acute medicine and surgery Flashcards
BOAS anaesthesia problem list
The airway itself-
Particularly vulnerable during pre-anaesthetic sedation, induction and recovery
Difficult intubation
Regurgitation/Aspiration-
Often have pre-existing inhalation pneumonia
Eyes – corneal sensitivity
Reduced CO2 sensitivity? - high co2 shown on capnograph
Hypoventilation/Hypoxemia
(Hyperthermia)
(Surgical location and monitoring)
BOAS anaesthesia - Premedication
Opioids a good choice -
(avoid morphine)
If painful surgery-
Pethidine
Methadone
If non-painful surgery-
Butorphanol
Buprenorphine
Anaesthesia starts with premed- monitor from this point!
Try not to rush, prepare thoroughly before starting
Omeprazole routinely administered
Pre-oxygenate (if not stressed)
If possible, pull tongue out – frees the soft palate
BOAS anaesthesia – Sedative choice
Short-acting
Antagonisable
Low dose to effect-
(Dex)medetomidine
?Acepromazine
Particularly useful post-BOAS surgery
Anticholinergic if no 𝛼-2 agonist
BOAS anaesthesia - Induction
Inject induction agent (you choose)
Normal speed -
keep head raised
Regurgitation risk (suction)-
USE A LARYNGOSCOPE- Allows larynx visualisation
Use a smaller endotracheal tube than you expect!
Consider use of bougie or endoscopy-
Dog urinary catheter placed between arytenoids
‘Railroad’ a small ET tube over the top
Consider V-Gel if intubation impossible to allow emergency tracheostomy
BOAS anaesthesia - Maintenance
TIVA vs Inhalant?
Ventilatory Support – generally high PaCO2
Analgesia plan - local, systemic- Steroids vs NSAIDS
Monitoring
Corneal protection
preventing Regurgitation during induction
Keep head raised, suction/cotton buds ready
Intubate as normal and inflate the ET tube cuff
Avoid red rubber ET tubes
Routine use of omeprazole, maropitant plus metoclopramide infusions
boas patients often habe hiTL HERNIA THAT ACTS AS RESOUVOIR
BOAS patients – Recovery procedure
Sedation (acepromazine followed by alpha-2 agonist or vice versa)
Analgesia (NSAIDS* +/- opioids)
*caution if steroids - paracetamol
Oxygen supplementation
Monitoring plan
Leave IV cannula in situ
Maintain in sternal recumbency
EXTUBATE LATE - after the head is raised
Very well tolerated!
Check for regurgitation prior to extubation
Be prepared to re-intubate-
Have full induction kit ready
Have spare (smaller) tubes ready
Have tracheostomy kit ready
Six-month-old pug recovering from routine castration. On extubation; screaming/gurgling, thrashing, SPO2 estimated 94%, pale mucous membranes. What do you do initially?
- Wait it out, try to pull tongue forward
- Re-anaesthetise and intubate
- Sedate with ACP
- Sedate with (dex)medetomidine
- Administer IV fentanyl and oxygen
- Re-anaesthetise and perform a tracheostomy
- Sedate with (dex)medetomidine
the problem here is delerium or pain- alpha 2s treat both of those to a good degree
Patient regurgitates post extubation. Still quite sedated What would you do initially?
- Raise the head
- Lower the head
- Suction the oropharynx
- Swab the oropharynx
- Re-anaesthetise
- Start steroids and antibiotics
- Lower the head
stille sedated patients cannot swallow and so lowering the head may be enough
Six-month-old pug recovering from routine castration. On extubation; screaming/gurgling, thrashing, SPO2 estimated 74%, cyanotic mucous membranes. What do you do?
- Wait it out, try to pull tongue forward
- Sedate with ACP
- Sedate with (dex)medetomidine
- Administer IV fentanyl and oxygen
- Re-anaesthetise and intubate
- Re-anaesthetise and perform a tracheostomy
- Re-anaesthetise and intubate
always in the case of cyanosis
When to re-intubate?
SPO2 consistently ‘low’ on room air-
If reading 80 something, then consider oxygen / re-intubation- Pulling tongue out assists readings
Obvious respiratory effort/distress. Head + neck extended
Cyanosis
Paradoxical breathing
Diabetes mellitus- Anaesthetic considerations
Stabilised vs. non-stabilised?
Surgical procedure (emergency vs. elective)
Chronic organ damage (renal/hepatic)
Usually older patients +/- weight loss
Hyperglycaemia dehydration/acidosis
Ketoacidosis
Hypertension
Immunosuppression
Maintain glucose within a range that ensures gradient into glucose-dependant tissues (brain, kidney tubules, erythrocytes, intestinal mucosa)
Prevent ketoacidosis
Maintain stable fluid balance
Rapid return to normal function post-op
Prevent sepsis
Diabetes mellitus- Pre-operative preparation
Admit at least 24 hours prior to surgery
NB hospitalisation may ‘destabilise’
Assess glucose, hydration, electrolytes and renal/hepatic parameters – correct as necessary
Ensure regular medication is adhered to
Perform CBC – sepsis risk
Ensure scrupulous aseptic precautions when blood sampling and placing iv cannulae
Diabetes mellitus- Peri-operative glucose management – general points
Aim is to maintain normoglycaemia (3.5-6 mmol/l) or slight hyperglycaemia (maximum 12-16mmol/l)
Need to monitor glucose every 20-30 minutes (neurological damage)
Treat mild hypoglycaemia with 5-10 ml/kg/hr of dextrose saline (4.3% dextrose in 0.18% saline)
NB 2 aseptic cannulae required
One for fluid administration
One for blood sampling
Admit day before surgery for assessment
Ensure patient is first on the list
1-2 hours before surgery give 1/3 -1/2 normal insulin dose
???food withdrawal???
Take blood sample for glucose estimation at induction
Give peri-operative glucose infusion as necessary
Aim to complete surgery before glucose nadir
Feed ASAP after recovery
Alternatively, rigid approach
For unstable keto-acidotic patients
Intravenous glucose and insulin are infused continually – see later
Requires constant glucose monitoring using a ‘bedside’ monitor plus dedicated personnel
Treating glucose derangements
Hypoglycaemia – 5% dextrose or hypertonic glucose (central line needed)
Formula – mls of hypertonic (20 or 50%) glucose needed = D-O/A x 200 x kg
Hyperglycaemia – if over 16 mmol/l – glucose free solutions plus 0.5iu/kg soluble insulin iv
Monitor closely
Diabetes mellitus-Anaesthetic drug selection
Avoid hyperglycaemic drugs – 2 agonists and glucocorticoids (?)
Commonly available drugs are suitable – ACP, opioids, propofol, alfaxalone, inhalation agents and nitrous oxide
Use short-acting drugs to allow return to normal
Extradural techniques are useful (if already familiar)
Diabetes mellitus- Ancillary care
Crystalloid infusions (glucose saline or CSL) – 5-10ml/kg/hr
Close monitoring of physiological variables – don’t forget the animal at expense of glucose
Offer food as soon as animal is recovered
Continue to monitor glucose during recovery
Return to normal regime asap
Unstable keto-acidosis during anesthesia
Usually emergencies – poor GA candidates
Maintain on a triple infusion until patient can be stabilised later-
Insulin; 0.5-1 iu/kg/hr
Potassium; 0.5mmol/kg/hr
5% Dextrose saline; 5-10ml/kg/hr
Plus, constant monitoring
NB insulin may be absorbed onto plastics
Feline hyperthyroidism- Anaesthetic considerations
Euthyroid (treated) or hyperthyroid
Increased oxygen demand and carbon dioxide production
Increased cardiac workload – tachycardia, arrhythmias, hypertrophy – demand hypoxia
Secondary organ failure and weight loss common – in particular RENAL disease
Surgical site close to vital structures
Post-operative hypocalcaemia
Maintain oxygen delivery to organs
Maintain renal perfusion
Avoid anything which may cause arrhythmias or compromise cardiac function
Maintain normothermia (weight loss and increased metabolic rate)
Maintain all other measured parameters within normal limits
Thorough history (duration likelihood of secondary changes) and physical exam
Assess for cardiac failure (arrhythmias, ascites etc)
CBC and biochemistry (renal/hepatic parameters in particular)
Arterial blood gas/pulse oximetry
Feline hyperthyroidism- Pre-operative preparation
Ideally euthyroid for 2 weeks prior to GA
If signs of cardiovascular disease are present, consider blockade
If signs of cardiovascular failure are present – consider something like diltiazem (Hypercard) (Ca channel blocker to treat hypertension), diuretics, oxygen, cage rest etc
Feline hyperthyroidism- Anaesthetic drug selection
If euthyroid, anaesthetics chosen do not need to deviate from familiar protocols!
If hyperthyroid presented for emergency procedures
Avoid drugs which increase sympathetic stimulation eg ketamine (?)
Avoid arrhythmogenic drugs or those which increase cardiac workload eg atropine
pre-med-
ACP (up to 0.03mg/kg im) or midazolam (0.25mg/kg im) plus a vagomimetic opioid – eg methadone (0.1-0.2mg/kg im) – usually provides adequate pre-operative sedation
+/- Alpha-2 agonist LOW dose
Safety of 2 agonists has been questioned and some advocate they should be avoided unless necessary (cat behaviour)
Antimuscarinic drugs (atropine, glycopyrrolate) should be avoided
Feline hyperthyroidism- Induction
Should be accomplished ‘without stress’
If possible provide oxygen for 3-5 minutes beforehand and monitor ECG
Propofol and alfaxalone are both satisfactory
Avoid ketamine – sympathetic effects
Inhaled agent induction is slow and stressful due to the high cardiac output - AVOID
Feline hyperthyroidism- Maintenance
Inhaled anaesthesia. Isoflurane or sevoflurane do not sensitise the myocardium to catecholamines and may be the agent of choice
Due to increased metabolic rate, 100% oxygen should be provided
Constant close monitoring of measured parameters and, ideally, ECG analysis should be provided by dedicated personnel
Feline hyperthyroidism- Recovery
Cats are usually hypothermic so provide adequate warmth – forced warm air heaters are ideal but protect the eyes
Extubate early but check patency of airway and assess for Horner’s syndrome and laryngeal paralysis
Continue oxygen therapy into the recovery period
Analgesia - ?NSAIDs
Iatrogenic hypoparathyroidism
Clinical signs – muscle tremors, tetany, restlessness and seizures
Monitor blood calcium for at least 48hours
Emergency calcium therapy – 10mg/kg iv elemental calcium (as 10% calcium gluconate). If signs recur infuse 1mg/kg/hr. Monitor ECG for bradycardia
Various vitamin D compounds are available but they vary in speed of onset
Canine hypothyroidism- Anaesthetic considerations
Reduced cardiac performance – bradycardia, low contractility, low volume of distribution
Lowered thermoregulatory ability
Anaemia – reduced tissue oxygen delivery
Obesity – low FRC and tidal volumes
Lethargy - ?need for premedication?
