1
Q
Infectious causes of acute diarrhea in adult horses
A
- Salmonella (S. typhimurium, others)
- Neorickettia risticii
- Clostridium difficile
- Clostridium perfringens
2
Q
Toxic causes of acute diarrhea in adult horses
A
- NSAID overdose (right dorsal or generalized colitis)
- Cantharadin (blister beetle) toxicity
- arsenic
- antibiotic associated
3
Q
Misc. causes of acute diarrhea in adult horses
A
- grain overload
- sand enteropathy
4
Q
What factors determine infection risk with Salmonella?
A
- organism virulence
- if horse has any risk factors
- antibiotic administration
- immunocompromised
- underlying GI disease (colic)
5
Q
Pathogenesis/dissemination of salmonella infection
A
invades epithelial cells, causes massive inflammation in lamina propria, often found in mesenteric LN & liver, may cause septicemia (particularly foals)
6
Q
What organism causes Potomac Horse Fever?
A
Neorickettsia risticii
7
Q
What cytotoxins are involved in the pathogenesis of clostridiosis?
A
Cytotoxin A, Cytotoxin B
8
Q
How does the life cycle for Neorickettsia risticii and infection of horses work?
A
- infects trematodes
- aquatic snails, and aquatic insects are intermediate hosts for infected trematode larvae
- horses ingests aquatic insects affected with trematode metacercaria
9
Q
What cells does Neorickettsia risticii infect?
A
macrohages, monoctyes
10
Q
What is the primary cause of clostridiosis in adult horses?
A
Clostridium difficile
11
Q
What factor predisposes horses to development of clostridiosis?
A
antibiotic treatment
12
Q
What is the pathogenesis of clostridiosis?
A
severe epithelial damage -> hemorrhagic colitis
13
Q
What would be contraindicated in a cantharidin toxicity case?
A
mineral oil-will INCREASE absorption
14
Q
What are some specific ways mucosal injury occurs when talking about specific causes of acute diarrhea in adult horses?
A
- Damage to enterocytes by microbial or chemical toxins (clostridia, cantharidin, arsenic, lactic acid from fermented carbohyrates)
- cell death of enterocytes (Salmonella)
- NSAIDs damage mucosa by inhibition of homeostatic prostaglandins
15
Q
Hypersecretion is what type of fluid loss?
A
isotonic
16
Q
Consequences of high volume fluid loss include:
A
- dehydration
- electrolyte & acid/base imbalances
- hypoproteinemia
17
Q
Laboratory findings associated with acute diarrhea
A
- mature neutropenia & leukopenia (early) or neutrophilia with leukocytosis (late)
- usually left shift
- thrombocytopenia
- hyperfibrinogenemia
- hypoproteinemia
- hypoglycemia
- hyponatremia
- hypokalemia
- hypocalcemia
- metabolic acidosis (if poor perfusion or bicarb loss)
- azotemia
- high anion gap/lactic acidosis
- elevated liver function tests
- relative polycythemia
18
Q
Diagnosis for Salmonella
A
- fecal culture-at least five samples
- +/- fecal PCR
19
Q
Diagnosis of Potomac Horse Fever
A
- buffy coat PCR
20
Q
Diagnosis of Clostridiosis
A
- C. difficile*
- fecal cytotoxin immunoassay best
- C. perfringens*
- culture & PCR for toxins
21
Q
Diagnosis of cantharadin toxicity
A
- ID blister beetles in the hay
- catharidin assay-urine best/preferred, especially if alive; can do feces or GI contents
22
Q
Situations where colloids are beneficial
A
- vascular leak syndrome
- tissue edema
- poor cardiac output/perfusion
23
Q
Appropriate fluid therapy if dehyration is mild (<5%)
A
- oral fluids with salt supplementation
24
Q
Appropriate fluid therapy if dehydration is moderate (6-8%)
A
- oral fluids with salt supplementation
- might need to administer by NG as well
- stimulation of thirst with salt paste
- IV administration may or may not be needed; may consider colloids
25
Appropriate fluid therapy if dehydration \>8% or horse is hypotensive
* IV fluids necessary
* isotonic crystalloid bolus then constant infusion
* hypertonic saline mayb e useful to restore circulating volume and increase BP
* colloids
26
What are anti-inflammatory/analgesic considerations with acute diarrhea situations?
