Hepatic and urinary Flashcards
diagnostic tests for hepatic disease- Hepatic enzymes
– hepatocellular (ALT, GLDH, AST) vs cholestatic (ALP, GGT). They may be increased with hepatocellular damage or cholestasis respectively (remember non hepatic causes of elevations are very common).
diagnostic tests for hepatic disease- diagnostic tests for hepatic disease
increased in hepatic inflammation (globulin) or neoplasia (globulin)
- decreased in severe liver disease (albumin and globulin) e.g portosystemic shunt (PSS).
diagnostic tests for hepatic disease- Bilirubin
pre-hepatic, intra-hepatic, post-hepatic
diagnostic tests for hepatic disease- Bile acid stimulation test
(do not perform in icteric patients)– test of liver function.
diagnostic tests for hepatic disease- increased in cholestasis
-
decreased in severe liver disease, portosystemic shunt
diagnostic tests for hepatic disease- Blood glucose
decreased in liver failure, hepatic tumours
diagnostic tests for hepatic disease- Coagulation factors
may be prolonged in hepatic failure
diagnostic tests for hepatic disease- Haematology
mild non regenerative anaemia in chronic disease; microcytosis in PSS
diagnostic tests for hepatic diseas- Urinalysis
bilirubinuria suggest hepatobiliary disease (especially cats); urate uroliths in PSS.
diagnostic tests for hepatic disease- Imaging
radiography,
ultrasonography- most usefull inforst opinion, CT.
diagnostic tests for hepatic disease- sampling
Cytology (FNA), biopsy (percutaneous
u/s guided trucut, vs
biopsy at laparoscopy
vs biopsy at
exploratory laparotomy).
Rex, 10 year old MN Labrador retriever, fully vaccinated, no history of travel outside of the UK. Progressive history over the past few months of decreased appetite, lethargy and diarrhoea.
Physical examination: there is a weight loss of 4Kg since last checked 6 months ago.
he is diagnosed with chronic hepatitis, how would you go about disgnosisng this
Problem list: diarrhoea
weight loss
lethargy and decreased appetite are likely to be secondary problems.
You decide to perform haematology, biochemistry and urinalysis. (Haematology shows a mild, non-regenerative anaemia. Biochemistry shows elevated ALP and ALT and reduced albumin. Urinalysis: USG is 1.036 and no abnormalities are identified.)
this shows hepatic disease likley
Abdominal ultrasonography is performed to further investigate your ddx. From this, you identify that:
The liver is subjectively small.
The liver is hyperechoic compared to the spleen (normally, it is hypoechoic).
The liver appears heterogenous with small hypoechoic nodules.
Abdominal ultrasonography is performed to further investigate your ddx. From this, you identify that:
The liver is subjectively small.
The liver is hyperechoic compared to the spleen (normally, it is hypoechoic).
The liver appears heterogenous with small hypoechoic nodules.
chronic hepatitis (CH) treatment
lack of evidence, ACVIM consensus statement from 2019 suggests a combination of ursodeoxycholic acid; SAMe; vitamin E; and possibly immunosuppressive agents (prednisolone; azathioprine; cyclosporine).
cause isiopathic so difficult
History: Buttons, 9 yo FE DLH. Indoor cat only, fully vaccinated. No history of travel outside of the UK. A three day history of acute onset lethargy and anorexia.
Physical exam: QAR, rectal temperature is elevated, 39.6, mucous membranes are icteric, she has a slight skin tent and tacky mucous membranes. HR is 180 and RR is 28 bpm. The rest of the physical exam is unremarkable.
she is diagnosed with a gall bladder infection, how would you go about doing this?
You decide to perform biochemistry, haematology and urinalysis. (Biochemistry show an increase in ALT, ALP, GGT and bilirubin, and a mildly elevated urea.. Haematology shows a left shift neutrophilia (meaning increased numbers of immature/band neutrophils) and there is a mildly elevated Hct and total RBC. Urinalysis is positive for bilirubin.)
findings suggest a hepatic or post hepatic cause
Ultrasonography identifies a diffuse patchy echogenicity and a thickened gall bladder wall and distension of the bile duct, but rules out extrahepatic biliary obstruction.
Biopsy performed by percutaneous ultrasound-guided trucut, following normal coagulation time results.
Treatment: antimicrobials, ideally based on C & S from bile or hepatic tissue. If not possible, E.coli is the most common isolate. Amox/clav would be a sensible choice and supportive treatment (IVFT, SAMe, UCDA, analgesia)
Icterus/jaundice
Also termed hyperbilirubinaemia. It is a yellow discolouration of the body tissue resulting from the accumulation of excess bilirubin.
