CMS- Cardiorespiritory and dental and GIT Flashcards

Question

Confirmation of Freedom from Disease form strep. equi

Answer 1

When all clinical signs have resolved & Three negative nasopharyngeal swabs OR negative on bilateral guttural pouch samples (PCR) Clearance testing should commence approximately four weeks after the last clinical signs of strangles have been observed.

Answer 2

Expensive - only perform where high index of suspicion Feline PCR on a conjunctival/nasal swab Chlamydia felis, Calicivirus, herpesvirus, M. felis, B. bronchiseptica Canine PCR on a swab Adenovirus, parainfluenza virus, herpes virus, distemper virus, B. bronchiseptica, Mycoplasma spp. Small Mammals B. bronchiseptica PCR and culture; Guinea pigs and rabbits. Rabbits – B. bronchiseptica, P. multocida, Chlamydia spp. Reptiles Tortoises – herpesvirus, Mycoplasma spp, picornavirus; PCR on a swab. Snakes - Adenovirus, Reovirus, Arenavirus, Paramyxovirus/Ferlavirus, Nidovirus; PCR and EDTA blood sample. Chlamydia psittaci

Answer 3

Can sometimes be done conscious with the head directed towards the floor. Otherwise do under GA – protect the airway!!! Collect material into a sterile kidney dish for cytology and culture (bacterial, fungal) Can be therapeutic e.g. with disinfectant or to flush out a FB.

Answer 4

Not as useful for sample collection as a nasal flush. Deep swab better sensitivity – around the level of the medial canthus of the eye in rabbits. Generally done under deep sedation or GA to get deep enough sample.

Answer 5

Poorly sensitive for nasal passage and sinus changes; often subtle. Useful to assess dental disease

Answer 6

Cross-sectional images avoid superimposition of structures  much better assessment of the nasal cavities and sinuses. Useful for SOL where and endoscpe cannot be passed. Necessary for surgical planning e.g. for neoplasia. Requires GA

Answer 7

Can use a rigid endoscope; flexible preferred for pharyngoscomy. Requires deep plane of GA. May ned to flush nasal passages first to facilitate visualisation. Risk of haemorrhage. Uses: Visualize masses, fungal plaques, foreign bodies Biopsy Sample for fungal culture May be therapeutic: Removal of foreign body or polyp Aspergilloma debulking Targeted flushing with treatment e.g. antifungal.

Answer 8

Usually done as extension of rhinoscopy. Flexible endoscope retroflexed behind the soft palate for inspection of the caudal nasopharynx. Uses: Evaluate length of soft palate. Look above soft palate for mass, polyp, foreign body, stenosis etc.

Answer 9

Can be dramatic. Emergency management: Reduce BP - cage rest, sedation Reduce bleeding - ice packs on, packing of the nose with adrenaline soaked sponges. Ongoing management Severe cases may require treatment for hypovolaemic shock or even blood transfusion Need to identify and treat underlying disease Common underlying causes: Coagulopathy Invasive nasal diseases, eg Aspergillosis, neoplasia  blood vessel rupture. Trauma e.g. FB, penetrating I jury

Answer 10

Dogs: See Canine infectious respiratory disease lecture Cats: Calicvirus and herpesvirus Tortoises: Herpesvirus Snakes: adenoviruses, herpesviruses, ranaviruses, iridioviruses, reovirus and picornaviruses. Ferrets: Influenza Some have a very poor prognosis e.g. snake viral diseases. Usually rely on the immune system clearing the infection May  lifelong carrier status (calicivirus, herpesvirus etc.) treatment- Supportive treatment: Anti-inflammatory drugs (NSAIDs most common) Nebulisation (F10, saline, mucolytics) Mucolytic (e.g. Bromhexine) Fluid therapy Supportive feeding Specific treatment: Feline herpesviruses – ocular topical preparations (human preparations off license) or systemic (famiciclovir or feline omega interferon) reported Chelonia – acyclovir reported for use in herpesvirus infection

Answer 11

Primary bacterial disease = rare: Bordetella bronchiseptica (Dogs, cats, G. pigs) Pasteurella multocida (rabbits) Mycoplasma spp. (birds, chelonia, rats) Chlamydia (birds, cats) Also commensals; require a stressor to induce disease. Also common as 2o infections Treatment: Systemic antibiosis TMPS, tetracyclines and fluorquinolones all effective against P. multocida and B. bronchiseptica. Chlamydia and mycoplasma have no cell wall so tetracyclines and fluoroquinolones indicated. Systemic mucolytics (bromhexidine) Anti-inflammatory drugs (NSAIDs most common) penicilin and cyclosporins effective against pasturella- but mainly a pathogen of rabbits and these antibiotics caise dibiosis in rabbits Supportive care: Nebulisation Saline and/or mucolytics (e.g. acetylcysteine) to aid removal of exudate. Antiseptics e.g. F10 Assisted feeding (rabbits, G. pigs) Fluid therapy Prevention of primary bacterial disease Vaccination: B. bronchiseptica - dogs and cats, intranasal administration. P. multocida – rabbits (commercial situations) Reduces symptoms but doesn’t prevent disease. Reduce stressors Bacterial infection usually 2o to underlying pathology: Viral or fungal infection Dental disease (esp rabbits) Foreign body Neoplasia Trauma Hypovitaminosis A- birds Treatment: As for primary disease Treat underlying condition

Answer 12

Aspergillosis most common by far in the UK. Dogs = usually immunocompetent (cf disseminated aspergillosis), birds = usually an underlying condition Forms granulomas in the nasal cavity (dogs), syrinx (birds) and lower airways. Granuloma debulking essential to success of treatment – often done at time of rhinoscopy. Topical treatment: Irrigation post-debulking +/- nebulisation with antifungal agents. Antifungals - Amphotericin B, terbinafine, azoles (clotrimazole, enilconazole) F10 Systemic treatment: Azoles (itraconazole, voriconazole, ketoconazole) Amphotericin B Terbinafine Supportive care: Treat 2o infections Liver support (SAMe and silybin) GI support (diet, probiotics) Monitoring Bloods (hepatic enzymes, WBC count)

Answer 13

Topical treatment: Irrigation post-debulking +/- nebulisation with antifungal agents. Antifungals - Amphotericin B, terbinafine, azoles (clotrimazole, enilconazole) F10 Systemic treatment: Azoles (itraconazole, voriconazole, ketoconazole) Amphotericin B Terbinafine Supportive care: Treat 2o infections Liver support (SAMe and silybin) GI support (diet, probiotics) Monitoring Bloods (hepatic enzymes, WBC count)

Answer 14

Common FB: Cats: Grass blades Dogs: Grass seeds, stones? Small mammals and chelonia: Hay Primary treatment = removal. Tx of 2o infections Systemic anti-inflammatory (NSAIDs)

Answer 15

Pharyngeal trauma e.g. stick injury External trauma e.g. bite wounds to muzzle Symptomatic treatment: Removal of stick if present - will require GA if penetrating. Analgesia Tx 2o infections

Answer 16

Rare in dogs; result of chronic inflammation  hyperplasia. Common in cats Benign masses arising from the lining of the middle ear. Can extend up into the external ear canal or down into the nasopharynx. Removed via traction in the first instance. Surgical access – Incision through the mid-line of the soft palate (avoiding the distal 5 mm) or bulla osteotomy.

Answer 17

Adenocarcinoma = most common. Other epithelial tumours (carcinoma, squamous cell carcinoma) also relatively common. Radiotherapy = treatment of choice Surgical resection/reduction and chemotherapy reported, may be suitable for some cases. Median survival time 10-18 months

Answer 18

Radiographs = poorly sensitive; possibly useful for mass or FB; best without ET tube CT = better sensitivity, may be used to assess airway lumen. MRI = useful for soft tissue lesions  airway narrowing.

Answer 19

May be due to infection (e.g. KC complex), irritation (e.g. smoke inhalation), trauma etc. Treatment usually symptomatic: Anti-inflammatory drugs (NSAIDs for mild cases, steroids for severe). Treat any underlying infection where possible. In very severe cases, inflammation may  laryngeal oedema and complete or partial obstruction. Oxygen supplementation, sedation, or GA with intubation or tracheotomy may be required.

Answer 20

Most useful test in most cases. Larynx evaluated for: Normal function (bilateral abduction during inspiration) Thickening Masses associated with arytenoids or vocal folds Presence of everted laryngeal saccules Extraluminal masses compressing airway Laryngeal collapse

Answer 21

Internal (e.g. from FB) or external (e.g. bite wound, choke chain injury). Commonly  partial or complete obstruction due to oedema. Need to check for cartilage fractures Complications: Laryngeal paralysis or collapse. Fibrotic and granulomatous tissue secondary to severe or chronic damage  stenosis.

Answer 22

Less common than nasopharyngeal or tracheal. May -> complete or partial obstruction, or just irritation. Treatment: Removal and anti-inflammatory drugs, treatment of 2o infections. In acute obstruction tracheostomy may be indicated – see later frequently present as emergancies etih as inncident took place or after tissus have swolen and obstruction has occured Emergency treatment: Oxygen administration. Sedation/anesthesia. Intubation/tracheostomy Corticosteroids to reduce oedema Antibiotics (if infected) Surgical treatment: To repair severe soft tissue damage, including removing foreign bodies e.g. penetrating stick injuries. To repair discontinuous laryngeal cartilage fractures (high risk of granulation tissue  stenosis) To manage 2o laryngeal paralysis

Answer 23

common in older dogs roaring noise Failure of arytenoid and vocal fold movement during the respiratory cycle, particularly decreased or absent abduction during inspiration. Result of: Intrinsic laryngeal muscle innervation disease or damage. Disease or injury of the dorsal crico arytenoid muscles or the arytenoid cartilages. Generalised neuropathy (cats) usually ideopathic The rima is progressively obscured by the collapsing corniculate (upper arrows) and cuneiform (lower arrows) processes of the arytenoid cartilages. The epiglottis may also collapse towards the rima. Symptoms: Inspiratory stridor (“roaring”, dysphonia (altered bark), and exercise intolerance most common symptoms. Cyanosis and collapse in severe cases. Dysphagia also reported. Diagnosis Clinical signs, signalment, laryngoscopy

Answer 24

Emergency management: As per trauma Medical management: Anti-inflammatory drugs (NSAIDs in mild cases, steroids in severe) Rarely successful Surgical management: Laryngoplasty (“tie back”) Laryngoplasty (“tie back”) Surgical abduction of the arytenoid cartilage -. enlargement of the rima glottidis . Unilateral generally provide sufficient increase in glottis diameter to reduce symptoms. May be performed bilaterally if needed but increases risk of aspiration.

Answer 25

Rare Advanced imaging, biopsy and histopathology required for diagnosis. Benign masses may be removed (care re:larynx function); malignant masses may be managed surgically, or via radiotherapy or chemotherapy depending on type.

Answer 26

Neck radiographs used to evaluate for tracheal collapse, foreign body, hypoplasia,and stenosis. Thoracic radiographs help rule out pulmonary or cardiac disease. CT more sensitive for structural abnormalities, masses etc.

Answer 27

Useful in evaluating tracheal collapse. Shows real time changes in tracheal diameter. Can be done conscious (observation of dynamic changes as the dog breaths or coughs) or under GA (negative pressure applied to the ET tube)

Answer 28

Used for: Evaluating dynamic disease e.g. tracheal collapse. Diagnosis of extraluminal or intraluminal masses. Diagnosis and removal of foreign bodies. Obtaining cytology and biopsy samples. Endoscope usually passed through ET tube to maintain airway patency under GA.

Answer 29

Small volume of sterile saline instilled into trachea then re-aspirated. Samples can be used for cytology, culture, and to identify parasitic organisms. May be performed via the oral cavity under GA, either blind or via endoscopic visualisation. Conscious technique also described. or Small volume of sterile saline instilled into trachea then re-aspirated. Samples can be used for cytology, culture, and to identify parasitic organisms. May be performed via the oral cavity under GA, either blind or via endoscopic visualisation. Conscious technique also described.

Answer 30

As per laryngitis; due to infection, irritation, trauma etc. Treatment usually symptomatic: Anti-inflammatory drugs (NSAIDs for mild cases, steroids for severe). Treat any underlying infection where possible. Small FB can  irritation without obstruction and may require removal.

Answer 31

Can be complete or partial obstruction. Common in small psittacines e.g. cockatiels (millet seeds) Can be very dramatic e.g. dogs and rubber balls! Treatment: Removal and anti-inflammatory drugs, treatment of 2o infections. In acute obstruction tracheostomy (mammals) or air sac tube (birds) may be indicated.

Answer 32

Internal (e.g. from FB or inappropriate ET tube use) or external (e.g. bite wound, choke chain injury). All cervical bite wounds should be assessed for airway damage. Penetrating injuries: Require surgical repair Minor injuries – debridement, primary closure +/- fasciomuscular repair. Major injuries (non-viable tissue or excessive size) – tracheal resection and anastomosis. Iatrogenic tracheal tears and pressure necrosis: Usually from ET tube cuff overinflation and/or excessive repositioning without disconnecting GA circuits during procedures. May resolve with strict cage rest (esp cats). Surgery may be primary closure (tears) or anastomosis (necrosis) Supportive care: Analgesia, antibiosis if needed, airway maintenance. Tracheal stenosis = common sequale, esp for anastomosis.

Answer 33

Usually secondary to injury (iatrogenic, traumatic) or neoplasia, rarely congenital. Initial treatment = symptomatic (oxygen, anxiolytics) Mild cases: Dilation with balloon catheter or bougie under endoscopic of fluoroscopic guidance. High risk of recurrence Stent placement Used to retain opening of stenotic area and for palliative management of malignancies Placed under fluoroscopic guidance. Antitussives (e.g. butorphanol) Same procedures in tracheal collapse Surgical resection and anastomosis As for trauma Low dose pred may help prevent stricture formation following surgery.

Answer 34

In dogs can be acquired or congenital. Due to chondrodystrophy  collapse of the tracheal cartilage rings. Toy breeds esp Yorkshire terriers predisposed. Note: Also occurs in horses (Shetland ponies and mini-horses predisposed); Can be 1o or 2o, very rare.

Answer 35

Emergency management: Place animal in a cool, dark environment Supplemental oxygen Light sedation to reduce stress Cough suppression Corticosteroid Symptomatic treatment and management: Exercise restriction Maintain (or obtain!) good BCS Harness instead of collar and lead Treat concurrent respiratory disease. Remove respiratory irritants (e.g. cigarette smoke) Sedatives in stressful circumstances Conservative management: Coticosteroids- long term needs tapering Antitussives Antisecretory drugs Bronchodilators Antibiotics if indicated Surgical management: Extraluminal propylene ring prostheses. Intraluminal stent placement – see prev

Answer 36

Pathogenesis: Abnormal respiratory anatomy due to shortened faces and reduced skull size without proportional reduction of soft tissues. Features of BOAS: Stenotic nares and nasal passages Overlong soft palate Laryngeal saccule eversion +/- ccollapse Tracheal hypoplasia Acute collapse may occur, especially in hot weather. Emergency management: Supplemental oxygen Sedation Corticosteroids Emergency intubation or tracheostomy Cool, dark environment +/- active cooling if hyperthermic.

Answer 37

Management Weight management Avoid walks at hot times of day. Anti-inflammatory drugs may be used to control airway oedema and maintain patency. Management of GI signs (thought to be induced by constant aerophagia) Surgery Indicated in all cases where CS persist despite medical management, and any animal presenting with acute respiratory distress as a direct result of BOAS. Variety of procedures which can be performed in isolation or combination, depending on the individual presentation. Correction of stenotic nares Resection of aberrant turbinates Soft palate resection Laryngeal sacculectomy Laryngeal tie-back Prevention – this is an entirely human made problem! Breed for respiratory function: The Kennel Club/ University of Cambridge RFG Scheme was introduced in January 2019 Grades BOAS severity to guide breeding choices- 0 to 3. Validated in the Bulldog, French bulldog and Pug so far Consists of a clinical assessment of the upper airway with an exercise stress test. Dogs must be over 1 year of age prior to assessment; results are valid for 2 years then reassessment required. No analogous scheme currently for cats.

Answer 38

immune state- what are they vaccinated agianst? how are they vaccinated, collostrum managment housing- housed togther? quality of housing? housing system age of calves? timeline- onset, progression conclusion history of disease changes in behaviour managment- dry cow, partuition and post- partum

Answer 39

post mortem dead calves asses sickly live animals asses non diseased animals calf factors= respiritory defences assess housing- bedding, ventilation, clenliness, size, shared housing, maixed age groups?

Answer 40

were they bought in? raised on farm? relationship farmer has with suppliers? biosecurity measures for cows that are bought in? housing managment age timeline of disease

Answer 41

Blood pressure Blood tests- Haematology/biochemistry Cardiac biomarkers Electrocardiography (ECG) Ultrasonography (focused/emergency thoracic ultrasound, echocardiography) Radiography

Answer 42

Assess cardiac output Hypotension (particularly in DCM) Hypertension (cats, MMVD) (Be aware of stress/white coat effect) Therapeutic considerations Antihypertensives Risks/contraindications e.g. ACEIs in hypotension Doppler/Oscillometric/Invasive

Answer 43

Haematology/Biochemistry Not directly useful in evaluating cardiac disease Systemic conditions Therapeutic considerations Renal values/electrolytes

Answer 44

Cardiac Biomarkers NT-proBNP Troponin Aims Screening Differentiating cardiac v respiratory Prognostication Less useful for Staging Assessing cardiac function Diagnosing specific disease

Answer 45

Evaluate cardiac stretch Natriuretic peptides synthesised by the brain (BNP), heart (ANP) and other organs (CNP). Release stimulated by atrial/ventricular stretch Two major pathways of effects: Vasodilatory – reduce BP Renal - natriuresis and diuresis (Actions generally oppose those of RAAS) Can measure concentrations of N-terminal portions (NT-proANP/BNP) BNP used more often, commercial assays available Increase with severity of disease Elevated values associated with worse outcome Can be assessed quantitatively or qualitatively

Answer 46

Quantitative – numerical value External lab – useful for screening, not emergencies In house quantitative machines also available (Woodley Vcheck) Cats: <100pmol/L – not compatible with increased myocardial stretch/stress >100pmol/L – increased stretch/stress, further investigations indicated >270pmol/L – respiratory signs are likely secondary to CHF Dogs: <900pmol/L – not compatible with increased myocardial stretch/stress 900-1800pmol/L – increased stretch/stress, further investigations indicated >1500pmol/L in MMVD – increased risk of CHF in the next 12 months >1800pmol/L – likely to have clinical signs of heart disease Breed variation Dobermans >735pmol/L – increased risk of DCM Labrador up to 2000pmol/L may be normal

Answer 47

Qualitative – positive/negative Use: Differentiating cardiac from respiratory disease in dyspnoeic patients Good for emergencies Especially if unable to image Idexx Feline ProBNP snap 99.5% accuracy for >100pmol/L 95% accuracy for >270pmol/L

Answer 48

Troponin complex involved in actin-myosin interaction (C, T and I subunits) Troponin-I (cTnI) is normally bound to troponin-T, detaches in response to sarcomeric injury Elevated circulating cTnI is a specific indicator of myocardial injury/hypoxia or cellular necrosis Increases with severity of disease Elevated values associated with worse outcome/prognosis Extremely high values seen in myocarditis, sustained ventricular arrhythmias Day to day utility – unclear Limited use in myxomatous mitral valve disease, congenital disease Of some use in patient with unusual presentation Dilated phenotype in a non-typical breed (or in a cat) Hypertrophic phenotype in a young cat May suggest acute inflammatory process

Answer 49

Arrhythmias Physical exam critical Remember arrhythmias can be present in non-cardiac disease, especially in dogs Also preclinical disease, especially dobermanns, boxers

Answer 50

Ultrasound is the gold standard test for diagnosing cardiac disease Thoracic ultrasound (TFAST/POCUS) Emergency Dyspnoeic patients Differentiate cardiac from respiratory conditions Left atrial enlargement Identify pleural effusion, pericardial effusion, B-lines? Measurements? Subjective? Ultrasound is the gold standard test for diagnosing cardiac disease Thoracic ultrasound (TFAST/POCUS) Emergency Dyspnoeic patients Differentiate cardiac from respiratory conditions Left atrial enlargement Identify pleural effusion, pericardial effusion, B-lines? Measurements? Subjective?

