640 Obesity Surgery, 11, 2001 © FD-Communications Inc.

Obesity Surgery, 11, 640-642

Background: Biliopancreatic diversion (BPD) wasdesigned to avoid the serious complications ofjejunoileal bypass (steatohepatitis and hepatic fail-ure). Although this is today considered a safe andeffective procedure, a few reports of patients whodeveloped steatohepatitis and subsequently died inhepatic failure exist.

Methods: We report a morbidly obese patient whodeveloped subacute hepatitis resulting in hepaticfailure 1 year after BPD.

Results: Because of irreversible liver failure thedecision to perform a liver transplantation wasmade. The patient underwent emergency liver trans-plant and lengthening of the common limb. Thecourse of liver transplantation and the patient’srecovery were uneventful.

Conclusion: Severe liver disease may rarely followBPD. Liver transplantation and lengthening of thecommon bowel may be performed to treat thesepatients.

Key words: Morbid obesity, bariatric surgery, biliopancre-atic diversion, liver transplantation, subacute hepatic fail-ure

Introduction

Operations for morbid obesity may have occa-sional serious complications. Jejunoileal bypassprocedures formerly performed to correct this,occasionally worsened hepatic steatosis and fibro-sis and resulted in hepatic failure. Vertical bandedgastroplasty was also considered a satisfactory pro-cedure for weight loss in morbid obesity, but hasoccasional complications from the gastrointestinaltract, besides complications from other systems.The current surgical procedures of choice (ie. bestclinical outcome with lowest complication rate) formorbid obesity involve gastric bypass with gastro-jejunostomy and biliopancreatic diversion (BPD).Liver damage following BPD for obesity is a rare,dangerous and, when left untreated, potentiallyfatal complication This is the first case report ofacute liver failure after BPD treated successfullyby means of liver transplantation.

Case Report

A 41-year-old woman who weighed 120 kg (height162 cm, BMI 46) was referred for obesity surgery,

Case Report

Liver Transplantation in a Case of Steatohepatitisand Subacute Hepatic Failure after BiliopancreaticDiversion for Morbid Obesity

Julio Castillo, MD, PhD1; Emilio Fábrega, MD, PhD1; Carlos F.Escalante, MD, PhD2; Juan Carlos R. Sanjuan, MD, PhD1; Luis Herrera,MD, PhD1; Fernando Hernánz, MD, PhD1; Esteban Martino, MD, PhD1;Fernando Casafont, MD, PhD1; Manuel Gómez Fleitas, MD, PhD1

1Liver Transplantation Unit and 2Obesity Surgery Unit, Hospital Universitario “Marqués deValdecilla”, Santander, Spain

Reprint requests to: Dr Julio Castillo, Servicio de CirugíaGeneral II, Hospital Universitario “Marqués de Valdecilla”, AvdaValdecilla s/n, Santander 39008,Spain. Fax: 34-942 203733;e-mail: jcastillod@mundivia.es

Obesity Surgery, 11, 2001 641

Transplantation after BPD

due to obesity hypoventilation syndrome, venousinsufficiency and daytime somnolence, after non-operative attempts at weight reduction had failed.She was a cigarette smoker (4-6 per day). Therewere no known drug allergies. She did not drinkalcohol. There was no history of diabetes, drugabuse or blood transfusions. Preoperative studies,including abdominal ultrasound, chest x-ray,spirometry and serum ALT, AST, alkaline phos-phatase, bilirubin and albumin were normal. Sheunderwent BPD using Scopinaro’s classic tech-nique and cholecystectomy in February 1999.Liver biopsy only demonstrated mild macrovesicu-lar steatosis.

Two months after surgery she had lost 20 kg andall liver function tests were normal. Six monthslater, her weight was 73 kg. She had mild diarrhea,and, again, ALT, AST, alkaline phosphatase, biliru-bin and albumin levels were normal. However, twomonths later she had about ten stools daily,weighed 69 kg and ALT was 1200 IU/L, AST 800IU/L, alkaline phosphatase 294 IU/L and totalbilirubin 3.3 mg/dl. Malabsorption tests demon-strated bacterial overgrowth. Pancreatic enzymeswere then prescribed.

She was hospitalized in February 2000 after atwo-month history of vomiting, diarrhea (morethan ten stools daily), weakness, abdominal painand distension and myalgia. She appeared chroni-cally ill, temperature was 36.5 ºC, jaundice andascites were noted, and the liver was palpable onabdominal examination. Hematocrit was 35.6,white cell count 10,600, platelets 120,000,Prothrombin Activity 53%, serum bilirubin 13.4mg/dl, AST 302 IU/L, ALT 283 IU/L, alkalinephosphatase 476 IU/L, albumin 2.7 mg/dl, glucose64 mg/dl, transferrin 102 mg/dl, and cholesterol133 mg/dl. Immunologic tests for hepatitis A, Band C virus, CMV, Herpes simplex, Varicela-Zoster, HIV, Epstein-Barr and Toxoplasma werenegative. ANA, AMA and AML were also nega-tive. Serum copper concentration and urinary cop-per excretion were normal. Doppler ultrasound,CAT and MRI showed signs of chronic hepatic dis-ease and ascites, with no signs of portal hyperten-sion. Contrast enema and upper gastrointestinalradiographs were normal. Transjugular hepaticbiopsy demonstrated submassive hepatic necrosis,early nodule formation, periportal and lobular neu-

trophilic infiltrates and cholestasis. Because the patient accepted oral intake and

medication, there was no need for total parenteralnutrition. Enteral nutrition with protein restrictionwas given to prevent protein intake-inducedencephalopathy. However, over the next few daysher condition slowly deteriorated; facial edema andgeneral confusion developed; later, grade III andIV encephalopathy and flapping appeared, togetherwith 15% prothrombin activity and 5% factor Vactivity. She underwent orthotopic liver transplan-tation in April 2000, using the piggy-back tech-nique. During the operation, an ileojejunal latero-lateral anastomosis was constructed, shortening thetotal bypass length to only 40 cm.

