Hepatology Flashcards
Name the liver disease traditionally associated with administration of biologic agents to horses.
Theiler’s Disease; Serum Sickness; Acute Serum Hepatitis.
What is the proposed aetiologic agent of Theiler’s Disease?
Theiler’s Disease Associated Virus.Family: Flaviviridae.NB following the initial report in 2012 this virus has not been isolated from additional cases HOWEVER a new (unnamed) virus has been isolated from all subsequent Thriller’s Disease serum samples tested.
The liver has a large reserve capacity. What percentage of functional liver tissue must be removed before regeneration and recovery are no longer possible?
80%.
In what Rappaport zone does the most hepatocellular regeneration occur?
Zone 1 (the portal area).
Name two agents that inhibit normal liver regeneration?
Pyrollizidine alkaloids and antineoplastic drugs; anti-mitotic.
List three factors which may inhibit liver regeneration.
- Fibrosis bridging the liver lobules.- Loss of a stroma to build on.- Lack of portal blood supply.
Fasting hyperbilirubinaemia can be seen in horses in the absence of liver disease. What is the highest bilirubin concentration usually correlated with fasting alone and is this unconjugated or conjugated bilirubin?
6mg/dL unconjugated bilirubin.
What is the mechanism by which icterus occurs in liver disease?
Failure of uptake, conjugation or excretion of bilirubin.
What is the mechanism by which weight loss occurs in liver disease?
Energy demand greater than energy absorbed or metabolised.
What is the mechanism by which ascites occurs in liver disease?
Portal hypertension and lymph leakage caused by cirrhosis or veno-occlusion.
What is the mechanism by which change in liver size occurs in liver disease?
Nodular hyperplasia, tumour, cirrhosis, fatty degeneration.
What is the mechanism by which diarrhoea occurs in liver disease?
Bile deficit malabsorption or intestinal oedema secondary to portal hypertension.
What is the mechanism by which pruritus occurs in liver disease?
Retention of bile salts.
What is the mechanism by which dermatitis occurs in liver disease?
Hepatogenic photosensitisation.
What is the mechanism by which CNS signs occur in liver disease?
Heptic encephalopathy.
What is the mechanism by which tenesmus (+/- rectal prolapse) occurs in liver disease?
Hepatic encephalopathy.
What is the mechanism by which change in faecal colour occurs in liver disease?
Bile pigment deficit or undigested fat.
What is the mechanism by which haemorrhage occurs in liver disease?
Failure to synthesise clotting factors II, V, VII, IX, X.
True or false: icterus is a common findings in cattle with liver disease.
False. Rare unless biliary blockage occurs.Most common cause of icterus in ruminants is haemolysis.
Which clinical signs are reported in cattle (but rarely in horses) with liver disease?
Ascites, diarrhoea, tenesmus, rectal prolapse.
Describe the pathophysiology of ascites in cattle with liver disease. How can the peritoneal fluid be classified?
i) Venous blockage –> portal hypertension –> increased hydrostatic pressure.ii) Increased production of hepatic lymph high in protein (>3g/dL) –> leaks out of liver sinusoids (which are permeable to plasma proteins) –> interstitial space –> peritoneal cavity.Modified transudate; protein may be relatively high (3-3.5g/dL).
Describe the progression of skin lesions in cattle with hepatic photosensitisation.
White areas of skin become erythematous, then thickened with keratin crusts, then necrotic.
Describe the pathophysiology of hepatic photosensitisation in cattle with liver disease.
Plant matter is ingested –> bacteria in GIT degrade chlorophyll to phylloerythrin –> travels by portal circulation to liver –> conjugated and excreted in bile BUT with cholestasis some phylloerythrin will be be carried to the skin where it acts as a photodynamic agent.
Why does the faecal colour remain unchanged in adult cattle with liver disease but may be lighter in calves with liver disease?
