) Not seen in newborns but has been seen in foals as young as 2 days of age. In rare cases deep ulcers can perforate leading to death Diagnosis – gastroscopy. Treatment PPI – omeprazole +/- Sucralfate Prophylaxis – acid suppression may lead to GI disturbances

Answer 204

Persistence after birth of the tubular connection between the bladder and umbilicus During gestation is patent to drain the bladder in to the allantoic sac Urachus should close at birth with rupture of the umbilicus aetiology- Not really known Failure to close at birth Or re-establishment of patency: Inflammation, infection, excessive physical handling – e.g. lifting, or early severance or ligation of the umbilical cord. Seems to develop secondarily in ill neonates Important to differentiate between patent urachus with concurrent omphalophlebitis. Transabdominal ultrasound of umbilical remnants for further evaluation / identification of infections/abscessation.

Answer 205

Many uncomplicated cases will resolve with supportive care, routine umbilical disinfection, and systemic antimicrobials if needed. Umbilical dips multiple times/day Foals without evidence of umbilical sepsis, chemical cautery of the umbilical stump silver nitrate applicators or swabs dipped in 7% iodine solution. Foals with septic umbilical structures / non responders > Surgical resection of umbilical remnants

Answer 206

Physiological anaemia (↑ blood volume) * Increased oxygen demand * ↓ FRC and ↑ alveolar ventilation- * Rapid uptake and offloading of anaesthetic gas * Enlarged/full abdomen- * Intermittent positive pressure ventilation – IPPV - nearly always necessary * Poor venous return – reduced arterial blood pressure * Appear sedated (↑progesterone and ↑↑ blood-brain barrier permeability) * Appear more ‘sensitive’ to anaesthetic agents – care with ‘depth’ of anaesthesia * Reported decrease in anaesthetic requirement by 25-40% elayed gastric emptying * Decreased oesophageal sphincter tone * Lower pH of gastric contents – All lead to high potential for regurgitation and aspiration pneumonia * In humans = Mendelsons syndrome * Electrolyte disturbances * Exhaustion and pain

Answer 207

Viability – Hypoxia, hypercapnia, acidosis, drugs * Respiratory depression – Hypoxia, drugs, hypothermia, lack of stimulation * Hypoxia – Placental separation – Impaired maternal ventilation – Impaired maternal blood pressure * Hypercapnia

Answer 208

Virtual complete lack of drugs licenced in pregnant/lactating animals and in neonates * From NOAH; – Acepromazine – “Do not use in pregnant animals” – Methadone - “The use of the product is not recommended during pregnancy or lactation” – Propofol - “Use only according to the benefit/risk assessment by the responsible veterinarian” – Alfaxalone – “The safety of the veterinary medicinal product has not been established in cases where pregnancy is to be continued or during lactation Isoflurane – “Use only accordingly to the benefit/risk assessment by the responsible veterinarian” * Sevoflurane – “The safety of SevoFlo has not been established during pregnancy or lactation” * NSAIDs – “The safety of the veterinary medicinal product has not been established during pregnancy and lactation Use shorter acting or antagonisable drugs wherever possible * IF FAMILIAR apply local anaesthetic/opioid techniques – E.g. epidural blocks * Use minimum effective doses – But do not under-dose * Always supply fluid and oxygen support Premedication reduces maternal stress – Improves uterine blood flow * Premedication allows analgesia provision – Improves uterine blood flow * Premedication allows reduction in induction and maintenance agent dose – Reduces negative cardiovascular effects of these agents – Reduces foetal exposure to these agents Any anaesthetic drug can undergo placental transfer * Weak bases (e.g. local anaesthetics) may become ion trapped – Much worse if foetus is acidotic = hypoxic – Worse with repeated or high doses * Drug in foetal CNS depends on placental transfer plus foetal metabolism/clearance

Answer 209

Elective – Almost treat as ‘normal’ – Place iv cannula – I always premedicate and if accepted without stress pre-oxygenate – Prepare equipment, drugs and personnel in advance – Pre-clip if appropriate Emergency presentation – Stabilisation with fluids asap – Check electrolytes, pcv and tp and stabilise if necessary prior to induction – Premedication important to reduce dose of iv induction agents – Pre-clip if appropriate

Answer 210

(e.g. methadone, fentanyl) – Sedation and analgesia – Minimal cardiovascular effects * Maternal bradycardia treated with atropine/glycopyrrolate * Foetal heart relatively unaffected – not underautonomic control – Limited additional respiratory depression * ?Favour short acting fentanyl- possibly

Answer 211

may cause prolonged sedation and hypothermia in mother and neonate; generally avoided – However no increase in mortality in several studies

Answer 212

Xylaxine associated with significantly increased puppy mortality; generally avoided – In goats medetomidine reduces uterine blood flow by 50%

Answer 213

(midazolam/diazepam) – Rapidly cross placenta and accumulate in foetus – Associated with ‘floppy infant syndrome’ in humans – Similar depression seen in pups following midazolam, ketamine, enflurane anaesthesia * However specific antagonists exist – But may be ineffective in cats

Answer 214

Following IVFT initiation I use moderate doses of methadone (0.1-0.3mg/kg) IM 20 minutes prior to induction * Alternatively IV fentanyl 2-3μg/kg 2-3 minutes prior to induction * Monitoring starts at premedication! * ANY signs of maternal/foetal distress start oxygen therapy and induce anaesthesia

Answer 215

Inhalation techniques have been used following pre-oxygenation – Common to see struggling and stage II excitement – Risk of regurgitation and aspiration * Injectable to effect more controlled – Allows minimum effective dosing – Allows early control of airway

Answer 216

Maternal propofol 3x foetal concentration after 1 bolus = protein binding in the dam – Same residence times for mother and foetus – Not associated with poorer outcomes

Answer 217

Similar or better than propofol for mother and puppies * Better viability scores cv propofol at 60 minutes * Similar puppy survival rates at 3 months

Answer 218

compared to propofol – Improved maternal cardiovascular stability – More profound foetal depression * Intensive resuscitation often necessary – No differences in puppy surviva However, often given with benzodiazepines = detrimental

Answer 219

Regurgitation is a potential problem * Induce anaesthesia with the head raised Secure the airway as rapidly as possible with a cuffed endotracheal tube * Consider ‘Sellick’s manoeuvre’ Other problems on induction – Cardiovascular drug effects * Use minimum effective doses * Some advocate intravenous lidocaine immediately prior to induction to allow ease of intubation * Premedication will lower doses – Apnoea * Pre-oxygenate * Be prepared to apply IPPV * A familiar intravenous agent * Minimum effective dose * Given slightly faster than normal to allow rapid endotracheal intubation

Answer 220

soflurane vs sevoflurane in oxygen – Theoretically more rapid alterations in ‘depth’ with sevoflurane – Limited evidence of either being superior – Allows oxygen administration and IPPV * Nitrous oxide? – Controversial (potential for diffusion hypoxia?)

Answer 221

Intermittent positive pressure ventilation almost always necessary – Care to avoid overventilation * Hypocapnia ≡ uterine vessel constricƟon * Hypocapnia shifts oxyhaemoglobin curve to left * Neuromuscular blocking agents useful – Only use if familiar – IPPV mandatory – Ionised so do not cross placenta – Contribute to balanced anaesthetic technique Extra(epi) dural techniques give excellent analgesia * If unfamiliar can increase anaesthetic time * But allows induction agent time to clear * If using local anaesthetics reduce dose (reduced epidural space) and monitor for hypotension * 2-3mg/kg lidocaine often used * Extradural opioids have minimal systemic effects * 0.1mg/kg pf morphine often used * Blood pressure monitoring important – maintain uterine flow and administer fluids * Actively treat hypotension with fluids/pressors – Ephedrine/dopamine useful adjuncys * May see supine hypotension syndrome – Published evidence of improved blood pressure if mother tilted to left Sevoflurane or isoflurane in oxygen plus IPPV * Local anaesthetic techniques * Tilt to left (if surgeons happy) and fast surgery * Intravenous fluids given to maintain physiolo CONSTANT monitoring

Answer 222

* Virtually no published evidence regarding safety of analgesics in pregnant dogs/cats – Therefore often (incorrectly) avoided * Remember; Pain causes sympathetic stimulation and sudden reduction in uterine blood flow – Hypoxia = puppy mortality * We are responsible for the welfare of our patients Benefits of analgesia – Pain causes * Release of cortisol, catecholamines, pituitary hormones and therefore catabolic state * Wound breakdown * Hyperglycaemia and insulin resistance * Leukocytosis - neutrophilia * Cytokine production * Poor immune function * Reduced appetite Inadequate analgesia is associated with decreased milk production in the dam Caesarean Section – Analgesia * NSAIDs very useful in dam as no CNS depression – Identified as cause of reduced neonate survival * Often given after neonate removal * Only 1-2% of maternal dose passes into milk – NSAIDs considered safe for breast feeding human infants – Some advocate gastroprotectants to neonates but no direct evidence Caesarean Section – Analgesia * Full mu agonist opioids provide excellent analgesia to mother * Repeated doses could accumulate in neonates – Theoretical risk of respiratory depression * Naloxone administered into umbilical vein or sublingually very effective should this occur – Butorphanol is also a mu receptor antagonist – I have used this successfully into umbilical vein

