Horses 2 Flashcards
acute colitis how bad, success rate, how often get diagnosis and complications
- Emergency - due to possible cardiovascular collapse due to fluid loss into the gut
- Expensive to treat
- ISOLATION
- Treatment can be unsuccessful - 70% success rate
- Definitive diagnosis in 20-30% cases
- Complications
○ SIRS
○ Laminitis
○ DIC, MODS, death
what are the 7 main differential diagnosis for acute colitis
1) salmonella
2) clostridium
3) antimicrobia-assoacited colitis
4) potomac horse fever
5) viral - coronavirus
6) cyasthostomiasis (parasite)
7) non-pathogenic - grain overload and right dorsal colitis (NSAID toxicosis)
Salmonella and clostridium causing acute colitis what types, how infectious
- Salmonella ○ Many serovars, groups B and C most common (horses) - not clinically important which serotype present ○ Highly contagious -> important ○ Invade mucosa, produce enterotoxins - Clostridium ○ C. perfringens § Types A and C most common in horses § Produce α toxin (type A), β and β2 toxins (type C) ○ C. difficile § Two main toxins: A & B
What occurs with antimicrobial-associated colitis and potomac horse fever in terms of causing acute colitis
- Antimicrobial-associated colitis
○ Overgrowth of pathogens due to disruption of normal colonic flora
○ ANY antimicrobial, some more likely than others - Potomac Horse Fever (Neorickettsia risticii)
○ North America – certain geographical locations, spreading. Seasonal, complex life cycle.
○ Within the bloodstream - leads to bi-phasic fever
○ Organism invades monocytes; evades immune response, travels to colon
○ Predilection for large colon mucosal epithelial cells → loss of microvilli
in terms of acute colitis how does viral, parasites and non-pathogenic disease cause
- Viral
○ Coronavirus
§ Cell invasion → necrotizing enteritis (crypt and tip necrosis), villus attenuation, fibrin deposition (pseudomembrane formation), microthrombosis and haemorrhage - Cyathostomiasis (parasite) – mass emergence
○ Physical disruption of mucosa due to larval cyst rupture, inflammatory response - Non-pathogenic
○ Grain overload
§ Overgrowth of lactate-producing species, physical damage of acid on mucosa
○ Right dorsal colitis – NSAID toxicosis
§ Lack of protective PGs, vasoconstriction, ischaemia, ulceration, (necrosis)
acute colitis how important is the diagnosis
REGARDLESS OF THE CAUSE, CLINICAL APPEARANCE IS THE SAME - smell, haemorrhagic, non-haemorrhagic
YOU CANNOT MAKE A DIAGNOSIS BASED ON CLINICAL SIGNS ALONE
Pathogenis in the colon what are the 4 main effects
1. Disruption to caecal and colonic mucosa → abnormal fluid and ion transport ○ Malabsorption ○ Hypersecretion ○ Combination ○ Inflammatory cells – release inflammatory mediators → stimulate direct and indirect secretory responses 2. Inflammatory response in colon ○ “Leaky” capillaries § Colonic oedema § Loss of albumin into colon § Leakage of bacterial toxins into circulation – COMMENSALS + pathogens ○ Infiltration of leukocytes § Produce inflammatory mediators 3. Fluid shifts ○ Secretion, malabsorption → fluid sequestered in colon, lost in diarrhoea →cardiovascular effects § Hypovolaemia § Poor perfusion 4. Electrolyte loss -> Na+, K+, Cl
SIRS when/how occurs
- Gut and blood in close alignment
○ Gut - gram negative and gram positive bacteria
○ Blood - albumin and white blood cells - Inflammation of the layer
○ Bacteria can move into blood (not common) more common is the endotoxins moving into the blood
○ Albumin moving into gut from blood
○ Loss of blood
In SIRS after bacteria moves into the blood what occurs
- Toxins interact with white blood cells -> cascade within WBC resulting in inflammatory cytokines -> activate coagulation -> loss of platelets