In adult cattle other pigments like chlorophyll contribute to the colour of the faeces.In calves with simple GITs, much of the faecal colour comes from stercobilin, a metabolite of bilirubin, so with cholestasis faeces may be lighter in colour.
What clinical signs may be seen in ruminants with hepatic encephalopathy which are not reported in horses?
Tenesmus, rectal prolapse, excessive vocalisation.
List the hepatocellular leakage enzymes that are measured in cattle and whether or not they are liver specific.
- Aspartate aminotransferase (AST) - many tissues including muscle and erythrocytes.- i-iditol deyhydrogenase (IDH=SDH) - liver specific; acute liver dz; may be normal in chronic liver disease.- Glutamate dehydrogenase (GLDH) - acute liver dz; may be normal in chronic liver disease.- Lactate dehydrogenase (LDH) - many tissues including muscle and erythrocytes; acute liver dz; may be normal in chronic liver disease.
List the enzymes that if elevated indicate cholestasis in cattle and whether or not they are liver specific.
. Gamma glutamyltransferase (GGT) - also in pancreas, mammary gland, kidney tubues and other duct epithelium; elevated in calves after drinking colostrum; remains elevated for weeks.- Alkaline phospatase (ALP) - also in bone, intestines, placenta and macrophages; variable elevation with liver disease in ruminants.
Outline liver function tests performed in cattle.
- High ammonia concentrations.- Low BUN (produced in liver), however may also be low in anorectic/fasted cattle as rumen bacteria use urea for protein production.- Clotting factor abnormalities in terminal dz.- Hypoalbuminaemia (albumin T1/2 cattle 16.5d) and hyperglobulinaemia in chronic dz.- Bilirubin: liver damage –> inc unconjugated (indirect) bilirubin i.e. direct:total direct:total > 0.5. Inc bilirubin NOT consistent finding in cattle with liver disease, unlike other species.- Bile acids: hour to hour fluctuation occurs in cattle, therefore have to be VERY high to indicate liver dz i.e. > 126 umol/L beef cattle, > 88 umol/L dairy cattle.- Sulfobromophthalein excretion: 2mg/kg BSP IV; blood samples T=0, 5, 7, 9, 11 minutes; T1/2
Describe the landmarks for percutaneous liver biopsy in cattle. When is a liver biopsy contradicted in cattle?
- Insert biopsy needle at the intersection between a horizontal line drawn cranial from the middle of the paralumbar fossa and the 11th ICS on the RHS.- When a liver abscess is suspected.
Describe the aetiology of Black Disease. What species of animal is most frequently affected?
- Dz caused by toxins elaborated by Clostridium novyi type B; typically present in the soil, also sometimes identified in the GIT and liver of ruminants grazing affected pastures.- Massive liver damage –> anaerobic environment in liver –> growth of Clostridium novyi type C.- Liver insult is usually migrating liver flukes therefore seasonal occurrence related to liver fluke cycle.- Sheep > cattle, goats, horses > pigs.
Describe the pathophysiology of Black Disease.
- Alpha toxin enters cells by endocytosis and inhibits ras and rho guanosine triphosphatases by glycosylation.- Beta toxin is a necrotising and haemolytic phospholipase C (lecithinase).- C. novyi spores ingested, cross GI wall, disseminated through macrophage system incl Kuppfer cells.- Localised anaerobic conditions in liver e.g. fluke damage –> spores germinate, proliferate, release toxins and create zones of coagulative necrosis in the liver.- Toxins enter circulation and cause damage to neutrons, vascular endothelium and other tissues –> sudden death.
Describe the clinical signs of Black Disease.
- Typically peracute death.- Lethargy, depression, anorexia, fever, recumbency, venous congestion darkens skin.- Death in hours in sheep and 1-2 days in cattle.
Describe the typical necropsy findings in an animal that has died from Black Disease.
