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502 Cards in this Set
- Front
- Back
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Colic |
-Clinical finding, not a diagnosis |
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Colic behaviors
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-Lip curl
-Pawing ground -Flank watch -Kicking at abdomen -Lateral recumbency -Rolling -Violent -Can be anywhere from mild to severe and anywhere inbetween -Everyone has a different idea of what “panful” is -Need to be very specific about clinical signs with history -Animals display pain differently also! |
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Other causes of pain that could look like “colic”
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-Thoracic or pulmonary disease
-Cardiac pain -Urinary pain -Reproductive issue --uterine --testicular |
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Functional causes of colic
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-Inflammatory: |
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Simple obstruction causing colitis
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-Fecolith
-Enterolith -Impaction -VERY common |
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Epidemiology of Colic
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-Diseases that cause colic are common cause of death (11%)
-Very common disease -2-5% require surgery, many can be managed medically in the field -Studies determine associations, not cause --need to beware of comfounders, factors associated with the risk factor and disease but are NOT causal |
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Risk factors for colic in horses
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-Signalment: no sex or use of horse is associated with prevalence
-Specific types of colic may be gender related --large colon volvulus in brood mare --inguinal hernia |
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Breed predispositions for Colic
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-Thoroughbreds |
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Age and colic prevalence
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-Foals are less likely to develop colic than older horses
--less likely to have surgical lesions -Less likely to get inflammatory lesions or obstructions -Risk is increased with age --not a linear relationship, but exists |
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Populations that get specific types of colic lesions
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-Stall confined adult horses: cecal impaction
-Older horses: strangulating lipoma -Young horses with parasitic issues: intussusception -Foals: ulcerative disease |
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Geography and types of colic
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-No association between geography and overall incidence of colic
-Specific types of colic happen in specific areas -Sand colic: coastal areas -Enterolithiasis: western US -Ileal impactions: Bermuda coastal grass Hay -Grass sickness: dysautonomia and |
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Feeding to prevent colic
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-No good answer!
-Increased incidence of colic with high amounts of grain or concentrates -Forage is associated with decreased risk of colic -Recent change in feed doubles risk for colic -No association between feed type and colic -Association with poor quality hay? Round bales? -Access to potable drinking water is important |
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Management and colic incidence
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-Increased stable time increases risk for colic |
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Exercise and colic
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-Event/racehorses may be at increased risk for colic |
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Parasites and Colic
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-Association between de-worming and incidence of colic is variable
--resistance? Efficacy? Dose? -May be an association between tapeworms and incidence of colic -Incidence of worms has increased recently |
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Medical history and Colic
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-Previous history of colic is a risk factor for recurrent episodes of colic
-Previous colic surgery is associated with increased risk of colic -Need to know if a horse has colicked before! -Look for a colic incision |
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Teeth and Colic
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-anecdotal evidence
-Dental disorders are associated with esophageal obstruction and simple impaction or obstruction -Dental prophylaxis is recommended |
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Information needed from owner for colic work-up
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-Signalment
-Age -Breed -Other locations lived -Job/Use -Feeding practices, grazing management, exercise, parasitic control --changes in management -medical history --colicked before? How many times? Resolution? -Dental care |
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Information about a specific colic episode
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-Specific clinical signs
-Duration of clinical signs -Degree of discomfort, describe behavior -Medications already administered --what, route, how much --response to medications -Restricted feed, do not feed until you know what is going on! -Manure production |
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Botulism vs. Colic
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-Horses with colic seem to roll more often
--are not quiet when they go down -Horses with botulism fasciculate, quiver, go down and are quiet |
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Colic work-up
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-GOOD history
-Physical exam -Pay close attention to: --GI motility --Abdominal distension --Cardiovascular stability --comfort level -Rectal examination -Nasogastric tube and check for reflux -Abdominal ultrasound -Abdominocentesis -Gastroscopy |
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Rectal Exam for colic case
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-Large colon: feel sacculations and band |
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Abnormal findings on rectal exam in colic case
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-large viscous distension |
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Nasogastric tube and reflux in colic case
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-Create a siphon
-Look at character of the reflux and amount of reflux -Was there a change in comfort after reflux was taken off? -Decrease in heart rate after removal of reflux? |
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Things administered via nasogastric tube
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-Water
-Electrolytes -Mineral oil -Diocytl sodium succinate (DDS, detergent that breaks up impactions, can also cause inflammation) -Psyllium for sand colic -Bismuth subsalicylate (pepto bismol) |
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Abdominocentesis for colic case
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-Increased nucleated cell count and increased total protein
-Normal nucleated cells: less than 5,000 cells -Normal protein: ;ess than 2 g/dL -If concerned about ruptured viscus, abdominocentesis is really helpful -Also look at lactate |
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Initial therapy for colic case
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-Pass nasogastric tube
-Administer water, electrolytes, lubricant --Only give if there is no reflux -IV fluid therapy --colloids, crystalloids, hypertonic saline -Administer analgesics/antispasmotics --banamine |
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Analgesics/Antispasmotics used in colic cases
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-Flunixin meglumine (banamine)
-Buscopan -Xylazine -Butorphanol -Detomidine |
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Indications for surgery in a colic case
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-Response to therapy
-Painful even after gastric decompression, persistent pain -Needs repeated administration of analgesics, painful animal -Repeated rectal exam with abnormal findings or worsened findings -Absent borborygmi -persistent tachycardia, HR more than 60 bpm |
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When to refer a colic case
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-Failure to respond to sedation or analgesia
-Prolonged clinical signs with no improvement -Violently uncomfortable horse -Horse with significant reflux -Horse with significantly abnormal rectal examination findings |
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Equine Exploratory Surgery
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-Done in a very routine way
-Start with cecum, should appear first -Most is related to large colon and small intestine, most often where issues occur -Also want to palpate stomach, pylorus, spleen, liver, kidney --nephrospenic ligament -Duodenum cannot be exteriorized |
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The Cecum
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-First organ noted on abdominal incision
-Sits mostly on right side of abdomen -Occupies majority of the right side -Can feel sacculations and ventral/medial band on palpation --ventral and medial bands fuse near apex -Attached to the dorsal body wall at base -Located between the ileum and large colon -About 1m long -Apex is near ventral midline -Highly sacculated organ with 4 bands -Dorsal body wall attachment is important! -“Tourguide” to abdomen, allows location of ileum to look at the rest of the small intestine |
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Cecum communication
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-Communicates with right ventral colon via cecocolic orifice
--caudal part of cupula -Cecocolic fold runs from lateral aspect of the right ventral colon to lateral band of the cecum --identify to figure out if things are twisted --determines proper or improper position of cecum and colon |
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Large colon in the horse
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-Originates at cecocolic orifice in right ventral colon
-Ends in transverse colon, cranial to root of the mesentery --cannot exteriorize -Occupies majority of the equine abdomen -Can exteriorize most of the large colon, starting with pelvic flexure -Sternal flexure between right ventral colon and left ventral colon -Pelvic flexure between left ventral colon and left dorsal colon -Diaphragmatic flexure between left dorsal colon and right dorsal colon |
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Normal large colon in horse
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-Pelvic flexure on left
-should feel cecum on right |
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Equine Colon Anatomy
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-Need to know the normal position to know if position in normal
-Need to know which oart of the colon you are looking at or exteriorizing -Important for repositioning the colon back in the abdomen |
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Small intestine
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-Important to examine from aboral to oral, NEED to go in order!
--start with ileum -Can find simple obstructions, entrapment, strangulations, inflammatory process |
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Ileum
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-Enters cecum on ventral and medial aspect
--ileocecal orifice (not visible) -Ileocecal fold goes from antimesenteric surface of the ileum to the dorsal band of the cecum --once ileocecal fold is found, can locate and evaluate small intestine --Makes a V between ileum and cecum |
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Anatomic features of the ileum
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-dorsal Anti-mesenteric band
-Unique vascular pattern --ileocecal artery is parallel to the ileum (branch of cranial mesenteric artery) --know the start of the jejunum because vasculature becomes arcuate |
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Evaluating the Jejunum
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-Arcuate blood supply from cranial mesenteric artery
-25m long -Duodenocolic fold at junction of duodenum and small colon/transverse colon jct -Duodenum is attached to the dorsal body wall -Trace jejunum |
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Duodenocolic Fold
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-Between duodenum and colon
-Not able to be exteriorized during surgery, can only palpate |
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Evaluating the Duodenum
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-1m long
-Travels caudal to the root of the mesentery -Runs cranially towards the stomach along the right side of the body wall -S-shaped sigmoid curve near pyloris --contains duodenal papilla with bile and pancreatic duct -Usually not a site of disease |
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Evaluation of the stomach on colic surgery
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-Palpate the pylorus, has muscular valve-like feel
-Should have palpable lumen -Located on left of midline -Pylorus and esophageal sphincter are very close together -Feel for duodenal thickening, inflammation, or stricture -Pyloric thickening or stricture -Gastric foreign body or outflow obstruction |
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Transverse colon
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-Termination of right dorsal colon
-Ends at the small colon -Runs from the right side of the body to the left -Cannot exteriorize or visualize, but needs to be palpated --make sure nothing is wrong! -Attached dorsally to body wall -Common site of simple obstruction --enterolith, fecolith, trichophytobezoar, sand impaction, gravel impaction, firm feed material |
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Anatomy of the Small Colon
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-Transverse colon runs into the small colon, which becomes the rectum
-Fan-shaped mesocolon, 80-100cm at midpoint -Can exteriorize most of it, just not oral and aboral ends -About 4m long -Broad mesenteric and anti-mesenteric bands -Usually feel fecal balls and sacculations -Need to be careful with palpation, has a lot of fine vessels and arcuate vasculature -Common site of simple obstruction -can be entrapped or incarcerated -subject to trauma, inflammatory processes, or neoplasia |
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Evaluation of the Liver
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-Cranial to the stomach
-One of the largest organs in the horse --right lobe, left lobe, quadrate lobe, caudate lobe (largest, part of epiploic foramen) -Typically very stable with 6 ligaments supporting position in abdomen -Right lobe atrophy can occur with certain types if displacements -Cholelithiasis is possible -Neoplasia (biopsy) |
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Epiploic Foramen
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-Potential opening to the omental bursa
-Commonly associated with small intestinal entrapment -Borders: --caudate lobe of the liver --caudal vena cava --pancreas and hepatoduodenal ligament --Portal vein -Not visible -Some big anatomic vessels in the area! Need to be careful! |
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Evaluation of the Spleen
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-Caudodorsal to cranioventral placement, falciform shape
-50cm long, 25cm wide -Important vascular structures -Phrenic nerve enters from visceral side at the hilus -Nephrosplenic ligament is most important |
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Other structures to evaluate during colic surgery
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-Kidneys
-Bladder -Reproductive tract -Diaphragm |
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Structures that cannot be exteriorized during colic surgery
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-Base of the cecum
-Right dorsal colon -Transverse colon -Oral and terminal 30cm of small colon -Terminal ileum -Duodenum, pylorus, stomach -Much viscera (spleen, liver, bladder) |
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Evaluating structures not accessible through ventral midline incision
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-Laparoscopy
-Flank incision --uterine torsion --kidney --nephrosplenic space ablation -17th or 18th rib resection --typhlectomy |
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Colic Surgery Summary
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-Not a visual sport! |
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Rumen
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-Finely tuned fermentation vat
-Can collect rumen samples to see how rumen is doing --Stomach tube, sample acidity can be modified by saliva, saliva is alkaline --needle into rumen through body wall -Normal pH: 6-7, just a little acidic -Look at protozoa for an indication of rumen health --protozoa die first if there is an issue --should see 5-10 protozoa swimming around in rumen in healthy cows |
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Rumenocentesis
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-Needle into the rumen from the body wall
-Easy to do, can do with one person --stomach tube needs 2 people at least -More representative sample of rumen -Do not have alkaline saliva throwing off pH of the sample -May cause cellulitis or infection of the needle path |
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Rumen Fistula
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-Allows re-seeding of the rumen, transfaunation
-Permanent hole in the rumen and body wall |
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Bloat
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-Distension of the rumen
-ALL rumen diseases involve bloat -Failure to eructate is most common cause of bloat in cows --Can also be due to increased gas production, but rarely |
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Rumen lactic acidosis
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-“Grain overload”
-Over consumption of carbohydrates -Results in over-production of acids --Excessive and rapid production of acids -Gradual increase in carbohydrate allows cow rumen to adapt, microbial population changes over time -If left unchecked, animal will eat grain to its heart’s content |
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Situations leading to rumen lactic acidosis
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-“Grain overload”
-Break into the grain storage room -Access to pasture with grains and weeds -Feeding accident -Bully cow in group feeding situation -New arrival into herd, sudden change in diet -Feedlots -Dairy lactation diet |
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Pathogenesis of Rumen lactic Acidosis
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-“Grain overload”
1. Ingestion of carbohydrate 2. Rapid fermentation of carbohydrate leads to production of volatile fatty acids (VFAs) --acetate, butyrate, proprionate, lactate 3. Initial drop in pH occurs due to rapid fermentation and production of VFAs --pH drops to 5.5 4. Gram- bacteria and protozoa die (lactate consumers) --lactate producers are favored with low pH, Strep bovis --lactate is no longer consumed, but is produced 5. Lactic acid accumulates in rumen, pH drops below 5.5 |
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Rumen and acid
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-Rumen does not have defensive factors against acid
