lecture 18-21.pdf

Lecture 18: Equine GI sx ● Colic = abdominal pain ● Colic is a symptom, not a disease ● Possible sources: ○ GI ○ Hepatic ○ Urinary ○ Reproductive ○ Peritoneum ○ ANYTHING IN THE ABDOMEN ● 4 sources of pain: ○ Stretch (distension) ○ Tension ○ Inflammation ○ Infarction ○ Transmitted by mechanical (stre...

Lecture 18: Equine GI sx ● Colic = abdominal pain ● Colic is a symptom, not a disease ● Possible sources: ○ GI ○ Hepatic ○ Urinary ○ Reproductive ○ Peritoneum ○ ANYTHING IN THE ABDOMEN ● 4 sources of pain: ○ Stretch (distension) ○ Tension ○ Inflammation ○ Infarction ○ Transmitted by mechanical (stretch, tension, infarction) and chemical (inflammation) receptors ● Stuff that looks like colic, but isn’t: ○ Myositis ○ Pleuropneumonia ○ Laminitis ○ Ataxia ○ Dementia ● Small intestine: ○ Duodenum, jejunum, and ileum ○ Ileum is more muscular and has antimesenteric band ■ Connects to dorsal band of the cecum via ileocecal fold ○ Vascular arcades: ■ Major jejunal vessel ■ Arcuate vessel ■ Vasa recta ● Cecum: ○ 4 bands (teniae): ■ Dorsal and medial go to apex ■ Dorsal band > ileocecal fold ■ Lateral band > cecocolic fold ○ Ileocecal valve ○ Cecocolic valve ● Large colon: ○ Flexures ○ Pelvic flexure is narrow- important site for obstruction ● Small colon: ○ Long, fatty, mesentery ○ Attach to duodenum via duodenocolic ligament ● Stomach lesions: ○ Ulcers ■ Presenting complaints vary by age ● Adults: off feed, bruxism, low grade colic (often chronic), poor performance ● Foals: colic, bruxism, ptyalism ○ Dramatic ■ Dx: ● Gastroscopy or empirical response to tx ■ Can cause rupture ● Dx at laparoscopy or necropsy ■ History of chronic of high dose NSAID use ● Inhibit production of protective prostaglandins ■ Typically occurs in the non-glandular squamous epithelium ● Margo plicatus, lesser curvature ■ Tx: ● Antacids ● Sucralfate ○ Band Aid- won’t fix the problem, but will help them feel better ● H2 antagonists ○ Zantac or pepcid ● PPI ○ Omeprazole- gastrogard/ulcergard ■ Tx of choice ○ Impaction ■ Occurs secondary to ingestion of: ● Excessive amount of dry fibrous material ● Feeds that swell (such as wheat, barley, sugar beet pulp) ● Materials that form a mass ○ Persimmon seeds or mesquite beans ■ Dental disease increases risk ■ More often mild/chronic, but may be acute/severe ■ Dx: ● U/S ○ Enlargement but little reflux abstained or when the reflux consists primarily off feed ○ Endoscopy ○ Exploratory celiotomy ● Tx: ○ Lavage via NG tube ○ Diet coke ○ NPO until impaction is cleared ■ Risk of gastric rupture ○ Neoplasia ○ Gastric outflow obstruction ■ Pyloric stenosis ■ Pyloric mass (associated w/ ulcers or neoplasia) ○ Risk of rupture secondary to ulcers, impactions, or other obstructions ● Small intestinal lesions: ○ Strangulating: ■ Epiploic foramen entrapment ● Margins: ○ dorsal/craniodorsal- caudate lobe of the liver (near vena cava) ○ Cranioventral: portal vein ○ Ventral: gastropancreatic fold ○ +/- normal clinical signs of SI strangulating lesions ○ Most occur left to right ○ 50% of cases involve both ileum and jejunum ■ Jejunum alone: 30% ■ Ileum alone: 20% ○ Cribbing appears to be a predisposing factor ○ Fatal hemorrhage from rupture of the portal vein is an important surgical complication ○ Associated w/ decreased long term survival after sx ■ Pedunculated lipoma ● Causes obstruction when pedicle wraps around intestine ● Older horses are at greatest risk ○ 14-19 years old ● Arabians at higher risk ● Affected horses are not necessarily overweight ● 90% are found in the SI ○ 10% found in small colon ● Once identified- must cut stalk ● R & A of affected intestine ● Post op complications common ○ Post op ileus ■ Intussusception ● Acute form: sudden onset, progressively severe abdominal pain ● Subacute: anorexia, depression, intermittent colic ● Dx: ○ U/S ○ Sx ● Most commonly caused by abnormal motility ○ Other causes: ■ Heavy ascarid ■ Enteritis ■ Tapeworms ■ Abrupt dietary change ● Tx: ○ Sx ■ Will often require R & A ■ Inguinal/scrotal or umbilical hernia ● Inguinal/scrotal: ○ Most are indirect ■ Passes thru vaginal ring into vaginal tunic ○ Direct hernias are more common in foals ○ Adults: acquired and irreducible with a short segment of bowel affected ○ Foals: congenital and reducible with a long segment of bowel affected ○ Predisposed breeds: standardbreds, tennessee walkers, saddlebreds ○ Inguinal incision ■ Unilateral castration recommended ● Umbilical: ○ Most common strangulating lesion involves only the antimesenteric wall of the ileum ■ Parietal (Ritcher’s) hernia ● Becomes non reducible and painful to palpation ■ Volvulus ■ Mesenteric rents ■ Gastrosplenic ligament incarceration ■ Mesodiverticular band (vitelline anomaly) ■ Strangulating lesions are ALWAYS surgical ○ Non-strangulating: ■ Ileal impaction ● Most commonly primary condition of normal ileum ● Most common in SE U.S. related to feeding coastal bermuda grass hay ● Also been associated w/ tapeworm infection ● May be able to palpate rectally ● Early: can tx medically; sx often required later ■ Ascarid impaction ● Parascaris equorum ○ Roundworms ● Usually foals < 6 months ● Commonly affected foals have been administered dewormer within past 24 hours ● Dx: ○ Fecal ○ Sx/necropsy ● Tx: ○ Sx indicated if obstruction ○ Analgesics + lube ● Poor prognosis ● Prevention: ○ If heavy: use staged kill technique ■ ½ dose of dewormer 1st ■ 3 weeks later give 2nd tx ■ Duodenitis-proximal jejunitis (proximal enteritis) ● Hallmark: large amounts of NG reflux ○ > 48 L in 24 hours ● Fundamentals of tx: ○ Frequent decompression via NG tube ○ Medically manage electrolyte abnormalities, dehydration, etc. ○ NPO until c/s resolve ■ Never oral fluids ● Serious complications due to endotoxemia (including laminitis) can occur ● Horses with enteritis may still require sx (if uncontrollable pain) ■ Muscular hypertrophy of the ileum ■ Neoplasia ■ Gastroduodenal obstructions ■ Intestinal inflammation and fibrosis ■ Lesions may be surgical- often the dx is made at surgery ● Obstruction/strangulation vs proximal enteritis: ○ Obstruction/strangulation: ■ Any age ■ Intense pain that progresses to depression ■ Strangulation: rectal palpation- more likely to have tightly distended loops of SI ■ Hypomobile, moderately - marked distended bowel on U/S ■ Peritoneal fluid: serosanguinous fluid ○ Proximal enteritis: ■ Rarely young horses (<1.5 years) ■ Intense pain that progresses to depression ■ Sick- may have a fever and leukocytosis or leukopenia ■ Volume of reflux is usually greater than in obstruction ■ After gastric decompression: will improve attitude and HR ■ Peritoneal fluid: increased TP Lecture 19: Equine Sx 2 ● Cecal lesions: ○ Impaction: ■ Most common cecal disease ■ Multifactorial: ● Poor dentition ● Poor hay quality ● Decreased water intake ● Tapeworms (Anoplocephala perfoliata) ● Hospitalization prior to sx, particularly ortho ○ NSAIDs, anesthesia, immobilization ■ Dx: ● Rectal palpation ○ Best to dx early ■ High risk of rupture ■ Often happen w/o warning ■ Tx: ● Hydration ● +/- mineral oil ● AVOID: ○ Xylazine ○ Butorphanol ● Promotility agents are controversial ○ Neostigmine is not recommended ● Sx probably best for moderate-severe impactions ○ Intussusception (cecocecal, cecocolic) ○ Volvulus or torsion ○ Infarction ○ Neoplasia ○ Cecal rupture: ■ Commonly secondary to cecal impaction ● Large colon lesions: ○ Large colon tympany: ■ Gas colic, spasmodic colic ■ Gas colic is due to excessive fermentation ■ Most common large colon dz and cause of colic in horses ■ Bowel distension