Hepatobiliary Flashcards
What is hepatorenal syndrome?
Renal failure secondary to portal HTN- pathophys poorly understood.
OLiguria with Na and water retention in the setting of liver failure (acute or chronic) + not due to another cause.
Manage with octreotide/ terlipressin (Tx port HTN) and dialysis
Fatal without liver transplant (or dialysis).
Pathophys poorly understood.
Ascitic paracentesis: PROCEDURE
INDICATIONS
- New (diagnostic)
- Symptomatic
- SBP suspected
PROCEDURE
- Roll slightly to left
- USS: find fluid pocket in LLQ (1/3 way ASIS to umbi)
- Local
- Z track technique
DIAGNOSTIC:
- 60ml syringe on 20G needle (or spinal)
THERAPEUTIC:
- Advance stylet/catheter combo whilst aspirating
- Take off sample
- Attach to 3-way and bag
- Send samples
- Monitor
-
Give albumin 20% if >5L off
—> 100ml for every 3L - Stop once minimal (or 6h)
- Occlusive dressing + lie on other side
COMPLICATIONS
- Usual
- HypoNa
- Hypovolaemia
- Hepatorenal syndrome (>5L)
Analysis of ascitic fluid:
APPEARANCE
Clear- normal
Cloudy- peritonitis
Blood- traumatic tap or haemorrhage
Milky- Chyle/ lymph
BIOCHEM
Cell count
Protein/ albumin
Glucose
Lipase/ amylase
MICROSCOPY
SAAG >1.1, protein <30 = transudate (systemic)
SAAG <1.1, protein >30 = exudate (local)
SAAG (serum albumin - ascitic albumin)
What ascitic tap finding is DIAGNOSTIC of SBP?
Absolute PMN count >250
WCC >100 with >50% PMN
But not essential for Dx
Turbid
SAAG <1.1
+ gram stain/ culture
Spontaneous Bacterial Peritonitis (SBP)
Not entirely understood:
—> Portal HTN
—-> Mucosal oedema
——> bacterial translocation (E coli, enterococcus, S. Pneumoniae)
Mortality 30-50%. Don’t miss!!
Presentation very variable
Classic triad: fever, abdo pain, increasing ascites = uncommon!
Suspect in anyone with ASCITES plus ANY other feature
Management:
- Ascitic tap
- Ceftriaxone 1g daily
- Certain patients also get +- albumin
Define ‘conjugated’ vs ‘unconjugated’ hyperbilirubinaemia:
Normal = 85% unconj, 15% conj.
<20% conj = UNCONJUGATED
—> prehepatic
—> hepatocellular dysfunction
Can cross BBB and cause kernicterus
>50% conj = CONJUGATED
—> hepatocellular injury
—> intrahepatic obstruction
—> post hepatic obstruction
Doesn’t cross BBB, but can enter urine
Often signifies dangerous cause
Causes of UNCONJUGATED hyperbili:
Haemolysis
Excessive bruising
GI haemorrhage
Congenital: Gilbert, Crigler-Najar
Bowel obstruction (increased enterohepatic cycling)
Neonatal and breastmilk jaundice
Causes of CONJUGATED jaundice:
HEPATITIS
- Viral (A, B, C)
- Toxic
–> OD (paracetamol, Iron)
–> Idiosyncratic (isoniazid, fluclox)
- Alcoholic
- Autoimmune
Acute liver failure
INTRAHEPATIC OBSTRUCTION
- Cirrhosis (Wilson, ETOH, primary)
- Cholestasis (pregnancy)
- Dubin- Johnson, Rotor
- Infiltrative
- Haemochromatosis
- Budd-Chiari
POST HEPATIC OBSTRUCTION
- Gallstones
- Cholangitis
- Pancreatic head Ca
- Ampullary Ca
- Biliary atresia
- Biliary sclerosis
- Strictures
Causes of ISOLATED hyperbilirubinaemia:
Gilbert’s
Haemolysis
What is the significance of dark urine and pale stools?
Indicated OBSTRUCTIVE cause of bili:
Dark urine means must be conjugated
Pale stools means bile not being excreted
Diagnostic work up of jaundice (adult):
INVESTIGATIONS
- Bilirubin- conj and unconj
- LFTs
- Urine:
–> any bili ABNORMAL
–> If present, must be CONJ
Be guided by:
1: CONJ VS UNCONJ
2: LFT PATTERN
—> Isolated
—> with hepatocellular pattern
—> with cholestatic pattern
Ultrasound, ERCP/MRCP
‘First line’ liver screen: Paracetamol, Hep A, B, C.
‘Second line’ liver screen
What tests are on a ‘liver screen’?
LFT
Cong/unconj bilirubin
Synthetic:
Glucose
Albumin
Coags
Infective:
Hep A,B,C,D,E
CMV
EBV
Autoimmune:
- ANA
- AMA
- ANCA
- Anti kidney/liver/smooth musc
- IgM/ IgG
Specific:
- Fe panel (Haemochromo)
- Ceruloplasmin/ Copper (Wilson’s)
- Alpha1 antitrypsin
- Paracetamol
NEONATAL jaundice:
Common + usually benign:
–> ‘Physiological’ (immature)
–> ‘Breastmilk’ (components) and ‘breastfeeding’ (low initial intake)
–> Bruising
Abnormal if onset:
<24 hours
- Haemolysis
- Sepsis
>2 weeks
- Above
- Biliary atresia
- Hypothyroidism
Abnormal if conjugated:
- Biliary atresia (Dark urine, pale stools)
- Hepatitis
INVESTIGATIONS
- Serum bilirubin (conj + unconj)
- Blood group and DAT (Coombs)
+/- Film
+/- Haemolytic screen
+/- LFTs
+/- USS
+/- Sepsis screen
+/- TFTs
Plot on nomogram
Phototherapy until 50 below line (check 6-12 hrly)
Hydrate and feed frequently
Check again 12h for rebound
Features and management of Hepatic Encephalopathy:
- Confusion/ coma
- Asterixis
- Hyperreflexia
- Clonus
- Babinski +
Ammonia levels don’t correlate that well.
Grades 1-4: mildly drowsy –> coma
Reduce enteric production + resorption of ammonia:
- Lactulose 30ml PO- 2hrly until bowels open, then QID
+
- Metronidazole PO
Broad management of acute liver failure:
- Work up cause
-
Encephalopathy
–> Lactulose, metro or rifaxamin -
Liver function
–> Stop toxics
–> Dose-adjust
–> Fentanyl, ketamine okay -
Synthetic function
–> Hypoglycaemia
–> Albumin
–> INR/bleed -
Portal HTN
–> Terlipressin/ octreo -
Ascites
–> Paracentesis
–> Na restriction + diuretics (give albumin, not NaCl) -
Hepatorenal syndrome
–> Monitor for, optimise nephrosafety -
Definitive
–> Tx specific cause
–> Refer to Transplant Centre
Clinical features of chronic liver disease:
- Cachexia
- Jaundice
- Bruising
- Scleral ichterus
- Hepatic fetor
- Gynaecomastia
- Ascites
- Distended superficial abdominal veins
- Spider naevi
- Palmar erythema
