---start---- donaldson equine colic Goals: learn incidence of medical and surgical colic causes of, risk factors assoc. w/, colic evaluation and tx of colic in the field do not attept to learn all the causes; lean rather the principles of managing horses with colic. Incidence of colic: common. 25-50% of emergency equine calls most resolve with medical mgmt. location of lesion and cause remain unknown from 11/1/95-11/1/98: 182/436 equine emergency calls were for "colic" for 87% of colic cases in one report, dx was made on PE. 5% at sx, 6% at necropsy. your hands, eyes, ears are important! What is Colic? **** colic is a sign of a disease, not a diagnosis or specific dz entity!! *** colic == manifestation of abdominal pain (due to some other problem) sign vs symptom - symptom = what person describes, subjective; sign = objectively visible sign of something mechanisms of pain: 1. superficial (pinprick), deep (broken arm), visceral (poorly localized) for example, someone may think they feel chest pain from gastric ulcers. 2. mechanical, thermal, inflammatory localization of pain; referred pain: referred pain - pain in chest may radiate down arm, pain in abdomen may be referred into chest. superficial and deep pain are well localized, visceral pain is poorly localized. signs of colic are numerous, and easily confused with signs of pain in other areas: pawing, lying down and getting up frequently, stamping, kicking at abdomen, looking at flanks, restlessness, rolling, stretching out, posturing as if to urinate, sweating, playing in water, anorexia, shifting weight, self trauma, tenesmus, depression. slide: one horse who used to kick out with one leg to the side with each bout of recurrent colic. cause unknown. note signs occur with other diseases: pawing may occur with anxiety, one horse at the Radnor hunt was pawing during an episode of tying up. Evaluation of horse with colic: signalment - age, breed, sex, use of horse - may predispose to certain diseases, examples: age: foals - ascarid impactions; old horse - neoplasia breed: Arabs - enteroliths; standardbred - inguinal hernia sex: stallions - inguinal hernias; mares - breeding/parturition trauma use: racehorse - gastric ulcers; pleasure horse - mgmt by owner - less likely to have colic; mgmt by trainer more likely to have colic! History - owner will call and say "come see this colicky horse" but you must decide if the horse really has abdominal pain or not. the history frequently contributes a large portion of the information allowing us to make a diagnosis. history taking is very very important. allow owners to describe exactly what they have seen that makes them suspect the horse has colic. try not to interrupt the client so much. Let client tell you what they saw, while you watch the horse, see what it is actually doing. see if it goes along with colic. find out duration and severity of signs - owner may have noticed mild changes yesterday and more severe today, or normal until an hour ago; appetite - with low grade chronic pain may keep eating, with severe acute pain may stop; feces - character, quantity - some obstructed horses will still pass feces. get other recent history (change in training level - racehorse on stall rest for injury), past medical history, any meds (NSAIDs like phenylbutaone may cause ulcers), anthelmintic schedule (regular worming? appropriate intervals? parasitism is underinvestigated as a cause of colic - parasites can affect GI motility, blood flow, may cause hypersensitivity reaction), pasture condition (sand colic), stocking density, diet and changes in diet (pasture horse suddenly given feed, sometimes chronic colic cases resolve with diet changes as one horse changed from corn to a less volatile grain did); recent transportation (may cause dehydration); dental care (check teeth!); geographic location (NJ shore, predisposed to sand colic; poisonous plants in some areas; location may influence diet, parasites; enteroliths occur more in CA; SE US more ileal impactions on bermuda grass hay, etc); other sick animals on farm (parasite problem, salmonellosis, toxic element in feed, monensin poisoning could present this way though usually heart signs; strangles - abd abscess), changes in activity (very common risk factor for colic), previous colics (horses that colic once are more likely to colic again), farm type and management (riding schedule changes, feeding schedule changes, appropriate handling measures, high stocking density might predispose to parasitism, lots of transient horses maybe more infxns dz), weather (full moon? horses less likely to drink cold water, prefer warm water. more common to see impactions in cold weather). other causes of "colic" remember mechanisms of pain - if visceral pain, probably will manifest b/c of stretching of an organ. viscera being stretched by mass, gas, fluid, impaction of ingesta, foreign body. or, may be due to inflammation or ischemia. limits exist in how animal can show pain look at owner's interpretation - may help you decide each organ system has a painful process that may mimic GI pain: liver (abscess may be painful, cholelithiasis is classic liver dz associated with pain, anorexia, fever), urinary (urolithiasis, obstruction), thoracic (esophageal reflux, pleuritis), CNS (rabies can present initially as anorexia or dysphagia; other encephalitis), musculoskeletal (exertional myopathy, laminitis), reproductive (impending parturition looks just like colic). initial exam of horse with colic: depth of history taking will depend on severity of pain. if severe, rolling, thrashing, you don't take a long history