Answer 51

Aims Presence of CHF Cardiomegaly/staging Concurrent disease Cough Less useful for: Risk of impending CHF Cardiac function Diagnosing specific disease Looking for CHF Stabilise! In emergencies ultrasound better If uncertain but unstable trial medication? Sedation MMVD patients are usually safe to sedate/anaesthetise Usually have good cardiac output/blood pressure/systolic function Cats, patients with DCM Ideally assess function Butorphanol 0.1-0.3mg/kg IM,IV Alfaxalone/propofol Cardiomegaly/staging Very useful if echocardiography not available Subjective/objective Vertebral heart score (VHS) Vertebral left atrial score (VLAS)

Answer 52

Objective assessment of LA size Draw from the centre of the ventral aspect of the carina to the most caudal aspect of the LA Measure the length of this line in vertebral body units, starting at T4

Answer 53

28-44 (lower end for athletes)

Answer 54

MOST ARE NORMAL Physiological, due to high Parasympathetic (VAGAL) tone Atrioventricular Block Sinus arrhythmia Sinus bradycardia Siniatrial Block Sinoatrial Arrest Abolished with increased sympathetic tone- light exersise, slight stress profound cases ARE abnormal

Answer 55

ABNORMAL Pathological Supraventricular or Ventricular- Premature depolarisations Tachycardia Fibrillation Inflammatory, degenerative, metabolic, toxic aetiologies

Answer 56

s1- lub- start of systoly, av valves- qrs s2- dub- end of systole, sl valves closing- t s-3 very small squeek sound- ventricles recoiling s4- contraction of the atria- comes in just before s1- p

Answer 57

regularly ireegular heart rhythm 1)second degree AV block- blocked p waves without qrst complex p-p interval is the same- san firing fine but avn not transmiting to ventricles 2)The most common physiological dysrhythmia of horses 40% of horses have 20-AV block on 24-hour ECG monitor 3)Long pauses (SA block/arrest) and variation in length of diastole (Sinus bradycardia and sinus arrhythmia) are less common, but can all occur in normal horses When is it not normal? If present during exercise (not abolished by inc. sympathetic tone) Advanced 20-AV block - RARE - Pathological process creating conduction block at AV node - Horse will demonstrated exercise intolerance or collapse Pathological heart blocks are usually associated with inflammatory or degenerative changes at the AV node

Answer 58

ventricles not contracting with signals from san avn will fore them independantly every 20 seconds or so will show on ECG as random qrs complexes independent of P waves AV-dissociation: Rapid SA discharge (due to reduced cardiac output) Slower rate of Ventricular ‘escape’ complexes (approx. 20/min) Horses present with severe exercise intolerance and frequent collapse Treatment Anti-dysrhythmic medication – used with caution (with 24-hour ECG monitoring) Anti-inflammatories (dexamethasone 0.1 – 0.2 mg/kg IV) if evidence of inflammatory cause Definitive long-term therapy - Placement of Pace-maker

Answer 59

Tachydysrhythmias- Pathological Supraventricular or Ventricular Premature depolarisations Tachycardia Fibrillation Inflammatory, degenerative, metabolic, toxic aetiologies Supraventricular (SVPD)- supraventricular premature depolarisation Originate in atria - signal came form somewhere separate to SA node Usually conducted through AV- normal QRS complex seen on ECG Isolated SVPD at rest not uncommon eloctrolite imbalence post exersisse seen as a normal qrs without p wave that interups regular interval- shows they are atrail in nature Ventricular (VPC)= ventricular premature complex Originate in ventricles- follows different pathway through heart Abnormal QRS complexes- different to surrounding ones Isolated VPCs can occur at rest, during exercise or in the immediate recovery phase post-exercise Frequent VPCs, or ‘runs’ of VPCs are abnormal

Answer 60

1) Atrial Fibrillation- most common 2) ecg- irrecular intervals between qrst complex with no p waves and varience on baseline. the atria are fibrilating creating F waves (bumpy apearence of base line) atrail contraction into ventricles is lost and so cardiac output slightly reuced- ventricular contraction good but irregular

Answer 61

1) Atrial Fibrillation- most common 2) ecg- irrecular intervals between qrst complex with no p waves and varience on baseline. the atria are fibrilating creating F waves (bumpy apearence of base line) atrail contraction into ventricles is lost and so cardiac output slightly reuced- ventricular contraction good but irregular Lone (primary) AF Horses are predisposed to AF due to; High resting vagal tone Large atrial mass In combination with any of the following; Shortening of the effective refractory period Atrial inhomogeneity Presence of SVPDs 0.3% Prevalence in Thoroughbred racehorses Clinical Signs of Lone AF- Reduced athletic performance Prolonged respiratory recovery after exercise Normal resting HR Low grade cough Typical findings on auscultation Irregularly irregular rhythm, absence of S4 Sustained AF Persistent AF which presents at rest and during exercise Paroxysmal AF Sudden and transient AF that spontaneously reverts to normal sinus rhythm when not exersising- hard to diagnose- in exersise ecg

Answer 62

Usually occurs during strenuous exercise Will revert to normal within 24-48 hours post-exercise Diagnosis Definitive = resting ECG recording at time of paroxysm Post-reversion; Exercising ECG 24hr Holter ECG Frequent SVPDs at rest, or during exercise provides supportive evidence for AF

Answer 63

AF that occurs as a consequence of underlying structural cardiac disease; Mitral Valve insufficiency ->Left atrial enlargement-> increases capacity of electrical signals Primary myocardial disease Clinical Signs More profound exercise intolerance Resting tachycardia Other signs of heart disease – loud cardiac murmurs Structural remodelling of myocardium and inability to treat underlying condition means AF will be permanent

Answer 64

Horses with sustained, uncomplicated lone AF may be candidates for conversion to sinus rhythm. Success of cardioversion will depend on; Duration of AF- Prolonged AF -> Structural and electrical remodelling of atria Horses with AF > 4months have significantly higher rate of recurrence Presence of underlying disease: Horses with existing cardiac disease are poor candidates for conversion, evidenced by; Resting HR > 60bpm Loud cardiac murmurs (significant regurgitation) Structural changes on echocardiography Only ever done in hospital environment with continual ECG monitoring Quinidine - Prolongs the effective refractory period Given orally (via NGT) @ 22mg/kg every 2hrs for max 4 doses Conversely can be Proarrhythmic (severe tachycardia) Severe GIT, respiratory and neurological complications can occur- colic common Electrocardioversion- Transvenous cardiac electrodes placed across atria, prior to defibrillation under GA Only available in a couple referral centres in UK electrode plcaed via jugular vein shock administered as ventricles depolarising- r wave if delivered at any other time horse may be killed

Answer 65

Horses with - prolonged, sustained AF - mild underlying heart disease - refractory AF Can be successfully managed Require regular exercising-ECG recordings Absence of frequent or sequential premature depolarisations Evidence of regularity of R-R interval during exercise Level of exercise dictated by maximal HR achievable – often moderate Severe cases should be retired. regular ecgs every 6-12 months. check for ventricular changes

Answer 66

Physiological regurgitation- Some degree of regurgitation can be found in horses with normal valves, or in horses without murmurs Atrioventricular regurgitation is recognised in fit athletic TBs No association with racing performance Pathological regurgitation- Congenital - valvular dysplasia Degenerative - endocardiosis Inflammatory/infectious- endocarditis Idiopathic

Answer 67

diastolic murmenrs will completely cover over other heart sounds and murmer will be there fro most of the cycle systolic murmers will be shorter

Answer 68

Examination- Historic or clinical indicators of cardiovascular insufficiency Murmur characteristics – localisation Echocardiography- When to investigate? Valves – Position, shape, movement Regurgitant jet – Doppler; size, direction & velocity (severity of regurgitation) Cardiac structure – Chamber size; evidence of compensatory change. Electrocardiography- Investigate for the presence of any concurrent dysrhythmias

Answer 69

diastolic Most common – high prevalence (5-8%) Common in middle age Usually degenerative form blood leaks into ventricles and usually dosent effect horse too badly Assessing severity: Loudness of murmur Quality of arterial pulse - Hyperkinetic pulses- cardiac output increased due to increased blood in ventricles Monitor progression with serial echocardiography If no structural change – good prognosis for general riding, may need to be retired at wors Poor prognosis; Compensatory left ventricular overload Higher risk of ventricular dysrhythmias

Answer 70

Second most common regurgitation Prevalence of 2.9 – 3.5%. Higher in Thoroughbreds Most likely form of valve regurgitation to lead to congestive heart failure Due to pulmonary hypertension (increased atrial pressure) Also risk factor for AF Investigate if - higher grade murmur - loud 3rd heart sound - in high level exercise

Answer 71

Most common congenital cardiac defect in horses Common in Welsh mountain ponies Defect (‘Hole’) is normally in membranous portion of septum Blood flows from left  right Loud & course pansystolic murmur audible on right side (4th ICS) Also often a murmur audible on left side associated with increased flow out of pulmonary artery louder murmer indicates smaller hole and therefore better prognosis Prognosis Depends on size and position of defect Horses with small defects can have successful athletic careers Poor prognosis associated with; Larger defects; As measured on echocardiography Evidence of right ventricular overload Reduced velocity of shunt flow Increasing pressure in right ventricle

Answer 72

Dysrythmias 2nd-degree AV block is very common and completely normal at rest Atrial Fibrillation is the most common dysrhythmia in horses and will affect athletic performance Dysrhythmias should be thoroughly assessed in any active horse Murmurs Aortic and mitral regurgitation are relatively common Often exist in normal horses, functioning at high athletic ability Mitral regurgitation more likely to cause significant secondary changes Loud murmurs, progressive murmurs or murmurs associated with clinical signs should definitely be investigation

Answer 73

A- At risk (e.g. CKCS, chihuahua, etc) B1- Degenerative mitral valve changes present, normal LA and LV dimensions B2- Degenerative mitral valve changes present, LA and LV dilation C- Congestive heart failure (past or present) D- Congestive heart failure refractory to standard therapy

Answer 74

A- At risk (e.g. CKCS, chihuahua, etc) B1- Subclinical – normal left atrium/mild enlargement B2- Subclinical – moderate/severe atrial enlargement (i.e. increased risk of CHF/thromboembolic disease) C- Congestive heart failure (past or present) D- Congestive heart failure refractory to standard therapy

Answer 75

A- At risk (e.g. CKCS, chihuahua, etc) B-Occult DCM – morphological or electrical changes. No evidence of CHF but may experience syncope B1- Electrical abnormalities (suspected to be due to DCM) B2- Left ventricular systolic dysfunction +/- chamber enlargement +/- electrical abnormalities C- Congestive heart failure (past or present) D- Congestive heart failure refractory to standard therapy

Answer 76

Pimobendan- Phosphodiesterase III inhibitor, calcium sensitiser "Dual-action inodilation" Improved inotropy (muscle contraction) and vasodilation Improved cardiac output Delays onset of clinical disease (MMVD, DCM) Improves survival (MMVD, DCM) DCM – PROTECT study (2012) MMVD – EPIC study (2016) Pimobendan group had longer time to endpoint Pimobendan also improved survival Pimobendan Stage B2 DCM/MMVD 0.1-0.3mg/kg BID anecdotally used TID in advanced CHF (off label) One hour before food/empty stomach Food decreases bioavailability Rapid peak effect Pimobendan What about cats? Limited evidence supporting a clear benefit Consider in CHF Be careful in patients with obstructive cardiomyopathy

Answer 77

given in Stage B2 DCM/MMVD 0.1-0.3mg/kg BID anecdotally used TID in advanced CHF (off label) One hour before food/empty stomach Food decreases bioavailability Rapid peak effect Pimobendan What about cats? Limited evidence supporting a clear benefit Consider in CHF Be careful in patients with obstructive cardiomyopathy

Answer 78

Stage B2 Spontaneous echo contrast (smoke) Increased left atrial size Reduced left atrial function Clopidogrel 18.75mg SID NB: very bitter Aspirin 81mg every 2-3 days Rivaroxaban 2.5mg SID

Answer 79

Largely same for dogs and cats Control congestion (backwards failure): diuretics Improve output (forwards failure): pimobendan Suppress RAAS: ACE Inhibitors/spironolactone

Answer 80

Loop diuretics (ascending loop of Henle): Furosemide Torasemide- good for patients with right sided heart faliure due to higher bioavailability than furosemide Thiazides (distal convoluted tubule): Hydrochlorthiazide Potassium-sparing (collecting duct): Spironolactone Amiloride Diuretics Most important part of CHF therapy Furosemide – first line? Start around 1-2mg/kg BID (can give TID) Maximum total dose around 12mg/kg/day (8mg/kg/day helpful cutoff for refractory/stage D?)

Answer 81

Short duration of action Long term tolerance (diuretic resistance) Not completely absorbed (~50%)

Answer 82

Long duration of action (SID dosing) Reduced likelihood of resistance? High bioavailability (~100%) good for patients with right sided heart faliure due to higher bioavailability than furosemide First line vs refractory Personal choice? Upcard: licensed product, about 20x more potent than furosemide transition from furosomide once refractory Torasemide transition 1/20 of the total furosemide daily dose e.g. if a dog is receiving 20mg BID (i.e. 40mg/day), the equivalent dose is 2mg/day 0.1-0.6mg/kg SID

Answer 83

Aldosterone antagonists- spironolactone ACE Inhibitors-benazepril etc Angiotencin receptor blockers RBs-telmisartan(somitra)- no cardiac license but licenced for renal disease

Answer 84

ACE Inhibitors Benazepril most common in UK Enalapril, ramipril, etc Long history of use, limited evidence base? Theoretical benefit in opposing RAAS Combined with spironolactone (Aldosterone antagonists)_ (Cardalis) May reduce the rate of CHF progression May reduce LA pressure Risks: Decreases systemic blood pressure Decreases the GFR Can cause hyperkalaemia (theoretically) Use with caution in azotaemic/hypotensive patients dual therapy vs tripple therapy- possible lack of support for using this

Answer 85

Aldosterone antagonist – opposes RAAS Potassium-sparing “diuretic” (very limited diuretic effect) Alone or combined with ACEI Shown to improve survival in dogs with MMVD and CHF Evidence of benefit in cats Quadruple therapy (furosemide, pimobendan, ACEI, spironolactone) currently recommended for patients in CHF – MMVD, DCM Cats: furosemide + clopidogrel +/- ACEI, spironolactone, pimobendan

Answer 86

Quadruple therapy (furosemide, pimobendan, ACEI, spironolactone)

Answer 87

furosemide + clopidogrel +/- ACEI, spironolactone, pimobendan

Answer 88

Pimobendan May be a candidate for valve repair under bypass May be a candidate for transcatheter edge-to-edge repair (TEER)

Answer 89

Diuretic (furosemide or torasemide) Pimobendan, benazepril, spironolactone May be a candidate for valve repair under bypass May be a candidate for TEER

Answer 90

Diuretic (torasemide) +/- hydrochlorothiazide Pimobendan, benazepril, spironolactone May be a candidate for valve repair under bypass Likely not a good candidate for TEER May benefit from transseptal puncture

Answer 91

Surgery preferred in humans with mitral regurgitation due to primary valvular disease “When surgery is considered, mitral valve repair is the surgical intervention of first choice when the results are expected to be durable according to the Heart Team evaluation since it is associated with better survival compared to mitral valve replacement” Medical treatment is palliative in its nature Reduction in clinical signs; can reduce or stop diuretics 93% survival at 38 months postop

Answer 92

(Mitraclip, V-clamp) “Transcatheter mitral valve implantation for severe PMR is a safe alternative in patients with contraindications for surgery or high operative risk.” Patients for whom repair is not an option (finances, few centres)

Answer 93

Chinese group (Hongyu Medical Technology) manufactured a device (V-Clamp), similar to human Mitraclip Excellent results in Shanghai CSU are having great success in USA (70 cases, 90% 12m survival) Few centres in Europe; Willows the only hospital in the UK

Answer 94

Management of Acquired Heart Disease paliative procedure Left atrial decompression Minimally-invasive, reduces LA pressure Reduction in pressure in dogs reported for dogs ith advanced refractive heart failure

Answer 95

CAUSE OF MORTALITY Multi-factorial disease complex – infectious agents, environment, stress on the host (c.f. triad of disease causation!) Younger animals mostly, but adult cattle can also be affected Main cause of mortality in young cattle globally Probably the highest economic impact of any infectious condition of cattle in UK – est. cost of £60-80M per year Risk (trigger) factors involved housing-Inadequate ventilation and high stocking densities. Mixing of ages in same air space. transport- Major stressor. Strong association between transport and BRD morbidity. Passage through a livestock market – mixing of animals. ‘Shipping fever’. weather conditions- Sudden or extreme temperature changes. Lack of wind affecting air movements and ventilation in housing in Autumn/Winter. husbandry practices on farm- Stressors such as castration, dehorning, weaning, mixing batches, market purchases and mixing of cattle from different sources. Vaccination/Immune status-Initial colostrum intake and quality. Use of vaccine and according to data sheet. Improper storage of vaccine rendering ineffective. Genetics- Some breeds may have more resistance to BRD. Sucklers calves may have more resistance than dairy BRDC: Antibiotic + NSAIDs = better treatment outcomes? Short-term perhaps, but seemingly not longer-term

Answer 96

Dull, lethargic - pyrexia Lack of appetite - reduced feed intake - low rumen fill (‘look empty’) Increased respiratory rate (tachypnoea), difficulty breathing (dyspnoea) Coughing often a feature (but not for ‘shipping fever’) Nasal and ocular discharges Upper and lower respiratory tract may be involved, but we are usually focussed on LRT

Answer 97

have synergistic effects Bovine herpese virus 1 bovine respiritory syncytial virus bovine diarrhoea virus bovine adenovirus bovine corona virus mannheimia haemolytica pasturella multiocida hisophilus somni mycoplasma bovis ureaplasma spp.

