Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
162 Cards in this Set
- Front
- Back
|
What factors protect the stomach in the horse?
|
1 - glandular mucosa
2 - stratified squamous epithelium |
|
|
How does the glandular mucosa protect the horse stomach?
|
-secrete mucus or bicarb
-increased blood flow (GPGE2) - rapid epithelial restitution |
|
|
What is the most commonly injured part of the stomach?
|
stratified squamous epithelium
|
|
|
What are factors that contribute to ulcer formation?
|
-gastric acid secretion
-pepsin secretion |
|
|
What is gastric acid secreted by?
|
parietal cells of glandular mucosa
|
|
|
What is pepsin secretion caused by?
What does it do? |
-pro-enzyme secreted by by chief cells,of the glandular mucosa
-activated by acid pH and digests protein |
|
|
What are 6 main causes of ulcers?
|
1 - NSAIDS (depresses PGE2 synthesis)
2 - stressors like disease 3 - training, breeding, showing 4- high grain (textured) 5 - unknown 6 - H. pylori? |
|
|
What percent of sick foals get ulcers?
What is the most common type? |
25-50%
-squamous epithelium |
|
|
What percent of race horses get ulcers?
|
66%
-squamous most common -glandular is less than 20% |
|
|
What are CS of ulcers in foals?
|
-colic
-don't want to eat -gas/diarrhea -teeth grinding |
|
|
What are CS of adults with ulcers?
|
-picky appetite, weight loss
-similar to foals BUT -adults DON'T GET DIARRHEA |
|
|
What are ways to diagnose gastric ulcers?
|
- gastroendoscopy
-fecal occult blood (young only) -gastric mucosa permeability test |
|
|
Why is fecal occult blood not a good test for gastric ulcers in adult horses?
|
colonic flora digestion of blood
|
|
|
What is a positive gastric mucosa permeability test?
|
presence of sucrose in urine at 120 minutes indicates a gastric mucosal injury because sucrose must be broken down before it is absorbed
|
|
|
How do you treat gastric ulcers?
|
1 - change lifestyle
2 - change feed (increase roughage, continuous feeding) 3 - consider medications (cost, daily frequency, response) 4 - if medications are a consideraton (treat at least 3 weeks and recheck) |
|
|
What 4 drugs could you use for gastric ulcers?
|
1 - omeprazole
2 - ranitidine 3 --cimetidine 4 - sucralfate |
|
|
What are 3 medical disorders of the SI?
|
1 - duodenitis - proximal jejunitis (DPJ)
2 - proliferative entropathy 3- Rhodococcus equi enteritis |
|
|
What is duodenitis-proximial jejunitis?
|
-inflammation and thickening of the proximal small intestine
-excessive fluid and electrolyte secretion into the small intestine -diminished SI motility -accumulation of lg. volumes of fluid in SI and stomach |
|
|
What are 3 general causes of DPJ in the horse?
|
-infectious
-dietary indiscretion (over eating, rapid change in diet) -ambient heat, exercise |
|
|
What are 4 infectious causes of DPJ?
|
1 - Clostridium difficile and C. perfringens
2 - Salmonella species 3 - Enteric bacteria like E. coli (rare) 4 - parasitic (rare) |
|
|
What do DPJ and SI surgical lesion have in common?
|
NG tube reflux
-elevated protein in abdominocentesis |
|
|
What is the difference between DPJ and SI surgical lesion on US?
|
DPJ - moderately distended SI, thick walls, some motility
SI surgical lesion - VERY distended SI, walls not thick, little motility |
|
|
What is the difference in the MM between DPJ and SI surgical lesion?
What is the diff in HR? |
DPJ - dark pink to red
- SI surgical lesion - pink to purple DPJ - 60-70 and SI surgical lesion is 60 to over 100 |
|
|
Which condition has a fever - DPJ or SI surgical lesion?