and discuss minutiae. you control pain as best you can, get TPR basic PE before sedation if possible. talk about it later. some analgesics affect GI motility, be careful. if horse isn't that painful, you can do more detailed careflu history. watch horse while talking to owner. assessment of pain: onset, severity, duration - examples: sudden and acute, chronic and gradual, etc. severity - violent, mild, etc. severe depression w/o pain may indicate bowel necrosis or rupture pain may be intermittent (spasmodic) or continuous self trauma may be present - some studies show this is associated with poor px. if horse requires analgesia - do brief PE first, TPR, CV status, abdominal auscultation - then short acting analgesic/sedative, nasogastric intubation. if not, watch horse from distance PE: cardiovascular system - need to assess, check for hypovolemic shock heart rate: tachycardia - occurs due to pain, hypovolemia (to maintain CO), acidosis, toxins, anemia, endotoxemia (important - this alone will cause tachycardia) peripheral pulses: poor if poor perfusion extremities: cold if poor perfusion mms - pale, hyperemic, cyanotic? crude estimate of cv function. pale with anemia or pain-induced vasoconstriction, hyperemic w/sepsis, endotoxemia, vasodilation; cyanotic due to poor oxygenation - DIC, huge abdominal distension impeding ventilation, poor CO. CRT hydration - skin turgor, jugular refill, crt anyway - assess that stuff, look for shock ---break--- abdominal auscultation and percussion(!!!) auscultation kind of an art. listen for frequency of sounds, absence of sounds, location and quality of sounds. fluid, gas, sand affect sounds - sand causes seashore sounds in cranial ventral abdomen. repeated evaluation is important, abdominal distension. interpretation of presence of borborygmi - there can be churning, moving ingesta around, without actually causing progressive motility. again, repeated evaluation is important. motility may stop, or start. lack of any sound each time is very concerning, complete ileus is associated with ischemia, inflammation, severe obstruction. so focus on cardiovascular and GI evaluation but do not forget all the other stuff - musculoskeletal, CNS, dentition especially. horse could have rabies, pericarditis, exertional myopathy slide: this horse was "colicking" last year, laying down in stall. seemed sort of stiff. intern went out - patchy sweat on either side of withers, tie shaped. also hypoalgesic in that area - no sensation there. also, he had no real withers! he fractured the withers, was in pain. the sweating and hypoalgesia was from nerve root compression. skin/sweat gland innervation is partly sympathetic. so do a complete exam. listen for pleuritis, check for laminitis, myositis, look at teeth. nasogastric intubation: so horse is there, you think you need to try this - what do you do? well, when do you do it? it can be therapeutic and diagnostic. no real contraindication other than potential bleeding from trauma passing tube. no reason not to do it, though not always needed. if large volumes of fluid are present in stomach you can get them out. if you do, you knwo what the problem might be - obstruction, ileus. where might obstruction be? small intestine...duodenocolic ligament is present so if colon is full and displaced, may put tension on duodenum and cause reflux so other lesions might create some gastric reflux but most severe ones are from proximal lesions. use sense of smell - if really foul, could mean necrosis. look - yellow, bloody,ascarids coming out of the tube? also, rarely - reflux in horse occured, bucket used to collect it - found a lot of sand in it. make sure your tube goes into the stomach. sometimes people lavage the distal esophagus. it's an easy mistake, try not to make it. you want to get stomach contents - bile, hay, oats, whatever. significance of excessive gastric reflux - probably a proximal lesion, often surgical. some medical. refer the horse, with tube in place. hard to manage these horses on the farm. Rectal exam: when to do, when not to do? when not to do: if you are afraid. be safe. ensure your safety first. also ensure horse's safety - if too fractious, can't do. risk of rectal tear. make sure it is indicated. when to do: when it is indicated (?) develop a routine. you only feel the caudal 1/3 of the abdomen. make sure you feel all of the possible parts you can. you can palpate cecum, pelvic flexure of large colon, uterus, accessory sex glands, inguinal rings, bladder, lymph nodes, left kidney and spleen right next to left kidney; dorsally the terminal aorta and internal and external iliac. on right, cecal bands. abdominal wall. evaluate feces - mucus, parasites, diarrhea, dry/fibrous, poorly digested, sand, blood (occult) limitations of exam- you're only feeling caudal part of the abdomen. now, use all the info you've obtained to synthesize a plan. history, degree of pain, PE results, NG tube, rectal results. also repsonse to analgesia - does mild analgesic help or not? so think of options. you won't know the exact problem but you can assess severity. present ALL the options. many times, owners have elected to try any available therapy even if you think they'll never go for it. additional dx: indications: many things can be done on farm, some only at hospital. if you think something else is going on you can try: hematology: CBC - RBC, WBC, platelets - the PCV/TS of hypovolemic horse will be increased. if horse has secretory diarrhea, for example - PCV and TS both rise - hemoconcentration, hypovolemia. PCV/TS very useful test. with severe inflammatory