Answer 223

Premedicate with methadone 0.1-0.2mg/kg * Rapidly place an extradural block if possible – Lidocaine plus morphine – +/- incisional block with lidocaine * Administer an extra 0.1-0.2mg/kg methadone after neonatal removal * Administer full dose of meloxicam or carprofen after neonatal removal * Assess pain carefully in recovery period and at home

Answer 224

Apgar scoring can guide resuscitation – Heart rate, respiratory effort, muscle tone, reflexes and colour are scored – Can be used as guide to puppy distressonsider – Warmth – Vigorous body rubbing – Suction and removal of membranes – Oxygen (low heart rate = hypoxia) +/- IPPV – GV26 acupuncture point * In general avoid doxopram – Increases myocardial oxygen demand

Answer 225

Airways of the mammalian lung consists of a branching tree of blind ending tubes. This design creates physiological problems. Mammalian lung contains two types of airways: Conducting - carry air to and from respiratory airways. Respiratory - responsible for gaseous exchange with blood. The cough receptors are located mainly on the posterior wall of the trachea, pharynx, and at the carina of trachea, the point where the trachea branches into the main bronchi. The receptors are less abundant in the distal airways, and absent beyond the respiratory bronchioles

Answer 226

Puppies- infectious respiratory disease Toys and miniatures- tracheal collapse Young dogs < 2 years- Angiostrongylus Westies, SBT- IPF Older dogs- laryngeal paralysis, chronic bronchitis, neoplasia

Answer 227

Dyspnoea in any position other than standing or erect sitting – usually due to bilateral pulmonary oedema

Answer 228

Dyspnoea in one lateral recumbency but not the other – unilateral lung or pleural disease, or unilateral airway obstruction e.g. unilateral pleural effusion Often seen in patients when in hospitalised and in lateral recumbency Can be dramatic deterioration so always be vigilant for this

Answer 229

Respiratory muscle fatigue leading to opposing movements of the chest and abdominal wall. e.g. inspiration the caudal ribcage collapses inward and the abdominal contents are displaced caudally. Can occur in may cases of respiratory disease but is generally a poor sign. Cats very good at hiding severe respiratory disease As a result this species is commonly presented with severe apparently acute onset clinical signs

Answer 230

Thoracic palpation Presence of - apex beat, rhonchi, masses, deformities, pain (e.g. rib fractures) Thoracic auscultation Hindered by purring, panting, growling! Use both sides of your stethoscope Normal sounds Inspiratory – soft, low pitched Expiratory – none or softer and lower pitched Abnormal sounds may or may not be associated with abnormal breathing patterns. Crackles – ‘sweet wrappers’ (rales) – Dry or moist Moist – CHF and most prominent on inspiration (right hilar position 1st) – usually some resp distress Dry – acute or chronic –e.g. IPF Wheezes (high pitched) and rhonchi (low pitched) narrowing of airway (bronchi/trachea) Can be inspiration or expiration but most commonly expiration Determine the density of a part by tapping the surface with a finger Best for larger dogs and cats Determine whether the tympanic sounds created by the chest wall are normal, increased or decreased e.g pleural effusion – dull below fluid line and normal above it There are many different causes of increased and decreased tympanic sounds on percussion

Answer 231

History – is the animal coughing or having respiratory difficulty/changed character Clinical examination Routine haematology and biochemistry Specific blood tests - e.g. serum Pro-BNP concentration Blood gas evaluation Diagnostic imaging Thoracic radiographs, fluoroscopy, CT, Ultrasound, scintigraphy, MRI Tracheal washes/Bronchoscopy Lung FNA/biopsies NB these are often older dogs with concurrent disease other tests as clinically indicated!

Answer 232

Minimum database of biochemistry and haematology Always of value in respiratory patients Determines if underlying systemic condition present/likely Anaemia Eosinophilia, neutrophilia Use of assays such as NT-ProBNP to determine between cardiac and respiratory causes of coughing Blood gas evaluation (arterial and venous) Enables determination of oxygenation, ventilation/perfusion mismatching and acid-base balance Handheld analysers available Hypoxaemia – PaO2 <80mmHg Equations for determining effective perfusion and oxygenation of blood in standard texts Caution as sample for PaO2 needs to be arterial and taken in the absence of air

Answer 233

Thoracic radiographs Where thoracic disease is suspected thoracic radiographs (at least 2 views) should always be taken Radiographs should only be taken when the patient is stable enough to do so! Severely dyspnoeic patients should be stabilised prior to radiographs in all but extremely exceptional circumstances Can consider horizontal beam radiographs for patients too dyspnoeic to lay down Aids with fluid identification and free gas Radiation safety issues may preclude this approach Fluoroscopy Valuable to assess dynamic integrity of airway Thoracic CT Advantages over radiographs Increased sensitivity (high resolution CT: 300 micrometers) Spatial assessment of disease Value to differentiate pleural, extrapleural and mediastinal disease Disadvantages Unable to perform easily in conscious patient Increased costs and limited availability thoratic ultrasound- lines found indicate pathology

Answer 234

Tracheal wash – why would you perform this? Main indication is for patients suspected to have large airway disease Now recognised to provide information about the small airways as well when cough reflex retained Can be either trans-tracheal (TTW) or endotracheal (ETW) TTW benefits as cough reflex retained therefore better information from lower airways Indicated in patients that you have concerns about anaesthetising Is less sensitive than BAL but is easier to perform and can be carried out in the conscious patient.

Answer 235

Diffuse airway disease Small- medium dogs Red rubber catheter with tip removed 0.9% warmed saline 5-30ml aliquots amount 2-5ml/kg more sensitive than traceal washing but patient must be anesthetised BAL fluid- 40-50% recovery Froth and floaters Direct and cytospin smear EDTA (cytology and PCRs) Plain (culture)

Answer 236

Site specific sampling Mucosal inspection Airway collapse FB retrieval can diagnose Tracheal collapse indications- Investigation of unexplained clinical signs To obtain diagnostic samples Evaluate radiographic lung lesions Assessment of airways Treatment of airway disease Relatively safe procedure Diagnostic for a number of conditions Allows collection of samples Allows removal of foreign material contraindications- Care with hyper-responsive airways e.g. cats with allergic bronchial disease Dogs with wheezing suggesting airway spasm Unstable cardiac failure / arrhythmias Care in those patient with tracheal obstruction Haemorrhage – increased risk with: Pulmonary hypertension Uraemia Coagulopathies Neoplasia/gross lesions

Answer 237

Sterilisation - according to manufacturers recommendations If unusual / repeated bacteria isolated swab scope Care of scope – very delicate Fibreoptic or video Under GA as prevents scope damage Airway diameter vs scope diameter important Not the same therefore as humans or horses Sternal recumbency Elevate head so nose is parallel to the table Monitor with pulse oximetry / end tidal capnography Small dogs and cats can’t use ET tube Pass endoscope directly through larynx – extreme care Intravenous anaesthesia – propofol/alfaxan Urinary catheter to deliver oxygen with manual ventilation Preoxygenation for 30-45 seconds Extensive evaluation can be difficult Use systematic approach to examine the structures Collect samples using Saline lavage – bronchoalveolar lavage (BAL) Surface brushing (cytology brush) Biopsies – care with technique Samples submitted for Culture – bacterial/mycoplasmal/fungal Viral isolation PCR for infectious organisms e.g. mycoplasma Cytology BAL for lobar or diffuse lower airway disease or interstitial lung diseases 0.9% sterile saline solution Bacterial swabs Sterile plain tubes (plastic) EDTA tubes BAL catheter Urinary catheter Continuous suction device Syringes An assistant! Formalin Pre-oxygenate – 2 minutes in compromised patients Lodge endoscope in small airway Instil sterile saline via catheter Volume not been established various amounts depending on author/clinician preference For medium to large dogs ~25ml per lobe (2 lobes washed) For small dogs and cats ~10ml per bolus (up to 4 sites) Immediate suction after instillation of fluid If too much suction then causes airway collapse and damage (100-170mmHg pressure max) Care with suction chambers as more likely to damage cell morphology Repeat boluses in same position First bolus has largest amount of material from large airways Lavage several lobes Coupage whilst fluid is being instilled Good quality sample Foam on top – due to surfactant in fluid >50% of fluid retrieved In one study mean volume retrieved was 48% 1 Retrieval volume should increase with each subsequent lavage

Answer 238

Dog urinary catheter or feeding tube (5-6F) Ensure end hole only Sterile ET tube Y connector Dog in dorsal recumbency Pre-oxygenate Place tube as far as will go until feel resistance 20-25ml saline and 5ml of air in dogs 20ml per bolus in 4kg cat – 2-3 sites 7/9 patients right caudal lung lobe (2/9 LCLL)

Answer 239

100% Oxygen for 5-10 minutes Gentle positive pressure ventilation May aid with opening of atelctatic alveoli If previous stable patient does not respond to oxygen consider: Obstruction of ET tube Bronchospasm - bronchodilator Pneumothorax Normal to auscultate crackles for up to 24 hours post BAL

Answer 240

URT and large airways are not sterile have commensal bacteria Numbers are increased in dogs with reduced clearance Quantitative culture – rarely performed in veterinary medicine, can be requested Evidence of infection Intra-cellular bacteria* Growth from BAL fluid Neutrophilic inflammation on cytology