Diminished drug metabolism
Muscle wastage
Associated conditions – DM, Addison’s disease, megoesophagus
Goals of anaesthesia
Maintain oxygen delivery to tissues
Maintain ventilation
Maintain cardiac output
Maintain normothermia
Avoid regurgitation
Ideally establish normal thyroid hormone levels with medical management for at least 2 weeks
Canine hypothyroidism-Pre-anaesthetic medication
Mentally depressed animals may require no sedation
A positive chronotropic opioid – pethidine at 3-5mg/kg im – is useful
Some authors consider ACP unwise – prolonged sedation, vasodilation and hypothermia
Anticholinergics (eg atropine 0.02-0.04mg/kg iv) may be useful but may best be reserved for intra-operative bradycardia
Canine hypothyroidism-Induction
Prolonged circulation time and reduced volume of distribution – CARE with doses and WAIT for effect
Commonly used agents are suitable
Rapid placement of cuffed ET tube essential
Canine hypothyroidism-Maintenance
Isoflurane or sevoflurane recommended – nitrous oxide inclusion is useful
Intermittent positive pressure ventilation should be applied
Monitoring should be stringent and performed by dedicated personnel – in particular paying attention to blood pressure and temperature
Fluids should be infused as normal
In recovery – keep warm and maintain oxygen delivery
Hyperkalaemia
May be seen as a result of;
Renal failure
Addisonian crises
Iatrogenic administration
‘Blocked cats’
Urinary tract trauma/bladder rupture
Clinical signs;
Vomiting/diarrhoea
Weakness/lethargy
PUPD
Bradycardia
Treatment of Hyperkalaemia
Intravenous fluid therapy to restore normal electrolyte levels and treat dehydration or low blood pressure
Calcium gluconate 10%-
Protects against cardiotoxic effects by stabilising the cardiac membrane potential
Insulin and glucose: Shifts potassium from the extracellular to the intracellular compartment
Sodium bicarbonate-
Corrects metabolic acidosis and shifts potassium from the extracellular to the intracellular compartment
Albuterol-
Administered via inhalation to shift potassium from the extracellular to the intracellular compartment
Anaesthetic Management of Hyperkalaemia
treat!
Beware of underlying conditions (hypovolaemia, concurrent trauma)
STRONGLY recommended to correct BEFORE anaesthesia!
Why Are Emergency Patients A Challenge?
Emergency patients have minimal ‘physiological reserves’ to tolerate the stress of anaesthesia
Vital that we fine tune the anaesthetic to minimise effects of the condition
But basic principles still apply
In fact they become more important
Unstable cardiorespiratory system
- Altered circulating fluid volume
- Metabolic derangements
Time pressures and patient status- May limit comprehensive preanaesthetic examination
Potentially unknown/limited history
Emotional and financial pressures from the owners
Anaesthetic Challenges With GDV Cases?
Electrolyte imbalances (potassium and calcium) with cardiac arrhythmias- Correct haemodynamically significant arrhythmias before induction if possible
Hypovolaemia
Respiratory compromise
Possible regurgitation and aspiration
Pain and distress
Metabolic acidosis and increased lactate
Most (all) critical patients require some form of pre-operative stabilisation
Intravascular access via a patent cannula
Rapid administration of anaesthetic, analgesic and emergency drugs
Pre- and intraoperative fluids
Possibly 2 FL cannulae in GDV cases
Fluid stabilisation +/- additives
Appropriate drug therapy
Shock rates’ of CSL – a bolus of 2x 15ml/kg over 2 x 10 minutes plus potassium infusion (separate line)
premed for GDV case
Potentially unnecessary if the patient is obtunded
Drugs such as the alpha-2 agonists which have major cardiovascular effects should generally be avoided
Although the emphasis is usually on correcting the underlying condition quickly it is always necessary to ensure good analgesia in any surgical patient
Full mu-agonist opioids are the drugs of choice
Pethidine (meperidine) administered intramuscularly is often a good choice- Short acting, excellent analgesia with some sedation, minimal effects on the cardiovascular system
Methadone or morphine suitable but may cause a degree of bradycardia and emesis
Following premedication monitor the patient for adverse effects
Induction Of Anaesthesia in gdv case
Have emergency drugs (doses calculated) to hand plus syringes/needles
Any induction agent can be used
Emphasis on minimal effective
doses to allow endotracheal
intubation
For example-
Calculate the full dose of an agent such as propofol, but only administer quarter of the dose over 30 seconds = SLOW
In most patients this will be sufficient to allow intubation
Propofol or alfaxalone +/- a benzodiazepine such as midazolam may allow a reduction in the propofol dose
Fentanyl effective with minimal effects on cardiac output but may cause apnoea
Etomidate does not alter cardiac output, but causes profound adrenal suppression
Ketamine with benzodiazepine potentially useful
In the emergency case I prefer to use familiar agents given to effect
Recovery of gdv case
Closely monitor cardiorespiratory status
Check temperature regularly - Hypothermia common cause of delayed recovery
Assess glucose -Particularly in septic patients
Analgesia should be given as necessary to ensure patient comfort
Appeared very unsettled – causes could be;
Pain
Dysphoria
Nausea
Full bladder
Anxiety
Performed Glasgow Short Form Pain scale
example-
Pain score = 8
Greater than 5 indicates inadequate analgesia
Max received an ‘MLK’ infusion
MLK = constant rate infusions of
Morphine at 0.1mg/kg/hr
Lidocaine at 1mg/kg/hr
Ketamine at 0.12mg/kg/hr
Neurological Diseases of Pigs
Non-Infectious -
Water Deprivation/ Salt Poisoning
Infectious - Direct -
Glasserella parasuis
Streptococcus suis
Oedema Disease
Infectious – Indirect -
Congenital Tremor
Salt Poisoning’ – Water Deprivation
Water Requirements -
Rule of Thumb – 1L per 10Kg of bodyweight
i.e. 60Kg pig is drinking approx. 6L water per day!!
Direct correlation with feed intakes
Excess Dietary Salt-
Hopefully unlikely – more a problem when waste products fed
Care salt blocks
Sudden Water Deprivation -
Frozen pipes, Leak, Low Water Pressure
Clinical Signs -
Gait Abnormalities
Recumbency
Extension of the Neck
‘Convulsions’
Blind
Diagnosis -
Assessment of Diet and Water Delivery System
Histopathology is Pathognomic – Preserve Brain
‘Meningoenchepahlitis with oedema and eosinophil infiltration’
Epidemiology -
Is the problem – in one pen? In Multiple pens? And what water lines feed these?
Other ‘tell tail’ signs – is there tailbiting?
Treatment / Control -
Rehydration may exacerbate the problem!
Rehydrate slowly
Fix the issue and prevent it from happening again
Glasserella parasuis
Gram negative coccobacillus
‘that requires V factor, but not X Factor’ (D.Taylor, Pig Diseases 8th Edition, 2006)
Previously known as Haemophilus parasuis
Very common globally
Mainly affects pigs post weaning when maternal antibodies begin to wane
Disease Presentation Part One
Acute -
Temperature
Lameness – Multiple Joints affected
Neurological – Head Extension, Recumbency
Respiratory – may be associated cough or shallow breathing
Mortality Spike
Post Mortem -
Fibrinous Pleuritis
Fibrinous Pericarditis
Fibrinous Peritonitis
Yellowish-Green Joint Fluid
Diagnosis -
Clinical Presentation
Isolate the bacteria for PCR – Hard
Glasserella parasuis- Treatment
Doxycycline / Penicillin / TMPS / Amoxicillin – Water Soluble and Individual Injection
Anti Inflammatories – Water soluble and individual injection
Control / Prevention
Target Trigger Factors – Draughts, Cold, Concurrent Conditions
Vaccination – Sows or Piglets
Streptococcus suis
Many strains worldwide - Zoonotic
Cause of joint ill in piglets (not a neurological problem)
Most common strain is Type 2 – Septicaemia -> Meningitis
Responsible for Neurological signs post weaning
Nervous Signs – Tremor, Paddling, Opisthotonus
Clinical Presentation:
Post Weaning
Increased Respiratory Rate
Nervous Signs
Acute mortality rise
Pathology – Bronchopneumonia with Interlobular Oedema
Fibrin Strands – Pleural and Peritoneal cavity
Vegetative Endocarditis
Diagnosis: Clinical Signs, PM findings, Tonsillar Scrapes, Microbiology
Treatment: Very Sensitive to Penicillin, Palliative Care (Heat Lamp, Enema, Low light Levels), Fever
Control:
Target Trigger Factors – Draughts, Cold, Concurrent Conditions, Stocking
Vaccination – S.suis Poorly immunogenic and no cross protection from commercial S.suis Type 2 vaccine
Autogenous vaccination can be considered
Oedema Disease
Clinical Presentation-
Acute mortality rise
Pigs with good Body Condition Score
Neurological signs
Diet Change
No Fever
Puffy eyes, Odd Squeal
There is often no Diarrhoea!
Diagnosis -
Ropes – Saliva for PCR
Bacterial Isolation – Faecal / Gut Contents
Treatment
Acute cases – Antibiotics individual injection or water soluble
Neomycin, Apramycin
Control
Vaccination
Organism
Toxin
Zinc Oxide
Breeds
Congenital Tremors in pigs
Hypomyelinogenesis
Cerebellar hypoplasia
Limited Mortality
Stops when the pig is sleeping
Normally seen in Gilt litters
Infection in partum
pig Vaccines
Example:
Sows
Pre Service – Erysipelas, Parvo Virus & Leptospira Protect the Pregnancy
Pre Farrowing – E.coli and Clostridia Protect the piglet (colostrum)
Example:
Piglets
At weaning – Mycoplasma hyopneumoniae, PCV2, PRRS(live)
Post weaning – Oral Live Attenuated Lawsonia vaccine
There is no typical plan: Most commonly farms will vaccinate against Porcine Circo Virus 2 and Erysipelas, Parvo +/- leptospiraDiseases of the Piglet - Infectious Disease
Diseases of the Piglet - Infectious Disease - Necrotic Enteritis
- Clostridium Perfringens Type C
- Small Intestinal Haemorrhage
- D+, Sudden Death
- First 24 hrs
Diagnosis
Toxin ELISA (on intestinal Contents)
Gross and Histological Pathology
Beta Toxin
Epidemiology/Pathogenesis
- Infection from sow at birth
- Ingestion of Clostridia
- Toxin Release Necrosis
Treatment or Prevention? -
- Acute Outbreaks: Mortality of up to 100%,
- Colostral Immunity!!
