Case Conversations Flashcards
Bright, good appetite, one horse is really dyspnoeic, 2 or 3 depressed and inappetant
*Mucopurulent nasal discharge. Enlarged submandibular LNs– some have ruptured
Most likely???
E. Streptococcus equi equi- Strangles
Unlikely to be viral because of big LNs
B- farm workers (fomites)
C- Soil-maybe
D- Asymptomatic carrier
E- vet maybe
F- neighboring horse maybe
Strangles
Isolating horses– 3 groups– really contagious, incubation period of a few weeks.
D- definitely
Treating with antibiotics difficult to penetrate abscesses… so organisms left in the core of the abscess so those animals often have a relapse
** do not recommend to vaccinate– type III hypersensitivity
Strep equi zooepidemicus
Lower resp tract, but upper resp tract commensal
Strangles
D- absolutely not!!
What do you do?
A. CBC, biochem, urinalysis
B. Biopsy tongue ulcers
C. Biopsy hind limb
D. Blood cultures
E. Nasal swab for viral culture
F. PCR samples for viruses
A. CBC, biochem, urinalysis
A B C D
Not C and not H
Primary diagnosis?
Vasculitis and cellulitis secondary to:
- drug or vaccine reaction
b. severe cat bites
c. post dental bacteraemia
d. virulent systemic disease (VSD)
e. something else
D. Virulent systemic disease
What is VSD?
People carry it around– they don’t sneeze it into the next cage
VSD, what did the hospital do?
VSD
D. Vaccines are not effective depending on the strain– Calicivirus changes strains all the time
A, B, C all right
WHICH of the following clinical signs are prevalent and/or important?
A. Dullness
B. Inappetance
C. Coughing
D. Dyspnoea
E. Snezing
F. Hyperexcitability
G. Mortality
Coughing, sneezing, mortality
C- clinical exam
B and D
Unlikely to be bacteraemic– down the trachea
Factors that contribute to the development of respiratory disease in a group of animals in a feedlot
12 yo MN shih tzu
Loud, harsh cough intermittently for 6 months
Terminal retch and swallow, slowing down on walks
Eating and drinking ok
* General appearance- BAR, normal temp, normal RR RE
Coarse crackles and occasional expiratory wheeze, coughs on tracheal palpation, productive
Low heart rate, II/VI left apical systolic cadiac murmur, pulses normal
BCS 7/9
Chronic canine bronchitis
BAL: inflammatory cells, some RBCs
Higher WCC, neutrophilia, eosinophilia, monocytosis, increased TS
Blood gas: PaO2 - 90 mm Hg; PaCO2- 40 mmHg (NORMAL)
Treatment:
* Anti-inflammatory GCs, methylxanthine bronchodilator, consider antitussives, manage allergens, irritants and air quality and humidity of the home, treat infection if present, weight loss, limit stress/ excitement, consider nebulisation and coupage, can be treated but not cured, long term prognosis guarded
12 yr old MN shih tzu, heavy breathing, not eating, weight loss
Last 24 hours breathing heavily, dull lethargic, starting to slow down on walks, several soft infrequent cough
Quiet, alert, responsive, normal temperature,
RR = 60 with moderate increase in effort
Diffuse soft crackles
162 HR, grade V/VI left apical systolic murmur, pulses normal
BCS 3/9
Left sided congestive heart failure
* high ALT, ALP, neutrophilia, lymphopenia
Blood gases: PaO2- 60 mmHg, PaCO2- 25 mmHg
Treatment
* Supplemental oxygen and minimal stress
* 2-4 mg/kg frusemide IV q 1-2 hours until RR < 30, then 1-2 mg/kg po BID-TID
* consider venodilator or systemic vasodilator if frusemide alone is not effective
* MOnitor RR/ effort, potassium concentration, PCV/TP and renal parameters
* Can be treated but not cured, long term prognosis guarded
6 yr FS westie, heavy breathing, bringing food/ water up
* Breathing heavily last 24 hours
* Dull, lethargic, Brought up intact biscuits covered in clear fluid soon after eating
* Drank and brought the water straight back up
* General appearance- quiet, alert, responsive
* Temp 40 C
* Resp 60 with moderate increase in effort, MM hyperaemic, diffusely harsh lung sounds with crackles cranioventrally on the right
CVS- HR 162 MMs hyperaemic, CRT 0.5 seconds, no murmur, pulses tall and wide
BCS 4.5/9
Aspiration pneumonia with megaoesophagus
Leukocytosis, bands, neutrophilia, monocytosis, inc. TS, inc. TP, Moderate toxic change
Blood gas: PaO2- 60 mmHg, PaCO2- 25 mmHg
Treatment:
* Supplemental oxygen and minimal stress
* Broad spectrum antibiotics
* BAL or blind BAL for culture and susceptibility testing
* Restrictive IV fluid therapy
* Nebulisation and coupage
* Consider bronchodilator if acutely dyspnoeic and bronchospasm suspected
* Prognosis for resp disease is good but must carry out investigation for underlying cause when stable
12 yr FS westie, heavy breathing, coughing and slowing down over the last few months, weight loss