- Neutrophils express L selection molecules and endothelial cells produce E selection molecules
- White blood cells attach to the endothelial lining and move into the gut
○ Blood sample -> low albumin, low white blood cell
Problem list for acute enteritis cases
- Diarrhoea ○ Infectious (vs. noninfectious) - Hypovolaemia/ haemoconcentration ○ Fluid loss in diarrhoea - Hypoproteinaemia ○ Protein-losing enteropathy - SIRS (“endotoxaemia”) Secondary to GI compromis - Thrombocytopenia ○ Hypercoagulable state - Leukopenia/neutropenia ○ SIRS - Mild azotaemia ○ Pre-renal/renal/post-renal ○ Probably pre-renal - Hyperglycaemia ○ Stress ○ Severe disease
Acute enteritis diagnostic plan what need to submit
- WILL need to start treatment before results back
○ OFTEN don’t get an answer, need to tell the owners - Samples to submit
○ Faeces
§ Clostridial toxins
§ Salmonella PCR/culture (series of 5) -> one negative doesn’t indicate horse is negative
□ Shed in varied quantities, intermittently
§ Parasitology
○ If PHF season/area
§ EDTA blood – PHF PCR
§ Serum – PHF IFAT
+/- Ultrasound - can help assess oedema
What are the 4 main complications of acute colitis and when at risk
- Laminitis - most common - ANY CASE ○ All colitis cases at risk ○ PHF, grain overload big risks - Coagulopathy ○ Thrombophlebitis – consequence of SIRS - Hypertriglyceridaemia - Rectal prolapse - really oedematous rectums straining to pass large amounts of diarrhoea
Acute enteritis treatment plan, what is generally needed and not needed
- Largely supportive, VERY EXPENSIVE
- Referral generally required
- ISOLATION
- Long-term IV catheter
○ IV crystalloid fluids
○ Anti-inflammatory treatments - Antimicrobials – generally NO
Supportive - reduce laminitis, anti-diarrhoeals, anaglesia, anti-endotoxin treatment
Acute enteritis describe the supportive/preventative measures needed
○ Reduce risk laminitis
§ Ice boots (how long?) -> a few days after white cell count normalises
○ Anti-diarrhoeals
§ Di-tri-octahedral smectite (Biosponge®)
○ Probiotic?
§ Saccharomyces boulardii
○ Analgesia
§ Control colic pain
□ Usually due to ileus, dysmotility, (colon infarction)
§ NSAIDs (not in right dorsal colitis (RDC)- caused by NSAIDS)
□ Look a lignocaine and opioids
○ Anti-endotoxin treatment??
§ (Hyperimmune plasma) -> 50:50 in literature, risks that have with transfusions
§ Flunixin meglumine (not RDC) -> works on the clinical effects -> WORKS
acute enteritis prevention and monitoring plan
Prevention - Isolation - Separate at-risk groups - Don’t mix horses and cattle (Salmonella) - Feed roughage ASAP following GI compromise e.g. colic - Don’t use antimicrobials when unnecessary Monitoring plan - Regular monitoring is essential ○ Cardiovascular parameters ○ PCV/TP ○ Lactate ○ Diarrhoea frequency, volume ○ Electrolytes ○ CBC Monitor for complications
foal diarrhoea difference to adults, result, treatment and how to balance referral and management on farm
- Easier to diagnose - generally higher identification of the pathogen
- Neonates do become bacteraemia (useful to take blood culture)– consequences
○ Sepsis
○ Septic joints/other synovial structures
○ Omphalitis - umbilical structures - Treatment largely supportive, still expensive
- Referral vs. management on farm
○ Severity of disease (i.e. intensity of required treatment)
○ Ability and knowledge of owners/farm managers
What are the 3 initial things need to do to diagnose a foal with diarrhoea
- Signalment – age esp. important
- History
○ Farm size
○ Gestation and birth
○ Post-partum period
○ Adequate passive transfer?
○ Duration of diarrhoea?
○ What is it doing now?