Prevention and Control -
Management Colostrum Management, Neonatal Care
Environment Hygiene at Farrowing, Temperature of Farrowing Room (indoor vs Outdoor?)
Health Sow/Gilt Vaccination, Gilt Acclimation
Vaccination -
Why? Colostral Antibodies Toxin
Who & When?
Sow - 3 weeks pre farrowing
Gilts – 6 and 3 weeks pre farrowing
Diseases of the Piglet - Infectious Disease - Coccidiosis
- Isospora suis
- 4-21 days of age
- Preventable if toltrazuril given before day 4
- Combined iron product available
(i.e. Baycox Iron / Forcerris)
Diseases of the Piglet - Infectious Disease -Enteric Colibacillosis
E.coli
- From 24hrs old
- Acute
- Wasting, Dehydration
infectious diseases of piglets at weaning
Streptococcus suis
Glasserella parasuis
Clostridum difficile
Clostridium perfringens Type A
Diseases of the Piglet - Infectious Disease -Enteric Colibacillosis – Neonatal Diarrhoea
E.coli
- From 24hrs old
- Watery/Creamy Yellow D+
- Wasting, Dehydration, Mortality
Diagnosis:
- E.coli culture
- Virulence Factors: Fimbriae F4, F5, F6
Epidemiology:
- At Farrowing (from sow to piglet)
- Low Colostrum intakes
- Poor Colostrum Quality
- Poor hygiene (at farrowing, between litters)
Treatment or Prevention?
- Acute Outbreaks: Piglets must be treated, Orally
- Chronic clinical cases: Prevention
Mortality can be up to 70%
Fimbriae allow adhesion to the Gut wall
Treatment: Oral Apramycin, Paramycin, Injectables – Will they target the pathogens in the gut
Prevention and Control
Management Colostrum Management, Neonatal Care
Environment Hygiene at Farrowing, Temperature of Farrowing Room (indoor vs Outdoor?)
Health Sow/Gilt Vaccination, Gilt Acclimation
Vaccination
Why? Colostral Antibodies
Who & When?
Sow - 3 weeks pre farrowing
Gilts – 6 and 3 weeks pre farrowing
Farrowing Room Temperature – 21degrees (ish) Piglets require 28-30degrees, Sow needs to eat and won’t at higher temperatures so always looking at trade offs
Diseases of the Piglet - Infectious Disease -Joint Ill’
- Streptococcus suis (Type I)
- 7days to weaning
- Swollen Joints, Temperature, Tremors, Sudden Death
- Bacteraemia
Diagnosis
Clinical Cases
Bacterial Culture – Brain, Joints, Heart Blood -> serotyping
Epidemiology / Pathogenesis -
- Sow
- Needle Transfer
- Carrier Animals (tonsils Type II
Treatment or Prevention? -
- Acute Outbreaks: Treat whole litter Penicillin
-Vaccination?
Homologous Strain Only Autogenous Vaccination
Be aware we can also see Type II in the farrowing house but hopefully this is something that was covered in the Neurological diseases lecture
Prevention and Control
Management Colostrum Management, Neonatal Care
Environment Hygiene at Farrowing, Temperature of Farrowing Room (indoor vs Outdoor?)
Health Sow/Gilt Vaccination, Gilt Acclimation
Autogenous vaccination-
Herd Specific Pathogen
Homologous Strain
Cascade
Commercially Streptococcus suis Type II vaccines do exist, however there is no cross protection so it is a good candidate for Autogenous vaccination. This must be only be applied under the cascade,
Diseases of the Piglet- Iron Deficiency Anaemia
Why?
- Outdoor Vs Indoor?
Diagnosis-
Pale Piglets up to 28 days of age
Haemocue:
<90g/L – Anaemic
90-110g/L – Sub Clinical
>110g/L – Optimal
A Treatment that is a prevention…
Sow milk is pretty iron deficient by all accounts
Reference values provided by CEVA animal health
Diseases of the Piglet- Coccidiosis
7-11days old (Lindsey et al., 2012)
- Yellow Pasty D+
Diagnosis -
Clinical Signs
Detcetion of Oocysts in piglet Faeces
Treatment-
Toltrazuril / Combined
Treatment or Prevention?-
Toltrazuril 24-72hrs of age
Hygiene
Where are the Oocysts coming from?-
Sow/Gilt is a reservoir for infection
Preventative Measures in pigs - Teeth Clipping
Legislation exists, there are many other additions depending on the scheme, one example is Red Tractor which 95% of the pigs in the UK are sold under
Why do we do it? – Born with 8x very sharp outward facing teeth, needle teeth
Veterinary Derrogation required
Why?
Facial Necrosis
-Extremely Painful
-Welfare Issue
Teat Damage
-Welfare Issue
Preventative Measures in pigs – Tail Docking
Why?
Tail Bites are a Welfare Issue
- Painful
- Open Wound
- Hard to Heal
- Lead to Secondary Infections (Public health concerns)
Not all farms tail dock and as an industry we are trying to move away from this practice. However, whilst enrichment helps tail biting will occur in any system. When it is epidemic it is very hard to treat and animals suffer.
There are many risk factors and it is not black and white
types of external acute haemorrhage in the horse
Castration
GP mycosis
Lacerations
Umbilical loss in foals
Easy to recognise
Not always easy to quantify, especially in a moving animal
types of internal acute haemorrhage in the horse
Uterine artery rupture
Mesenteric artery rupture (strongyle migration)
Tumours - haemangiosarcoma, splenic disease
Thoracic large vessels rupture in racehorses
Renal haemorrhage
Rib fracture (esp. foals)
Much harder to detect
Absence of visible blood loss
Can also be difficult to quantify
Abdomen/ Thorax
Broad ligament/ uterus
Intestinal lumen – Increased BUN/ normal creatinine
Coagulopathy is a rare cause of haemorrhage in the horse but can be an issue after haemorrhage (consumptive coagulopathy)
signs of haemorrhagic shock in the horse
Tachycardia
Tachypnoea
Cold extremities
Anxiety or depression (obtunded)
Pale mucous membranes/ prolonged CRT
Weak arterial pulse
Flow murmur (dec. blood viscosity)
Sweating
Colic / abdominal distension (intra-abdominal haemorrhage)
Decreased CVP / arterial pulse pressure/MAP
clinicla pathology of haemoragic shock in the horse
Hyperlactataemia (impaired tissue oxygenation) most sensitive indicator in acute blood loss
Hypoproteinaemia
Anaemia
PCV and TP may be normal in acute blood loss-
Not very sensitive in early stages
Splenic contraction can maintain PCV in acute stages
PCV and TP remain normal until fluid redistributes from the interstitial spaces (takes up to 12 hours)
Serial monitoring required
TP changes first ( 4-6 hours post insult)
Treat based on clinical signs not PCV!
Estimating blood loss in horses
Blood volume is estimated as 8% of body weight
500kg horse = 0.08 x 500 = 40 L
In horses’ general guidance acute loss of > 30% (> 12 L in a 500kg horse) of blood volume. Signs of hypovolaemic shock
-> Blood transfusion
describe the presentation of a horse with less than 15% (6l in 500kg horse) blood loss
normal heart rate
normal resp rate
normal capillary refil time
normal blood pressure
other physical exam findings- possible mild anxiety
describe the presentation of a horse with less than 15%-30% (6l-12l in 500kg horse) blood loss
increased heart rate
increased resp rate
mildly prolonged capillary refill time
normal blood pressure
other physical exam findings- mild anxiety
describe the presentation of a horse with less than 30%-40% (12l - 16l in 500kg horse) blood loss
moderatly to severly increased heart rate
increased resp rate
prolonged capillary refill time
decreased blood pressure
other physical exam findings- anxious or depressed; cool extremities
describe the presentation of a horse with less than >40% (>16l in 500kg horse) blood loss
severly increased heart rate
increased resp rate
Very pale mucous membranes
sever hypotension
other physical exam findings- obtunded; cool extremities
Management of acute haemorrhage in horses
Control blood loss if possible
Administer appropriate fluid therapy
Prepare for blood transfusion if estimate greater than 30% blood loss
(Do not drain haemothorax/abdomen unless respiratory distress (thorax))
Internal haemorrhage there is recycling of up to 2/3 RBC’s and most of protein
Management of acute haemorrhage in horses- 1. Control blood loss
Surgical ligation / pressure-
Pressure bandage / tourniquet (distal limb)
Manual pressure
Ligation of testicular artery
Packing of sinuses
Not always possible-
Intraabdominal haemorrhage
Guttural pouch
Pro-coagulants-
Topical:
Chitosan (e.g. ‘Celox’ gauze/granules/’Hemcon’)
Kaolin based gauzes (e.g. ‘QuikClot’)
Smectite (‘Woundstat’)
Absorbable for smaller areas:
Gelatin (‘Gelfoam’) (mechanical)
Fibrin sealants (‘Surgiflo’) ( biologic)
Are they superior to standard packing/ pressure?
Side effects? (embolisation)
Stabilise clots:
Antithrombolytic Drugs- Inhibit fibrinolysis and stabilise clot
Two options
Aminocaproic acid
Tranexamic acid -
Better evidence to support use (mainly in humans – little data in horses)
8 X more potent than aminocaproic acid
Therapeutic doses in horses have been shown to be much lower in horses than humans
Reasonably cost effective
topical procoagulants for use in acute haemorage in horses
Chitosan (e.g. ‘Celox’ gauze/granules/’Hemcon’)
Kaolin based gauzes (e.g. ‘QuikClot’)
Smectite (‘Woundstat’)
Absorbable procoagulants for use in acute haemorage in horses
for smaller areas:
Gelatin (‘Gelfoam’) (mechanical)
Fibrin sealants (‘Surgiflo’) ( biologic)
procoagulants for use in acute haemorage in horses- IV formalin
No evidence to support use
factors to consider when deciding on appropraite fluid therapy for accute heamorage in horses
Is the haemorrhage controlled or uncontrolled?
What are the practicalities to consider for “in the field” use?
Don’t forget coagulation factor replacement
Is there a suitable donor available if required?
Commercial haemoglobin-based fluids – availability? Expense?
Uncontrolled bleeding-
Persistent hypotension is very dangerous.
Aim of treatment should be to support the circulating blood volume to the minimum required for adequate tissue perfusion until haemorrhage is controlled.
ballaence between adiquate perfusion and potential to worsen bleeding
The use of crystalloids / synthetic colloids in the face of uncontrolled haemorrhage can:
Dilute RBC/clotting factors
Increase blood pressure – destabilise clot, increase bleeding?