Pre-hepatic: enhanced bilirubin formation, usually due to haemolysis. Ddx include primary IMHA and secondary IMHA e.g feline haemotropic mycoplasmosis (FHM, previously termed feline infectious anaemia or haemobartonellosis).
Hepatic: the liver is unable to clear the daily bilirubin load due to impaired hepatic function. Ddx e.g neutrophilic and lymphocytic cholangitis (cats); FIP (cats); leptospirosis (dogs); chronic canine hepatitis; hepatic lipidosis (cats); diffuse neoplasia.
Post-hepatic: biliary system is unable to excrete bilirubin via the FGI tract, ddx include biliary obstruction (ddx e.g cholelithiasis; severe pancreatitis, or e.g ruptured common bile duct or gallbladder).
Haematology (regenerative/pre regenearative anaemia) is key is helping to identify pre-hepatic causes, and imaging and biochemistry to differentiate hepatic (usually ALT is proportionately higher than ALKP) from post-hepatic (ALKP proportionately higher than ALT) causes.
Pre-hepatic jaundice
enhanced bilirubin formation, usually due to haemolysis. Ddx include primary IMHA and secondary IMHA e.g feline haemotropic mycoplasmosis (FHM, previously termed feline infectious anaemia or haemobartonellosis).
hepatic jaundice
the liver is unable to clear the daily bilirubin load due to impaired hepatic function. Ddx e.g neutrophilic and lymphocytic cholangitis (cats); FIP (cats); leptospirosis (dogs); chronic canine hepatitis; hepatic lipidosis (cats); diffuse neoplasia.
post-hepatic jaundice
biliary system is unable to excrete bilirubin via the FGI tract, ddx include biliary obstruction (ddx e.g cholelithiasis; severe pancreatitis, or e.g ruptured common bile duct or gallbladder).
History: Rocky, A 16 week old ME Yorkshire Terrier. Small compared to litter mates, seems disorientated at times, drinks a lot.
Physical exam: neurological exam: slightly reduced mentation, otherwise no neurological deficits are detected, small for age but the rest of the examination is unremarkable.
he is daignosed with a protosystemic shunt- how would you go about doing this?
You perform haematology which shows a mild anemia with a microcytosis (low MCV). Biochemisty shows a reduced urea and albumin and elevated ALT and AST. Urinalysis shows a low USG and is otherwise normal.
You perform a bile acid stimulation test which shows that bile acids are elevated. This is suggestive of a porto systemic shunt.
Following discussion with the owner, referral is arranged, where a CT scan confirms an extrahepatic portosystemic shunt between the portal vein and the caudal vena cava.
Treatment: following medical stabilization, surgery is performed to close the shunt. Rocky makes an excellent recovery, and survival rates are around 95%.
What if surgery had not been an option?
Medical treatment includes: - diet change, to reduce the amount of protein and feed only high quality, highly digestible protein diets.
- lactulose (decreases ammonia absorption, unfavourable environment for toxin producing bacteria to reduce ammonia production)
- sometimes antibiotics (metronidazole, amoxicillin), to alter the bacterial population of the GI tract away from toxin producing bacteria)
treatment fo portosytemic shunt
Treatment: following medical stabilization, surgery is performed to close the shunt. Rocky makes an excellent recovery, and survival rates are around 95%.
What if surgery had not been an option?
Medical treatment includes: - diet change, to reduce the amount of protein and feed only high quality, highly digestible protein diets.
- lactulose (decreases ammonia absorption, unfavourable environment for toxin producing bacteria to reduce ammonia production)
- sometimes antibiotics (metronidazole, amoxicillin), to alter the bacterial population of the GI tract away from toxin producing bacteria)
Interventions for hepatic disease
Specific diagnosis vs supportive care
Supportive care:
Diet: high quality protein, highly digestible: prescription hepatic diets, possibly with protein supplementation (cottage cheese, chicken) or prescription diet for GI disease. Monitor protein on biochemistry and body weight.
Interventions for hepatic disease- Antioxidants
oxidnet stress occurs in liver due to decrease blood flow?
limited evidence
- SAMe (S-adenosylmethionine)
- Vitamin E
- Silymarin (milk thistle)
- Zinc
Interventions for hepatic disease-Choleretics and bile acid modifiers
- UDCA (ursodeoxycholic acid)
Stimulates bile flow which reduces cell
damage and oxidative stress + immunomodulatory action.