* Loud, harsh cough intermittently for 6 months, breathing heavily, coughed up white foamy material with trace of blood this mornign, starting to slow down on walks, decreased appetite, weight loss
* quiet, alert, responsive, normal temp, RR 60 with mod increase in effort, pale pink MMs, diffusely harsh lung sounds, HR 162, grade II/VI left systolic cardiac murmur
BCS 3/9
Metastatic Pulmonary Neoplasia
Anaemia, high platelets, leukocytosis, neutrophilia, monocytosis, increased TS, increased TP, increased ALT, ALP, AST, hypoglycaemic, hypercalcaemia
Mild toxic change
Blood gases: PaO2- 60 mmHg, PaCO2- 25 mmHg
Treatment:
* Supplemental oxygen as needed (clinical signs + SpO2 or arterial blood gas to determine)
* Chemotherapy likely little impact
* Palliation with NSAIDs or corticosteroids, antitussives
* Treat secondary infections
* Consider appetite stimulants
* Pain management as needed
* Long term prognosis is poor
3 yr ME Jack Russel, heavy breathing, collapsed, protracted seizure and now heavy breathing, is sometimes dull after eating, small compared to littermates, general appearance- laterally recumbent, mentally altered, hypersalivating
* high temp 40C
* RR 60, MM cyanotic, marked increase in effort, diffusely harsh lung sounds and generalised crackles
CVS- HR 180, MM cyanotic, tacky, CRT 2.5 seconds, pulses short and narrow
Neuro- pupils responsive, no menace, normal spinal reflexes, non-ambulatory
BCS 4.5/9
Non Cardiogenic pulmonary oedema
Anaemic, neutrophilia, lymphopenia, decreased urea, hypoglycaemia, low cholesterol, increased AST, increased CK, increased PT, increased APTT
Mild microcytosis, WBC morphology unremarkable
Blood gases: PaO2- 60 mmHg; PaCO2- 25 mmHg
Treatment
* Supplemental oxygen and minimal stress
* Furosemide can be considered
* Positive pressure ventilation with PEEP as needed (clinical signs + SpO2 or arterial blood gas to determine)
* Investigate/ manage primary cuase
* May worsen before it improves, likely to recover over 48-72 hours, long term prognosis for resp disease is good but must carry out investigation for underlying cause when stable
3 yr ME Jack Russel, heavy breathing, white gums, coughed up pink foamy material with frank blood, not eating/ drinking, normally very active farm dog, works in the paddocks during the day, kennelled overnight, toxins or trauma?
* Weakly standing but orthopnoeic, quiet but responsive, normal temp
RR 60, MM pale, pattern is rapid and shallow with paradoxical movement, reduced breath sounds ventrally with crackles dorsally, mild right epistaxis noted
CVS- HR 180, MM tacky, unable to assess CRT, regular rhythm, pulses short and narrow, BCS 4.5/9
Vitamin K antagonist rodenticide toxicity
Anaemic, neutrophilia, lymphopaenia, decreased TS, increased urea, hypoalbuinaemia, extremely high PT, high APTT
PaO2- 60 mmHg (decreased), PaCO2- 50 mmHg (slightly elevated)
Treatment:
* Supplemental oxygen and minimal stress
*PPV with PEEP as needed (clinical signs + SpO2 or arterial blood gas to determine)
* 15-20 ml/kg FFP (or whole blood if very anemic)
* Vit K1 5 mg/kg initially then 2.5 mg/kg BID (duration, dependent on agent)
* Return for recheck PT 48 hours after vit K1 supplementation is completed
* Monitor RR/effort, PCV/TP, BP, PT/aPTT
* Long term prognosis is excellent
3 yr ME Jack Russell struggling to breathe, collapsed, found collapsed in the yard, weak with rapid breathing, normally very active, works in the paddocks during the day, kennelled overnight, possible access to toxins/ trauma
* Laterally recumbent, dyspnoeic, appears panicked, profoundly weak, normal temp, RR 60 with minimal chest movement, then agonal just after presentation, MM cyanotic, lung sounds were quiet prior to respiratory arrest
CVS- HR 180, regular moist unable to assess CRT, pulses tall and wide
Neuro- dilated pupils, depressed spinal reflexes, non-ambulatory, profoundly weak
BCS 4.5/9
Low platelets, leukocytosis, neutrophilia, lymphopenia, monocytosis, increased phosphate, increased urea, increased creatinine, hyperglycaemic, increased ALT, increased AST, off the charts CK, off the charts PT and APTT
Blood gas- PaO2- 52 mmHg, PaCO2- 78 mmHg
Treatment
* supplemental oxygen, minimal stress
* Immediate intubation and PPV required
* Tiger snake antiserum, repeated vials until anti-venom detection kit shows negative resulto n blood
* Fluid therapy and nursing support
* monitor coagulation times, CK, renal function
* Long term prognosis is good
* MBSA: generally flat, trollied in
* hypoperfusion (moderate)
* Irregular rhythm, HR 188
* distended and tympanic abdomen
* Tachypeic but lungs clear
Medications??
* Gastrointestinal protectants, prophylactic antibiotics, analgesia, fluids
C. 80 ml/kg (cat is 60 ml/kg) (60% is body water)
Two methods of gastric decompression
When would you choose butorphanol?