Answer 98

More than 125 named Mycoplasma species Generally host-specific, a few are opportunist zoonoses Small: cell = 300-800nm Nutritionally fastidious, dependent on host. TCA cycle is absent, cannot synthesise own amino acids, nucleotides or fatty acids. No cell wall – very unusual- affects antibiotic use in cattle- Respiratory infections - pneumonia Mastitis Eye infections Joint infections Reproductive infections Otitis (inner ear – head tilt) / Meningitis calf pneumonia, arthritis, mastitis, infective keratoconjunctivitis Many Mycoplasma species can produce biofilms: This helps them to survive: Host immune responses Disinfectant treatments Antimicrobial treatments In the environment Also no cell wall – limits Tx options

Answer 99

M. haemolytica bacteria part of the normal bacterial flora of the bovine resp. tract If conditions are right for the bacteria they can invade the lungs and set up a severe inflammatory response and bronchopneumonia – aged 1 month to 2 yrs generally Often associated with prior/concurrent infection with viruses or Mycoplasma bovis M. haemolytica is particularly associated with ‘shipping fever’ or ‘transit fever’ in cattle (formerly also known as pasteurellosis – NB name change for the bacterium) Clinical signs often seen about 2 weeks after sale and transport Similar clinical signs seen with Histophilus somni infections in cattle

Answer 100

Bovine herpesvirus 1 (BHV-1) Can affect adults as well as youngstock i.e. all ages Severe outbreaks occur where the disease enters a non-immune herd for the first time Highly contagious disease with severe inflammation of the upper respiratory tract may lead to serious primary or secondary pneumonia clinical signs- High morbidity in group – spreads fast – sudden onset Copious (quickly purulent) nasal and ocular discharges Erosions on nasal septum – severe nasal inflammation Conjunctivitis Pyrexia – inappetence Animals very depressed Halitosis – trachea severely affected Frequent coughing Reluctant to allow handling of larynx/trachea Differentiate URT from LRT signs – rhinotracheitis, no lung sounds Adult cows may abort and there is often a reduced fertility until herd immunity develops Animals suffering from IBR are highly susceptible to secondary bacterial infections Acute disease in milking cows usually accompanied by a severe and prolonged drop in milk production (up to 10 days) Differentials – Mannheimia, Malignant Catarrhal Fever (MCF), [bluetongue] Once infected, the majority of cattle in the herd become carriers (even if vaccinated) and can excrete the virus when stressed (Herpes virus) Herds where IBR is endemic suffer mainly from low-grade problems associated with calf pneumonia, decreased fertility and occasional abortions Vaccines available e.g. Bovilis® IBR Marker Live (MSD), Hiprabovis IBR Marker Live (Hipra), Rispoval IBR-Marker Live (Zoetis), Tracherine (Zoetis) Vaccinate to prevent or in the face of an outbreak Procaine penicillin for supportive therapy in clinical cases; NSAIDs

Answer 101

Dictyocaulus viviparus) – ‘husk’ – coughing - vaccine available (Bovilis Huskvac, MSD) – initial vaccination protocol and then exposure to low levels on pasture boosts immunity, which should preclude need for boosters

Answer 102

(Atypical Interstitial Pneumonia) - an intoxication from lush pasture after poor plane of nutrition – adult cattle in late summer/autumn - Sudden onset resp. distress with pulmonary oedema – tachypnoeic, not coughing, temperature normal, salivation, outstretched neck with mouth breathing, usually multiple animals – deaths possible - Conversion of amino acid L-tryptophan in rumen to 3-methylindole by microbes – enters bloodstream and damages lung tissue

Answer 103

ORC tends to be the term used in sheep rather than ORDC Same principles apply – complex mix of aetiological agents present in natural microbial flora, triggered into causing disease due to stressors Ovine respiratory symptoms - causes- Bacterial agents: Mannheimia haemolytica Bibersteinia trehalosi Pasteurella multocida Mycoplasma ovipneumoniae Viral agents: Parainfluenza 3 (PI3) Ovine pulmonary adenocarcinoma (Jaagsiekte) Maedi-Visna

Answer 104

Bacterial agents: Mannheimia haemolytica Bibersteinia trehalosi Pasteurella multocida Mycoplasma ovipneumoniae Viral agents: Parainfluenza 3 (PI3) Ovine pulmonary adenocarcinoma (Jaagsiekte) Maedi-Visna Others – e.g. lungworm – Dictyocaulus filaria in sheep (milder than in cattle – chronic cough)

Answer 105

Mannheimia haemolytica (formerly P. haemolytica) Most important respiratory pathogen in sheep – septicaemic and systemic forms Often acute – sudden deaths – (in lambs up to 3 months - septicaemia) Pneumonia in adult sheep – rare unless predisposing factor such as OPA Temperature +41°C, dull, respiratory signs Also Pasteurella multocida Type A – rare in UK, mostly septicaemia in young lambs Systemic ‘pasteurellosis’ due to M. haemolytica: Major economic importance in UK Acute onset depression, lethargy and inappetence in adults - apart from flock Pyrexia Septicemic ‘pasteurellosis’ – sudden death in lambs up to 12 weeks old At post-mortem – often overlying fibrinous pleuritis with lung consolidation Vaccines – often combined with Clostridial disease protection: Ovivac P Plus (MSD), Heptavac P Plus (MSD). Also Ovipast Plus (MSD). Note Clostridial disease as differential for sudden death in unvaccinated lambs.

Answer 106

Bibersteinia trehalosi (formerly known as Pastuerella trehalosi) – sheep only Most common form in recently-weaned (older) lambs - August to December, aged 5-12 months Sudden deaths after moving onto weaning/sale/movement and turn out onto brassicas or improved pasture after poor plane of nutrition e.g. weaned off hill ground, moved to lowland for fattening Treatment – oxytetracycline Vaccines – may be combined with Clostridial disease protection: Ovivac P Plus (MSD), Heptavac P Plus (MSD) ; Ovipast Plus (MSD)

Answer 107

Most infections are mild or non-clinical Mainly young and growing lambs affected

Answer 108

(atypical Mycoplasma pneumonia) Mycoplasma ovipneumoniae Mild to severe respiratory disease – primarily coughing, reduced weight gain Probably mixed infections (Mannheimia, PI3) – respiratory complex Often housed / intensively kept sheep

Answer 109

Contagious tumour – respiratory transmission Jaagsiekte sheep retrovirus (JSRV) – no cure – one of the ‘iceberg diseases’ Causes the development of tumours in the lung Lungs become very heavy and produce large quantities of fluid Incubation period: Several months up to 2 yrs Secondary bacterial infection common e.g. M. haemolytica - pneumonia Clinical signs: Weight loss Laboured breathing, especially during exercise – lagging behind ‘Wheel-barrow test’ – large quantities of fluid drain from the nose Spread from animal to animal via infected expired air droplets and fluid

Answer 110

Viral disease of adult sheep that can cause two syndromes: Maedi – respiratory (most common) – interstitial pneumonia Visna – neurological signs - encephalitis and wasting – rarer form Incubation period: 2 – 5 years Mainly transmitted from dam to lamb via colostrum; air-borne indoors between adults; highly infectious No vaccine and no cure – fatal. Also causes Caprine Arthritis Encephalitis (CAE) in goats Notifiable disease in Northern Ireland; endemic in GB – test and cull – accreditation scheme

Answer 111

Mainly growing and finishing pigs – huge global economic impact Main organisms involved: Mycoplasma hyopneumoniae (Enzootic pneumonia) Pasteurella multocida Actinobacillus pleuropneumoniae Porcine circovirus (PCV) Swine influenza viruses (SIV) Porcine reproductive and respiratory syndrome virus (PRRSV) Global distribution - important economically Causal organism: Mycoplasma hyopneumoniae (as part of PRDC) Clinical signs mainly seen at 8 – 20 weeks, although infection contracted much younger (often around 2 wks) Normally low grade chronic soft cough; unless get secondary infection Very high morbidity, low mortality - bronchopneumonia Incubation period about 2 weeks Barking cough – especially when disturbed in the pen Gradual spread between pigs, unless a naïve herd become infected – c/s in all ages of pig, including adults Lasts +/-50 days Depression of growth rate and feed conversion Outcome - uneven size depending on clinical impact and recovery rate lung leasions- reactive lympnodes

Answer 112

menigitis and pneumonia in pigs leaison covers whole lung

Answer 113

Infected sow can pass on infection to piglets around 14 days of age Carrier pigs Aerosol transmission for up to 3 km Direct contact and aerosol transmission within herds Disease in non-immune herds – importance of vaccination Treatment/control: Diagnosis based on: clinical signs, ELISA tests, post-mortem findings, lung scoring at slaughter Antibiotics active against M. hyopneumoniae (NB no cell wall) Vaccination e.g. Suvaxyn M. hyo (Zoetis); Stellamune Once, (Elanco) Vaccination reduces clinical signs, lung lesions and antibiotic use, with improved performance in terms of FCR

Answer 114

LESS COMMON cause of pneumonia in horses Viral Pneumonias Equine Influenza Equine Herpes Virus Equine Arteritis Virus Rhodoccocus equi equi infection in weanlings Complications from URT viral URT infections

Answer 115

Most Pneumonias in horses result from; Contamination of the LRT with bacteria from URT- stomach tubing, dysphagia, inhibition of normla clearance mechanisms Compromise to normal respiratory defence mechanisms; Inhibition of normal clearance mechanisms Inhibition of phagocytosis by alveolar macrophages Bacterial Pneumonias usually result from; TRAVEL (Transit Fever)- stress, poor ventilation, shairing airspace, horse has haed held up for long time so natural drainage usually done during grazing is impeeded Aspiration- Choke Dysphagia Iatrogenic Other risk factors General Anaesthesia Exercise/Stress Trauma Pulmonary lesions are usually distributed throughout cranioventral lung fields - Consolidated lung fields Inflammation and infection invariably spreads to pleura and pleural cavity; Fibrinopurulent Ple1ural Exudate Pleural adhesions Abscessations PROGNOSIS- Reported survival rates ranging between 43 to 76% Affected by; Inciting cause Pathogen(s) involved Localisation within ling field Time until diagnosis/treatment large amount of fibrenousa dhesions in pleural cavity = poorer prognosis

Answer 116

Premonitory signs associated with inciting cause? e.g. URT signs Signs associated with systemic inflammatory response Pyrexia, lethargy, depression, exercise intolerance, weakness. First sign could be Pyrexia (Pyrexia of Unknown Origin) Thoracic Pain (Pleurodynia) Abducting elbows, low head carriage, grunting Stilted gait, reluctance to lie down/turn Respiratory Signs – VARIABLE! Increased respiratory rate and effort Soft cough, may be inhibited by thoracic pain diagnosis- Thoracocentesis edta- Cytology: establish nature of effusion, screen for possible neoplasia, total protien transport/ blood culture media-Bacteriology: Very useful to guide antimicrobial therapy Biochemistry rarely used

Answer 117

procaine benzyle penecillin- g+ve aerobes gentamicin- g-ve aerobes metronidazole- anarobes thoratic drainage Supportive Therapy- Intravenous Fluid Therapy Non-steroidal Anti-inflammatory therapy Oxygen Therapy (rarely done) Enteral/Parenteral Nutrition Monitoring Ensure patency of chest drains Frequent ultrasonographic assessment

Answer 118

RIGHT FORELIMB- red LEFT FORELIMB- yellow (LEFT) HINDLIMB- green Right lateral recumbency (if possible) Use spirit (clip fur?) Minimise electrical interference Untangle wires

Answer 119

Is there a P for every QRS? Is there a QRS for every P? Regular or irregular? Does the QRS look normal?

Answer 120

Atrial fibrillation - Always irregular Atrial flutter - Usually irregular, sometimes regular Usually regular- Accessory pathways Atrial tachycardias Junctional tachycardias

Answer 121

Most common canine arrhythmia (14% of canine arrhythmias) Very common in DCM (Big) dogs Less common in cats multiple constant electrical impulses originate in the atria- the larger the atria the more chance this has to occur (big dogs) multiple electrical impulses originate within the atria- av node bombarded and ,many signalspass to ventricles and cause tachycardia Typical physical exam findings Irregular rhythm - chaotic Variable pulse quality, pulse deficits Usually persistent (can be paroxysmal) Usually fast (>140bpm if untreated) Lone AF af in the absense of structural heart disease. contrivercial in dogs and warrents monitoring ecg- Irregular narrow complex tachycardia No P waves Completely irregular baseline fibrillations Rapid rate Loss of atrial ‘kick’ contributing to ventricular filling Shorter diastole – less time for filling Poor output Can result in CHF (decompensation) Worsens prognosis Treat CHF Rhythm control vs rate control Rhythm control Restore sinus rhythm – rarely attempted Rate control

Answer 122

Rate control Diltiazem modified release (0.5-2.5mg/kg TID) – slow conduction through SAN/AVN Digoxin (0.003-0.007mg/kg (3-7 µg/kg) PO BID) – negative chronotropy Dual therapy usually superior to monotherapy Digoxin (3-7 µg/kg BID) Start with low dose, titrate up Measure serum levels frequently 3-7d after initiation/dose change 6-8 hours post pill If concerned about toxicity Target 0.6-1.2ng/mL (trough level) Renal values and electrolytes Digoxin toxicity GI signs Lethargy, anorexia, vomiting, diarrhoea Care in anorexic patients/patients with pre-existing GI signs Myocardial toxicity Arrhythmias 2nd/3rd degree AV block (Supra)ventricular arrhythmias Digoxin toxicity – risk factors Renal disease – reduced clearance Hypokalaemia – digoxin binds same site on Na+/K+-ATPase Cachexia – digoxin is muscle-bound Obesity – poorly lipid soluble – dose based on lean weight Ascites – digoxin does not distribute into ascitic fluid If you suspect toxicity Treatment: STOP digoxin for at least 24-48hrs, measure serum levels, restart at lower dose Treat symptomatically – CARE WITH FLUIDS Going forward Monitoring Mean heart rate – rate control Holter Train owners to measure themselves Target: <125bpm (<155 in clinic?)

Answer 123

Supraventricular Tachycardias Quite similar to atrial fibrillation in pathophysiology and management Flutter/fibrillation spectrum instead of multiple sites of electrical impulses in the atria there is one- usually around tricuspid valve, in a lcosed loopthat perpetuates impulses Rapid REGULAR atrial rhythm, (atrial rate 300-500bpm) No P waves Flutter waves- more uniform, sawtooth apearence with no returne to baseline ventricular rhythm may be regullar or irregular Occurs with atrial enlargement

Answer 124

Management As with AF – rate control Fast rates – poor cardiac output, acceleration of heart disease Diltiazem +/- Digoxin Amiodarone Radiofrequency ablation of flutter circuit- Rarely performed Management As with AF – rate control Fast rates – poor cardiac output, acceleration of heart disease Diltiazem +/- Digoxin Amiodarone Radiofrequency ablation of flutter circuit Rarely performed

Answer 125

Atrial fibrillation Atrial flutter Accessory pathways: 200-300bpm Atrial tachycardias: 200-300bpm Junctional tachycardias: 100-160bpm

Answer 126

Travels through normal ventricular conduction pathway ECG: P waves abnormal (P’) or absent Normal (tall, narrow) QRS complexes (unlike VPCs) Exercise intolerance Inappropriate panting CHF – predominantly right-sided Weakness/collapse Gastrointestinal signs Tachycardia can be persistent or paroxysmal

Answer 127

Sustained HR>200bpm (>260 cats) Vagal manoeuvre- press on eyes, carotic massage, press on nose (cats) Provide diagnostic information May terminate rhythm Precordial thump Treat any underlying cardiac disease Diltiazem (0.05-0.1mg/kg IV over 5-10mins; repeat to effect, up to maximum of 0.25-0.35mg/kg) Esmolol (25µg/kg/min CRI, or 0.5mg/kg IV bolus over 1 minute) Oral sotalol (0.5-3mg/kg PO BID) Oral management Diltiazem modified release (0.5-2.5mg/kg PO TID) Sotalol (0.5-3mg/kg PO BID) Atenolol (0.3-1.5mg/kg PO BID) – not if CHF Amiodarone (PO/IV)- anaphalixis, oral toxicity Echocardiography Tachycardia induced cardiomyopathy 24hr Holter ECG Baseline, response to treatment Electrophysiology study

Answer 128

Ventricular premature complexes (VPCs) Accelerated idioventricular rhythm (AIVR) Ventricular tachycardia Cardiac disease Extracardiac disease Neoplasia (splenic, hepatic) GDV SIRS/Sepsis Toxins Anaemia Trauma Cats – nearly always due to primary cardiac disease

Answer 129

Short R-R interval - PREMATURE Non-sinus (no P wave) Wide (‘bizarre’) QRS complex Isolated – do not require treatment ectopic beat originates somewhere else in ventricle- can no longer depolarise normally and so ventricles are depolarised by self induction which is slower causeing wider complexes couplet- two in a row on ecg bigeminy- alternating sinus and ventricular waves trigeminy - sinus beat followed by two vpcs

Answer 130

AIVR Four or more consecutive VPCs 70-160bpm Paroxysmal or sustained Not an emergency Doesn’t require antiarrhythmic treatment Investigate systemic disease/underlying cause Common following abdominal surgery

Answer 131

Four or more consecutive VPCs > 160-180bpm Paroxysmal or sustained If sustained and causing reduced cardiac output (seen in clinical signs- weak lethargic)- EMERGENCY - Lidocaine boluses (2mg/kg/IV)

Answer 132

Sinus node dysfunction (SND)/Sick sinus syndrome (SSS) Atrioventricular block Clinical signs Non-specific – lethargy Syncope/collapse Heart failure

Answer 133

Complex disorder of entire cardiac conduction system (not just SA node) Fibrofatty replacement of nodal tissue Various ECG consequences Sinus bradycardia/arrest AV block Tachycardias (brady-tachy syndrome) Middle-aged to older dogs Typically small breeds WHWT, miniature schnauzers, Cocker spaniels Asymptomatic – Sinus node dysfunction Symptomatic – Sick sinus syndrome Collapse Diagnosis ECG – may need long recordings (>2min) 24hr Holter ECG Atropine response test- 0.04mg/kg IV Vagolytic – increase in heart rate (>50% or >140bpm) within 30 minutes May predict response to oral anticholinergics

Answer 134

Management -only if symptomatic, i.e. SSS Medical – anticholinergics Theophylline, propantheline, hyoscyamine, terbutaline If positive response to atropine Surgical Pacemaker implantation

Answer 135

Bradycardia Delay in AV conduction Prolonged PR interval >0.13s dogs, >0.09s cats Not clinically significant May reflect increased vagal tone

Answer 136

Bradycardia Transient interruption of AV conduction Non-conducted P waves Type I Physiological Wenkebach phenomenon Prolongation of PR interval before block Type II Pathological? Fixed PR interval Clinical consequences depend on grade, frequency of block

Answer 137

Complete interruption of AV conduction Non-conducted P waves Escape beats Emergency – pacemaker implantation necessary

