A 43-year-old woman underwent liver transplantation for alcoholic cirrhosis (MELD real 19).
A 54-year-old male cadaver whose graft was extracted according to the standard technique and placement in Wisconsin solution.
A wedge biopsy was taken during extraction and showed 30% macrosteatosis without fibrosis.
Cold ischemia time was 210 min. During recipient hepatectomy, the vena cava was preserved using the piggy-back technique.
No transfusion of blood products was required during implantation or ICU stay.
Triple therapy with TAC-MR (Advagraf®, Astellas Pharma US, Il), mycophenolate mofetil and prednisone was prescribed as a regimen.
Initially, the post-transplant course was characterized by mild hepatic dysfunction that responded favorably to alprostadil 0.03 mcg/kg/min for 3 days.
Because the patient was seropositive for cytomegalovirus (CMV) and the receptor was negative, we started CMV prophylaxis with valganvir 450 mg/12 h.
At the third week after transplantation, the patient developed jaundiced skin and mucous membranes, abdominal pain, ascites and hepatomegaly.
Analytical evidence of stasis associated with infratherapeutic plasma levels of tacrolimus (5.50 ng/ml).
Analytical values were: total bilirubin: 3.47 mg/dl; AST: 31 transferase: 61 UI/l; alanine aminotransferase: 74 UI/l; INR: 5 IU/dl normal; ultrasound: 25 UI/dl).
The anatomopathological study of transjugular biopsy performed on the 24th day post-transplant (PTD) revealed a "duct post-rejection cell with moderate inflammatory signs.
Hydaline, centrolobar, obstructive sinus syndrome
The rejection activity index (ARI) (5) was 7 (2+3+2).
Simultaneously, we optimized tacrolimus plasma levels and administered 3 boluses of 1 g of intravenous methylprednisolone 24 h.
However, ascites increased and tacrolimus reached toxic plasma levels (between 30 and 15 ng/ml for 18 days despite consecutive decreases in the dose of TAC-MR).
He required repeated evacuating paracentesis, volume expansion with intravenous albumin and diuretic treatment.
The ascitic fluid study revealed a transudate with negative cultures (including mycobacteria after 90 days) and a serum-ascitic albumin gradient > 1.1 g/dl, compatible with portal hypertension.
Deterioration of liver function continued and was associated with acute renal failure (total bilirubin: 1.23 mg/dl; allergic rhinitis/transferase: 100 IU/l; alkaline creatinine clearance: 1346 mg/dl).
A cardiac study ruled out right ventricular failure.
Median CT angiography confirmed the absence of portal venous obstruction or at the level of suprahepatic drainage.
To define the severity and prognosis of POS we measure pressures and quantify the gradient of portal hypertension.
Unfortunately, we could not perform the measurement because, after performing an evacuating paracentesis, the patient presented a sudden deterioration of the general condition.
When a hemoperitoneum was suspected, an urgent exploratory laparotomy was performed, which resolved satisfactorily.
We took advantage of a new liver graft biopsy, which confirmed the worsening of SOS by the development of extensive centrilobular fibrosis with partial resolution of acute rejection (ARI = 4).
The patient was included in the transplant list, and 51o TPD underwent retransplantation without incidents.
The new immunosuppression consisted of quadruple therapy with basiliximab, mycophenolate mofetil, prednisone and delayed introduction of MD-CT.
Pathological examination of the explant revealed evident bridges of fibrosis between the centrolobular veins and the portal space.
Some centrilobular veins had been totally replaced by fibrous material.
Numerous portal venules showed fibrotic changes, indicative of portal hypertension.
The patient had a post-transplant failure due to mild rejection and acute renal failure.
She was discharged 29 days after retransplantation.
He is currently being studied for suspected biliary strictures of the anastomosis.
The evolution of the case presented is summarized in Figure 4.