Additionally synthetic colloids have been shown to cause: hypocoagulation in humans/horses
But if no blood products are immediately available crystalloids are indicated in the face of severe haemorrhage as a salvage procedure
Management of acute haemorrhage 2. Hypotensive resuscitation where the bleeding has not stoped or there is no certainty the bleeding has stopped
Has the haemorrhage stopped?
No/Unsure:
‘Permissive hypotension’: “Provide enough perfusion pressure to vital organs such that function is maintained while keeping blood pressure below the normal range in the hope that clot formation will not be disrupted”
Aim to maintain MAP ~ 60mmHg, SAP<90mmHg
Give maintenance isotonic crystalloids – 2-3ml/kg/hr.
Hypertonic saline generally contraindicated in uncontrolled haemorrhage
Consider blood transfusion: for any ‘transfusion triggers’:
These are guidelines. They need to be balanced against the clinical picture, practical limitations and what fluids are available to you
Management of acute haemorrhage 2. Hypotensive resuscitation In cases where the bleeding has stopped
Definitive haemostasis (e.g. clamping of an external bleeding vessel) -
Fine to expand volume using crystalloids, hypertonic saline, blood as dictated by the clinical picture. If crystalloids are used, volume administered should be at least as great as the estimated blood loss. Can give initial bolus ( 10ml/kg rapidly)
Clinical signs, PCV, and laboratory evidence of tissue hypoxia can then be used to determine the need for transfusion.
Unstable control e.g Clot / uterine artery/ haemothorax-
Cautious replacement of circulating volume – Blood ideal as not diluting Rbc’s. You would be more concerned about rapid volume expansion in these cases.
Care not to displace clot / cause haemorrhage via increased blood pressure
Management of acute haemorrhage 2. Hypotensive resuscitation- drug options
Acepromazine-
Controversial
Theory: systemic vasodilation effect – lower blood pressure - reduce haemorrhage.
But if blood loss persists it will worsen the hypotension.
Only use if stable cardiovascular function
Probably not recommended in acute haemorrhage
Management of acute haemorrhage 2. Hypotensive resuscitation- Blood transfusion
Transfusion triggers
>25% - 30 % blood volume lost
Signs of hypovolaemic shock
PCV <20% / Hb<7g/dL (in acute bleed) ( < 12% in chronic anaemia)
Lactate >4mmol/L
These are guidelines and should be used in combination with the clinical picture
equine bood donors
Large healthy gelding > 500kg. Good temperament.
Minimum PCV of 35%, and a total protein 6.0 g/dL (60 g/L).
No universal donor as 8 equine blood groups and > 30 different factors
Ideally be negative for the Aa and Qa alloantigens (most antigenic)
Avoid mares that have had foals or horses who have themselves previously received a transfusion
Donkeys and Mules have RBC antigen “donkey factor”. Can not act as donors and can only receive horse blood if free from anti donkey factor Ab
May not be necessary in emergency situations when the recipient has had no prior exposure to blood products
Routine crossmatching evaluates haemagglutination
Haemolytic reactions are not detected unless rabbit complement is added
Major crossmatch-
Donor’s RBCs and the recipient’s serum
Minor crossmatch -
Recipient’s RBCs and the donor’s serum
Up to 20% of the donor horse’s blood volume can be collected at one time.
For a 500kg horse who has 40 L of blood this = 8L
Often, we are using client owned horses so typically we collect less than 20%
Crystalloid fluids can be given to replace blood volume, and are recommended when greater than 15% blood volume is collected
Transfusion Volume and Technique in horses
Calculating the deficit-
Equation may only be used if the horse’s PCV accurately reflects the blood loss
((normal PCV- animal PCV)/normal PCV) x Blood volume
Blood volume = 0.08 x body weight
example-
500 kg TB racehorse – normal PCV = 35%
Presents with a PCV of 10 following an episode of acute haemorrhage
((35-10) ⁄ 35) x (0.08 x 500) = ?
(25/35) x 40 = 28.6 L
Aim to deliver 30 – 50% of the deficit as volume has already increased through mobilization of interstitial fluid, voluntary intake of water, and administration of intravenous fluids
(0.3 – 0.5) x 28.6 = 8 – 14 L
The volume to be transfused may be limited by the volume of blood that can be safely removed from the donor horse
Warm to room temperature
Filter giving set
Pre-transfusion examination ( HR/RR/ Temp)
SLOW (<0.5ml/kg/hr for 10-15 mins)
Monitor for reaction
reactions-
Usually in first 15 minutes
More common after multiple transfusions
Agitation, tremors, urticaria, pruritis, piloerection, colic, nasal oedema, pulmonary oedema, weakness, collapse, tachycardia, tachypnoea, dyspnoea, pyrexia, death
STOP
Consider use of corticosteroid or antihistamine
Or in severe cases adrenaline
Decide necessity to try to cautiously continue
If re-starting, do so SLOWLY
If reaction recurs, STOP and find another donor….
when should you refer a colic
Classification of Colic-
“Medical Colic”
“Surgical Colic”
Inconclusive-
Schedule Re-examination
Avoid Flunixin
Call the Referral Centre
Persistent pain despite analgesia
Progressive abdominal distension
Tachycardia (>60bpm)
Signs of hypovolaemia
Absence of borborygmi
Abnormal rectal findings
Gastric reflux (>4L)
Preparation Prior to Referral for colic
Decompress stomach- NG tubein situ?
Analgesia
Report of treatment administered
Directions for owner
Rug and bandage limbs
investigaion of colic in a hospital setting
Observation- Pain assessment- colon torsions post foaling are particulary painfull
Establish a baseline
Watch loose
External examination
“Safety First”- prepeare sedation- xylozine- controls situation
Belly Tap-
Blood Work-
Stomach Tube-
Ultrasonography-
Rectal Exam-
Cardiovascular Assessment-
TPR – Remember the T!- pyrexia big diagnostic- often not surgical
Heart Rate (N.B. Buscopan suppresses parasympathetic innervation causing tachycardia- don mistake for diagnostic)
Pulse Quality
Peripheral Skin Temperature
Mucous Membranes (inc. CRT)
Skin Turgor
“Stableside PCV”
History-
Signalment
Immediate colic history
Previous colic history
Management or feeding changes
Recent travel or exercise
Dentistry
Worming history
Concurrent illness
“Windsucking”
Pregnancy
Gastrointestinal Auscultation-
Appreciation of “Normal”
Hypermotility
Hypomotility
Caecal contractility (“The Flush”)
Tympany
Sand
Abdominal Ultrasonography for colic
Accurate assessment in patients with abdominal pain
Particular value:
Small patients
Lack of adequate restraint
Excessive straining
Rectal tears
Advanced pregnancy
Alcohol saturation without clipping-
Cotton wool and container
Spray bottle
Clipping-
Draft breeds
Ponies
Donkeys
Individual horse-to-horse variation
Low frequency (2-5MHz) curvilinear transducer-
Ideal
30cm depth
Rectal transducer-
10-12cm depth
Distended SI often dependent
Peritoneal fluid assesment
Machine Settings-
Image optimization-
Frequency
Time-gain compensation controls
Depth settings
Overall gain
Key principles-
Scan with the highest frequency that will allow adequate penetration
Depth settings should be adjusted frequently – dependent on structure of interest
Larger horse will require a lower frequency than foal or fit TB
Limited Technique-
Ventral abdomen
Left caudal ICS (renosplenic window)
FLASH Technique-
Fast
Localised
Abdominal
Sonography of the
Horse
Full Examination
Paralumbar fossa/flank region
Tuber coxae to stifle
ICS (5-17th)
Ventral lung margin to costochondral junction
Ventrum
Sternum to inguinum
Costochondral junctions to midline
FLASH Scanning for colic
Fast
Localised
Abdominal
Sonography of the
Horse
Seven Topographical Locations:
Ventral abdomen
Gastric window- 10-15th ICS,
Ventral to the lung,
Gastric contents not normally visible
, Splenic vein useful landmark,
Occasionally SI loops in this region- Gastric Distension
Splenorenal window-
Predominant feature of the LHS
Can extend to the right of midline
Left kidney deep to spleen- (Paralumbar fossa- 15-17th ICS)
Homogenous echogenicity- Hyperechoic relative to liver and kidney
Nephrosplenic Entrapment (LDDLC)
Left middle third of abdomen
Duodenal window- Right kidney 14-17th ICS, Descending duodenum -Ventral to the right kidney, Deep to right liver lobe in 11-17th ICS
Right middle third of the abdomen
Thoracic window
Rectal Examination for colic
“Safety First”
Spasmolytic
Lubrication
Sedative
Twitch
Stocks
Appreciation of “Normal”
Examination of the faeces-
Consistency
Sand
Mucus
Parasites
Systematic Examination
Quadrant System
Clockwise starting Left Dorsal
what can be felt upon Rectal Examination of the horse– Left Dorsal
Spleen – caudal edge
Nephrosplenic ligament
Nephrosplenic space
Left kidney – caudal pole
Aorta
Root of mesentery – smaller horses
what can be felt upon Rectal Examination of the horse- Right Dorsal and Right Ventral
Duodenum -
Rarely palpable
Distension
Caecum-
Ventral and medial taenia
Dorsocaudal-ventrocranial
Inguinal Ring- especially in stallions
what can be felt upon Rectal Examination of the horse- Left Ventral
Pelvic Flexure
Left dorsal colon- No palpable taenia or haustra
Small colon- Faecal balls
Inguinal ring
Bladder
Reproductive tract
what can be felt upon Rectal Examination of the horse- Abnormalities
Distended Small Intestine
Displaced Intestine
Tympany
Taut Mesenteric Bands
Impaction-
Large or Small Colon
Caecum
Decision for Surgery in colic cases- Principles
Emergency
Often a definitive diagnosis is not possible (or necessary)
Exploratory Laparotomy = Diagnostic +/- Therapeutic
Better to operate and comprehensively examine the abdomen than to miss a surgical lesion.