-Abomasum can resist acidic conditions, rumen cannot -Rumen wall will become ulcerated, which leads to bacterial translocation into blood stream and septic shock -Metabolic acidosis results due to absorption of acid, systemic absorption -Large accumulation of small molecules in the rumen changes osmotic pressure, pulls water into rumen --results in 3rd spacing, dehydration, and hypovolemia --Rumen will be big and fluid-filled |
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Clinical signs of Rumen lactic Acidosis
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-Acute onset
-Depressed animal -Cow looks colicky due to ulcerations in rumen --kicking at belly, grinding teeth -Dehydrated, sunken eyes -Tachycardia due to hypovolemia -Tachypnea -Rumen is distended, can ballot to feel big, distended rumen -Rumen atony, dorsal distension with rumen gasses, cow looks bloated -Diarrhea -Cow may look neurologic -Death! |
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Diagnosis of Rumen Acidosis
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-Rumenocentesis, look at pH
-Blood work --lactate (only measures human form, L-lactate) --pH --PCV, look for dehydration |
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Sequelae of Rumen Acidosis
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-Bacteria or fungi invade rumen wall
--mycotic rumenitis, fungi invade through denuded rumen wall (no treatment) --abscesses in rumen wall --liver abscess -Thiamin deficiency can lead to polioencephalomalacia -Laminitis |
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Treatment for Rumen Acidosis
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-Empty out rumen! Get rid of acid and wash walls
-Triage cows --ignore or euthanize recumbent cows with dramatically increased HR, will probably die anyway --Monitor cows that look OK --Focus on “middle group” of cows -With acute treatment, prognosis is good -Fluids, rumenotomy -Bicarbonate to buffer acids -Antibiotics to prevent liver abscesses and rumen abscesses --penicillin -Thiamin to prevent polioencephalomalacia -Rumen transfaunation |
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Traumatic Reticuloperitonitis
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-“Hardware Disease”
-Common in cows fed total mixed ration --nails, bailing wire, cows eat EVERYTHING -Usually causes localized peritonitis |
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Peritonitis in Cows
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-Infection of the peritoneal cavity
-In cows source of bacteria is usually endogenous --leakage of GI contents into peritoneal cavity -Reticulum: traumatic reticuloperitonitis -Perforated abomasal ulcer -Uterine perforation during dystocia -Pipette injury to uterus during AI or metritis treatment -Surgical complications |
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Clinical signs of Traumatic Reticuloperitonitis
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-Acute decrease in milk production
-Fever -Pain --Tachycardia --reluctance to move or walk, may look stiff --stands with elbows abducted to alleviate pain --No ventroflexion due to pain, withers pinch test may get a grunt -Bloat! |
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Diagnosis of Traumatic Reticuloperitonitis
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-Imaging (radiographs, ultrasound)
-Abdominocentesis (not usually done) -Blood analysis, look for fibrinogen |
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Treatment of Traumatic Reticuloperitonitis
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-Medical vs. surgical treatment
-Both have same recovery rate |
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Medical treatment of traumatic reticuloperitonitis
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-Antibiotics (penicillin, ceftiofur)
-Analgesia (Banamine IV) -Magnet to stop movement of metal -Restrict exercise -Cheaper, less invasive treatment -Metal stays in the body, can migrate and do more damage --eventually metal will corrode and dissolve |
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Surgical treatment of Traumatic Reticuloperitonitis
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-Rumenotomy
-Can confirm diagnosis, remove metal so it does not move anymore --remove cause of damage -Expensive! -More possible complications |
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Disseminated peritonitis in Cows
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-Septic shock
-Ascites due to inflammatory exudate and fluid in the abdomen -Look at PCV and TS for diagnosis --Normal: 32, 7.0 --dehydrated: 45, 8.2 (both are increased) --Disseminated peritonitis: 45, 5.0 (PVC is increased, protein is decreased) -“Splitting” of PCV and protein is a bad sign |
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Prognosis for Peritonitis in Cows
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-Localized peritonitis has good prognosis
-Disseminated peritonitis has poor prognosis |
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Rumen gas production
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-Gas is produced in lower liquid layer
-Gasses bubble up and become free gas in dorsal part of the rumen -CO2 and CH3 are most common gasses -Eructation releases gas --due to vagal nerve stimulation |
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Failure to Eructate in Cows
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-Most common cause of bloat in cows
-Can be mechanical, paralytic, or frothy -Need to be able to differentiate between free gas and frothy gas bloat! --pass a stomach tube, look for foam on end of tube |
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Mechanical bloat
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-Due to stenosis or obstruction of the esophagus
-Can be due to animal lying on its side or back --lateral recumbency, dorsal recumbency --Fluid blocks opening |
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Paralytic bloat
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-Anything that causes decreased smooth muscle contraction of the rumen
-Vagal nerve defecits -Botulism, tetanus, milk fever |
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Frothy Bloat
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-Causes viscosity and surface tension changes
--surface of the rumen changes -Foam cannot be eructated! -Related to diet --cattle turned out onto lush, leguminous pastures, rich in chloroplast production -Rumen expands, compresses diaphragm and chest cannot expand --Rumen compresses vena cava, reduces cardiovascular return, results in cardiovascular collapse |
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Treatment for Bloat
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1. Trocarize the rumen
--put hole in rumen at paralumbar fossa --temporary, emergency procedure --has complications, but can be life-saving 2. Poloxalene “therabloat” --detergent, breaks down foam --Give before emergency treatment 3. Put a stick in cow’s mouth --makes cow salivate, saliva has mucins that prevent bloat |
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Causes of Bloat in Cows
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-Lactic Acidosis
-Frothy bloat -Traumatic reticuloperitonitis -Esophageal obstruction -tetanus -Milk fever, hypocalcemia -Vagal indigestion |
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Vagal indigestion in cows
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-Chronic forestomach emptying disorder that results in decreased activity
-Type I: failure of eructation -Type II: failure of omasal transport, rumen is not emptying and continues to expand -Type III: pyloric obstruction, problem with abomasal emptying |
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Type I vagal indigestion in cows
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-Failure of eructation |
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Type II vagal indigestion in cows
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-Failure of omasal transport
-Usually due to abdominal adhesion --Adhesions prevent contraction and expansion of the rumen -Sequela of hardware disease -Can also be due to liver abscesses -Nerve endings in the wall of the reticulum are affected -“Papple” shape to cow, Apple on left and pear on right --dorsal and ventral distension on left --ventral distention on right --distention is due to rumen on the right |
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Type III vagal indigestion
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-Pyloric obstruction
-Displacement of abomasum --Secondary to RDA with volvulus --if goes on for too long can cause damage to nerves -Commonly lymphosarcoma that causes space-occupying lesion, obstructs pylorus -HCl builds up in abomasum, results in metabolic Alkalosis, acid is retained in the abomasum -“Papple” shape |
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Type II vs. Type III vagal indigestion in cows
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-Type II: allows abomasal emptying
--HCl will be normal -Type III: no abomasal emptying --HCl stays in abomasum, results in metabolic alkalosis -Both have poor prognosis! |
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Diagnosing bloat
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1. Pass stomach tube
--does not pass: esophageal obstruction --get foam, frothy bloat --get gas, move on 2. Check pH of rumen sample --pH less than 5.5: Lactic Acidosis/grain overload --pH 6-7 or slightly increased, move on 3. Check for pneumonia --present: type I vagal indigestion --absent: move on 4. Check for fever, pain, and acute onset --Present: traumatic reticuloperitonitis --absent: vagal indigestion type II or type III 5. Test Cl or bicarbonate levels --low Cl: type III vagal indigestion, pyloric obstruction --normal Cl: type II vagal indigestion, omasal emptying failure |
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Hepatic Lipidosis
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-“Fat cow syndrome” or “chronic ketosis”
-Excessive accumulation of triglycerides in the liver -Secondary to excessive fat mobilization from adipose tissue -Fat mobilization is induced from negative energy balance and hormonal changes -Multifactorial condition -Occurs in over-conditioned cows after parturition -Progressive depression and failure to respond to treatment of other concurrent diseases -Seems to be reversible in cows |
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Situations leading to negative energy balance
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-Lactation
-late gestation -Multiple fetuses -Malnutrition |
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Clinical signs of Hepatic lipidosis in Dairy cows
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-Over-conditioned cows, obese
-Cows that lose weight quickly -Depression, weakness, can lead to recumbency -Anorexia, decreased rumen motility -Decreased milk production -Other concurrent diseases --retained fetal membranes, metritis, mastitis, DA |
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Clinical signs of Heaptic Lipidosis in Beef cows
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-Poor body condition
-Long Hair coat -Recumbent but alert -Diarrhea |
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Clinical signs of Hepatic Lipidosis in Small Ruminants
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-Separation from the rest of the herd
-Depression, weakness leading to recumbency -Anorexia -Neurologic signs --appears blind --tremors --star gazing --Incoordination --circling --grinding teeth |
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Diagnosis of Hepatic lipidosis in cows
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-Ketonuria
-Elevated GGT, AST, SDH -Elevated serum free fatty acids and non-esterified fatty acids -Decreased serum triglycerides and cholesterol -Serum bile acids may be elevated (difficult to interpret in cattle) -Definitive diagnosis based on histopathology of liver biopsy |
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Liver ultrasound for hepatic lipidosis in cattle
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-Enlarged liver
-Rounded edges when they should be sharp |
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Liver Biopsy of cow with hepatic lipidosis
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-Cow needs to be restrained in standing stocks, sterile preparation of right 11th intercostal space
--intersection between line extending from tuber coxae and point of the shoulder and 11th intercostal space -Trucut biopsy needle -Definitive diagnosis based on histopathology of liver biopsy --some fatty infiltration is normal in post-partum dairy cows, but severe or marked infiltration is not normal |
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Pathogenesis of Hepatic Lipidosis in Cows
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-Liver is site of gluconeogenesis in cows, 85% of gluconeogenesis
-During negative energy balance, blood glucose drops and causes decrease in insulin:glucagon ratio -Hormone-sensitive lipases are activated, FFA, NEFA, and glycerol are released into bloodstream -In liver glycerol is used to produce glucose or can be recombined with FFA to make triglycerides -breakdown of FFA via b-oxidation results in excess acetyl CoA that is converted into ketone bodies -Liver is overwhelmed with mobilized FFAs, increased triglycerides are deposited in liver -Triglycerides do not leave liver --rate of hepatic triglyceride formation exceeds formation and release of VLDL into peripheral circulation |
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Treatment of Hepatic Lipidosis in Cattle
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-Remove cause of negative energy balance, if possible
--Treat underlying disease --Induce parturition or emergency C-section -Provide Energy: IV dextrose, CRI of 5% dextrose --may also give insulin -Propylene glycol: glucose precursor -Transfaunation, provides VFA as glucose precursor -Glucocorticoids can be given to induce gluconeogenesis, increase appetite, reduce milk production -Lipotrophic agents may help reduce lipolysis in adipose tissue |
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Insulin as treatment for hepatic lipidosis in cattle
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-Suppresses fatty acid mobilization
-Increases tissue uptake of glucose -Low dose of long-acting insulin -Need to keep a close eye on blood glucose! |
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Lipotrophic agents as treatment for Hepatic lipidosis in cattle
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-Choline, methionine, niacin
-May help reduce lipolysis in adipose tissue -May help increase fat mobilization in liver |
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Prevention of Hepatic Lipidosis in Cattle
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-Avoid obesity in dry cows
--keep BCS 3/5-4/5 -Improve dry matter intake arounf parturition --transition diet high in energy and adequate fiber -Prevent or treat post-partum diseases --milk fever, mastitis, metritis -Feed glucose precursor before and after calving --propylene glycol, niacin, etc. |
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Liver Abscesses in Cows
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-Can be seen in any species, ar more prevalent in ruminants
-Most common in beef cattle fed high carbohydrate diets (feedlot cattle) -Primary etiologic agent is Fusobacterium necrophorum --Arcanobacterium pyogenes, Streptococcus, Staphylococcus, and Bacteroides are also possible |
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Clinical signs of Liver Abscesses in Cows
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-Most are subclinical and diagnosed at slaughter
-Weight loss or decreased weight gain -Decreased milk production -Partial anorexia -Fever -Pain when moving or lying down -Diarrhea -Epistaxis, hemoptysis -Pneumonia, dyspnea -Photosensitization, icterus (rare) |
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Diagnosis of Liver Abscesses in Cows
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-CBC:
--neutrophilia --increased fibrinogen --Anemia is possible -Chem: --hyperglobulinemia --hypoalbuminemia --elevated GGT or AST -Post-mortem exam |
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Ultrasound for Liver Abscesses in Cows
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-Can identify if abscess is on superficial aspect of liver
-Abscesses appear as hypoechoic capsules enclosing an anechoic area of fluid and hyperechoic areas of pus -Cannot rule out liver abscesses based on negative ultrasound |
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Pathophysiology of Liver Abscesses in Cows
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-Necrophorum is part of normal rumen and intestinal flora
-Erosion of rumen epithelium due to grain overload, lactic acidosis, and rumenitis allows bacterial translocation -Bacteria Enters liver via portal vein -F. necrophorum produces leukotoxin, destroys leukocytes -In calves, can be due to umbilicus infection |
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Liver Abscess Sequelae
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-Encapsulated with connective tissue
-Can also erode large veins -May rupture into vein or form thrombus in caudal vena cava -Emboli can be carried to right heart and lungs, leads to hematogenous pneumonia with sepsis and pulmonary thromboembolism |
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Treatment of Liver Abscesses in Cows
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-Usually not done, usually not diagnosed until slaughter
-Prognosis is poor and long-term antibiotics have long meat withhold -If treating, treat with penicillin, ceftiofur, oxytetracycline, or macrolides -Supportive treatment --fluids, dextrose, transfaunation |
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Prevention of Liver Abscesses in Cows
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-Slowly increase grain fed over 3-4 week period
-Add long-stemmed or coarsely chopped hay, prevent rumen acidosis -Antibiotics can be added to cattle rations -Leukotoxin-based F. necrophorum vaccines can provide some protection |
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Liver flukes in Cattle
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-Most common liver fluke in ruminants is Fasciola Hepatica
-Most infections are from grazing in and around water and habitat that stays wet for more than half the year -South central states, Florida, Pacific NW -Life cycle has asexual multiplication phase in snail intermediate host -Transmission in southern states is higher during early spring and early summer -Transmission in western states is higher in late spring, summer, and fall |
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Clinical Signs of Liver Flukes in cows
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-Most often observed in late fall or winter, depending on geography
-most often subclinical -Reduced weight gain and poor feed efficiency -Decreased milk production -Longer dry period, longer to breed back -In severely infected animals may see weight loss, emaciation, depression, submandibular edema, anemia, rough coat, icterus -Migration of flukes across liver parenchyma forms necrotic tracts --primary predisposing factor for C. novyi (Black disease) and C. haemolyticum (Bacillary hemoglobinuria) infections |
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Diagnosis of Liver flukes
|
-Fecal float
-CBC/Chem: will see anemia, hypoproteinemia, mild eosinophilia --elevated liver enzymes, elevated bilirubin -Liver ultrasound and biopsy may help to rule out other liver diseases --may also be able to visualize migrating tract and biliary hyperplasia -Post-mortem exam may provide definitive diagnosis |
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Pathophysiology of Liver flukes in Cows
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-Anemia and hypoproteinemia due to feeding
-Cause direct damage to liver parenchyma during migration --biliary hyperplasia and fibrosis of liver parenchyma -Migration tract can predispose animal to infection by C. novyi and C. haemoliticum |
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Treatment of Liver flukes in Cows
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-Prevention is key!
