GIT Flashcards
Clinic signs of colic
Causes of abdominal pain
Pain as a guide to your approach to colic- mild
Mild- moderate pain guiding approach to colic
Approach to severe colic
Colic history taking
Interpretation of drugs given– analgesia with colic
* Flunixin- duration 12-24 hours, onset 40 minutes, potent visceral analgesic at high dose, improves appearance of MMs
* PBZ- duration 12-24 hours, onset approx 40 minutes, less potent than flunixin for colic pain, oral phenylbutazone: 2 hours for onset
* Buscopan- antispasmodic + weak NSAID, relatively poor analgesic cf others
Physical exam info colic
Abdominal distension likely caused by? Gut sound variation meaning what in colic??
NGT passing what in colic?? Lack of reflux?? Nose bleed?
Approach to colic
Rectal exam anatomy
Rectal exam safety
Rectal exam: findings– colic
Rectal exam– rectal tears
•
Mucosa only
•
Not normally a problem
•
No further rectal exams
•
Soften manure-
enteral fluids
•
Mucosa + submucosa +/
- muscularis
+/- serosa
•
Needs definitive management
•
Decrease GI spasm
- Propan
B
•
Cover w
abx
/NSAID-
Pen/Gent/
flunixin
•
Pack off to reduce contamination
•
Epidural (coccygeal NOT L-
S)
•
Damp cotton wool in stockinette
20cm oral to tear
•
Refer: clients likely to be distressed, common source of
litigation
Higher risk rectal exams
U/S investigation colic?
Abdominocentesis in colic
•
No fluid
No help
•
Clear
–light yellow
Normal
•
Sanguinous
Ischaemia
•
Turbid yellow
Peritonitis (see febrile colic)
•
Brown, large volume +/
- feed
Ddx
rupture/
enterocentesis
Clinical signs:
enterocentesis
generally
not problematic
Summary of colic 1
Large colon orientation
Medical management of equine colic
Causes of medical colic
* continuous/loud gut sounds
* mild to moderate or intermittent pain: spasmodic colic, spasmodic pain?
* Hypomotile (sometimes referred to as ileus- trust but confusing as ileus often implies more severe problem)
* Infrequent, quiet or absent gut sounds
* Stress
* Pain
* Change in routine/feeding
* Drugs (sedatives: multiple doses)
* Withholding feed
* No identifiable cause
Poor intestinal motility– functional or physical obstruction
Feed–> result in large colon impaction
Large colon impaction
Management of large colon impaction
Options for enteral fluids
Volume of enteral fluids
Impaction expected outcomes
Impaction unexpected outcomes
DDX colon v. caecal impaction
* Caecal impaction (surgical)
* Uncommon, key risk factors: management change in previous two weeks
* Typical history: Horse usually lives out, stabled for orthopedic dx, low grade colic 24 hrs +, pass manure but smaller amounts, ileocaecal gut sounds can still be present!
* hospitalization for orthopedic problems
Risk factors to impaction/ colic
* 5 cases per 100 horses per year “normal” frequency
* (1 case every 2 years in 10 horse yard)
* Higher risk populations
- high level competition/ TB racehorses
- exposed to many other risk factors
Nutritional factors of impaction/ colic
Nutritional risk factors of impaction/colic
* higher quantities of concentrates: increased risk for colic, anterior enteritis, colon impactions and displacements
* Pasture access generally reduces the risk: colon impactions, colic, fructans can vary with climate changes: may destabilise microflora causing problems from time to time
* Exception: sand colic (impaction) only in grazing horses
Cut lucerne hay/ lucerne chaff to a minimum if colic a problem in the past
Dietary changes summary posing risk for colic
Gastric ulceration in adults
* high concentrate/ low roughage diet
* Acidification of gastric contents
* Protective mat of roughage is lost
* Leads to ulceration
- squamous or glandular ulcers
- squamous more significant: above margo plicatus
Gastric ulceration diagnosis
Gastric ulceration treatment
* Omeprazole SID
* Ranitidine BID- TID
* Response to omeprazole may take 3-4 days
* Response to ranitidine usually quicker (24 hours)
* Consider repeat gastroscopy to guide treatment duration
* IF risk factors remain, maintenance dose advisable
NSAID induced ulceration??