Which one is more painful |
DPJ - fever
SI Surgical lesion, VERY painful unless ruptured, vs. DPJ that is only moderately painful |
|
|
What are the treatments for DPJ?
|
1 - relieve GI pressure (pass a tube, reflux every 2 hours)
2- fluid and electrolyte replacement therapy 3 - NSAID therapy 4 - prophylactic antibiotics 5 - anti-gastric ulcer medication |
|
|
What age horses does proliferative enteropathy occur in?
What is it caused by? |
-weanling to yearling foals
-Lawsonia intracellularis |
|
|
What is the pathogenesis of proliferative enteropathy?
|
-Lawsonia invades crypt cells of ileum
-causes mitotic division and hyperplasia -gut becomes thick and corrugated with limited brush border development -malabsorption -weight loss and hypoproteinemia (hypoalbuminemia) |
|
|
What is the history of proliferative enteritis?
|
adequate access to food, but poor weight gain
|
|
|
What are the PE findings of proliferative enteritis?
|
-small
thin with poor coat -quiet attitude -peripheral edema -skin lesions and other secondary infections |
|
|
What additional tests should be done to diagnose proliferative enteritis?
|
1 - CBC
2 - Blood Chem 3 - Abdominal US 4 - IFA test for serum antibodies |
|
|
What is seen on a CBC with proliferative enteropathy?
|
-hypoproteinemia
-+/- anemia |
|
|
What is seen on a blood chem with proliferative enteropathy?
|
-hypoproteinemia
-hypoalbuminemia |
|
|
What does an US look like with prolifferative enteropathy?
|
-thick, but not usually distended SI (as great as 6-12 mm wall thickness)
|
|
|
What is seen on an IFA serum antibody test with proliferative enteropathy?
|
titer greater than or equal to a:30 is diagnostic
|
|
|
What is the treatment for proliferative enteropathy?
|
-erythromycin +/-rafampin (dose dependent) for 6 weeks
-chloramphenicol -tetracyclines (ox (3-7 days) and doxy (17 days) -supportive care |
|
|
What age do foals get Rhodococcus equi?
|
2 - 5 months
|
|
|
What is enteric disease due to with R. equi?
|
extrapulmonary disorders associated with lymphatic infection
-pathogens resides in macrophages and gains access to other parts of the body through lymphatics (originating from the lungs) -usually GI disease follows pneumonia, but not always |
|
|
What are the HIstory and CS of a foal with R. equi enteritis?
|
1 - respiratory disease on the farm and or in the foal
2 - diarrhea 3 - weight loss 4 - low grade colic 5 - febrile 6 - anorexic 7 - other immune mediated diseases |
|
|
What will a CBC show with R. equi enteritis?
|
-leukocytosis
-neutrophilia -hyperfibrinogenemia -+/-thrombocytosis |
|
|
What will the US of the thorax and abdomen show in a horse with R. equi enteritis?
|
thorax = evidence of abscesses
abdomen = evidence of abcess, peritonitis, thick bowel |
|
|
What is the treatment for R. equi enteritis?
|
- same as pulmonary disease
- erythromysin -azithromycin -clartihromycin -combine with rifampin -treat one week after CBC is normal -watch for diarrhea in both foal and mare |
|
|
What is endotoxin?
|
gram neg bacteria
-part of the outer cell wall -shed when die or there is rapid replication -LPS has O antigen, Lipid A and PS Core |
|
|
What part of entotoxin is constant accross bacteria?
|
lipid A
-hydrophobic that is burries in cell membrane |
|
|
What part of entotoxin is variable between bacteria bacteria?
|
O-antigen, O chain
-hydrophilic - projects into the aqueous environment |
|
|
What 4 things does endotoxin do?
|
1 - binds to cell surface
2 - stimulates a number of pathways 3 - release of cytokines 4 - activation of gene transcroption |
|
|
What are low dose signs of endotoxemia?