NSAID
* could impede mucosal repair and potentially nephrotoxic
* use at lowest dose possible if used
Lidocaine
* very good analgesic (inhibits afferent neurons, sympatholytic), anti-inflammatory, promotes mucosal healing
* but must be given by CRI and monitored closely
27
What are some compounds that are sometimes given to aid mucosal healing?
* bismuth subsalicylate
* psyllium
* misopostol
28
Describe nutritional support for acute diarrhea cases in adult horses
* need to eat SOMETHING
* good quality grass hay/grass-best
* pelleted diet-reduces mechanical load on colon & readily digestible(should be high in roughage & low in soluble CHO)
* **avoid grains**-fermented to lactate
* enteral nutrition should be avoided
* parenteral nutrition is cost effective in severely hypermetabolic patients or neonates
29
When are absorbant powders indicated?
Cantharadin toxicity, clostridiosis(reduce absorption of endotoxins); only given to horses with intestinal motility
30
Metronidazole may be indicated for \_\_\_\_\_\_\_\_\_\_
clostridiosis
31
What is one undesirable side effect of metronidazole in some horses?
horses may stop eating
32
What antibiotic is recommended for *Neorickettsia risticii*?
Oxytetracycline IV preferred
can give Doxycycline PO
33
Possible antibiotics indicated for salmonellosis
* Chloramphenicol
* Enrofloxacin
34
What are some possible causes of chronic diarrhea?
* **#1-parasites** (particularly cyathostomes)-cause large intestinal inflammation & PLE
* inappropriate diet
* sand accumulation in ventral colon & cecum
* chronic salmonellosis
* right dorsal ulcerative colitis
* neoplasia-colon
* chronic peritonitis
* chronic liver or heart disease
35
Diagnostic plan for chronic diarrhea
* fecal exam for parasites
* evaluate for sand
* salmonella culture/PCR
* peritoneal fluid analysis for peritonitis or neoplasia
* rectal biopsy for IBD or neoplasia
36
Drug of choic for deworming cyathostomes
moxidectin
37
What is a good treatment approach for sand?
psyllium powder
38
What types of diets are appropriate choices for chronic diarrhea treatment?
* all hay
* complete pelleted feed
39
What are risk factors for NSAID toxicity?
* dehydration
* reduced blood flow to colon
* underlying disease
40
What is a classic finding associated with RDUC?
**hypoproteinemia/hypoalbuminemia**-d/t PLE
41
Differentials for intermittent colic with or without weight loss
* obstructive disease of GI tract
* gastric ulcers
* IBD
* neoplasia
* sand enteropathy
* parasites (cyathostomiasis)
* peritonitis
* dental disease
* EIA
42
What are the two cornerstones for treatment of RDUC?
1. diet modification
* low fiber roughage: pelleted; avoid hay, avoid grain, avoid grass
2. misoprostol to promote mucosal healing
43
What is the role of corn oil in RDUC treatment?
provides calories and possibly promotes healing by promoting prostaglandin production
44
What are the two forms of equine gastric ulcer disease?
1. squamous disease (EGUS)
2. glandular disease
\*can coexist
45
Perforating ulcers are most common in what age horses?
weanlings (4-6 months of age)
46
What are the normal protective factors to acid injury of stomach?
* saliva
* roughage mat
* mucus, epithelial integrity-PGs
* gastric emptying
47
Risk factors for squamous disease
* occupation/training (race & show horses)
* intermittent feeding, anorexia, withholding food
* stress (environment, hauling, stall confinement)
48
Risk factors for glandular disease
* Illness
* ICU foals
* post-op colics
* gastric outflow obstruction
* NSAID toxicity
* maybe *Helicobacter* infection
49
What is a classic sign of gastric pain?
pain associated with eating-may be reluctant to eat
50
What type of ulcers seem to be more painful?
glandular
51
What type of hay is the best as a buffer?
alfalfa
52
What is the H2 antagonist of choice in horses?
ranitidine
53
What is the most specific therapy to reduce acid production?
proton pump blocker-omeprazole(Gastroguard)
54
Sucralfate is most effective for ulcers in what part of the stomach?