-Routine fall or late fall/winter treatment --after end of transmission period -Flukicidal drugs: --albendazole --clorsulon |
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Neonatal Development of the Abomasum
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-Abomasum is primary stomach compartment during development
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Adult cow stomach Compartments
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-Rumen 80%
-Abomasum 8% -Omasum 7% -Reticulum 5% |
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Abomasal Anatomy
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-Abomasum is most distal stomach compartment
-Right side of midline, craniovental part of abdomen -Greater omentum connects to greater curvature of the stomach -Lesser omentum connects to lesser curvature of the stomach |
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Physiology of the Abomasum
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-Only gastric compartment with a glandular compartment
-Critical role in digestion -Secretes digestive juices and HCl -Normal pH 3.0 -Innervation via vagus nerve |
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Common disorders of the Abomasum
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-Left displacement LDA
-Right displacement RDA -Volvulus RVA -Abomasal ulcers (young cows, dairy cows) -Lymphosarcoma -Abomasal impaction (usually sand) -Foreign bodies (young animals) |
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LDA
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-Abomasum relocates to the left side of midline between rumen and body wall
-Most common surgical problem encountered in dairy cows --0.35-4.5% of all dairy cows -Sporadic in calves, dairy bulls, and beef cattle -ALWAYS check for a ping |
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LDA predisposing factors
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-Early lactation
--57% occur within the first 2 weeks after parturition --80% within the first month -Rapid diet change, rapid increase in feed concentrates -Concurrent disorders --hypocalcemia, ketosis, fatty liver, mastitis, retained placenta, metritis -Atony of the abomasum -Twins -Pregnancy displaces the rumen and at the end of pregnancy there is increased space in the abdomen |
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LDA Diagnosis
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-Decreased milk production and/or feed consumption
--Acute drop in milk production -Change in fecal character -Hypomotile rumen -Left-sided ping -Ketosis -Normal TPR unless concurrent disease is present -“Floating DA” -Can be low or high on the flank, be sure to ping the entire area |
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RDA
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-Abomasum dilates and floats dorsally on the right side of the cow between the liver and right body wall
-More rare than LDA -Pylorus moves ventral, stays caudal |
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RVA
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-Abomasum and attached structures rotate counterclockwise around an axis
-Axis is through center of the lesser omentum -NOT a torsion, wraps around the root -Always a clockwise rotation -Pylorus moves craniodorsally |
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RDA clinical signs
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-Decreased milk production or feed consumption
--Acute drop in milk production -change in fecal character -Hypomotile rumen -Ketosis -Normal TPR unless concurrent disease is present -Ping in middle of the right flank over 10-13th ribs -May or may not see abdominal distention -Sometimes are able to see the abomasum behind the last rib |
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RVA diagnosis
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-Same as RDA and LDA
-Cow is SICK! -Dehydration -Muscle fasciculations, teeth grinding -Abdominal distension due to fluid accumulation in abomasum -Rectal exam will have minimal feces, may or may not be able to palpate abomasum -Ping will extend further cranial -Succussion, ballotment with auscultation, “Fluid ping” -Over time wall of abomasum will become necrotic --probably will not rupture, but could |
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LDA/RDA lab findings
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-Acute LDA/RDA will not have any abnormalities
-Metabolic hypochloremic alkalosis --HCl is trapped in abomasum, H does not get into circulation -Hypokalemia -Hypocalcemia -Hyperglycemia or hypoglycemia -Ketonuria -Paradoxical aciduria |
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LDA/RDA Management
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-Surgical vs. medical
-Based on clinician preference and comfort level -Type of displacement, always cut a RVA -Cow factors -Economics -Facilities -Assistance available |
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Medical management of LDA/RDA
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-Roll cow to reposition the abomasum
-Give laxative and Ca -Cheap, no surgical skills needed -High incidence of recurrence -Not an option for RDA or RVA -Need to lay cow down, need people -Only really done for LDA |
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Surgical Management of LDA/RDA
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-Open surgery:
--right flank omentopexy/pyloropexy --Right paramedian abomasopexy --Left flank abomasopexy -Blind approach: --toggle --blind stitch -Laparoscopy: assisted abomasopexy |
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Supportive treatment for LDA/RDA
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-Give in addition to surgical treatment
-Correct Dehydration, oral or IV fluids -Correct electrolyte and acid-base disturbances -Correct ketosis (dextrose, propylene glycol) -Correct all other concurrent diseases -Give saline! |
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Prognosis for LDA/RDA
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-Very good with surgical correction if there are no concurrent diseases
-Most return to lactation level |
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Prognosis for RVA
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-Depends on degree of damage to abomasal wall and metabolic abnormalities
-May have permanent damage to vagal nerve -May have irreversible stretching of abomasal wall, results in vagal indigestion syndrome --if there is damage to the abomasal wall, will never regain normal motility -50% have post-op complications |
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LDA/RDA/RVA prevention and Control
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-Introduce concentrates and silage before calving
-Increase particle size of feed, add forage -Prevent hypocalcemia -Prevent or detect periparturient diseases early |
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Abomasal Ulcer Predisposing Factors
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-intensive management practices
-Stress --parturition, change in housing, change in feed, concurrent diseases -high starch diets, concentrates, corn silage -Lymphosarcoma -Misuse or overuse of NSAIDs -Bacterial contribution has not been proven |
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Non-perforating Abomasal Ulcer: Type I
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-Perforation is not complete
-Hard to diagnose, always a suspicion -Mucosal and some submucosal tissue loss -May be able to diagnose with ultrasound -Focal mural thickening -Local serositis -Animal will be anorexic with decreased rumen motility -Possible low-grade fever -Grinding teeth |
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Non-perforating Abomasal ulcer with severe blood loss: Type II
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-Ulcer is in area of a vessel
-Penetration of mucosa and submucosal blood vessel -Hemorrhage into abomasum -Partial anorexia and decreased rumen motility -Pale mucus membranes, tachycardia, cold extremities -Melena -Commonly seen with lymphosarcoma -Rarely perforates |
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Abomasal Perforation with local peritonitis: Type III
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-Looks like traumatic reticuloperitonitis
-Penetration from mucosa to serosa -leakage of abomasal contents -Localized peritoneal reaction with adhesions -Anorexia -Low-grade fever -Decreased or absent rumen motility -Localized abdominal pain -Ultrasound should show localized peritonitis -Omentum patches and seals holes |
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Abomasal Perforation with diffuse peritonitis: Type IV
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-Penetration from mucosa to serosa
-Widespread contamination of peritoneal cavity with abomasal contents -Significant exudates in peritoneal cavity -Fibrin deposition -Total anorexia -Fever, then hypothermia -Ileus -Possible diarrhea -Tachycardia -Dehydration -Shock -Recumbent animal with grunt on respiration -Usually die very quickly -Fulminant, acute peritonitis |
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Diagnosis of Type I abomasal ulcer
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-Often lack any detectable signs
-Suspect if cow is at-risk, poor appetite, decreased weight gain, decreased rumen motility -May have positive fecal occult test -Thickening of abomasal wall on exploratory surgery or ultrasound |
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Diagnosis of Type II abomasal ulcer
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-Suspect if there is melena and anemia
-If secondary to lymphosarcoma, may see BLV serology -May have atypical or neoplastic lymphocytes on abdominocentesis -Wall of abomasum is severely thickened |
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Diagnosis of Type II abomasal ulcer
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-Suspect if there is anorexia, fever, pain in craniovental abdomen
-CBC will show elevated fibrinogen, leukocytosis, and elevated protein -Abdominocentesis is diagnostic unless peritonitis is chronic and localized -Abdominal ultrasound may be useful -Exploratory laparotomy |
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Diagnosis of Type IV Abomasal ulcer
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-Suspect if there are acute signs of illness, shock, diarrhea, or hypothermia
-CBC will be normal to low --serum protein in the face of hemoconcentration, elevated fibrinogen -Abdominal ultrasound will show large volume of free abdominal fluid -Abdominocentesis should confirm diagnosis |
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Medial treatment for Abomasal ulcers
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-Broad spectrum antibiotics
--guide with abdominocentesis and culture -Give blood transfusion if needed, PCV less than 15 -Antacid use is usually debatable, can be helpful in young calves because they are still basically monogastric --Oral antacids are inactivated in the rumen --IV antacids are preferred, but are cost prohibitive and not sure if they work or not -Mucosal protectants are inactivated in rumen -Supportive treatment with fluids and nutrition -Address concurrent diseases, reduce high-starch feeds |
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Surgical Treatment for Abomasal Ulcers
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-Medical treatment |
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Prevention of Abomasal Ulcers
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-Minimize stress in early lactation |
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Bovine Laparotomy Approaches
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-Right paralumbar fossa, right flank
-Left paralumbar fossa, left flank -Right paramedian |
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Indications for Right paralumbar fossa bovine laparotomy
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-Exploratory surgery when you suspect there is a problem on the right
-“ADR” cow -GI obstruction -Low Cl, metabolic alkalosis -Rumen chloride -Abdominal ultrasound -Abdominal distension -Colic signs -Ping on the right -Scant feces or no feces -Abnormal rectal exam or abnormal abdominal ultrasound -Small intestinal disorders -Cecum and colon srugery |
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Surgeries for LDA
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-Right flank incision
-Omentopexy -Pyloropexy |
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Surgeries for RDA/RVA
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-Omentopexy or pyloropexy
-Standing surgery is preferred with RVA --sick cow should not be put onto back |
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Small intestinal disorder surgery in cows
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-Right side surgery
-Hemorrhagic bowel syndrome -Intussusception -Small intestinal torsion at mesentery root |
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Cecum and colon surgery in cows
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-Cecal dilation or volvulus
-Atresia coli in a calf -Go in on right side |
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Standing anesthesia in a cow
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-Inexpensive
-Need standing stocks -Anatomy is in normal location, easier to identify things -Cow can go down! |
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General anesthesia in a cow
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-Expensive
-Done in referral centers only -Aspiration and muscle or nerve damage are concerns -More controlled environment |
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Preparation for standing surgery in a cow
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-Restraint is key!
--stocks of chute --alter --sedation is usually not needed, increases risk that cow will go down -Clip and aseptically prepare area -Local anesthesia: line block -Regional anesthesia: inverted L, Proximal paravertebral, distal paravertebral |
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Sedation drugs for bovine standing laparotomy
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-Acepromazine (0.03-0.05 mg/kg IV)
-Xylazine (0.02-0.05mg/kg IV) -Detomidine (0.01-0.02 mg/kg IV) |
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Line block in cows
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-Injection of analgesic agent directly on surgical site
-Infiltrate all layers --skin, muscles, peritoneum --may need a spinal needle hide is so thick -Convenient, easy -May cause tissue edema or affect healing -Anesthesia is only in a limited area |
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Inverted L anesthesia in cows
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-Blocks all nerves entering the surgical site
-Regional block -Vertical line: caudal to the last rib -Horizontal line: ventral to the transverse processes of the lumbar vertebrae -good for fat cows, small calves, and small ruminants -Need to do many injections! Lots of poking the cow |
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Proximal Paravertebral Anesthesia in Cows
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-Block as close to the spinous processes, hit nerve before dorsal and ventral branches split
-Deposit analgesic close to the intervertebral foramen -Blocks T13, L1, L2 -Inject at anatomical sites L1, L2, L3 -Gives regional anesthesia -Paralyzes lumbar and flank muscles, leads to relaxed flank -More difficult to execute |
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Distal Paravertebral Anesthesia in Cows
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-Lateral approach to the nerves
-Anesthetizes nerves after nerve has divided into dorsal and ventral branches -Blocks T13, L1, L2 -Anatomical sites L1, L2, L4 |
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Surgical Approach to Bovine Laparotomy
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-Ventral incision in middle of paralumbar fossa
-3-5cm ventral to transverse processes of lumbar vertebrae -Extends ventrally 20-25cm -3-5cm caudal to last rib |
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Incision of Bovine Laparotomy
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1. Skin
2. External abdominal oblique muscle 3. Internal abdominal oblique muscle 4. Transverse abdominal oblique muscle and peritoneum -Should see greater omentum, duodenum runs horizontally across incision within the omentum |
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Greater Omentum in Bovine
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-“Omental Sling”
-Suspended from dorsal roof -“Curtain” that divides right side of abdomen and caudal abdomen |
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Guidelines for Bovine Exploratory Laparotomy
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-Be systematic
1. Caudal abdomen should have: --reproductive tract, urinary bladder, left kidney (will feel like it is on right of midline), Descending Colon, Rectum 2. Cranial abdomen: --liver and gallbladder, should have smooth edges without adhesions or abscesses --gallbladder is often full in anorexic animals --Abomasum should be along right ventral body wall, fundus contains fluid ingesta --Pylorus is firm, sits at 9th and 10th costochondral junction, can be exteriorized 3. Palpate for adhesions or abscesses between reticulum and body wall or diaphragm 4. Identify omasum, caudal and medial to reticulum --firm and filled with ingesta 5. Find duodenum, ascending and descending --runs horizontally across incision, covered by superficial sheet of greater omentum 6. Find right kidney, dorsal to descending duodenum |
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Bovine Intestinal tract aboral to Abomasum Exploratory laparotomy
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1. exteriorize apex of cecum
2. Identify ileocecal junction 3. Identify proximal colon, ascending loop and spiral colon 4. Feel small intestine |
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Bovine abdominal Anatomy on the Left
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-Rumen
--dorsal sac, omental attachment -Spleen: sits dorsally and cranially on rumen -Check for LDA |
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Closing Bovine Laparotomy
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1. Body wall closure:
--#2 absorbable suture, simple continuous --peritoneum and transverse abdominal muscle closed together --internal abdominal oblique and external abdominal oblique closed together 2. Skin closure: --#2 non-absorbable suture, simple continuous/ford interlocking --leave several simple interrupted sutures at most ventral aspect of incision --leave penrose drain at ventral aspect of incision if contaminated surgery 3. Remove sutures after 15 days |
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Left paralumbar Fossa/Left Flank with Rumenotomy
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-Rumenotomy due to grain overload or toxicity in small rumimants
-Same as right flank approach, just on left -Exteriorize rumen with moist sponges before cutting into rumen --Prevent ingesta from going into abdomen -Use #1 suture material and simple continuous or cushing’s pattern for rumen -Avoid having a leaky weak point at ventral edge of invision |
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Rumen Board/Weingarth Apparatus
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-Board that can be secured to the skin of the cow
-Use non-traumatic clamps on wall of rumen, secure rumen outside of the body -Rumen hooks allow rumen to be hooked to the board, keep rumen out of the body |
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Closure for Rumenotomy
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-Double inverting pattern on rumen, double cushing
--#2 absorbable suture material -Close body wall same as right flank approach --peritoneum and transverse abdominal muscle, internal and external transverse abdominal muscles, skin -Leave penrose drain in bottom of incision for drainage |
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Right paramedian approach for cows
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-Mainly for abomasal pexy
-Make incision right in the area of the abomasum -Make incision midway between umbilicus and xiphoid process, just to right of midline -Will not have great exposure to anything besides omentum |
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Layers in right paramedian approach
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1. Skin
2. External sheath of rectus abdominus muscle 3. Rectus abdominus muscle 4. Internal sheath of rectus abdominus muscle 5. Peritoneum |
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Right paramedian closure
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1. Peritoneum, internal sheath of rectus abdominus, rectus abdominus, and external sheath of rectus abdominus are closed in same layer
--#2 absorbable material --simple continuous or simple interrupted pattern 2. Skin closed --#1 or #2 non-absorbable or absorbable material in simple continuous pattern |
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Post-operative management for Bovine laparotomy
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-Antimicrobials:
--contaminated surgery --field surgery --suspect bacteremia or endotoxemia --Only use antimicrobials legal to use in food animals! Think about withdrawal -Anti-inflammatory drugs (Banamine) -Fluids -Electrolytes -DExtrose |
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Right flank Omentopexy/Pyloropexy
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-Standing surgery
-No assistance needed -Good exposure of the abdomen -All types of displacements can be addressed -Can be difficult for inexperienced surgeons -Recurrence is more common -Poor exposure of the abdomen itself, can only see the pylorus |
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Steps in Right flank Omentopexy/Pyloropexy
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1. Incision
2. Explore abdomen, look at the rest of the abdomen --helps to diagnose underlying causes and prognosis 3. Localize abomasum 4. Decompress abomasum if LDA using needle attached to long piece of tubing --go in parallel and tunnel, then into lumen --prevents contamination of peritoneal cavity with abomasal fluid 5. Position abomasum correctly --cup abomasum, push down, then under rumen --“L” shaped motion --do not pull on omentum to reposition --easier to reposition RDA, basically repositions itself with deflation 6. Identify the pylorus by pulling gently on abomasum and finding attachment 7. Omentopexy and closure |
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Omentopexy Closure
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-Put pexy 1 hand distance behind the pylorus
-First layer is peritoneum and transverse abdominal muscle -Include bites of omentum in each stitch --“wedge” omentum into incision -Simple continuous pattern with absorbable material -Internal and external abdominal oblique muscles sutured together -Skin sutured last |
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Pyloropexy closure
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-Same as omentopexy, but do not go into pyloric mucosa and lumen! Stay in submucosa
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Complications of Right flank Omentopexy/Pyloropexy
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-Recurrence
-Infection of incision -Outflow obstruction at pylorus if pyloropexy is not properly placed |
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Right paramedian abomasopexy
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-Secure stabilization of the abomasum, abomasum itself is being pexied
-Easy surgical procedure -Works for all types if displacements -Good exposure of the abomasum, can see ulceration and adhesions -Have to put cow in dorsal recumbency, need assistance to lay cow down --not ideal for pregnant or very sick cows, lame cows -hard to reposition volvulus -Ventral incision, more prone to infection and herniation -Poor exposure of the rest of the abdomen, everything is covered by omentum |
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Right paramedian abomasopexy preparation
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-Lie cow down
-Need sedation, 30-45mg xylazine IV --conservative dose, can increase with experience --decreases stress for all involved -Clip and prepare ventral abdomen -Local line block along incision site |
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Right paramedian abomasopexy surgical approach
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-15-20cm incision 4-5cm caudal to the xiphoid
-Parallel and 3-4 cm to the right of midline -6 skin layers to go through -Abomasum usually floats to the top/replaces itself and is easy to decompress --exteriorize greater curvature of the abomasum into incision before recompression |
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6 skin layers in right paramedian abomasopexy
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1. skin
2.Subcutaneous Fascia 3. Thick external fascia of rectus sheath 4. Rectus Abdominus muscle 5. Thinner external fascia of rectus sheath 6. Peritoneum |
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Right praamedian abomasopexy closure
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-Close cow and include abomasum in 1st layer
-Only want to close the seromuscular layer of the abomasum, do not want to go into lumen --Pinch abomasal wall before taking a bite -Simple continuous pattern with #2 absorbable material --Will form adhesions regardless of the suture type |
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Right paramedian Abomasopexy Complications
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-Aspiration pneumonia
-Musculoskeletal injuries -Incision hemorrhage (avoid milk vein!!) -Dehiscence -Herniation, usually abomasum herniates through incision -Fistulation -Recurrence -Always need to worry when putting cown on her back without intubation or withholding food |
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Left flank abomasopexy
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-Standing procedure
-Can address adhesions between abomasum and left body wall or rumen -good for cows in later gestation -Need to have long arms! -Only works for LDA -Poor exploration of the rest of the abdomen, rumen is in the way -Need capable assistant to help with suture placement |
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Preparation of left flank abomasopexy
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-Standing procedure
-Clip and prepare left paralumbar fossa -Clip and prepare 20x20cm area cranially and ventrally on right side of cow -Flank anesthesia: paravertebral, inverted L, Line block -Ventral abdomen anesthesia: local anesthesia, 3-4cm to right of midline and 4-5cm caudal to sternum |
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Left flank abomasopexy surgical approach
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-Same as for right flank, just on left
-Localize abomasum -Place sutures in abomasum and deflate abomasum -Position abomasum into correct location -Tack abomasum through body wall on ventrum -Close left flank incision, standard closure -Cut ventral sutures in 10-15 days |
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Complications of left flank abomasopexy
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-Accidental damage to milk vein
-Entrapment of omentum or small intestine -Improper positioning of abomasum, can lead to partial outflow obstruction -Fistulation -Recurrence -Incisional infection |
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Toggle or Blind stitch/blind tack to correct LDA
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-Inexpensive and quick solution
-Secures abomasum without doing actual surgery -Do not know that you are for sure pexying the abomasum -Blind technique, can be risky! -requires dorsal recumbency -Requires assistance -ONLY for LDA! -No exploration of the abdomen |
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Toggle Pins Preparation
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-Clip and prepare abdomen before rolling cow
-Roll cow, secure legs and head -Anesthesia is not usually needed -Once the cow is on her back, work quickly! --some gas escapes from abomasum with rolling, and gas is needed to find the abomasum and secure it to the body wall |
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Toggle pin surgical procedure
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-Need to work QUICKLY!