Answer 138

General Approach Maintain cardiac output Avoid hypo/hypertension Avoid excessive tachy- or bradycardia Avoid increases in myocardial workload Avoid myocardial depressants and arrhythmogenesis Maintain oxygenation (ventilation – but IPPV can be detrimental- can impare output through lungs) Maintain good fluid balance – avoid over infusion In general THOROUGH pre-op exam and if poss. echo: establish baseline Red flags = increased resting HR and RR BIG anaesthesia concern = enlarged L atrium – assoc’d with poor outcomes THOROUGH history concentrating on exercise tolerance ?cv orthopaedic issues The ‘car park’ test Avoid stress (sedation, analgesia, calm environment) Try to treat prior to GA if possible Pre-oxygenate (stress free) Cautious IV fluids

Answer 139

Common in older patients- adult ckcs Leads to pulmonary congestion/oedema, Left Volume volume overload and eventually right sided failure Pre-oxygenate Keep HR same - Tachycardia ↑ regurg fraction, bradycardia ‘stretches’ the valve Avoid positive inotropes (↑ workload and regurg fraction) Aim for small decrease in afterload (which drug?)- Avoid ketamine, alpha-2 agonists Avoid arrhythmias (? Anti-arrhythmic drug?) Maintain preload but not excessive IPPV may treat pulmonary congestion/oedema

Answer 140

Cardiac inotropy is inhibited and CO is HR dependent Avoid big changes in HR Ensure adequate filling pressures (fluids) and afterload to ‘work against’ Often require dobutamine (positive inotrope) infusion to maintain BP Hyperthyroid cats often have gallop rhythms and hypertension – ensure adequate preload and avoid sympathetic stimulation Some advocate avoiding ketamine in these cases

Answer 141

Multiple causes Remember ’golden 12 hours’ before contusions develop Usually a cause – rarely primary cardiac disease Ensure all other parameters are wnl Ensure good analgesia – opioids drugs of choice Consider antiarrhythmics only if significant- Check BP/ pulse oximeter/pulses/CO2 Lidocaine, β-blockers, amiodarone, magnesium Avoid sympathetic stimulation- pain ect Recover if arrhythmia is significant and not responding to treatment

Answer 142

Typically necessary in patients with 3rd degree AV block Often myocardium itself is ok Try pre-treatment atropine/glycopyrrolate/ Isoproterenol Pre-oxygenate Use nothing to lower heart rate – pethidine often used External pacing leads placed prior to induction = major risk time

Answer 143

Usually, L to R shunt unless reverses (very poor prognosis if this happens) Pulmonary oedema/overload and pulmonary hypertension Systemic hypotension with very low diastolic- Typical hyperdynamic pulses and caudal blue mm’s Eventually LV overload and hypertrophy- May develop L atrial dilation – major red flag Eventual RV hypertrophy Avoid shunt reversal – systemic hypotension and pulmonary hypertension- IAAs vasodilate and IPPV increases pulmonary blood pressure – caution Prevent hypothermia (often young) Avoid worsening of shunt (hypoxia, high carbon dioxide, pain) Maintain HR – pethidine often chosen as opioid of choice Pre-oxygenate Analgese – especially if open chest ligation Beware of Branham reflex – sudden bradycardia after shunt ligated- Overstretch of L ventricle or sudden ↑ ABP ≡ baroreceptor reflex

Answer 144

pethidine, alfaxalone t/e, sevoflurane in oxygen, opioids as necessary, careful IPPV (increases pulmonary pressure) I pretreat with glycopyrrolate – Branham's sign

Answer 145

ACP, Opioid, propofol induction, maintain with isoflurane in oxygen Maintenance fluids only unless clinically hypovolaemic

Answer 146

pethidine/low dose methadone plus atropine/glycopyrrolate, ketamine/bzd induction prepared to pace, isoflurane in oxygen for maintenance

Answer 147

The diagnosis and management of respiratory conditions can be challenging Animals are difficult to assess without causing additional stress to the patient (restraint etc) Stress may worsen the respiratory distress and exacerbate the hypoxaemia Often these animals have very advanced disease before clinical signs appear - large respiratory reserve The perioperative period is critically important and often these cases are relatively easy to manage once anaesthesia has been induced ! The serious conditions presenting with respiratory distress in the dog may include: Upper airway obstruction Trauma Pneumonia ARDS or ALI Pulmonary thromboembolism Pulmonary oedema Neoplasia The serious conditions commonly presenting with respiratory distress in the cat include: Asthma & chronic bronchitis Pulmonary oedema Pleural effusion Pneumonia (less common) Neoplasia & polyps Prior to anaesthesia the focus should be on Minimising stress Providing oxygen Trying to draw up a list of differentials based on the clinical signs & a brief physical examination

Answer 148

Provision of oxygen is always beneficial However it may be stressful- difficult in large animals Review the different ways of providing oxygen: flow by, mask, nasal prongs etc and the FIO2% that is possible with different methods Rarely an animal needs emergency anaesthesia and IPPV Most of the information about drugs and approach to anaesthesia is pertinent to respiratory cases & cardiac cases In critical cases! Flow-by easiest- Place O2 line 1-3 cm from patient’s nose/mouth 6-8 l/min = FIO2 of 0.25-0.4 Rapid airflow not tolerated by some Mask (?smear with cat food) 6-10l/min = FIO2 0.35-0.55 Reservoir bag + 8-10l/min = 0.5-0.8 Leakage in brachycephalic dogs and cats & poor cooperation - ?worthwhile?

Answer 149

Patients with respiratory disease include those with airway/muscular disease and the inability to ventilate and those with primary lung disease and the inability to oxygenate (and some have both) Hypoventilation is common in anaesthetised patients (why?) This is detrimental as many respiratory conditions already have underlying hypoventilation (neoplasia, trauma, collapsing trachea) Vital to keep the airway patent - worsens the ability to ventilate- Place an ET tube (why is it so much better than a mask?) Care with kinking of tube & secretions Avoid drugs that may cause bronchospasm During anaesthesia of these patients, dead space can be increased because In respiratory disease dead space can be larger CO drops and pulmonary artery pressure decrease IPPV can compress pulmonary capillaries in bits of the lung Long ET tubes and large masks (not a good idea) Bronchodilators If the anaesthetised patient is breathing spontaneously these dead space changes may be significant because of the smaller tidal volumes V/Q mismatch is also exacerbated The inhalants make this worse due to attenuation of hypoxic pulmonary vasoconstriction (prevents perfusion through poorly ventilated alveoli) An FIO2% > 30-35 will usually prevent this becoming critical, but PaO2 values may be significant less than normal. (What is the usual PaO2? And how is this related to FIO2%) Commonly shunt causes hypoxaemia (venous admixture) Anatomic (tetralogy of fallot R-L shunting) V/Q mismatch approaching zero, ie pulmonary disease; pneumonia, torsion, pyothorax, D.R., abdominal pressure, haemorrhage etc Simply shunt = mixed venous blood returned to the arterial side of the circulation Increasing FIO2% usually has NO beneficial effect (can you work out why?) Anaesthesia can increase shunt fraction because it decreases FRC (functional residual capacity)- recumbency & relaxation of the diaphragm and thoracic muscles, and the forward movement of the diaphragm In addition, the FRC is accompanied by atelectasis and small airway closure An occasional large breath or ‘sigh’ during anaesthesia may help to decrease the amount of small airway closure

Answer 150

Includes upper airway obstruction, laryngeal paralysis, tracheal collapse, neoplasia, foreign body Animals are anxious and have increased respiratory effort (vicious cycle  distress)- Also Bernoulli effect Can be hyperthermic Paradoxical inward movement of thorax on inspiration Difficult to examine Often benefit from low dose sedation (anxiolysis) with phenothiazine and opioid. (Care with respiratory depressants in brachycephalic dogs) Dogs often improve after acepromazine Oxygenate, secure IV access Cool, administer fluids, anti-inflammatory agents Have a range of ET tubes, long narrow ET tubes available for bulldogs, also stylets, swabs, and laryngoscope as intubation may be challenging Titrate drugs – can use drug combinations to reduce overall dose of induction agent Secure airway, and inflate cuff

Answer 151

Intraoperatively these patients may require extubation and re intubation to facilitate surgery Occasionally a temporary tracheostomy needed BOAS dogs tolerate an ET tube for a significant period of time as they are recovering When extubating the cuff is not deflated completely to encourage any secretions or blood to be pulled forward Post op - close attention to the airway is necessary, occasionally animals decompensate during recovery and require re intubation/anaesthesia

Answer 152

These are not usually emergencies Understand the pathophysiology of the disease you suspect or have diagnosed Complete clinical examination Further diagnostics can be helpful: Haematology (? 2nd polycythaemia) Pulse oximetry & arterial blood gases Thoracocentesis Xrays Bronchoscopy There is a long list of conditions with neural or chest wall disorders that once anaesthetised can decompensate rapidly See table on next slide, try to fill in the response column PaCO2 rises with hypoventilation, acidosis and hypoxaemia also develop The risk of this decompensation can be minimised by closely monitoring these cases and providing oxygen and being very careful with sedatives and pre-meds

Answer 153

Increasing FIO2% sufficient in some Some require intubation & IPPV Other require drug therapies too (‘clean, dry & widen airway’) Antibiotics Bronchodilators Diuretics PDE inhibitors, beta 2 agonists, antihistamines, antimuscarinics Anti inflammatories Anti-tussives Mucolytics Pre med (low dose acepromazine + opioid) or Ketamine + midazolam (cats) Preoxygenate IPPV cautiously during anaesthesia 100% O2 with low inflation pressures

Answer 154

Blunt thoracic trauma can result in pulmonary contusions which compromise gaseous exchange Cage rest and oxygenation Occasionally require emergency anaesthesia & IPPV (very low pressures - otherwise everything is made worse) Enthusiastic blood volume expansion in animals with contusions may -> pulmonary oedema Giving diuretics then may reduce the circulating blood volume & increase alveolar dead space

Answer 155

Chronic bronchitis – review the pathophysiology XS mucus -> infection Atelectasis -> hypoxaemia -> polycythaemia & cor pulmonale Hypoventilation -> chronic hypercapnia -> densensitised to CO2 Bronchospasm & bucking (hypersensitive reflexes) V sensitive to respiratory depressants (sedatives and anaesthetics) Hypoxic respiratory drive (CO2 rises -> narcosis) Humidify the gases (why? what do cold dry gases do to the airway?) & provide IPPV (why?) Higher airway pressures, care with trauma Slow inspiratory cycle Long expiratory pause MV increased (as alveolar dead space is increased) Leave ET tube in as long as possible in recovery O2 Doxapram infusions (some texts suggest) Dispose of breathing system if infection is suspected

Answer 156

Review the pathophysiology Bronchoconstriction can be caused by Chronic bronchitis Local irritants Asthma Pre/intra op Oxygen Bronchodilators Antispasmodics Steroids Antihistamines Beta 2 agonists – terbutaline very useful in cats Avoid stress

Answer 157

Check oxygen source and ventilation of horse ?IPPV necessary- Often WORSENS oxygenation Switch down the inhalant Consider the position of the horse Improve cardiac output if possible Consider a beta agonist such as salbutamol/albuterol (down the ET tube)… doesn't always work Recover the horse

Answer 158

Poor dentition Abnormal oesophageal anatomy Dry feeds Failure to soak sugarbeet Adequate water provided Carrots and apples chopped into small pieces Greedy eaters? Try flat stones or salt blocks in feed bins to slow eating down

Answer 159

What most owners expect… ‘food coming from the nostrils’ But also includes… Hypersalivation Retching Inappetant Colic signs Coughing And also… Dull Head down and extended Take a history: Feeding regime Normal husbandry Details of dental treatment Horses use diagnosis- Take a history: Feeding regime Normal husbandry Details of dental treatment Horses use Failure to pass a nasogastric tube is diagnostic…. complications- Inhalational pneumonia Uncommon Contamination from food and oral cavity materials: - mixed population of different bacteria - penicillin, gentamicin and metronidazole to cover gram positive, negative and anaerobes *sterile tracheal wash culture and sensitivity to adapt therapy if no improvement* Inhalational pneumonia Ulceration of the mucosa of the oesophagus +/- muscular layers of the oesophagus (sometimes deeper) Fibrous (scar tissue) strictures can last days/weeks May lead to: - Stricture – poor prognosis requiring conservative dilatation or surgery - Fistula – most resolve resolve spontaneousy – may need surgery - Diverticulum – signs of recurrent choke Inhalational pneumonia Ulceration of the mucosa of the oesophagus +/- muscular layers of the oesophagus (sometimes deeper) Megaoesophagus: Difficult to assess with endoscopy Best diagnosed with contrast radiographs No treatment- management only: - sloppy mashes - feed from a height with front limbs on a step to help emptying the oesophagus via gravity Prevention- Adequate water provided Carrots and apples chopped into small pieces Greedy eaters? Try flat stones or salt blocks in feed bins to slow eating down

Answer 160

Note: Most cases resolve spontaneously Mild cases Sedation Detomidine/Romifidine + Butorphanol NSAIDs –reduce inflammation of the mucosa Intravenous buscopan (hyoscine butylbromide)– short term muscle relaxation ACP? Lower the head and prevent aspiration of impacted feed into the lungs Moderate (most cases you will see) As previous + Gentle lavage Persistent cases… As previous: sedation + buscopan + lavage This may take up to 1hr to clear If treatment fails- Don’t panic! Refer for: - endoscopy/gastroscopy – evaluate the cause of obstruction (a fb may need surgical removal) - Treatment of severe food impaction under general anaesthesia: More controlled lavage, with a cuffed ET tube to protect the airways from food material. The table can be tilted to help emptying of the food material with gravity and larger volumes of fluid can be used. Subsequent management… Soaked/sloppy feed for 12-24hours In severe cases oesophageal endoscopy can allow assessment of the oesophageal mucosa after an impaction has been treated

Answer 161

Rabbits and hystrichomorphs All teeth elodont Incisor and cheek tooth issues common. Myomorphs Elodont incisors, brachydont cheek teeth Primarily incisor issues Hedgehogs and ferrets Brachydont teeth Dental pathology more similar to dogs and cats.

Answer 162

Hereditary Overgrowth due to insufficient wear through gnawing (myomorphs) secondary to cheek tooth elongation (rabbits and hystrichomorphs) Trauma -> malocclusion -> abnormal growth

Answer 163

Due to insufficient dietary fibre (all) +/- nutritional osteodystrophy (rabbits). Insufficient attrition -> Overgrowth +/- incisor malocclusion Bridging (hystrichomorphs) Spur formation -> lingual and/or buccal lacerations. Due to insufficient dietary fibre (all) +/- nutritional osteodystrophy (rabbits). Vitamin D +/- calcium deficiency -> Osteomalacia Weak teeth with defective enamel Thinning and loss of supporting alveolar bone Aberrant tooth growth (apical elongation)

Answer 164

Elodontomas common in degus, prairie dogs and squirrels.

Answer 165

Important part of any rabbit consultation. Areas to assess: Facial symmetry Jaw palpation External soft tissues Incisors Oral cavity exam Ocular examination Facial symmetry Jaw palpation External soft tissues Incisors Oral cavity exam Ocular examination Limited: Soft tissues Recalcitrant patients! Only a small proportion of the tooth is visible above the gingiva. If symptoms suggestive of dental disease are present, but conscious dental exam is normal, imaging is indicated

Answer 166

Always under GA Minimum four views required: Lateral 2x lateral obliques Dorsoventral lateral allows assesment of dental lines- roots will be misaligned with pathology obliques- Separate out the dental arcades for individual assessment. Dorsoventral view- Mineralisation of chronic inflammatory tissue visible in this image

Answer 167

Gives more in depth information regarding individual teeth. Useful for surgical planning (3D modelling) More sensitive for otitis media and nasolacrimal pathology

Answer 168

Clipping e.g, with nail trimmers, is never appropriate. Can cause the tooth to shatter -> sharp edges +/- soft tissue trauma. May also damage the germinal tissue -.> future abnormal growth. Diamond cutting disc = preferred trimming instrument Usually done conscious or with mild sedation. Care re:pulp cavity and soft tissues

Answer 169

Permanent cure for malocclusion Radiographs recommended first to assess tooth shape (especially in chronic cases) Periodontal ligament broken down with a crossley luxator or a 16g needle, bent to mimic the curve of the incisor Can be very difficult where teeth are highly dystrophic or ankylosed. Complications: Tooth regrowth Abscess formation Remember: rabbits have six incisors!

Answer 170

Conscious burring or rasping of cheek teeth is becoming increasingly requested by clients, especially for guinea pigs. This is not an appropriate technique for the management of cheek tooth disease. The RWAF and BVZS released a joint position statement in 2023, “BVZS position statement on the use of anaesthesia in rabbit, guinea pig and chinchilla dental procedures March 2023” which I recommend reading for further details.

Answer 171

Lingual (lower arcade) and buccal (upper arcade) spurs can  significant soft tissue trauma and pain. Guarded dental burrs preferred method of removal. Molar cutters recommended by some authors burs have risk of lacerating facial atery- can be fatal and cant be used along side intibation molar cutters may be quicker but can shatter teeth

Answer 172

Stops problem teeth from growing, so the stop producing spurs but still retain a functional crown. Lower arcade teeth only except the most caudal cheek tooth as the apex is inaccessible. Plan using palpation of protruding apices +/- radiography Procedure: Incise skin over the ventral aspect of the mandible Dissect away and overlying tissues Remove any bone overlying the apex (scalpel blade or hypodermic needle). Pick out germinal tissue with a hypodermic needle, then flush the hole with methylated spirits to destroy any remaining germinal tissue. Close the subcutaneous tissue and skin in two layers, leaving the hole in the bone open.

Answer 173

Mostly rabbits More complicated than incisors. Easiest in mobile teeth which have lost periapical bone support. Also commonly performed for teeth involved in abscesses. Intraoral and extraoral techniques described

Answer 174

Usually in teeth which are already mobile and not abnormally shaoed on radiographs. Peridontal ligament broken down using a rodent molar luxator, and molar forceps used to remove. Harder than it sounds!

Answer 175

Indications: Otherwise immobile teeth repeatedly causing spurs. Fractured teeth Ankylosed teeth Cases of osteomyelitis or abscessation. Skin is incised over the affected tooth and a bone burr is used to expose the tooth root and unerupted crown.

Answer 176

Abscesses = end stage sequalae to apical changes. Always require surgical excision, ensuring full removal of the abscess capsule. Basic principles: Plan carefully All associated teeth should be removed. Necrotic tissue, including bone, must be fully debrided away. Usually marsupialised, sometimes closed with antibiotic impregnated beads in place. Post op antibiosis based on culture of the abscess capsule. Analgesia essential – NSAID + opioid

Answer 177

Agamids (bearded dragons and water dragons) and chameleons most commonly affected Acrodont teeth Soft diets  calculus formation  periodontal disease. Calcium deficiency (NSHP) may also contribute. Infection may  osteomyelitis due to the anatomical attachment of the teeth to the bone of the jaw. Diagnosis: Clinical examination Radiographs Culture and sensitivity Biopsy Treatment Dental scaling Antibiosis Analgesia Topical antiseptic Euthanasia

Answer 178

Stress, pain, and/or obstruction > Reduced gastrointestinal motility > Slow gastric emptying Fermentation of gastrointestinal contents Decreased fluid and nutrient absorption

Answer 179

Dehydration and impaction of the stomach contents Gas production, especially where caecotrophs are present in stomach contents Gastric dilation  Gastric ulceration Necrosis Perforation Peritonitis True gastric obstruction of the pylorus now known to be rare; desiccation of gastric contents is almost always secondary to stasis.