How long will signs last if only a single dose? |
-restless, depressed, inappetant, febrile, absent GI sounds
-mild to moderate evidence of CV compromise -8-12 hours |
|
|
What are high dose signs of endotoxemia?
|
-circulatory collapse
-stuporous and anorexic -signs of dehydration -poor pulses, cold extremities -fever, then hypothermic -sweat, shiver, muscle fasciculations -may have evidence of coagulopathy (petechia or clotting) -infarcts and associated signs followed by bleeding tendencies |
|
|
What does a CBC and Chem look like with endotoxemia?
|
- leukopenia, neutropenia, left shift, toxic changes
-lymphopenia if severe -hyperglycemia followed by hypoglycemia -hemostatic disorders (reduced platelets and prolonged bleedign time) |
|
|
What does a lactate of 2-4 mean?
4-5? |
-significant disease
- severe disease so monitor closely |
|
|
Why do endotoxin specific treatments often not work?
|
-only work before LPS exposure
|
|
|
What are 3 specific common treatments for endotoxemia?
|
1 - NSAIDs: Flunixin meglumine
2 - Pentoxyfyline (effect may be blocked by NSAIDs) - up regulation of prostacycline 3 - polymixin B (good prior to LPS exposure) |
|
|
What are 5 general treatments for endotoxemia?
|
1 - early, aggressive CV resuscitation
2 - laminitis prevention 3 - remove cause 4 - neutralize circulating endotoxin 5 - block inflammation caused by endotoxin |
|
|
In treating endotoxemia, you want to start with CV resuscitation. What does this entail?
|
1 - volume expansion (polyionic solutions 20-40 ml/kg/hr; plasma, heta starch)
2 - electrolyte replacement: bicarbonate, potassium, calcium |
|
|
When giving a polyionic solution, what should you monitor?
|
-BP, PCV, plasma protein concentration, ascultate lungs
|
|
|
What is the "laminitis prevention bundle" when treating endotoxemia?
|
1 - fluids
2 - cryotherapy 3 - flunixin meglumine 4- pentyoxifyline 5 - plasma with heparin 6 - insulin with glucose and check blood glucose every 2-4 hours |
|
|
In adults what are likely culprits of the source of endotoxemia?
Foals? |
- GI lesions
- Gram neg infection in other viscera (pleuropneumona, hepatic abcess, abdominal abcess, pyelonepritis) Gram neg septicemia or local (umbilical) |
|
|
What are 2 methods to neutralize circulating endotoxin?
|
1 - hyperimmune plasma and serum (contains antibodies against endotoxin)
2 - polymixin B (attacks the endotoxin - binds to LPS) - give slowly over 15 min. and monitor for renal injury |
|
|
What 10 drugs inhibit endotoxin induced inflammation?
|
1 - NSAIDs (flunixin meglumine)
2 - methyl xanthine derivatives (pentoxyfylline) 3 - corticosteroids 4 - heparin 5 - scavengers of reactive oxygen species 6 - allopurinol 7 - DMSO 8- Naloxone 9 - PAF inhibitor 10 - Ketamine CRI |
|
|
How does banamine act to decrease inflammation associated with endotoxemia?
|
-blocks formation of COX 1 and 2
-nonspecific therefore renal and gut injury is possible |
|
|
How does pentoxifylline act to decrease inflammation associated with endotoxemia?
|
-suppress macrophage inflammatory cytokine production like TNF
-reduce production of IL-10 (antiinflamatory) -reduce neutrophil activation -increase RBC deformatbility (reduce clot formation associated with laminitis) |
|
|
How does corticosteroids act to decrease inflammation associated with endotoxemia?
What do you risk with high doses? |
-inhibit TNF production
-stabilize cell membranes -prevent neutrophil activation -laminitis |
|
|
How does heparin act to decrease inflammation associated with endotoxemia?
|
-block micro-thrombi formation, but unfractionated form also causes RBC agglutination in horses
-recommended low molecular weight heparin -blocks micro-thrombi formation but doesn't agglutinat platelets |
|
|
How does allopurinol act to decrease inflammation associated with endotoxemia?
|
-hydroxyl radical scavenger
0inhibits xanthine oxidase |
|
|
What are the 2 benchmarks for predicting a prognosis in endotoxemia cases?