Answer 241

Inhaled medications: Corticosteroids Bronchodilators Nebulisers Oral therapy: Anti-inflammatories- Corticosteroids, NSAIDs, anti-leukotrienes Bronchodilators- Terbutaline Theophylline Antibiotics, anthelminthics Mucolytics – N-acetyl cysteine (NAC) delevery- Mask Spacing device/chamber Metered dose inhaler (MDI) inhaled medications?- Management of chronic airway disease Minimal absorption into systemic circulation Less systemic side effects – particularly steroids Faster onset of action

Answer 242

Beta 2 agonist Salbutamol (albuterol in USA) Salmeterol – longer acting medication Corticosteroids Fluticasone Beclomethasone Inhibition of mast cell degranulation (unclear efficacy in dogs and cats with airway disease) Cromolyn sodium/sodium cromoglicate Salbutamol (ventolin) Beta 2 agonist Fast onset of action Lasts >3hrs Cleared renally following metabolism in tissues and blood (esterases) 10-20% inhaled reaches lower airways SE: tachycardia, arrhythmias, tremors Why are inhaled medications valuable Reduces systemic exposure to GC Dose of GC required is lower Reduces systemic side effects Effective in acute situations Acute respiratory distress – beta agonists Evidence for efficacy Humans – extensive evidence Veterinary – increasing evidence Inhaled corticosteroids – Bexfield et al 2006 Inhaled bronchodilators - Kirschvink and others 2005 disadvantages- Expensive Time consuming Owner compliance Patient compliance

Answer 243

Inhaled bronchodilator Beta 2 agonist Fast onset of action Lasts >3hrs Cleared renally following metabolism in tissues and blood (esterases) 10-20% inhaled reaches lower airways SE: tachycardia, arrhythmias, tremors

Answer 244

Fluticasone propionate Flixotide in UK Slowly absorbed from lung Long dwell time in lungs Rapid first pass metabolism in liver Less systemic side effects Long half life Least bioavailable Side effects Oral infections e.g. candidiasis, coughing, wheezing

Answer 245

Most chronic bronchitis cases do not have bacterial infection as a causal agent If there is secondary infection requires immediate therapy due to compromised resistance mechanisms Antibiotics indicated if C&S results +ve, or if intracellular bacteria seen on BAL cytology Empirical treatment then initiated prior to culture results Care if using fluoroquinolones with theophylline as they inhibit metabolism increase concentration of theophylline – risks toxicity Antibiotic selection should ideally be based on C&S Require high concentration in the lungs Need to penetrate, dissolve in blood-bronchus barrier Lipophilic antibiotics penetrate this best Needs to be effective against respiratory pathogens Ideally a/b should be bacteriocidal May need to select combination a/b e.g. complex pneumonia/mixed infection Ensure adequate treatment period at least 4-6 weeks for severe/chronic infections – CRP? Primary infection is uncommon in dogs Secondary respiratory tract infections common in chronic bronchitis, compromised mucociliary clearance Good airway penetration Drugs reach airway by passive diffusion Favourable characteristics- Lipophilicity and low Mr Few drugs reach same conc as plasma Depends on nature of organism Mycoplasma inherently resistant to certain antibiotics as no cell wall – choices include macrolides and fluoroquinolones, can consider tetracyclines No current evidence that inhaled antibiotics have any efficacy and so oral medication always required However may have a role to play in B. bronchiseptica infections

Answer 246

Can be useful to help reduce mucus accumulation in chronic bronchitis and other conditions with compromised muco-ciliary clearance Bromohexine – increases lysosyme activity and IgA concentration in experimental studies Licensed product – bisolvon NAC – Effective at breaking mucin disulphide bonds no current published efficacy data Anecdotal evidence some evidence for efficacy when administered orally between 125-600mg B-TID PO Cannot be nebulised as causes bronchospasm

Answer 247

Fluoroquinolones are concentrated significantly in canine alveolar macrophages good penetration into airway Macrolides are reasonably well concentrated into respiratory tract Azithromycin very good distribution into pulmonary tissues Metronidazole accumulates well in bronchial secretions Drugs with long half life accumulate in secretions – e.g. doxycycline Lincosamides – accumulate well in phagocytes Penicillins have relatively poor distribution into bronchial tissue Some are better than others e.g. amoxicillin > ampicillin Cephalosporins – variable penetration depending on generation although better than penicillins Tetracyclines – reasonable concentration in secretions relative to plasma

Answer 248

This is often seen +/- cough/cyanosis/noise F.B. Neoplasia Trauma/haemorrhage etc Laryngeal paralysis/trauma/granuloma BOAS - long soft palate, stenotic nares, larynx collapse Tracheal or bronchial collapse Extra-luminal mass lesions - thyroid, abscess, lymphoma Asthma/bronchospasm (cat) Nasopharyngeal polyp (cat)

Answer 249

URT obstruction Loss of thoracic capacity Pulmonary parenchymal disease Non-CRS conditions Metabolic/physiologic

Answer 250

This can be seen with and without cyanosis * Pleural effusion - blood, pus, chyle, true/modified transudate * Pneumothorax * Neoplasia - pleural or mediastinal * Ruptured diaphragm * Abdominal abnormality - severe ascites/mass * Gross cardiomegaly

Answer 251

Ultrasound very sensitive at detecting fluid Transudate Modified Transudate FIP Pyothorax Exudates Chylothorax Haemothorax

Answer 252

Clear, watery analysis- Prot <25 g/L Cells < 1.5 x 109/L causes- Hypoalbuminemia

Answer 253

Straw coloured; serosanguinous; slightly viscous analysis- Prot >25 g/L Cells < 5 x 109/L Cytology may identify neoplastic cells. causes Right sided or biventricular CHF Diaphragmatic rupture Neoplasia

Answer 254

Blood (bloody) Non-septic inflammation (viscous, straw coloured) Septic inflammation (viscous, turbid, purulent) Chylous (milky) analysis- Prot > 25 or 30 g/L Cells > 5 x 109/L Blood, mesothelial cells Neuts, macrophages, mesothelial cells Neuts (degenerate), bacteria, macrophages, mesothelial cells TG fluid > TG plasma Pl. fluid Chol/TG ratio <1 Small lymphocytes causes- Trauma, Neoplasia, Coagulopathy, Lobe torsion Chronic chylothorax, Neoplasia Rupture Oes., FB, Pyothorax, Fungal infection Idiopathic, CHF, CrVC obstr, Trauma, lobe torsion

Answer 255

Clinical signs of pulmonary parenchymal disease Usually increased inspiratory and expiratory effort Cough may or may not be present Can see less frequently hemoptysis, collapse/syncope or cyanosis Occasionally minimal signs of respiratory disease are noted even with severe pathology- Particularly in cats Aspiration pneumonia- Pulmonary oedema

Answer 256

Inhalation of material into the lower airway- Stomach contents with variable amounts of particulate matter Care with nursing recumbent patients Outcome depends on nature and amount of aspiration pH, bacterial contents, volume, particle size- Chemical aspiration – pneumonitis Large volumes of fluid – drowning event PEG fluids (bowel prep) – pulls interstitial fluid into the lungs Primary infection due to aspiration is less common- This usually occurs as a secondary event due to damage

Answer 257

Consequence of various conditions Increased hydrostatic pressure Reduced oncotic pressure Increased vascular permeability Impaired lymphatic drainage This leads to fluid accumulation in the interstitium and subsequently in the alveoli at a rate that exceeds removal- Ventilation perfusion mismatching and hypoxaemia Cardiogenic or non-cardiogenic - main difference is type of fluid Cardiogenic is low protein due to increased hydrostatic pressure without increased vascular permeability Non-cardiogenic is the result of lung damage which increases vascular permeability

Answer 258

result of lung damage which increases vascular permeability Importantly hypoalbuminaemia rarely causes pulmonary oedema due to efficient pulmonary lymphatics Lymphatic damage is more likely to cause a chylous effusion rather than pulmonary oedema Neurogenic form (along with electric shock) – pathophys. unclear but thought to be due to intense pulmonary vasoconstriction and inflammation both increase vascular permeability Most common cause is pulmonary epithelial injury Pulmonary inflammation and oedema leading to respiratory compromise are termed acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) The difference is determined by severity (ARDS>ALI) Presentation – signs may be delayed after insult for up to 72 hours Moist cough (may produce froth), orthopnoea, cyanosis Harsh BV lung sounds with crackles are typical Radiographs – unstructured interstitial pattern and peri-bronchial can progress to alveolar, often caudo-dorsal Therapy – caution as animals clinically fragile Address underlying cause, treat ARDS/ALI Oxygen supplementation Sedation may be required (caution with resp depression) Support – keep affected lung dependent Diuretics less effective for non-cardiogenic oedema but still indicated

Answer 259

Ideally do not move the horse before veterinary assessment Provide instructions on controlling haemorrhage +/- remove foreign bodies from the foot If distressed, perform brief examination (CV and neurological) Sedate with α2 agonist Succinct history Known trauma/sudden onset at exercise? If unknown cause, when was the horse last seen normal? Is the horse stabled or turned out with other horses? Coaptation? Transport? Immediate euthanasia? Second opinion!- beva guidleines