-Locate the abomasum, ping -Place pins, toggle goes into the lumen of the abomasum -re-auscult for ping, place 2nd pin 5cm caudal to initial site -Decompress before pulling out trocar -Tie both sutures together and leave space for swelling -Let cow up, roll onto left side first, and auscult for ping on left and right -Cut sutures in 10-15 days --fibrous adhesion should be holding abomasum in place -If toggle fails, needs surgery! |
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Toggle Pin Complications
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-recurrence |
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Normal Umbilical anatomy
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-1 umbilical vein, originates from the liver |
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DDx for Umbilical mass
|
-Umbilical hernia
-Simple umbilical abscess, Omphalitis -Umbilical abscess with infection of umbilical remnants --urachal abscess --omphalophlebitis --omphaloarteritis -Patent urachus (rare in cattle, common in foals) -Urachal cyst -Hematoma |
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Umbilical hernia
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-Can be hereditary or due to infection
-Do not fix in breeding bulls! If hereditary, can be passed on to a lot of cows -Hernial ring: body wall defect -Hernial sac: what hangs down -Hernial content: omentum, abomasum, rumen, small intestine --mostly omentum -Size of hernia is based on hernia ring/body wall defect |
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Diagnosis of Umbilical hernia
|
-Palpation of a reducible mass with circumferential hernia ring
-Evaluate for abscess -Evaluate for strangulation --rare in cattle --will see abdominal pain, metabolic derangements |
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Conservative Management of Umbilical Hernia
|
-For small uncomplicated hernas
--less than 2-3cm -daily digital palpation -abdominal support bandages -local injection of irritants around hernia ring, cause reaction and swelling/fibrosis around hernia -hernial clamps or elastrator bands (be careful not to clamp something you should not) |
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Anesthetic considerations for herniorrhapthy
|
-Withhold hay 24-36 hours
-General anesthesia for large or complicated hernias or hernias in older animals -Local anesthesia for field situations or small, uncomplicated hernias -Sedation: xylazine, ketamine, triple drip -Epidural anesthesia: --0.15ml/kg 2% lidocaine --0.05 mg/kg xylazine -Local anesthesia |
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Herniorrhaphy Surgical Technique
|
-Make Fusiform incision on skin around umbilicus
-Dissect subcutaneous tissues down to the hernia sac and ring -Enter abdomen just lateral to the umbilical stalk --allow digital palpation of intraabdominal structures --do not go cranial or caudal, may hit umbilical remnants -Incision of abdominal wall is continued in fusiform fashion --trace umbilical ring --bleeding indicates good tissue --Do not take off too much tissue, just go right to the edge -May need to do resection and anastomosis of incarcerated small intestinal tissues -Simple continuous pattern or inverted cruciates on body wall --#1 or #2 vicryl or PDS -Subcutaneous tissues closed with simple interrupted sutures --0 or 2-0 vicryl -Skin closed with interrupted pattern --#1 absorbable or non-absorbable material |
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Details about Umbilical Hernias
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-Infection is #1 cause of recurrence/failure of hernia repair
-Peri-operative systemic antimicrobials are highly recommendded in field situations -Do not use non-absorbable suture material on the body wall, absorbable suture is a must! (Vicryl or PDS) -Limit bulky feeds for about 1 week post-op --prevent excessive tension on repair -Belly bands or abdominal support is also helpful |
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Uncomplicated Umbilical Abscess
|
-Usually happens right around birth
-Infection secondary to: --direct contact with contaminated environment during neonatal period --Hematogenous spread secondary to septicemia/bacteremia --Usually goes from umbilicus to body, but can go from body to umbilicus -Most common bacterial isolates: --Arcanobacterium pyogenes (Truperella) --E. coli |
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Diagnosis of Umbilical Abscess
|
-Digital palpation of external stalk
-Deep abdominal palpation --rule out concomitant infection of umbilical structures -Ultrasound, will show hyperechoic flocculent material |
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Management of Umbilical Abscesses
|
-Drainage and lavage or abscess cavity
-Systemic antimicrobials -Surgical resection of abscess cavity -Drainage should be performed before surgery! --about a week before, do not want contamination |
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Umbilical Abscess with Infection of Umbilical Cord Remnant
|
-Urachal abscess is most common
--cord extending caudal to umbilicus -Omphalophlebitis: --systemic signs of infection, pneumonia --cord extending cranial to umbilicus -Omphaloarteritis --can be unilateral or bilateral --cord extends caudal to umbilicus |
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Urachal abscess clinical signs
|
-Unthrifty animal
-Fever -Umbilical mass -Pollakiuria -Pyruia -Sediment on vulva |
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|
Urachal abscess Diagnosis
|
-Deep abdominal palpation
-Abdominal ultrasound -Urinalysis -Chemistry panel, look at BUN and Creatinine |
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|
Management of Urachal Abscess
|
-Lance and lavage abscess before surgery
-Systemic antimicrobials --Penicillin, ceftiofur --Cystitis and Pyelonephritis are not uncommon -General anesthesia is needed for surgery |
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Surgical management of Urachal Abscess
|
-Draining tract is oversewn to prevent contamination of surgical site
-Surgical approach is the same as for an opened herniorrhaphy -Enter abdominal cavity just lateral to umbilical stalk --prevent entering urachal abscess -Adhesions to omentum are carefully dissected --CAREFULLY -Isolate urachus, follow to the bladder --be careful not to penetrate urachus while dissecting -Apex of the bladder and urachal remnant are removed -Apex of bladder is closed -Abdomen is closed in regular fashion |
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|
Omphalophlebitis Clinical signs
|
-Umbilical mass
-Unthrifty -Fever -Signs of bacteremia or sepsis -Pneumonia and other systemic signs are present --liver abscess |
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|
Diagnosis of Omphalophlebitis
|
-Deep abdominal palpation
-Ultrasound exam: liver abscesses -Blood cultures |
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|
Management of Omphalophlebitis
|
-Lance and lavage external abscess if needed
-Systemic antimicrobials -Stabilize patient before general anesthesia |
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Surgical management of Omphalophlebitis
|
-Initial surgical approach is same as for urachal abscess
-Be careful when opening abdomen -Umbilical vein is carefully dissected up to the liver --DO NOT enter umbilical vein! -Trace, ligate, remove umbilical vein -Need to establish drainage -If infection is restricted to the umbilical vein, resect en bloc -If infection extends to liver abscess, umbilical vein is marsupialized with body wall |
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|
Omphaloarteritis diagnosis and clinical signs
|
-Looks same as urachal abscess (fever etc.) |
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|
Management of Omphaloarteritis
|
-Lance, lavage |
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Prevention of umbilical problems
|
-Clean calving areas |
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|
Camelid forestomach anatomy
|
-3 compartments
-Esophagus enters C1 only -All 3 compartments are glandular -No papillae in C1 -C3: only distal 1/5 has enzyme acid secretion --C3= “abomasum” |
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|
Track of Camelid GI system
|
-3 compartment stomach to duodenum
-Duodenum becomes small intestine, SI is perimeter of omental sling -Ileum and cecum -Centripetal loops of spiral colon, followed by centrifugal loops of spiral colon -Rectum and anus |
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Camelid Liver
|
-Right side of the abdomen
-Fimbriated border -Usually do not have a gallbladder -Bile duct opening is 16-20cm from the pylorus |
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Camelid Pancreas
|
-Caudal to the liver
-Flat structure, 15-20cm long and 3-6cm wide -Pancreatitis has been reported --Associated with equine herpes virus? |
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|
Painful camelid sigs
|
-Very variable!
-May not outwardly display discomfort at all -Camelids are very focused on herd behavior, isolation indicates pain -Tenesmus, lots of time straining over dung pile or frequent visits to dung pile -Cush when painful |
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|
DDx for camelid pain
|
-GI issue
-Uterine torsion -Urinary issue |
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Clinical signs of colic in a camelid
|
-Restlessness
-Cush in awkward position --legs extended, lateral recumbency -Frequent change in position -Abdominal distension -Tenesmus -Failure to pass normal manure -Regurgitation |
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Common causes of colic in new-world camelids
|
-Mechanical:
--simple obstruction without vascular compromise --strangulating obstruction -Inflammatory/metabolic: --enteritis --Peritonitis --Ulcerative disease (C3 or C1) --Forestomach acidosis --Hepatic lipidosis -Reproductive disease --uterine torsion and complications associated with correction --post-partum complications -Urethral obstruction |
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|
History of colic in camelids
|
-History is very important
-Management changes --feed, housing, transport, herd changes -Behavior changes -Stage of gestation, if applicable -Last urination -Last defectaion -Tenesmus |
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|
Physical exam od camelid colic
|
-Signs of severe inflammation/SIRS
--toxic sclera, fever --tachycardia, tachypnea --cardiovascular stability and perfusion -Abdominal distension, pain on palpation -Behavior on admission -Rectal exam |
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|
Hematologic and biochemical Analysis of camelid colic
|
-Complete hematological evaluation
-Chemistry profile --electrolytes, liver enzymes -Blood gas analysis, acid/base status -Whole blood or serum lactate -Serum amylase and lipase |
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|
Abdominal Radiographs for Camelids
|
-May see impacted C1 or C3
-Intestinal distension -Suspicion of peritonitis -Diaphragmatic hernia |
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|
Abdominal ultrasound for Camelids
|
-C1 takes up most of the left ventral abdomen, can see transverse pillar
-C3 occupies most of right ventral abdomen -Wall thickness should be 2-4mm -Intestinal structures are best seen in lower right paralumbar fossa --ascending colon has largest diameter |
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Abdominocentesis for Camelids
|
-Right paracostal approach may be most useful for obtaining peritoneal fluid
-Insert needle or teat cannula -Viscera may obscure ventral or paramedian approach --significant ventral abdominal fat -Ultrasound guidance |
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|
Passing tube on Cameilds
|
-Good diagnostic tool for colic
-Analyze C1 fluid --pH and Cl |
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|
Obtaining C1 fluid from camelids
|
-Orogastric method
--use soft speculum --aspirate contents --pass protected tube -Percutaneous method --clip and aseptically prepare left cranial abdomen --16 gauge, 7.5cm needle, 20cm caudal to the last rib -Insert needle perpindicular to the body wall |
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Common causes of acute GI disease in camelids
|
-Proximal obstruction
-Distal obstruction -Ruptured viscous -Peritonitis without rupture -Necrotizing enteritis |
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Proximal obstruction in camelids
|
-Intraluminal bezoar
-Infiltrative SI disease -Strangulating SI disease -May have milder signs of discomfort -Significant abdominal distension -May regurgitate or salivate -Normal rectal exam, decreased fecal production -Hypochloremic metabolic alkalosis -Hypokalemia is also common --sample of C1 fluid will have Cl more than 40 mEq/L -On ultrasound abdominal cavity will be filled with C1 |
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Etiology of proximal intestinal obstruction in camelids
|
-Bezoar, Impaction
-Strangulating obstruction -Clostridial enteritis -Infiltrative bowel disease --inflammatory or neoplastic |
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Prognosis for Proximal intestinal Obstruction in camelids
|
-Poor survival compared to distal obstruction
-Improved survival with trichophytpbecoar duodenal obstruction --suspect in camelids older than 1 year --Hypochloremic metabolic alkalosis --right paracostal surgical approach --good prognosis |
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|
Distal Intestinal Obstruction in Camelids
|
-Signs of colic are often severe
-Tenesmus -Decreased fecal output or no fecal output -Abnormal rectal findings |
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|
Diagnostics for Distal intestinal Obstruction in Camelids
|
-Hypokalemia is common
-Abdominal radiographs may show distended spiral colon or cecum -Abdominal ultrasound may show increased abdominal fluid, distended colon or cecum --big distended loops -Will be able to feel on rectal exam |
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|
Etiology of Distal intestinal obstruction in Camelids
|
-Spiral colon fecolith
--centrifugal loops -Impaction of spiral colon or cecum -Spiral colon torsion --mesenteric torsion -Ileocecal intussusception |
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|
Prognosis for Distal intestinal Obstruction in camelids
|
-Survival is better than proximal obstruction
-More prompt surgical intervention -Less metabolic derangements, may not appear as sick |
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|
Initial stabilization of camelid with colic
|
-IV fluid therapy
--give 20ml/kg bolus, then re-evaluate --maintenance rate 3-4 ml/kg/hour -Evaluate resuscitation --peripheral perfusion, skin turgor, lactate, urine production -Look for subtle behavioral changes -Correct any electrolyte imbalances -Monitor fecal production -Re-evaluate frequently! |
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|
Indications for surgery in Camelids with colic
|
-Clearly abnormal rectal exam
-Significant radiographic or ultrasonographic abnormality -Change in abdominocentesis -Does not respond to medical management -PAIN |
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|
Surgical intervention for colic in camelids
|
-Ventral midline celiotomy is most common
-Suspect proximal intestinal obstruction, right paracostal approach is recommended -Laparoscopy is lesion specific -Success depends on lesion and duration of clinical signs --distal impaction and simple obstruction have best prognosis -Torsion of mesentery/spiral colon carry poor prognosis |
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|
Forestomach acidosis in Camelids
|
-Depression, diarrhea, weakness, ataxia
-Tachycardia, tachypnea -Metabolic acidosis -C1 fluid will have low pH, less than 5.5 --May be yellow and foul-smelling --few protozoa, bacterial overgrowth is present, gram+ bacterial species |
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|
Treatment of forestomach acidosis in camelids
|
-IV fluid therapy with sodium bicarbonate
-Orogastric tube to relieve bloat -Transfaunation -Additional treatment of banamine or antimicrobial theraphy -Success rate is 66% survival with aggressive treatment |
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|
Ulcerative disease in camelids
|
-Diagnosis of exclusion
--depression, anorexia, bruxism, weight loss, isolation behavior -C3 is most commonly affected --more likely to perforate than C1 |
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|
Diagnosis of Ulcerative disease in camelids
|
-Abdominocentesis will be normal or mildly inflammatory
-CBC and chem will be normal |
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|
Treatment of ulcerative disease in camelids
|
-0.4 mg/kg omeprazole IV
--Oral omeprazole does not change C3 pH -Pantoprazole -Reduce stress! |
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|
Peritonitis in Camelids
|
-Ruptured viscous, can be C1 or C3
--Strangulating obstruction -No rupture, will not find perforation on exploration --streptococcus zooepidemicus |
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|
Hepatic lipidosis in Camelids
|
-Females may be over represented
-Usually occurs in animals 6-10 years old -Weight loss, anorexia, isolation from herd -Neurologic signs present in 25% of cases -Diagnose via chemistry profile, abdominal ultrasound, and liver biopsy --Increased GGT, ALP, Bile acids, and AST --may be hyperglycemic or hypoproteinemic -Liver biopsy will show vacuolation of hepatocytes and biliary perforation |
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|
Treatment of Hepatic lipidosis in camelids
|
-IV fluid therapy
-Partial parenteral nutrition -Decrease stress and metabolic demands -Attempt to eliminate other illnesses -Poor prognosis |
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|
Pancreatitis and pancreatic necrosis in Camelids
|
-Vague clinical signs:
--anorexia, lethargy, recumbent, signs of colic -Comparison of amylase and lipase levels in peritoneal fluid relative to serum -Association with equine herpes virus type 1? |
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Important thoughts on Camelid GI
|
-Persistently painful camelid should be explored |
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|
Camelid General Information |
-Foregut fermenters |
