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http://dx.doi.org1550-7289/r 20

*CorrespondAlcoy, Alicante

E-mail: a.ba

Surgery for Obesity and Related Diseases ] (2014) 00–00

Case report

Liver failure and transplantation after duodenal switchAniceto Baltasar, M.D.a,*

aClinica San Jorge, Alcoy, Spain

Received February 6, 2014; accepted February 12, 2014

Abstract Liver failure (LF) and liver transplant (LT) are rare after a biliopancreatic diversion/duodenal switch

/10.1014 A

ence:0380ltasar@

procedure for obesity, but occasionally it may happen. Two clinical cases are presented. One patient,18 years ago, had LF, but a liver donor could not be found, and the patient died. The second patient,2 years ago, received a successful LT and is now well and asymptomatic. Careful follow-up,medical management and surgical intervention may prevent the occurrence of LF. Transplantationand bowel reversal may be necessary. (Surg Obes Relat Dis 2014;]:00–00.) r 2014 AmericanSociety for Metabolic and Bariatric Surgery. All rights reserved.

Keywords: Biliopancreatic diversion; Duodenal switch; Liver failure; Liver transplant

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Morbid obesity (MO) is a condition reaching epidemicproportions all over the world. Bariatric surgery is the mosteffective management of MO.Nonalcoholic fatty liver disease (NAFLD) has become

the most common cause of chronic liver disease worldwide[1]. Nonalcoholic steatohepatitis (NASH) represents 1 ofthe most common histologic findings in MO patientsundergoing liver biopsy. NAFLD usually improves withbariatric surgery, but occasionally NAFLD may appear afterthe bariatric procedure [2].Histologic features of NASH (steatosis, necroinflamma-

tory activity, and portal fibrosis) are similar to those foundin other conditions such as liver disease after jejunoilealbypass and alcoholic fatty liver. The mechanisms of injuryon the MO remain undefined and the risk of progression tocirrhosis is controversial [3].Unrecognized or recognized cirrhosis is not necessarily

an absolute contraindication to bariatric surgery, providedthere is good hepatic function and no evidence of severeportal hypertension (corrected portal pressure o12 mmHg). NASH-related cirrhosis has been shown to improve

16/j.soard.2014.02.013merican Society for Metabolic and Bariatric Surgery. All r

Dr. Aniceto Baltasar, Clinica San Jorge, Olivar 55,4, Spain.aecirujanos.es

with all forms of bariatric surgery. The best option in manyof these patients appears to be a restrictive procedure [4].Biliopancreatic diversion/duodenal switch (DS) is prob-

ably the more effective operation to treat MO with the bestlong-term results related to weight loss [5–7]. Prachandet al. [8] had 54% excess weight loss with gastric bypassand 68% with DS while Strain et al. [9] reported a 16.5BMI drop in the gastric bypass and 23.8 with the DS. Liverfailure (LF) and liver transplant (LT) has been rarelyreported after DS [10].Baltasar et al. [11] in 2004 reported 10 cases of severe

liver impairment on 470 MO patients operated with DS(93 of them laparoscopic DS) followed during 9 years and1 patient had LF.

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Case reports

Case #1

A 41-year-old woman with a body mass index (BMI) of58 (kg/m2) had a DS in April 1995, and she had a very largefatty liver. The alimentary limb (AL) was 260-cm long andthe common channel (CC) was 65 cm. She did well untilJune 1995, 3 months later, when she was readmitted to auniversity hospital for persistent vomiting and had a BMI of48. Liver function tests were abnormal (AST-155 IU/L;

8384ights reserved.

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A. Baltasar / Surgery for Obesity and Related Diseases ] (2014) 00–002

ALT-91; AP-621 IU/L), and at this time a percutaneousliver biopsy showed NASH (grade III steatohepatitis with-out necroinflammatory activity or portal fibrosis). In August1995, she was readmitted with a BMI of 39, and she wastreated successfully with total parenteral nutrition andbiliary and pancreatic supplements and had a liver biopsyof mild NASH.She was readmitted again in October 1995 with severe

jaundice and alteration of liver function tests (TBil-18.9,DBil-12.6, ALT-123, AST-236, AP-644, INR-1.64) andwas transferred to a transplantation service with progressivealteration of bleeding profile. The clinical course of thepatient rapidly worsened with encephalopathy. She wasurgently placed in red-call alert for transplant, but she diedof LF while waiting for a LT donor (no postmortem liverexamination is available).

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Case #2

A 33-year-old, female with a BMI of 49 had uneventfulLDS in March 2008 with a 260-cm AL and 65-cm CC. Fivemonths later, she was healthy and asymptomatic with aBMI of 26. On November 2009, 20 months after the initialsurgery, she became progressively jaundice with T-bilirubin-508 (0–18 mmol/L), direct bilirubin-217 (0–8mmol/L), prothrombin time-17, INR-6.5. LF with brainsymptoms developed within a week, and she went intocoma. She received an orthotopic liver transplant. Thepathologic report at the time of LT was disappearance ofhepatocytes, cholangiolar metaplasia, and severe bile stasis.The AL length was increased while the BPL was shortenedto make a CC 4200 cm. Today, 4 years later, her albuminis 3.4, she is asymptomatic with a BMI of 23, and her liverprofile is normal.