|
6 hours
24 hours |
|
|
What are COMMON causes of weight loss in the horse?
name 6 due to poor management |
1 - poor dentistry
2 - inadequate deworming program 3 - inadequate access to fresh water 4 - inadequate diet 5 - competition for feed 6 - stress |
|
|
What are UNCOMMON causes of chronic weight loss?
|
1 - inflammatory disease
2 - infectious disease 3 - neoplasia 4 - malabsorption/maldigestion (manifestation of inflammatory or neoplasia) |
|
|
Other than a routine PE and checking the teeth, what should be included when investigating chronic weight loss?
|
1 - diet
2 - water 3 - rectal exam 4 - fecal parasite and sedimentation for sand 5 - MAYBE blood work and abdominocenteis |
|
|
Is a normal liver plapable on rectal exam?
|
no
|
|
|
What things do you feel for on a rectal exam?
|
-viscera (size, position)
-bowel for thickness -palpate ascending aorta, internal iliac |
|
|
Say that you can't really diagnose weight loss in the horse. Where should you start for management of this problem?
|
1 - change diet
2 - decrease work 3 - deworm 4- float teeth 5 - change management of horse (separate feed) 6 - monitor weight on regular basis |
|
|
What are the 3 main functions of the liver?
What are important products? |
-synthesis
-metabolism -excretion -albumin, glycogen, clotting factors |
|
|
Why is prognosis poor with liver disease?
|
because 60-80% is lost before CS are seen? Marked ability to regenerate.
|
|
|
What are common presenting signs with liver disease?
|
-photosensitization - most common (white area of face)
-yawning -hepatoencepalopathy (head pressing) |
|
|
What are rule outs for icterus?
|
-conjugated bilirubin
-inappetance (unconjugated) |
|
|
What will a CBC tell you with liver disease?
|
-icteric
-infection - increased WBC - hypoalbumineic (panhypoproteinmia) |
|
|
When do you start worrying about increase in leakage enzymes?
|
3x increase and other CS - acute disease
|
|
|
What are the 5 hepatocellular enzymes to look at?
Which one is THE most specific for liver injury in the horse? |
1 - SDH - most specific with very short half life (24 hours) so good to monitor and elevations mean active disease
2 - AST 3 - LDH 4 - GGT 5 Alk Pos |
|
|
What is AST specific for?
|
muscle, liver, RBCs
-long half life -sensitive but not as specific |
|
|
Where does LDH come from?
What else do you need in order to interpret it? |
liver and muscle
-need concurrent CK -intermediate half life |
|
|
What is the most USEFUL hepatobiliary enzyme in the horse and why?
|
GGT
-comes from the biliary system, GI, pancreas, renal so accurate indication for biliary diseae -BUT, not good for monitoring becuase can stay elevated for a long time |
|
|
What is elevated in foals under 45 days?
|
GGT
|
|
|
What lab values show evidence of liver disease?
|
-decreased albumin
decrease BUN decreased glucose increased bilirubin increased trigycerides -cloudy serum |
|
|
What are common finding of bilirubin with liver disease, biliary obstruction and hemoytic disease?
|
- rise in unconjugated and conjugated
-conjugated often greater than 25% |
|
|
What will be elevated in icteric horses without liver disease?
|
bile salts
-not altered by feeding - >20 is indicative of liver disease even in icteric horses |
|
|
What may be most useful in monitoring recovery of liver function in the horse?
|
- ammonia
-this is likely not the cause of encephalopathy in the horse |
|
|
Whare the hepatocelllar leakage enzymes?
|
SDH - most specific and acute
AST - less specific, longer half life LDH - none specific and intermediate half life |
|
|
What are the hepatobiliary enzymes?
|
GGT: less specific and long half life
Alk Pos |
|
|
Where do you enter for a percutaneous liver biopsy?
|
11-14 IC space -- then do histo and culture
|
|
|
What is the initial therapy for liver disease?
|
-fluids and glucose
-electrolytes (potassium) - decrease ammonia (neomycin, mineral oil, lactulose) -min. stress -sedate -change diet (decrease protein) |
|
|
What are causes of Theilers Disease (Serum Hepatitis) that causes acute hepatic necrosis?
|
1 - prior equine biologics (tetanus antitoxin)
2 - dietary or environmental toxin 3 - idiopathic |
|
|
When is Theiler's Disease most common?