Pain
Response to Analgesia
Clinical Examination
Diagnostic and Procedural Findings
Indications Surgery IS Needed in colic cases
Pain-
Uncontrollable and/or severe
Poor/transient response to flunixin meglumine or detomidine
Requires further analgesia
Gastric reflux-
>4L yellow fluid
Rectal Findings-
Distended small intestine
Distended and displaced large colon
Distension that cannot be relieved medically
Palpable foreign body or mass
Auscultation- Absent intestinal sounds
Peritoneal Fluid-
Increased total protein
Presence of red blood cells and degenerate neutrophils
N.B. Indicators of hydration or perfusion are not specific for diseases requiring surgery
Heart rate
Mucous membrane colour
CRT
PCV
Plasma protein concentration
Indications Surgery IS NOT Needed in colic cases
Pain- Depression or lack of pain
Temperature - >39.2°C
Complete Blood Count- Neutrophilia or neutropenia
Auscultation- Progressive intestinal sounds
causes of colic that can be identified on exploratory laparotomy and
Strangulated Pedunculated Lipoma
Epiploic Foramen Entrapment
Large Intestinal Displacement
Intussusception
Neoplasia
Anastomosis
a surgical connection between two structures. It usually means a connection that is created between tubular structures, such as blood vessels or loops of intestine. For example, when part of an intestine is surgically removed, the two remaining ends are sewn or stapled togethe
Postoperative Complications in colic surgery
Within 48 hours of surgery:
Incisional/surgical pain
Persistent ischemic bowel,for example, ileal stump
Continuedischemia/reperfusion injuryof bowel
Leakage at anenterotomy or anastomosissite
Postoperative ileus
Recurrentdisplacement
Within 2-7 days of surgery:
Obstruction at ananastomosis (e.g.,haematoma,impacted ingesta)
Delayed adaptation at the anastomosis
Peritonitis/anastomoticleakage
Postoperativeileus
Large colonimpaction
Gastriculcers
Greater than 7 days after surgery:
Adhesions
Recurrence of previous problem, e.g. colon displacement
Incisional Infection-
Culture and sensitivity
Drainage and lavage
Broad spectrum antimicrobials
Abdominal bandage or hernia belt
Incisional Herniation-
Significance dependent on size of hernia and intended use of horse
Hernia belt or abdominal bandage
Box rest
Herniorrhaphy- 3-6 months post colic surgery
Thrombophlebitis-
Catheter Removal
Culture and Sensitivity
Antimicrobial therapy
Topical treatment- DMSO? Diclofenac?
US Monitoring
post op care for colic
NSAID
Incisional management +/- suture removal
Rehabilitation-
6w box rest
6w small paddock rest
Postoperative complications?
canine stomach
Located in the cranial region of the abdomen caudal to the liver.
Ingesta enter the stomach via the cardia and exits though the pylorus.
The stomach is a dilation of the alimentary canal involved in initial stages of digestion.
Cellular lining of the stomach produces various substances involved in digestion.
It is entirely glandular in the dog.
many blood vessels that feed the spleen are assosiated ith the stomac so torsion can inflame the spleen
describe the parts and function small intestines of the dog
Located in between the stomach and large intestines.
Made up of the duodenum, jejunum and ileum.
Adapted for digestion and absorption of nutrients.
Duodenum-
Begins cranially in the RHS of the abdomen and runs caudally, then turns left (caudally to the mesenteric artery) and the courses cranially on the left of the midline. Bile and pancreatic ducts empty into the cranial portion.
Jejunum-
Longest portion of the SI.
Sits within the mesojejunum therefore allowing the jejunum to reside throughout the abdomen.
Ileum-
Shortest position of the SI.
It can be difficult to tell it apart from the jejunum. One way of identifying the ileum is identifying the artery running along the boarder of the ileum. This is located 180 degree from the ileum’s attachment to its mesentery.
the further along the small intestine the harder it is to operrate
describe the parts and function large intestines of the dog
Terminal portion of the intestinal tract connecting the SI to the anus.
Compromised of the caecum, colon, rectum and anal canal.
Caecum-
A diverticulum in the initial portion of the colon involved in absorbing water.
Colon-
Comprised of the ascending, transverse and descending colon.
Involved in nutrient and water absorption.
Located in the dorsal abdomen starting on the RHS coursing cranially then passing to the LHS and courses caudally to the left side of the abdomen into the pelvic vanity.
opening of the large intestine is not a small practice procedure- large risk of septic peritonitis
foreign bodies may be able to be milked to the anus
Approach to GI emergencies- initial assesment
Initial goals are to assess for shock (hypovolaemic and distributive most common) and localise the problem.
Assessing for shock:
Heart rate
Pulses
MM colour or CRT time changes
Temperature
Respiratory rate and effort
If shock is identified, this needs to be addressed asap.
See previous lectures:
Approach to triage
Fluid therapy
Diagnosis of shock
Localising the problem – many disease processes can present with gastrointestinal signs:
Cardiac disease -> vomiting, abdominal distension
Hepatic and pancreatic disease -> vomiting, diarrhoea, and/or abdominal pain and distension
Urogenital disease -> vomiting, abdominal pain
Splenic disease -> abdominal pain and/or distension
Endocrine disease e.g. DKA -> vomiting, diarrhoea
Musculoskeletal disease, e.g. IVDD spinal pain can present as abdominal pain.
Full history and clinical examination is always indicated
Approach to GI emergencies- Diagnostic tests
Radiography -
Plain
Contrast
Abdominal ultrasound-
Abdominal focussed assessment with sonography for trauma (A-FAST)
Survey abdominal ultrasound
Peritoneal fluid tap
Haematology and biochemistry
Approach to GI emergencies- Radiography
First choice for suspected obstructive disorders e.g. foreign body, GDV
Plain radiographs often enough for diagnosis.
Oesophageal foreign body-
Poorly defined opacity in the dorsocaudal lungfield.
DV radiographs would show this on the midline, increasing suspicion that it resides within the oesophagus rather than a lung.
First choice for suspected obstructive disorders e.g. foreign body, GDV
Plain radiographs often enough for diagnosis.
GDV-
Dilation without volvulus – no compartmentalisation of the stomach
Dilation and volvulus – gas is compartmentalised by a band of soft tissue.
Intestinal foreign body-
Gas distension of the intestines - white arrows
Foreign body (corn cob)- red arrow
No gas beyond the foreign body
Intestinal linear foreign body-
Plication of the small intestine due to a linear foreign body (white arrow heads)
Contrast studies are used less often in emergency presentations, but may help identify strictures, partial obstructions, or intussusceptions in less urgent cases.
Intestinal stricture due to neoplasia:
Loops of small intestine of normal diameter.
Dilated loop of small intestine.
Abrupt termination after the most dilated loops of intestine.
Feces present in colon
More useful than radiographs when effusion is present.
Approach to GI emergencies- Abdominal ultrasound
More useful than radiographs when effusion is present.
Can pick up more subtle changes e.g. intestinal stricture due to neoplasia, intussusception etc.
A-FAST used to detect free fluid for sampling or where a bleed is suspected.
Approach to GI emergencies- Peritoneal tap
Usually ultrasound guided to avoid accidental organ perforation.
Used to distinguish type of free fluid present within the abdomen.
Peritoneal lavage reported as a diagnostic tool where fluid is present in volumes too small to sample/ultrasound is not available – rarely done now.
Approach to GI emergencies- Haematology and biochemistry
Primarily used to rule out other causes of GI signs, and to assess for any abnormalities which need to be corrected prior to further investigations or surgery.
Primarily used to rule out other causes of GI signs, and to assess for any abnormalities which need to be corrected prior to further investigations or surgery.
Changes with GI disease:
Dehydration -> ↑HCT and TP, azotemia
Upper GI obstruction -> metabolic alkalosis due to loss of H+, K+, and Cl- in the vomit.
Infectious disease -> WBC changes.
See previous clinical pathology lectures, in particular:
Electrolytes and Acid Base
Proteins, liver and pancreas
Haematology
Approach to GI emergencies- Fluid therapy
See previous lectures:
Approach to triage
Fluid therapy
Diagnosis of shock
Used primarily to correct dehydration.
Try and take ongoing losses into account (v+ and d+)
Important to correct shock, and electrolyte abnormalities prior to general anaesthesia in surgical cases.
Approach to GI emergencies- Antiemetics
Antiemetics:
Primarily used in medical cases e.g. dietary indiscretion or infection.
Use of antiemetics contraindicated where obstructive disorders are suspected as they may hide signs of ongoing nausea.
Maropitant:
Neurokinin 1 (NK1) receptor antagonist; centrally mediated anti-emetic.
Some evidence may be better for vomiting than nausea e.g. in CKD cats.
Exception = motion sickness
Effective against emetogens (drugs which induce vomiting)
Ondansetron:
Serotonin receptor antagonist; central and peripherally acting antiemetic.
Developed to treat chemotherapy induced nausea; effective for both vomiting and nausea.
Human drug, use in animals is off license.
Metoclopramide:
Dopamine receptor antagonist, plus serotonin receptor antagonist at higher doses; centrally acting antiemetic.
More effective in dogs than cats
Prokinetic in the proximal GI tract – contraindicated with suspected obstructive disease.
Approach to GI emergencies-Gastroprotectants
H2 receptor antagonists (ranitidine, famotidine):
Decrease gastric acid production
Increase GI motility
Proton pump inhibitors (omeprazole):
Decrease gastric acid production – more effective than H2 antagonists
Sucralfate:
Binds to ulcer sites, creating a barrier and preventing further erosion.
Stimulates bicarbonate and PGE production (mucosal defense) and binding of epidermal growth factor (mucosal repair).
Works best in acidic environments.
Approach to GI emergencies- Antimicrobials
Not indicated in mild cases of vomiting or diarrhoea.
Amoxicllin/clavulanate:
Indicated perioperatively when entering the GI tract, but use post-surgery should only be continued if there is a therapeutic indication.
First choice for haemorrhagic diarrhoea where there is a risk of sepsis (including parvovirus infection).
Metronidazole:
Commonly used for haemorrhagic diarrhoea as it has secondary GI anti-inflammatory effects.
Studies have not been able to demonstrate a significant benefit to using metronidazole in these cases.
May be indicated where there is a known Giradia or Clostridia spp. infection
Oesophageal obstruction common causes and diagnostics
Common foreign bodies:
Bones and corn cobs
Chew toys and rubber balls
Rawhide
String
Sharp metal objects e.g. sewing needles and kebab skewers.
Common sites:
Thoracic inlet
Heart base
Where the oesophagus passes through the diaphragm.
Presenting signs
Choking/gagging
Increased salivation
Regurgitation
Lethargy, dyspnoea and coughing 2o to aspiration pneumonia
Possibly sequale:
Aspiration pneumonia
Oesophageal perforation/necrosis (see image)
Mediastinitis, pleuritis, and pyothorax
Radiographs - preferred
Radiolucent FB may require contrast (sterile, water-soluble iodinated agent)
Allows assessment of lung fields for evidence of aspiration pneumonia etc.
Oesophagoscopy-
Direct visualisation of the foreign body
Oesophageal obstruction treatments
Treatment = removal under GA with a cuffed ET tube.
Endoscopic removal:
Requires air insufflation – care re:oesophageal perforation.
Flexible or rigid (easier) endoscope + blunt forceps to remove per os.
Otherwise, gentle pressure can be applied to try and move the FB into the stomach then -> gastrotomy.
Surgical removal:
Gastrotomy (if FB can be moved into the stomach) - less risky than thoracotomy.