*Mu antagonist
* short duration of action
* not a good choice if going to surgery because not a pure mu agonist
Morphine side effects?
* histamine release, hypomotility
* Why you choose methadone over morphine
Buprenorphine
* partial mu agonist– more analgesic than butorphanol but less analgesic then methadone
* lasts 6-8 hours
* prevent pure mu agonist from working because it has a high affinity for the mu receptor and makes it hard to go to a pure agonist later
* takes 30-40 minutes to take effect
Ketamine?
* good analgesia without cardiovascular compromise
* not as good as a pure opioid agonist
* possible drug to consider GDV, just not pre-op in the ICU
Fentanyl? Fentanyl patch?
* Disadvantage: short acting– 30 minutes
* advantage– IV vs having to go IM
* Short acting, can give more later especially if completely wrong
* Fentanyl patch- slow release
What can you hit by accident?
Can hit the spleen, but you may get blood anyway so dont necessarily assume you’ve done so
** if it untwists before you take your RADs, you have more time to stabilize the patient– so you do this before RADs!
* restores CV compromise
Right lateral– if you don’t get answer then go to right, left later, and VD
Take another view!!
* Hypoventilation- Diaphragm- definitely anaesthetic complication potential
* Hyperventilation- Acidaemia, pain
* Hypoxaemia- hypoventilation in the extreme could lead to hypoxemia– we give them 100% oxygen so what breaths they do take
* Hypotension- it was just in shock- crystalloids go get redistributed into the peripheral tissues– so if we don’t keep an eye on the fluids in the process of correcting run the risk of hypotension… almost all anaesthetic drugs cause cardiac dysfunction
* Hypertension– highly unlikely, pain would be the main reason
* Hypothermia- inhaled anaesthetic gases cooled, cold table, shave off fur, alcohol to prep them… etc.
* Hypokalaemia– unlikely, you can see with more chronic GI things but this is acute and potassium was fine on bloods
* Acidemia
* Alkalemia- not as likely
* Cardiac dysrhythmias- ventricular (VPCS/ ventricular tachycardia)– myocardium suffered ischaemia therefore has to heal
Propofol- super short acting, cardiac, post induction apnoea
Midazolam- muscle relaxation, reduces the dose of propofol you need (all side effects of propofol are dose related)
1 mg/kg of propofol followed by midazolom followed by propofol to effect
* Ketamine- increases circulating catecholamines, he can maintain a high heart rate when presented means he still has sympathetic drive (NOT A WRONG CHOICE but possibly don’t give because it has arrhythmias– so increasing the amount of circulating adrenalin may increase arrhythmias)
Management/ monitoring for a GDV
Lactate into the entire body after recirculation
Pathognomonic – Right sided clockwise GDV
* reach to the far side of the dog will find pylorus, bring pylorus up with the right hand, pushing down with the left hand
* Decompress if it is really dilated to make space
* can move the spleen to make space too
assess viability of tissue– change in colour, change in texture (feels thin), ecchymotic haemorrhage– brush stroke blue, dark red color
* resection with non-viable tissue– observe for 5 minutes to see if it is picking up again, check for pulse.
* GI stapler for resection OR partial gastrectomy
Which gastropexy type?
A. Belt-loop
B. Incisional
C. Circumcostal
D. Tube
Incisional- less time consuming, less fiddly (leave mucosa and sub mucosa intact– through the seromuscular layers)
Post op GDV considerations
* Fluids- avoid positive fluid balance– don’t continue high rates unless required
* Nutrition asap– unusual for them to eat sooner than 24 hours (>24 hours start to consider how to get them to eat– nasoesophageal tube?? to get the enterocytes working)
* Haemodynamic monitoring (ECG- arrhythmias, MABP)
* Resp monitoring
* Analgesia
* Ongoing monitoring– did you take enough stomach out??
Post op analgesia in the hospital?
Generally spend several days in the hospital even if they are doing well (arrhythmia, breakdown of tissue, were in shock, etc.)
* Fentanyl patch– takes 12-24 hours to kick in (in the ICU you wouldn’t choose Fentanyl patch– unreliable absorption because transdermal, some dogs last 2 days-3 days)– shave the hair, prep the skin, water tight adhesion that stays clean
** Fentanyl patch– not in cats!!
* Lignocaine infusions– analgesic– anti-endotoxic so if you had a patient with significant necrosis… also it can help with persistent arrhythmias– the longer they are on it, can make you nauseaus but intra operatively higher dose then post operatively in the ICU– otherwise drool, won’t eat as quickly
* Fentanyl infusion more common post operatively
* NSAID- no if you’ve resected a massive part of the stomach, can cause GI problems and renal problems (after 2-3 days might be fine)
3 yo TB racehorse
* 4am found rolling
Trainer gave 2 ml ACP IV
No change at 10 minutes
Trainer gave 10 ml flunixin
What do you do first?
Give detomidine for analgesia and to get physical exam done
History– don’t do first– horse is painful
* physical exam- HR, RR, temp, g/s, MMs– dangerous at this time
How you interpret?
a. Not surgical: r/v 3 hours
b. Impaction- MM
c. Early sxl lesion
d. Don’t have enough info to decide
Duration of colic short and pretty painful
Elevation in HR is minimal
Can’t make a call it is not surgical yet, too early
* Impaction- hasn’t passed manure but don’t know that is the primary lesion yet
Mgt of impaction– enteral fluids– but if SI obstruction would distend SI more… so wouldn’t want to do too much
Could be early surgical
DON’t have enough info!!!