Answer 180

Gas production due to fermentation > intestinal dilation. Caecal tympany may occur where large volumes of gas are present in later stages of stasis. Very painful > Depression Complete anorexia Frantic chewing of wood, paper or bedding Audible tooth grinding

Answer 181

Occurs in both foregut and hindgut, i.e.: Decreased carbohydrate absorption from the small intestines. Decreased supply of nutrients to the caecal microbiota, resulting in decreased volatile fatty acid production and absorption from the caecum. Results in negative energy balance. Free fatty acids mobilised from adipose tissue and transported to the liver. Eventually results in hepatic lipidosis

Answer 182

Clinical signs on history Clinical findings Blood glucose Radiography Haematology and Biochemistry Urinalysis Ultrasound Clinical signs on history- Decreased appetite Decreased faecal output Lethargy/depression Tooth grinding Abnormal posture Uneaten caecotrophs (lagomorphs) Clinical findings- Decreased or absent gut sounds Firm/doughy stomach on palpation Pain on careful abdominal palpation Pain can be difficult to assess – use rabbit grimace scale Other clinical findings may point to the underlying reason for stasis Blood glucose- Normal range 5.5-8.2mmol/L (BSAVA Rabbit medicine manual) Study in 2012 (Harcourt-Brown and Harcourt-Brown): Medical stasis: 8.5mmol/L +/-3.3 Surgical stasis: 24.7mmol/L +/- 5.4. Therefore BG >20 = more likely to a have a serious condition requiring surgery. NOT DIAGNOSTIC IN ISOLATION Radiography- Orthogonal views looking for GIT dilation +/- evidence of obstruction (gas dilation which abruptly ends). Stomach with impacted contents and a halo of gas commonly seen. Sequential radiographs looking for movement of gas may be useful. Serial radiographs can demonstrate movement of gas through the GIT. Presence of gas in the caecum indicates that no obstruction is present, or that it has moved through into the caecum and should now pass through uneventfully. Haematology and Biochemistry- Apart from glucose measurement blood testing tends to be non specific for GI disease. More useful for evaluating underlying conditions. Urinalysis- Also non specific for GI disease. More useful for evaluating underlying conditions. Ultrasound- Tricky in hindgut fermenters due to the large amount of gas in the normal rabbit GIT, which is exacerbated in GI stasis. May be useful, especially for finding obstructions, pancreatitis, peritonitis etc.

Answer 183

Fluid therapy Supportive feeding Analgesia Pro-kinetics Fluid therapy- Oral vs subcutaneous vs IVFT Combined oral and IVFT for non-obstructive cases, IVFT only in obstruction Daily maintenance requirements 70-100ml/kg/day Care re:pulmonary oedema Supportive feeding- Only in non-obstructive cases Critically ill patients – Lafeber emeraid Oxbow critical care fine grind Nasogastric tube can be placed if patients will not tolerate syringe feeding

Answer 184

Fentanyl/fluanisone 0.5 ml/kg IM is the licensed dose to produce anaesthesia 0.2-0.25ml/kg SC reported in literature for analgesia (BSAVA manual of rabbit surgery, dentistry and imaging) Ketamine CRI may be considered where severe pain present. One off dose of 10mg/kg IM used to reset central sensitisation to pain stimuli. Meloxicam 0.6mg/kg BID SC Gastric ulcer risk? Buprenorphine 0.05mg/kg q6hr IM Decreased GI motility?

Answer 185

Not in obstruction Ranitidine 4-6mg/kg Acts on the entire GIT (oesophagus to colon). Also decrease acid secretion so helps prevent gastric ulceration. Metoclopramide 0.5mg/kg Only acts on the proximal GIT (oesophagus, stomach and small intestine) Cisapride 0.5-1.0mg/kg Acts on the oesophagus, stomach, small intestine, and colon. May potentiate the effect of ranitidine

Answer 186

Most common cause in lagomorphs is pellets of impacted fur, ingested foreign bodies e.g. Synthetic fibres, dried less common. Other causes of obstruction include tumour, stricture, adhesions, and strangulation. Stabilisation is essential in the first instance. Analgesia – opioids preferred in obstruction Fluid therapy - IVFT Antibiosis – Broad spectrum cover for anaerobes and gram negatives indicated e.g. metronidazole and trimethoprim/sulfamethoxazole combinations, particularly where the GIT will be or has been entered. Foreign bodies may spontaneously or intermittently resolve, especially hair pellets (‘moving foreign body’) Ex-lap indicated where the obstruction is not resolving. Need to identify the cause of the obstruction and decide if operable or if euthanasia is indicated. Indications for euthanasia: Devitalised/necrotic intestine (end to end anastomosis carries a very poor prognosis in small mammals). Inoperable tumour causing constriction. Rupture of the intestines with evidence of peritonitis. It is often possible to milk foreign bodies through the small intestine into the caecum. If enterotomy is required prognosis is poorer as it is difficult to create a leak-proof repair without causing a stricture. Prognosis for cases requiring anastomosis is very poor. If enterotomy is necessary, ideally to move the foreign body to an area of healthy gut prior to making an incision. GIT should be occluded to minimise leakage of intestinal contents. Saline soaked sterile swabs should be around the GIT to minimise contamination. Enterotomy incisions are made along the antimesenteric border of the intestine. Incisions should be repaired with 4/0 or 5/0 monofilament suture material e.g. moncryl in a simple interrupted pattern. After repair incision sites should be leak tested using sterile saline and a 25g needle. Omentalisation can be attempted (often unsuccessful in lagomorphs due to the small size of the omentum) As for medical stasis: Analgesia (opioids +/- nsaids and ketamine) Fluid therapy (IVFT) Prokinetics Nutritional support (emeraid critical care) +/- Antibiosis (metronidazole and sulfa/trim combinations) Nursing care post operatively is paramount – best achieved in a hospital setting at least initially.

Answer 187

Cyathostomin spp considered the equine parasite of most epidemiological and clinical significance Over 50 different species identified Direct, non-migratory life cycle Ingested larvae develop (L3 L4) within mucosal crypts of the large colon Early L3 larvae can arrest their life cycle when conditions outside the host are suboptimal for development Mass eruption of the EL3 larvae can result in clinical disease – Larval Cyathostomiasis clinicla signs-

Answer 188

>5yrs Rapid weightloss Diarrhoea Ventral oedema Abdominal pain Signs of endotoxaemia Colic? Rapid death!! Early L3 provoke a fibroblastic response Presence of larvae -> infiltration of lymphocytes, eosinophils, plasma cells and mast cells. This leads to marked oedema, submucosal haemorrhage, ulceration of the mucosa, in severe cases haemorrhage of the instestine. Inflammation and loss of mucosal barrier -> increased permeability and protein loss to the intestinal lumen. Inflammatory changes in the intestinal mucosa -> altered motility resulting in diarrhoea and abdominal pain. Severe diseases occurs when large numbers of parasites erupt. risk facotors- Large numbers of encysted larvae simultaneously develop and exit the LI mucosa. “mass emergence” occurs in late winter/early spring Usually young horses, but can be any age. Poor pasture management +ineffective anthelmintic treatment Treatment with ivermectin with heavy mucosal burdens -> LC Anthelmintic resistance diagnosis- Haematology and biochemistry  neutrophilia Hypoalbunaemia ? Anaemia, hyperglobinaemia, increased AP? DDx for any PLE US for thickened colon or caecum? FEC is of limited benefit: egg numbers do not correlate with larvae! Small red worm ELISA?

Answer 189

Supportive to address fluid and protein loss Immunosuppressive doses of prednisolone 1mg/kg 24-48hrs prior to anthelmintic treatment Moxidectin or 5 day Fenbendazole? NSAID if pyrexic Antibiotics? Co-grazers? prevention- Was monitoring and treatment in place? Which drugs were used and when and how much? Effective against mucosal larvae? Poo picking occurred? If apparent adequate control strongly suspect resistance! Perform FECRT

Answer 190

bacterial contamination (secondary to colic, castration ect) -> inflamation -> ++ peritoneal fluid, ++ cellularity, ++protien, fibrin deposition-> increaed permiability: more toxins and bacteria enter-> impared organ function pain, innapitence, SIRS, hypovolemia, cv comp

Answer 191

inflamation of the peritoneal lining clinical signs non specific and vairiabe- chronic vs acute potentially life threathening primary vs secondary septic or not diffuse or foca acute or chronic most common presentations- secondary, acute iffuse and septic or primary, difuse and non septic varitey of bacterial species invoved common causes- collic- ishemia allow toxin leackage sprea of infection from other areas- liver kidney, internal abcesses urogenital injury internal parasite migration iatrogenic blunt or penetrating trauma rarley secondary to viral infection acute- depression, colic, inapitence, pyrexia, stiff, boarded abdomen, congested mucous membranes, tachycardia, tachypneaa, reduced gut sounds, reduced fecal output, sweating, diarrhoea chronic- depression, chronic intermitent colic, anorexia, weight loss, reduced exersise tolerance, intermitendt pyrexia dxx- colic, pleuroneumonia, poat operative pain following laperotomu, abdominal abcessation, abdominal neoplasia laminitis, haemoperitoneum, uterine perfusion, myopathies, pyelonephritis

Answer 192

heamotology- wbcc decreased in actue disease with neutropenia later on tere may be an increase with left shift pcv may be increase- haemoconcentration- or may be deceease in chronic disease due to bone marrow depression biochem- hypoprotienaemia (low albumin)- loss of protien into abdomin hyperprotienaemia ( dehydration / increase in globulins in chronic cases elevation in acute phase protiens SA/ fibrinogen (chronic electrolite istuebances/ metabolic acidosis increase in blood lactate >2mmol-1

Answer 193

should be clear enough to read newspaper throug should be straw colourded- not orand/ re/ brown/ green total cell count should b 0-5x10^8/l. in peritonitis generally over 100- 90% neutrophils may have decrease glucose may have increased lactate marignal chnges occur after castration or abdominal surgery so be aware

Answer 194

shows increased volume of peritoneal fluid generally hypoechoic, may be foci present (fibrin tags or ahesions) may also be used to guide aspiration may also identify unerlying cause

Answer 195

prompt, agressive treatment traet primary cause, eliminate infection- broad spectrum- penecillin, gentamicin, metronidaxol reverse hypovolemic and endotoxic shock/ correct metabolic and electrolyte abnomalities, control pain correct dehydration and hypoprotenamia peritoneal labage- nutriotional support fluid therapy contole pain- nsaids, anti endotoxic drugs- flunixin meglimine nasogastric intubation can provide pain relif via decompression prognosis gaurded- gut rupture hopeless localised adhesions or absessation- chronic iill thrift and recurrent coli

Answer 196

Exotic pet mammals are more prone to lower GI disease than upper GI disease. GI stasis important – covered elsewhere. Diarrhoea is a rare but serious condition in exotic pet mammals. Rabbits – true diarrhoea vs uneaten caecotrophs Primary infectious disease = more urgent, but otherwise similar to dogs and cats. Enterotoxaemia/antibiotic induced dysbiosis = life threatening condition.

Answer 197

Often mistaken for diarrhoea. Caecotrophs may be soft or not ingested for many reasons: Inappropriate diet +/- obesity most common.- causes runny hard to eat caecotrophs and also physical trouble reaching perineam Dental disease Musculoskeletal - trouble reaching perineaumdisease Upper respiratory tract disease Urinary tract disease

Answer 198

Caused by Clostridium spp. (C. spiriforme primarily) or E. coli overgrowth -> enterotoxin production -> enteritis. AKA antibiotic induced dysbiosis, but other factors can also predispose to overgrowth: Low fibre diets Carbohydrate overload Excessive dietary protein Clinical examination: Diarrhoea: mild (early) -> severe, watery diarrhoea. Early stages – quiet demeanour, GI pain, dehydration. Peracute and acute – collapse and death. Diagnosis Clinical signs and history Faecal gram stain- Clostridium spiroforme is spiral, Clostridium difficile is rod Faecal culture Post mortem examination DDx – infectious enteritis, mucoid enteropathy (rabbits), megacolon Infectious enteritis – all species Mucoid enteropathy – rabbits Megacolon – rabbits Heavy metal toxicity – all species Diagnostic process as for enterotoxaemia plus imaging (radiographs) and haematology and biochemistry testing. For more information see Chapter 12: Digestive system disease, In the BSAVA Manual of Rabbit Medicine.

Answer 199

Supportive care- Fluid therapy- be careful! desert adapted species- rabbits- 100ml/kg/day 50% iv, 50% oral Maintain body temperature- can overheat easily Nutritional support Probiotic and high fibre supplement Encourage fibre intake i.e. provide good quality hay and encourage intake. Analgesia- Opioids preferred as they slow GI motility as well as providing pain relief. Spasmolytics- Help decrease abdominal pain Metamizole/butylscopolamine (buscopan) Loperamide Both off license use Metronidazole- Indicated for anaerobic infections including Clostridia spp. Risk of CNS toxicity at high doses Causes marked decrease in food intake in Chinchillas Cholestyramine- Ion exchange resin which binds to enterotoxins and reduces their effect of the GIT. Off license – human preparation. prevention- Care with antibiotic selection. Consider the use of a fibre +/- probiotic supplement alongside antibiotic use in susceptible species (especially rabbits, guinea pigs, chinchillas, and hamsters) advise on dieat

Answer 200

Indicated for anaerobic infections including Clostridia spp. Risk of CNS toxicity at high doses Causes marked decrease in food intake in Chinchillas very unpalatabe

Answer 201

Ion exchange resin which binds to enterotoxins and reduces their effect of the GIT. Off license – human preparation. more palitable than metronidazole

Answer 202

Birds, especially psittacines, are commonly presented for routine beak trimming at veterinary practices. Beak trimming is only indicated where there is beak overgrowth (as a result of poor husbandry) or where the beak is malformed. neaoplasia, liverdisease- can lead to malformation of beak

Answer 203

Regurgitation and vomiting = similar ddx to cats and dogs therefore should be worked up in a similar manner. Differences include: Crop = additional potential site for pathology to occur. Behaviour regurgitation needs to be considered can be behavioural

Answer 204

Regurgitation = a mating behaviour in many psittacine species. Parrots are commonly hand reared to make them a more friendly pet as an adult -> confused parrots who try and pair bond with their owner. Accompanying behaviours: Aggression (‘mate’ and or nest guarding) Excessive vocalisation Masturbation (especially males)- cam lead to prolapse Feather destructive behaviour Treatment requires breaking the bond humanely: Avoid sexual behaviours (full body stroking, feeding from the mouth). Reward only non-sexual behaviours. Increase enrichment and interactions with other family members. Reduce environmental stimulus to breed (decreased day length, lower calorie diet)

Answer 205

Most commonly seen in backyard poultry: Sour crop Crop impaction Still relatively common in exotic avian species: Burns (crop feeding food which is too hot) Infection (bacterial, viral, parasitic, and fungal all reported) Severe crop burn  fistula.

Answer 206

Disruption of the normal crop flora -> candida overgrowth. Predisposing factors: Inappropriate diet Antibiotic use GI stasis -> delayed crop emptying. Diagnosis = clinical signs + abundant yeasts on crop cytology Treatment- Crop emptying and flushing – via inversion (high risk) or crop tueb. Treat underlying conditions where appropriate. Oral anti-fungals – Nystatin- POOR ORAL ABSORBTION so goood to treat crop Supportive care – probiotics (poor evidence), GI stimulants e.g. metoclopramide (if non-obstructive ileus present)

Answer 207

Oral anti-fungals POOR ORAL ABSORBTION so goood to treat crop

Answer 208

Causes: Ingestion of long grass, hay, string etc. GI hypomotility Diagnosis on clinical presentation (distended crop full of hard or doughy contents) Treatment: Conservative – poor prognosis and high risk of aspiration- may result in euthanasia Ingluviotomy - local used to numb skin over crop and uisision made and contents removed. soft food =should be fiven to avoid pressure on wound send contents for cytology to target antifungal or antibiotics

Answer 209

Common chamber for excretion -> faeces, urates and urine all expelled concurrently Polyuria commonly mistaken for diarrhoea by clients. Normal droppings = separate brown faeces, white urate, and liquid urine Polyuria= Brown faecal portion and white urates still formed, but floating in a large pool of liquid urine. Polyuria. Brown faecal portion and white urates still formed, but floating in a large pool of liquid urine.

Answer 210

Biliverdinuria Biliverdin = 1o bile pigment of birds. Liver disease or dysfunction  increased plasma biliverdin  yellow-green or lime-green urates. Do not confuse with dark green urates – associated with anorexia (usually faecal portion of droppings is absent) Investigations: Haematology and biochemistry Imaging Specific disease testing Treatment depends on underlying cause

Answer 211

Differentiate from seed spilled onto faeces. Due to malabsorption Diagnostics: History and CE Faecal examination Imaging Specific disease testing H&B less useful Treatment will depend on underlying cause.

Answer 212

Reptiles exhibit many gastrointestinal diseases which can be investigated in the same manner to traditional companion animal species: Stomatitis (≈ gingivitis) Diarrhoea Regurgitation Other disease processes are investigated and/or treated differently in reptiles cf of other species: Anorexia Constipation

Answer 213

Reptiles with anorexia can survive much longer and are usually presented much later than mammals and birds. Need to differentiate physiological vs pathological causes. Physiological: Brumation/hibernation Male snake breeding season anorexia Gravid/nesting females Sit and wait predators Pathological anorexia may be related to stress, an underlying disease condition and/or poor husbandry.

Answer 214

Extremely common in UK garden tortoises. Due to poor hibernation practice: Insufficient temperature control -> tortoises waking up and re-entering hibernation repeatedly -> exhaustion of glucose stores. Excessive hibernation length (>3m) -> leucopenia on waking. Diagnostic approach: History and clinical exam Haematology Biochemistry prevention- Provide correct husbandry Keep the animal in the preferred optimal temperature zone (POTZ) for that species. Provide UVB via an appropriate method (see BIAZA UVB Tool) Provide food to encourage intake. Prevention is with good hibernation practice: Health check including faecal parasitology Preparation period- 4 weeks Temperature controlled hibernation period- use fridge, allow air into fridge every day Close monitoring Limit hibernation length- max of 3 months for adults- 2 weeks for under 6 years old mustl limit ddue to production of white blood cells- not produced during hibernation so too long can cuase immune deficiency

Answer 215

Rehydration- Most important aspect of treatment Must correct dehydration BEFORE feeding Epicoelomic or intraosseus fluids in first instance, switching to oral once urine has been produced. 2x maintenance (40ml/kg/day) until urine production, then 20ml/kg/day Antibiosis Injectable as enteric absorption unreliable. Ceftazidime most commonly used- 3rd gen cephalosporin but better with side effects for tortuses Feeding - If eating does not resume, supportive feeding should be initiated. Oesophagostomy tube preferred for ongoing feeding. Increase food slowly to avoid refeeding syndrome.- usually doen for months

Answer 216

injectable as enteric absorption unreliable. Ceftazidime most commonly used- 3rd gen cephalosporin but better with side effects for tortuses

Answer 217

Infrequent defecation very common in reptiles – perceived as normal. Diagnostic approach: Husbandry history Clinical exam Faecal examination H&B Imaging Prevention: Correct husbandry Maintain hydration

Answer 218

Treatment: Water and KY enema Bathing Fluid therapy Treat underlying issue Lactulose reported but rarely necessary.