Thoracotomy – usually requires referral
End-to-end anastomosis – may need to be performed where there is severe damage to the oesophagus.
Medical treatment post-removal:
Sucralfate
Anti-inflammatories
H2 antagonists/proton pump inhibitors
+/- antimicrobials
Feed a soft diet
Feeding tube
Where damage is severe.
Needs to enter the GIT beyond the point of damage.
Gastric dilatation and volvulus presentation and diagnostics
The phone call:
“My dog is trying to vomit, but nothing is coming up.”
Common signalment:
Large breed, deep chested dogs (but also reported in smaller breeds and cat less commonly)
Guinea pigs
Serious condition – mortality 10%-45% in treated animals.
Presenting signs
Non-productive retching (dogs)
Abdominal distension
Lethargy and collapse in later stages
Clinical examination:
Dyspnea and/or tachypnoea
Tympanic anterior abdomen
Tachycardia, +/- dysrhythmia
Weak pulses
Pale mucous membranes and prolonged capillary refill time (CRT)
Possible sequale:
Cardiac arrythmias (ventricular premature complexes and ventricular tachycardia)
Endotoxaemia
Gastric necrosis -> peritonitis and/or septic shock
Electrolyte and acid base disruptions.
Disseminated intravascular coagulation.
Diagnosis
Radiographs (see prev)
Orogastric intubation
Gastric dilatation and volvulus treatment
Initial treatment
Gastric decompression (orogastric tube or percutaneous) +/- lavage
Treatment/management of shock
Manage dysrhythmias
See previous lectures:
Fluid therapy
Anaesthetic management of emergency patients
Anaesthetic dysrhythmias
Anaesthetic considerations – see Ian’s lecture
Aims of surgery:
1. Identify and remove damaged or necrotic areas of the stomach and/or spleen.- Partial resection of necrotic stomach
Complete or partial resection of necrotic spleen.
2. Correct stomach position- Clockwise rotation = most common, but always check
3. Adhere the stomach to the body wall to prevent recurrence0 Incisional and belt loop gastropexy = most common
Post surgical care:
Continue monitoring electrolytes, acid base, and ECG for 24-48 hours post-surgery.
Fluid therapy until oral intake is sufficient to prevent dehydration.
Analgesia – opioids
Small, soft, low fat meal should be offered 12-24 hours after surgery
Anti-emetic (maropitant) if needed.
Proton pump inhibitors if ulceration present.
Prokinetics?
Antibiotics?
Prevention-
Feed more, smaller meals
Avoid stress during feeding
Do not use an elevated feed bowl.
Avoid breeding from dogs which have suffered from, or have immediate relatives which have suffered from, GDV.
Restrict exercise before and after meals?- no studies but often said
Prophylactic gastropexy?- recomended by some surgeons
Gastric and intestinal foreign body presentation and diagnostics
The phone call:
“My dog/cat is vomiting everything up, even water.”
Gastric foreign bodies only tend to present as an emergency if causing an outflow obstruction or perforation.
Intestinal foreign bodies almost always present as an emergency.
Linear foreign bodies can be both.
Common signalment:
Younger animal, known scavenger
Clinical examination
Dehydration
Signs of shock (tachycardia, poor pulses, poor perfusion)
Abdominal pain
Palpable abdominal mass
Pyrexia
Possible sequale:
Perforation ->peritonitis +/- septic shock
Sepsis +/- DIC without perforation
Diagnosis-
Clinical exam – palpate abdomen and check under the tongue (linear) for evidence of FB.
Radiographs (plain or contrast)
Ultrasonography
Gastroduodenoscopy (may also be therapeutic if FB can be retrieved)
Haematology and biochemistry – used to assess systemic state rather than as a diagnostic test.
Gastric and intestinal foreign body treatment
Medical treatment:
Induction of vomiting?
Feeding fibre/psyllium?
Serial radiographs?
Fluid therapy and correct electrolyte and acid base abnormalities – see previous lectures
Analgesia – opioids
Antibiotics –cephalosporins or amoxy/clav.
Foreign body retrieval:
Gastric and duodenal FB – possibly endoscopic retrieval.
Surgical – gastrotomy, enterotomy, or both.
Always check the entire GIT when performing an ex-lap, stomach to colon – it is possible to have multiple foreign bodies!
Try and milk foreign bodies to an area of healthy tissue before making the incision.
Linear FB may require multiple incisions.
End-to-end anastomosis required where tissue is non-viable
Post operative care:
Ongoing fluid therapy.
Continue monitoring and correcting electrolyte abnormalities.
Start feeding a low fat diet from 12 to 24 hours post-surgery.
Antiemetic if needed
Proton pump inhibitors if ulceration present.
presenting signs of a foreign body- Gastric – acute
Vomiting
Dehydration
Hypovolemic shock
presenting signs of a foreign body-Gastric - chronic
Intermittent vomiting
Weight loss
Possibly asymptomatic/incidental finding
presenting signs of a foreign body-Small intestine - proximal
Vomiting
Dehydration
Hypovolemic shock
presenting signs of a foreign body- Small intestine - distal
Intermittent vomiting
Dehydration
Weight loss
Anorexia
Intussusception- presentation and diagnostics
GSDs and Siamese cats appear predisposed
Intussusception = a ‘periscoping’ of the intestines.
The phone call:
“My puppy/kitten is really quiet and doesn’t want to eat. They’ve vomited a few times too.”
Signalment:
Young animals, especially common post-parvoviral infection or parasitic enteritis.
Older animals, often associated with intestinal masses (esp cats).
Presenting signs:
Vary with site and severity of the intussusception.
Acute(less comon): Scant, bloody diarrhoea, vomiting, abdominal pain, mass on abdominal palpation.
Chronic: Intractable, intermittent diarrhoea, depression, anorexia, and emaciation.
Diagnosis
Radiographs: Plain often unhelpful, contrast more useful in some cases (thin ribbon of material seen at the site of the intussusception)
Abdominal ultrasound – most useful.
Haematology and biochemistry
Faecal analysis
Intussusception treatment
Medical treatment:
Treatment of any underlying condtion
In acute cases may need to stabilise as per intestinal foreign bodies.
Percutaneous correction may be possible in rare cases; high risk of recurrence
Common sites:
Ileocolic
Jejunojejunal
Surgical treatment:
Manual reduction +/- enteroenteropexy
End-to-end anastomosis
Manual reduction:
Apply gentle pressure on the neck of the intussusception while ‘milking’ the apex out of the intussusceptiens.
Avoid excessive traction – push on the intussuscipiens more than pull on the intussusceptum.
Enteroenteropexy-
Prevents recurrence of intussusception.
Place small intestinal in a series of gentle loops from the distal duodenum to the distal ileum.
Bends must be gentle to prevent obstruction.
Place sutures to secure the loops, engaging the submucosa, muscularis, and serosa, 6 to 10 cm apart.
Resection and anastomosis is indicated if:
A mass is detected.
It is not possible to manually reduce the intussusception.
The tissue is no longer vital.
Any part of the blood supply is disrupted during reduction.
Post operative care:
As for foreign bodies
Mesenteric volvulus/torsion
The phone call:
“My dog is collapsed. Their stomach is swollen and they are passing blood from their anus. They seemed fine a few hours ago.”
Rare, and almost always fatal.
Prompt recognition and surgical intervention is vital.
Diagnosis = challenging as c/s non-specific and progress rapidly
Radiographs may show uniform distension of the majority of the GIT, but by this stage most of the intestines will be necrotic.
Partial volvulus may allow time for surgical intervention and correction, but euthanasia often indicated.
Acute haemorrhagic diarrhoea Syndrome (AHDS) diagnostics and presentation
The phone call:
“My dog/cat is passing bloody diarrhoea!”
Differentials:
Parvovirus
Clostridial endotoxicosis (2o to other infections, dietary indiscretion etc.)
Coagulopathy e.g. rodenticide toxicity
Intussusception
Foreign body intestinal trauma (uncommon)
Signalment:
Parvovirus = unvaccinated puppies
Other ddx = middle aged, small breed dogs most commonly reported but possible in any dog.
Rare in cats
Presenting signs:
Haemorrhagic diarrhoea
Distinguish from melaena and haematochezia, neither of which should present with diarrhoea.
Parvovirus: Watery with mixed fresh and digested blood
AHDS: raspberry jam consistency
+/- vomiting and/or haematemesis
Anorexia
Lethargy
Clinical examination:
Dehydration
Hypothermia more common than pyrexia
Tachycardia (2o to dehydration and hypovolaemia)
Canine AHDS index has been devised to assess the clinical significance of disease.
Mortier et. Al. 2015 reported AHDS score <2 can be discharged from hospital, Hall 2023 extrapolated this to any score <2 does not require hospitalisation.
Ideally need to make a clinical judgement based on the individual case.
Image credit: Hall, E., 2023. Dealing with haemorrhagic diarrhoea in dogs. In Practice, 45(9), pp.516-531. is a table for assesing clinical significance of ahds
AHDS Treatment
AHDS is mostly self limiting with supportive care, therefore not essential to get a definitive diagnosis in most cases.
Exception = parvovirus. Always test if any clinical suspicion due to highly infectious nature and risk to other dogs
Diagnosis – lots of options
main-
Haematology and biochemistry
Faecal analysis
SNAP test for parvovirus
secondary-
Basal cortisol or ACTH stimulation test (hypoadrenocorticism)
Coagulation profiles (bleeding disorders/rodenticide toxicity)
Pancreatic specific lipase (pancreatitis)
Imaging – non-specific, may be useful if neoplasia or pancreatitis present
Serum protein C (marker of intestinal inflammation) - not useful for diagnosis but serial monitoring may have a prognostic value
Haematology and biochemistry-
Highly variable
Haemoconcentration due to dehydration, progressing to decreased PCV
Inflammatory leukogram (AHDS) or leucopenia (parvovirus)
Hypoproteinaemia
Hypokalaemia
Pre-renal azotemia
Faecal parasitology useful but faecal culture not as the bacteria commonly implicated in AHDS are also present in healthy individuals
Faecal antigen SNAP test for parvovirus – false negatives sometime occur.
Parvovirus PCR also available, serology less useful in practice
Most cases will resolve with supportive care:
Fluid therapy: Correct dehydration and hypovolaemia, then maintenance.
Antibiotics: Only where there is evidence of sepsis (amoxy/clav)- Widespread use of metronidazole in haemorrhagic diarrhoea is not indicated – see earlier.
Dietary modification: – traditionally food was withheld, but studies have shown “feeding through” with a low fat, easily digestible diet decreases morbidity and hastens recovery
Antiemetics: e.g. maropitant
Analgesia: opioids
Supplementary treatment options:
Protectants and adsorbants e.g kaolin - frequently used, but weak evidence for efficacy
Pro-, pre- and postbiotics – limited evidence for use, but unlikely to do harm.