Soo… rectal and U/S.. transverse of the SI.
Definitely small intestinal because the U/S picture is not normal
** Not likely AE because there was no reflux– AE causes functional obstruction of the proximal SI so reflux is often present a short time after onset. The horse was not febrile though this doesn’t always occur with AE and he had said NSAIDs which could decrease temp slightly and give a false reading: despite 38C is well within normal range
* The level of pain may also be more than expected with AE though this is unreliable. I would expect some motility in the U/S picture with AE but stasis with a physical obstruction. AE is less common than a physical obstruction though a racehorse is fed a large amount of concentrates which is a risk factor for AE
A. NGT/ rectal: 2-3 hours
* Reflux may or may not be present at this time: it depends on the site of obstruction. Passing a NGT is an important part of any colic work up or reassessment but absence of reflux does not rule out SI obstruction in the early stages of colic
Repeating the rectal exam is an important part of re-evaluation of a colic and SI distension may not be palpable: if present it is most often in the midline as stacked fluid filled tubes travelling transversely across the abdomen but the mesentery is long so dilated loops can be anywhere. Tension on the medial band of the caecum or pain when it is palpated occurs if the caecum is being pulled out of place due a lesion involving the ileum though this is not a particularly sensitive or specific finding.
Which is most appropriate COA?
A. Fecal culture
B. rumen pH
C. Abdominocentesis
D. Exploratory laparotomy
E. Wither pinch test
B. Rumen pH
Lactic acidosis
What if it was 5.5? We would need to go back to clinical exam
When would abdominocentesis be helpful? If it is chronic
Exploratory lap?
Wither pinch test? Peritonitis
JD- culture takes weeks because slow growing.. culture used as the definitive test
Salmonellosis- yes; fetid diarrhoea, pyrexic– 95% confident in diagnosis. Sensitivity of culture… revolting salmonella faeces… does not survive transport to the lab very well. 80% with Salmonella would come back with Salmonella. (cost of C&S- $10)
E. coli scours- no
Mycotic rumenitis
Grain overload- no
A
Give oxytet for 5 days IF the cow is showing systemic signs– this cow had a temp of 39, not normal in Warnabol in winter
* In general the enterobacteria that get into the blood are not sensitive to Penicillin
* Baytril- by law do not use in food producing animals in Australia– can’t use it against the label
* Tolfenamic acid- NSAID- 2 day duration of action in cattle, cheaper than Meloxicam
* Low pH and want to correct that.. so either Sodium bicarb or Mg carbonate or both.
* 2 liters of hypertonic fluids followed by 20 L of water orally– appropriate fluid therapy– but this cow doesn’t need it, she is standing up
4 stages of acidosis
Cow is down- antibiotics and fluids
low rumen pH need to buffer
Compromise of gut wall if systemica effects
A. 5 liters of Hartmann’s IV quickly
B. 15 L of Hartmanns quickly IV
C. 2 L of hypertonic fluids IV and 20 L of electrolyte solution
D. 2 liters of hypertonic fluids and 20 L of water orally
E. 2 liters of hypertonic fluids and 20 L of water with 200g NaHCO3
blood volume of a cow? 40 L in 500 kg cow (8%)
Is she down because she is dehydrated?
She is down because she is acidotic and she is in shock, therefore circulatory collapse therefore not enough volume of fluid to fill capillaries….
Hartmann’s doesn’t treat acidosis well in cattle
* Animals that are dehydrated– extracellular space is dehydrated–idea of hypertonic solution is to draw fluid from the EC space to the IV space… where there is no fluid in the EC it can make them worse… however in cases of shock, hypertonic fluids are very useful… so hypertonic would be OK.
* So D or E??
- Use sodium bicarb because we want to fix the acidosis too.
A. 5 liters of Hartmann’s IV quickly
B. 15 L of Hartmanns quickly IV
C. 2 L of hypertonic fluids IV and 20 L of electrolyte solution
D. 2 liters of hypertonic fluids and 20 L of water orally
E. 2 liters of hypertonic fluids and 20 L of water with 200g NaHCO3
5 liters of Hartmann’s combined with flunixin.
5 liters to 40 L enough of a circulatory boost to get them going again. Don’t give too much end up with haemolysis.
** 2 L of hypertonic with electrolytes… reason for electrolytes… when you give hypertonic fluids IV and then oral fluids into the rumen… want to make easy path of fluid for fluids to get into the blood stream… putting electrolytes in will potentially slow that down
* use electrolytes in a dehydrated cow but not hypertonic solution for a dehydrated cow.
Diarrhoea last week, eating OK, not depressed, no straining or blood, normal temp, green poo, no grain, watery, sub mandibular oedema
A. Salmonella
B. Liver Fluke
C. JD
D. Simple indigestion
E. E. coli scours
F. BVD
Diet? Can always be change in diet of an individual cow because the cow before her didn’t eat and she got a double ration
* milk? dropping off
* JD?