- Tissues in much more advanced state of autolysis than would be suggested by time of death.- Fluid in pericardial sac, thoracic and peritoneal cavities.- Endocardial and epicardial haemorrhage.- Urine grossly normal.- Liver swollen and congested with single or multiple foci of hepatic necrosis (yellow to white) surrounded by broad area of hyperaemia.- C. novyi type B is identified in liver samples: gram stain from impression smear, culture, toxin ID, fluorescent antibody ID of the organism.
Describe the treatment of Black Disease in ruminants.
- Tx usually not attempted due to peracute nature of dz and very poor px.- High doses penicillin and oxytet IV then IM, IV fluids.- Outbreak: vaccinate herd +/- prophylactic ABs.
Outline strategies for prevention or control of Black Disease in ruminant herds.
- Proper fluke control (see fluke notes).- Vaccinate with Clostridial bacterins/toxoids s/c –> short period of protection (5-6mo) therefore if calves vacc before 3-4mo give again at weaning; in non-fluke areas give once before time of peak fluke transmission; in areas with longer fluke season vaccinate twice per year.- Carcasses of animals dying from Black Dz should be removed, buried deeply or burnt.
Describe the aetiology of Bacillary Haemoglobinuria (aka Redwater Disease). What species of animal is most frequently affected?
- Clostridium novyi type D (Clostridium haemolyticum).- Clostridium novyi type D is typically present in the soil, also sometimes identified in the GIT and liver of ruminants grazing affected pastures; regional distribution but may occur in unusual areas after flooding.- Massive liver damage –> anaerobic environment in liver –> growth of Clostridium novyi type D and toxin production.- Liver insult is usually migrating liver flukes therefore seasonal occurrence related to liver fluke cycle (Summer and early Autumn in USA).- Sheep, cattle, goats > horses.
Describe the pathophysiology of Bacillary Haemoglobinuria.
- C. novyi spores ingested, cross GI wall, disseminated through macrophage system incl Kuppfer cells.- Localised anaerobic conditions in liver e.g. fluke damage –> spores germinate, proliferate, release toxins and create zones of necrosis in the liver.- Toxins enter circulation –> intravascular haemolysis, icterus, haemoglobinuria, endothelial damage –> death.- Beta toxin is a phospholipase C that causes localised hepatic necrosis, intravascular haemolysis and damage to the capillary endothelium.
Describe the clinical signs of Bacillary Haemoglobinuria.
- Most common animals > 1yo; peracute death.- Depression, anorexia, fever.- Breathing may be rapid or shallow.- MM pale and icteric.- Blood thin and coagulates slowly.- Blood from nostrils, mouth, rectum or vagina.- Severe haemoglobinuria/port wine urine.–> recumbency, bloat, death.
Describe ante-mortem diagnostic tests and the typical necropsy findings in an animal that has died from Bacillary Haemoglobinuria.
- Anaemia, inc AST, TBili and GGT; haemoglobinuria.- Generalised icterus; subcut petechial and ecchymotic haemorhages, oedema and emphysemia; red-tinged abdominal and thoracic fluid; haemorrhages on serosal surfaces, epicardium and endocardium; spleen enlarged; LNs congested and haemorrhagic; lungs filled with blood-tinged fluid; advanced autolysis.- Pathognomonic lesion = ischaemic hepatic infarct. Centre of coagulative necrosis up to 30cm diam with zone of hyperaemia at its interface with viable liver tissue.
Describe the treatment of Bacillary Haemoglobinuria in ruminants.
- Rarely attempted due to acute nature of disease.- First choice high dose penicillin IM or IV; second choice tetracycline IV; fluids; blood transfusions as needed.
Outline strategies for prevention or control of Bacillary Haemoglobinuria in ruminant herds.
- Proper fluke control (see fluke notes).- Vaccinate with Clostridial bacterins/toxoids s/c –> short period of protection (5-6mo) therefore if calves vacc before 3-4mo give again at weaning; in non-fluke areas give once before time of peak fluke transmission; in areas with longer fluke season vaccinate twice per year.