Faecal microbiota transplantation – rarely performed. Little information available on safety and efficacy
Prevention
Parvovirus - vaccination
Otherwise difficult due to wide range of factors which could potentially be involved
Prognosis
Parvovirus – guarded even with treatment
AHDS– generally good with treatment, can be fatal if left untreated.
Parvovirus
Barrier nursing essential!
Supportive treatment:
Fluid therapy
Antibiotics (amoxicillin, amoxy/clav) – usually neutropenic, antibiorics indicated as high risk of sepsis
Antiemetics e.g. maropitant
Gastroprotectants (H2 antagonists or proton pump inhibitors)
Nutritional support
Severe cases: Blood transfusion (anaemia)
Antiviral treatment:
Virbagen Omega
“For the reduction in mortality and clinical signs of parvovirus (enteric form) in dogs from one month of age.”
Monoclonal antibody treatment:
Recently released by Elanco in the US- no uk release date
“Neutralises canine parvovirus in vivo by selectively binding and blocking the virus from entering and destroying enterocytes.”
Hyperthermia
“Hyperthermia results from increased muscle activity, increased ambient temperature, or an increased metabolic rate.”
May be further categorised into:
Heat stroke/exhaustion
Exercise induced
Malignant hyperthermia (medication/anaesthetic induced).
Stress induced hyperthermia common in cats
Pyrexia
“Pyrexia occurs when the hypothalamus resets the body’s thermoregulation to a higher point than normal, resulting in physiological mechanisms which increase body temperature.”
Can be due to infectious, immune-mediated, or neoplastic disease
Rectal temperature >39.2oC
Pyrexia of unknown origin:
Pyrexia with no obvious cause following diagnostic tests and which has shown no response to treatment with e.g. antibacterials, NSAIDs, steroids etc.
differentails for pyrexia
Vaccine reaction
May be a trigger for immune mediated disease
Infectious diseases in non-vaccinated animals e.g. FeLV, cat flu, parvovirus, leptospirosis, kennel cough etc.
Environment:
Hunting – Toxoplasma gondii, Salmonella spp.
Travel history – Leishmaniasis
Ectoparasite control:
Tick borne disease e.g. Babesia, Erhlichia, Anaplasma
Flea-borne disease e.g. Bartonella
Exposure to other animals
Infectious disease e.g. FIV, FeLV, infectious gastroenteritis, kennel cough, cat flu
Injury e.g. abscess or cellulitis following a bite wound
Any other clinical signs which could narrow down which body system is involved:
Gastrointestinal tract
Urinary tract
Neurological system
Respiratory system
Pancreas
Cardiac system
Musculoskeletal system
trail treatment for pyrexia of unkown origin in cats
Conservative treatment:
NSAIDs – only if no dehydration OR correct dehydration first.
Fluids – subcutaneous or oral rehydration
Antibiotics – especially in cats where a cat bite is suspected but no bite wound can be found
NOTE: Cefovecin (Convenia) – long acting third generation cephalosporin which is massively overused in these cases. Not a first line drug!
Retrospective study of 106 cats presented with pyrexia:
FIP most common diagnosis by far.
Infectious disease most common cause, followed by inflammatory, then neoplastic, immune mediated, and misc causes less common
Cats:
Cat bite abscess
Acute viral and uncomplicated bacterial infections e.g. cat flu, gastroenteritis etc.
trial treatment for pyrexia of unkown origin
Conservative treatment:
NSAIDs – only if no dehydration OR correct dehydration first.
Fluids – Usually oral rehydration
Antibiotics
Less clear cut than in cats
The most common infectious conditions are acute viral or gastrointestinal infections – antibiotics not indicated for either.
Retrospective study of 140 juvenile dogs presented with pyrexia:
Steroid responsive meningititis-arteritis most common diagnosis, followed by immune mediated polyarthritis.
Immune mediated conditions most common, followed by other non-infectious inflammatory conditions, then infectious.
Dogs
Acute viral and uncomplicated bacterial infections e.g. kennel cough, gastroenteritis etc.
Steroid responsive meningitis-arterititis - now being recognised much more frequently in first opinion practice
Steroids:
May be trialled where clinical signs are suggestive of SRMA and further investigations are not an option.
Need to be wary re:infectious causes of pyrexia – could become worse
investigation pyrexia of unkown origin
Retrospective study of 106 cats presented with pyrexia:
FIP most common diagnosis by far.
Infectious disease most common cause, followed by inflammatory, then neoplastic, immune mediated, and misc causes less common
Retrospective study of 140 juvenile dogs presented with pyrexia:
Steroid responsive meningititis-arteritis most common diagnosis, followed by immune mediated polyarthritis.
Immune mediated conditions most common, followed by other non-infectious inflammatory conditions, then infectious.
Where to start?
Choose tests which give you the most amount of information first:
Haematology and biochemistry
(FeLV and FIV SNAP test for cats)
Urinalysis
Choose tests which give you the most amount of information first:
Thoracic and abdominal radiographs
Abdominal ultrasound
Faecal analysis?
If an underlying cause has still not been identified or confirmed, move on to more specific tests.
Immune testing-
Saline auto-agglutination or Coombs test for IMHA
Antinuclear antibody (where evidence of two or more immune mediated disease processes is present)
Rheumatoid factor where an erosive polyarthropathy is present.
Acetylcholine receptor antibodies if myasthenia gravis is suspected.
Cytology-
FNA of masses
Cerebrospinal fluid tap – where meningitis is suspected
Arthrocentesis – where polyarthrtitis is suspected
Bone marrow aspiration and biopsy – where bone marrow disease is suspected e.g. where panleukopenia is present on haematology
Infectious disease testing
Outdoor cats (esp hunters): Toxoplasma gondii IgG and IgM, tick-borne disease PCR panel (Borrelia, Ehrlichia/ Anaplasma etc.), Bartonella PCR
Cats with anaemia: Infectious anaemia panel (Haemotrophic Mycoplasma spp.)
Dogs with a travel history: Vector borne disease PCR panel (Leishmania, Babesia, Ehrlichia etc.)
Most cases will require:
Fluid therapy
Anti-inflammatories – either NSAIDs, or steroids where immune mediated disease is present
Otherwise, treatment will depend on the underlying disease.
If a diagnosis has still not been reached, consider referral.
Cats:
Cat bite abscess
Feline Infectious peritonitis
Toxplasma gondii
Dogs:
Heat stroke
Steroid responsive meningitis-arteritis
Immune mediated polyarthritis
Cat bite abscess
Presentation:
Lethargy
Anorexia
Pyrexia
+/- focal swelling or draining abscess (head, neck, rump, legs and paws = common sites)
Diagnosis based on history and clinical signs
Treatment depends on presentation
Cat bite abscess - treatment
Release pus:
Open (if not already draining) and flush with sterile saline (20ml syringe and 19g needle)
If abscess is extensive or painful, sedation or GA may be necessary
Owners should bathe the wound at home (saline or chlorhexidine) to keep it open and encourage further drainage.
Analgesia
Meloxicam – analgesia and anti-pyretic.
Opioids – if dehydrated
Fluids
Mild dehydration - single s/c bolus
Moderate to severe dehydration - IVFT
Antibiotics
Only if pyrexic and/or systemically unwell
Base on inhouse cytology if possible
Feline infectious peritonitis
Immune mediated disease which develops in some, but not all, FCoV infected cats
Presentation:
Signalment: Cats <3 or >10 years old from a multi-cat environment (e.g. breeding cattery or shelter). Recent stressor also common.
General signs: Anorexia, lethargy, pyrexia, weight loss, pale and/or jaundiced mucous membranes.
Presentation (cont):
Wet form: Effusions - Peritoneal (65%), pleural (10%), or bicavity (25%)
Dry form: Varies with organ system affected. Occular and CNS signs most common (60%), remainder involve abdominal organs
Diagnosis is challenging, as many cats will be infected with FCoV without developing FIP.
Clinical suspicion is raised by:
Consistent history, signalment and clinical signs (wet form especially)
Haematology: Non-regenerative anaemia, lymphopenia, IMHA.
Biochemistry: Hyperglobulinaemia, hyperbilirubinaemia in the absence of significant changes to other liver enzymes
FCoV serology and PCR not diagnostic as not all infected cats develop FIP, but high titres may be indicative
Gold standard: Immunostaining of FCoV antigen within macrophages in effusion or tissues + histopathological changes consistent with FIP.
Prognosis grave – currently no cure.
FIP treatment
Treatment options:
Immune mediated disease so currently therapy aims at modifying the immune response using steroids.
Interferon (virbagen omega) shown to be ineffective for FIP
Antiviral drugs targeting FCoV replication now being investigated but not yet available.
Toxoplasma gondii
Clinically silent in the vast majority of cats, self-limiting intermittent diarrhoea in approx. 20%
Rarely, severe acute and chronic forms of disease will develop:
Acute: Pyrexia, anorexia, CNS signs, multifocal inflammation.
Chronic: Vague, recurrent illness, chorangioretinitis is common.
Possible breed disposition -Norwegian forest cat, Birman, ocicat and Persian cats.
Clinical suspicion is raised by:
History (hunting) and clinical exam findings consistent with multifocal inflammatory disease.
High T. gondii IgM and IgG (ideally rising titres taken 2-4 weeks apart)
H&B and urinalysis not useful for diagnosis, but may show which organ systems are effected.
Definitive diagnosis:
Detection of tachyzoites in tissue biopsies or cytology samples.
Immunohistochemistry or immunofluorescence on histology samples.
Toxoplasma gondii treatment
Primary treatment: Clindamycin BID for 4 weeks
Supportive treatment:
Fluid therapy if dehydrated
Appetite stimulants e.g. mirtazapine.
Ocular inflammation – topical glucocorticoids
Care re:systemic immunosuppressants
Elimination of the parasite is very difficult, and recurrence is common.
Heat stroke
Almost always due to
Exposure to high environmental temperatures (e.g. hot car)
Recent physical activity, usually in hot weather.
Presenting signs:
Continuous panting +/- cyanotic mucous membranes
Hypersalivation
Stiffness
Collapse in severe cases
check bloods continuously to moitor renal function
Steroid responsive meningitis-arteritis
Most common form of canine meningitis.
Typical presentation:
Young dog
Pyrexia
Neck pain with no other neurological deficits
Less common signs include cranial nerve deficits and, in chronic cases, deficits associated with spinal cord damage.
Diagnosis is often made on signalment and clinical examination alone.
Haematology: Leucocytosis with left shift
Biomarker: C-reactive protein (non-specific for inflammatory disease)
CSF cytology:
Most important diagnostic test.