Answer 260

Full history- Previous lameness Shoeing Current medication Full clinical examination- Posture Obvious swelling, deformity or asymmetry Wounds Determine which limb(s) affected Assess the degree of lameness Clean the limbs Palpation: Swelling or synovial effusion Wounds inc. Small wounds Digital pulse amplitude FBs in foot (N.B. check frog sulci) Hoof tester application Pain on flexion/extension Reduced/abnormal range of motion Crepitus

Answer 261

Most common causes: Subsolar abscessation Laminitis Cellulitis Synovial sepsis Fracture Tendonitis Tendon laceration/rupture Myopathy diagnostics- Radiography- Suspected Fracture/Joint Subluxation Wound Assessment Laminitis Ultrasound- Assessment of Tendon and Ligament Injury Wound Assessment Diagnosis of Pelvic Fractures Synoviocentesis- Suspected synovial sepsis MRI- Penetrating injuries to the foot Further assessment of other distal limb injuries Scintigraphy- Suspected pelvic/stress fractures (esspecially whre radiographically scilent) Serum biochemistry +/- urinalysis- Suspected myopathy/rhabdomyolysis

Answer 262

Clinical signs- Severe lameness Heat Pulse amplitude Hoof testers Coronary band palpation Aetiology- Bruising Foot conformation Penetrating wounds “White Line” disease Laminitis Keratoma

Answer 263

+/- ASNB Remove Shoe Subsolar exploration Tetanus prophylaxis Topical antiseptic Foot bandaging AnalgesiaPeriarticular Cellulitis

Answer 264

Broad spectrum antimicrobial treatment NSAID Dexamethasone Cryotherapy Physiotherapy Bandaging more common in horses training pon sand very acute swelling on hock very painfull

Answer 265

General physical examination Haemorrhage? Other injuries? Careful attention to anatomical location Visual examination Digital exploration with gloved hand Radiography Ultrasonography

Answer 266

differentail for acute lameness associated with kick injury may be assosiated with small wound very painfull

Answer 267

Clinical Signs: Acute-onset/progressive severe lameness If draining, variable lameness +/- wound adjacent to synovial structure Heat, pain and swelling Synoviocentesis remote from wound Collect sample Cytology Culture and sensitivity Distend with sterile saline/contrast- can see the state of the bursa- egress from a wound? Concurrent antimicrobial found on the front of the shoulder, abouve the foot, below the elbow and in the hoc

Answer 268

Antimicrobial NSAID Tetanus prophylaxis Clipping Pack wound KY Jelly to haircoat Clean skin (not wound) with soap Local Anaesthesia! Bandaging Referral Arthroscopic assessment and lavage under GA wound closure- trying to aschive sealed system devride woun

Answer 269

Primary (First Intention) Closure Delayed Primary Closure Delayed Secondary Closure Second Intention Healing

Answer 270

Surgical Debridement Judicious! N.B. Vital structures Mechanical Debridement Tap water Sterile polyionic fluid Hydrogen peroxide Chemical Debridement Hypertonic saline (20%) Biological Debridement Maggots

Answer 271

he use of casts, splints, bandages, or slings to help stabilize fractures or luxations, reduce postoperative swelling, or help to protect wounds

Answer 272

Flexor Tendons Suspensory Ligament Extensor Tendons- less of a concern. can return to work even without surgery. can cause necrosis if vasculature compromised but not comkon presentation affect on athetisism?- External Coaptation

Answer 273

a piece of devitalized bone that has been separated from the surrounding bone during the process of necrosis. acts as foreign body complication o wounds

Answer 274

infiltration of air underneath the dermal layers of skin not common but ay be seen with axillary wounds

Answer 275

Infection Presence of foreign material Exuberant granulation tissue- very common in horses Necrotic tissue Movement Loss of blood supply Poor oxygenation Loss of tissue Systemic health disorder Tumour transformation

Answer 276

Medial > Lateral Involve Diaphysis Spiral Propensity for catastrophic failure Recovery Perioperative

Answer 277

Avoidance of general anaesthesia Reduce catastrophic fracture or implant failure Improved: Haemostasis Soft tissue dissection Surgical exposure Operator orientation Cost Patient Selection Patient Preparation Location Equipment Chemical Restraint Team- Surgery Nursing Imaging Anaesthesia

Answer 278

Short acting sedative by titrated continuous infusion- ⍺2-agonists Multimodal analgesia: Local anaesthesia NSAID Opioid- Morphine Caudal epidural analgesia Intraprocedural monitoring

Answer 279

Clinical Examination: Palpation (inc. with limb elevated) Observe postural changes Wounds – possibility of tendon laceration Ultrasonography Treatment: Rest and controlled exercise Cold therapy Anti-inflammatory medication Compression and coaptation Intralesional therapy- Stem cells

Answer 280

Optimal Treatment: Debridement and repair under GA Call the referral centre

Answer 281

This can be seen with and without cyanosis * Pleural effusion - blood, pus, chyle, true/modified transudate * Pneumothorax * Neoplasia - pleural or mediastinal * Ruptured diaphragm * Abdominal abnormality - severe ascites/mass * Gross cardiomegaly

Answer 282

Physical lung injury Thoracic trauma Pulmonary contusion - ventilation perfusion mismatch Chest wall damage and pain Thoracic radiographs to evaluate all thoracic structures Lag phase Supportive care with supplemental oxygen ASAP Other treatment as required – e.g. stabilisation of the thoracic wall, analgesia

Answer 283

Drowning Aspiration of liquid Immediate consequences result from hypoxaemia Alveoli fill with fluid – dilutes surfactant and leads to alveolar collapse and intrapulmonary vascular shunting leading to V-Q mismatching Reduced compliance and inflammation leads to ARDS worsening hypoxaemia Systemic complications of lactic acidosis and hypercapnia More common in dogs than cats Underlying cause laryngeal disease, seizure whilst swimming Unable to exit water

Answer 284

EBN is more common in dogs, with reactive eosinophilic airway disease occurring in cats Typically young adults ?huskies/malamutes and Rottweilers?? Acute or chronic presentation – usually coughing Can also see weight loss Radiographs show diffuse bronchointerstitial pattern although can see alveolar patterns (can be dense infiltrates) Circulating eosinophilia in ~50% dogs – some will have hypereosinophilic syndrome BAL for diagnosis – caution to look for parasites, neoplasia and fungal disease Treatment – prednisolone 1-2mg/kg daily Outcome often very good unless other organs involved in which case prognosis guarded

Answer 285

Typically WHWT and other terriers (Staffordshire BT) Middle aged to older dogs History Insidious onset Chronic breathlessness which is slowly progressive Coughing can be a feature Exercise intolerance Owner may notice cyanosis Can cause syncope Clinical examination Crackles throughout the lung fields Prolonged expiratory phase with expiratory effort. Diagnosis of IPF Suggestive clinical signs Diffuse crackles on auscultation, dyspnoea, coughing Thoracic radiographs Generalised interstitial lung pattern +/- right sided cardiomegaly, +/- pulmonary hypertension CT – method of choice in humans Typical ground glass appearance – diffuse increase opacity without loss appearance of blood vessels. Bronchoscopy BAL samples are either normal or show low cellularity Rules out other inflammatory conditions – primarily CB Lung biopsy is the only method of definitive diagnosis Relatively poorly understood compared with human fibrotic lung diseases In absence of biopsies, efficacy of treatment difficult to determine Serum and BALF Endothelin I concentration Osteopontin serum concentration is higher in diseased WHWTs Has shown good sensitivity and specificity for determination between IPF and CB and EBP BALF concentrations of ActivinB higher in IPF dogs Serum and bronchial epithelium CCL2 and CXCL8 higher in WHWT cf. other breeds (CCL2 increased in affected WHWT) Procollagen type III is elevated in BALF in dogs with IPF Surfactant P concentration may be reduced in some dogs with IPF This is an important surfactant with strong hydrophobic properties mutation of the SP-C gene is recognised in humans to be associated with familial forms of interstitial lung disease S100A9 has shown high specificity for IPF relative to other interstitial lung diseases in humans

Answer 286

Success of therapy depends largely on whether active inflammation present Symptomatic treatment Avoid collars, harness only, avoid smoke inhalation Inhaled therapy Bronchodilator, corticosteroids Oral therapy Bronchodilators - especially if concurrent airway collapse Corticosteroids Additional immunosuppressive medication Azathioprine and cyclosporin No evidence of clinical efficacy Management of pulmonary hypertension* Phosphodiesterase inhibitors Sildenafil, tadalafil Pimobendan Antibiotics as necessary Anti-fibrotics (e.g. colchicine) Theoretically slows collagen deposition and reduces production of profibrotic cytokines No evidence for efficacy of these in veterinary patients No evidence of improved outcomes in humans either

Answer 287

Coagulopathies Clinically - anaemia, subcutaneous haematomas, internal haemorrhages, prolonged bleeding from wounds or after surgery Thrombocytopenia, prolonged APTT and OSPT, elevated D-dimer (previously measurement of FDPs was used) –via consumptive coagulopathy – chronic DIC Studies have shown deposition of immunoglobulins, complement and fibrinogen in pulmonary vessels Also causes immune mediated thrombocytopaenia Similar pathophysiology can lead to thrombopathia Parasite releases – or stimulates host to release – factors that modulate blood clotting? Neurological dysfunction Paresis, depression, seizures, spinal pain, behavioural changes, ataxia and loss of vision have been described Associated with aberrant nematode migration or subdural haemorrhage secondary to coagulopathies Why are the signs of A. vasorum so diverse? Adult antigens Cause Type III hypersensitivity (immune complex deposition) Complement activation Immune infiltrate in lungs and other tissues Egg deposition/L1 Pulmonary inflammation/granuloma formation Pulmonary arteriolar vasoconstriction End arteritis and fibrosis of vessels SNAP test Se 95% Sp 94% PCR – on BAL or pharynx swabs Modified Baermann flotation: Pooled faecal samples over a three-day period or repeated sampling increases accuracy