and pain ■ Risk factors: ● Cribbing ● Recent exercise change ● Ineffective deworming regimen ● Hx of travel ● High carb diet ■ Dx: ● Rectal exam ■ Typically respond to conservative tx: analgesics and temporary withholding of food ○ Impaction: ■ Second most common large colon dz ■ Can be caused by feed, sand, gravel ■ Tends to occur in places where the diameter of the GI tract changes dramatically ● Pelvic flexure ● Junction of right dorsal colon and transverse colon ■ Risk factors: ● Same as cecal impaction and tympany ■ Dx: ● Most frequently on rectal exam ■ Tx: ○ ○ ○ ○ ○ ● Medical: ○ Oral +/- IV fluids, analgesia, oral laxatives, temporary withholding of food ○ Early/mid impactions typically respond to medical management in 24-48 hours ● Large impactions often require sx ■ Sand impactions: ● Often present as chronic mild diarrhea ○ Transient diarrhea ● AXR needed ● Rupture is a major concern ● Major risk factor is feeding on ground w/ sandy soil Enterolith: ■ Primarily struvite crystals and magnesium ammonium phosphate ■ Ingested FB can act as nuclei for formation of enteroliths ■ Single enteroliths tend to be spherical ■ Flattened surfaces are highly suggestive of multiple enteroliths ■ Can cause acute, persistent colic OR intermittent low grade colic due to intermittent obstruction ■ Most commonly located in the right dorsal colon, transverse colon (hard to get out), and small colon ■ Sometimes dx by AXR ■ Tx: ● Always surgical Nephrosplenic entrapment: ■ Dx: ● Rectal exam and/or AUS ■ Large colon is displaced dorsally and to the left and becomes stuck in the nephrosplenic space ■ Often impaction is present ■ Medical management: ● Phenylephrine to shrink spleen + jogging ○ May be a possible complication of fatal hemorrhage ● Rolling ○ Requires GA and lots of help Right dorsal displacement: ■ Initiated by retropulsive movement of impacted pelvic flexure and migration of the large colon to the right ■ Large colon located between the cecum and the body wall ■ Cannot palpate the pelvic flexure on rectal exam ■ May be able to resolve medically ● If no response- sx Strangulating large colon volvulus: Large colon displacement/volvulus: ■ Volvulus: ● </= 270 degrees- non-strangulating ● >/= 360 degrees- strangulating ○ If < 360 degrees may also be described as right dorsal displacement or left dorsal displacement/nephrosplenic entrapment (NSE) ● Rotation most commonly occurs at/or proximal to the cecocolic ligament ○ Twist must be palpated to determine direction for correction ● NSE can cause strangulation of the entrapped portion of the colon ○ Large colon volvulus: ■ Most painful and devastating GI disease ■ Risk factors: ● Broodmares ● Recent parturition ● Diet changes ● Recent access to lush pasture ■ Usually clockwise direction as viewed from behind the horse ● Palpation intra-op to confirm ■ Pathology linked to colonic wall devitalization via ischemia and/or congestion > fluid sequestration in the lumen > bacterial translocation and massive endotoxin release into systemic lymphatics and vasculature > septic/endotoxic shock ● Early referral and prompt sx intervention significantly improves prognosis ○ Right dorsal colitis ○ Mural infarction ● Small colon lesions: ○ Non-strangulating obstructions: ■ Fecal impaction (or meconium impaction in foals): ● Most commonly reported lesion of the small colon ● Same risk factors as other impactions + salmonella ● Typically a diffuse impaction rather than focal ○ Different than large colon ● Meconium impaction: ○ Neonates ○ Progressive abdominal distension and pain ○ Persistent straining can lead to patent urachus and/or ruptured bladder ○ Tx: ■ Fluids ■ Warm lubricated based enemas ■ Rarely need sx ■ Fecalith: ● Isolated intraluminal impaction ● Chronic focal intraluminal