ABSTRACTS from 16th International COnference on ... - CRRT Online

Educational Objectives:
E13
Liver and the Kidney 2: Principles of Extracorporeal Hepatic Support
Andrew Davenport MD, FRCP
8:15-9:45
Wednesday, February 15
1. to understand why clotting occurs in extracorporeal circuits in patients with liver failure
2. to understand why some therapies can be complicated by hypoglycaemia
3. to understand the limitation of lactate and citrate as anionic buffers in patients with hyperacute liver failure
Content Description:
Patients with hyperacute liver failure are at increased risk of cerebral oedema and intracranial hypertension.
Conventional haemodialysis leads to an acute fall in plasma urea and other small solute concentrations during the
first hour of treatment. This rapid fall in osmolality leads to a gradient between the plasma and the brain, as
water moves twenty times faster than urea, such that water can flow along a concentration gradient <strong>from</strong> the
plasma into the brain, so increasing cerebral oedema, and resulting in brain stem coning in severe cases. Thus
slower therapies such as CRRT are preferable in cases of hyperacute liver failure. However the Achilles heel of
continuous dialysis/haemofiltration circuits is circuit clotting, so that they become intermittent therapies rather
than continuous, In acute liver failure, the liver fails to sythesise some of the natural anticoagulants (antithrombin,
proteins S & C), and hepatic necrosis leads to inflammatory reaction and increased release of tissue factor.
So although these patients often have abnormal prothrombin times, they are often procoagulant, with increased
risk of extracorporeal circuit clotting.
Patients with acute liver failure may be unable to maintain glucose homeostasis and are at risk of hypoglycaemia.
Thus to prevent hypoglycaemia, dialysates and or replacement solutions should contain glucose.
Traditional aemofiltration and dialysates for CRRT have been lactate based, or more recently citrate has been
introduced as an anticoagulant. Lactate and citrate are then indirectly converted through to bicarbonate and so
correct metabolic acidosis. However if the rate of metabolism through to bicarbonate is reduced due to hepatic
insufficiency, then the patient will become acidotic if the continued losses of bicarbonate and lactate/citrate by
the dialyzer/haemofilter exceed the rate of conversion through to bicarbonate. Thus in cases of hyperacute liver
failure bicarbonate based dialysates and reinfusion fluids are often required.
Suggested Reading:
Davenport A. Continuous renal replacement therapies in patients with liver disease. Semin Dial. 2009 Mar-
Apr;22(2):169-72
Davenport A, Tolwani A. Citrate anticoagulation for continuous renal replacement therapy (CRRT) in patients
with acute kidney injury admitted to the intensive care unit Nephrol Dial Transplant plus 2009; doi:10.1093/ndtplus/sfp136
Agarwal B, Shaw S, Hari MS, Burroughs AK, Davenport A. Continuous renal replacement therapy (CRRT) in
patients with liver disease: Is circuit life different?J Hepatol. 2009 Jun 24
Davenport A, Will EJ, Davison AM Hyperlactataemia and metabolic acidosis during haemofiltration using lactate-buffered
fluids Nephron. 1991; 59(3):461-5
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