* Parasitic tx? No.
Salmonella– unlikely– faeces would stink, depressed, first clinical sign is the cow goes off her feed, in herds with outbreaks– 20-40 cases… cows come into bail, if above 39C and not eating- treat
Liver fluke– could be, a bit old
JD- likely diagnosis, 7 is classic age, no other signs, sub mandibular oedema… Johne’s ELISA… Finding fluke eggs would not rule out Johne’s.
NOT Simple indigestion, E. coli scours, BVD– if you suspected could do ELISA on milk vat to check for antibodies but unlikely in this cow
A, B, C (within 1 week of suspicion so wait for the test)… can send the cow to knackery that has a positive ELISA but clinically normal
JD cause problems in humans?? Current thinking– people in both camps.
Incidence in WA CD, incidence in farmers is no different to the normal population
b. 12 DSE/ha
based on classes of animals have on the land
How can you tell farm is appropriately stocked? Based on French equation– below
** a bit on the lower side with stocking rate
What is a high total worm count in a lactating Merino ewe?
10-20,000 or more is a high total worm count
Age related immunity… ewes may not be the best indicator.. wethers also would have developed immunity. Not lambs with low WEC– wouldn’t get enough sensitivity, so not very representative. Lambs with high WEC >1000epg– selective tx. If drenches do work… would see a change.
E. random lambs- if their avg. WEC > 200 epg
August and taking into account all we have learned
E. Mainly Teladorsagia and Trichostrongylus
** often occur in mixed infections
Haemonchus isn’t such a problem in August– mainly at warmer times of year (in this region that is!)
Outbreaks in warmer regions depending on how much rainfall
Adjusting to delete Haemonchus (since that isn’t our biggest problem not) to show effects of scour worms
Now it has taken out a drench group!! Before we would have considered it useful but not anymore
Smart grazing- wethers or less susceptible group of stock at a high stocking rate
Grass is drying off, sheep go in 2.5 x normal stocking rate, stay in there for a month (December)– short grass, lots of eggs will die… then in February 2nd drench–wethers at 2.5 x normal stocking rate, stay in there a month… then in March-May (autumn break)–we want eggs to die… weaners in their first winter contributes to weaner ill thrift….
drenches need to be strategic
Control release capsules–expensive and can eructate but rare…. high enough dose to kill larvae.. but at some point drops below effective dose. How do we manage that?? Product says it lasts for 90 days… so before 90 days is up… 8 weeks in do WEC and see if it is increasing, if so give a drench of a different class… increase level of protection and decrease developing resistance.
DSE changes massively depending on whether you have small or large sheep
20 DSE/ha
wether- 1.1 because they are quite big
1st september- lambing
2nd december- weaning
How old is oldest lamb at weaning?
B. 13 weeks
SHould be marked before weaning– at about 8 weeks from the start of lambing
A. pretty much spot on
WHAT SHOULD YOU NEVER GIVE TO A GOAT?
GOATS ARE NOT LITTLE SHEEP
Is 327 normal for this mare? sounds a bit short
We are thinking- is there an unhealthy uterine environment?
Vaccination? Are management practices good enough?
Urination defication?
Was milk leaking prior to birth?
** No lethargic after normal first 36 hours
Normal temp
RR slightly high, HR is a little high
Yes it has urinated and defecated
Rule out/ less likely (gray)?? No NI, Meconium impaction, Enterocolitis
I don’t know yet, I need more info!
E
Hct– high for a foal
Fibrinogen– inflammation
Neutropenia– overwhelming inflamm?? Sepsis!!! I’m worried
* Split differential (normal WCC)
Hyperglycaemia- stress
Creatinine– like to see lower– we are worried about nephropathy (NE?? due to ischaemia)
** often born with high CK but would have expected to have come down by now
Also, treatment??
A- YES SEPSIS
PREMATURE
trifecta.. very possible
Tx for sepsis as it could kill them first
Broad spectrum AMs– which ones?? We are thinking about the kidneys
Worried about oedema of the brain, GIT and kidneys
Mildly dehydrated– 20-30 mL boluses stretch out over an hour so not too much
Careful monitoring and nursing
NE?? then thinking about GIT function
Do we refer this foal??? If we don’t need continuous fluids, then could manage on the farm, does the foal need to be looked at every 2 hours? Do we have the staff?
How long are we going to monitor? With sepsis we treat well beyond resolution of clinical signs– weeks rather than days
Incomplete ossification– risk of crushing and damaging
Foals sometimes do have some incomplete ossification but this is an abnormal amount and it is impossible to keep from loading
next slide presenting problems
What do you do now?
Bacterial, viral or protozoa
Necropsy could help you decide… culture.. viral cause may not be able to tell– hard to get a fresh enough carcase
What do you do now?
Cleaning and rotating calves– hygiene
Sick ones out
Resus and fluid management– addressing dehydration and electrolyte imbalances
Calves with diarrhoea
Moderate skin tenting– 10% dehydration… 30-35 kg– needs 3 L of fluid
D.
Campy is hard to culture
you’d need to tell them you suspect specifically
Any more ideas?