glandular
55
What is a specific therapy you could try in refractory cases of ulcers?
oral doxycycline-use as anti-inflammatory
56
Causes of primary impaction (choke)
* poor quality feed
* poor mastication
* dehydration/lack of saliva
* greedy eaters
57
Causes of secondary impaction/obstruction (choke)
* corn cob, apple, other FB
* stricture (congenital or acquired)
* diverticulum
* neoplasia
* abscess or granuloma
* inclusion cysts
* vascular ring anomaly
* motility dysfunction-megaesophagus
58
Prepharyngeal dysphagia is called \_\_\_\_\_\_\_
"quidding"
59
Clincal signs associated with choke
* anxiety
* hypersalivation
* nasal discharge including feed material, saliva, water
* cough
* gag, extend neck when eating
* mass/swelling in cervical region
* dehydration
60
What could cause a functional obstruction leading to choke?
esophagitis
61
Treatment plan for choke
* Clear obstruction:
* lavage under heavy sedation (detomidine)-single NG tube; keep head lower than thoracic inlet
* lavage under general anesthesia-double NG tube
* sugery may be necessary to remove FB, masses, etc.
* hydrate
62
Fluid of choice when dealing with choke
0.9% saline with bicarbonate added as needed
63
What effect does detomidine have on esophageal motility?
* decreases waveform duration
* increases transit time
64
Dietary management of horse after choke
Remember esophageal motility will be reduced for a few days post-obstruction
* pelleted diet **slurry**-may need to feed permanently if choke was secondary (e.g. stricture, mass)
* 2-3% BW per day divided into six feeedings
* corn oil supplemenation
* **avoid** hay, grass until function is normal; reintroduce slowly when appropriate
* salt supplementation if salivary loss continues
65
Complications of choke
* aspiration pneumonia-can be severe if bacterial infection occurs
* rupture-proably fatal
66
Follow-up protocol for choke
* re-scope after relieving obstruction-look for mucosal injury or underlying disease/causes
* if ulcerated:
* NSAIDs??-prevent stricture
* sucralfate
* re-scope 14-30 days if injury to mucosa is seen
67
Etiology of proximal enteritis
none definitively known:
possibly *C. difficile*, other bacteria, mycotoxins suggeted
68
Pathophysiology of proximal enteritis
* mucosal barrier damage
* hypersecretion (due to inflammation)
* **functional ileus** of proximal GI tract--\>gastric fluid accumulation
69
Distinguish between proximal enteritis and small intestinal obstruction
* **Fever** with proximal enteritis; not with SIO
* loops on rectal palpation are non-turgid with PE but **turgid** with **SIO**
* Peritoneal fluid of SIO (if strangulating) has high WBC/RBC; PE does not
* animals with **PE will respond to gastric decompression** while animals with **SIO remain painful** after gastric decompression
* gastric fluid with **PE-fetid, orange-red, large volume (\>10L)**; SIO-green-yellow fluid (bile)
* ultrasound: **PE-thicker wall and smaller diameter than SIO**, **some motility. SIO: diameter 6-10 cm, wall**
* PE-GGT, Tbili, ALP, AST usually elevated; not with SIO
70
Therapeutic principles for PE
* analgesia
* usually flunixin meglumine (low dose) & lidocaine CRI; butrophanol also option
* **gastric decompression**
* fluids-hydration/electrolyte balance
* sepsis/endotoxemia
* prokinetics
71
Differential diagnosis for proximal enteritis
* peritonitis
* small intestinal obstruction
* gastric outflow obstruction
* salmonellosis
72
Antibiotics given in the case of proximal enteritis? rationale?
* Metronidazole is given sometimes since Clostridiosis is potential etiology
* give broad spectrum antibiotics if neutrophil count is very low (b/c increased risk of infections)
73
Why is it useless to give omeprazole when horse is still refluxing?
it needs to be absorbed in SI to have effects; omeprazole is drug of choice once motility has returned
74
What are some prokinetics that may be tried to return motility and combat functional ileus?