The biopsy of the explanted liver demonstratedsigns of submassive hepatic necrosis, with intensecholestasis (+++) and steatosis. The course of herliver transplantation and recovery were uneventful.When the patient was discharged, all liver functiontests were normal, and have remained so.

Discussion

Non-alcoholic steatohepatitic liver failure has beenreported as a fatal complication following BPD.1,2

The postoperative progressive deterioration of theliver enzymes may be the first sign of liver decom-pensation in these patients. Therapeutic approachesfor this complication include total parenteral nutri-tion, surgical reversal, and the ambulatory adminis-tration of an uncoated pancreas extract with a highprotease content taken with protein-rich meals.3

Early recognition and adequate treatment may pre-vent more serious complications. However, insome cases, the condition continues to decline,with the onset of acute hepatic failure in subjectswith no such previous disease. The previouslyreported patients died.1,2 They had not been con-sidered as suitable candidates for liver transplanta-tion, mainly on the basis of malnutrition and tech-nical problems related to previous surgery.1 Basedon the good results that we obtained with the casethat we report here, we believe that liver transplan-tation and simultaneous lengthening of the com-mon intestinal limb may be performed in thesepatients.

642 Obesity Surgery, 11, 2001

Castillo et al

References

1. Grimm IS, Schindler W, Haluszka O. Steatohepatitisand fatal hepatic failure after biliopancreatic diver-sion. Am J Gastroenterol 1992; 87: 775-9.

2. Langdon DE, Leffingwell T, Rank D. Hepatic failureafter biliopancreatic diversion. Am J Gastroenterol

1993; 88: 321.

3. Antal S. Treatment of protein malnutrition and

uncontrollable diarrhea following biliopancreatic

diversion with pancreas extract Viokase. Obes Surg

1993; 3: 279-283.

(Received January26, 2001; accepted July 13, 2001)

The fact that an adverse event may occur after anoperation does not necessarily mean that the eventis a specific complication of the operation. A com-plication exists when an event occurs regularly,even if rarely, in all large series, with a frequencysufficient to recognize a causal relationship and toformulate pathogenetic hypotheses. This is not thecase for liver failure after BPD. BPD has beenwidely performed in the western world for morethan 20 years, with some published series exceed-ing 1,000 operated patients and many exceeding100, and in none of these series has a single caseof BPD-related liver failure been reported.

Antal claims that pancreatic enzymes may pre-vent and reverse the elevation of serum transami-nases following BPD, but he has never reported acase of liver failure in his series.1

The two cases reported in the letter by Langdonet al2 were patients with multiple previous gastricrestrictive procedures (and therefore uncompliantby definition), who had received elsewhere (andthis means without an adequate follow-up) anundescribed (and then unknown) operation. Thevery peculiar history of these patients, including“50” stools daily, migrating Angelchick prosthesis,iatrogenic hepatic coma, TV screen explosion andsurreptitious alcoholism, makes it difficult to under-stand what happened. Interestingly, both patientshad normal serum transaminases and neither hadthe type of liver histology seen after JI bypass.

On the contrary, the patient reported by Grimm etal3 (again operated on elsewere), is a well-docu-mented, although unexplained in its pathogenesis,case of fatal liver failure that occurred after anapparently primary BPD. Nevertheless, it was theonly reported case with more than 5,000 BPD pub-lished by that time, and the author could not sug-gest any specific cause/effect relationship betweenBPD and liver failure.

Almost 10 years have elapsed since then, andthe published cases have risen to more than10,000. The interesting case report above byCastillo and associates (the first case reported bythe same group that performed the BPD) is alsowell documented. Yet, it is again without any expla-nation and, added to the one by Grimm et al3, itmakes two cases out of more than 10,000 BPDs inmore than 20 years.

Non-alcoholic steatohepatitis in the obesepatient is well known. It may be aggravated, even ifexceptionally, by weight loss no matter how it isobtained, and, in conjunction with some known andsome unknown co-factors, it may lead to liver fail-ure.

Although a few cases of postoperative acutepancreatitis were reported after BPD, nobody con-siders it to be a specific complication of BPD butrather a generic complication of gastric surgery oreven of general surgery. Similarly, the handful ofreported cases of unexplained liver failure afterBPD should be considered as a complication ofobesity, or of weight loss, or at the very most of sur-gically-induced weight loss, and not as a specificcomplication of BPD.

Nicola Scopinaro, MDProfessor of Surgery

Genoa, ItalyReferences1. Antal S. Treatment of protein malnutrition and uncon-

trollable diarrhea following biliopancreatic diversionwith pancreas extract Viokase. Obes Surg 1993; 3:279-283.

2. Langdon DE, Leffingwell T, Rank D. Hepatic failureafter biliopancreatic diversion. Am J Gastroenterol1993; 88: 321.

3. Grimm IS, Schindler W, Haluszka O. Steatohepatitisand fatal hepatic failure after biliopancreatic diver-sion. Am J Gastroenterol 1992; 87: 775-9.

Liver Failure

Invited Commentary