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|
Gastric issues in Horses
|
-Uncommon, except gastric ulcers
-Variable history and clinical signs --can present with colic, dysphagia, bruxism, ptyalism, inappetence, weight loss, lethargy -Need to do gastroscopy for diagnosis --requires holding horse off-feed for 12-24 hours -Sonography, contrast radiography, and nuclear scintigraphy may be helpful diagnostics |
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|
Equine Gastric Lesions
|
-Ulceration
-Gastric dilation -Rupture -Impaction -Neoplasia -Pyloric stenosis |
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|
Gastric Dilation in Horses
|
-Uncommon
-Stomach fills with gas, becomes distended -most common cause is small intestinal obstruction -Highly fermentable feed can be a cause -Racing, swimming, and post-gastroscopy can also be causes of dilation |
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|
Gastric neoplasia in Horses
|
-Not common, but can happen
-Gastric squamous cell carcinoma is most common -Marked weight loss, inappetence, lethargy, dysphagia -50% can be diagnosed based on abdominocentesis and cytology -Most are diagnosed with gastroscopy -No treatment for squamous cell carcinoma |
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|
Pyloric stenosis in Foals
|
-Duodenal pyloric outflow obstruction
-Foals 3-5 months old -Present for regurgitation of milk out of nares, dysphagia -Bruxism, colic, aspiration pneumonia -Treat with gastro-jejunostomy |
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|
Causes of Gastric Rupture in horses
|
-Small intestinal obstruction
-Impaction -Ulcers -Nasogastric feeding or water -Idiopathic -Usually ruptures along greater curvature |
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|
Clinical signs of horse with gastric Rupture
|
-Dull
-Sweating -Muscle fasciculations -Reluctant to walk -Tachycardia, tachypnea, nostril flare -Fever -Absent borborygmi -Leukopenia -High PCV, low total protein --“splitting” -High blood lactate -Diagnose via sonography and peritoneal fluid analysis --can see ingesta swirling around in abdomen |
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|
Diagnosis Gastric Impaction in Horses
|
-Sonography
-Gastroscopy -Surgery -Necropsy, will see muscle hypertrophy and fibrosis of stomach wall --stomach was not completely normal |
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|
Clinical signs of gastric impaction in horses
|
-Present for colic
-Bruxism, dysphagia -Cannot actually get tube into stomach |
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|
Treatment of Gastric Impaction
|
-Try to treat medically, do not do well with surgery
-Withhold feed -Gastric lavage -Low survival rate due to stomach rupture after impaction |
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|
Small intestine lesions in horses
|
-Variable percentage of colic cases, can be 50%
-Most are strangulating lesions/obstructions --distal jejunum and ileum -Need to decide if it can be managed medically or if it is a surgical condition ASAP! --want to go to surgery early, decreases amount of bowel that needs to be resected |
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|
History and Physical exam for small intestine lesions in horses
|
-Variable pain, can start mildly painful
--strangulating lesions are persistently painful --abrasions indicate pain -no Abdominal distention --unless volvulus of root of small intestinal mesentery -Heart rate is usually elevated, tachycardia (56-76 bpm) -increased Respiratory rate (tachypnea) and nostril flare -Rectal temp will be within normal limits -Mucus membranes are variable -Borborygmi will be absent with strangulating obstruction --strong correlation between absence of gut sounds and need for surgery |
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|
Ancillary tests for Small intestinal issues in horses
|
-Nasogastric intubation (therapeutic and diagnostic)
-Examination per rectum --dilated loops of small intestine -Abdominal sonography -Peritoneal fluid analysis --nucleated cell count --protein concentration --lactate --if serosanguinous, take to surgery! -PCV/TS -Lactate: idea of general peripheral perfusion --if high, 10+, bad news --3-7, gray zone --less than 1 = good -Glucose: if high look for strangulating obstruction -Plasma chloride: low in horses that are refluxing |
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|
Peritoneal Fluid lactate
|
-Should be the same as the plasma
-If higher lactate in peritoneal fluid, strong indication for surgery |
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|
Duodenitis in horses
|
-AKA proximal jejunitis, anterior enteritis
-Acute inflammation of duodenum and proximal jejunum -Distended small intestine on rectal exam -Nasogastric reflux is pathognomonic --48L of reflux in 24 hours --8L at any one time --3l/hour for more than 12 hours -Peritoneal fluid: --normal color and cell count --increased protein -Usually not painful, prevent dull -Take to surgery to confirm diagnosis |
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|
Treatment for Duodenitis in horses
|
-Medical treatment: IV fluids
-Exploratory celiotomy -Prognosis is 60-80% positive, but can be variable -Expensive to treat -Can possibly develop laminitis as sequelae |
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|
Causes of Ileal Impaction in Horses
|
-Coastal Bermuda Grass Hay
--cut late has high lignin content --SE USA -Weather changes -Water intake -Anoplocephala perfoliata tapeworm |
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|
Clinical signs of Ileal Impaction
|
-Intermittent moderate to severe pain
--responsive to analgesic drugs -Physical exam is within normal limits -No reflux or distended small intestine -Can progress to persistent pain and no response to analgesics -Small intestine becomes more and more distended, may start to get reflux -Decreased borborygmi -Eventually animal is dehydrated and in shock |
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|
Diagnosis of Ileal impaction in horses
|
-Geographical region (southeast US)
-Feeding history --Coastal hay Bermuda grass -Abdominal pain-Reflux -Palpation per rectum -Abdominal sonography -Normal peritoneal fluid lactate that over time increases as bowel becomes devitalized |
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|
Medical management of Ileal Impaction in horses
|
-Can only do it diagnosis is made and abdominal pain and small intestinal distention does not progress
-IV fluids, electrolytes -Oral fluids, mineral oil -Analgesic drugs -Buscopan |
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|
Indications for Surgery in case of Ileal impaction in horses
|
-Persistent or moderate to severe pain
-Small intestinal distension -nasogastric reflux -Cardiovascular deterioration -Increased peritoneal fluid lactate |
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|
Surgery for Ileal impaction in horses
|
-Massage contents into cecum
-Sodium carboxymethylcellulose to lubricate surface -Ileal enterotomy may be needed -Ileal hypertrophy may require jejunocaecostomy (ileal bypass) |
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|
Post-operative care for Ileal impaction in horses
|
-Anthelmintic treatment to prevent tapeworms
-Avoid feeding coastal hay |
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|
Ascarid Impaction
|
-Non-strangulating impaction in horse small intestine
-Typically seen in foals, 3-4 months old -Most occur after deworming due to rapid death of worms -Can rupture! -Can result in abscess, intussusception, volvulus, etc. |
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|
Ileal neoplasia
|
-Lymphoma is most common
|
|
|
Eosinophilic enteritis in horses
|
-Can be focal or diffuse
-Not common at NBC -Non-strangulating lesion |
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|
Ileal hypertrophy in horses
|
-Uncommon
-Muscular hypertrophy -Cause is unknown -Usually have to resect or bypass -Non-strangulating lesion |
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|
Intramural or mesenteric hematomas in horses
|
-Intramural usually causes obstruction
-Mesenteric can affect blood supply to the intestine -Non-strangulating lesion |
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|
Intra-abdominal abscesses in horses
|
-Cause adhesions with small intestine stuck to it
-bastard strangles -Non-strangulating lesion |
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|
Strangulating lipoma in horses
|
-Pedunculated lipoma
-Benign fat tumors on pedicle/stalk -Lipoma wraps around a piece of bowel or can form a knot -Most common in mature or geriatric horses, late teens and 20’s or older --older horses that come in with colic have strangulating lipoma until proven otherwise -Ponies and Arabians are predisposed -Surgical treatment: --jejunojejunostomy --jejunocecostomy -Prognosis is generally good, especially with early surgical intervention |
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|
Epiploic Foramen Entrapment
|
-Bowel gets stuck in vestibule of omental bursa
--goes left to right, and gets stuck -Usually occurs in 10-15 year old horses -Thoroughbreds and warmbloods are more common -Surgical correction is needed -Affects distal jejunum and ileum --jejunojejunostomy or jejunocecostomy -Do not want to tear portal vein during correction! -Good prognosis with minimal recurrence rate --epiploic foramen closes with surgery? |
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|
Intussusception
|
-Bowel telescopes into another section of bowel
-Jejunojejunal and ileocecal are most common -predisposing factors: --enteritis --tumor, leiomyoma --Anoplocephala perfoliata tapeworm -Diagnose based on ultrasound -Jejunojejunostomy and jejunocecostomy |
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|
Ileal Volvulus in horses
|
-180 degree rotation around the mesentery
-Primary: associated with younger horses -secondary, due to some underlying cause -Segmental: -Mesenteric root: distended, violently painful -Correction via surgery --if segmental, can resect and anastomose --if at mesenteric root, may need to euthanize if bowel is not viable |
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|
Inguinal/scrotal hernia bowel incarceration in horses
|
-Direct or indirect
--direct: directly through body wall --indirect: goes through inguinal ring -Adults/acquired indirect is most common -Direct/ruptured direct can occur -Can be congenital in foals (indirect) -Tennessee Walking horses and Standardbreds are most common -Surgical emergency! Damage to body wall -May be able to fix laparoscopically -Can be due to strenuous exercise, breeding, or trauma |
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|
Umbilical incarceration Hernias in Horses
|
-Uncommon for bowel to herniate, usually fat or omentum herniates
-Can be small or large intestine --usually just one wall (Richter’s hernia) --Wall can necrose, end up with enterocutaneous fistula -Diagnose with ultrasound and clinical signs --3-6 month foal with history of umbilical hernia, colic, and firm hernia -Surgical intervention! -Usually bowel is viable |
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|
Diaphragmatic hernias in Horses
|
-Congenital or acquired
-Uncommon -Small intestine is most commonly involved -Respiratory distress is common instead of signs of colic -Diagnose via ultrasound and radiographs -Need to correct surgically --most animals are euthanized --poor prognosis |
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|
Misc. strangulating obstructions in horses
|
-Incarceration in gastrosplenic/gastrohepatic ligament
-Mesodiverticular band -Meckel’s diverticulum -Strangulation through a rent -Adhesions |
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|
Post-operative management of Colic cases
|
-Broad spectrum antimicrobials
--usually less than 48 hours -Banamine -IV fluids and electrolytes -Nasogastric tube to make sure they do not have reflux -Motility modifying drugs, lidocaine -Feeding, start grazing immediately and gradually increase over time |
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|
Post-operative complications with small intestinal surgery in horses
|
-Post-operative reflux
--secondary to ileus or obstruction at anastomosis -Adhesions -Inappetence is a bad sign after surgery |
|
|
Anatomy of the equine large colon
|
-3.5-4 meters long, very long!
-HUGE capacity -Only attached at base, right dorsal colon --rest is free to move about abdomen, can cause problems -Cecocolic ligament -Ventral colon has sacculations -Dorsal colon has bands -Colic branch of ileocolic artery and vein give blood supply, also right colic artery and vein |
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|
Tympany in horses
|
-Gas/spasmotic colic
-Very common, 65-75% of colic cases -Mild to moderate pain -Unremarkable physical exam -Gas distention felt on rectal exam, may feel normal -Give banamine and maybe sedation (xylazine, butorphanol if needed) -Hold off feed -Enteral fluids -Good prognosis, but will recur |
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|
Intraluminal colon obstruction in horses
|
-Non-strangulating obstruction
-Can be ingesta, sand, enterolith, foreign material -Pelvic flexure/left ventral colon and right dorsal colon are most common locations --more than just narrowing, may also be motility issues -Mild to moderate pain -Mild to severe abdominal distention --abdominal distention is common in colon issues -Physical exam is initially unremarkable, progresses --tachycardia, tachypnea, fever, decreased borborygmi -Rectal palpation is good for diagnosing pelvic flexure impaction |
|
|
Sand colic vs. sand impaction
|
-Sand colic/sand enteropathy:
--chronic sand in intestinal tract --recurrent colic, weight loss, low protein --diarrhea -Sand impaction: sand is causing an obstruction --very geographic |
|
|
Enteroliths
|
-Common cause of obstruction in horses
|
|
|
Ingesta impaction in colon in horses
|
-Most common form of impaction
-2nd most common form of colic -Left ventral colon is impacted, near pelvic flexure -Due to poor quality feed, poor dentition, reduced water intake, parasitism, change in management exercise or diet, recent shipping, recent illness -Recent changes! |
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|
Classic colic impaction
|
-Winter:
--decreased exercise, decreased water, poor hay/feed -Mild signs of pain, not rolling violently -Physical exam within normal limits for the most part -Diagnose via rectal palpation, can feel impaction |
|
|
Treatment for Colic impaction in horses
|
-Fluids
-Electrolytes -Mineral oil -DSS (breaks down ingesta?) -Withhold feed, do not want to add to impaction -Walk -Analgesics as needed, banamine -medical management as long as animal is passing manure, not becoming distended, no reflux, and have borborygmi -Prognosis is good to excellent -Need to monitor closely during medical treatment!! |
|
|
Causes of mortality in colic impaction cases
|
-Take animal to surgery that has a massive, fluid-filled, friable colon
-If animal goes to surgery, go early! |
|
|
Sand Impaction in horses
|
-Very geographic
--CA, CO, FL, MI, NJ -Horses fed on the ground -Colic, gas distention -May be able to auscultate in ventral abdomen, “sea washing over beach” -May see sand in feces, fecal sand sedimentation -Radiographs and ultrasound |
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|
Treatment for sand impaction in horses
|
-Metamucil or Sand Clear
-Surgery! Sand can do some real damage to the colon --could rupture colon |
|
|
Enteroliths
|
-Most common in California
-Struvite concretions: NH4, Mg, Phosphate -Usually has a nidus -Genetic predisposition -Can be round or polytetrahedral --polytetrahedral indicates stones rubbing on each other --Perfect sphere indicates just one stone -Radiographs can be helpful for diagnosis -Treatment: surgery! -Prognosis is good --unless it is left and there is a rupture! |
|
|
Foreign Body Impaction in Horse Colon
|
-More common in younger horses
-Bailing twine -Nylon -Socks -Rubber fencing -Any non-digestible material --sits in colon (usually right dorsal colon) and becomes mineralized --once mineralized, causes obstruction -Usually painful on presentation with abdominal distention |
|
|
Right Dorsal Displacement of the Colon
|
-Most common displacement
-Can rotate counterclockwise or clockwise -Colon displaces between the cecum and right body wall -Diagnose with rectal palpation and ultrasound --colonic artery is on wrong side of the body -Colon is displaced around the base of the cecum |
|
|
Treatment for Right Dorsal Displacement of the colon
|
-Medical treatment
--IV fluids -Surgery --decompress and reposition -Excellent prognosis -Recurrence is common |
|
|
Left Dorsal Displacement of the Colon
|
-“Nephrospenic entrapment”
-Colon is displaced between the spleen and left body wall -Colon rotates 180 degrees, goes between spleen and left body wall, becomes stuck over nephrosplenic ligament -Diagnose via rectal palpation --feel kidney, colon, and spleen --often can only feel gas-distended colon -Spleen may be displaced ventrally -Rectal findings + ultrasound gives diagnosis |
|
|
Left Dorsal Displacement of the Colon treatment
|
-Medical management
--IV fluids --enteral fluids --phenylephrine, causes vasoconstriction, decreases size of spleen, and allows colon to roll off of nephrosplenic ligament -Surgery if persistent pain --push spleen axially, lift colon off from top of the spleen -Rolling under general anesthesia -Excellent prognosis -Recurrence is common |
|
|
Nephrosplenic space ablation
|
-Prevention for nephrosplenic entrapment
-Put in mesh between kidney and spleen -Prevents entrapment |
|
|
Large Colon Volvulus in horses
|
-Most serious cause of colic in horses
-Usually occurs towards the base of the ceco-colic ligament --360 degree volvulus most commonly -Proximal bowel is usually not ischemic -Severe pain and distention -Most often counterclockwise rotation, right at the base of the colon |
|
|
Large colon volvulus clinical signs
|
-Brood mare that foaled recently
-Violently painful -Marked abdominal distention -Tachycardia -Dry, dark mucus membranes -Prolonged CRT -Cool extremities -Hemoconcentration, increased PCV -Hyperlactatemia -Azotemia -Poor tissue perfusion! Animal goes into shock quickly! -Fair prognosis |
|
|
Large colon volvulus treatment
|
-Immediate surgical intervention!
