My patient has a pre op Portal vein Embolization had a laparoscopic trisectionectomy and wedge of left lateral sector. Initially did well postop, home in 2 weeks. Has had a very slow worsening of hyperbilirubinemia (cong and mostly uncong) and some ascites and anasarca as outpatient.
Readmitted 2 weeks ago with total bili of 375, now at 650 (no prev liver disease, minimal lifetime alcohol intake, folfox for 4 months post colon resection). Ultrasounds show IHDs normal size, ERCP shows no bile leak. With NJ protein-restricted tube feeding, the ammonia levels are rising from 31 to 67 over 2 weeks.
INR has been 1.3 for about 6 weeks postop, but rising to 1.4 with a recent UTI. He has not been encephalopathic. Albumin levels of 15 have been bolstered with twice daily albumin infusions for two weeks to a level of 35, but the patient is anasarcic. Creatinine was 140 2 weeks ago, is slowly worsening and is now 212; jumped with each of 2 paracenteses.
He is stagnant, with worsening bilirubin. Is there any evidence for intervening to improve whatever liver dysfunction is driving this patient's course?
What about inflow and outflow veins of the remnant? Are they OK? Is there any kinking of the LHV?
No, flow is all OK and liver remnant must be twice of preop size; significant growth.
Thx.
I had female pt with similar problem after anterior approach RT for huge intrahepatic cholangiocellular Ca, but the problem was considered to be some kinking of the LHV. The patient improved slowly and the treatment was similar to yours plus keeping left lateral decubitus position on the bed, low doses of dopamine, LMW heparine, methionine and UDC. Probably it can be helpful to check for common hepatotropic viruses and drugs that can damage the liver.
i expect that this patient may do OK in the long run, as long as we are very careful to address any infections early etc and to watch all indices. However, I wondered if there are ideas of things that we may try to improve the bilirubin metabolism (since that seems to be the measurable derangement of greatest imoortance), as a way to minimize the morbidity. The patient is on NJ feeds with minimal protein and a good hepatic mix of amino acids, but with the amonia rising now, we have started lactulose (did not do so previously as the drawbacks of dealing with diarrhoea and potential perianal problems in pt with anasarca).
Liver size increase sometimes does not imply increase of liver function.
Kinking (as A. Julianov said) is a good idea.
If thing get worse, you should have in mind MARS
Sometimes congestion of the liver remnant can be missed and regarded as hypertrophy. You can check also the angle between LHV and sagittal plane on preembolisation and posthepatectomy CT scans in order to evaluate the change in position of LHV.
It sounds like your patient has all the features of post-op hepatic failure and apart from ruling out any correctable technical issues (as discussed above) the management centres around optimised medical therapy. According to the numbers you gave above (Bili, INR, creatinine) your patient has a MELD score of 32 so is very sick indeed.
Even though the liver remnant has grown physically the regenerative pattern is cholestatic and functional recovery generally takes many months. During this time sepsis is a major risk, and any significant episode of sepsis can trigger hepato-renal failure, followed closely by multi-organ failure.
Maintaining nutrition is important and there is not good evidence that a low protein diets protects against encephalopathy or uraemia. I would be aiming to provide 25-40kcal/kg/day including 1-1.2gm/kg protein. Na restriction is important and if you are giving albumin make sure it is salt poor (ie 20% albumin). Judicious use of diuretics (aldactone and frusemide) to control ascites - hyponatraemia and worsening renal function are the limiting factors for diuretic therapy. Look out for spontaneous bacterial peritonitis (diagnostic tap if suspected) and avoid large volume paracentesis if SBPis suspected. If renal function is worsening rule out sepsis and consider using terlipressin which is effective in patients with HRS.
What was the initial resection for? Did she have normal liver to begin with? MARS was suggested above - this does improve biochemical parameters in liver failure but unfortunately has not been shown to not change patient outcome. Is the patient a transplant candidate?
You must list this patient for liver transplant as salvage procedure, if oncological criterion is met
I observed this isolated hyperbilirubinemia on mulitple occasions in patients after PVE and PVL and especially in ALPPS. It is a form of PHLF with a specific presentation. The prognosis is generally poor, especialy in elderly patient once they get an infection. The voluemtry cut off of an sFLR of 30% is entirely unreliable to prevent this form of PHLF. And NOT JUST because livers may grow because of congestion and edema. Rather becasue true hypertrophy does not result in functional hypertrophy in some cases. I think the solution is the use of HIDA scans following the result of the Amsterdam group to measure uptake function prior to resection: I hope it will soon become standard, because I think this complication can be avoided by determing volume AND funtion prior to extensive liver resections.
Splenic artery ligation, although benefit may be lost this late on
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