Summary of medical management of colic
Referral and euthanasia of colic cases
Treatment options for colic
Approach to colic
Tx of RDD? LDD?
Why is it important to differentiate anterior enteritis from physical obstruction of the SI? What is anterior enteritis?
Hallmark of AE? Why?
Hypomotility: fluid accumulates
Treatment of anterior enteritis?
What is done at surgery in a non strangulating lesion?
What is done at surgery for strangulating lesions?
How much SI can you safely resect? What do you have difficulty accessing? Complications?
Complications of LI resection? What will happen if non viable? Another reason for resection?
Post operative management surgical colic
Early post op complications
* Ileus
- functional obstruction due to dysmotility (inflammation)
- most typical after SI R&A
- Colic (pooling intestinal fluid: distension)
- Reflux, CV support (fluids), anti-inflammatories
- duration unpredictable
- monitor with U/S
* Endotoxaemia
- bacterial absorption across damaged mucosa
- injected/ congested MMs
- Increased HR, colic, +/- fever
- Laminitis
- IV fluids/ CV support
- Hyperimmune plasma ($$$)
- Polymixin B (nephrotoxic, with care)
- Laminitis prophylaxis: sole support/ ice boots
* Adhesions
* Inflammation: gut, foreign material, excess handling etc
* SI least tolerant
- 5 days to years after surgery
- Obstructs lumen
- Axis for volvulus: present as colic
- Can resect some
* Minimise the risk: good surgical technique, early intervention
Post operative management after discharge in colic
After discharge from equine colic complications
* infection delays healing
* strain before healing is complete: acute dehiscence (hospitalised horses), hernia formation (weeks-months)
* Prolong duration in a box
* because healing is slower with infection– manage the infection
* +/- supportive bandage
* Reccurrence
* LI: displacement/ volvulus- up to 15% following initial lesion; >50% following second
* SI: rate not well established, EFE < 5%
Prognosis of SI resections
Prognosis of LI volvulus? LI displacement?
Summary equine colic
Young horses general DDX
Aged horses abdominal DDX
Aged horse characteristics for DDX abdominal problems
* related to poor dentition
- impactions
- especially donkeys: long lived
* Donkeys very stoic
* Rarely roll or paw
* Note subtle behavioural changes
* Metabolsim of NSAIDs is faster
* But be careful of masking signs
Colic in breedin stallions
Breeding animals colic in a broodmare
* uterus can twist: uterine torsion (last 2 months)
* Relatively uncommon
- diagnosis: rectal palpation of broad ligaments
- ligament crosses uterus obliquely in direction of torsion
- left ligament horizontal and headin cranial
- right ligament vertical and heading below uterus (less reliable)
- = clockwise torsion
- Counterclockwise also possible
Options for correction of colic in a broodmare
Recently foaled broodmare colic likely DDX
* Uterine artery rupture (particularly in older broodmares, very painful)
- NSAIDs, careful sedation to calm
- Tranexamic acid: antifibrinolytic (10mg/kg in 1L IV)
* +/- blood transfusion
- decided by: lactate > 4, HR 80, Hb< 8 g/dL, PCV < 15% (unreliable in acute stage)
- can lose approx. 11 L without need to transfuse
- 1/3 of blood volume: b. vol. = 8% body weight
* Recently foaled
- foal can damage uterus during foaling: uterine tear, uterine fluid (sterile) in abdomen–> presents as peritonitis 1-3 days after foaling: low grade fever, full, mild colic, inflammatory abdo tap…. may require surgical closure and abdo lavage
OR can damage GI tract
- necrosis or rupture of GI tract (high bacterial load)
- Present as peritonitis BUT: severe inflammation and endotoxaemia
- cannot be treated effectively: euthanase
Risk period post foaling for what??
Recently foaled (within 3 months) broodmare most likely– surgical emergency
Travelling colicky broodmares
Australia’s geographical influence of colic
* enteroliths: concretions of various minerals
* form in large colon
* luminal obstruction when large
* chronic +/- acute colic
* ingesta and gas build up oral to obstruction, pressure necrosis possible
* Require surgical removal
* WA, NSW, QLD
* Infectious agents– QLD/NSW– HV can present as colic
* uncommon but 100% mortality
What infectious agent can show up as colic?