Answer 219

cliniical exam routine cbc and biochem serum cortison +- acth stimulation diet trial faecal culture =/- parasitology gastro biopsy endoscopic biopsy

Answer 220

Most common suspected cause of acute diarrhoea, especially in dogs. Spoiled food, inappropriate treats, change in diet etc. Usually only symptomatic treatment required; see PCP lecture.

Answer 221

Usually presents as chronic diarrhoea Diagnosis and treatment is via an exclusion diet. Need to take a thorough dietary history to allow selection of an appropriate exclusion diet: Single, novel protein and carbohydrate source (even if hydrolysed diets used) No treats, flavoured medications, toothpaste etc. Response is normally rapid (2-3 weeks) Wait 12 weeks before rechallenging with previous foods one at a time (optional)

Answer 222

Wide range of potential pathogens: Bacterial – Salmonella, campylobacter, clostridia etc. Viral – Parvovirus, distemper (paw pad hyperceritosis, coronavirus Protozoal – giardia, cryptosporidia, Toxoplasma, Tritrichomonas foetus, isospora Parasitic – roundworms, tapeworms, hookworms Faecal parasitology (parasites and protozoa) Faecal culture? Specific testing: Often offered as panels for different species: Canine: CPV, CDV, Enteric Coronavirus, Salmonella, Giardia, Cryptosporidia, C.jejuni, Clostridium perfringens enterotoxin Feline: FPV, Feline Coronavirus, Salmonella, Giardia, Cryptosporidia, Toxoplasma, Tritrichomonas foetus, C.jejuni, Clostridium perfringens enterotoxin Check individual labs for sample requirements. viral testing usually more clinically significant becuse pathonogenic bacteria can be fond in low levels in healthy animals

Answer 223

Treatment will depend on which disease(s) are involved: Parasitic disease: Most treatments will treat multiple types of intestinal parasite – check datasheets Fenbendazole covers for nematodes, cestodes and giardia so most appropriate option for trial treatment. Protozoal disease: Giardia – Fenbendazole Isospora – TMPS or anti-coccidiostats e.g. toltrazuril Cryptosporidia – usually self-limiting Bacterial disease: Mild cases: supportive care only Acute diarrhoea with suspected bacteraemia – amoxy/clav Campylobacter spp. - Erythromycin Other bacteria – Metronidazole (esp Clostridia spp.) or tylosin. Avoid broad spectrum or second line antibiotics!

Answer 224

Fenbendazole

Answer 225

Fenbendazole

Answer 226

TMPS or anti-coccidiostats e.g. toltrazuril

Answer 227

Mild cases: supportive care only Acute diarrhoea with suspected bacteraemia – amoxy/clav Campylobacter spp. - Erythromycin Other bacteria – Metronidazole (esp Clostridia spp.) or tylosin. Avoid broad spectrum or second line antibiotics!

Answer 228

Viral disease: Primarily supportive care. Anti-viral therapy - recombinant feline interferon, experimental drugs.

Answer 229

Definitive diagnosis on histopathology: Idiopathic inflammatory bowel disease Lymphangiectasia Granulomatous colitis Diagnosis of exclusion: Antibiotic responsive

Answer 230

Catch all term used to describe several conditions which meet the following criteria: Persistent GI signs, including diarrhoea Histological evidence of intestinal inflammation No response to diet trial. Lymphoplasmacytic = most common Eosinophilic, neutrophilic, granulomatous and mixed inflammation also reported.

Answer 231

Immunosuppression = mainstay of treatment Usually prednisolone, taper to lowest effective dose Ciclosporin may be useful in refractory cases Diet: Highly digestible and/or exclusion diets usually recommended. Supplementation with folates and cobalamin may be required. Manage dysbiosis Pre-, pro- and post-biotics Metronidazole or tylosin in severe cases Once symptoms controlled, may be possible to wean patient off therapy and maintain by dietary manipulation alone.

Answer 232

Differential for Protien Loosing Enteropathy (others = IBD and neoplasia) Causes: 1o congenital (rare) Obstructive neoplastic or inflammatory lesions of lymph system. 2o to hypertension (systemic disease – see later) Lymph build up in vessels  Loss of lymph across enteric mucosa  protein (mainly albumin), lipid and lymphocyte rich fluid in GIT  osmotic diarrhoea. Protein (albumin) loss exceeds liver synthesis-> Hypoalbuminaemia-> Decreased plasma osmotic pressure-> Ascites and oedema

Answer 233

Guarded to poor prognosis long term Management: Diet low in fat, high in good quality protein. Supplementation of fat-soluble vitamins (A, D, E, K). Anti-inflammatory therapy (oral prednisolone ). Metronidazole if secondary bacterial overgrowth present.

Answer 234

Aka histiocytic ulcerative colitis Predisposing factors: Breed + genetic lines Age (<2 years) Inflammation and invasive E. coli seen on histopathology Treatment = enrofloxacin SID for 4-8 weeks. Important to confirm diagnosis prior to starting antibiotic therapy

Answer 235

Not common; young, large breed dogs appear susceptible. Diagnosis of exclusion Treatment: Antibiotic choice: metronidazole or tylosin Dietary support Supplements Faecal microbiotal transplantation- risk of transefering pathogens, generally referal option

Answer 236

Antibiotic choice: metronidazole or tylosin may only require one treatment, may require multiple. only time you try suddently stopping antibiotics

Answer 237

Lymphoma most common, adenocarcinoma and mast cell tumour also reported. Clinical signs: Chronic, progressive diarrhoea Palpable abdominal mass +/ obstruction (focal masses) Hypoalbuminaemia (PLE) Weight loss Diagnosis: Imaging (ultrasound, radiography) Biopsy (FNA vs surgical)

Answer 238

Focal masses with no metastases: Mass resection with end-to-end anastomosis. Diffuse masses: Chemotherapy Complete remission may be possible with T cell lymphosarcoma. Palliative care: Prednisolone, nutritional support, anti-emetics, appetite stimulants, gastro-protectants, supplementation.

Answer 239

Pancreatitis and triaditis Endocrinopathies, most commonly hypoadrenocorticism (Addison’s disease) and hyperthyroidism (increased blood pressure???). Other systemic diseases (hepatic, renal, cardiac) Exocrine pancreatic insufficiency Drug induced

Answer 240

Most commonly -> idiopathic atrophy of pancreatic acinar tissue.- Less commonly following chronic pancreatitis, rarely congenital pancreatic hypoplasia. All -> lack of pancreatic digestive enzymes _> maldigestion -> polyphagia, weight loss, and steatorrhea +/- coprophagia. Definitive diagnosis based on bloods (Tripsin Like Immunoreactivity) +/- biopsy

Answer 241

Treatment: Pancreatic enzyme replacement Highly digestible diet, +/- fat restricted Cobalamin/vitamin B12 supplementation Small intestinal bacterial overgrowth = common sequale- metranidazole

Answer 242

NSAIDS Inhibition of COX-1 prostaglandins -> loss of gastrointestinal protective mechanisms, disrupting the mucosa and -> vomiting and diarrhoea. Antibiotics Disrupts the microbiome -> overgrowth of pathogenic bacteria e.g. E. coli and clostridia -> production of enterotoxins -> diarrhoea. Antifungal and chemotherapy drugs: Cytotoxic - affect rapidly dividing cells first, e.g. GI epithelial cells. Treatment: Withdrawal of the drug (where possible) Symptomatic

Answer 243

Usually 2o to major surgical resection; may be transient or permanent. Rare as a congenital condition. Removal of the ileocaecocolic junction= increased risk. May improve with fat restricted diet Supplementation with fat- and water-soluble vitamins and minerals required. Small intestinal bacterial overgrowth = common sequale.

Answer 244

Questions to consider: Is the diarrhoea acute or chronic Are you dealing with an animal that is systemically well? What are the immediate concerns in terms of patient stabilisation? Is the aetiology potentially infectious/ zoonotic? What is the most logical approach to diagnosis/ further investigations What are your treatment options – general/ specific/ +/- cost implications? What is the likely prognosis?

Answer 245

Due to inflammation of large colon and caecum (colitis/ typhlocolitis) Disruption of the mucosal barrier Altered motility Hypersecretion of fluid. Exact pathophysiology may vary with underlying aetiology. Underlying aetiology may only be established in < 50% of cases. Tachycardia Pyrexia Depression Tachypnoea Altered mucous membrane colour Delayed capillary refill time Poor jugular refill Ventral oedema Inappetence Weight loss Colic Sweating Muscle fasciculations Muscle weakness Laminitis. ** In some cases, diarrhoea may not be present at presentation

Answer 246

Salmonella species Clostridium species Cyathostominosis Equine coronavirus Potomac horse fever (not UK)

Answer 247

Drug-related (ie, NSAID toxicity, antimicrobial-related) Carbohydrate overload Sand enteropathy Toxins (e.g., acorn, cantharidin [blister beetle]) Dietary change CHO overload: lactate overproduction in the colon and subsequent colon mucosa damage and hyperosmolarity of the colon contents. > sepsis and laminitis Acorn toxicity results in acute onset clinical signs including haemorrhagic diarrhoea, colic, and renal dysfunction NSAID toxicity and sand enteropathy can cause acute diarrhoea, but more commonly result in chronic diarrhoea Potomac horse fever (PHF) Neorickettsia risticii – North America but also Europe. Watery diarrhoea and pyrexia. Affected horses commonly develop laminitis.

Answer 248

Healthy horses may shed salmonella asymptomatically Ubiquitous in the environment Invasion genes – encode proteins that cause ruffles in enterocyte membrane and Salmonellae become interiorized. Without invasion there is no response (opportunistic) Clinical signs: severe, acute enterocolitis, profuse diarrhoea, signs of endotoxaemia including pyrexia and tachycardia, and profound neutropenia Risk factors: Colic / GA / Hospitalisation/ Abx therapy/ Stress/ Transportation/ Intercurrent infection Often individual horse but contagious so clusters can occur Zoonoticq

Answer 249

(C difficile and less frequently C perfringens) Ubiquitous in the environment and can be a normal part of the equine intestinal Disease is caused by proliferation of toxigenic strains C difficile most common cause of antimicrobial-associated diarrhoea. Clinical signs: range from moderate illness with diarrhoea, pyrexia, depression and inappetence, to a rapidly fatal per acute colitis. Risk factors: Colic / GA / Hospitalisation/ Abx therapy/ Stress/ Transportation/ Intercurrent infection C difficile is a significant cause of diarrhoea in people

Answer 250

Equine coronavirus (ECoV) previously recognised in foals but now also adult horses. Individual cases and outbreaks of disease Clinical signs: pyrexia, lethargy, and anorexia; however, diarrhoea and colic are also reported. Encephalopathic signs secondary to hyperammonaemia. Mortality low – most horses recover (supportive care for encephalopathy if present) Fairly uncommon in the UK

Answer 251

Blood work Assessment of hydration, electrolyte and acid base abnormalities Ideally CBC and full biochemistry but minimally PCV/TP. Initial leukopenia characterised by neutropenia +/- lymphopenia. WBCC often re-bounds later in disease process PCV and TP (care) can help to determine hydration status PCV > 45% associated with decreased survival Serum biochemistry + electrolyte changes hyponatraemia, hypochloraemia, hypokalaemia, hypocalcaemia and metabolic acidosis. Prerenal or renal azotaemia Total protein and albumin often decreased (may be masked by dehydration) Elevation of blood lactate levels (dehydration or endotoxaemia) Elevation of Serum amyloid A and fibrinogen (varies with duration) fecal analyisis- salmonella- serial samples for Faecal PCR and culture Clostridium difficile- toxin a and B Toxin ELISA Clostridium perfringens- endotoxin toxin eliasa coronavirus- faecal pcr Neorickettsia risticii- faecal and vlood pcr Abdominal ultrasonography: Assess intestinal wall thickness, intestinal motility, stomach size, volume and appearance of peritoneal fluid Abdominal radiography/ (faecal sedimentation) Sand enteropathy

Answer 252

Aims : Modify the inflammatory response, replace the loss of fluid, protein and electrolytes. Mainstays: Fluid therapy, anti-inflammatory and anti-endotoxic medications, and laminitis prophylaxis Cost implications: Intensive treatment in a referral hospital setting can have significant financial implications and can easily reach similar costs as surgical treatment of colic fluid therapy- In general, i.v. fluids are required. Enteral fluids in mild cases Commercially available, balanced, polyionic crystalloid solutions, such as lactated Ringer’s, best choice for fluid resuscitation and maintenance requirements. In severe cases can use hypertonic saline ((2 to 4 ml/kg of 7.2 per cent solution) This must be followed by appropriate volumes of isotonic fluids to prevent cellular dehydration. Regularly reassess patient/ electrolytes/ protein levels Hypoproteinaemia is common > oedema formation, so these horses often need plasma +/- colloids (possible risks?) Limiting inflammation and endotoxaemia- Flunixin meglumine: Low dose? Full dose? Risk/benefit Polymyxin B: prevents the interaction of LPS with inflammatory cells and the initiation of the proinflammatory cascade. Risks? Intestinal binding agents: Di-tri-octahedral smectite (Bio-Sponge; Platinum Performance) binds bacterial exo- and endotoxins including C difficile toxins A and B and C perfringens enterotoxin. Laminitis prophylaxis: Digital cryotherapy (ice boots) Treatment of acute diarrhoea in adult horse is controversial and may decrease survival . May actually increase the shedding time in cases of Salmonella Use only in the case of identification of certain pathogens Clostridial associated diarrhoea : metronidazole. Cases with severe neutropenia and/or evidence of septic foci. Potomac horse fever (PHF) Neorickettsia risticii : oxytetracycline Probiotics: weak evidence of clinical benefit. Faecal transfaunation “ Poo soup” shown to be effective in treating C difficile infection in people. Risk of disease transmission.

Answer 253

Flunixin meglumine: Low dose? Full dose? Risk/benefit Polymyxin B: prevents the interaction of LPS with inflammatory cells and the initiation of the proinflammatory cascade. Risks? Intestinal binding agents: Di-tri-octahedral smectite (Bio-Sponge; Platinum Performance) binds bacterial exo- and endotoxins including C difficile toxins A and B and C perfringens enterotoxin. anitimicrobial therapy?- Treatment of acute diarrhoea in adult horse is controversial and may decrease survival . May actually increase the shedding time in cases of Salmonella Use only in the case of identification of certain pathogens Clostridial associated diarrhoea : metronidazole. Cases with severe neutropenia and/or evidence of septic foci- jugular vein thrombophlebitis Potomac horse fever (PHF) Neorickettsia risticii : oxytetracycline Laminitis prophylaxis: Digital cryotherapy (ice boots)

Answer 254

Diarrhoea that has been present for at least 7 to 14 days. Persistent or intermittent. Often mild or no signs of systemic disease. Usually associated with large intestinal (colon and caecum) disease, +/- small intestinal involvement. Not uncommon that a diagnosis is not reached despite extensive diagnostic investigations. Weight loss Ventral/ peripheral oedema Pyrexia Colic +/- Inappetence / reduced feed intake +/- Depression Increased Borborygmi

Answer 255

infectious- Cyathostominosis/ Parasitism Lawsonia intracellularis (weanlings) Chronic Salmonellosis Peritonitis non-infectious- Idiopathic colonic dysfunction/ undifferentiated/ dysbiosis Inflammatory bowel disease (IBD) Sand enteropathy NSAID toxicity Intestinal neoplasia (lymphosarcoma) Chronic Disease (Liver/ renal / CHF/ hyperlipaemia)

Answer 256

Clinical signs: Progressive weight loss, recurrent colic and slow-onset chronic diarrhoea Infiltration of the intestinal mucosa and submucosa by abnormal cells. Classification based on predominant cell type Granulomatous enteritis, lymphocytic - plasmacytic enteritis and eosinophilic enteritis. MEED: A more severe form of eosinophilic enteritis also exists that results in eosinophilic infiltration of other organs including the liver, lungs and skin Alimentary lymphoma is the main differential diagnosis for IBD Ultrasonography and rectal examination may reveal a thickened intestinal wall. Definitive diagnosis of IBD or lymphoma requires histopathology of intestinal biopsies

Answer 257

Primarily affects weanling and yearling horses between August and February Clinical signs: include lethargy, weight loss, pyrexia, diarrhoea and peripheral oedema. Marked hypoproteinaemia and hypalbuminaemia, and ultrasonographic evidence of small intestinal thickening Confirmed using faecal PCR

Answer 258

In regions with sandy soil/ low grass levels. May also present as acute D++ or predominantly as colic (may be recurrent) Dx radiography (faecal sand sedimentation tests are unreliable)

Answer 259

Prolonged or excessive NSAID use can result in mucosal ulceration and oedema of the right dorsal colon, known as right dorsal colitis (RDC).