Answer 288

A. Vasorum - management Over recent years products have become licensed Previously no licensed products available in UK Licensed products: Advocate (Bayer), Prinovox (Virbac) spot on - (Imidacloprid and Moxidectin) 2.5mg/kg spot on as a single dose Milquantel (MSD), Milbemax (Elanco), Milbactor (Ceva) – milbemycin oxime and praziquantel 0.5mg/kg milbemax orally Given 4 times at weekly intervals Studies have also used 2 doses a month apart in the pre-patent period Unlicensed products: Fenbendazole – effective but unlicensed used at 25-50mg/kg orally for 7-21 days, some people suggest treating at weekly intervals every 3 weeks for 3 treatments Some clinicians start with a low dose to reduce the complications of acute treatment deterioration from massive worm death and liberation of worm Ag – 20mg/kg orally Levamisole and ivermectin also effective but unlicensed alternative products are equally effective and licensed with fewer potential side effects So how do we treat A. Vasorum? Need to counsel owners about the risks of beginning therapy for Angiostrongylus Considerations for supportive treatment in addition to anthelminthics with infections that have been identified Bronchodilators Aid with airway hyperresponsiveness Corticosteroids May reduce tendency for acute deterioration after beginning anthelminthic therapy Phosphodiesterase inhibitors – for ongoing PH Cage rest and possible oxygen therapy if dyspnoea present Considerations for haematological dyscrasias May be ongoing despite therapy for angiostrongylus

Answer 289

Affected cats present with a cough Allergic airway disease Reactive bronchoconstriction may also result Can have air trapping and severe dyspnoea Expiratory dyspnoea (bronchoconstriction affects expiratory phase more than inspiratory) May auscultate expiratory wheezes Air-trapping: diaphragm flattened, “barrel” chested Minimise stress Provide humidified oxygen (in incubator; oxygen cage) Give IV steroids (e.g. dexamethasone 1 mg/kg) Bronchodilators e.g. Terbutaline (0.01 mg/kg IM or IV) Consider MDI admin. of bronchodilators (salbutamol) Severe, life-threatening distress: Adrenaline (0.1ml of 1:1000 IV or via ET tube)

Answer 290

Salbutamol (VentolinR) (100 mcg/dose) 1 puff bid or as required Effective within 5 minutes, lasts ~ 4 hours. Give as required. Fluticasone (Flixitide) (125 mcg/dose) 2 puffs bid Long term control of inflammation. No systemic effects Takes 10 – 14 days for peak effect

Answer 291

Try and keep cats away from environmental allergens (e.g. soft furnishings, bedrooms, carpeted rooms etc.). Allow cats outdoor access if possible. Avoid very warm, dry environments. Bronchodilators: e.g. Terbutaline (2 agonist) (Oral: 1.25 mg per cat q. 12 hours) Prednisolone: Initial dose 5 mg/cat sid; taper dose once signs controlled. Aim for alternate day medication. A/B rarely indicated.

Answer 292

Pulmonary thromboembolism- Acute onset dyspnoea Few radiographic signs Hypercoagulable states- Trauma/surgery Sepsis/DIC HAC/exogenous corticosteroids HypoT4 IMHA Glomerulonephropathies Pulmonary hypertension

Answer 293

can present open-mouthed/panting/shallow breathing * Hyperthermia/heat stroke/fever * Obesity * Excitement/fear/stress/pain/shock * Parturition/false pregnancy/eclampsia * Anaemia/abnormal haemoglobin * Acidosis * CNS disease * Endocrine dz, e.g. HAC & steroid tx, hypert4 * Neuromuscular disease

Answer 294

is when the dog is overreaching for their intended location f the ataxia is caused by a lesion in the cerebellum, the dog will walk with an exaggerated “goose-stepping” gait

Answer 295

all four limbs effected cerebellar signs normal postural restions normal proprioception spacistity tremours mostly effectis coordination

Answer 296

will show with other vestibular signs- head tilt proprioception will be abnomal if central

Answer 297

upper motor neuron signs- isses with proprioception paresis

Answer 298

mix or cerebellar and vestibular sigs- dysmetric gauite, loss of balence, wide base stance, intention tremour presetns in 1st year o life MRI- sometimes shows cerebellar atrophy post mortem fianl diagnosis autosomal recessive mode of inheratence- do not breed no treatment supportive care and pysiotherapy if animal and owners are coping- prognosis varies depending on clinical signs can repeat mri and neuro exams to monitor progression- mri may not be needed

Answer 299

can cause megaoseophagus and thymoma typically present with severe weakness after only a few minutes of exercise. This weakness might affect all four legs or only affect the back legs. It is frequently preceded by a short stride stiff gait with muscle tremors. effects neuromuscular junction often aqured, can be congenital a simple (though not inexpensive) blood test can be done to check for antibodies against acetylcholine receptors. It is called an AChR test. medical managment- anticholinesterasic agensts- oral or im immunosupressive- prednisolone, ciclosporin( best choice if asp pneumonia form megoesophagus) need intensive nursing- chair to eat Tensilon test: A Tensilon test may be used if MG is suspected, but you are still waiting for antibody test results. This test involves providing an IV medication, and if the dog is MG-positive, then it will temporarily improve their muscle strength gaurded prognosis- espessially with aspiration pneumonia antibosy titers and chest x-rays for moitoring chance for reocurance

Answer 300

with focal forebrain leasions neuro signs will show on the oposite side of the bosy to the leasion they may circle towards the leasion

Answer 301

a type of progressive myoclonic epilepsy that is inherited in an autosomal recessive manner and typically presents in previously healthy adolescents with new onset seizures, which are usually myoclonic, occipital, or generalized tonic-clonic. typical jerking of head- spontanious or triggered may voacalise these progresss to epilepsy treatment is symptomatic- as seasures triggered by light- goggles antiseasire meds not fatal but progressive- blind, ataxia- may require euthanasia LD is unique because of the rapid neurological deterioration of the patients and the appearance in brain and peripheral tissues of insoluble glycogen-like (polyglucosan) inclusions, named Lafora bodies (LBs)

Answer 302

temp- 398-40 resp- 8-18 heartrate- 60-100 mm might be pale

Answer 303

CSF Analysis Imaging- * Radiograph * Myelography * CT scan * MRI * US * Scintigraphy Electrodiagnostic

Answer 304

Suspected inflammatory CNS disease- * Meningitis * Meningo-myelitis * Meningo-encephalitis * Before myelography * Multifocal * Suspected inflammatory CNS disease Infectious * Viral * Bacterial * Protozoal Non infectious * SRMA * MUO SITES: -CISTERNA MAGNA -LUMBAR Contraindications- Raised Intra Crainial Presure Conformation- * Chiari-like malformation * occipital dysplasia Coagulopathy

Answer 305

At the practice: * Cell count * Semi-quantitative protein analysis Specialised lab: colect in edta tubes * Cytology * Protein analysis * PCR * Others

Answer 306

Fracture/ subluxation Infectious Neoplasm Congenital Anomaly

Answer 307

* Intrathecal injection of non-ionic contrast agent Injection- * Cisterna magna * Lumbar (L5-L6-L7 PROS: * cost * visualisation from C1-L7 * dynamic studies CONS: * risks * technical difficulty * limited information Survey radiographs * CSF collection Injection of contrast- * 0.3- 0.5 ml/Kg Lateral/VD/ oblique Views COMPLICATIONS- neurological deterioration * seizures * cardio-respiratory depression

Answer 308

when compared to MRI- soft tissue and bone indows transverse aquisition reconstruction- 2d -3d nonionic iodinated contrast quick x-rays exposure indications- * Spinal trauma (more accurate than radiographs) * Acute head trauma(bone and acute haemorrhage) * Chest and abdomen evaluation * Middle/inner ear (tympanic bullae) * IVDD (CT and/or myelo-CT) Hansen Type I > Type II * Spinal malformations (+/- MRI) * Surgical planning (implants- 3D printing) * When MRI cannot be used (metal in the body)

Answer 309

when compared to ct- better soft tissue details requres anesthesia longer duration more exprensive Sequences: * T2W * T1W * T2* (haemorrhage) * STIR (fat s uppression) * FLAIR (fluid suppression) * T1W + C lanes: Sagittal, Dorsal and Transverse IV paramagnetic agent: Gadolinium Gold standard advanced imaging modality for the nervous system * Brain * Spinal cord * Peripheral nerves

Answer 310

Abnormal head position Weakness and ataxia Seizures Paralysis and paresis Important to remember that ‘normal’ may be different for different species

Answer 311

severe hyperextension of the head and neck leading to an extreme arched pose.

