Teaching clinic: 2 cases of cirrhosis HBV Flashcards
Which is the first step in the management of ascites for in-hospital patient? * Bedrest * Fluid restriction * Salt restriction * Diagnostic paracentesis * Diuretic therapy
- Diagnostic paracentesis (Exclude SBP)
Ascites physical properties
Physical properties
* Colour
- straw
- blood-stained (3 bottle tests: uniformly blood stained
- chylous: (TB kidney) must check lipoprotein (hyperlipidemia), malignancy (gynecological/lymphoma cauasing lymphatic obstruction)
* Protein - may be as high as 40 g/L without special significance
* Rate of reabsorption - 900 ml/day (In tense ascites, may to 1.5 l/day)
* WCC < 500/mm3 (< 250 PMN)
* Malignant cells < 10% positive in malignant ascites
If CA lung pleural fluid: will have 80% chance of picking up malignant cells
Mx of ascites
- Diagnostic paracentesis in every patient for white cell count
- Salt restriction (1/2-2g/day)
- Fluid restriction (0.8-1L/day)
- (a) Diuretics: spirolactone (not 1st line in other fluid retention causes such as cardiac: furosemide). K+ sparing. High incidence of gynectomastia especially in alcoholic cirrhosis. Amiloride can be used for male
(b) Proximal loop diuretics if (a) insufficient. Bumetadine (Burinex) furosemide absorption unreliable in portal hypertension
(c) albumin infusion (increase intravascular oncotic pressure) and IV diuretics
Oliguria: <500ml/day
Insensible water loss: 600-800ml (undetectable water loss i.e. skin and lungs)
Complications of therapeutic paracentesis
- shock
- electrolyte disturbance
- uraemia
- infection (HO dirty finger)
- encephalopathy
- protein depletion
Safety of therapeutic paracentesis?
Abd tap of 4-6L is safe
* With albumin infusion and/or
* If patient has peripheral edema
(1) and (2) can prevent intravascular volume depletion
NB
* Bleeding from puncture sites
* Sepsis
* Perforation of caecum with right sided punctures (sigmoid colon more mobile due to sigmoid mesentery)
Which other physical sign is most likely to be present? * Bilateral basal crepitations * R pleural effusion * L pleural effusion * Hard nodular hepatomegaly
- R pleural effusion
None of the above
Effect of diuresis in SBP
Leads to selective condensation of ascites H2O with
* Increase in protein content
* Increase in lymphocytes because of long life span
* Constant PMN because of short lifespan
Lymphocytes: lifelong
PMN lifespan: 3-7 days
More ascitic protein means less opsonic activity which means more prone to SBP
What is max tapping for pleural effusion?
AE of overtapping?
1L per day, if more the collapsed lung will have decreased surfactant –> will result in reexpansion pulmonary edema
Most common cause of reexpansion pulmonary edema is when there is pneumothorax with delayed admission
SBP mechanism
If known cirrhotic: just describe the protein as low (<10g/L) or high
Clinical features of SBP
Common: 10-20%
* P. U. O.
* Encephalopathy
* Abdominal S/S - none to marked
* Diarrhoea
* Hypothermia
* Asymptomatic
* May be fatal/recurrent
dx of SBP
- WCC (do differential count) :
- > 500 WBC / mm3 suspicious
- > 250 PMN / mm3 in pts with S/S of SBP
- > 500 PMN / mm3 in asymptomatic pts
- Culture (usually G-ve or streptococci; may be neg.): gut in origin (not likely to be anaerobic)
pH<7.3 suspicious (if blood pH not acidotic)
pH<7.15 poor prognosis
Arterial/ascitic fluid pH gradient of 0.10
Tx of SBP
Broad spectrum 3rd gen cephalosporin: exponential fall in PMN count after initiation of antibiotics
Duration of treatment: 5 days
Can stop antibiotics as soon as PMN count <250/mm3
Prevention of recurrence of SBP
Ofloxacin
- incompletely absorbed by gut
- highly active against gram neg bacilli
- low activity against anaerobes
- rarely causes bacterial resistance
- low side-effects
Long term use of quinolones increases the risk of ESBL enterobactericacae
Use rifaximin if quinolone resistance
Which antibiotic well absorbed by gut and used for systemic infections, requires double dosage?
Metronidazole for amoebiasis
The cause of the LFT deterioration is :
* Acute graft rejection
* Acute-on-chronic graft rejection
* CMV infection
* Post-transplant lymphoproliferative disorder
* Emergency of lamivudine resistant HBV
- Emergency of lamivudine resistant HBV (YMDD mutant)
Cant be graft rejection: within 1 hours
Not on chronic graft rejection
CMV would not present with hyperbilirubinemia
PTLD: EBV clonal expansion (would present with lumps and bumps)
TDF warnings
- Slightly greater decrease in bone mineral density suggesting increased bone turnover
- HypoP and osteomalacia secondary to proximal renal tubulopathy can also occur
Benefits of TAF
– Comparable viral suppression (HBV DNA <29 IU/mL)
– Improved rates of ALT normalization
– No resistance development
– Rates of HBeAg loss and seroconversion similar
Less toxicity: decline in hip and spine BMD with improved bone biomarkers
Well tolerated in HBeAg-ve and +ve patients
Can be used in pregnancy now (small studies)
What is the most likely histologic finding?
* Subacute fulminant hepatitis
* Re-development of cirrhosis
* Fibrosing cholestatic hepatitis
ALT and AST not elevated: so not subacute fulminant hepatitis
Redevelopment of cirrhosis can occur within a year if reinfected. Cirrhosis of the liver would not lead to this degree of cholestasis (increased bilirubin)
Ans: fibrosing cholestatic hepatitis
Features of fibrosing cholestatic hepatitis
Histology of explanted liver
* Prominent loss of hepatocytes
* Portal expansion by fibrosis
* Hepatocytes
- diffuse marked balloon degeration
- cholestasis excess HBsAg in cytoplasm and excess HBcAg in nuclei
- Dx - Fibrosing cholestatic hepatitis
Pathogenesis of fibrosing cholestatic hepatitis
- Pathogenesis
- primary cytopathic effect of HBV dysregulation of viral transcription
- Increased HBV mRNA → viral Ag in endoplasmic reticulum → cell death
- Rapid graft failure and death
- Rapid recurrence with re-transplant
Prevention of recurrent HBV in liver transplant
- Indefinite high dose HBIG – 65-80% effective
- Lamivudine – depends on rate of resistance developing
- Low dose HBIG + nucleoside analogue - >90% effective; current practice in most >90% centres
Monotherapy with entecavir/tenofovir for liver transplantation is a viable option