Answer 260

Refer to “on demand” lecture can present as chronic diarrhoea

Answer 261

History May provide clinically relevant information Age, deworming history, administration of NSAIDs, soil type Blood work Findings depend on the underlying aetiology Dehydration is less common than in acute diarrhoea PCV may be decreased (anaemia of chronic disease) WBCC – normal or increased (contrast to initial leukopenia in acute D++ cases) SAA/ Fibrinogen – normal or increased Hypoproteinaemia and hypalbuminaemia most common findings Electrolytes may be normal but deranged in severe cases Other changes may reflect underlying disease e.g., liver disease, renal disease, hyperlipaemia Faecal analysis- Fibre length: poor mastication /altered digestion Microscopy: FWEC not useful for larval cyathostominosis but may see larvae PCR for chronic Salmonella or Lawsonia (weanlings) Dental examination- Poor mastication > Diarrhoea Abdominal ultrasonography- Assess intestinal wall thickness (2-4 mm normal) thickened in IBD/ neoplasia/ NSAID toxicity (RDC) Volume and appearance of peritoneal fluid (peritonitis) Rectal examination - Assess intestinal wall thickness, position and size of the large colon and abdominal organs, and abnormalities of lymph nodes Abdominocentesis - Indicated in cases accompanied by hypoproteinaemia or pyrexia Inc. in WBCC/ protein levels indicates inflammatory process/ peritonitis Cytology for abdominal neoplasia – neoplastic cells rarely exfoliate into the abdomen so -ve result does not exclude neoplasia. Oral glucose absorption test- Indicated in cases of diarrhoea where malabsorption is suspected (e.g., IBD or neoplasia) Administer 1 g/kg glucose as a 20 per cent solution by NG tube in unsedated horse. Collect blood samples. Glucose levels should double from the baseline at 90 to 150 minutes and return to resting by 360 minutes **Many factors can influence the results, including intestinal transit, age and hormonal and metabolic status Abdominal radiographs- Identify sand within the large colon. Biopsy - Rectal or duodenal – IBD/ neoplasia

Answer 262

Often possible to complete diagnostic tests before developing a treatment plan Non-specific therapies- Codeine phosphate (1–3 mg/kg administered orally every eight to 24 hours) Prolongs intestinal transit time and decrease faecal water content. Dietary manipulation can improve or even resolve chronic diarrhoea in many cases. E.g., reduction in the moisture content ( decrease grass increase hay). Change often recommended on basis of suspected aetiology Antimicrobials- Rarely warranted. Exceptions Lawsonia / peritonitis

Answer 263

Tetracyclines (e.g., oxytetracycline) or macrolide antimicrobials. (***Care re colitis in older animals with macrolides)

Answer 264

Antimicrobials broad spectrum or as directed by C&S

Answer 265

Corticosteroids Dexamethasone (0.05–0.1 mg/kg i.v/ i.m q 24 hours) Prednisolone (0.5–1 mg/kg po q 24 hours) Azathioprine (1–3 mg/kg p.o q 24 hours)

Answer 266

Psyllium (1 g/kg) and magnesium sulfate (1 g/kg) combined with water and administered via a nasogastric tube q 24 hours for four days +/- mineral oil. Hay diet

Answer 267

Misoprostol (2.5–5 µg/kg administered orally every 12 hours) Sucralfate (10–20 mg/kg administered orally every six to 12 hours)

Answer 268

Dietary manipulation/ Faecal transfaunation/ Probiotics?

Answer 269

acute- Salmonellosis (S. Dublin, S. Typhimurium) Winter dysentery (Coronavirus) Carbohydrate overload – acute acidosis Malignant Catarrhal Fever Bovine Viral Diarrhoea (BVD) – infection in naïve animal/herd chronic- Johne’s disease (paratuberculosis) SARA – Subacute Ruminal Acidosis Mucosal disease (BVDV) – up to about 2 yrs generally Parasitic Gastroenteritis (PGE) – usually subclinical in adult beef and dairy cows Fasciolosis – Fluke Fasciola hepatica Renal amyloidosis (rare) Upper alimentary tract squamous cell carcinoma (typically older beef cows – bracken in hill areas)

Answer 270

Increasing and common problem in high-yielding dairy herds Digestive disorder – suggested as possibly the most important nutritional disease of dairy cattle (Enemark, 2009) Leads to metabolic acidosis – lactic acid levels high Substantial economic costs linked to reduced milk production, decreased efficiency milk production, premature culling and increased fatalities in dairy cows Common sequelae of SARA in a dairy herd: Rumenitis Metabolic acidosis Reduced Dry Matter Intake (DMI) Abomasal displacement and ulcers Laminitis Bloating of rumen Reduced fertility Two distinct risk groups in the dairy herd: Cows in early lactation exposed to high energy rations too quickly – low rumen pH <=5.5 Cows in mid-lactation on high feed intake, sensitive to sudden changes in feed composition or delivery Faeces can be bright yellowish colour with unusual sour smell and appear foamy with gas bubbles and more than usual amounts of undigested fibre or grains Intermittent diarrhoea - inadequate digestion and fast passage of feed through the gut

Answer 271

Sudden overload of carbohydrate e.g. animal accessing a concentrate feed store or mistake in mixer feed wagon Colic signs – restless Distended abdomen due to bloat and large, fluid-filled static rumen Become weak and ataxic, teeth grinding, anorexic Increased resp. rate due to metabolic acidosis Profuse watery diarrhoea can develop after 24 hrs Rapid carbohydrate loading of rumen – lactic acid production – pH drops below 5.5 Marked increase in rumen liquor osmolarity with fluid drawn in - dehydration Low rumen pH reduces motility – stasis - bloat Lactate absorbed into circulation – metabolic acidosis Damaged rumen mucosa – absorption of toxins – seeding of infection to liver possible

Answer 272

High fatality rate in severely affected animals – treatment can be attempted More basic approach: Oral or IV fluids, antibiotic therapy (bacteraemia due to rumenitis), IV vitamins More adventurous: Rumenotomy – surgical approach to remove rumen contents – but need to prevent leakage into abdomen in a recumbent animal: Niehaus (2008): https://doi.org/10.1016/j.cvfa.2008.02.011 Rumen lavage – administering large volumes of water to rumen and then trying to siphon off again through wide-bore stomach tube

Answer 273

Most common isolate in cattle in UK - Salmonella Dublin More common in dairy herds than suckler herds It can cause differing clinical pictures on farms depending on which class of cattle are most affected: Adults – abortion, diarrhoea, milk drop, (septicaemia) Calves – diarrhoea, septicaemia, pneumonia, arthritis, meningitis 1. Acute salmonellosis can occur in adult animals. They can develop enteritis with diarrhoea and pyrexia. Especially S. Typhimurium. 2. Chronic salmonellosis - adult animals - repeated episodes of diarrhoea with loss of condition. Animals can shed intermittently – carrier animals, making eradication from the herd difficult. S. Dublin infection is especially prone to carrier state in adults – stress trigger. 3. Salmonella spp. infection causes abortion in cattle infected in late pregnancy – especially with S. Dublin. 4. Septicaemia - usually young animals. Develop a high temperature and can die very quickly. Recovered animals can become carriers – intermittent shedders – stress of calving Chronic problem of Salmonella outbreaks on a farm often due to carrier animals and this would require screening of entire herd to find the source Excreted in faeces, milk, urine, saliva, vaginal discharges S. Dublin can survive for up to 6 years in dried faeces (Plym-Forshell & Ekesbo, 1996) Bought-in cattle can be a source of introducing infection to a clean herd Study found 40% of dairy herds in GB showed evidence of infection on bulk milk testing (Henderson et al. 2022: Prev. Vet. Med., 208, 105776) - widespread Zoonotic – infection usually contracted from handling sick or carrier animals or aborted material Abortions in last trimester of pregnancy with retained placenta and possible metritis – most often caused by S. Dublin Bulk milk tank testing good way of simple herd surveillance at farm level Vaccine available to help control the disease in cattle Importance of on-farm within-herd biosecurity and hygiene – isolation of cases if possible

Answer 274

Bovilis® Bovivac® S (MSD Animal Health) ‘For the active immunisation of cattle in order to induce serological and colostral antibody production against Salmonella Dublin and Salmonella Typhimurium and in the face of an outbreak to reduce Salmonella Typhimurium infections when used under field conditions as part of an overall herd management programme. Bovilis Bovivac S may also contribute to reducing S. Typhimurium contamination of the environment.’

Answer 275

Mycobacterium avium paratuberculosis (MAP) Chronic disease, normally seen clinically in cattle aged 4 yrs + (but can shed before clinical signs) A major problem globally - dairy and beef herds Bacterium infects macrophages of Peyer’s patches of small intestine – chronic granulomatous enteritis Is it zoonotic? – increasing volume of evidence from human medicine Young calves more susceptible than adults – infected up to about 1 year old Faecal-oral - main transmission route – usually dam to calf, or other infected dam in group calving pen Ingested through colostrum/milk; contaminated surfaces – udder, calving pen floor, pasture, soil, water, feed Infected semen – shared bull In utero infection possible ‘ICEBERG’ PHENOMENON – hidden burden of infection on the infected farm Cattle susceptible to infection up to about 1 year of age, but the earlier they get infected, the worse the subsequent lesions – must reduce calf exposure stages- scilent, subclinical, clinical, advanced- diarrhoea at htis stage may take years to progresImmune response involves massive inflammatory cell infiltration into intestinal wall – thickening and destruction of villi Progressive malabsorption leading to weight loss and chronic diarrhoea (eventually) – but causing lot of harm before we get to that point! Cases often culled prematurely before see obvious ‘classic’ clinical signs: Decreased milk yield in dairy cattle; increased risk of lameness and mastitis; infertility – culled from herd earlier as lame, mastitic or barren Many dairy herds in GB now testing milk regularlys

Answer 276

Can cause a variety of conditions (diarrhoea, respiratory disease, subfertility, abortion, congenital disease, Mucosal disease) Immunosuppression a significant feature Major economic importance in the UK herd and internationally Normally a mild enteric disease in calves/cows (more severe form – Type II) BVDV infection in a naïve, unvaccinated and previously unexposed animal or herd can result in a transient diarrhoea There may be pyrexia, dullness and milk drop in dairy animals Non-pregnant cattle – clinical recovery and seroconversion, protection for up to 3 yrs But there could be further problems in pregnant cattle, depending on stage of gestation - abortion or the persistently infected calf BVDV can cause Mucosal disease (MD) in persistently infected animals – the ‘trojan horses’ of BVD MD stems from in-utero infection of calf with BVDV from naïve dam - PI Outcome depends on time of infection: First month – usually early abortion 2 – 4 months – persistent infection (PI) of the foetus 5 – 9 months - abortion, congenital abnormalities or normal healthy calf Also causes immunosuppression and low-grade infertility and subfertility in endemically-infected herds Vaccines - normally given to breeding heifers at least 2 months before first service (Bovilis BVD, MSD; Bovela, Boehringer). Booster vaccinations. Important to identify and remove PI animals from the herd (antigen positive / antibody negative in blood tests) BVD - National control voluntary programmes (England, Wales) and compulsory with legislation – identification and removal of PIs (Scotland, NI)

Answer 277

BVDV can cause Mucosal disease (MD) in persistently infected animals – the ‘trojan horses’ of BVD MD stems from in-utero infection of calf with BVDV from naïve dam - PI Outcome depends on time of infection: First month – usually early abortion 2 – 4 months – persistent infection (PI) of the foetus 5 – 9 months - abortion, congenital abnormalities or normal healthy calf Persistently infected animals are the main source of infection for the rest of the herd. PI animals normally do not grow well – ‘poor doers’ – prone to other infections Virus mutates to cytopathic virus in PI animal and produces Mucosal disease – infection & necrosis of all gut-associated lymphoid tissue – ulceration of alimentary tract, oral cavity – severe diarrhoea, mucopurulent nasal discharge, oral and interdigital erosions and death/euthanasia – PIs must be detected and removed asap

Answer 278

Vaccines - normally given to breeding heifers at least 2 months before first service (Bovilis BVD, MSD; Bovela, Boehringer). Booster vaccinations. Important to identify and remove PI animals from the herd (antigen positive / antibody negative in blood tests) BVD - National control voluntary programmes (England, Wales) and compulsory with legislation – identification and removal of PIs (Scotland, NI)

Answer 279

Bovine coronavirus (BCoV) – detected in faeces and nasal secretions Significant economic impact globally (production losses) Epizootic herd outbreaks of watery diarrhoea with dark blood, usually during the winter housing period Extremely high morbidity in naïve herds (up to 100% affected), virtually zero mortality Pyrexic, depressed, anorexic, milk drop (can be up to 70%) Supportive treatment only – usually recover in few days, outbreak over in 1-2 weeks Norway only country in world to have a national control programme

Answer 280

More common to see beef/suckler cattle with severe fluke infestations compared to dairy - more likely to be areas of endemic fasciolosis Intermediate host – Galba truncatula mud snail Can lead to chronic diarrhoea and weight loss in cattle Differentials – Salmonellosis, Johne’s disease

Answer 281

Bacterial: [MAP: Johne’s disease] – but diarrhoea not common in sheep, in contrast to cattle Salmonella spp. Parasitic gastroenteritis (PGE) – NB Periparturient rise in ewes after lambing Others: Concentrate overfeeding - acidosis

Answer 282

Adult sheep (and goats) – highly prevalent in UK, but often ignored and greatly under-diagnosed Rarely get diarrhoea until terminal stages – many sheep will be shedding MAP without obvious signs Chronic weight loss is most obvious sign – thin ewes around 3-4 yrs old Poor fleece quality also seen Infertility - often culled as barren ewes before development of other signs Diagnosis – group blood tests – hypoalbuminaemia (loss of albumin from damaged intestine), blood ELISA (low sensitivity, high specificity), post-mortem signs, (faecal samples – poor diagnostic power) Vaccine available for sheep and goats (Gudair, Virbac: Clinical particulars - Gudair emulsion for injection for sheep and goats (noahcompendium.co.uk)) – offers best long-term control prospect

Answer 283

One of most common causes of neonatal diarrhoea in beef and dairy herds May cause high mortality in outbreaks, usually in calves aged 8-14 days old Incubation 1-3 days – fast spread Concurrent infection with Cryptosporidium makes diarrhoea worse Very watery green/yellow faeces Can collapse, severely dehydrated with sunken eyes, acidotic Need IV fluid therapy if collapsed and acidotic – can add bicarbonate to fluids to counteract acidosis Colostrum and pen hygiene Rotavirus is zoonotic – and genetic reassortment is possible between animal and human strains

Answer 284

Another common cause of neonatal diarrhoea ETEC strains of E. coli possess the K99 antigen They do not invade the intestinal mucus and villi remain intact – but toxin draws hypersecretion of fluids into gut Typically calves at 1-3 days old Sudden onset profuse yellow-white diarrhoea (no blood or mucus) Quickly dehydrated and recumbent – fluid therapy Bovilis® Rotavec® Corona Emulsion for Injection for Cattle (MSD Animal Health)- For the active immunisation of pregnant cows and heifers to raise antibodies against E. coli adhesins F5 (K99) and F41, rotavirus and coronavirus

Answer 285

For the active immunisation of pregnant cows and heifers to raise antibodies against E. coli adhesins F5 (K99) and F41, rotavirus and coronavirus. While calves are fed colostrum from vaccinated cows during the first two to four weeks of life, these antibodies have been demonstrated to: - reduce the severity of diarrhoea caused by E. coli F5 (K99) and F41 - reduce the incidence of scours caused by rotavirus - reduce the shedding of virus by calves infected with rotavirus or coronavirus. Onset of Immunity : Passive protection against all active substances will commence from the start of colostrum feeding. Duration of Immunity : In calves artificially fed with pooled colostrum, protection will continue until colostrum feeding ceases. In naturally suckled calves, protection against rotavirus will persist for at least 7 days and against coronavirus for at least 14 days.

Answer 286

Trivacton 6 (Boehringer Ingelheim):Clinical particulars - Trivacton 6 (noahcompendium.co.uk) Lactovac (Zoetis): Uses - Lactovac suspension for injection (noahcompendium.co.uk) Bovigen Scour Emulsion (Virbac): Clinical particulars - Bovigen Scour Emulsion for injection for Cattle (noahcompendium.co.uk) Bovilis® Rotavec® Corona Emulsion for Injection for Cattle (MSD Animal Health)

Answer 287

Most common isolate in cattle in UK - Salmonella Dublin More common in dairy herds than suckler herds It can cause differing clinical pictures on farms, with a range of possible symptoms Usually calves aged 2-6 weeks, often high morbidity and mortality in affected groups Septicaemic form - Develop a high temperature and can die very quickly before being noticed (within 6-12 hrs) Typical signs if enteric: Dull, anorexic, pyrexic, grey pasty faeces with fresh blood and mucus Older calves may develop diarrhoea – foul-smelling with mucus May also develop pneumonia or meningitis – may even be the primary presenting sign Surviving calves often grow poorly, with polyarthritis and gangrene of extremities possible – ear tips, tail tip zoonosis!

Answer 288

Fluid and electrolyte therapy to counteract the dehydration caused by the diarrhoea – mainstay of treatment May need intravenous fluid therapy depending on condition and economic value Antibiotics are used in the treatment of systemic Salmonella cases – note the AMR and AM stewardship implications – but calves often have bacteraemia and other clinical signs, so may be more justifiable than adults Vaccine widely used: Clinical particulars - Bovilis® Bovivac® S (noahcompendium.co.uk)

Answer 289

Protozoal disease – especially Cryptosporidium parvum Common in UK, across Europe and globally - endemic Oocysts ingested (as low as 25 for infective dose) and parasite multiplies in small intestinal mucosa leading to diarrhoea (mucus, blood and straining) Mainly seen in beef/dairy calves from 4 – 6 weeks up to about 6 months of age Associated with intensively stocked, unhygienic conditions (indoors and outdoors) – very stable oocyts in environment Increased risk in mixed age groups (suckler cows/calves) and mixed with lambs

Answer 290

Halofuginone is an oral solution for calves (Halocur, MSD; Stenorol Crypto, Huvepharma NV; Kriptazen, Virbac) - best for prophylaxis, but also licensed for treatment – administer to newborn calves from 24-48 hrs on infected farms to reduce shedding and improve calf outcomes Control aimed at reducing stocking density and improving environmental hygiene: - Regularly moving feed and water troughs and prevent faecal contamination - Bedding management - Clean and disinfect all buildings with products that kill oocysts - difficult

Answer 291

Calves – Eimeria alabamensis, E. bovis, E. zuernii Infection causes loss of epithelial cells and villous atrophy Severe cases - sudden onset profuse diarrhoea containing mucus and fresh blood. Straining and potential rectal prolapse. Temperature normal. Chronic cases – wasting and poor appetite in animals < 1 yr old Low-level infections can produce immunity for the future, and even clinically normal animals may shed coccidian oocysts Sources of infection – sporulated oocysts in watercourses, contaminated sheds or on pastures

Answer 292

hygiene; medication: decoquinate e.g. Deccox 6% Premix for Medicated Feeding Stuff for Sheep & Cattle (noahcompendium.co.uk); diclazuril e.g. Vecoxan® 2.5 mg/ml Oral Suspension (noahcompendium.co.uk); toltrazuril e.g. Cevazuril® 50 mg/ml, oral suspension for piglets and calves. (noahcompendium.co.uk)

Answer 293

Key features: Infection may be inapparent – subclinical Can cause diarrhoea, pyrexia and death (septicaemia) Any age, but most common in weaners and growers Serotypes found in pigs are also zoonotic Any age of pig can be affected clinically Fever to 41C in acute scenario Diarrhoea can initially be yellow, but blood can be introduced later - often foul smelling Pigs with diarrhoea rarely die but may be stunted with necrotic ear tips Rectal stricture syndrome possible later – distended abdomen Salmonellae enter pig herd via introduced breeding stock, feed, water supply, fomites, vectors such as rodents and wild birds Salmonella spp. are transmitted in faeces and resist drying in environment – long survival even in dust – needs effective C&D Carriage in tonsil and terminal ileum – chronic shedding controle and prevention Hygiene - all-in all-out housing and effective disinfection Isolation of affected pigs - quarantine Rodent control – mice and rats Exclude birds (but what about outdoors?) Pasteurised feed supplies - should not be contaminated Treat cases and cull chronically-affected animals Pigs carry salmonellae on tonsils and in caecum until slaughter Possibility of faecal contamination of carcase after slaughter Salmonellae in pork can cause human foodborne infections ELISA tests on meat juice allows herd detection at abattoir How best to control? Primary production or after slaughter?