Describe the aetiology of hepatic abscess in cattle.
- Dairy (up to 40-60% herd) and beef (1-95%; ave 20-30%).- Feed related; inc incidence in grain-fed cattle.- Polymicrobial; anaerobes predominate; Fusobacterium necrophorum (gram -ve, anaerobic rod) > Trueperella pyogenes (Gram +ve, facultative anaerobe, rod) > Bacteroides, Clostridium, coliforms, Pastuerella, Prevotella, Staph, Strep etc.- F. necrophorum is normal rumen flora –> utilises lactic acid to produce VFAs and also digests ruminal epithelial and feed protein.- Hepatic abscesses occur most commonly in ruminants.
Describe the pathophysiology of hepatic abscess formation in cattle.
- Major virulence factor of F. necrophorum = leukotoxin which is cytotoxin to PMNs, macrophages, hepatocytes and ruminal epithelial cells.- F necrophorum subspecies necrophorum is more toxin (i.e. elaborates more leukotoxin) than funduliforme (occurs more often in mixed infections).- F. necrophorum +/- other bacteria enter liver through portal v (most common), hepatic a, umbilical v, bile duct system or direct extension (e.g. FB in reticulum pokes liver).- Acid-induced rumenitis –> damage to rumen wall (aggrivated by foreign objects in feed) –> invasion and colonisation of ruminal wall –> rumen wall abscesses –> bacterial emboli enters portal circulation –> liver abscess.- F. necrophorum has many virulence factors which overcome aerobic environment and phagocytic mechanisms to establish abscesses in liver: leukotoxin may evade phagocytosis and –> release of lysosomal enzymes and organ metabolites from damaged phagocytic cells; LPS and platelet aggregation factor –> IV coagulation; haemolysin –> impairment of oxygen transport.
Describe the clinical signs of hepatic abscessation in cattle.
- Most often only detected at the time of slaughter.- Occasionally abscesses rupture –> peritonitis OR erode into CVC –> CVC syndrome.- Anorexia most common clinical signs (if any).
Describe ante-mortem diagnostic tests used to diagnose hepatic abscessation in cattle.
- General CBC/chem not good indicators of presence of liver abscesses, however in experimentally infected animals inc TP, TBili, GGT and SDH occur.- Ultrasound MAY visualise abscess but limited by window.
Describe the typical necropsy findings in a bovid that has died from a hepatic abscess.
- Abscesses are well encapsulated, pus filled, with thick, fibrotic walls; range from 2-3mm to 15cm diameter.- Can be one to hundreds within the liver distributed equally in superficial and deep zones.- Abscesses eventually become sterile and are replaced by fibrous scars.- Histo: pyogranulomatous lesion with necrotic centre, encapsulated, surrounded by an inflammatory zone.
Describe the treatment of hepatic abscessation in cattle.
- Seldom practical; cattle with clinical sequelae e.g. CVC syndrome are usually culled for slaughter.- Typically F. necrophorum and T. pyogenes are susceptible to penicillins and macrolides.
Outline strategies for prevention of hepatic abscessation in cattle herds.
- Feed additives are approved for prevention in feedlot cattle: bacitracin methylene disalicylate, chlortetracycline, oxytetracycline, tylosin (most effective - reduces incidence by 40-70%) and virginiamycin.- Vaccine (F. necrophorum leukotoxoid and T. pyogenes bacterin reduced incidence and severity but not available.- Feed management to dec incidence of rumen acidosis: gradual adaption to high-grain diets, avoid under or over feeding, increased feeding frequency, increased roughage content, provide adequate bunk space and fresh water.
What are potential sequelae of hepatic abscessation in cattle?
