A simple description of a less understood topic in Intensive Care Medicine. Aim to make understanding and management easy for the residents and prevention steps for all ICU workers.
3. Introduction
• HRS is the development of renal failure in Pts
with advanced chronic liver disease(eg. portal
HTN due to cirrhosis, severe alcoholic
hepatitis, or (less often) metastatic tumors
• HRS occasionally happened with fulminant
hepatitis, who have portal HTN & ascites.
4. Pathogenesis
Progression of liver failure
&
portal hypertension
↑Arterial
vasodilatation
↓Effective arterial BP
Moderate Na
retention
Severe water
retention & ↓ Na
Central Hypovolemia
↓Cardiac
output
↑Chronotropic
function
Extreme Hepato-renal Syndrome
5. Types
• Type 1:
• Increase in serum creatinine >2.5mg/dl
(221 micromol/L) or 50% decrease in Cr. Clearance
<20ml/min. during a periods of less than 2 weeks.
– Rapidly progressive and very poor short term outcome.
• Type 2:
• Increase in serum creatinine>1.5 mg/dl, without
meeting criteria of type 1.
– refractory ascites is usually present.
– Slower I progress but prognosis is not bad as type 1.
6. Prognosis
• Worst of all complications
of cirrhosis.
• Median survival in type
1 to 2 weeks
• Median survival in type 2:
up to 6 months
7. Risk Factors
It may happen spontaneously, but there are
many triggers include:
- diuretic resistance ascites
- large volume paracentesis without
albumin replacement (15%).
- SBP (20%).
8. Major Criteria
– Advanced chronic hepatic failure and portal hypertension
– Serum Creatinin > 1.5 mg/dl or 24 hours urine creatinin
clearance < 40 ml/min
– Absence of shock, massive GI or renal fluid losses,
exposure to nephrotoxic drugs, hypovolemia & ongoing
sepsis
– No sustained improvement in renal function following
diuretic withdrawal & volume expansion with 1.5 litres of
isotonic saline
– Proteinuria < 500 mg/dl
– No evidence of obstructive uropathy or parenchymal renal
disease
10. Differential Diagnosis
• Glomerulonephritis and vasculitis:
– IgA nephropathy, renal disease associated with hepatitis B & C.
• Obesity with DM
– Who have NASH and diabetic nephropathy.
• ATN:
– 10-20% of patients with AKI in the setting of cirrhosis have ATN.
ATN with FENa ……
• SBP in absence of septic shock can be associated with HRS
(expert opinion).
• Pre-renal azotemia:
– In cirrhotics induced by GI fluid losses, bleeding, or therapy with
a diuretic or NSAIDs.
11. Factors playing role in the management of HRS
• Is the recovery expected in short term?
• Is the pt. admitted to the ICU?
• Which drugs are available for HRS?
• National and regional variability.
• Is the pt. a candidate for liver transplantation?
12. Treatment
• Patient in ICU:
Initially, we have to start:
o norepinephrine(0.5 – 3 mg/kg) with the goal of raising MAP:10
mmHg.
o albumin for @ least 2 days (1 g/kg per day or 100 gm
maximum).
o IV vasopressin may also be effective, starting at rate of
0.01 units/min & titrating upward as needed.
• Patient not in ICU: (terlipressin + albumin)
o Terlipressin:1 to 2 mg / 4 to 6 hrs).
o albumin: for 2 days (1 g/kg per day [100 g maximum]), followed
by 25 to 50 grs / day until terlipressin therapy is discontinued.
13. Treatment
• If terlipressin is not available:
(midodrine + octeriotide + albumin)
o Midodrine orally (starting @ 7.5 and increasing
the dose /8 hr. up to a maximum of 15 mg t.d.s).
o Octreotide is either given intravenous infusion
(50 mcg/hr) or S/Q (100 to 200 mcg t.d.s)
o Albumin is given for 2 days as an IV bolus
(1 g/kg /day [100 g maximum]), followed by 25 to
50 grs /day until midodrine & octreotide therapy
is discontinued.
14. Treatment
• In highly selected Pt. who fail to responds to
medical therapy:
• Transjugular intrahepatic porto-systemic shunt
is some times successful.
o TIPS: has numerous complication.
o TIPs: needs contrast so CRRT should be considered
particularly if serum creatinine >1.5 mg/dL.
o TIPS should be considered only as a last resort in
selected patients.
15. Treatment
• In patients who fail to
– respond to the above therapies,
– develop severely impaired renal function
– are candidates for liver transplantation
– have a reversible form of liver injury
– are expected to survive
• The recommendation is
– to start dialysis as a bridge to liver transplantation
or liver recovery.
16. Treatment
• Other therapies:
Misoprostol
N-acetylcysteine
ACE inhibitors
None of these approaches are consistently
associated with benefit.
Peritoneovenous shunt:
no more recommended because of lack of long term
benefit and high rate of complication.
17. Prevention
• As the HRS regularly developed in Pt. with systemic
bacterial infection and/or alcoholic hepatitis, so the
following intervention can help to prevent HRS:
o IV albumin in Pt. with SBP 1.5g/kg in the 1st day and
1g/kg in the 3rd day of antibiotic.
o It will reduce the incidence of renal impairment and mortality.
o Norfloxacin:
A randomized trial reported significant benefits with the
oral administration of norfloxacin at 400 mg/day.
Norfloxacin was associated with the following significant
benefits:
- decreased one-year probability of SBP (7 versus 61 percent) and
hepatorenal syndrome (28 versus 41 percent), and
- improved survival at three months (94 versus 62 percent) and
one year (60 percent versus 48 percent).
18. Conclusion:
• HRS can happen with advanced CLD and also with fulminant
hepatitis.
• Diuretics will cause azotemia but not HRS.
• HRS diagnosis needs good history and clinical diagnosis after
exclusion of other DD.
• Starting medical therapy depends on drug availability and Pt.
Position (ICU VS. medical ward).
• TIPS: should be considered as a last resort because of most Pt.
are not suitable for operation, numerous complication related
to the procedure, and needs for CRRT before and after the
procedure.
• CRRT should be started for Pt. expected to responds to
medical therapy or as a bridging to liver transplant.