colitis, WBC can go up or down - up initially, down if severe due to sequestration of WBC at lesion site or at postcapillary endothelium due to margination because of endotoxemia. early DIC -> thrombocytopenia serum biochemistry: TP, electrolytes, creatinine, pH, enzymology, fibrinogen severe inflammatory bowel lesions can cause loss of protein into feces - protein losing enteropathy, hypoproteinemia. hypocalcemia can occur, hypokalemia can occur with enteropathies. obstructive urolithiasis can be suggested by elevated creatinine level, or prerenal azotemia could exist. low pH -> lactic acidosis, loss of bicarbonate via GI lesion. enzymology - liver, muscle. can r/o exertional myopathy, cholelithiasis. fibrinogen - if chronic problem, will be elevated; if acute, won't be elevated yet. abdominocentesis - sampling peritoneal fluid detects what is going on in abdomen. look for inflammatory mediators, WBC, RBC, TP, cytology. if strangulating lesion, RBC may be present; cytology is key. if lesion is very acute you might have severe necrosis and bacteria present - septic peritonitis - without big WBC response. cytology is often overlooked. fecal - parasite/culture; UA: parasites, enteric infections ultrasonography: transrectal, transcutaneous: evaluate palpable masses and nonpalpable areas. endoscopy - to detect gastric ulcers exploratory celiotomy/laparotomy - the ultimate diagnostic. sometimes the fastest way to find out what is going on. consequences of severe GI dz in the horse: *** inflammation or ischemia of the gastrointestinal tract leading to loss of fluid and absorption of endotoxin.the combination of hypovolemia and endotoxemia may lead to shock and multiple organ system failure. prevention and early treatment are KEY to survival. *** once you pass a certain point, no tx helps. endotoxemia - endotoxin in blood. different from septicemia - viable microorganisms circulating. septicemia is usually accompanied by endotoxemia, but endotoxemia can occur w/o septicemia. SIRS: systemic inflammatory response syndrome - systemic response to release of vasoactive inflammatory mediators, regardless of origin. shock: inadequate tissue oxygenation, frequently due to poor perfusion. tx endotoxemia, SIRS, shock: restore CO, give crystalloids, hypertonic saline which is rapid and cheap - low volume hypertonic 7.4 % saline will increase CO by a direct mechanism and will pull fluid into the intravascular compartment. must follow with large volumes of isotonic fluids colloids: plasma, synthetic colloids - albumin, ATIII, fibronectin, alpha MacG the synthetic ones can be given rapidly; but plasma has a lot of valuable stuff in it (albumen, ATIII, fibronectin, alpha macroglobulin, etc) cardiac support - beta-adrenergics inhibit endotoxin - hyperimmune plasma, polymyxin b inhibit endotoxemia mediators - give flunixin meglumine (banamine), pentoxifylline (Trental). inhibit free radicals: dimethyl sulfoxide (DMSO) managing abdominal pain in horses: why provide analgesia? so they don't hurt themselves, because it is kind, so they do not hurt us, to decrease physiological response to pain- decrease catecholamines which vasoconstrict; get rid of pain effects on GI motility choosing an analgesic: duration, toxicity, efficacy, side effects must all be considered. in acutely painful horse use something rapid-onset, short-acting. later on, after you have a dx, you can use more analgesics or longer acting ones. toxicity - NSAIDs will have toxicity in right dorsal colon and in kidney. efficiacy - how potent is it? alpha2 adrenergic agonists: these are most often used. rapid onset, short acting, very potent analgesics. they create profound ileus, though. that's good in some cases - if you have an impaction you are rehydrating. xylazine, detomidine opioid agonist/antagonists: butorphanol is most common. also potent narcotic. these decrease GI motility too. relatively short acting - about an hour. NSAIDs: flunixin meglumine is good for GI/visceral pain evaluate if the pain is really of GI origin carefully evaluate to rule out need for hospitalization treat pain and shock investigate and treat cause, if needed. case: 17 yr old arab gelding fall 1998 use: companion owner noticed horse getting up and down several times in pasture PE: NR, standing quietly with owner detailed history obtained good worming program, adequate pasture, no change in routine. only thing noticed is a creek going through the yard. infectious colitis in horses can occur sometimes during the year associated with river waste...potomac horse fever. enteritis associated with ehrlichia. hmm. horse showing no signs of pain or compromise at this time, though. systemically seems healthy. rectal not indicated. plan: watch for recurrence call owner next day - horse is fine, out grazing, no problem. this is a common scenario. transient pain, no problems. NBC spring 1995 12 y.o TB mare, foaled 2 days ago, now mild colic, anorexia, fever. gave flunixin and refered to NBC. PE T 101, p 48, RR 12, sl depressed, not eating, sl hyperemic mms, GI sounds decreased. foaling was normal rectal exam normal; repro tract feels normal, speculum exam normal. no GI reflux. PCV/TS -normal. CBC: mild leukocytosis, chem: elevated fibrinogen. u/s - echogenic peritoneal fluid present. abdominocentesis - WBC, protein elevated. cytology - mostly neutrophils, some degenerate, occasional intracellar bacteria. septic peritonitis? give fluids, antibiotics not helping. exploratory celiotomy - part of small colon is necrotic and ischemic mesentery present. trauma during foaling most likely. nonresectable. euthanized. ----end----