- Septic cardiac and pulmonary emboli.- Sudden death secondary to rupture of liver abscess, with septic embolisation to the right side of the hear.- CVCT syndrome: phlebitis caused by extension of liver abscess involving CVC –>
Describe caudal vena cava thrombosis syndrome.
- Phlebitis caused by extension of liver abscess involving CVC –> thrombus forms anywhere between liver and R atrium (most often where CVC enters diaphragm –> CSx.- CSx range from sudden death caused by rupture of CVC to pulmonary embolism, pneumonia, infarction, endocarditis, hemoptysis and epistaxis.
Describe hepatic telangiectasia (‘sawdust liver’) in cattle.
- A focal degeneration in liver lobular circulation characterised by red-brown foci 1-5mm in diameter.- Microscopically hepatocytes are distorted and sinusoids congested.- Does not cause clinical signs but –> liver condemnation.- Hypothesised pathogenesis: necrotising hepatitis, ischaemia, dilation of Disse spaces, reduced density of reticulin framework, vit E-Se deficinecy, alteration of the anti-sinusoidal barrier, immune-mediated disease.
How common are primary liver tumours in large animals?
Very rare. 0.011% of animals in one slaughterhouse study.
Liver tumours may occur following metastasis from another organ. What is the most common metastatic tumour of the bovine liver?
Lymphosarcoma.
What primary tumours have been described in cattle and what clinical signs are associated with their presence?
- Hepatocellular carcinoma.- Anorexia and weight loss of weeks to months duration.- Elevated liver enzymes and polycythemia.
What is the mode of inheritance of haemochromatosis in Salers cattle?
Homozygous recessive.
Describe the pathophysiology of haemochromatosis in Salers cattle.
Inappropriate absorption of iron from the GIT –> hepatic storage (iron overload) –> eventual loss of hepatic function.
What clinical signs and clinical pathology abnormalities are reported in Salers cattle with haemochromatosis?
- Decreased weight gain, poor BCS, dull hair coat, loss of incisor teeth, +/- diarrhoea.- Increased concentrations of liver enzymes, total serum iron concentration, total iron binding capacity and saturation of transferrin (>60%).- Liver iron concentration >5000ug/g (ppm) (84-100).
What histopathologic changes are reported in the liver in Salers cattle with haemochromatosis?
Brown pigment that stains for iron in hepatocytes and Kupffer cells; marked hepatic fibrosis.
What treatments are reported for haemochromatosis?
- Reducing iron storage through phlebotomy –> reported improvement in some calves, but one hiefer failed to reduce liver iron concentrations following removal 160L blood over 12 months.- Deferoxamine used in humans to reduce iron accumulation.
What is the most common liver fluke found in production ruminants?
Fasciola hepatica.
Describe the life cycle of Fasciola hepatica.
- Vector: lymnaeid snails found in mudbanks and temporary water bodies, springs, streams etc; typically environments that stay wet >6mo –> fluke infections.- Lifecycle of snail host and fluke occur when wet, T>10C; seasonal transmission in winter and spring SC/SE US and late spring to fall NW US.- 600 growing degree days (e.g. 42d >25C) required for complete intramolluscan development –> release of cercariae that encyst as infective metacercariae –> ingested by ruminants –> burrows through SI into peritoneal cavity –> liver parenchyma (feeds) –> bile duct (matures to adult and reproduces) –> GIT –> eggs laid in faeces –> miracidia hatch in water and find snail. - Exponential propagation under favourable environmental conditions –> explosive seasonal outbreaks; major economic impact late autumn/winter when animals are under nutritional stress.- Tranmission ended by 2 weeks of summer heat, drought, or sustained cold winter weather.
What fluke load is required for economic loss in cattle and what load for clinical signs?
- Economic loss: 10-40 flukes/animal possible; >40 probable.- Clinical signs: >200 flukes/animal.
What clinical signs are observed in cattle with a high liver fluke load?