DDX febrile colic
8 yo TB, quiet/ lying down approx 12 hours
Little manure passed today (reduced LI motility? Large colon impaction?)
Temp 39C
No drugs given so far
Occasional flank watching/ dull– low grade abdo pain
HR 48
MMs salmon pink– no CV compromise (expected given low grade pain)
Temp narrows DDX down: SI/ LI/ Peritoneal cavity
- ddx colitis, anterior enteritis, peritonitis
- fever rules out routine LC impaction
- could occur secondary to dysmotility
…. Suspect primary peritonitis: cytology G-ve pleomorphic rods (consistent with A. equilli)
- treatment: bacterial infection– ab penicillin +/- gentamicin
- low grade colic: NSAIDs
- little manure (inflammation in abdo slows motility)– enteral fluids
- expect normal physical exam within hours
- re-evaluate after 5 days with abdo tap
- not necessary in many cases
** not a GI catastrophe– we know this because they are not CV collapsed
- not colitis because gut sounds are not increased early on… loose manure/dxa on rectal.. peritoneal fluid rules out
Not anterior anteritis because no reflux
Take home points colic by signalment
Acute colitis pathophysiology
Approach to acute colitis
Presentation:
* Dull, purple MM, CRT > 3 sec, HR = 80, T = 37.1 C, Cold extremities, poor pulses, slow jugular refill time, diarrhoea in tail, fluidy hypermotile borborygmi
Problem list
* Diarrhoea- infectious v. non-infectious (this case is likely infectious)
* Hypovolaemia/ haemoconcentration- fluid loss in diarrhoea
* Hypoproteinaemia- protein losing enteropathy
* Endotoxaemia (now called SIRS because there are lots of possible bacterial toxins involved, not just endotoxins– absorption across compromised colon)- secondary to GI compromise
* Thrombocytopaenia- hypercoagulable state
* Decreasing WBC/ neutrophil counts- SIRS
* Mild azotaemia- pre-renal/renal/post-renal
* Hyperglycaemia- stress, severe disease
DDX:
* Salmonella, Antimicrobial associated colitis, Clostridium (difficile or perfringens), Potomac Horse Fever (Neorickettsia risticii)- North America, Grain overload, Right dorsal colitis- NSAID toxicity, Cyathostomes- mass emergence
** Most of these appear clinically the same!!!
(GI rupture, Severe septic peritonitis)
** Takes fibrinogen 24-48 hours to peak, expect it to be normal in an acute case
Diagnostic plan:
* Will need to start treatment before results back– often don’t get an answer
* Samples to submit: faeces- clostridial toxins, Salmonella PCR/culture, parasitology, If PHF season/area– EDTA blood for PHF PCR, serum- PHF IFAT….
* U/S
** most of the time we don’t get an answer, most of treatment is supportive anyway
Salmonellosis
Clostridiosis
Antimicrobial associated colitis
Potomac horse fever
Diagnosis and Prevention of Potomac Horse Fever
Grain overload
Peritonitis
Diagnosis and Prognosis of Peritonitis
Complications of acute colitis
Treatment plan for acute colitis
Prevention of acute colitis
Treatment of acute colitis
* analgesia:
- Control colic pain: usually due to ileus, dysmotility, (colon infarction)
- Lidocaine CRI
- Butorphanol
- NSAIDs (not RDC)
* Anti-endotoxic treatment
- Plasma
- Polymyxin-B
- Pentoxyfylline
- Flunixin meglumine (not RDC)
Monitoring of acute colitis
* Salmonella PCR- negative
* Clostridial toxin assay- negative
* PHF PCR and serology- negative
* Coagulation panel:
- decreased ATIII, prolonged PTT, PT
- Thrombocytopenia
Day 4
- HR decreased to 40, firmer cowpie faeces, severe leukopenia/neutropenia, polymyxin B, flunixin dose dropped
Day 5
- HR 36-40, soft formed faeces, regeneration neutrophils, biosponge discontinued, oxytet discontinued, flunixin and ice boots discontinued
Day 6
- pentoxyfylline discontinued
- discharged from hospital
- $10,000
Foal diarrhoea basics
Approach to the foal with diarrhoea
Approach to the foal with diarrhoea physical exam
Approach to the foal with diarrhoea problem list
