Masato Nakasuji and MJ Bookallil, Anasth Analg 2000; 91: 1351-5.

Reviewed by: R. Prasad, MD

Conclusion
Hyperkalemia just after revascularization correlates with anhepatic...

• hyperkalemia (preexisting)
• acidosis due to low CO
• decreased liver lactate uptake (severity of liver dz)
• NOT with extent of preservation injury or cold ischemia time

Methods

• 64 patients, OLT, 1/98-12/99.
• Excluded: h/o cardiac dz, CVVHD during OLT
• Anesthetic: Isoflurane, pancuronium, oxygen, air. Solumedrol 500mg. Warm acetate Ringer's solution. Saline-washed PRBC (with bicarb) via RIS. CaCl to maintain iCa 1 mmol/L, K+ if K < 3.5 mmol?L after revascularization.
• Surgery: Iced UW solution for liver preservation. All had venovenous bypass. Graft liver suprahepatic VC end-to-side with recipient IVC (piggyback method).
• Patients divided into 2 groups based on serum K at 1-min postrevascularization
• Group 1: <5.5 mmol?L
• Group 2: >= 5.5
• Compared several factors between groups, inclucing preop factors, K level during OLT, hemodynamics, ABG/lactate, creatinine clearance, Hgb/EBL.

Results
Group 2 ...

• Preop Variables - Groups similar, except liver dz indicators slightly worse:

• K higher during hepatic dissection, remained higher till 60 min after revascularization (no hyperkalemic arrests).
• pH slightly lower, base balance more negative, lactate higher, and CO lower during anhepatic and early neohepatic phases

• IVC pressure lower after IVC clamping (Group 2 = 19 mmHG vs. Group 1 = 23 mmHg)

• Hemodynamics (PACW, CVP, SVRI)
• EBL, PRBC/FFP before revascularization
• Creatinine clearance and K intake/urinary excretion
• Preservation injury (based on serum AST levels)

Discussion
Slightly worse liver condition in Group 2 makes it a bit more difficult to interpret ... decreased lactate uptake from worse liver dz would explain the worse (lactic) acidosis, which would tend to increase serum K before revascularization. Also, worse dz may cause increased collateralization (reflected in lower Group 2 IVC pressure after cross-clamp), so these sicker patients may not need as much of a fluid bolus prior to clamping (prerevascularization transfusion volume was ~20% lower). Therefore, there may be less hemodilution, with consequent increase in K with revascularization, compared with Group 1.
What does this mean for practice?

• Avoid hyperkalemia while anhepatic? - Nothing new here.
• Avoid acidosis while anhepatic? - Again, nothing new. Lactic acidosis related to preexisting liver disease - can't do anything about severity of pt's liver disease. Of course, avoid LR.
• Avoid low CO while anhepatic? - Should we push CO even higher, even if BP is considered acceptable? Give more volume to try to hemodilute?