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Discussion

LF leading to death or LT after bariatric surgery is rare.Castillo et al. [12] reported the first successful LT after BPDon a MO (BMI 46) female patient who lost 2 kg in 2months (BMI 38) and had a BMI of 28 at 6 months andsubacute hepatitis was diagnosed. A transjugular hepaticbiopsy demonstrated submassive hepatic necrosis, earlynodule formation, periportal and lobular neutrophilic infil-trates, and cholestasis. Her condition deteriorated; facialedema and general confusion developed; and later, grade IIIand IV encephalopathy and flapping appeared, togetherwith 15% prothrombin activity and 5% factor V activityresulting in LF 1 year after BPD. She underwent orthotopicLT in April 2000, using the piggyback technique, and sherecovered. During the operation, an ileum-jejunal side-to-side anastomosis was constructed, shortening the totaldiversion length to only 40 cm.Lowell et al. [13] wrote about the jejunoileal bypass (JIB)

a MO technique, developed in the late 1960s, but is now

abandoned because of a high rate of complications, includ-ing cirrhosis. Lowell et al. [13] reviewed their experience ofJIB and LT in 380 consecutive adult patients since 1985,and 4 patients underwent LT. The mean duration of timefrom JIB to LT was 22.3 years. All patients had compli-cations, in addition to their liver disease, related to the JIB,which included nephrolithiasis, cholelithiasis, vitamin defi-ciencies, renal insufficiency, and d-lactic acidosis. Onepatient had the JIB taken down before LT, which precipi-tated acute liver and renal failure, necessitating urgenttransplantation. One patient, who had the JIB taken downat the time of LT, developed recurrent MO, while the other3 patients did not. The patient who did not have the JIBtaken down did not develop recurrent liver disease and hasbeen followed-up with monthly liver function tests andyearly biopsies. Lowell et al. [13] concluded that theincidence of patients who require LT after JIB might beon the increase. Takedown of the JIB may also precipitateacute liver failure in the cirrhotic patient. JIBs takedownshould be accomplished either at the time of LT or after LT.The LT patients with decompensated cirrhosis after JIBhave demonstrated excellent early results. LT recipients arealso at risk for recurrent MO after takedown of the JIB.Våge et al. [14] reviewed 36 JIB patients, from 1971–

1976 at 425 years. Ten patients (28%) had their shuntreversed. With 1 exception, these patients quickly regainedweight, and 5 (50%) of them died. Meanwhile 23 patientswith an intact JIB were alive. When the optimal shuntlength for the individual patient is found, JIB maintains asubstantially reduced weight for 25 years. Vitamin andmineral deficiencies are common, but no serious clinicaldeficiency states where seen. Still, no bariatric grouprecommends JIB any longer.Geerts et al. [15] surveyed LT incidence after MO surgery

in Belgium. An enquiry was sent to all Belgian livertransplant centers to investigate the occurrence of subacuteand chronic LF after bariatric surgery. After weight-reduction surgery, 10 patients in 3 Belgian transplant centerswere listed for LT due to severe hepatocellular failure. Nineof them had undergone a Scopinaro BPD operation, and onehad a JIB. The median time to develop LF was 5 years. Thepatient with JIB developed chronic LF after 25 years. Sevenpatients received transplants, 2 died awaiting a graft, and 1 isstill on the waiting list. After LT, 1 patient developed rapidreappearance of LF at 10 months, requiring retransplanta-tion. Two recipients died shortly after LT due to multiorganfailure. The remaining recipients were doing well. Accordingto this survey, the BPD operation carries a potential risk ofLF. However, because there were only 10 cases, the actualincidence of BPD-induced LF is unknown. He advised strictfollow-up of liver function and timely dismantling of BPD.Grimm et al. [16] also reported a BPD patient whodeveloped steatohepatitis and subsequently died of LF.Sgambato et al. [17] had a 42-year-old woman (BMI 54)

who underwent biliointestinal bypass (BIB) for severe obesity

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Liver Failure and Transplantation After DS / Surgery for Obesity and Related Diseases ] (2014) 00–00 3

in 2012. Nine months later, she experienced diarrhea and arapid weight loss of 70 kg with 41% BMI reduction. Atadmission, she had jaundice with pale mucosa and splenome-galy. Due to the rapid liver decompensation she underwentorthotopic LT and reversal of the BIB. Her subsequentcondition was a satisfactory clinical improvement.Sagredo [18] described a 28-year-old obese woman who

developed acute LF and had a LT 11 months after gastro-plasty with intestinal resection and a gastrojejunal anasto-mosis. A liver biopsy was performed after the surgery andrevealed severe steatohepatitis and fibrosis.In contrast, the DS procedure developed in the early