Contraindicated in biliary obstruction - risk gall bladder rupture.
offlicence
Interventions for hepatic disease-Antimicrobials
Use only when history, physical exam and
further diagnostics are suggestive of
an infectious aetiology
A good example of when they are indicated:
Leptospirosis (take urine/blood sample for PCR test
before starting antimicrobials to avoid false negatives). Penicillins
or doxycycline.
Interventions for hepatic disease- Anti-inflammatories (corticosteroids)
Indications
Biopsy evidence of ongoing inflammation, e.g lymphocytic cholangitis in cats.
No fibrosis or early/mild fibrosis
Infectious causes ruled out as far as possible.
Contraindications
Known of suspected infectious cause
Advanced, bridging fibrosis or non-inflammatory fibrosis (no benefit and increased risk portal hypertension (PH))
Ascites (in animals with liver disease this is usually caused by portal hypertension. CS can precipitate GI ulceration and HE, and increase water retention).
HE (CS lead to protein catabolism and production of ammonia, worsening HE)
Acute hepatitis (usually infectious or toxic aetiology, and high risk GI ulceration)
portal hypertension …..
PH occurs due to increased resistance in the portal circulation and/or increased portal venous flow.
Causes can be pre-hepatic, hepatic or post-hepatic
Portal pressure is rarely measured directly (definitely not in first opinion practice!), and the diagnosis is inferred from the development of complications of hepatic disease, including multiple acquired PSS, ascites and HE.
Hepatic surgery, cases of hepatic compromise-
Pre-surgical considerations-
Anaemia
Hypoproteinaemia
Hepatic encephalopathy
Extended coagulation times
Ascites
Dehydration
Prophylactic antibiotics
A large ventral midline abdominal incision from xiphoid cartilage caudally. The falciform ligament should be removed.
Balfour abdominal retractors
An assistant can retract caudally on stay sutures placed in the greater curvature of the stomach to facilitate manipulation of the liver.
Common first opinion hepatic surgeries: biopsy; partial lobectomy
Hepatic biopsy at exploratory laparotomy
For peripheral lesions: - place a loop of absorbable suture around the tip of the liver lobe and tie tightly (remember surgeons knot). Empty suture packet can be used as a cutting board. Resect approx. 5mm distal to the suture, place in formalin and obtain C & S sample from hepatic tissue.
For focal lesions: punch biopsy. Haemorrhage can be really well with e.g lysosypt (a collagen haemostat) which is left in place. Place biopsy sample in formalin and C & S as above.
Both techniques: ensure haemostasis before
routine abdominal closure.
when to refer for hepatic disease
Portosystemic shunts
Definitive diagnosis?
Imaging?
Anesthetic and surgical training, e.g biliary surgery
Biopsy – percutaneous ultrasound
guided, laparascopic
Inpatient care provision in first opinion
practice– registered veterinary nurses,
OOH arrangements etc.
infectious causs of diarrhoea in foals age 0-14 days
SEPTIOCEMIA!!
Viral infection-
Rotavirus
Coronavirus/adenovirus (Uncommon, usually seen in immunocompromised foals)
Bacterial infection-
Clostridium difficile
Clostridium perfringens
Escherichia coli (rare)
Salmonella
Fungal Infection -
Candida/Mucor spp. (Rare: usually seen in
immunocompromised foals)
Protozoal infection-
Cryptosporidium spp
non-infectious causs of diarrhoea in foals age 0-14 days
Foal heat diarrhoea
Nutritional causes (such as errors in feeding or lactose intolerance)
Perinatal asphyxia syndrome/ HIE
Necrotising enterocolitis
non-infectious causs of diarrhoea in foals age2 weeks- 2 months
Nutritional causes (such as errors in feeding or lactose intolerance)
Luminal irritants (such as sand enteritis)
Gastric ulceration
infectious causs of diarrhoea in foals age > 2 months
Viral infection-
Rotavirus
Coronavirus/adenovirus (Uncommon, usually seen in immunocompromised foals)
Bacterial infection-
Clostridium difficile
Clostridium perfringens
Escherichia coli (rare)
Salmonella
Lawsonia intracellularis
Rhodococcus equi ( rare: more commonly respiratory disease)
Fungal Infection -
Candida/Mucor spp. (Rare, usually seen in
immunocompromised foals)
Protozoal infection-
Cryptosporidium spp
Parasitic infection -
strongyloides westeri (uncommon)
infectious causs of diarrhoea in foals age2 weeks- 2 months
Viral infection-
Rotavirus
Coronavirus/adenovirus (Uncommon, usually seen in immunocompromised foals)
Bacterial infection-
Clostridium difficile
Clostridium perfringens
Escherichia coli (rare)
Salmonella
Fungal Infection-
Candida/Mucor spp. (Rare: usually seen in
immunocompromised foals)
Protozoal infection-
Cryptosporidium spp
Parasitic infection-
strongyloides westeri (uncommon)
non-infectious causs of diarrhoea in foals age > 2 months
Nutritional causes (such as errors in feeding or lactose intolerance)
Luminal irritants (such as sand enteritis
Gastric ulceration
Foal heat diarrhoea ( 75-80% foals)
Self-limiting condition in foals aged 5 days to 15 days
No signs of systemic disease, and continue to suckle well
Aetiology remains speculative
Changes in mares’ milk around time of first oestrus?? Unlikely as occurs in orphan foals too.