Can outbreaks occur? |
fall
yes |
|
|
What age does Tyzzer's Disease occur in?
|
Foals from 7-40 days old
|
|
|
What is the etiology for Tyzzer's Disease?
|
Clostridium (Bacillus) piliformis
-mare is the carrier and it is present in the soil |
|
|
What does Tyzzers Disease cause and what are the CS?
|
-peracute hepatic necrosis
-CS: septic, concurrent signs of hepatitis |
|
|
What does equine neonatal herpes cause?
|
perinatal infection that causes weak or stillborn foals
CS: early or term foal, weak at birth, abnormal lung sounds, die in hours or few days |
|
|
What type of plants cause chronic liver disease with acute exacerbation?
|
-pyrrolizidine alkaloids
-cumulative toxicosis (5% BW) |
|
|
What is diagnostic of pyrrolizidine alkaloid toxicosis on necropsy?
|
megalocytosis, cell death, fibrosis
|
|
|
What plants can cause trifoliosis (photosensitization)?
|
-Aslike clover (Trifolium hybridum_
-Kline grass (Panicum coloratum) - RED Clover -toxic baled or on pasture |
|
|
What type of weather is assoicated with photosensitization?
|
humid - so toxicity varies from year to year
-helps mycotoxin grow |
|
|
What liver problem is assoicated with photosensitization?
|
biliary fibrosis and hyperplasia
|
|
|
What are CS of a cholelith?
|
-recurrent, progressive colic
-+/- fever -jaundice -weight loss -hepatoencephalopathy --photosensitization |
|
|
What age horses get choleliths?
|
>9
|
|
|
What type of horses get hyperlipemia?
What is the inciting cause? What is the prognosis? |
ponies, donkeys, miniature horses, drafts
- anorexia -poor - best to prevent |
|
|
What nutritional support can you provide horses with hyperlipemia?
|
5% glucose
maintenance fluids slurry by NG tube 30 cc oral Karo Syrup (short term, may cause diarrhea0 |
|
|
What type of horse is affected by hyperlipidemia?
|
fat horses of any type (not breed specific)
-better prognosis thatn hyperlipemia |
|
|
Who has high triglyceritdes - hyperlipidemia or lyperlipemia?
|
hyperlipemia
|
|
|
What does plasma look like with hyperlipidemia?
|
usually clear (not opaque)
|
|
|
What is the treatment for hyperlipidemia?
|
increased energy in ration or IV fluids
|
|
|
Adult diarrhea in the horse is a disease of what?
|
cecum and large colon
|
|
|
What is the function of the LI?
|
1 - fluid resorption
2 - Sodium Transport 3 - Bicarbonate secretion and absorption 4 - microbial/protozoal/funcal flora 5 - VFAs from fiber (insoluble carbohydrates) 6 - ammonia production |
|
|
What does injury to the LI cause: Name 6 things?
|
1 - watery manure
2 - acidemia 3 - hyponatremia (and hypokalemia) 4 - nutrients loss (weight loss) 5 - hypoproteinemia, hypoalbuminemia 6 - endotoxemia |
|
|
What are general inflammatory causes of diarrhea?
|
-infectious
-toxins -IBD (infiltrative) -Secondary to other diseases |
|
|
What are infectious inflammatory causes of diarrhea in the horse?
|
-Salmonella
-PHF -CLostridiosis -Endoparasitism |
|
|
What are toxic inflammatory causes of diarrhea in the horse?
|
-catharidin
-NSAID -Antimicrobials (erythromycin, TMS, tetracycline) |
|
|
What type of bacteria is Salmonella and what is the most common in the horse?