Approach to the foal with diarrhoea
Clinical pathology
Diarrhoea DDX foals
Diagnostics diarrhoea foal
* diagnostic faecal samples- slightly more rewarding in foals than adults
- Salmonella PCR/culture
- Clostridial toxin assay– +/- gram stain
- Rotavirus ELISA or LAT
- Parasitology- acid fast (protozoal diarrhoea)
* Older foals– Lawsonia- IPMA, Rhodococcus- culture, PCR for VapA
** won’t necessary culture the cause of diarrhoea- commonly culture E. coli from foal blood but not a common cause of diarrhoea– has to do with leakage from common bacteria from the GIT
Clostridiosis in foals
* Usually not associated with prior AM use in foals
* Sporadic cases, outbreaks
* Prevention
- Good hygiene and biosecurity
- clean mare’s udder
** Acute onset common, tends to be associated with haemorrhagic diarrhoea but not always
Salmonellosis in foals
* loves to get into blood and then into joints…
Rotavirus in foals
* Diagnosis:
- ELISA or latex agglutination
- EM of faeces or tissues
- Virus isolation from faeces or tissues
* Treatment
- Supportive, non-specific: lactase supplementation (can use human lactase supplementation)
** tips of intestinal villi producing lactase to break down lactose, so can develop lactase deficiency that remains after the virus is gone
Cryptosporidium in foals
Nutritional diarrhoea in foals
Foal heat diarrhoea
Rhodoccocus equi in foals
Treatment: macrolide + rifampin
- erythromycin, azithromycin, clarithromycin
* Supportive care, address respiratory disease
* Prevention: hyperimmune plasma in first 1-2 days of life for foals on endemic farms, minimize dust/ particle spread, separate sick foals
Other causes of diarrhoea in foals
Treatment of foal diarrhoea
* Antidiarrhoeals: D-tri octahedral smectite, bismuth subsalicylate
* Gastroprotectants- omeprazole
* Allow to nurse v. withholding from mare- lactase enzyme replacement if villous damage suspected
* Topical barrier tx (mimize scalding)
Colic in foals- tucking front legs up, turning their head. Normal sleeping is on their side with legs straight out
Approach to the horse with chronic diarrhoea
Physical exam
- usually no signs of systemic inflammation
- usually not febrile
- often not hypovolaemic
- Diarrhoea cowpie to liquid, variable volume and frequency
- +/- colic signs
- ventral oedema
* Clinical pathology
* CBC– normal… PCV may be increased (hypovolaemia), decreased (anaemia of chronic disease), or normal… TP is often decreased
* Biochem- electrolytes, organ function, triglycerides
DDX Chronic diarrhoea
Right dorsal colitis causes
Right dorsal colitis common problem list
Diagnosis of right dorsal colitis
Right dorsal colitis treatment and prevention
Sand enteropathy
Common problem list of sand enteropathy
Diagnosis of sand enteropathy
Sand enteropathy treatment
Prevention of sand enteropathy
Cyathostomiasis
Diagnosis of Cyathostomiasis
Treatment and prevention of Cyathostomiasis
Inflammatory bowel disease
Inflammatory bowel diseases common problem list
Four recognized types of inflammatory bowel disease
Diagnosis of IBD
* Abdominal U/S
* Rectal biospy
* Intestinal biospy (if colic surgery)
* Can be elusive
Glucose absorption test
Treatment of IBD
Alimentary lymphosarcoma
Diagnosis of Alimentary lymphosarcoma
Equine proliferative enteropathy
Equine proliferative enteropathy diagnosis
Equine proliferative enteropathy treatment
Approach to clinical parasitic disease
* Physical exam
- obvious signs: poor body condition, poor haircoat, diarrhoea, ventral oedema
- normal?
Problem list clinical parasitic disease
Common equine parasites
Large strongyles
Small Strongyles
Small strongyles diagnosis and treatment
Ascarids– name most common?
Ascarids treatment and epi
Strongyloides??
Pinworms in horses?
Lungworms?
Common cestode in horses?
Gasterophilus
Ivermectin, Abamectin?
Moxidectin?
Febendazole?
Oxfendazole, oxibendazole?