Acute phase = pleocytosis, non-degenerated neutrophilic granulocytes, increased protein content, and a negative microbiological culture.
Chronic phase: Predominant cell type changes to lymphohistiocytic cells (lymphocytes and macrophages) – risk of false negative results.
MRI: Useful to rule out other common ddx
Steroid responsive meningitis-arteritis treatment
Prednisolone = 1st line treatment for moderate to severe cases.
NSAID (carprofen) use has been reported for mild cases with CSF cell counts <200 cell/uL.
Azathioprine may be used as a second line drug in combination with prednisolone.
Immune mediated polyarthritis
Can be primary (idiopathic) or secondary to another inflammatory condition which -> immune complex formation
Presenting signs: reluctance to walk, altered gait (stilted, “walking on eggshells”) or lameness, multiple swollen, painful joints.
Non-specific presenting signs: pyrexia, lethargy, inappetence, vomiting, diarrhoea.
Definitive diagnosis is based on arthroscopy of at least three joints demonstrating:
WBC > 3000/uL
Neutrophils > 10%
TP > 2.5 g/dL
Negative culture
BUT because IMPA can be 2o, a full suite of baseline tests are recommended to evaluate for underlying inflammatory conditions
Immune mediated polyarthrtitis treatment
Prednisolone = 1st line treatment for IMPA, +/- azathioprine as per SRMA.
Major differential for IMPA is septic arthritis, therefore recommended to wait for culture results before starting prednisolone.
Opioid analgesia should be started while waiting for results.
“Lily”, a six year old entire Neapolitan mastiff bitch, is presented with a 3 day history of lethargy, inappetence, and polydipsia and polyuria.
What other history questions do we want to ask?
when was her last season
how much exactly is she drinking
are there any other animals in the house? could she have been ated
eating? vomiting? dihorea?
have you noticed any clinical signs
any acess to toxins?
“Lily”, a six year old entire Neapolitan mastiff bitch, is presented with a 3 day history of lethargy, inappetence, and polydipsia and polyuria.
What are we going to be looking for on clinical examination?
temperature
pulse
respiritory
mucous membranes- colour, crt, moinstness
vulvar exam- discharge? cytology? open or closed cervix
palpate abdomen
mamary gland
“Lily”, a six year old entire Neapolitan mastiff bitch, is presented with a 3 day history of lethargy, inappetence, and polydipsia and polyuria.
shes 6% dehydrated
uncomfortable in the abdoen
normal ympnnodes
open cervix
small volume of puralent foul smelling discharge
raised temperature
What is your primary differential?
pyometra
Oestrogen stimulation of the uterus, followed by periods of progesterone influence
-> Synthetic progesterones (alazin highly predisposes dogs to pyos, should be spayed) administered over long periods
OR
Oestrogens given for misaligment
Endometrial proliferation, uterine glandular secretions, cervical closure and decreased myometrial contractions
Cystic endometrial hyperplasia/endometrial hyperplasia
Secondary invasion with bacteria (often E. coli)
<- Underlying UTI, renal disease etc. may predispose to infection
Neutrophilic inflammation, accumulation of pus within the uterus, +/- septic shock, decreased responsiveness to ADH polyuria
Pyometra - pathogenesis
Open vs closed pyometra-
Open: Pus drains out of the cervix
Closed: Pus is trapped within the uterus, higher risk of rupture and sepsis.
Closed pyometra is almost always an emergency requiring surgery.
May consider medical management of open pyometra in certain cases-
Mild symptoms
Valuable breeding bitches
Animals with increased anaesthetic risk (geriatric, underlying health concerns)
Note: High risk of recurrent pyometra after the next season when medical management used- should be bred or spayed before next season
involvment of-
repro system
renal system- interfirence with antidiuretic hormone from pyo
toxins interfiere with ADH
immune system- acumulation of neutorophils in uterus can deprive other areas of the
“Lily”, a six year old entire Neapolitan mastiff bitch, is presented with a 3 day history of lethargy, inappetence, and polydipsia and polyuria.
you suspect pyometra
What diagnostic tests do we want to perform?
Haematology and biochemistry
Cytology (vaginal discharge)
Ultrasound
Culture and sensitivity
“Lily”, a six year old entire Neapolitan mastiff bitch, is presented with a 3 day history of lethargy, inappetence, and polydipsia and polyuria.
you suspect pyometra
you perform-
Haematology and biochemistry
Cytology (vaginal discharge)
Ultrasound
Culture and sensitivity
What changes might we expect to see?
Haematology and biochemistry- neutropenia, leukocytocis, anemia, azotemia
Cytology (vaginal discharge)- degen neutrophils adnf bacteria
Ultrasound- fluid filled uterus
Culture and sensitivity- +++
“Lily”, a six year old entire Neapolitan mastiff bitch, is presented with a 3 day history of lethargy, inappetence, and polydipsia and polyuria.
you suspect an open pyometra
her symptoms are mild
Based on our clinical picture, what treatment options do we have?
sue to her age and her relative stability surgical managemnt would be the most appropriate
it is unlikly she would be bred from any more
what does medical managemtn for pyometra look like
antibiotics- amox/clav
fluid therapy- stabalise
protaglandin- colprostenol
galastop- cabergoline- medical treatment of closed pyo- dopamine agonist
alizin- algiprestone- progesterone receptior antaonist- relaxes cervix to allow puss out
licenced for abortion but off licenese use for . three doses at days 1,2 and 7
cloporestol- prostaglandin
in combo with alepredistone
not licensed in dogs
causes luteolusis and uterine contactions
pyometra in Hamsters, rats and mice
Most commonly affected species.
OHE indicated – short oestrus cycle means recurrence almost inevitable.
Medical management usually attempted prior to surgery to decrease GA risk.
Antibiotic choice = fluorquinolones
Fluids – s/c
“Cookie”, a three year old Golden Retriever bitch, is presented for a whelping check. An ultrasound performed by a home visit service counted nine puppies, but only five have been delivered and Cookie is no longer straining.
What other history questions do we want to ask?
are the puppies doing ok?
when did she start?
whe was the last puppies passes?
did the straining stop when the last puppie was born or some time fter?
how long between each puppies?
has there been any stressors?
how many placentas has she passed? is there one for each puppie?
what diet has she been fed?- puppie food is best
has their been any discharge?
has the bitch whelped previously? were their issues? is thier known issues in this line
“Cookie”, a three year old Golden Retriever bitch, is presented for a whelping check. An ultrasound performed by a home visit service counted nine puppies, but only five have been delivered and Cookie is no longer straining.
she strained for some time after the last puppy and then stopped
What are we going to be looking for on clinical examination?
tpr
mm
whats her consition?- exhasted ect
mentation
abdominal palpation
check vaginal canal
can we feel a puppy?
fetal heart rate
“Cookie”, a three year old Golden Retriever bitch, is presented for a whelping check. An ultrasound performed by a home visit service counted nine puppies, but only five have been delivered and Cookie is no longer straining.
low temo
vestibule is dilated on palpation- no puppy in canal- weak fergusons response (contration in response to pressure)
puppies palpated within abdomen
maternal heart rate is 48
foetal hear rate is 208
What is your primary differential?
absence or weakness of fergusons respone increases suspision of hypocalcemia
puppies are not in distress- too high heart very uncommon
uterine inertia
Dystocia pathophysiology
Maternal factors:
Primary uterine inertia – multifactorial, genetic disposition suspected.
Secondary uterine inertia – multifactorial, hypocalcaemia/hypoglycaemia play a more prominent role.
Birth canal abnormalities (breed conformation, stricture, masses etc.)
Foetal factors:
Size mismatch (large puppy, small bitch)
Malformations
Malposition
Inertia = most common reason for dystocia across breeds, birth canal conformation/size mismatch more common in brachycephalics
“Cookie”, a three year old Golden Retriever bitch, is presented for a whelping check. An ultrasound performed by a home visit service counted nine puppies, but only five have been delivered and Cookie is no longer straining.
low temp
vestibule is dilated on palpation- no puppy in canal- weak fergusons response (contration in response to pressure)
puppies palpated within abdomen
maternal heart rate is 48
foetal hear rate is 208
you suspect dystocia
Define and refine the problem!
What type of dystocia do we have?
Secondary uterine inertia – multifactorial, hypocalcaemia/hypoglycaemia play a more prominent role.
“Cookie”, a three year old Golden Retriever bitch, is presented for a whelping check. An ultrasound performed by a home visit service counted nine puppies, but only five have been delivered and Cookie is no longer straining.
you suspect secondary uterine inersia
What further diagnostic tests should we perform?
bloods- check calcium levels- low calcium levels does not rue out hypocalcemia as cellular calcium levels not shown
check ketones- hypoglycemia- pregnancy toxemia
check how many puppies left
“Cookie”, a three year old Golden Retriever bitch, is presented for a whelping check. An ultrasound performed by a home visit service counted nine puppies, but only five have been delivered and Cookie is no longer straining.
you suspect secondary terine inertia
Based on our clinical picture, what treatment options do we have?
medical managment-
calcium- increases strenth of contraction
10% calcum gluconate soluiton as slow IV . can be done sc but potential side efects. oral ineffective
give calcium and wit before gic=ving oxytocin- more time if given subcut
oxytocin- increases frequency of contrations
microdoses more effecteive than higher doses
can be given sc, im or iv 30 min for up to 3 soses
give both in all cases regardless of bloods
glucose if hypoglycemic
3 rounds of medical managment then go for c section
bsava maual has step by step process
palpation to manilpulat epuppies nto canal but not likley as no puppie in birth canal
4 puppies is about the limit for mediclal intervention as mother will be fatigued
labour should not be too prolonged if trying medical managment
do not make a dog contract on a suck puppies
surgical options- obstructive dysticua
non obstructive with greater than 4 puoppies
pre operative fluids recomended
oxytocin can be given after c section aid uterine involution and milk let down
use intradermals to prevent puppies form interfering with sutures
use abdominal lavage, pre operative antibiotics- amox-
ongoing antiobiotics recomended
may recomed dpay at time of c-section- increased surgical time? increased infection risk? decreased mothering behaviour- increase in pain, unkown reasons?
previos opinion is not to do spay but more modern retrospective analysis says risk is not as increased as previously feared
eventual spay should be recomended as dog is poor breeding candidate- calium suplimentation durign pregnacy not shown to help.
“Barney”, an eight year old male entire Dwarf Lop rabbit, is presented with acute onset enlargement of the scrotum. He flinches when the area is palpated, and appears lethargic.
What other history questions do we want to ask?
has he been fighting?
has he been bred from recently?
what other rabbits does he live with?
eating? drinking? urinating? faeces?