--within 2-3 hours --typically involves the whole colon --resection is a debulking procedure -Decompress and de-rotate --usually have to do multiple times -Colonic viability assessment -Enterotomy vs. resection --remove digesta -Once untwisted, determine whether it should be recovered or euthanized -Fair prognosis, high recurrence |
|
|
Large Colon Volvulus Medical treatment post-op
|
-Can be very challenging
-IV fluids, crystalloids and colloids --often have protein-losing enteropathy -Analgesia -Anti-endotoxin therapy (polymixin B) -Ischemia and re-perfusion injury treatment (difficult) -Fair prognosis |
|
|
Colitis
|
-Differential diagnosis for colic
-Often attributed to salmonella or clostridium -Antimicrobial associated C. difficile |
|
|
Colitis presentation
|
-Can present like a colic
-Abdominal pain and distention -Often have a fever (can differentiate from volvulus etc.) -May be colicky initially, becomes dull and inappetent -May have diarrhea -Mild to severe disease -Protein may be inappropriately low -Low sodium and Cl may be present |
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Colitis treatment
|
-IV fluids! Crystalloids and colloids
--often have protein-losing enteropathy -Anti-endotoxin therapy --polymixin B, J5 plasma -Metronidazole for clostridium species -Anti-diarrhea --peptobismol, biosponge |
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Right dorsal colitis
|
-Specifically right dorsal colon
-Associated with any NSAID -History of mild colic, diarrhea, inappetence, weight loss -Occult blood -Hypoproteinemia! Protein losing enteropathy! -May see melena or occult blood in feces -on ultrasound right dorsal colon may appear thick, rest of the colon is not thick |
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Treatment for Right dorsal colitis
|
-IV fluids
-Parenteral nutrition -Corn oil, high omega-3 fatty acids -Psyllium -Low-residue feeds -Occasionally need bypass/resection, last resort! --big surgery |
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Horse Cecal Anatomy
|
-Sits in left caudal abdomen
-1m long -30L capacity -Base cannot be exteriorized but can be seen -4 cecal bands (lateral, medial, dorsal, ventral) -ceco-colic ligament from lateral cecal band -Ileocecal fold from dorsal cecal band |
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Cecal Tympany
|
-Gassy cecum
-rectal palpation: gas-distended viscous on right side of the abdomen --attached to body wall -Can manage medically with IV fluids |
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Cecal Impaction
|
-VERY serious! Has chance of rupture!
-Slightly painful animal, maybe not painful -inappetent -Decreased defecation -Can be dry, firm --coastal Bermuda grass hay -Liquid ingesta -Predisposing factors: --general anesthesia --surgery --NSAIDs --stall confinement --hospitalization |
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Cecal Impaction diagnosis and medical treatment
|
-Diagnose via rectal palpation and ultrasound examination
--want to make sure it is in the cecum! -ideally should be brought to surgery, but can medically manage -Feed restriction -Oral water and electrolytes -Mineral water -DSS -IV fluids -Analgesia -Motility stimulants --neostigmine --erythromycin |
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Cecal impaction surgical treatment
|
-Do if HR increases, starts to sweat, etc.
-Best to do immediately! If ruptures, cannot do anything! -Typhlotomy: empty colon -Complete or incomplete bypass --jejunocolostomy --ileocolostomy -Cecocolic anastomosis, gives cecum another “exit” -Variable prognosis |
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Typhlotomy
|
-Exteriorize cecum and empty it out
-Need to make sure the cupula is empty! -Cecal impaction, anastomosis -Use impermeable drapes and carboxymethyl cellulose --adheres to digesta and helps with removal -Make incision 10-20cm long -Close with 2-0 or 0 synthetic absorbable suture -Can also stable closed |
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Cecal Rupture causes
|
-Cecal impaction
-Parturition -Anoplocephala perfoliata tapeworms |
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Cecal rupture clinical signs
|
-Rapid development of signs of shock
--cardiovascular deterioration --tachycardia -Pain -Diagnose on rectal examination, ultrasound -Peritoneal fluid analysis -Diagnose on surgery or necropsy -FATAL! |
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Cecal rupture on rectal palpation
|
-positive pressure in the abdomen
--should be negative pressure -Grittyness/crepitus under fingers |
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Cecal intussusception in horses
|
-Ceco-cecal and ceco-colic
-Associated with dysmotility -Anoplocephala perfoliata tapeworms -Eimeria leukarti -Organophosphates -Mural abscess -Can be acute or chronic -May have signs of recurrent colic -Can be difficult to correct! --typhlectomy --cecal bypass if it cannot be reduced --enterotomy with right ventral colon |
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Cecal Torsion
|
-Rare!
-Involves cecum and large colon -Congenital abnormalities -Severe abdominal pain -Correct via partial typhlectomy |
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Cecal Infarction/Thromboembolism
|
-Associated with strongylus vulgaris and cyathastomes
--went away for a bit, but is recurring due to resistance -Usually severe pain -Correct via surgery, typhlectomy --can resect if an isolated incident, often is a more disseminated process |
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Indications for Typhlectomy
|
-Ischemic necrosis
-Severe adhesions -Abscesses -Neoplasia -Severe contamination -Ligate medial and lateral cecal arteries and veins, within medial and lateral cecal ligaments -Occlude lumen with Doyan clamps, resect -0 synthetic absorbable suture -Full-thickness simple continuous suture or cushing pattern |
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Small colon Anatomy
|
-“Descending colon”
-4m long -6-8cm diameter -Has sacculations |
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Small colon impaction
|
-Most common lesion in small colon
-Fecalith or impaction -Ponies, female horses, and older horses -More common in fall and winter -Poor quality roughage -Insufficient water intake -Poor dentition -Inadequate mastication -Lack of exercise -Parasitism -Usually do not feel on rectal palpation -Localized obstruction, gas distention, intestinal necrosis |
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Diagnosis of small colon impaction
|
-Winter, pony
-Fecal palpation can feel small colon filled with impactions --long, tubular impactions -Fecallith is an isolated ball --usually occurs more proximal in the small colon --can result in intestinal necrosis |
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Medical management of small colon impaction
|
-IV fluids
-Enteral fluids (has a long way to go) -Can be difficult to manage medically, especially if not addressed early |
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Surgical management of small colon impaction
|
-High enema: hose in rectum, massage impaction out
-Enterotomy --ultimately less traumatic? Can end up with strictures -pelvic flexure enterotomy |
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Complications of surgical management of small colon impaction
|
-Adhesions
-Re-impaction -Salmonellosis |
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Small Colon Impaction types
|
-Phytobezoars: plant material + concretion
-Trichobezoars: hair + concretion -Phytoconglobate: foreign material + concretion -Rope, twine, plastic, rubber, halters, hay nets, tire treads can all act as nidus |
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Enterolith locations
|
-Right dorsal colon
-Transverse colon -Small colon -NOT in cecum or small intestine |
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Meconium Impaction
|
-Newborn foals |
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Meconium Impaction
|
-Newborn foals |
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Atresia coli
|
-Very uncommon
-DDx: meconium impaction |
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Rectal Prolapse in Horses
|
-Can tear blood supply to small colon
-Will develop septic peritonitis -If prolapse more than a foot, consider mesocolon tear |
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Rectal tears in Horses
|
-Blood on rectal palpation, bad news!!
-Inform client immediately -Sedate the horse and give lidocaine enema or buscopan IV --helps relax rectum -Evacuate the rectum -Assess tear |
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Grade 1 rectal tear
|
-Mucosa and submucosa
-Muscle layers and serosa are intact |
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Grade 2 rectal tear
|
-Muscle layers involved in tear
-Mucosa and submucosa are intact, serosa is intact -“Theoretical” -May cause peri-rectal abscess --leads to obstruction later on |
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Grade 3a rectal tear
|
-Only serosa is left intact
-Tear through mucosa, submucosa, and muscle layers -Very deep tear, not quite all the way into the abdomen but might as well be |
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Grade 3b rectal tear
|
-Full thickness tear, mesorectum is left intact
-Feces can dissect up into mesorectum and open into abdomen |
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Grade 4 rectal tear
|
-Full thickness
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Treatment for rectal tears
|
-Antimicronials (Penicillin, gentamicin)
-NSAIDs -Tetanus toxoid -Epidural anesthesia -Rectal packing to prevent contamination -Prepare horse to be shipped to a surgical facility! --call and ask if they want rectum packed |
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Rectal tear surgery
|
-Suture tear per rectum |
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Small colon Enerotomy
|
-Thick anti-mesenteric band |
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Diagnosis of enteric disease in Swine
|
-Case history
--age, gradual or acute onset, duration, number of animals sick -Physical exam -Necropsy specimen selection --choose untreated, live animals showing signs for less than 1 day --fecal, serology, culture are all important --Sample jejunum, ileum, colon/cecum, stomach, mesenteric lymph nodes, liver |
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Drugs prohibited from extra-label use in food animals
|
-Chloramphenicol: idiosyncratic aplastic anemia
-Clenbuterol: allergic reactions and death -Diethylsylbestrol: carcinogen -Nitromidazoles: carcinogens -Furazolidone, Nitrofurazone, other nitrofurans: carcinogens, mutations -Sulfonamide drugs -Fluoroquinolones -Glycopeptides: MRSA -NSAIDs: phenylbutazone, except in very young dairy animals |
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Agents isolated from Neonatal diarrhea in pigs
|
-E. coli (45.6%)
-Isospora suis (23%) -Rotavirus (20.9%) -TGE (11.2%) -Other (0.1-2%) |
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Causes of diarrhea
|
-Ingestion of poorly absorbable material, bulk-forming laxative
-Stimulation of mucosal intracellular enzymes by bacterial toxins or other factors -Disrupted integrity of small intestine mucosa, villous atrophy -Increased intestinal motility -Local lymphatic or venous obstruction |
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Types of diarrhea in pigs
|
-Dysentery: mucus, blood
-Osmotic: malabsorption -Secretoy: usually due to toxins --enterotoxin, endotoxin --transfer water into lumen |
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Colibacillosis
|
-Enterotoxigenic E. coli (ETEC)
-Fimbral adhesions K88, K99, 987P, F41 --needs to attach in intestines before it releases enterotoxins --can genetically select for pigs that lack receptors for certain E. coli adhesins -#1 cause of neonatal diarrhea in pigs less than 5 days old -Causes edema disease in weaned pigs, 1-2 weeks old -“traveler’s diarrhea” in humans |
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Colibacillosis pathogenesis
|
-Piglet ingests organism from dam or littermate
-Bacteria attaches to enterocytes via adhesins -Enterotoxins released -Increases electrolytes released into GI lumen --bicarbonate, Na -Osmotically pulls water into the lumen -Causes dehydration, metabolic acisosis, diarrhea -Works quickly in neonatal pigs, piglets do not have a lot of resources and are easily dehydrated |
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Clinical signs of Colibacillosis
|
-Profuse, watery diarrhea
--brown, yellow, or clear -Dehydrated animal -Gaunt, depressed, fecal staining -Death 24-48 hours after onset of signs |
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|
Necropsy of Colibacillosis
|
-Usually no gross lesions
-Microscopic submucosal edema -Fecal pH greater than 8 --release of bicarbonate into lumen increases pH -Lumen bacterial cultures |
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Treatment/Prevention/Control of Colibacillosis
|
-Commercial bacterins to sow pre-farrowing
--sow produces antibodies which are transferred to neonates in colostrum -Antimicrobials, oral and injectable --gentamicin, neomycin, ampicillin -Electrolytes -Immunization (make sure farm is storing and using vaccines appropriately) -Sanitation -Genetics -Probiotics for gut maturation? |
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|
Transmissible Gastroenteritis (TGE)
|
-Coronavirus, FIP-like
-Virus is stable if frozen, can survive the winter --hearty, stable virus -Can be transmitted by starlings, cats, dogs, humans -Easily transmitted from farm to farm -Epizootic is more common, also enzootic form |
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Transmissible gastroenteritis TGE pathogenesis
|
-Pig ingests virus, inhalation is also possible
-Virus invades and replicates in small intestine -Atrophy of jejunal villi --loss of villi, virus is shed into the environment with villi -Shed for 2-3 weeks -Causes decreased digestion and malabsorption --maldigestion |
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History/clinical signs of Transmissible Gastroenteritis (TGE)
|
-Diarrhea in pigs of all ages in naïve herd
-Diarrhea in piglets 1-8 weeks old in endemic herds --gilt litters only, sows develop immunity and pass immunity onto offspring in colostrum -May or may not see vomiting --One of the only pig diseases that results in vomiting and diarrhea -High morbidity and mortality, especially in young pigs --young animals will die -Profuse, watery diarrhea -Dehydrated pigs |
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Necropsy specimens of Transmissible gastroenteritis TGE
|
-Thin-walled small intestine
-Jejunal villus atrophy -Fecal pH less than 7 -Virus isolation in peracutely infected pigs --need to get pigs early to see virus -Serology for monitoring |
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Treatment/Prevention/Control of Transmissible gastroenteritis TGE
|
-Supportive treatment
--generally young pigs become chronic poor-doers --older pigs get treatment to minimize secondary infections form bacteria -Immunize sows pre-farrowing, allows transfer of antibodies in colostrum -Quarantine and test all incoming animals -Strict biosecurity! |
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|
Porcine Epidemic Diarrhea virus (PEDv)
|
-Serious, highly contagious swine disease
-Enveloped, single-stranded RNA virus --coronavirus, similar to TGE --very resistant organism -Need very strict biosecurity and vaccination regime -No cross protection -First discovered in UK in 1971, asia 1982, USA 2013 -32 states currently have + herds, including PA and MD --Hawaii also -SIGNIFICANT economic losses in pigs, especially young pigs |
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Porcine Epidemic Diarrhea Virus Pathogenesis (PEDv)
|
-Pig ingests virus, usually fecal-oral
-Virus invades and replicates in small intestine -Incubation is short, 12-24 hours -Atrophy of jejunal villi -Virus is shed for 7-10 days -Causes decreased digestion/maldigestion and malabsorption |
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|
History and clinical signs of Porcine Epidemic Diarrhea Virus (PEDv)
|
-Diarrhea in all age pigs in naïve herd
--all pigs are susceptible -Vomiting and diarrhea in sows and gilts -Severe diarrhea in 1-8 week old piglets --endemic herds will have diarrhea in recently weaned piglets -high morbidity and mortality in suckling and recently weaned pigs -Profuse, watery diarrhea -Dehydrated pigs! |
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|
Necropsy specimen of Porcine Epidemic Diarrhea Virus (PEDv)
|
-Looks a lot like TGE, different type of corona virus
-Thin-walled small intestine -Jejunal villus atrophy -Virus isolation in peracute infected pigs -PCR on feces, fresh intestinal samples, or swiffers -Immunohistochemistry, histopathology of fresh and fixed tissues |
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Treatment Prevention Control of PEDv
|
-Supportive treatment
--young pigs become chronic poor-doers --older pigs can be treated to minimize secondary infections -2 new vaccines are available -Quarantine or test all incoming animals -Strict biosecurity! -Disinfection of facilities --clorox, VirkonS, 1 stroke Environ, Tek-tol -Feed, trailers, transport personnel need to be disinfected |
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|
Rotaviral enteritis
|
-Rotavirus, RNA virus
-Ubiquitous, expect to see on farms, especially farms with poor management -Ingested from sows -Causes villous atrophy, similar to TGE --maldigestion and malabsorption -Synergism with other pathogens makes definitive diagnosis difficult |
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|
Rotavirus History and clinical signs
|
-Seen in pigs 3 days to 8 weeks of age
--corresponds to decline in lactogenic antibodies -Low mortality, variable morbidity -Transient diarrhea (yellow) -Dehydration -Vomiting -Can survive with good supportive care |
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|
Treatment, Prevention, Control of Rotavirus
|
-Electrolyte replacement
-Antibiotics to control secondary infections -Good sanitization is essential, decrease the challenge dose -Immunize sow -Practice all-in-all-out management |
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|
Coccidiosis
|
-Isospora Suis protozoa
--Eimeria is also a possible pathogen, but less common -Oocysts are hearty in the environment -Generally see in mixed infections |
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|
Coccidiosis Pathogenesis
|
-Oocyst is ingested, usually from other scouring young pigs
-Oocytes mature, hatch, and invade/destroy enterocytes of small intestine --5-7 days -internal and external maturation of oocutes -Malabsorption ensues |
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|
History and clinical signs of Coccidiosis
|
-5-21 day old piglets
-Diarrhea will be whitish yellow, pasty -Gaunt piglets -Slow recovery -Variable morbidity and mortality |
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|
Coccidiosis necropsy specimens
|
-Thickened jejunal and ileal walls
-Villous atrophy -Impression smears |
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|
Treatment, prevention, and control of Coccidiosis
|
-Prevention and control are key!