1990s has only had anecdotal reports associated with LF.To date, LT after DS remains an extremely rare occurrence.D’Albuquerque et al. [19] claims that any MO surgery

that promotes malabsorption, such as gastric bypass andBPD techniques, may have complications associated withthese procedures and LF that have been observed withincreasing frequency. They reported 3 patients who, 7–24months after bariatric surgery, had LF for which LT wasconsidered to be indicated. LT was undertaken in 2 of thepatients, and the third patient died while waiting for thisprocedure. They discussed the possible causes of thisuncommon and poorly understood complication of surgeryfor obesity. One possibility is that it might arise because ofprogression of steatohepatitis. An alternative concept is thatthis complication may be secondary to rapid, massiveweight loss. Marceau et al. [20] reported 1 patient withLT after DS, and 10 years later he is alive and doing well.Auclair et al. [21] has recently reported a LT after 1

uncomplicated DS in a patient with a BMI of 54. LFoccurred 8 months after the procedure as the patientdeveloped progressive encephalopathy, which had started3 weeks after the onset of jaundice. The liver showed anacute hepatitis with confluent bridging necrosis, mixedinflammatory infiltrates, and significant ductular reaction.A subacute LF was diagnosed, and the patient was listed forLT because of increasing coagulopathy and worseningencephalopathy. Neither reversal of the BPD nor length-ening of the common limb was performed. The patient isdoing well, and she remains clinically well 20 monthsafter LT.Butte et al. [22] claimed that sleeve-forming gastrectomy

(SFG), a restrictive procedure, can be successfully used inLT recipients who require later MO surgery, becausehistologic regression of steatosis and normalization of liverfunction tests and glucose levels usually occur.Sarr [23] had a DS done in a young 22-year-old female

(BMI 73) with portal hypertension, Noonan and metabolic Xsyndrome, including insulin resistance, dyslipidemia, sleepapnea, and markedly decreased mobility, and cirrhosis of theliver. This procedure seemed [24] controversial because arestrictive procedure, such as a SFG, as the first stage shouldbe offered to a patient who may require later a LT. We haveperformed 6 LSFG in patients with unsuspected cases of

granular liver cirrhosis, instead of using the LDS, and noneof them had any postoperative consequences.We [11] reported on 10 patients with 470 DS cases who

developed hepatic impairment with a single LF patient.Later on, in the following 459 cases, we had a secondpatient with LF and that made 11 cases of severe liverimpairment in 929 DS (416 LDS), an incidence of 1.18%.The 2 cases of LF made the incidence of LF to be .21% inthe whole group.Because LF is such a serious condition, what type of

alternative can be offered to any patient with hepaticimpairment before a LF happens? Prevention at surgery isoffered by Hess [25], measuring the whole small bowelbefore any BPD surgery and calculates the CC as 10%, theAL as 40% and the BPL as 50%. The final cause of the LFcondition should be related to 3 main conditions: a)preoperative functional liver impairment; b) reducedcaloric-protein intake; and/or c) malabsorption.The surgeon first needs to be aware that although this is a

rare condition, it is so important that early management isoffered to the impaired patient before a LF occurs. Thepostop patient should be properly fed by oral and parenteralintake including proteins, sugars, vitamins, and so on.If there is no proper and quick improvement, the

malabsorption component should be reversed! Increasingthe CC loop length is not a complex procedure. Thesimplest way in our opinion [26] is to join side-by-sideAL and BPL 100-cm proximal to the RNY jejunal-ileumanastomosis, the so-called “kissing-X” anastomosis used forthe protein-caloric malnutrition, and the operation should bedone by laparoscopy. Full reversal of the small bowel to theoriginal position is quite a complex procedure and so isincreasing the AL by adding an extra length from the BPL.If the condition appears within the context of chronic low

proteins, anasarca or caloric-protein malnutrition, then thesimplest and quicker resolution of this condition is to carryout the kissing-X by the open laparotomy approach,because we have the experience [27] that the small bowelwall may be too thin and can be injured by the laparoscopicinstruments on the mesenteric border where transmuraldiverticula formation occurs due to the weakness of thesmall bowel wall.

Conclusion

LF and LT are rarely reported as the complication of DSsurgery. The incidence of liver impairment is 1.28% in ourpatients and LF requiring LT is .21%. This severe compli-cation should be considered to provide early diagnosis andmedical management with nutritional support and carefulfollow-up. In case of progression detected by an increase inthe liver impairment and coagulopathy, reversal of theshort-bowel syndrome and malabsorption should be done,leaving only the restrictive part of the DS. If the patientdevelops a full-blown LF, then early referral for LT to a

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transplant center should not be delayed and partial or fullreversal of the BPD done at the time of transplantation.

Disclosures

The authors have no commercial associations that mightbe a conflict of interest in relation to this article.

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