* lidocaine CRI
* Metaclopramide-CRI best to avoid neurologic side effects, mania
* Erythromycin
* Bethanechol used to be used
75
How to institute feed/water back to horses recoving from proximal enteritis
* NPO while refluxing \>2-4L q4 hr
* can give small amounts of water when no significant amount of reflux for 24 hours
* water tolerated--\>graze every few hours for 24 hours
* grazing tolerated--\>small amounts of hay/complete pelleted feeds, slowly increasing over 2-3 days
* parenteral nutriaion is an opeion if NPO \>72 hours
76
Complications that can arise from proximal enteritis
* laminitis
* ulcers
* peritonitis
* adhesions
* renal failure
* DIC
* liver fibrosis
77
Etiology of proliferative enteropathy?
*Lawsonia intracellularis*
78
Transmission of proliferative enteropathy
fecal-oral from horse to horse
79
Lay term for proliferative enteropathy
"hose pipe gut"
80
Pathophysiology of proliferative enteropathy
infection of GI epithelial crypt cells--\>epithelial proliferation in small intestine--\>secretion, malabsorption, PLE
81
What age horses are affected by proliferative enteropathy
1-7 months old
82
Clinical signs associated with proliferative enteropathy
* rapid weight loss
* diarrhea, often + melena
* peripheral edema
* mild to severe colic
* lethargy
* anorexia
83
Lab findings associated with proliferative enteropathy
* panhypoproteinemia
* leukocytosis
* anemia of chronic inflammation/blood loss(non-regenerative)
* maybe electrolyte and acid base imbalances, depending on diarrhea
84
Antemortem test of choice for proliferative enteropathy
serology
85
Why is fecal PCR for *L. intracellularis* not very sensitive?
animals are not frequently shedding
86
Ultrasonographic findings assoc. with proliferative enteropathy
* thickened small intestine
* limited motility
87
Treatment options for proliferative enteropathy
* erythromycin, may be combined with rifampin
* azithromycin
* oxytetracycline or doxycycline
* chloramphenicol if erythromycin fails
* colloids (plasma or hetastarch)
* fluid support if needed
88
Causes of IBD
* an inappropriate immune response to a pathogen or antigen
* appropriate immune response to a persistent pathogen or antigen
89
How does the segment affected by IBD impact clinical signs seen?
Small intestine--\> malabsorption syndrome
Large intestine --\> diarrhea
Protein-losing enteropathy regardless of segment
90
What is a differential for IBD?
alimentary lymphosarcoma
91
What is the most common form of IBD?
lymphocytic/plasmacytic
92
Classifications of IBD
Eosinophilic
Granulomatous
Lymphocytic/plasmacytic
93
Pitting edema under the chin is often seen with what disease?
IBD
94
Lab findings associated with IBD
* anemia of chronic inflammation
* hypoalbuminemia, hypoglobulinemia
* possible leukocytosis
* eosinophilia-rarely, but lucky if found
* lymphocytosis-rarely
95
Weight loss is NOT common with what form of IBD?
eosisinophilic colitis
96
Dermatitis may be an associated finding with what form(s) of IBD
* granulomatous enteritis
* multisystemic eosinophilic epitheliotropic disease
97
What type of IBD is most likely to have diarrhea as a clinical sign?
MEED
98
Which form of IBD is most likely to produce colic?
eosionophilic colitis
99
Chronic weight loss in an adult horse should prompt what diagnostic test?
coggins
100
How does peritoneal fluid analysis help determine peritonitis vs. neoplasia?
* neoplasia: glucose and pH similar to that of plasma
* peritonitis: glucose and pH lower than plasma
101
What immunosuppressive treatments can be given in the case of IBD?
* Dexamethasone IV or IM since oral abs. poor
* Prednisolone PO
102
Causes of peritonitis
* intestinal rupture
* internal abscess (usu. mesenteric LN or liver)
* gram negative enteric bacteria, Actinobacillus equuli mixed with Streptococcus zoopidemicus or equi, R. equi in foals)
* primary infection
* cholangiohepatitis & bile duct rupture
103
Peritoneal fluid findings with peritonitis
High WBC, protein, fibrin present
104
What antibiotics are often first choice in the treatment of peritonitis?
aminoglycoside/penicillin combination
105
What antibiotic would be indicated with peritonitis due to suspected peforation?
metronidazole
106
When might a rectal biopsy be helful in making a diagnosis?
MEED or granulomatous enteritis
Equine Med & Surgery
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