Colostrum management
Rotavirus vaccine precalving
C
Nursing well
not crying persistently
being mothered well
sleeping together (no one on their own)
Birth weight
Primary cause– options other side
First litter– B
B- warm the puppies, then they might suckle themselves
Assess is she producing milk?
D. first week (lower second week)
Physical exam and post mortem
Weigh the pups
Faecal smear/ faecal float
Colostral transfer– bloods– ALP– 30 x increase when they have colostrum from the bitch
TP/ TS- first week or two they are lower than in an adult, in weeks to come gets into adult range
Check glucose
Good history
Poor husbandry
What reflexes do you check on the exam?
A or E (rule out the others)
** RR in neonates starts to become more normal after
E
Suspect aspiration pneumnia– dehydrated, hypothermic
why not Enrofloxacin? Impacts how cartilage develops and other effects as well
Amoxicilin first choice
Gippsland in late January
Outbreak of diarrhoea in a mob of 5 month old Merino weaners
Diarrhoea responds partially to Cydectin drench but has recurred and the mob now has a scouring ill thrifty tail of 40% of animals
Several weaners have died in the last week, prompting the farmer to bring 3 sick weaners in to the clinic for you to examine
Biochem, body weight, faecal exam, hydration, generally good physical exam, trace mineral status maybe not at first but if the farmer wants
** Low WEC now suggests drenching was effective
* Oxytet effective for most bacterial infections
** also consider managing and preventing e.g. lower stocking rates, improve nutrition
Most likely ddx bacterial enteritis– worms– Trichostronglyus rugatus, T. vitrinus, T. axei, Teladorsagia
Abamectin– Effective, the rest have too much resistance
What are the presenting problems? DDX?
* diarrhoea
* Sudden death
* Illthrift
* Scours
* Large tail on mob
DDX: worms, nutritional scours, bacterial, protozoal, acidosis
- Barbers pole worm
- Black scour worm
- Campy
- Cu deficiency… etc.
Bench marks for poor performance: mortality rate (2.7%) over 3 months (2% annually; 4% annually for weaners), body weight
* OJD in 3–>4 yo ewes– expected– not necessarily related to the deaths
* perinatal mortality is the problem- unk cause– skinny ewes are going to be the ones that die anyway, so doesn’t necessarily help
* this infection has been on the property 5-10 years: long incubation period
* source: could be cattle but not as likely, neighbors (drainage: water flowing from the neighbor), possibly rams but less likely
What questions do you want to ask?
History of dental care, vaccination history and deworming
*teeth floated every 6 months, up to date on vaccines, dewormed with ivermectin and pyrantel every 6 weeks
* Demeanor, other signs of systemic disease? BAR but generally poor appetite
In the past FECs normal– and CBC and biochem normal in the past– given Trimethoprim sulpha
Show horse
* problem list?
Must try moxidectin to take care of encysted cyathostomes
DDX
Extra- intestinal causes
* Pneumonia/pleuropneumonia
* Recurrent Airway Obstruction
* Extra-abdominal abscesses
* Chronic renal disease
* Chronic liver disease
* Pituitary pars intermedia dysfunction
* (Extra-abdominal) Neoplasia
* Severe musculoskeletal disease
Diagnostic tests?
Abdo U/S intestinal wall thickness, free fluid in the abdo?
Limitations– only see what’s right up against the body wall in a horse
Sector probe
Linear probe
Pretty normal
IBD but can’t rule out intestinal neoplasia
Treatment would not change– Corticosteroids but the prognosis would change
** Caution owner regarding laminitis, infections
* Slowly wean to lowest effective dose
Slinky 12 yo female speyed DSH
History of weight loss
Poor coat
Tachycardia 220 bpm
Thyroid nodule
Hyperthyroidism
Grade 3/6 left parasternal systolic cardiac murmur…. thyrotoxic cardiomyopathy, hypertension, HCM, RCM, DCM, unclassified anaemia
D. (E. good idea too)
Rule out?
R/O renal disease, protein losing enteropathies, diabetes mellitus
Equivocal result then…
A. Repeat TT4 in 2 weeks
Pros and cons of each GOOD EXAM QUESTION
But A.
Carbimazole with food can help
Could swap to Methimazole
Unlikely another disease
Doing nothing- may self resolve but giving with food better to try
What will you do now?
D. No change– important to warn the client of this potential… now we KNOW he has renal disease and we can tackle that too
E. Radioactive iodine
CKD 2 unmasked but stable like most cats
Stress Leukogram
Plasma volume expansion
Issues with perfusion with kidney and liver– hypoxic injury
Hypersegmented neutrophils beacuse of cortisol- they hang aroudn longer
Electrolyte changes aren’t common with CHF but they are with DCM
Fuzzy, hazy lungs– the line is probably just fat
* Diagnosis
Sinus rhythm with intermittent single abnormal ventricular complexes in between where the p waves should be starting (earlier)
Normal heart beat and normal cardiac output
Rate and CO will be normal
Few p waves with QRS
Wide and bizarre
Fits with ventricular origin- Ventricular tachycardia
Polymorphic- starts from different origins
ECG- heart appears to stop for a period of time
CLin path- CV disease often doesn’t give specific things secondary changes
Lipaemic serum– predisposed breed and no other signs to cause this… stress leukogram makes sense, the dog isn’t well
Would not make a diagnosis of sick sinus based on clin path
Heart murmur– big atrium on imaging (not always)
Min Schnauzer predisposed– normal thorax otherwise
Pace maker will kick in when the animal becomes bradycardic, doesn’t do much for tachy part– so still lose some of these patients over time for rhythm abnormalities
160- moderate for big breed dog
Lowish body temperature
Localized to right forebrain
Sinus rhythm with the occasional VPC– cardiac output isn’t compromised– rate is a little fast
Clin path- reticulocytosis- regen anaemia– abnormal shapes fit shear injury of red cells– might have DIC on the list– would fit with Haemangiosarcoma. Low protein- internal bleeding from a mass in the abdomen. Liver issues – either mets or hypoxic injury.