Answer 312

twisting of the neck which leads to a tilted head position, usually used to refer to a rotational movement of the head out of the normal position. One of the most common presentations of neurological disease in NTCAs Most common cause across species = ear disease (peripheral)- Otitis media +/- externa Aural polyps Aural neoplasia Central disease most common in rabbits (E. cuniculi) but can also be due to neoplasia (especially rats) Need to differentiate between peripheral and central disease Peripheral disease – investigation and treatment as per ear disease Central disease: Signalment Neurological examination Serology MRI Cerebrospinal fluid analysis

Answer 313

there are concurrent signs of CNS disease there is horizontal, vertical and rotational nystagmus- fast phase in any direction and changes with head position no facial nerve paralysis no horners syndrome

Answer 314

there are no concurrent signs of CNS disease there is horizontal and rotational nystagmus- fast phase away from leasion and no changes with head position possible facial nerve paralysis possible horners syndrome

Answer 315

Signalment- Younger (infectious) vs older (neoplasia) Species (E. cuniculi in rabbits, pituitary adenoma in rats) Neurological examination- Modified neurological examination has been validated in rabbits For other species standard neurological exam can be performed but interpret with care Serology- Paired titre testing for E. cuniculi (rabbits, rarely guinea pigs), Toxoplasma gondii (ferrets and meerkats, rarely other species) Serology commonly used for E. cuniculi. Always do IgG and IgM wherever possible. IgM indicates recent infection, raises suspicion that CS are due to E. cuniculi. If only IgG preset, then ideally need to demonstrate rising titres. MRI Most useful to look for neoplasia. Not often performed – expense and practical considerations Cerebrospinal fluid analysis Collection very challenging in NTCAs due to size and anatomical differences from dogs and cats. Cytology – generally non-specific inflammatory changes PCR testing for specific diseases (e.g. E. cuniculi, toxoplasma) may be useful

Answer 316

(rabbits, rarely Guinea pigs) Treatment: Fenbendazole licensed in rabbits at 20mg/kg q24h for 28 days. Prevention(?): 20mg/kg q24h for 9 days to prevent E. cuniculi symptoms during times of stress – evidence for this is very weak. Supportive care: Benzodiazepines if stressed, treatment for GI stasis, prophylactic antibiosis?

Answer 317

Treatment: Cabergoline (galastop) - dopamine D2 receptor agonist which inhibits prolactin secretion - has been shown to reduce tumour size in functional pituitary adenomas. Supportive care: Environmental modification (ramps, deep bedding to cushion falls etc.)

Answer 318

Can be seen in the end stage of any disease process (“death posture”) Specific diseases commonly causing opisthotonos: Paramyxoviruses (Newcastle disease in poultry, pigeon paramyxovirus, Ferlavirus in snakes) Arenavirus (inclusion body disease) in snakes Adenovirus in lizards (chameleons and bearded dragons) Thiamine deficiency Do we investigate? Viral disease- Specific PCR’s are available for paramyxoviruses (various species), arenavirus (snakes) and adenovirus (lizards) Remember paramyxoviruses in birds are notifiable! Thiamine deficiency- History – animals being fed previously frozen fish – and clinical signs.

Answer 319

Viral diseases - No treatment available, consider euthanasia. Prevention more important: All: Housing should be destroyed or thoroughly disinfected with a viricidal disinfectant. Arenavirus: Control snake mites Pigeon paramyxovirus: Annual vaccination Newcastle’s disease: Vaccination available but only provides short term immunity.

Answer 320

Treatment: Thiamine supplementation via the food. Prevention: Supplement all marine fish with thiamine when feeding; proper defrosting method; feed freshwater fish rather than marine species; or feed alternative prey (e.g. rodents, but will need to make them smell like fish!)

Answer 321

Any systemic condition Heavy metal toxicity (birds) Nutritional causes: Hypocalcaemia/NSHP (all) Thiamine deficiency (piscivores) Biotin deficiency (egg eating species) Infectious causes: Viral diseases in snakes/lizards Bornavirus (birds) Emergency management should be instigated where animals present collapsed. Warmth- Most collapsed NTCAs will by hypothermic – large surface area to volume ratio Use a variety of methods Reptiles – POTZ Care:hyperthermia and burns. Fluids- Oral rehydration is indicated where animals are able to swallow and where there is no clinical dehydration present. Parenteral fluids (subcutaneous, intravenous, intraosseous, or epicoelomic) indicated for complete collapse and where clinical dehydration is present. Glucose- Only in birds and mammals. Oral if able to swallow, as part of fluid therapy otherwise Calcium- Reptiles, psittacines (AGP), and callitrichids Oral usually sufficient unless the animal is so weak it is unable to swallow, or if seizures or tetany is present, in which case IV administration is recommended General investigations: H&B Imaging (radiographs, ultrasound) There is often a high index of suspicion for the cause of weakness and atxia in NTCAs due to signalment and history. Other diseases can be easily ruled out early on.

Answer 322

Lead and zinc = most common Waterfowl: Spent lead shot, lead fishing weights Psittacines: chewing the bars of galvanised zinc cages, lead curtain weights and lead paint. Presenting signs: Non-specific: Weakness, lethargy, depression, weight loss. GI signs: Anorexia, crop stasis, regurgitation, diarrhoea. Urinary: PU/PD, haematuria, biliverdinuria. Neuro signs: Circling, twitching, sezures Diagnosis: Radiographs: Metal density material in GIT (not always) Haematology: Non-regenerative anaemia, basophilic stippling rarer in birds than other species. Toxicology: Blood lead or zinc levels increased. Treatment aims to remove or chelate the heavy metal, and to support the bird during recovery. Supportive care: Supplemental heat, fluid, nutritional support, anti-seizure medication if necessary. Chelation: Calcium EDTA, Dimercaptosuccinic acid (DMSA), D-Penicillamine all reported. Calcium EDTA preferred, but currently unavailable. All require daily or twice daily injection – can be very stressful. Removal: If metal is visible in the GIT then removal via endoscopy, surgery, or gastric lavage should be attempted. Bulking agents such as psyllium husk have been used in cases where retrieval is not possible to aid passage through the GIT.

Answer 323

Seizures common, particularly with parrots and callitrichids Reptiles tend to become progressively weak. Emergency management as above + analgesia: Opioids: Morphine, methadone, or tramadol in reptiles, buprenorphine in mammals, butorphanol in birds. NSAIDs: Meloxicam. Care re:dehydration and renal disease. If seizures present, considered benzodiazepines. Prognosis is guarded to poor in advanced cases, and euthanasia should be considered. Supportive care- Environmental modification to reduce the risk of falls Fluid and nutritional support Calcium and vitamin D supplementation Analgesia Correct husbandry

Answer 324

Aetiological agent causing proventricular dilatation disease. Clinical signs: Neuro signs: Ataxia, difficulty perching, seizures, blindness, GI signs: Weight loss, crop stasis, regurgitation, proventricular and intestinal dilatation, maldigestion. Birds can be infected with bornavirus and not develop PDD. Diagnosis: Radiographs: Dilation of the proventriculus seen on plain or contrast radiographs RT-PCR: Feather calamus or whole blood. Often used as a screening test, but false negatives can occur. Histopathology: Definitive diagnosis. Performed on crop biopsy ante-mortem, or on post mortem sampling. Characteristic myenteric ganglioneuritis lesions.

Answer 325

There is currently no cure and very few treatment options for PDD Cyclooxygenase-2 Inhibitors Used for anti-inflammatory effects to improve QOL Celocoxib = treatment of choice, meloxicam and robenacoxib have anecdotal evidence supporting their use. Cyclosporin Anecdotally may decrease clinical signs in cases refractory to COX-2 inhibitors Immune suppressant, so prophylactic antibiotic and antifungal treatment recommended. Gabapentin For cases where seizures, ataxia, or feather plucking behaviour are present Adjunctive therapies: Prokinetics e.g. cisapride and metoclopramide Provide high quality, easily digestible diet Antibiotics and antifungals (2o infections common) EFAs Minimise stress – ensure correct husbandry and prevent breeding Vaccination has been shown to be effective experimentally but is not currently available.

Answer 326

Any systemic condition – end stage symptom. Common specific causes of seizures in NTCAs: Lead toxicity Hypoglycaemia Hypocalcaemia Toxin exposure – medications (multiple), Teflon (birds), avocado (birds). Bornavirus (birds) Emergency management is similar to that for weakness and ataxia: Warmth Oxygen administration Fluids +/- glucose Calcium: Especially for known high-risk species (AGP, callitrichids). Give IV to avoid aspiration. Benzodiazepines: Diazepam or midazolam can be administered IV or IM to stop seizure activity. Full history is essential: Husbandry Medications Toxin exposure Appetite Any other clinical signs Haematology and biochemistry Radiographs Ultrasound

Answer 327

At-risk individuals: Any inappetant small mammal or bird Ferrets with insulinoma Treatment consists of glucose administration while the underlying cause of the hypoglycaemia is investigated. Insulinoma (pancreatic B-cell tumour) = second most common neoplasm of ferrets

Answer 328

Diagnosis: Ultrasound: Requires a high definition machine and a skilled operator due to small tumour size in most cases. Histopathology: Definitive diagnosis, but difficult to achieve in practice. Clinical diagnosis: clinical signs of hypoglycaemia, and low blood plasma glucose concentration that responds to glucose administration. Treatment: Surgery: In otherwise healthy individuals where surgical planning via imaging has been possible. Diazoxide: Human drug for insulinoma, reduces insulin secretion. Preferred treatment option. Corticosteroids: increase hepatic gluconeogenesis and decrease glycogenolysis BUT unwanted side effects common Management: Owners are encouraged to train the ferret to allow at home blood glucose monitoring, enabling prompt intervention for hypoglycaemic episodes as they occur.