§ Is it up and nursing or dull and not nursing - Physical exam
○ Mentation
○ Cardiovascular status
○ Signs of sepsis/bacteraemia
§ Joints
§ Umbilicus
§ Petechiae
○ Evidence of not nursing well
○ Colic? - distention of small intestine, colon or disruption to movement
Foal diarrhea what is the general problem list and clinical pathology findings
Problem list - Dull/lethargic - Not nursing - Diarrhoea - Colic - Petechiae - Injected mucous membranes, slow CRT - Cold extremities - Slow jugular refill Clinical pathology findings - CBC - Fibrinogen - Biochemistry - Venous blood gas - IgG (neonates) - may be normal at 24 hour mark but if septic may use as energy so then begin to decrease
What are the 9 main differentials for neonatal foal diarrhoea
- Salmonellosis
- Clostridiosis – usually perfringens – often haemorrhagic - can be so severe than become anaemic
- Coronavirus
- Rotavirus
- Cryptosporidium
- Enterococcus durans***
○ New discovery in terms of being pathogenic - Nutritional – orphans especially
- FOAL HEAT
- Parasitic – Strongyloides
What are the 4 main differentials for older foals/weanlings
- Strongyles
- Ascarids
- Rhodococcus
- Equine proliferative enteropathy/Lawsonia (weanling age, usually chronic)
Foal diarrhoea diagnostics what needed and what differentials can it rule in or out
- Blood culture as become bacteriaemic
- Ultrasound
○ Colicky foals
○ Intussusception
○ Intestinal wall thickening, Intestinal contents
○ Umbilical infection
○ Surgical lesion? - 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) - cryptosporidium
Foal diarrhoea diagnostic what to add for older foals and why
○ Rhodococcus – culture, PCR for VapA
§ PCR Good at ruling out but not ruling things in
Rotavirus how common in what age, clinical signs and what does it cause
- Most common in foals 5 days – 4 weeks old
- Clinical signs variable – diarrhoea usually watery, yellowish/greenish, non-fetid
- Causes denuded villi, crypt hyperplasia, and combined secretory/malabsorptive enteritis
○ Temporary lactase deficiency - need lactase replacement therapy
Cryptosoridium how host-specific, importance, causes, diagnosis, treatment and prevention
- Non-host specific protozoa
○ ZOONOSIS! - Implicated as cause of foal diarrhoea
○ BUT isolated with same frequency from normal and diarrhoeic foals - Generally self-limiting, resolves in 5-14 days
- Diagnosis: acid fast stain (faecal sample)
- Treatment generally supportive
- Strict hygiene!
Nutritional diarrhoea what foals generally occurs in, causes and best treatment options
- Usually orphan foals
- Incorrectly mixed milk replacer
- Too much milk replacer
- Electrolyte abnormalities
- Correct feeding practices
- Nurse mare if available - best, otherwise goat milk is a good replacer
Foal heat diarrhoea what age group, why, results and treatment
- Foals aged approx. 7-9 days (may be 4-14 days)
○ Occurs around same time mare’s “foal heat”
○ Generally when foals are coprophagic (normal) - Foal remains systemically healthy
- Diarrhoea self-limiting
- Usually no treatment required
○ monitor
Rhodoccus equi what cause in foals and 2 other causes of diarrhoea
- Usually pneumonia (pulmonary abscesses), but many extrapulmonary manifestations ○ Ulcerative colitis 1) Sepsis, neonatal encephalopathy ○ Period of poor perfusion to GI tract ○ Treat primary problem, supportive care 2) Intestinal nematode parasites ○ Older foals/weanlings
What are the treatment options for foal diarrhoea
- Long term IV catheter
- IV fluids – replacement crystalloids
○ Care – electrolyte disturbances
○ Colloids? Generally not - Plasma – FPT, sepsis
- Systemic antimicrobials – broad spectrum, parenteral, preferably IV
○ Cephalosporin – 2nd or 3rd generation
○ Penicillin + aminoglycoside (if renal function OK)
○ Add metronidazole (PO) if concerned Clostridial - Anti-diarrhoeals
○ Di-tri-octahedral smectite
○ Bismuth subsalicylate - Gastroprotectants? - not done
○ Omeprazole - Allow to nurse vs. withholding from mare
○ Lactase enzyme replacement if villous damage suspected - Topical barrier Tx (minimise scalding) - like nappy san for babies
In general what are more likely colic causes in young horses (neonates) and immature horses
Young horses
- First manure getting stuck (meconium impaction)
- congenital abnormalities of the gut (atresia coli)
Immature
- Prone to infectious problems
- Enteritis (small intestinal)
- Parasitic
○ Ascarid impactions of the small intestine (foal lecture)
○ Intussusception (association with worms)
Aged horses and colic what breds, what type of lesions and why
- Often quite stoic- esp pony breeds
- Consider lesions that take time to develop (>15 years old)
○ Tumours
§ Benign: pedunculated lipoma: strangulate SI**
§ Malignant (uncommon)
□ Lymphoma
□ Adenocarcinoma
Aged horses with colic what looking for and what often related to especially in what species
- Look for evidence of previous, more severe abdo pain
○ Trauma/skin off head - Or related to poor dentition
○ Impactions
○ Esp donkeys: (long lived) -> generally lose multiple teeth leading to impaction
§ Donkeys very stoic - generally just lay down -> DON’T IGNORE IF GO OFF FEED
§ Rarely roll or paw
§ Note subtle behavioural changes
§ Metabolism of NSAIDs is faster -> lasts half the time of horses
□ BUT: be careful masking signs
aged horses with colic does it change their prognosis
Age does not reduce prognosis if in good health
- BUT: Consider concurrent dx
- Cushings syndrome inhibits healing
Previous laminitis?