|
gram neg
- S. typhimurium -also Krefeld, Anatum, INfantis, Dublin |
|
|
What are the history and CS of Salmonella?
|
-exposure (rain, runoff, ect. )
- stress/signalment -other affected horses -antimicrobials, dietary change, ect. -acute onset |
|
|
What are the 4 "diseases" of Salmonella?
|
1 - inactive disease
2 - severe fibrinonecrotic typhlocolitis 3 - sudden death 4 - septicemia in foals |
|
|
What does an animal look like with severe fibrinonecrotic typhlocolitis caused by Salmonela?
|
-MM are brick red to purple
-endotoxic shock: cold limbs and muzzle -CBC: neutropenia, left shift diarrhea |
|
|
What is the most sensitive test to diagnose Salmonella?
|
Fecal PCR
|
|
|
What 3 methods can be used to diagnose Salmonella?
|
1 - fecal culture
2 - rectal mucosal biopsy 3 - Fecal PCR |
|
|
If a fecal culture of Salmonella is negative after 5 daily consecutive cultures, what is the chance that the horse does NOT have Salmonella?
|
95%
|
|
|
What is the broth to use when culturing Salmonella?
|
selenite broth
|
|
|
What is the treatment for Salmonellosis?
|
1 - IV fluids
2 - plasma (adults 5 L and foals 1-2 L) 3 - NSAIDs: flunixin meglumine - breaks inflammatory cascade |
|
|
What can you use for electrolyte replacement with Salmonella?
|
-bicarb
-potassium - free choice water -salt lick |
|
|
Why do you use antibiotics with salmonellosis?
|
prevent systemic dissemination
|
|
|
What drugs would you use to treat Salmonella?
|
-fluoroquinolones - carefule in young animals due to cartilage damage
- Aminoglycocytes like gentamicin - make sure well hydrated |
|
|
How long should you isolate new horses?
|
2-4 weeks
|
|
|
Do horses shed for the rest of their lives?
If not, how long do hey shed? |
- no host adapted species of salmonella
1-3 months (as long as 2 years -infected shed lots in feces |
|
|
What is the agent that causes PHF?
What are its features? |
Neorickettsia risticii
-Anaplasmataceae family - Intracellular (macrophages, colonic/SI epithelium, colonic mast cells) -small, gram neg cocci -Darck Blue with Romanowsky's stain |
|
|
How are horses affected with PHF?
|
ingesting infected trematode or infected aquatic insects
(near water) |
|
|
What is the history of an animal with PHF?
|
-warmer time of year
-unvaccinated -nearby water source |
|
|
What are CS of PHF?
|
-like Salmonella
-biphasic fever (2-4 days then 10-14 days) -laminitis -vaccinated: fever, hypoproteinemia, laminitis, but generally milder |
|
|
How is PHF diagnosed?
|
1 - paired titers (IFA or ELISA) -- significant change in titer
2 - PCR - org. in buff coat |
|
|
When doing paired titers to diagnose IFA, how far apart do you take the samples?
What may interfere? |
2-4 weeks - freeze and send at same time (CS take 14 days so titer is already on the rise)
-vaccination |
|
|
What specific treatment is there fore PHF?
|
- oxytetracycline (don't give out of vein, give slowly)
-Doxycycline (may not be well absorbed) -supportive care like Salmonella -relapses can occur |
|
|
Is the PHF vaccine fully effective?
|
no - attenuates CS
-also multiple strains so may get a different one |
|
|
When do you vaccinate for PHF?
|
spring and mid-summer
|
|
|
Why do NSAIDS damage the colon?
|
-inhibit COX-1 and COX-2 and reduce prostaglandins
-colon needs them for BF and restoration of epithelium -causes increased injury and delayed healing |
|
|
What are CS of NSAID toxicity?
|
- low grade coli
-soft manure -low grade fever -hypoprotein and hypoalbumin -ventral edema |
|
|
Where are lesions most common with NSAID tox?
|
ritght dorsal colon
|
|
|
What is the prognosis for NSAID tox?