-Can be very frustrating, common disease with no approved treatment in US -Anticoccidials are not available -Need to break the cycle of the disease -Anti-microbials for secondary infections -better sanitation, eliminate porous surfaces like wood -All-in-all-out strategy |
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|
Clostridial enteritis
|
-Clostridium perfringens type C
--types A, B, and Difficile are also present --Difficile is difficult to treat and eliminate from the herd -Spore-forming -Common in USA -Variable morbidity and mortality -Causes necrotic enteritis |
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|
Clostridial pathogenesis
|
-Ingestion of bacteria from sow
-Adherence to jejunal villi -Production of toxins, beta toxins and others --toxins are pore-forming, cause tissue necrosis -Animal will be dead in as little as 12 hours after infection |
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|
Clostridial history and clinical signs
|
-3-21 day old suckling piglets
-Diarrhea --bloody diarrhea in young piglets, less than 7 days old due to necrosis --older piglets, 7-10 days, mucoid diarrhea -Necropsy specimen will show red, swollen small intestine and gas (clostridia produce gas) -Culture for definitive diagnosis |
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|
Clostridial treatment, prevention, control
|
-Individual treatment with penicillin, ampicillin, amoxicillin
-Give anti-toxin, not used often -Immunize sows pre-farrowing --toxoid for C, get antibodies in colostrum -Sanitization -Prophylactic antimicrobials to the sow or piglets at processing -If using medicated feeds, they need to come from a place that has a medicated feed license |
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|
Swine Dysentery
|
-Brachyspira hyodysenteriae spirochete
--Brachyspira pilosicoli -Not common in US or Canada --quarantine and testing has decreased incidence in US -Variable morbidity and mortality -Introduced into a group via introduction of carrier animals |
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|
Pathogenesis of Swine Dysentery
|
-Ingestion of spirochete from sow or other animals
-Spirochete invades colonic mucosa -Irritation and necrosis occurs in colon, leads to catarrhal, hemorrhagic colitis -Decreased water absorption due to fluid loss, electrolyte imabalnce |
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|
History and clinical signs of Swine Dysentery
|
-Pigs 2-6 months old, grower/finisher stage
--can also see in younger pigs -Diarrhea will be yellow to gray and soft -Bloody scours -Chronic, watery, fibrin, mucus, blood flecks in diarrhea -Gaunt animals but not otherwise depressed -Pigs will continue to drink |
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|
Necropsy specimens in Swine Dysentery
|
-Swollen, hyperemic colon and cecum
-Mucus, fibrin, bloody contents to bowel --mucohemorrhagic -Direct observation of organism in GI tract |
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|
Treatment, prevention, control of Swine Dysentery
|
-Antimicrobials
-If acute, Denagard in water -If chronic or not acute, meds in feed --carbadox, lincomycin, tiamulin -Pretty easy to treat! -Only accept animals from negative herds -Depop-a-repop --Treatable disease, but treatment is costly, depop can be a more efficient option -Isolate poor doers |
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|
Salmonellosis in Pigs
|
-Salmonella species:
--S. choleraesuis, causes diarrhea --S. typhimurium, causes respiratory disease -Asymptomatic carriers can be problems form time to time -Organism can survive for months in warm, moist areas -Zoonotic potential -Commonly seen in older pigs, grower/finisher pigs |
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|
Salmonellosis Pathogenesis in Pigs
|
-Pig ingests pathogen, or secretes pathogen if chronic
-Salmonella invades ileal mucosa -Enterotoxins and possibly endotoxins are produced -Causes hypersecretory diarrhea --decreased Na absorption, increased Cl secretion |
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|
History and clinical signs of Salmonellosis in Pigs
|
-See in pigs 2-4 months old, grower/finisher pigs
-Probably due to a recent stress event that causes a carrier to start shedding -Feces are watery, yellow -Quickly spreads through the pen -May also see signs of septicemia -Variable morbidity and mortality -Lots of unique characteristics --finisher pigs affected --can treat with antibiotics (keep aware of withdrawal times) --“button ulcers” in cecum colon and ileum |
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|
Necropsy specimens of Salmonellosis in Pigs
|
-Gross lesions: |
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|
Post-mortem lesions of Salmonellosis
|
-Chronic infection: Necrotic foci
--intestinal “button” ulcers --epiglottis --larynx -Congenital infection: --cerebellar hypoplasia --thymic atrophy --deformities of the head and legs |
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|
Treatment, prevention, control of Salmonellosis
|
-Injectable antimicrobials decreases severity
-Decrease stressors -Immunization/vaccinate --intranasal, injectable, oral -Prophylactic antimicrobials in feed or water --carbadox, neomycin -Purchase salmonella free pigs, or at least try! |
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|
Porcine Proliferative Enteropathy (PPE)
|
-Lawsonia intracellularis
--Necrotic enteritis, intestinal ademomatosis, garden hose gut -Pig specific -Intestines become so thick they feel like a garden hose |
|
|
Pathogenesis of Porcine Proliferative Enteropathy (PPE)
|
-Pig ingets organism, organism invades glandular epithelial cells
-Intracellular organism -Cells do not mature, do not shed --leads to thickened mucosa of the small intestine mostly -Characteristic lesion, disease is ONLY present in PIGS |
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|
History and Clinical signs of Porcine Proliferative Enteropathy PPE
|
-See in weaned through adult pigs
--usually grower/finisher pigs -Insidious in the herd -Diarrhea can be variable and intermittent -Blood in stool, frank or partially digested blood -Pallor -Variable morbidity, mortality is low -Mostly causes production problems |
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|
Necropsy specimens for pigs with Porcine Proliferative Enteropathy PPE
|
-Intestinal hemorrhage
-Thickened intestinal wall -Can see in small or large intestine -Have to do histopathology to identify the intracellular bacteria --comma-shaped bacteria |
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|
Treatment, Prevention, Control of Porcine Proliferative Enteropathy PPE
|
-Injectable Tylosin for individual pigs
--Usually treatment is given too late and animal does not fully recover from garden hose gut -All-in-all-out -Selected early weaning -Immunization --in water, need to make sure the water is free of debris etc., other antibiotics -Pulse medication --tetracyclines, virginiamycin, tiamulin in water and feed --give before stress events (shipping, regrouping, moving, ear tagging, etc.) |
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|
Porcine Circovirus type 2 (PCV2)
|
-Relatively new viral disease
-Kills pigs in late finishing stage -Outbreaks in Europe in late 1990s, Canada in 2004, US in 2005 -A and B versions, B is more lethal -Very stable virus, hard to kill -Seems to have gone away |
|
|
History and clinical signs of Porcine Circovirus type 2 (PCV2)
|
-Tends to strike in final needing stages of production, older pigs
-Many producers are unaware until it is too late -May suffer 20-40% death loss of pigs at 10-12 weeks of age --pigs just stop growing, hit a wall -Extreme and sudden weight loss -Labored breathing -Jaundice and diarrhea -In severe cases, may see skin lesions, immune suppression, neurological deterioration, kidney failure, death |
|
|
Pathogenesis of Porcine Circovirus 2 (PCV2)
|
-Spreads rapidly
-All routes of spread are unknown --for sure spreads via direct contact --oronasal, fecal urinary contact -Multiple routes of spread |
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|
Control, prevention, treatment for Porcine Circovirus 2 (PCV2)
|
-Several vaccines available, appear to have good efficacy
-Adequate colostrum intake during first 36 hours -All-in-all-out, full partitions between pens -Reduce batch mixing and cross-fostering --decreases mortality but exacerbates some diseases |
|
|
Trichuriasis (Whipworms) in pigs
|
-Trichuris suis
-Pig ingests eggs, eggs develop in cecal and colonic mucosa -Causes irritation and secondary infections -Catarrhal enteritis -See in pigs 2-6 months old -More common in pigs housed outside -Generally group performs poorly as a whole -May see diarrhea, may be mucoid or bloody |
|
|
Necropsy and specimens from Trichuris suis
|
-Presence of larvae in mucosal scrapings
-Worms in cecum --3-8cm long worms -May see eggs in feces on fecal exam |
|
|
Treatment, prevention control of Trichuris suis
|
-Anthelmintics
--dichlorvos, fenbendazole --ivermectin does NOT work! -Sanitation |
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|
Gastric ulcers in Pigs
|
-Multifactorial pathogenesis
-finely ground feed, less than 400um in diameter -Stress: anxiety, crowding, fasting, shipping, etc. -Increase in gastric acidity leads to hyperkeratosis or parakeratosis |
|
|
History and clinical signs of gastric ulcers in pigs
|
-See in weaned pigs, more than 8 weeks old
-Anorexia, unthrifty animals -Anemia, melena -Sudden death -on necropsy, see pallor pig --blood in stomach, ulceration in pars esophagea area of stomach -Sudden death after stress event |
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|
Treatment, Prevention, Control of gastric ulcers in pigs
|
-Prevention: control risk factors
--feed appropriate particle size and reduce stress -Add fiber to diet? -Genetically mediated? -Give melatonin? -Omepazole/ulcergard? |
|
|
Post-weaning scours in pigs
|
-Due to recent dietary changes and maturation of digestive system
--switch from milk to solid feed -Environmental stressors -Usually associated with pathogenic agent |
|
|
History and clinical signs of Post-weaning scours in pigs
|
-Diarrhea within 1 week post-weaning
-Variable morbidity and mortality --depends on endemic pathogens |
|
|
Treatment, prevention, control of post-weaning scours in pigs
|
-If associated with a pathogen, give antibactieral treatment
--if you know the pathogen only! -Maintain hydration status, give animals enough water -Environmental management -Pre-weaning creep feed |
|
|
Baby pig Anemia
|
-Iron deficiency, insufficient amount of iron in milk
-Piglets become unthrifty and anemic within 5-10 days of age -Pale skin, dyspnea, edema, lethargy -Prevent with IM injection of 200mg iron at 1-3 days of age --1 injection should last until pig starts eating solid food -IN wild, pig picks up iron from soil by rooting around |
|
|
Mulberry heart Disease in pigs
|
-Vitamin E/Selenium deficiency
-Oxidative damage of the heart occurs -Lots of little red dots covering the heart -Myocardial necrosis and failure -Pericardial sac is filled with gelatinous fluid or fibrin -Myocardial or endocardial hemorrhage -Causes acute death -May be due to inappropriate dextran iron usage? -Prevent by supplementing selenium in feed in selenium-poor areas -Can also give vitamin E/Selenium injection |
|
|
Osteochondrosis in Pigs
|
-Osteochondritis dessicans
-Driven by genetic selection for fast-growing animals -Failure of endochondral ossification, leads to DJD -Defects in the articular epiphyseal complex -Commonly occurs in distal ulna or femur, proximal femur or humerus, scapula, lumbar vertebrae, ischial tuberosity |
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|
History and clinical signs of Osteochondrosis in Pigs
|
-Genetics are main predisposing cause!