Weight loss, emaciation, depression, anorexia, rough hair coat, anaemia, hypoproteinaemia, submandibular oedema, in rare cases mild icterus.Depression, anaemia and biliary hyperplasia results from high levels of proline, a product of fluke metabolism.
Describe the immune response of cattle to a liver fluke infection.
Partial acquired resistance developed by 5-6 months post-infection; few flukes survive after 1 year.
Describe the necropsy findings in cattle that die following liver fluke infection.
- Tortuous tunnels of coagulative necrosis that organise and fibrose –> diffusely fibrotic liver, esp in ventral lobe.- Fibrous tags associated with liver penetration 3-4d PI.- Proliferative cholangiohepatitis: bile duct fibrosed, thickened, irregularly dilated and stenotic; calcifies 20wk PI.
How can liver fluke infections be diagnosed in cattle antemortem?
- Faecal sedimentation; >10 eggs/2g –> high probability of heavy infections and economic loss. - F. hepatica eggs can be distinguished from Paramphistomum (non-pathogenic rumen fluke) eggs as they are amber (not grey), bigger, more rounded at the operculum end.
Outline treatment and control of liver fluke infections in cattle herds.
- Prevention is key to control as a small number of eggs can –> sig infection following replication in snails.- Single tx with flukicide following transmission period (late Autumn) to kills adults prior to nutritional stress of Winter +/- in Spring if high risk climate.- Only 2 drugs available in US (many others overseas with different activity): albenazole and clorsulon (2mg/kg)n are effective against adults in bile ducts; clorsulon (7mg/kg) effective against juvenile flukes over 6wk old in bile ducts.
Which fluke replaces Fasicola hepatica in tropical areas?
F. gigantica - larger, longer PPE (10-12wk), greater pathogenicity.
Describe the pathophysiology of Fascioloides magna (the large American liver fluke) infections in cattle.
- Seen in cattle that graze with deer (natural host); cattle = dead end host; snails = intermediate host.- Geographic distribution: Gulf states, Great Lakes, NW.- Intensive encapsulation response –> closed cyst (liver +/- other organs if aberrant migration), liver parenchyma and LNs have black pigmentation –> liver condemnation.- Closed cyst precludes diagnosis by faecal sedimentation.- High dose albendazole moderate effective tx.
Is cholelithiasis a clinical disorder of cattle?
Has been reported but very rare.
Is disease of the bovine gallbladder commonly reported?
No, it is rare.
What other diseases has obstructive gall bladder disease been reported with in cattle?
Abdominal fat necrosis, choleliths, fascioliasis, foreign bodies, hepatic abscesses, neoplasia (adenomas, adenocarcinomas > papillomas > lymphomas) and suppurative cholecystitis.
What fungal toxin is capable of causing cholangiohepatitis in cattle and sheep?
Sporidesmin, a fungal toxin from Pithomyces chartarum.
Gilbert Syndrome is an inherited disorder described in Southdown sheep. Describe the pathophysiology of this syndrome.
Failure of the unconjugated bilirubin to cross the liver cell membrane and be conjugated; most likely caused by a defect in carrier proteins or the conjugating enzyme –> hepatic bilirubin clearance is ~30% of normal.
What clinical signs and laboratory test abnormalities are seen in sheep with Gilbert Syndrome?
- Elevated conjugated and unconjugated bilirubin concentrations in serum.- +/- icterus.- BSP is not excreted into the bile.- Liver histo normal other than pigment in the hepatocytes.
Dubin-Johnson Syndrome is an inherited disorder described in Corriedale sheep. Describe the pathophysiology of this syndrome.
Failure of conjugated bilirubin to enter the bile canaliculi.There may be an impairment in excretion of other organic anions as well.
What clinical signs and laboratory test abnormalities are seen in sheep with Dubin-Johnson Syndrome?
- Elevated conjugated and unconjugated bilirubin concentrations in serum.- +/- icterus.- BSP clearance is delayed.- Liver histo: hepatocytes contain black, melanin-like pigment.