Targeting cestodes
D
What species have parasites that are 100% resistant to all anthelmintics?
- Acknowledge the problem- de-wormer resistance is a problem.. MLs are the only class of de-wormer that is uniformly effective
Goals- prevent and treat parasite related disease, prevent further resistance from developing. Horses are never parasite- free, the goal is control, not eradication
- Start performing FECs- shows number of eggs per gram of manure. Does not evaluate harmful larvae, tells you who needs to be dewormed and if your de-wormer worked
- Understand natural immunity– some horses have very good natural immunity against worms, will never get faecal egg counts above 100 EPG
- Save the refugia
- Pick the right drug
- Use the correct dosing interval
- Re-consider rotation de-worming
- use seasonal deworming
- Reduce larval numbers
- educate your friends
The number one goal of de-worming program is??
Key to strategic de-worming
What are refugia?
Picking the right drug for adult strongyles, tapeworms, encysted strongyle larvae, bots?
Why kill encysted larvae? With what?
De-worming every 8 weeks?
Faecal egg count reduction test?
re-consider rotation de-worming?
* only L3 larva is infectious
* takes 3-5 days from egg to L3 (Temperature dependent)
* L3 killed by cold and very hot weather
- so… no need to de-wrom in mid-winter (cold climates), mid-summer (hot climates)
- saves money
- better for the environment
- decreases worm resistance
Reduce larval numbers
Educate your friends
Cost of treating parasites in horses
Strategic deworming-recap
When are deciduous premolars and incisors shed?
Horse teeth numbering system
Triadan system
How to age horses with their teeth
Eruption times are given below:
Foals up to 2 year olds:
6 days: central incisors present
6 weeks: central and intermediate incisors present
6 months: all incisors present (corner incisors erupt)
12 months: dental star present in central incisors, corner incisors not in wear
18 months: corners in wear
24 months: dental star in all lower incisors, M2 present
Permanent dentition:
2.5 years: permanent central incisors erupted
3 years: centrals in wear
3.5 years: intermediates erupted
4 years: centrals and intermediates in wear
4.5 years: corners erupted
5 years: all incisors in wear (dentition complete at this age)
After 5 years the accuracy of ageing by dentition decreases as it relies on occlusal forces causing wear of the teeth. This can be affected by several other factors such as what the horse eats, genetics, and environmental factors. Ageing by teeth becomes more subjective as the horse gets older. This is an approximate guide:
6 years: cups disappear from centrals, oval shaped occlusal surface
7 years: small hook present on distal aspect of the upper corners. Cups present in corners only.
8 years: incisors oval, cups gone, dental star present in centrals
9 years: centrals round, corners oval, dental star for centrals almost in centre
10 years: Galvayne’s groove at gum margin of corners, centrals and intermediates round, corners oval
15 years: Galvayne’s groove halfway down corner incisor, centrals triangular, corners round. Bite plane starts to become more angled.
17 years: all incisors triangular, dental star round and in centre of incisors
20 years: Galvayne’s groove extends full length of corner incisor. Lower incisors may be worn almost all the way to the gum.
20+ years: Galvayne’s groove moves down the corner until it grows out.
Not all horses will develop a Galvayne’s groove, therefore the absence of this feature cannot be relied on to determine age.
Galvayne’s Groove
Oral and dental examination
* Haussman gag- full mouth gag
* light source
* Soft tissue as well
* Horses should be sedated before the Haussman gag is placed
Equine dental record
Rasping teeth (aka Floating teeth)
* upper arcade cheek teeth is wider than the lower arcade, therefore sharp edges tend to develop on the buccal side of the upper arcade, and the lingual side of the lower arcade. Sharp edges can cause ulceration of the buccal mucosa
* Sharp edges require rasping
* improving occlusion of the molars allows greater lateral excursion as the horse chews, allowing it to chew its feed adequately. When this doesn’t occur, the horse may drop clump of feed from its mouth as it eats, called “quidding”
Where do hooks commonly occur?
Hooks commonly develop on P2 on the upper arcade and M3 on the lower arcade. These also interfere with eating and require rasping. These hooks should not be confused with the “7 year hook”, which occurs on the corner incisor at around 7 years of age.
Incisors may also require rasping if malocclusions occur on these teeth.