Answer 329

Examples: Ivermectin in chelonia Fipronil in rabbits Pyrethrins in snakes and lizards Avocado in psittacine Teflon in psittacines Diagnosis based on thorough history taking – need to be aware of potential toxin for that species prior to the consult. Treatment consists of emergency management of the seizures, and removal of the toxin: Wash off e.g. topical antiparaciticides Gastric lavage Administration of adsorbents e.g. activated charcoal Generally not possible to induce vomition in NTCAs

Answer 330

Spinal trauma. Most common reason for paralysis/paresis in all species Especially common in rabbits Other, less common causes: Lead toxicity Marek’s disease (chickens) Botulism (waterfowl)

Answer 331

Most common in chickens; pheasants, turkeys and quail may also be affected. Classic form causes asymmetrical limb paralysis. Other presenting signs: Classic form: Weight loss, pallor, diarrhoea, and anorexia. Acute form: 24-72hr depression/stupor -> death Chronic form: immunosuppression  2o infections Other forms = less common. Diagnosis: Often made post mortem on histopathology. Antemortem diagnosis most often on C/S alone Prognosis is grave and there are no treatment options. Prevention via vaccination, but needs to be done before or just after hatching so rarely done in pet poultry.

Answer 332

Clinical signs occur due to toxin ingestion, which causes ascending flaccid paralysis. Most common in waterfowl, but can also occur in chickens, turkeys and pheasants. Outbreaks tend to occur in stagnant or poorly oxygenated water bodies during warm weather. Diagnosis generally made on history and clinical signs alone. Treatment: Remove source of toxin Supportive care: Fluids, nutritional support (care re:aspiration) Time! Severe cases (respiratory and cardiac symptoms) - euthanasia indicated.

Answer 333

Laminitis can arise in three general situations: Sepsis associated laminitis e.g., diarrhoea, retained placenta, starch overload Endocrinopathic laminitis (MOST COMMON) e.g., pituitary pars intermedia dysfunction, equine metabolic syndrome, excessive pasture consumption Supporting limb laminitis e.g., associated with a fracture or joint sepsis of the contralateral limb.

Answer 334

Tachycardia/ tachypnoea Bilateral forelimb lameness Leaning back on heels Bounding digital pulses Increased hoof wall temperature Pain on hoof testers Palpable depression at the coronary band alt presentation- more thorough lameness assesment required Lying down Non weight bearing on one leg Tied up? Colic? NOT ALWAYS TYPICAL STANCE! key distinguishing features- Reluctance to walk Short, stilted gait at walk Difficulty turning Shifting weight Increased digital pulse

Answer 335

a grading system for laminitis 0- no gait abnomalaties Grade I: Horses shift weight from one foot to the other or incessantly lift feet. Lameness is not evident at a walk, but at the trot horses will have a shortened stride. Grade II: Horses move willingly at a walk and trot but with a noticeably shortened and stabbing stride. A foot can be lifted off the ground without difficulty. Grade III: Horses move reluctantly and resist attempts to lift affected or contralateral feet. Grade IV: Horses express marked reluctance or absolute refusal to move.

Answer 336

Provide analgesia Provide foot support Treat underlying endocrinopathy or primary condition causing sepsis-associated laminitis or SLL NSAID’s – FIRST CHOICE Phenylbutazone 2.2 to 4.4 mg/kg IV or PO BID Flunixin Meglumine 1.1 mg/kg IV or PO BID Suxibuzone 3.1-6.25 mg/kg PO BID Meloxicam 0.6 mg/kg IV/PO BID Acetaminophen (paracetamol) 20-25 mg/kg PO BID If insufficient opiates can be used: Butorphanol Pethidine Morphine In most cases…MULTIMODAL…easier in a hospital setting NSAID + CRI lidocaine/ ketamine/ butorphanol/ a2 agonists This is not enough alone, you must support the foot! mechanical support

Answer 337

Decrease ambulation Transfer load away from the affected laminae Support the sole without causing solar vascular compromise Reduce the moment about the distal interphalangeal joint Reduce tension in the DDFT Several different types Trial and error depending on case Personal preference Cost? Shoe removal? Most important – box rest!! general principle is to provide support to the caudal region of the foot where the horse is naturally ptting pressure to avoid painful toe region reduce mechanical forces on laminae iBOX REST + Deep Bed Increase depth of bedding at least 20cm deep Ensure bedding extends to the door Shavings Sand? Shoe removal?- Yes or no? Standard shoes concentrate loading around the outside of the foot so should be removed. Can induce further mechanical damage Rasp clenches and pull each nail individually Must be on a deep bed/foot supports applied immediately may bevel toe of hoof minimise movement to reduce rotation of laminae frog supports- rolled up bang=dagr or comercial option- comercial better for small horses styrofoam supprot system- doesnt work well in deep bed, confroms to horses foot, desnt compress in small ponies so better in bigger horse equisoft- like styrofome but better for smaller horses Hoof Cast- Stabilise the entire foot Decrease the movement of the hoof capsule Reduce shearing forces on the laminae Ease breakover Acepromazine- Sedative effects Decrease ambulation Therefore reduce mechanical damage to the unstable laminae. Studies describe variable effects of increasing blood flow to the digit- vasodilation- outdated concept however

Answer 338

When? Sepsis associated laminitis Hoof temperature maintained at less than 10deg C for 72hrs Immerse the foot and pastern region in ice and water.

Answer 339

These are CRITICAL at an early stage to assess existing damage and act as a point of reference.

Answer 340

Deep digital flexor tendon tenotomy Paddock soundness- will not return to any sort of athletic ability Treat unresponsive cases Lost potential for future athletic ability Relieves tension on the pedal bone.

Answer 341

Congestive Heart Failure Aortic Thomboembolism Pericardial Effusion Arrhythmias

Answer 342

Increased cardiac filling pressures, causing venous congestion and extravasation of fluids Left/Right Sided Pulmonary oedema Pleural effusion (left/right sided in cats, right sided in dogs) Ascites Peripheral oedema Clinical signs: Tachypnoea/dyspnoea Reduced exercise tolerance Reduced appetite Lethargy Weight loss Abdominal distension Cough?

Answer 343

ESSENTIAL- TFAST/POCUS/etc +/-Thoracocentesis Furosemide Oxygen +/- Sedation BONUS- Blood pressure Biochemistry X-rays B lines = pleural effusion If you have tachypnoea/dyspnoea and left atrial enlargement can assume cardiac and treat accordingly If no improvement consider further tests

Answer 344

Oxygen- Flow by, cage, nasal prongs, etc Sedation- Butorphanol 0.1-0.3mg/kg IM/IV If painful, e.g. ATE cat, methadone 0.2mg/kg IM/IV Furosemide- Mainstay of treatment Loop diuretic 1mg/kg IV or 2mg/kg IM q4h/PRN. Or CRI 0.5-1mg/kg/hr Monitor RR overnight (<40breaths/min. Lower for big dogs?) Thoracocentesis- Diuretics will not fix significant pleural effusion Thoracocentesis is a day one skill, not a referral skill Inspiratory dyspnoea Pimobendan? If poor cardiac output/systolic function PO or IV (very expensive) Care in obstructive disease (cats, aortic stenosis) expensive Radiographs- ONLY IF STABLE After thoracocentesis Assess pulmonary oedema Concurrent disease

Answer 345

Clinical presentation Muffled cardiac sounds Ascites (right heart failure) Weak pulses, pulsus paradoxus Non specific – lethargy, weakness, exercise intolerance May present with acute collapse

Answer 346

Echo/T-Fast- Quick Most specific and sensitive Check for tamponade – right atrial collapse Masses

Answer 347

Pericardiocentesis- - This is the only treatment if there is cardiac tamponade DO NOT GIVE FUROSEMIDE The only exception – mild pericardial effusion in CHF- cats. not treating the pe here, treating the heart faulure do not want to decrease circulating volume Pericardiocentesis- Referral?- justafiable if stable If stable to travel Collapsed? Hypotensive? IV fluid boluses- support preload and cardiac filling IV fluid boluses ECG – ventricular arrhythmias Large bore 14G or 16G catheter with side holes (blade) Scapel blade Lidocaine Extension, 3 way tap Bowl

Answer 348

Devastating complication associated with feline heart disease Most commonly caudal aorta Forelimb less common Acute onset paresis/paralysis Pain Absent/diminished femoral pulses, cold paws, cyanosis Associated with severe heart disease Euthanasia not the wrong option Poor prognosis 55-66% of cats PTS/died during initial 24hrs 6/250 cats alive at 1yr Hypothermia, low heart rate, multiple affected limbs, absent motor function Long recovery period/permanent deficits Recurrence

Answer 349

Attempt to treat for 72hrs? Unlikely to deteriorate after, less likely to need opiates Pain relief Methadone 0.2-0.3mg/kg q4h Buprenorphine inadequate? Concurrent heart disease Furosemide Clopidogrel- 75mg initial dose following thrombus? 18.75mg SID Bitter – gelatin capsule/Easypill/treats etc Superior vs aspirin at preventing recurrence Aspirin- 81mg every 2-3 days If a cat has had a thrombus, prescribe both? Rivaroxaban- Factor Xa inhibitor 2.5mg SID Has been evaluated in combination with clopidogrel – well-tolerated Small study, mix of at-risk cats and cats that had had an ATE Low recurrence rate and no new thromboembolic events in the at-risk group Anti-clotting? Short term Tissue plasminogen activator- Only in peracute cases – dissolve clot Risk of reperfusion injury? Very expensive, limited evidence Low molecular weight heparin - Subcutaneous inj 80-150IU/kg TID-QID

Answer 350

Tachycardia Bradycardia Is the patient’s heart rate appropriate? Regular or irregular? Pulses! Logical approach to ECGs Is there a P for every QRS? Is there a QRS for every P? Regular or irregular? Does the QRS look normal?