stallion colic what need to consider and some diagnostics
- Consider reproductive organs: check testicles
- Enlargement (with colic) is either:
○ Testicle itself: testicular torsion
○ Something else in the tunic with it: herniation (SI) - Both ischaemic + painful
○ Ddx with palpation /ultrasound /rectal
○ Palpate small intestine through internal inguinal rings
Broodmare colic what need to consider and main differentials
- Broodmare: pre or post-partum?
- Pre-partum -> Pregnant causes
a. Foal movement can result in low gr colic
b. foaling/ate term abortion
c. uterus can twist: uterine torsion (last 2 months)
Post-partum
a. rupture of uterine artery
b. foal can damage uterus during foaling
c. can also damage GI tract
Foaled within 3 months - HIGH RISK - most common large colon volvulus (this until proven otherwise
Broodmare pre-partum what are the 3 common causes of colic how common and diagnosis
a. Foal movement can result in low gr colic
§ More common in maiden mares
§ Present as low grade /intermittent colic
b. Foaling / late term abortion
§ Vaginal discharge /open cervix -> ASSESS RECTALLY
§ (colic) More likely in later gestation when foal large
c. Uterus can twist: uterine torsion (last 2 months)
§ Relatively uncommon
§ Diagnosis: rectal palpation of broad ligaments - EASILY IDENTIFIED
□ Ligament crosses uterus obliquely in direction of torsion
□ Left ligament horizontal and heading cranial
□ Right ligament vertical and heading below uterus (less reliable)
® =clockwise torsion ( Counter clockwise also possible)
Uterine torsion leading to colic in broodmares pre-partum and what are the 2 main options for correction and what must be confident on
1) Surgical
® Standing flank laparotomy
® Midline caeliotomy - preferred for shorter people
2) Non-surgical
® GA (triple drip)
® Roll in opposite direction to torsion
® Advantages of non-surgical correction
◊ Financial
◊ Less invasive /no risk of incisional problems - especially when late in pregnancy - increase pressure on that surgical incision
- Must be confident in diagnosis and direction of torsion -> Risk uterine rupture
What is the most common cause of colic in broodmare that has recently foals, when occur, presentation and results
Rupture of uterine artery**- common
§ Moderate- violent colic (hemorrhage is painful)
□ Soon after foaling: up to 48hrs
□ BUT- have very pale mmbs (ddx GI cause)
□ Most often bleed into broad ligament (contained)
® Can bleed into abdomen/uterine lumen
◊ Can bleed out quickly -> not able to save generally
Rupture of uterine artery leading to colic in recently foaled broodmare what is the treatment options
□ NSAIDs, careful sedation to calm -> don’t want to drop blood pressure too dramatically
® Detomidine and top up if needed
□ Tranexamic acid: antifibrinolytic (10mg/kg in 1L IV) - stabilises the clot
□ +/- blood transfusion (indications below)
® Decided by: lactate>4, HR 80, Hb<8g/dL, PCV<15% (unreliable in acute stage)
® Can lose approx 11L without need to transfuse
® (1/3 of blood volume: b.vol = 8% body weight)
What are the 2 main things foals can do during birth that can lead to colic in broodmares post-partum, what occurs and treatment
1) Foal can damage uterus during foaling
§ Uterine tear
§ Uterine fluid (sterile) in abdomen
□ Present as peritonitis 1-3d after foaling: low grade fever, dull, mild colic, inflammatory abdo tap
§ May require surgical closure and abdominal lavage - place abdominal drains
2) Or can damage GI tract
§ Necrosis or rupture of GI tract (high bacterial load)
§ Present as peritonitis BUT: severe inflammation and endotoxemia
§ Cannot be treated effectively: euthanise
What is the highest risk period for broodmares, what generally occurs and most common cause, treatment
Highest risk period for broodmares -> Foaled within 3 months
- Moderate- severe colic (ischemia/signif distension)
- CV compromise (ischaemia)
- Abdominal distension (LI)
- MOST COMMON CAUSE -> Large colon volvulus until proven otherwise
○ Surgical emergency