Sheep and goats are more susceptible than cattle to development of disease following infection by liver flukes as they do not mount the same immune response. Describe the acute and chronic forms of fluke infection in sheep.
- Acute: fatal disease, ascites, abdominal haemorrhage, pallor and icterus associated with migration of 5-6000 immature flukes from liver parenchyma to bile ducts 6-10 weeks post-infection.- Chronic: burdens of >200 flukes; submandibular oedema, ascites, emaciation.
What differences are seen on histology of the liver in cattle and sheep following liver fluke infection?
Both have proliferative cholangiohepatitis. The bile duct wall becomes calcified in cattle ~20wk PI, but does not calcify in sheep.
Describe the difference in response to infection with Fascioloides magna (the large American liver fluke) in cattle and small ruminants.
- Cattle: encapsulation –> closed cyst in liver.- Sheep and goats: does not encyst -> migrates un-interrupted –> 1-2 flukes are enough to kill.
Is cholelithiasis a clinical disorder of sheep?
No.
Cassia occidentalis (coffee senna) causes myonecrosis in cattle. Horses usually succumb to failure of another organ following Cassia occidentalis ingestion prior to development of myodegeneration. Which organ is this?
Liver. Ref: Equine Vet. J. (2013); 45 (2) 240-244.
List clinical signs observed in horses following exposure to Cassia occidentalis seeds in their grain.
- Sudden death.- Pica.- Hyperactivity.- Circling.- Head pressing.- Central blindness.- Tongue protrusion.- Loss of facial sensitivity.- Proprioceptive deficits.- Mild to severe depression.- Inappetence.Ref: Equine Vet. J. (2013); 45 (2) 240-244.
What is the prognosis for survival in horses following a natural outbreak of Cassia occidentalise poisoning?
- Mortality: 60%.- Mares that survived recovered fully; pregnant mares did not abort.Ref: Equine Vet. J. (2013); 45 (2) 240-244.
Describe the lesions found following post mortem of horses that have ingested Cassia occidentalis.
- Enhanced lobular pattern visible on capsular and cut surface of liver.- Liver histology: centrolobular hepatocellular vacuolisation and necrosis with mild lymphocytic infiltration, hyperaemia and haemosiderosis.- Brain histology: perivascular oedema; Alzheimer type II astrocytes.Ref: Equine Vet. J. (2013); 45 (2) 240-244.
Hepatic encephalopathy is typified by clinical signs of forebrain disease. What alternate neurologic abnormalities have been reported as the presenting complaint in horses with HE?
- Ataxia, dysmetria, general proprioceptive deficits and UMN paresis with normal mentation/CN exam.Ref: Equine Vet. Educ. (2011); 23 (1) 5-10.
What are the landmarks for ultrasound visualisation of the liver? What are the landmarks for percutaneous liver biopsy in the horse (for use when ultrasound is unavailable)?
- Ultrasound: 9th-16th R ICS, 9th-11th L ICS.- Biopsy: 12th-14th R ICS ventral to a line drawn between the point of the elbow and the tuber coxae, directing the needle towards the opposite elbow joint and advancing the needle during expiration.Ref: J. Am. Vet. Med. Assoc. (2014); 245 (8) 939-943.
What are potential complications of percutaneous liver biopsy in the horse?
- Biopsy of diaphragm, lung or intestines; enterocentesis; pneumothorax; haemorrhage into the peritoneal or thoracic cavity.Ref: J. Am. Vet. Med. Assoc. (2014); 245 (8) 939-943.
In a study of 36 QH/QH cross horses, what percentage of horses:- Had liver visible in all the 11th-14th R ICS?- Had liver >3.5cm thickness in all the 11th-14th R ICS?- Lung, intestines or both in the place of liver in an ICS of interest?