pressure can compromise the bowel wall ○ Infarction or rupture ● May be difficult to palpate rectally ● Mini horses are predisposed ● Sx tx is always required ● Rectal tears: ○ Causes: ■ Iatrogenic ● Most common ■ Enemas ■ Meconium extraction via forceps ■ Misdirection via bleeding ■ Spontaneous tears ○ Risk factors: ■ Small horses ● Especially arabians ■ Horses that are straining ■ ■ ■ ■ Horses w/ colic Repeated rectal palpations Stallions and geldings Inadequate restraint and lube ○ Dx: ○ ○ ○ ○ ■ Blood on rectal sleeve ■ Loss of resistance ■ Careful palpation and colonoscopy ■ Signs of colic, peritonitis, and endotoxemia ■ PE ■ Abdominocentesis Grading: ■ Grade 1: ● Involves mucosa and submucosa ● Most common ■ Grade 2: ● Involves muscular layers, but mucosa and submucosa are intact ○ May get fecal impaction in resultant diverticulum ● Very rare ■ Grade 3: ● Involve mucosa, submucosa, and muscle ● Gross contamination may be contained but can still impact peritoneal environment ■ Grade 4: ● Involves all layers ● Gross contamination of the abdomen Non-sx tx: ■ Grade 3 or lower ■ Food deprivation ■ Gentle manual evacuation of the rectum ■ Broad spectrum abx ■ Flunixin meglumine ■ Laxatives and laxative diet ■ Cheap and effective First aid for more severe tears: ■ Address endotoxemia and peritonitis ● Broad spectrum abx ● Anti-inflammatories and anti-endotoxic meds (flunixin) ● IV fluids ■ Temporary rectal packing in horses that are being referred for definitive tx ● Can be challenging Suture repair: ■ Ideal when fresh ■ Easiest when close to anus ■ Techniques: ● Instrument suturing ● Blind direct suturing ● Deschamps needle ■ Can combine w/ bypass procedure ● Indicated for grade 3 and 4 ● Colostomy or rectal liner +/- colon evacuation ● Goals: ○ Reduce fecal contamination from grade 3s ○ Prevent fecal peritonitis from grade 4s ● Rectal liner: ○ Complications: ■ Sleeve tearing ■ Retraction of sleeve into rectum uncovering tear ■ Formation of rectoperitoneal fistula ● Loop colostomy: ○ Can be reversed ○ Flush water thru distal part of small colon ○ Not common ○ Prognosis: ■ Excellent w/ mild tears ■ Euthanized w/ severe tears Lecture 21: Liver disease in horses ● Hepatic insufficiency: ○ Large functional reserve (80% must be damaged before basic function is impaired) ○ Hepatic disease may be present w/o signs of hepatic failure (subclinical) ○ C/S: ■ Weight loss ■ Anorexia ■ Colic ■ Depression ■ Pyrexia ■ Icterus ■ Hepatoencephalopathy ■ Less common signs: ● Coagulopathy ● Edema, ascites ● See notes for others ● Icterus: ○ Hyperbilirubinemia ■ Deposition of pigment into tissues ■ Total serum bilirubin = indirect + direct bilirubin ■ Do not confirm w/ light yellow cast to MM and eyes when eating greens ● Hepatic encephalopathy: ○ Abnormal mentation accompanied w/ hepatic disease ○ C/S: ■ Forebrain disease: depression, head pressing, circling, hyperactivity, aimless walking, persistent yawning, ataxia, disorientation, central blindness ■ Progression to unpredictable aggressive or violent behavior interspersed w/ somnolence ○ Dx: ■ Forebrain signs ■ PE and chemistry ■ Increased blood ammonia ● Associated w/ hyperammonemia ○ Increased in CSF and in serum ○ MUST be on ice ○ Severity correlates w/ degree of hepatocellular damage ○ Post-mortem: develop alzheimer type 2 astrocytes ● Hepatic photosensitization: ○ Secondary photosensitivity ○ Decreased clearance of phylloerythrin ■ Accumulates in the skin where UV light induces free radical production and cell damage ■ Most prominent in non-pigmented areas ● Diagnosis of hepatic injury- labs: ○ Liver specific: ■ SDH ● Hepatocellular necrosis ● Highly specific ● Short half life; acute or ongoing damage ● Used less than GLDH at UIUC ■ GLDH ● Hepatocellular mitochondrial enzyme ● Marker of acute or ongoing hepatocellular damage or necrosis ● Short half life; more stable than SDH ■ GGT ● Biliary epithelium ● Marker of cholestasis ● Longer half life than SDH and GLDH ● Baseline values are higher in neonates (< 4 weeks) and donkeys ● Other sources: renal, pancreatic GGT ○ Liver function tests: ■ BA (normal: 6-10 umol/L) ● Correlates w/ function reserve of the liver ● Excellent screen for liver damage ● Increased: ○ Hepatocellular damage ○ Biliary obstruction ○ Portosystemic shunts ○ ○ ○ ○ ● Specific for the presence of liver disease NOT specific for type of disease ■ Not affected by short term fasting ■ Higher values are found in neonates ■ Values in excess of 25 umol/L are associated with poor prognosis in adult horses Non-specific labs: ■ Bilirubin, ALP (will be high in growing horses), AST, LDH ● Bilirubin: ○ Can be NORMAL w/ liver damage ○ Indirect (conjugated): ■ Increased in acute hepatocellular disease, not specific ■ Increased w/ anorexia, hemolysis, and GI disease ● Anorexia is one of the most common reasons for elevated bilirubin ○ Direct (conjugated): ■ More reliable indicator of liver disease (value > 25% of total bilirubin) ● Liver disease ■ Cholestasis: > 30% of tbili, urine positive ● ALP: ○ Chronic of cholestatic liver disease ○ Pregnancy, hemolysis, GI disease, growing animals- will all be increased ● LDH: ○ Also found in muscle ○ Isoenzyme (LDH-5)- acute hepatocellular disease ● AST: ○ Acute hepatocellular damage ○ Increases dramatically secondary to muscle damage ■ Ammonia, plasma proteins, hemostatic function, BUN, glucose ● Hyperammonemia: ○ Hepatic disease ○ PSS ○ GI disease (increased production) ○ Tx: ■ Lactulose (oral) ■ Metronidazole (rectal or oral) Ultrasound Liver biopsy ■ COAG profile BEFORE biopsy ■ Usually right side ICS 12-14 Most useful dx: ■ GLDH (or SDH) ■ GGT ● ● ● ● ■ Total and direct bilirubin ■ Bile acids ■ Liver US and biopsy Tx of liver disease: ○ High carb, low protein diet ○ Correct fluid deficits ○ Address acid-base and electrolyte imbalances ○ Address coagulopathies ○ Mineral oil or biosponge by NGT ○ Oral abx ■ Metronidazole ○ Fibrosis = poor prognosis Equine hyperlipidemia: ○ Increased triglyceride concentrations ○ Associated w/ negative energy balance ■ Breed: ponies, mini horses, obese donkeys ■ Stress: illness, late gestation, early lactation ○ Clinical manifestation: ■ Common: reduced water and feed intake, depression ■ Severe: diarrhea, colic, fever, ventral edema, cachexia ○ Definitive dx: ■ Increased serum triglycerides ○ Mild: ■ All breeds: TG 100-500 mg/dl ■ Not associated w/ lipidemia, fatty infiltrates, clinical signs are rare ○ Severe: ■ Adult: TG > 500 mg/dl ■ Lipidemia absent ■ Rare clinical signs and fatty infiltrates ○ Hyperlipidemia w/ severe hypertriglyceridemia: ■ Ponies, mini horses, donkeys ■ TG > 500 mg/dl ■ Lipidemia, fatty infiltrates, clinical signs Normal energy metabolism: ○ Glucose ■ Primary energy source ■ Stored in liver as glycogen ■ Stored in adipose as triglycerides ○ 2 key hormones ■ Hormone sensitive lipase ● TG metabolism (adipose) ■ Lipoprotein lipase ● TG (VLDL) tissue uptake Negative energy balance: ○ Decreased glucose utilization ○ Promotes gluconeogenesis, glycogenolysis, and lipolysis ● ● ● ● ● ○ Primary energy reserve is FA stores in adipose tissue ○ Increased activity of hormone sensitive lipase Hyperlipidemia: ○ Physiological stress exacerbates normal response to energy balance ■ Hormone sensitive lipase is further up regulated ○ Insulin resistance ○ Obesity = excessive FA mobilization ○ Excessive TG and VLDL production and accumulation in the blood Tx for hyperlipidemia and hepatic lipidosis: ○ Correct primary disease ○ Correct/prevent negative energy balance ■ Enteral nutrition (palatable