Answer 351

Sinus tachycardia Supraventricular tachycardia (SVT) SV premature complexes Atrial fibrillation/flutter VPCs Ventricular tachycardia Sick sinus syndrome Etc…

Answer 352

Ventricular premature complexes - VPCs Short R-R interval - PREMATURE Non-sinus (no P wave) Wide QRS complex Cardiac disease Extracardiac disease Neoplasia (splenic, hepatic) GDV SIRS/Sepsis Toxins Anaemia Trauma Cats – nearly always due to primary cardiac disease

Answer 353

Four or more consecutive VPCs > 160-180bpm Paroxysmal or sustained If sustained and causing reduced cardiac output - EMERGENCY

Answer 354

Lidocaine (2 mg/kg IV bolus – up to 8mg total, then CRI) Care in cats- can evelope neurotoxixity- neuro signs Check electrolytes - potassium Sotalol Amiodarone Electrical cardioversion

Answer 355

High grade second degree atrioventricular block Third degree atrioventricular block Sick sinus syndrome? Persistent atrial standstill Remember to check potassium!

Answer 356

Treatment for underlying disease Hyperkalaemia Chronotropic drugs- terbutaline, theophylline, propantheline Pacemaker- Seldom performed OOH Unstable high grade 2nd or 3rd degree AV block

Answer 357

equine grass sickness Cats – feline dysautonomia Dogs – canine dysautonomia Rabbits – mucoid enteropathy complex Hares – leporine dysautonomia ? Llamas ? Sheep – abomasal emptying disorder

Answer 358

Mortality ~1-2% UK horses annually High risk premises up to 8% mortality More EGS cases in England than Scotland Soil- Loam & sand > chalk High soil N & Ti Low soil Zn & Cr High grass Fe Climate- Increased sun days Increased frost days Lower average maximum temperature Recent cases of EGS on premises Many horses on premises Mechanical droppings removal Soil disturbance Grazing Young horses Native Scottish breeds Stallions vs mares Recent move Recent dietary change Recent stress Recent ivermectin treatment Factors which protect against EGS- High levels of antibodies to Clostridium botulinum type C Co-grazing with ruminants Regular grass cutting Manual removal of droppings Supplementary forage feeding It occurs in three forms: acute, subacute and chronic Acute and subacute are nearly always fatal Approximately 50% of chronic cases can survive with prolonged supportive care. Clinical signs of EGS reflect the degree and distribution on neuronal degeneration AGS – gastric reflux and/or SI distension + secondary LI impaction SAGS – secondary LI impaction CGS – none of above

Answer 359

These reflect the degree and distribution of neuronal degeneration. Acute - Dullness Tachycardia (>60-100bpm) Drooling saliva Mild -> moderate colic Muscle tremors and patchy sweating SI distension and nasogastric reflux due to functional ileus Dehydration +/- Fever Horses external appearance may not reflect disease severity Found in all forms of EGS- Bilateral ptosisis Dry scant faeces covered in inspissated mucus differentials- Other forms of colic Surgical colic Anterior enteritis Inflammatory enteritis Primary ileal impaction Gastric impaction Oesophageal choke Botulism Haemabdomen Hypocalcaemia Equine motor neuron disease Diagnosis based on history & clinical signs, by experienced vets is 98% accurate NB it is NOT 100% accurate Diagnosis of AGS more problematic than for SAGS & CGS Monitor progression of clinical signs over time Only if welfare permits Provide supportive care Repeated gastric reflux, analgesia, IVFT Inappropriate if horse has surgical colic

Answer 360

for equine grass sickness False positives Sedation Some breeds Botulism Very ‘sick’ horses False negatives Excitement (↑sympathetic tone) in a horse with Bilateral ptosis, phenylephrine is put in one of the eyes and if positive the ptosis suspected to be caused by EGS will resolve

Answer 361

Exploratory laparotomy Rule out surgical disorders Not 100% accurate SI inflammatory disease Economic & welfare considerations Microscopic examination of ileal biopsy (Milne et al 2010) 1cm long full thickness Formalin fixed 100% sensitivity & 100% specificity Cryostat 100% sensitivity & 73% specificity Formalin fixed jejunum 100% sensitivity & 73% specificity Time delay Resources Acute & sub-acute EGS is invariably fatal Intensive nursing of chronic cases gives 55% survival

Answer 362

Marked weightloss Dysphagia Rhinitis sicca Diffuse weakness Low head carriage Muscle tremors ‘elephant on a ball’ stance

Answer 363

Nursing care Analgesics (NSAIDs) Omeprazole Antimicrobials- aspiration pneumonia severe rhinitis sicca diarrhoea (metronidazole) Probiotics/prebiotics Appetite stimulants- glucocorticoids, brotizalam, diazepam, cyproheptadine Fluids

Answer 364

Clostridum botulinum type C/D? Studies on this stimulated a UK wide vaccine trial Mycotoxin? Certain fungi produce neurotoxin seasonally Certain climates and pasture Specific aetiology of EGS remains undefined… evidence for votulism theory- EGS -  detection frequency of botulinum in intestines  levels of type C botulinum toxin in intestinal contents & faeces  serum levels of antibodies to botulinum Ag Consistent with some risk factors Botulinum detected in cat food in feline dysautonomia outbreaks

Answer 365

Reluctance to move Weakness Stiffness Lethargy Pigmenturia – 90% of cases Hypothermia Tachycardia + irregular rhythym Pain of varying severity Sudden death!! Caused by acute degeneration in postural and respiratory muscles and sometimes the myocardium. Death can occur from cardiac failure caused either by extensive degeneration of the myocardium or indirectly by asphyxia, which results from diffuse pulmonary oedema caused by congestive heart failure and reduced ventilation that is associated with respiratory muscle necrosis .

Answer 366

Take a history: Recent grazing history Access to sycamore seeds/seedlings Sudden onset of signs Multiple animals affected Time of year Poor weather Clinical examination- Reluctance to move Weakness Stiffness Lethargy Pigmenturia – 90% of cases Hypothermia Tachycardia + irregular rhythym Pain of varying severity Sudden death!! Laboratory findings- Elevated muscle enzymes – CK, AST and LDH Hyperlipidaemia and Hyperglycaemia due to stress, catabolism, impaired lipid metabolism and increased hepatic gluconeogenesis. Pigmenturia – ensure to distinguish from haematuria and haemoglobinuria differentials- Colic Lameness- Arthritis Laminitis Endotoxaemia Neurological disease- Tetanus Botulism Rabies Spinal cord disease Grass sickness Meningitis Haematuria or haemoglobinuria - Trauma Exercise Cystitis Calculi Systemic haemolysis Urethral defects Bladder tumour Renal Haemorrhage PSSM Vit E or selenium deficiency Poisoning- Ionophores Organophosphate insecticides Carbamites Strychnine Immune-mediated myositis Prolonged recumbancy

Answer 367

Chances of survival 50:50!! Treatment must be immediate Horses get progressively worse over 24-48hours, so if caught when sign are mild transport immediately!! 24/7 supportive care needed Aim: Limit further muscle damage Restore circulating volume Correct acid-base and electrolyte disturbances Provide alternative energy substrates to muscle cells Analgesia High volume IV fluids (LRS) Protect the kidney from myoglobin-induced injury and NSAID induced renal effects Correct dehydration and acid-base disturbances. Continue until urine is yellow and horse no longer dehydrated Nutrition- Impaired lipid metabolism and shift from aerobic to anaerobic metabolism therefore focus on carbohydrate energy source: Glucose infusion Carbohydrate rich food little and often – grass, good quality hay, alfalfa Stomach tube if dysphagic Also… Vitamin E 5000IU/day orally Selenium 1mg/day orally Vitamin B2, Vitamin C and carnitine Supportive care- Keep warm and minimize stress NSAIDs Drain bladder Physiotherapy Turn recumbent animals – maintain in sternal prevention- Checking fields carefully for Sycamore leaves and seeds Fencing off areas where Sycamore seeds and leaves have fallen Hoover-up/pick up sycamore seeds off the pasture Turning horses out for shorter periods Provide extra forage (hay or haylage) especially where pasture is poor or grazing is tight Reducing stocking density so there is plenty of good grazing for every horse When a case is seen or suspected: Field mates should be removed from the pasture and blood tested Provision of antioxidants, B vitamins and amino acid supplements may be worthwhile in these cases Unfortunately outbreaks of disease are common. Mortality rates 40%-100% Most horses alive 5days post the start of clinical signs are likely to recover. Can go on to make complete recovery