Transcript Ascites in the cirrhotic patient with chronic renal failure

Ascites in the chronic renal failure
patient with cirrhosis
Dr.Rajeev Jayadevan
MD (Vellore), DNB (Medicine), MRCP(UK),
American Board Certification in Medicine
American Board Certification in Gastroenterology
Senior Consultant Gastroenterologist
Sunrise Hospital
Acknowledgements
1. Dr. Jayant Thomas Mathew MD, DM Consultant
Nephrologist, Amala Medical College
2. Dr. Sooraj Y.S. MD, DNB (Nephrology)
Consultant Nephrologist, Sunrise Hospital
3. Dr. Abi Abraham MD, DM
Consultant Nephrologist, Lakeshore Hospital
Outline
• Refresh our basic physiology about ascites and
discuss what is pertinent here
• Practical aspects of treating a patient with CRF
and CLD who has ascites
Ascites in CLD: some basic science
A major issue here is that kidneys retain Na and
H2O excessively. Why?
When kidneys of cirrhotic or heart failure
patients were transplanted, they stopped
retaining Na and H2O.
This meant that the signal for Na/H2O retention
came from outside the kidney.
What triggered Na/H2O retention?
• Could it be low total blood volume?
• No, because when measured, these patients
had normal or, even increased blood volume!
• Could it be low cardiac output?
• No, because, pregnancy has high output,
but the kidneys still retain Na and H2O!
Who, then, tells the kidneys to retain Na/H2O?
“Arterial underfilling.”
Can be from :
1. Decreased cardiac output
2. Arterial vasodilatation
Effective vs. Total blood volume
Estimates of blood volume distribution indicate that
85% of blood circulates on the low-pressure, venous side
of the circulation, whereas an estimated 15% of
blood is circulating in the high-pressure, arterial circulation.
Schrier, J Am Soc Nephrol 18: 2028–2031, 2007
How does cirrhosis lead to
arterial underfilling?
Vasoconstrictor
systems not
turned on
How to treat nephrogenic ascites
Patient with ascites, CLD and CRF.
Question:
Is the ascites from the liver
or the kidney?
How to differentiate
cirrhotic vs. uremic ascites
Cirrhotic
• Transudate
• Low protein
• High SAAG > 1.1
• Creatinine < 5
• Slow reaccumulation
Uremic
• Exudate
• High protein
• Low SAAG
• Creatinine > 5
• Rapid reaccumulation
HRS
Hypovolemia-induced
Parenchymal
Drug-induced
Ascites in CKD + CLD.
Why is treatment difficult?
Management difficult as:
1. Symptoms overlap
2. Creatinine value unreliable due to CLD
3. Diuretics don’t work as easily as in CLD:
“Diuretic Resistance”
Diuretics and the nephron
Mechanisms of diuretic resistance in CRF
1. Reduced basal level of fractional Na reabsorption
2. Enhanced NaCl reabsorption in downstream segments:
DCT hypertrophy: beyond the reach of Furosemide
3. Reduced delivery of diuretic to the kidney. Diuretics are
secreted by the organic anion transporters (OATS), in the PCT,
these get inhibited by Acidosis.
4. Hypoalbuminemia decreases delivery
of Furosemide and also increases
its metabolism to glucuronide
Hypertrophy of distal tubule
Exposure to
loop diuretic
1. Taller cells
2. Larger rounded nuclei
3. Taller lateral cell processes
DCT
Na
Due to prolonged action of Loop
diuretic in the Loop of Henle,
more Na gets absorbed by a
hypertrophied DCT
Loop diuretic resistance:
Curve shifts to the right
EFFECT
DOSE
NEPHROTIC SYNDROME = ALBUMIN IN LUMEN
Luminal
action
Measures to combat diuretic
resistance in CRF
1. Restriction of fluid intake 1.5 L daily
2. Maintain Sodium intake of 2 g daily
3. Use of escalating doses of loop diuretics up
to established ceiling levels.
4. Judicious use of a second diuretic acting at a
downstream site , but watch for ADR
5. Reducing renal proteinuria in nephrotic
syndrome using ACEI or ARB
J Am Soc Nephrol 13: 798–805, 2002
Diuretic resistance:
How to test?
If < 50 mmol urine sodium in 8 hours
after Lasix 80 mg IV:
Resistant.
HEPATOLOGY, Vol. 49, No. 6, 2009
Choice of loop diuretic:
LASIX
TORASEMIDE
vs.
•
•
•
•
•
•
Preferred
Better bioavailability
Predictable outcome
OD dosing
Does better than Lasix in the 6-24 hr interval
20mg as good as 80 mg Lasix
Choice of diuretic- 2
Spironolactone
• Be cautious
• Monitor K more closely
• Patients already on ACEI
or ARB, chance of spike in K
What if gynaecomastia?
Try Amiloride 10-40 mg/d.
Less effective, however.
Second-line agents
Triamterene, HCTZ,
Metolazone (2.5 - 5 mg OD)
are second-line agents used to treat ascites.
Choice of Fluids
• Be careful with saline: pulmonary edema
• Albumin/ Plasma are OK: they stay in the
intravascular space
Protein in diet: how much?
• In CKD not on dialysis: very conservative.
0.6-0.8 g/kg/day
• If on dialysis: can give more: 1.2 g /kg/day
Dialysis patient: what day to tap?
• Tap on non-dialysis days
• Heparin can cause bleed otherwise
Dialysis patient with ascites:
how to tap:
Large-volume paracentesis
with IV Albumin replacement
at 8 g Albumin per liter of ascitic fluid removed
FFP or Platelets before a tap…..?? No.
• Routine tests of coagulation do not reflect
actual bleeding risk in patients with cirrhosis.
• These patients regularly have normal global
coagulation because of a balanced deficiency
of procoagulants and anticoagulants.
AASLD guideline HEPATOLOGY, June 2009
Do not send CA-125 in patients with ascites
• Patients with ascites should not have serum
tested for CA-125.
• It will be elevated due to pressure on
mesothelial cells
CKD + Cirrhosis :
What dialysis: HD or PD?
Peritoneal dialysis:
•
•
•
•
Less hemodynamic instability
Less bleed risk
Less Hepatitis B/C risk
No published increased risk of peritoneal
sepsis although theoretical risk from cirrhosis
(Same rates of sepsis for CKD patients on PD, regardless of presence of
cirrhosis)
• 40% more expensive
Reinfusion of ascitic fluid into the
dialysis machine: PRECEED
2 HD patients with CLD and
refractory ascites: quick
improvement, well-tolerated
TIPS: any role?
Patients with parenchymal renal disease,
especially those on dialysis, may not respond as
well to TIPS as those with functional renal
insufficiency.
Michl P, Gulberg V, Bilzer M, Waggershauser T, Reiser M, Gerbes AL. Transjugular intrahepatic
portosystemic shunt for cirrhosis and ascites: effects in patients with organic or functional renal failure.
Scand J Gastroenterol 2000;35:654-657.
Main points:
Ascites in CKD and CLD.
1.
2.
3.
4.
5.
6.
7.
Rule out other causes of ascites
Diuretic resistance occurs in CKD
Furosemide or Torasemide mainstay
Use Spironolactone with caution
Be liberal with IV albumin
Avoid IV fluids like saline
Work closely with the nephrologist