|
guarded and depends on colon healing (3-6 months
-monitor blood protein and albumin concentration |
|
|
What is the treatment for NSAID tox?
|
-hard due to high bacterial load in the colon
-antimicrobials (metronidozole) -masoprostil -severe cases (fluids, PPP, endotoxic therapy) -chronic - prolonged turn out |
|
|
What is the function of the squamous mesothelial cells coated with a serous film that line the peritoeal cavity?
|
-decreases friction
-facilitated free movemetn |
|
|
What are common causes of invasion of the peritoneum that causes peritonitis?
|
-infectious = bacterial, viral, fungal, parasitc
-non-infectious = traumatic, chemical, neoplastic -in the horse = secondary GI compromise and transmural migration of bacteria |
|
|
What are the events leading to peritonitis?
|
1 - invasion of the peritoneum
2 - trauma to mesothelial cells 3 - initiates a complex inflammatory cascade that results in fibrin formation 4 - simply handling the bowel can initiate this disease |
|
|
What is the most common cause of peritonitis in the horse?
|
-secondary GI compromise
|
|
|
What are the common causes of primary peritonitis?
|
1 - proximal enteritis
2 - intestinal ischemia, compromise 3 - gastric, intestingal perforation 4 - hemorrhage 5 - uroperitoneum 6 - parasitic migration 7 - abcess (secondary to S. equi, R. equi) 8 - neoplasia 9 - parturition |
|
|
What is the history with peritonitis?
|
-varies based on associated disease
- severe disease: may have acute onset and rapid demise |
|
|
What are the most common CS with peritonitis?
|
1 - pyrexia
2 - anorexia 3 - abdominal pain (mild-moderate) 4 - decreased gut sounds 5 - +/- diarrhea or dry feces (evidence of disrupted motility) 6 - dehydration |
|
|
What additional test would you want to so in suspected peritonitis?
|
1 - rectal exam (serosa of the intestine is rough or gritty)
2 - abdominal US - increased cellularity and fluid, fibrin tags 3 - abdominocentesis --> cytology and culture |
|
|
What is the treatment for peritonits?
|
-aggressive
- stabilize the patient -ID and treat inciting cause - administer additional medications and treatments specially for peritonitis |
|
|
What does a normal abdominocenteis look like?
|
-clear yellow
-TP< 1 or 2.5 -cell count <5000 cells with 24-60% neutrophils) |
|
|
What is abdominal fluid is blood tinged?
|
evidence of compromised bowel or intraperitoneal viscera
|
|
|
What is abdominal fluid is frank blood/hemorrhage?
|
splenic or vascular injury
|
|
|
What is abdominal fluid is normal and clear but large volumes?
|
ascites or uroperitoneum
|
|
|
What is abdominal fluid is cloudy?
|
high cells associated with severe inflammation, compromised viscera, abcess, neoplasia
|
|
|
What is abdominal fluid has bacteria
|
septic peritonitis (ID the Source)
|
|
|
What are treatments specially for peritonitis?
|
- shock therapy
-broad spectrum antimicrobial (including anaerobes) (K-Penicillin, Gentamicin, Metornidazole) -Minimize inflammation and fibrin formation with: NSAIDs, Lidocain, DMSA, Pentoxyfilline -Peritoneal Lavage -Surgery |
|
|
Why is lidocaine used to in treatment of peritonitis?
|
prokinetic - prevents adhesions
-analgesic |
|
|
What are the benefits of a peritoneal lavage?
|
-reduce concentration of bacteria, inflammatory mediators
-remove degenerative neutrophils and cellular debris -eliminate accumulated blood -remove irritating foreign material -dilute adhesion forming substrates like fibrin, fibrinogen |
|
|
What are limitations of peritoneal lavage?
|
- may not reach entire abdomen
-may cause inflammation -may disrupt clots - use with extreme caution in horses with evidence of hemorrhage |
|
|
What is the prognosis of peritonitis?
What are complications? |
60% mortality - post colic surgery risk
complications: laminitis, diarrhea, ileus, fibrous adhesions |