Maturational changes in bacterial intestinal flora considered the most likely cause
Perinatal asphyxia syndrome (PAS)/ HIE in foals
Risk factors, dystocia, inadequate oxygenation following delivery
Hypothesis: hypoxic injury of the gastrointestinal tract may lead to ischaemic damage to the enterocytes.
May lead to diarrhoea, gastrointestinal reflux, intolerance of enteral feeding or abdominal distension
Necrotizing Enterocolitis (common in human babies)- in foals
Pathophysiology: Multifactorial. complex interaction of immaturity, gastrointestinal mucosal injury, enteral milk feeding and bacterial invasion
Severe weakness, inability to stand, colic, ileus, gastric reflux, intolerance to enteral feeding, shock signs.
Even with intensive care, the prognosis is poor.
Nutritional causes/ luminal irritants of diarhoa in foals
Ingestion of abnormal material e.g. sand
Incorrect formulation of milk replacer (orphan foals)
gastric ulceration in foals
D++ may be seen in association with gastric ulceration in foals.
Concurrent clinical signs bruxism, ptyalism, dorsal recumbency, colic, ill thrift, poor hair coat and lethargy
rota virus in foals
Most commonly detected infectious agent in foals.
Incubation period 1-4 days
Clinical disease: ranges from mild self-limiting diarrhoea to profuse watery diarrhoea with significant dehydration and electrolyte derangements. Milder disease in older foals
Most common 5-35 days of age.
Virus infects the epithelial tips of the villi of the small intestine, resulting in cell lysis, blunting of villous tips and decreased production of lactase.
Leads to lactose intolerance and prolonged diarrhoea.
Faecal-oral transmission. Highly contagious. Can persist in the environment for several months. Infected foals shed virus for up to 10 days.
Vaccination of pregnant mares may reduce outbreaks.
clostridium infection as a cause of diarrhoea in foals
Clostridium difficile and Clostridium perfringens (both can rarely be found in normal foals)
As with adults’ development of disease is associated with toxin producing strains of the bacteria.
Sporadic cases and “outbreaks” can occur.
Risk factors: previous use of antimicrobials, stressors e.g., hospitalisation, travel and weaning.
Can result in severe haemorrhagic enterocolitis in foals, with rapid progression and high mortality rates
Clostridium difficile is commonly associated with diarrhoea in humans
salmonella infection as a cause of diarrhoea in foals
Well recognised pathogens associated with diarrhoea and septicaemia in foals
Clinical signs include moderate to severe diarrhoea, pyrexia, depression and inappetence.
Foals with salmonellosis should be monitored closely for evidence of sepsis and for signs of localised infections such as uveitis, synovitis and osteomyelitis.
Unlike in adult horses all neonatal foals with enteric salmonellosis should be treated with systemic antimicrobials
Zoonotic
Lawsonia intracellularis
infection as a cause of diarrhoea in foals
Infection via accidental oral ingestion, main reservoir of infection wildlife.
Faecal shedding for 7‐17 days in infected foals 1-2 weeks organism survival in environment
Primarily affects weanling and yearling horses between August and February
Clinical signs: include lethargy, weight loss, pyrexia, diarrhoea and peripheral oedema.
Marked hypoproteinaemia and hypalbuminaemia, and ultrasonographic evidence of small intestinal thickening
Off label use of pig vaccine has been shown to be protective against clinical disease.