- 39%.- 0%.- 55%, 36%, 9%.Ref: J. Am. Vet. Med. Assoc. (2014); 245 (8) 939-943.
Describe clinical signs and diagnostic test abnormalities in a case of hepatic abscess in a 4yo Arabian cross mare (Ref: J. Am. Vet. Med. Assoc. (2015) 247 (1) 98-105).
- PE: Intermittent colic and fever, tachycardia, tachynpnoea, icterus.- U/S: irregularly marginated, hyperechoic walled region of heterogenous echogenicity in proximity to the L liver lobes.- CBC: leukocytosis, mature neutrophilia, hyperfibrinogenaemia- MBA: inc GLDH, TBili, SAA.Ref: J. Am. Vet. Med. Assoc. (2015); 247 (1) 98-105.
If an encapsulated hepatic abscess does not respond to medical management what surgical procedures may be attempted under standing sedation to resolve the abscess?
- Percutaenous drainage and lavage of the abscess.- Partial rib resection, abscess drainage, removal of necrotic hepatic tissue.Ref: J. Am. Vet. Med. Assoc. (2015); 247 (1) 98-105.
Which spirochete was reported to cause suppurative cholangiohepatitis in a 3.5 month old foal in Pennsylvania presenting with lethargy and dermatitis and how was the diagnosis reached?
- Bartonella hensellae.- CBC/Chem: mature neutrophilia, hyperfibrinogenaemia, inc GGT, SDH, TBili, BA concentrations.- Liver u/s: enlarged, diffusely increased echogenicity.- Histology: liver - neutrophils within hepatic zones forming micro abscesses; neut/lymph/plasma cells/spindle cells proliferation between hepatic cords; Warthog-starry stain –> pleomorphic, 3-7um long, curved, blunt spiral and beaded agyrophilic organisms; skin - photosensitisation.- PCR on liver biopsy sample.Ref: J. Vet. Intern. Med. (2014); 28 (4) 1341-1345.
Outline the treatment of Bartonella henselae cholangiohepatitis reported in a foal in a single case study.
- Antimicrobials: rifampin and TMPS for 4mo; GGT inc and PCR +ve on biopsy therefore swapped to minocycline for a further 3mo.- SAMe.- Pentoxyfylline.Ref: J. Vet. Intern. Med. (2014); 28 (4) 1341-1345.
What modality can be used to identify a congenital port systemic shunt in a foal if liver ultrasound findings are WNL?
- Computed tomography angiography (pre and post-contrast scans).- Ultrasound-guided percutaneous transplenic injection of agitated saline and simultaneous echo –> bubbles in RA/RV (bubbles should be absorbed by the liver parenchyma if no shunt is present). - Biopsy: severe lobular atrophy characterised by dec distance b/w portal areas and central vv, marked arteriolar proliferation, dilated portal lymphatic and periportal sinusoids; findings consistent with portal v hypoperfusion.Ref: J. Vet. Intern. Med. (2012;) 26 (1) 171-177.
What surgical techniques have been reported to successfully treat extra-hepatic congenital PSS in foals?
- Cellophane banding with titanium clips.- Surgical ligation (risk of fatal portal hypertension or haemorrhage).- Transvenous coil embolisation.Ref: J. Vet. Intern. Med. (2012); 26 (1) 171-177.
In a review of horses with liver disease diagnosed by liver biopsy and serum biochemistry, what factors were associated with non-survival and what was their sensitivity and specificity (if available)?
- Serum bile acid concentrations > 20umol/L; Sp 78%, Se 63% for short-term survival; Sp 81%, Se 57% for long-term survival; NB serial testing may improve sensitivity.- Histologic score >2; Sp 90%, Se 63% for short-term survival; Sp 96%, Se 64% for long-term survival. - Hypoalbuminaemia, hyperglobulinaemia.- Elevated fibrinogen and SAA concentrations.Ref: J. Vet. Intern. Med. (2015); 29 (2) 644-650.