--rapid growth rate and increased average daily gain -Abnormal gait or lameness -Generally in pigs more than 4 months old -Does not resolve with antimicrobial treatment --mycoplasma also affects joints and will resolve with antimicrobials |
|
|
Treatment, prevention, and control of Osteochondrosis in Pigs
|
-Analgesics, NSAIDs, steroids
--Not great for animals going into the food chain! -Genetic selection -Improved floor surfaces -Limit feeding? -Difference in treatment for show pigs vs. commercial pigs? |
|
|
Splay leg (Spraddle leg)
|
-Pig hind legs are splayed out, animal has difficulty standing and walking
-Abduction of hindlimbs or forelimbs -Congenital defect, genetic predisposition -Can be due to zearalenone in feed --estrogen-like hormone, causes joint laxity -Seen in piglets within hours of birth -Can be traced back to a specific boar, look in breeding records |
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|
Treatment, prevention, and control of Splay leg in pigs
|
-Genetic selection |
|
|
Equine Gastric Ulcer Syndrome (EGUS)
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-Disease complex associated with damage to esophageal, gastric, or duodenal mucosa
-Damage is due to HCl and pepsin -Became well identified with endoscopy and ability to visualize the stomach -Up to 93% of performance horses have EGUS --Profoundly affects condition and performance -Can be very painful -More than 50% of foals have been shown to have EGUS -Potentially fatal in foals |
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Prevalence and impact of EGUS in adult horses
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-Results in poor body condition
-Can disrupt training or impair performance -Can cause colic -Can have severe complications! |
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Prevalence and impact of EGUS in foals
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-Potentially serious health problems
-Severe complications or death -Foal has tendency to want to lie on back --may reduce “stretch” feeling or other pain -May affect growth and development -Bile ducts in duodenum may be affected as well if disease is advanced |
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Horse stomach anatomy
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-Squamous portion: large in the horse
--does not produce any acid -Pyloric portion -Sigmoid portion of the duodenum -Most ulcers occur in Squamous portion of the stomach or border between squamous (non-glandular) and glandular portions --along margo plicatus |
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Equine gastric acid secretion
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-horses secrete HCl continuously, even when not eating
--horses are designed to graze continuously -Gastric acidity is high in foals, even as young as 2 days old -Consumption of roughage decreases acidity in foals and horses --roughage absorbs acid -Grain and processed feeds increase serum gastrin, and possibly HCl secretion -HCl is secreted by H/K ATPase acid pump on parietal cell membrane --10-16 pumps per cell -Acid pumps are stimulated by histamine, gastrin, ACh |
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Parietal cell Physiology
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-H/K ATPase on membrane
-H is secreted into the gastric lumen |
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Cimetadine
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-H2-antagonist
-Blocks H2 portion of stimulus to acid pump on parietal cells -Reduced amount of acid, raised pH |
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Gastrogard
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-Omeprazole
-Blocks acid pump at level of all stimulants -Much more effective blocker of H ion secretion, blocks ALL stimulants |
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Antacids
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-Buffers, buffer HCl in stomach once it has already been secreted
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Risk factors for Gastric ulcers in Horses
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-Intensive training and exercise
--causes reduced gastric mucosal blood flow --increases gastric acidity? -Altered eating behavior due to training -Episodic feeding -Withdrawal of feed and hay -Grain concentrate vs. Hay -Stress! -NSAID use |
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Stress as a risk factor for gastric ulcers in horses
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-Physical stress
--illness, painful musculoskeletal disorder -Behavioral stress --stall confinement --transport --unfamiliar environment --social regrouping |
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NSAID drugs as risk factor for Gastric ulceration in horses
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-Phenylbutazone, banamine, other NSAIDs
-Inhibit prostaglandin production, interrupts mucosal blood flow --decreased blood flow to right dorsal colon -Associated with ulceration throughout the alimentary tract -Causes local toxicity -Not a direct association, but increases risk of ulceration with prolonged use |
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Clinical signs of EGUS in foals
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-Poor appetite or intermittent nursing
--should nurse every 1-2 hours -Colic -Poor body condition -Frequently lies on back -Bruxism, grinding teeth (due to gastric pain?) -Ptyalism, excessive salivation (psyalorrhea) -Diarrhea or history of diarrhea |
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Clinical signs of EGUS in adult horses
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-Poor appetite |
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Diagnosis of EGUS in horses
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-Gastroscopy
--ONLY reliable method of diagnosis! --withhold feed -Empirical treatment of clinical signs --use appropriate acid suppression, signs should resolve in 24-72 hours --continue to treat for 3-4 weeks -Lab findings: --fecal occult blood in neonatal foals --other lab tests are not diagnostic |
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Endoscopic Evaluation for EGUS
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-Need god endoscope
-2.5-3m long, 10-12mm diameter -Prepare patient by withholding feed 6-8 hours and no water 2 hours -Need an experienced “driver” -Need to make sure you are indeed in the esophagus! --tubular, longitudinal folds, muscular contractions |
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Scoring EGUS severity
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0: normal mucosa (no lesions)
--normal individual 1: mild ulceration, small single or multifocal lesions 2: moderate ulceration, large single or multifocal lesions --may start to bleed --mucus is not there, not shiny anymore 3: severe ulceration, extensive lesions that are often coalescing --often bleeding |
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Treatment of EGUS: 4 goals
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-Eliminate clinical signs
-Promote healing -Prevent complications -Prevent recurrences |
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Treatment of EGUS: 2 pronged approach
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-Management modifications
--change management routine to be more compatible with normal --reduce training level --diet modifications, limit periods of fasting, increase roughage and pasture turnout and quality hay, reduce grain concentrates -Medical therapy --control gastric acid (omeprazole) “no acid, no ulcer”, maintain pH above 4 --mucosal protectants (sucralfate) |
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Managing gastric Acid in Horses with medical Therapy
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-Neutralizing agents: antacids
--need to be given every 2 hours -Antisecretory agents work well, but only if there isn’t anything better --histamine H2 receptor antagonists --prostaglangin analogs --acid pump inhibitors |
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Advantages of Acid Pump Inhibitors
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-Profound gastric acid suppression
-Prolonged duration of action -Once-daily dosing -Well-studied in horses -No related health problems associated with treatment --no side effects -Prevents recurrence -Can maintain training program -Gastrogard: approved for use in horses |
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Anti-ulcer in horses Summary
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-EGUS is major cause of illness in adult horses and foals |
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Gastrogard
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-Treatment for EGUS
-Provides potent long-lasting gastric acid suppression in horses -92% response in dose confirmation trials -99% response in field trials -Wide safety margin in adults AND foals -Field trials in a variety of breeds confirmed efficacy, safety, and viability |
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Peritonitis in Horses
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-Inflammation of the peritoneal cavity |
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Organisms commonly cultured from Equine Peritonitis
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-E. coli
-Actinobacillus organisms -Strep equi -Strep zooepidemicus -Rhodococcus -Bacteroides -Peptostreptococcus -Clostridium -Fusobacterium |
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Causes of equine peritonitis
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-Idiopathic
-Perforation of the GI or urogenital tracy -Infectious disease (actinobacillus) is common cause in adult horses -Trauma -Iatrogenic after abdominal surgery |
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Diagnosis of Peritonitis in Horses
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-Local peritonitis: minimal clinical signs |
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Non-specific signs associated with peritonitis in horses
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-Depression
-Anorexia -Weight loss -Intermittent fever -Ventral edema -Intermittent abdominal pain -Mild dehydration -Large amounts of echogenic fluid can be found in abdominal cavity on ultrasound |
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Laboratory findings in Peritonitis in horses
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-Increased PCV
-Hemoconcentration -Protein loss into peritoneal cavity -increased proteins -Hyperfibrinogenemia -Increased creatinine concentration --pre-renal or renal azotemia -Metabolic acidosis -Total protein concentration and nucleated cell count is increased --20,000 to 400,000 cells/ul -Gram stain for initial evaluation and selection of antimicrobial agents |
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Treatment for Peritonitis in Horses
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-Manage primary disease |
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Clinical signs of Diarrhea in Adult Horse
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-Acute onset
-Fever -Diarrhea -Hyperemic membranes |
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DDx for diarrhea in adult horses
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-Acute onset: |
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Infectious Causes of colitis in horses
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-Salmonella
-clostridium (perfringes and difficile) -Potomac Horse Fever -Coronavirus |
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Salmonella in horse
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-Fecal-oral infection
-Fomites, people, etc. can spread -Has predisposing factors: --stress (shipping, hospitalization, surgery) -Invasive, invades mucosa of the colon |
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Clostridium in horses
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-History of antibiotic therapy and disruption of GI flora
-GI signs are inflammation of colon, looks just like salmonella -Culturing organism is not diagnostic --need to find toxins in feces |
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Potomac horse Fever
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-Causes diarrhea in horses
-Fever, diarrhea, laminitis -Rickesstial, neorickettsia recipii -Complicated life cycle --rickettseal organism infects trematode, infects snails --horse can ingest snails or mayfly that is infected via trematode -Causes bacteremia, spreads to colon |
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Potomac Horse Fever Risk factors
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-Pastured horse
-Exposure to aquatic insects -NOT surgical stress or transporation |
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Coronavirus in Horses
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-Causes sloughing of villous epithelial cells
-Seen in outbreak situations in horses -Fever, colic, diarrhea -Mortality is low |
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Sand as a cause of colitis in horses
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-NJ, DE
-Horses fed off the ground, grazing low pastrues -Sand settles in ventral colon -Irritates surface of the colonic mucosa, causes inflammation --Fluids leak into abdomen -Can translocate bacteria through damaged mucosa -Can diagnose via auscultation, need to listen for several minutes --“sand washing on beach” sound, specific sand sounds -Ultrasound and radiographs confirm diagnosis |
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NSAID toxicity and colitis
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-NSAIDs are cox inhibitors
--prevent prostaglandins -Some prostaglandins improve blood flow to kidneys and GI mucosa -Decreased blood flow may result in right dorsal colitis -Causes colic and diarrhea -Protein-losing enteropathy, can look at plasma protein concentration --drop indicates issue |
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Antibiotics and Diarrhea in horses
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-Antibiotics change colonic flora
-Disbiosis can occur, disrupts normal symbiotic relaitonships -Can cause diarrhea -Diagnosis of exclusion, with history |
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Pathogenesis of Diarrhea in horses
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-Inflammation of colonic mucosa is main issue that causes clinical signs
--can be invasion, irritation, etc. -Inflammation allows translocation of bacteria --bacteria or endotoxin gets into blood and causes systemic issues --endotoxin interacts with macrophages/neutrophils and causes release of cytokines -Cytokines activate COX enzymes, results in tissue destruction, vasodilation (results in ischemia) -Bacteria has LPS/endotoxin on cell membrane |
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SIRS
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-Systemic inflammatory response syndrome
-Bacterial endotoxins are released everywhere in the body -WHOLE BODY is responding to bacteria |
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Diagnostic tests for SIRS
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-Salmonella: culture or PCR
-Clostridium: toxin assay -Potomac horse fever: PCR on blood -Coronavirus: PCR on feces -Sand: sedimentation test of feces and auscultation, image on ultrasound -NSAID toxicity: history, ultrasound for thickening of right dorsal colon -Parasitism of encysted small strongyles: rule out and history -Anti-microbial associated: history |
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Diagnostic tests that help guide treatment for Diarrhea in horses
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-CBC/Chem, look for electrolyte derangements
--low Na, low Cl, low K -Metabolic acidosis -Elevated creatinine due to pre-renal azotemia or renal azotemia --compare with USG -Low WBC count in acute phase, margination of neutrophils -PCV will be increased, TP will be decreased --“splitting” -Elevated lactate, switch to anaerobic metabolism |
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Treatment for horse with Diarrhea
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-Can be specific or supportive
-Some DDx have specific treatments, some do not |
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Potomac horse fever treatment
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-Ocytetracycline
-Fever usually precedes diarrhea, if treat early enough with oxytetracycline, may avoid diarrhea |
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Clostridium in horse treatment
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-Anaerobe, give metronidazole
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Treament of Salmonella in horses
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-Treat with antibiotics? Debate!
-Antibiotics will further disrupt GI flora, makes it worse -Antibiotics will not change course of disease -Good for preventing or avoiding translocation of bacteria --treating other bacteria that is translocating from got -If neutrophil count is less than 1,000 (neutropenia), treat with antibiotics |
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Coronavirus diarrhea treatment in horses
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-No specific treatment, supportive care
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Sand diarrhea in horses treatment
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-Psyllium, Metamucil
--mobilizes sand from colon -Gradual elimination of sand over time |
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Treatment of NSAID toxicity in horses
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-No specific treatment
-Sucralfate to prevent ulceration, protect submucosa |
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Parasitism causing diarrhea treatment in horses
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-Anthelmintics
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Dysbiosis treatment in Horses
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-Fecal transplant
-Fecal cocktail from a normal horse, give via stomach tube to horse with dysbiosis |
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Supportive care for horses with Diarrhea
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-Replace fluids! Most important treatment
-Address endotoxemia --bind endotoxin: Polymixin B, E. coli hyperimmunized plasma (J5), activated charcoal, biosponge (clay product) -Combat effects of endotoxin, inhibit metabolic effects: --COX inhibitors (NSAIDs), pentoxyphylline, DMSO (free radical scavenger) -Probiotics -Prevent laminitis --ice feet (decrease metabolic rate in laminae) |
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Frank blood in horse feces
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-Clostridium
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Prognosis for Acute Diarrhea
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-Good
-Unless animal gets laminitis! Then prognosis is poor |
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Chronic Diarrhea
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-Chronic inflammatory bowel diseases
-Unknown etiology -Can involve small or large intestine -Characterized by infiltration of intestinal wall with inflammatory cells --unknown reason --causes thickening of the intestine, increases barrier to absorption of nutrients -Decreased absorption of nutrients, protein losing enteropathy -May or may not have diarrhea, depends on how the colon is affected -Characterized by whatever type of inflammatory cell is present -Diagnose via glucose absorption test and intestinal biopsy (need to do surgery) |
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Diarrhea in foals
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-DDx varies based on age of the foal
--different causes in different aged foals -1-6 days: neonatal sepsis and septicemia, ischemic enteropathy --failure of passive transfer -1 week-6 months: foal heat diarrhea, salmonella, clostridium, rotavirus (2 weeks) -6 months-1 year: Lawsonia intracellularis |
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Neonatal septicemia
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-In foals 1-6 days old, neonate
-Due to failure of passive transfer -Hyperemic mucus membranes -Dehydrated -Diarrhea (may not be worst of the clinical signs) |
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Ischemic enteropathy
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-Affects foals 1-6 days old, neonate
-Part of neonatal ischemia syndrome -GI is affected by decreased blood flow and ischemia -Results in ileus, bloat, reflux, diarrhea |
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Foal heat diarrhea
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-Affects foals 1 week old
-Unknown cause --mother’s milk composition changes? --GI flora in foal is starting to change -Foal gets diarrhea when dam comes back into heat -Self-limiting diarrhea, animal does not get too sick from it -Needs to be differentiated from more serious types of diarrhea --salmonella, clostridia --will not have hyperemic mucus membranes or petechiations in pinnae |
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Salmonella in foals
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-Can be really nasty!
-Affects joints -In foals over 1 week of age -Put on antibiotics! Antibiotic that will be effective against salmonella |
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Clostridium perfringens and difficile in foals
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-IN foals over 1 week old
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Rotavirus in foals
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-Affects foals more than 2 weeks-4 months
-Most common cause of diarrhea outbreaks in foals on breeding farms -Attacks villous intestinal tips, causes villous atrophy and --results in decreased fluid absorption and diarrhea -Dehydration also -Can be mild diarrhea or really severe and cause death --varies in severity from mild to fatal -Vaccine exists, give to mares in late pregnancy --increases antibody levels in colostrum --decreases incidence and severity |
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Rhodococcus Equi
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-Usually a respiratory infection, causes abscesses in lungs
-Can also cause mesenteric abscesses and result in diarrhea --also other extra-pulmonary sites affected -Tx: macroline --can cause antibiotic diarrhea |
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Antibiotic associated diarrhea in foals
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-Associated with rhodococcus equi treatment
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Macrolides causing diarrhea in horses
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-Adult horses are VERY sensitive!
-Mare can get diarrhea from macrolides just from licking foal, or from getting a small amount ingested |
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Parasites causing diarrhea in foals
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-Ascarids are main concern
-Starts around 2 months of age, ends around 6 months -Can cause impaction and colics after deworming during passing |
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Lawsonia intracellularis diarrhea in foals
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-6 months to a year of age
-Bacteria, intracellular --Can survive in soil -Causes proliferative enteropathy, mostly of the small intestine --thickening of epithelial cells in crypts of small intestine -“Garden hose gut” in pigs -Causes protein-losing enteropathy --Will see edema due to low protein -Diagnose with PCR in feces -Treat with oxytetracycline, doxycycline, chloramphenicol |
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Approach to diarrhea in foals
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-Triage into systemically sick animals and mildly sick animals
--based on DDx -Look at perineum and tail for diarrhea -If foal is still nursing and not dehydrated: --prevent gastric ulcers, sucralfate --maybe not proton pump inhibitors, want to maintain protective benefit of low pH -IV fluids if foal is sick and not nursing |
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Fluid volumes for horse
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-60% of horse is water
-Fluid compartment is divided into intracellular and extracellular fluids --intracellular compartment is larger, 40% of body weight -Extracellular fluid is divided into interstitial (extravascular) and intravascular -8% of body weight is blood -Horse is big and has a lot of water! Need to use large volumes to treat -Exchange of water and electrolytes between intracellular and interstitial fluid --slow exchange, needs ATP -Exchange of water and electrolytes between interstitial and intravascular fluids --rapid exchange, via diffusion, no energy needed --what is in blood is a good assessment of what is in interstitial space, but NOT what is in cells -Blood=interstitial fluid, NOT cellular fluid |
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How much water is needed for an animal?
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-1ml/pound/hour
-1L/hour for horses |
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Why do we give fluids?
|
-Restore intravascular volume, allow perfusion and cardiac output
--ensures delivery to the cells -May be needing a specific electrolyte or glucose |
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Estimating dehydration
|
-Mild: water deficit is 6%
-Moderate: 9% bw -Severe: 12% bw -Examine animal to determine mild, moderate, severe --based on clinical signs |
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Clinical signs of dehydration
|
-Oral mucosa and saliva may be tacky or sticky with mild dehydration, dry with severe dehydration
--may be cold with severe dehydration -CRT: should be about 1 second --moderate, 2-4 sec --severe: longer than 4 seconds -Skin tent, tissues lose pliability -Sunken eyes, eyeball recession --only shows up with moderate or severely dehydrated animals -Jugular vein refill delay -Temperature of extremities will drop -Recumbent animals are severely dehydrated animals |
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How fast can you give fluids?
|
-give half of calculated amount in a bolus over 1 hour
-Shock dose: 60ml/kg bolus -Continuously reassess clinical signs and lactate! |
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Routes of fluid administration
|
-Mild dehydration: can rehydrate with enteral fluids
-With more dehydrated animal, will probably need IV fluids -Can give SQ in small animals, not so much in large animals |
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Fluid types: Crystalloids
|
-similar composition to plasma
-Plasmalyte -Normosol R: has bicarbonate precursors -Lactated ringers -Saline 9%, has Na --use in animal that has hypochloremia and alkalosis -D5W: dextrose in water --maintenance fluid, but do not give too fast or will cause diuresis --NOT a resuscitation fluid -Do not give hypotonic fluids into vasculature |
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Electrolytes in Plasma
|
-Na: 140
-Cl: 100 -K: 4 (mainly intracellular ion) -Bicarb: 25 --Fluids do not have bicarbonate, have bicarbonate precursors --lactate, acetate, metabolized into bicarb in the liver |
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Hypertonic saline
|
-Concentrated saline |
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Hetastarch
|
-Hydroxy-ethyl cellulose |