feed; enteral feeding tube) ■ Parenteral nutrition ■ 5% dextrose supplementation ■ IVF (balanced electrolytes) ○ Inhibit fat mobilization and improve TG uptake by peripheral tissues ○ Exogenous insulin ■ Suppresses hormone sensitive lipase and activates lipoprotein lipase ○ Exogenous heparin: ■ Stimulates lipoprotein lipase and promotes TG metabolism Chronic megalocytic hepatopathy: ○ Pyrrolizidine alkaloid containing plants ■ NAVLE ■ 4 weeks-12 months after exposure ■ Histology: ● Megalocytosis ● Biliary hyperplasia ● Fibrosis ■ WILL DIE Clover poisoning: ○ Signs of liver disease, photodermatitis ○ Signs within 2 weeks of ingestion of diet > 20% clover ○ U/S: ■ Liver enlarged w/ rounded borders ■ Progress to small liver w/ fibrosis ○ Biopsy: ■ Biliary hyperplasia ■ Periportal fibrosis ■ Minimal bile obstruction Cholestasis: ○ Bacterial infection may precipitate ○ Triad of clinical signs: ■ Icterus, fever, colic ○ Dx: ■ Increased GGT ■ Bilirubin (direct > 30% of total) ■ Increased bile acids and globulins ■ Bilirubinemia ■ U/S: dilated bile duct +/- hyperechoic foci ○ Tx: ● ● ● ● ■ Long term abx therapy until GGT is normal ■ Sx: choledocholithrotripsy, choledochotomy Tyzzer’s disease: ○ Clostridium piliforme ○ Acute necrotizing hepatitis in foals 7-42 days of age ○ Non-specific signs of severe hepatic compromise ○ Sporadic outbreaks in foals ingesting contaminated feces or soil ○ Definitive dx: ■ Organism identification post-mortem ○ Highly fatal grave prognosis in foals Theiler’s disease: ○ Clinical signs appear 4-10 weeks after administration of biologic equine origin ■ Tetanus antitoxin ● Most common ■ Hyperimmune plasma or antiserum/antitoxin: botulism, anthrax, strangles, WEE, influenza ■ Vaccinations ■ Plasma for colloid support ○ C/S are variable and non-specific ■ Acute onset, rapid progression ■ Lethargy, anorexia, icterus, fever, encephalopathy ■ Marked increases in liver enzymes ○ 50-90% mortality ○ Histopathology: severe hepatocellular necrosis and degeneration ○ Potential viral association Newly discovered equine hepatitis viruses: ○ Equine parvovirus: ■ Hepatotropic ■ Consistently found in cases of Theiler’s disease ○ Flaviviruses: ■ Equine hepacivirus- elevated enzymes during active infection ■ Theiler’s disease associated virus- not likely cause of disease ■ Equine pegivirus-high seroprevalence- not associated w/ disease Toxic hepatopathy- acute: ○ Centrilobular (lowest O2 tension) or periportal (site of 1st exposure) ■ Dx of exclusion, h/o exposure, detection of toxin ○ Drugs- hypersensitivity, intrinsic toxicity, idiosyncratic ■ Erythromycin ■ Tetracycline ■ Diazepam ■ Corticosteroids ○ Iron toxicity (ferrous fumarate) ■ Oral administration to foals before ingestion of colostrum ○ Mycotoxins ■ Aflatoxin ■ Fumonisin ○ Plants ■ Ryegrass, lupine, etc. ● Chronic active hepatitis: ○ Idiopathic chronic progressive hepatopathy ○ Causes: ■ Autoimmune ■ Hypersensitivity ■ Bacterial- chronic cholangiohepatitis ■ Viral ○ Insidious onset of progressive liver failure ○ Clinical signs are often intermittent ■ Lethargy and depression ■ Exercise intolerance ■ Anorexia and weight loss ■ Colic ■ Icterus ■ Rare exfoliative coronary dermatitis ○ Dx: ■ Mildly increased GLDH and AST ■ Marked increase in GGT and ALP ■ Increased BA, TP, and direct bilirubin ■ BUN < 10 ■ U/S: ● Small liver, increased echogenicity (fibrosis) ■ Systemic inflammation ● Inflammatory leukogram +/- left shift ● Polyclonal gammopathy ■ Liver biopsy ● Histopathology ● Concurrent culture ○ Tx: ■ Supportive care ■ Corticosteroids ● If biopsy shows mononuclear inflammation ■ Abx ● Inflammatory infiltrate or positive culture ● Abx excreted in bile are preferred ○ Chloramphenicol ○ Ceftiofur ○ Ampicillin ■ Prognosis depends on cause, severity, and duration