Rhodococcus equi
infection as a cause of diarrhoea in foals
Primarily a respiratory pathogen, can cause extra-pulmonary disease including enterocolitis, abdominal abscessation, peritonitis and hepatitis
Parasitic Infection (uncommon)
infection as a cause of diarrhoea in foals
S westeri infects foals early in its life (transmission of larvae via ingestion of the mare’s milk), but its role in diarrhoea is questionable.
Cryptosporidium parvum has been identified in the faeces of foals with diarrhoea, primarily in those less than 1 month of age. Contagious and zoonotic.
Approach to diagnosis in Foal diarrhoea
Thorough history and clinical examination
Further laboratory testing is dependent on the age of the foal and severity of the clinical signs
Baseline clinical pathology:
Haematology
Proteins
Inflammatory markers
Serum Electrolytes
Renal enzymes/urinalysis (SG If less than 1.010 foal is hydrating itself)- foal being able to urinate in the first place is important in itself
Plasma Lactate
IgG (in young foals)
determining the aetiology of foal diarhoea
Faecal testing is important from a biosecurity point of view.
Tests based on the most likely agent given the age of foal
Many commercial labs offer “diarrhoea panels” but you should be happy about the most appropriate tests given the context of each case.
In many foals with diarrhoea, more than one pathogen can be involved.
A positive test does not always confirm that the particular agent is the underlying cause of the diarrhoea, as several pathogens can be found in healthy foals as well.
Additional diagnostics – hospital setting
Abdominal ultrasonography:
Assess intestinal wall thickness, intestinal motility, stomach size, volume and appearance of peritoneal fluid in addition to umbilical structures in younger foals (important focus of infection)
Abdominal radiography
Sand /gas
fluids in foals
In foals with evidence of hypovolaemia fluids are required.
Enteral (very mild cases with no reflux)
Intravenous (most cases):
The rate, volume and type of fluid administered depends on the degree of hypovolaemia, cardiovascular status and plasma protein concentration
Foals are not tolerant of large sodium loads, so hypertonic saline contraindicated
For initial resuscitation in almost all cases a balanced crystalloid (such as lactated ringers) is appropriate.
Common approach 10–20 ml/Kg over 20–30 minutes, and then repeat as indicated by response to therapy (normalisation of tachycardia, improved mentation, passing urine etc.)
However, foals are not tolerant of excessive fluid volumes so care must be taken to avoid fluid overload.
Frequent reassessment should be performed and used to guide fluid therapy (PCV/TP/Urine SG/ clinical signs)
colloids-
Synthetic colloids not advised: have been associated with the development of coagulopathies, renal failure and an ultimately worse outcome in humans
Hyperimmune plasma (our best option) provides plasma proteins but also immunoglobulins.
Essential in foals with failure of passive transfer, but any sick foal can rapidly consume immunoglobulins even if initially adequate concentrations.
Electrolytes
Electrolyte imbalances and acid-base disturbances are common
Correction crucial for recovery and is typically performed via intravenous fluid therapy
In more mild cases oral supplementation may be sufficient.
When should we use antibiotics in a case of foal diarhoea?
Foals under 2 weeks
Clostridial infection
Salmonella
Lawsonia
Choice of specific antibiotics and dose important
Consideration should be given to hydration status and renal function prior to starting any potentially nephrotoxic antimicrobials
antimicrobials for a treatment of Undifferentiated D++ in neonate / Salmonella
foal diarhoea
amikacin (25–30 mg/kg every 24 hours, i.v. or i.m.) and ampicillin (20 mg/kg every 6–8 hours, i.v. or i.m.)
or
ceftiofur (5–10 mg/kg, every 6–12 hours, i.v. or i.m.)
antimicrobials for a treatment of Clostridial infection
foal diarhoea
Metronidazole (dose varies with age)
antimicrobials for a treatment of Lawsonia intracellularis
foal diarhoea
oxytetracycline (5-10mg/kg i.v, every 12 hours).
Or
macrolide antimicrobials. (***Care re colitis in older animals with macrolides)
Analgesia therapy in foals with dirhoea
Analgesia
Foals with D++ may show colic signs associated with inflammation / distension
NSAIDs such as meloxicam/ flunixin (care re renal effects and effects on epithelial health)
Butorphanol 0.01-0.04mg/kg i.v.
Buscopan (N-butylscopolamonium bromide) 0.3mg/kg i.v.
Gastric ulcer therapy in foals
Prophylactic use of anti-ulcer medication is controversial in neonates/ less so older foals
Use of proton pump inhibitors has been associated with the development of diarrhoea in hospitalised foals (Furr et al, 2012)
Sucralfate 20-40mg/kg po every 6 hour is an alternative option in neonates