* you can see mets in the lungs on RG
Cannot completely rule out brain tumour
Splenic mass- sx is the only paliative– but if you have mets– progress rapidly- 1 month survival– not really improving outcome… can only palliate and confirm diagnosis
ECG- no abnormalities– QT segment prolongation perhaps– intermittent VPC possible
Clin path-left shift, inflammatory leukogram, toxic change- screaming inflammation, hyperglobulinaemia– supports inflammation. Knowing anorexic– lipaemia!! Film with toxic neutrophils, metamyelocytes and bands
imaging-aspiration pneumonia
Diagnosis- tick paralysis– take off the tick, anxiolytics, specific therapy to aspiration pneumonia
Cervical myelopathy
Clin path- stress leukogram, mild increase in CK
Thorax was normal- cervical spine narrowing of IVD space between three different places C6-C7 almost completely collapsed– heart different phases of the cardiac cycle
PE: depressed, unable to urinate, enlarged painful bladder, HR 100 bpm, vomits in consult room
ANSWER:DDx for FLUTD : iFLUTD, obstruction (Urolith / plug / clot / sloughed tissue / urethral spams / urethral inflammation: male, main rule out), UTI (rare in cats less than 10 years), congenital (unusual at this age) / acquired (e.g. scar), trauma (history?), neoplastic ( bladder, urethra, rare this age), prostate disease, extramural compression, neurological (need physical exam) (combinations)
+/- concurrent behaviour / CKD disease.
Regardless of cause, cats with FLUTD will present with similar signs
Slow heart rate, no P waves (increased PR), small QRS, spiked T wave – sinoatrial arrest
Get serum [K] down (Na Cl fluids to dilute, calcium carbonate, insulin (glucose), (bicarbonate)
Ensure extrude penis (S shape!).
Retropulse uroliths back into bladder with saline / lubricate flush (saline / LRS – isotonic and non irritating)
Sedate / GA – reduces the risk of iatrogenic trauma / infection, IV top ups PRN
Occ if sick enough, local
Occ distal urethral / penile plug can be Rx with penile massage
May decompress cystocentesis first – “buys time” to stabilize, makes catheterization easier
Open ended catheters, 5 French, soft pliable, aseptic non traumatic technique, sterile gloves, clip, clean, aqueous lubricant
Take time and repeated attempts, may need to “close proximal urethra” then release and flush
Lavage bladder to remove cellular, protein and crystalline debris
+/- Attached close urinary system : Cats with narrowed urethral lumen, persistent debris or detrusor atony more likely to re obstruct in the first few days – may benefit from indwelling catheter and closed collection system
If not possible cystocentesis and try later
If still not possible, perineal urethrostomy : however risks of Urinary incontinence, stricture, uroperitoneum, infection
Treat metabolic derangements
IV fluids (saline)
Expect post obstruction diuresis
Monitor lytes and adjust fluid therapy (e.g. KCl)
Control K
Acid-base
Opioid analgesia
Antibiotics/???
Ideally rads before catheterise (might not be possible)
Good serosal detail. Did not include distal urethra!!!!!
Radiodence uroliths – think struvite, calcium oxylate
Frequency: plugs > uroliths
Crystals in asymptomatic cats are normal. However Tiger is not asymptomatic. Struvite should make you think about UTI, plug or infection.
A ) Not in cats (true in dogs)
B) They can be disolved (oxylate can’t)
C) Struvite plugs are more common than struvite stones in cats – C is correct..
D) Calcium oxalate is more common to cause ureteral obstruction (cf. struvite causes urethral obstruction more commonly than calcum oxalate)
Aim for urine pH 5.9-6.1 for dissolution (e.g. Hill s/d then c/d, RC Urinary S/O) : Reduced Mg, P, Ca,
Determine number, size, location and density with repeatable plain radiographs. No antibiotics unless cultures indicate otherwise. Continue diet for 3-4 weeks past when radiographs clear. Urinalysis & radiographs q 2 weeks
AVOID if kitten, pregnant, lactating, using with urinary acidifiers, kidney disease, hypokalaemia, metabolic acidosis, heart failure, hypertension,
Aim to reduce risk of reccurence, increased water intake, lower USG, avoid predisposing causes, treat infections,
Aim for pH 6.2-6.4 for prevention (Hill’s c/d, RC Urinary S/O). USG < 1.030-1.035. : Once any Surgery has healed. Life-long!!!