Answer 294

Bacterial: E. coli spp. Salmonella spp. Clostridium perfringens Type B – lamb dysentery Protozoal: Coccidiosis Cryptosporidium Parasitic worms (to be covered later): e.g. Nematodirus battus, Teladorsagia, Trichostrongylus Viral: Rotavirus

Answer 295

endotoxaemia – E. coli Davies et al. (2017) - oral antibiotics were prescribed to 49% of British sheep flocks – now removed from market (Spectam Scour Halt) Presents as lethargy, unwillingness to drink, profuse salivation, abdominal distension, scouring in some later cases E. coli multiplies in small intestine – produces endotoxins More common in indoor lambing conditions, esp. triplets, esp. later in lambing season Delayed/inadequate colostrum predisposes Prevention – adequate colostrum, as soon as possible; hygiene Cases - Electrolyte solutions, supportive care – but often fatal – high mortality rate typical post mortem findings No milk in abomasum Abomasum distended with air Liver congested – toxic effects Retained meconium Pure growth E. coli isolated from intestinal contents

Answer 296

Cryptosporidium parvum also common in lambs as well as calves - not host specific Typically second half of lambing - build-up of oocysts in environment – can survive on pasture for months Faecal-oral infection route Mainly seen in lambs about 3-7 days old – profuse yellow-green diarrhoea, some mucus Lambs appear dull with tucked-up abdomen, reluctant to follow dam – can collapse Associated with intensively stocked, unhygienic conditions (indoors and outdoors) Oral fluid therapy for dehydrated lambs. Halofuginone not licensed for sheep.

Answer 297

Eimeria crandallis and Eimeria ovinoidalis of most importance in sheep Typically seen in lambs aged 4-8 weeks old – most likely age for clinical impact Poor appetite, diarrhoea, dehydration, poor growth rate, deaths Sporulated oocysts ingested – from pasture/shed, other older lambs, ewes excreting them around lambing (probably in that order of importance) Lambs may also be infected with Nematodirus battus or pasteurellosis, causing co-morbidity and increased likelihood of death Similar licensed treatments as for calves; environmental hygiene and management of feed troughs – move regularly

Answer 298

TRP traumatic reticulopericarditis Left Displaced AbomasumRight Displaced Abomasum RD(T)A Abomasal ulcers Abomasal impaction Hair balls Caecal dilation and torsion Bloat/red devil-emergency lecture

Answer 299

displacement of the abomasum from the right ventral floor of the abdomen to the left dorsal abdomen after a period of inappetence. How common are they: winter/early spring due to housing management. Incidence: 0.05–6%. Targets to be under-Yield dependent: <8000-8500kg/cow/year = 0 LDA >8,500 kg/cow/year = <2% LDA Cost: surgery £200-300, treatment costs, premature culling, reduced fertility. discarded milk, and reduced milk yield Gravid uterus pushes the rumen forward and restricts rumen volume, decreased DMI Three factors allowing the abomasum to move further left 1. The rumen fails to fill the void by the involuting uterus after parturition, 2. The omentum attached to the abomasum must have been stretched 3. Abomasal atony: Cause of atony: less clear. Increased VFA production, decreased smooth muscle tone associated with hypocalcaemia, accumulation of sand in the abomasum. High concentrate, low fibre diet-high VFA-inhibits abomasal motility & Also decreases rumen pH and increases rumen osmotic pressure. Reduced feed intake during the transition period Reduced fibre in transition diet The LDA causes minimal decrease in abomasal outflow A mild hypochloraemia, hypokalaemic metabolic alkalosis may be seen. ‘rumen vomiting’ Blood pH and bicarbonate levels are elevated, with a concomitant decrease in blood chloride concentration Signalment-dairy cows, most commonly in the first month after calving History: associated with concurrent disease (hypocalcaemia, retained foetal membranes, twinning, (endo)metritis, endotoxaemia), high concentrate/low fibre rations. high/low bcs, multiparous, Holstein, low dmi Clinical signs-variable, may be complicated by the presence of other diseases especially metritis, secondary acetonaemia. 2 presentations ‘types’- Acute: Clinical signs most severe when the LDA occurs with metritis 5-7d post calving, pyrexic, depressed, toxaemic, anorexic, depressed milk yield. hypocalcaemic episodes, diarrhoea. Drawn up abdomen and sunken flanks. Ribs prominent, moderate dehydration (5-7%) 2 presentations ‘types’- 2. Chronic: Cases occurring over 10days in milk, chronic endometritis, secondary ketosis. Often presented 15-30dim, history poor milk yield (50% reduced), reduced appetite, chronic weight loss (up to 50kg since calving, one BCS unit), slow and dull mentation, dry and staring coat, normal temperature, constipated/stiff faeces. Diagnosis: CE: over the 11th-13th left rib- LDA percussion (ping-gas:fluid interface) and succussion (slosh), +/- other conditions, metabolic alkalosis on urine dipstick. Confirmed by surgery or paracentesis of the displaced abomasal contents with a pH 2 and no protozoa, U/S. The distended abomasum occupies the cranio dorsal area of the left abdominal cavity (under the ribcage). Rumen movements can be heard caudally in the sublumbar fossa, Rarely palpate any structural abnormality on rectal exam-uncommon to palpate the caudal edge of the abomasum. Problem list Left 11th-13th rib space high pitched percussion ‘Ping’ and succussion ‘slosh’ +/- Mucopurulent vaginal discharge (Metitis) +/- High blood/milk/urine BHB (ketosis) +/- pyrexia Demeanour Toxaemia Dehydration Decreased milk yield Posture Weight loss Diarrhoea inappetence

Answer 300

Diagnosis: CE: over the 11th-13th left rib- LDA percussion (ping-gas:fluid interface) and succussion (slosh), +/- other conditions, metabolic alkalosis on urine dipstick. Confirmed by surgery or paracentesis of the displaced abomasal contents with a pH 2 and no protozoa, U/S. The distended abomasum occupies the cranio dorsal area of the left abdominal cavity (under the ribcage). Rumen movements can be heard caudally in the sublumbar fossa, Rarely palpate any structural abnormality on rectal exam-uncommon to palpate the caudal edge of the abomasum.

Answer 301

Treatment options: Rolling (+/- laparotomy) (£, <40% success)- Rolling takes time, safe floorspace, 3 people and may be only 40% effective at best. Risk of inhaling rumen contents and people being kicked start with rhs down, then onto back, jiggle abdomen and percuss for abomasum moving to the ventral abdomen, then roll onto left side down, jiggle, allow to stand, percuss to check abomasum has moved to rhs Pump with 40L electrolytes Treat concurrent disease laparotomy (right or both sides) (£££, highly successful)- Many methods-single/double sided laparotomy- omentopexy/ pyloropexy, toggle, laparoscopic Find your preferred method and do that well Pyloropexy omentopexy Toggle (££, greater risk of injury and peritonitis) Euthanasia- cull/fallen stock, economics +supportive therapy

Answer 302

Laparotomy (preferred method) Many methods-single/double sided, omentopexy, pyloropexy, Preoperative NSAID and antimicrobial Clip Local anaesthesia +/- sedation Surgical prep cow, yourself and kit Abdominal entry and ‘tourism’ +/- deflate the abomasum Correct the position of the abomasum Pexy omentum/pylorus and close abdomen Aluminium/antibiotic spray on the incision Pump with 40L electrolytes Treat concurrent disease Follow up phone call-eating, increased milk production, improved demeanour Laparotomy -pyloropexy clip Local anaesthesia Surgical prep cow, yourself and kit Abdominal entry and ‘tourism’ +/- deflate the abomasum Correct the position of the abomasum Pexy omentum/pylorus and close abdomen Aluminium/antibiotic spray on the incision Pump with 40L electrolytes Treat concurrent disease

Answer 303

Treatment options: + supportive therapy Treat concurrent conditions Ketosis-300ml oral propylene glycol sid/bid daily 3-5days, vitamin B12 daily 3 days, liver forte, choline, for BHB over 5mmol/L give 400ml 50% dextrose iv once Metritis-preoperative amoxicillin daily 3-5days, Mild-moderate dehydration: 40L Oral fluids (with electrolytes, calcium (improves abomasal motility) yeast, appetite stimulants, energy. Eg ‘Selekt Off Feed’) (Severe dehydration: add IV fluids 3L 7.2% hypertonic saline on day 1) Analgesia (and potential anti endotoxaemic properties) Preoperative NSAID –Ketaprofen/ meloxicam/ flunixin/carprofen High fibre diet for 5days post op, re introduce concentrates slowly

Answer 304

Rolling (+/- laparotomy) Rolling takes time, safe floorspace, 3 people and may be only 40% effective at best. Risk of inhaling rumen contents and people being kicked start with rhs down, then onto back, jiggle abdomen and percuss for abomasum moving to the ventral abdomen, then roll onto left side down, jiggle, allow to stand, percuss to check abomasum has moved to rhs Pump with 40L electrolytes Treat concurrent disease

Answer 305

Prompt identification and treatment of early metritis/retained placenta/ketosis Oral fluid therapy can help restore rumen volume and increase feed intake in a cow with reduced appetite Analgesia Herd level Provide long fibre in early post partum period eg hay Avoid high concentrate levels immediately following calving Dry/transition nutrition that reduces the risk of hypocalcaemia (eg acidifying DCAB diets) Prevent over fatness in dry cows/heifers-monitor bcs Dry/transition/fresh yard management Monitor rumen fill, Monitor energy (dry & fresh cows) Monitor post partum disease levels

Answer 306

Right dilated abomasum -Less common than LDA Incidence hard to define, dairy cows but rarely does occur in other cattle Cost similar to LDA Aetiology and pathogenesis is not fully understood, though probably due to atony caused by high concentrate feed leading to secondary fermentation (allowing inflation and movement). Proportionally fewer RDA occur in fresh cows than LDA, indicating that atony is involved rather than lack of rumen fill. Once atonic, feed, fluid and gas accumulate in the abomasum which cause it to be grossly distended. The distended abomasum cannot move left due to a full rumen so it moves dorsally right Target=0% Biochemical changes-similar to LDA, plus abomasum does not empty itself into the duodenum Signalment- primarily adult dairy cows in early lactation History: onset is insidious, inappetence, reduced milk yield, weight loss, some ketosis Clinical exam: dull, afebrile, Mild dehydration reduced rumen contractions (weak and irregular). elevated HR over 80bpm, Faeces reduced (may be diarrhoeic, foul smelling, melena), percussion and succussion of right abdomen over 8th-13th rib= right ping and slosh(15-20cm diameter), colic behaviour-lifting leg up to abdomen, flank watching. Distention on right abdomen, on rectal exam-feel distended lower right quadrant. Problem list: dull, afebrile, reduced rumen contractions (weak and irregular). Mild dehydration Faeces reduced (may be diarrhoeic, foul smelling, melena), elevated HR over 80bpm, percussion and succussion of right abdomen over 8th-13th rib= right ping and slosh(15-20cm diameter), colic behaviour-lifting leg up to abdomen, flank watching. Distention on right abdomen, on rectal exam-feel distended lower right quadrant.

Answer 307

CE: over the 8th-13th right rib- LDA percussion (ping-gas:fluid interface) and succussion (slosh), metabolic alkalosis on urine dipstick. Confirmed by surgery or paracentesis of the displaced abomasal contents with a pH 2 and no protozoa, U/S. The distended abomasum occupies the cranio dorsal area of the right abdominal cavity (under the ribcage). Rarely palpate any structural abnormality on rectal exam-uncommon to palpate the caudal edge of the abomasum.

Answer 308

Treatment options: Medical-mild/early cases Hyoscine-n-butyl (Buscopan)-spasmolytic IV Calcium-improve contractility of abomasum (oral/sc) Oral coffee-improve contractility of abomasum Metaclopromide -now banned in food producing species!!! (was used to enhance gastric emptying into the small intestines) Surgery-(recommended due to risk of ensuing torsion) Cardiovascular stabilisation pre-op Voyage of discovery-prepare for the unexpected! Euthanasia Low economic value or poor prognostic cases Prognosis-HR over 100 grave, 81.2% return to a productive life, 1wk post op success or not Prevention-individual and herd-careful concentrate feeding

Answer 309

Surgery-(recommended due to risk of ensuing torsion) Cardiovascular stabilisation pre-op 3-5L hypertonic saline IV, followed by isotonic saline IV or oral electrolytes. Preoperative NSAID and antibiotic Standing right flank laparotomy (similar to an LDA), care during incising the abdominal muscles that the dilated abomasum is not cut. On entering the abdomen, decide if it is torsed or not. Decompress the abomasum: deflate of gas/ remove excess fluid using a pipe and a stab incision through a purse string (remove pipe, tighten purse string and over-sew purse string with absorbable suture) Push the abomasum ventrally Pexy the pylorus/omentum as per an LDA Close the abdomen as per an LDA Post op: 40L oral electrolytes, propylene glycol, multivitamins

Answer 310

Right dilated and TORSED abomasum. Incidence-very low (clinician may see 1/year) Cost-similar to LDA, plus loss of animal Target-0% Cause- following right displacement, as yet unknown mechanical factors Following dilation and displacement phases, the distended abomasum may rotate around an axis through the centre of the lesser omentum. rotate clockwise or anticlockwise-the majority go anticlockwise, resulting int a 180-270degree torsion. If left uncorrected this positional change has the potential to produce an abdominal catastrophe, involving complete luminal obstruction and irreversible neurovascular damage or necrosis! Signalment-same as RDA History-torsion is more acute than RDA, patient condition deteriorates quickly over the next 12-24hrs. Sudden onset abdominal pain which may only last a few hours. ! Untreated animals die within 48-72hours (in real terms by the time you see this you have about 6hours to initiate meaningful treatment) from severe dehydration, shock and toxaemia. Clinical signs: HR increases rapidly, 100-120bpm, anorexia, no milk yield, due to peripheral circulatory collapse the cow is cold to touch, is hypothermic, toxic, pale mucous membranes, marked dehydration >8% due to sequestered fluid in the abomasum. right distention of the abdomen & ping, on rectal palpation can feel a distended viscous on the upper right quadrant. rectum is empty. Biochemical changes: similar to RDA, plus marked dehydration (haemoconcentration) is a prominent feature Problem list: Whole of the clinical exam………seriously sick! Differential diagnosis- vagal indigestion, pyloric obstruction by a phytobezoar, caecal torsion, perforated abomasal ulcer, intestinal obstruction/interssuseption, mesenteric torsion, pneuoperitoneum, pneumorectum, diffuse peritonitis, physometra. (in general RDA torsion is more sudden onset, circulatory failure, shock, right ping and slosh than the other differentials) Prognosis very guarded-grave = HR >120bpm, recumbent, >15% dehydrated. Similarly, prognosis declines if during surgery the abomasum is found to be oedematous, discoloured (blue/black indicating devitalisation), fibrin tags, atonic, or large volumes of fluid need to be drained before the torsion is corrected. TIMING IS KEY – sooner make a treatment decision the better outcome 67.3% return to productive life, 33% will develop vagal indigestion due to pressure/tension on the vagus nerve. Follow up: 1day, 3days post op and 1wk post op - success/not Prevention-hard to define due to unknown specific cause

Answer 311

Treatment options: Surgical Euthanasia Surgery Cardiovascular stabilisation pre-op 3-5L hypertonic saline IV, followed by isotonic saline IV or oral electrolytes. Preoperative NSAID and antibiotic Standing right flank laparotomy -care during incising the abdominal muscles that the dilated abomasum is not cut. On entering the abdomen, decide if it is torsed or not. Decompress the abomasum Establish the direction of the torsion: Aim to free the duodenum. Feel a relief of tension Pexy the pylorus/omentum and close the abdomen as per an LDA Post op: aggressive fluid therapy IV hypertonic fluids, IV dextrose, 40L oral electrolytes, propylene glycol, multivitamins

Answer 312

Corticosteroid i.v / po/ nebulised Corticosteroids affect numerous steps in the inflammatory pathway side effects- Laminitis?( Only if already have ID) GI ulceration? Risk in pregnancy Risk to owners? licensing- For the management of a range of inflammatory /allergic conditions by injection not orally or nebulised Superior efficacy – 1st line treatment. Less side effects if nebulised allowed in food producing horses

Answer 313

Corticosteroid Oral Corticosteroids affect numerous steps in the inflammatory pathway side effects- Laminitis?( Only if already have ID) GI ulceration? Risk in pregnancy licensing- Yes but severe asthma and only for 10 days Lower efficacy than dexamethasone allowed in food producing horses

Answer 314

Corticosteroid Inhaled Corticosteroids affect numerous steps in the inflammatory pathway side effects- Reduced compared to systemic treatment? licensing- No – Human medicine allowed in food producing horses

Answer 315

Corticosteroid Inhaled Corticosteroids affect numerous steps in the inflammatory pathway side effects- Reduced compared to systemic treatment? licensing- No – Human medicine More potent that beclomethasone and less sys absorption but expensive allowed in food producing horses

Answer 316

Corticosteroid Inhaled Corticosteroids affect numerous steps in the inflammatory pathway side effects- Very few – nasal discharge licensing- yes Pro drug converted by lungs. Far less systemic effects allowed in food producing horses

Answer 317

Beta (2) Agonist Oral/ iv Agonism of the beta (2) receptor leads to smooth muscle relaxation in the bronchioles. Sympathomimetic side effects- Tachycardia Sweating licensing- yes Also reduces inflammatory response and improves mucus clearance. Rapid tachyphylaxis Consider injectable formulation for ‘rescue therapy’ but in the severely hypoxic horse, balance the clinical benefit of bronchodilation against the risk of increasing myocardial oxygen demand following administration of beta-adrenoceptor agonist allowed in food producing horses

Answer 318

Beta (2) Agonist Inhaled Agonism of the beta (2) receptor leads to smooth muscle relaxation in the bronchioles licensed?- Human medicine side effects- Tachycardia Sweating Short duration of effect but can be used if resistant to clenbuterol or side effectst not allowed in food producing horses

Answer 319

Antimuscarinic/ parasympatholytic Inhaled antimuscarinic agent that antagonizes the effects of acetylcholine licensed?- Human medicine side effects- Tachycardia Sweating Rapid but short-lived effect allowed in food producing horses

Answer 320

parasympatholytic i.v Bronchoconstriction in equine asthma is a result of parasympathetic activation. Parasympatholytics block the action of acetylcholine at parasympathetic sites in bronchial smooth muscle. Therapeutic Effect: Causes bronchodilation licensed?- Y but for treatment of colic not asthma side effects- Fewer side effects than atropine Rapid but short-lived effect allowed in food producing horses

Answer 321

parasympatholytic i.v Bronchoconstriction in equine asthma is a result of parasympathetic activation. Parasympatholytics block the action of acetylcholine at parasympathetic sites in bronchial smooth muscle. Therapeutic Effect: Causes bronchodilation licensed?- Authorised for use in horses side effects- Ileus Mydriasis Tachycardia Dysrhythmias Rapid but short-lived effect allowed in food producing horses