Diet Minimise building blocks : Low Mg, low P. Avoid excessive salt. (If overweight consider increased fibre e.g. w/d). Usually don’t need urinary acidifiers.
Long term, urinalysis q 3-6 months. +/- abdominal imaging
Increase water intake : Can food, add water, flavoured ice cubes, 2-3 meals per day, water fountains, extra water bowls / sites (avoid excessive salt)
40-55% cats will relapse within 12 months (death, euthanasia)
21% of these will be put to sleep within 1 year due to recurrence
CF about 1% when fed Hill’s c/d! (reduced incident rate by 89% vs controls!).
40-55% cats will relapse within 12 months (death, euthanasia)
21% of these will be put to sleep within 1 year due to recurrence
Obesity
Indoor confinement
Sedentary lifestyle
High number of rainy days
Diet changes
Major public holidays
Changes to home population / routine / moving
Litter tray changes
Inadequate litter trays
Stress, nervous, fearful, aggressive behavior
Multi-cat households
Historical gastrointestinal disease
Dry food diets
Frequent / ad lib feeding
History: Age at neutering, current / previous response to medications, trauma?, previous urogenital disease, timing of incontinence, continuous or intermittent, awareness,
PE: Bladder size, tone, ability to express (care), palpate before / after voiding, observe voiding, perineal area, rectal (caudal bladder, urethra, anal tone, pelvic diaphragm), vaginal exam for strictures and mass. Neurological exam : perineal sensation, bulbospongiosus reflex, spinal and HL evaluation,
Incontinence with a small or normal sized bladder is usually caused by bladder hypercontractility (urge incontinence) or decreased urethral resistance.
2 min
Small bladder: USMI, detrusor hyperreflexia (bladder / urethral : infection, urolith, polyp, neoplasia, primary/idiopathic), congenital (ectopic ureters, vaginal stricture, patent urachus, urethrorectal and urethrovaginal fistulas, ureterocele, pelvic bladder, female pseudohermaphroditism
1 min
Urinalysis, C+S (free catch or cystocentesis?), imaging (ideally), CBC + biochem (MDB ideally), +/- urodynamic studies (later),
Rx infection – continues to relapse / recurrent
Improves with phenylpropanolamine : PPA: BID/TID PO, taper based on response, avoid if hypertensive, cardiac disease, arrhythmia, anxiety, pregnant, lactating, care if NSAID use, best initial response rate
Further improvement with Estriol – SID, 40-65% response rate, side effects oestrus like signs, vulva swelling, attraction of males, bone marrow suppression (can be very serious), endocrine alopecia, pyometra, oestrogen sensitive tumours. Avoid in males, young puppies, intact or pregnant bitches
Rx infection – continues to relapse / recurrent
Improves with phenylpropanolamine : PPA: BID/TID PO, taper based on response, avoid if hypertensive, cardiac disease, arrhythmia, anxiety, pregnant, lactating, care if NSAID use, best initial response rate
Further improvement with Estriol – SID, 40-65% response rate, side effects oestrus like signs, vulva swelling, attraction of males, bone marrow suppression (can be very serious), endocrine alopecia, pyometra, oestrogen sensitive tumours. Avoid in males, young puppies, intact or pregnant bitches
Ectopic ureters should be considered in dogs that have had urinary incontinence all their life (even if intermittent). It is most commonly diagnosed in large-breed young females (regardless of whether spayed or not)
Urine incontinence may not be always apparent, and may range from mild to moderate. In mild cases urine incontinence may not be seen at all and recurrent infections could be the only sign, or hydroureter is diagnosed as a first sign during abdominal ultrasonography.
Unilateral (70-80% cases), submucosal (95% cases), opening into urethra
Dx : Cystosocpy, IVU and CT
D
75-89% seen with other congenital abnormalities. This case with USMI. Infections are common. Usually female. Usually large breed young females. Lifelong / intermittent incontinence. Can void normally.
Rx cystoscopic guided laser ablation (up to 77% success without adjunctive medications), may need medical therapy, surgery (e.g. Neoureterostomy
. Up to 30-55% of dogs experience ongoing, however improved incontinence after surgery alone. 25-71% of dogs are continent after surgery with adjunctive medical therapy if required. 16% of dogs experience dysuria after neoureterocystotomy
Treatment is best done by specialists
Good exam question!!!
Larry
- 12 yo Warmblood gelding
- 2 week history of mild intermittent colic
- Unwilling to work/poor performance
- Occasional urine dribbling
- Frank blood in urine sometimes seen after work
- Physical exam findings
–Bright and alert
–Normal TPR
–Some blood-stained urine on hindlimbs
–No other abnormalities
•What is your problem list?
–Mild intermittent colic
–Unwillingness to work
–Urine dribbling
–Haematuria (frank blood) after work
–Blood-stained urine on hindlimbs
Larry
•What is your diagnostic plan?
–Urinalysis
–CBC/chemistry
–Palpation per rectum
–Transrectal ultrasound
–Cystoscopy
–Renal ultrasound
What are your treatment options?
A.Monitor and wait for it to resolve
B.Surgical excision under general anaesthesia
C.Break the urolith up endoscopically and wait for the pieces to pass through the urethra
D.Dietary management
Increased urea
