Liver Failure After Jejunoileal Shunt Maj Richard J. Andrassy, MC, USAF; Lt Col Roderick C. Haff, MC, USAF; Capt Richard W. Lobritz, MC, USAF Reports of fatty infiltration of the liver following jejunoileal shunt obesity and hyperlipemia are frequent. Cases of overt liver failure, in contrast, are rare and poorly documented following the various types of small bowel bypass. Fifteen months after jejunoileal bypass, a 41-year-old nonalcoholic woman whose preshunt liver function was chemically normal was found to have morbidly abnormal liver chemistry values. A biopsy examination demonstrated severe fatty metamorphosis bordering on frank cirrhosis. Reversal of her shunt led to return of her liver chemistry values to normal and reversal of the morphologic changes noted at biopsy examination. Close follow-up of patients subjected to small bowel bypass for obesity or hyperlipemia is mandatory. If liver function abnormalities persist for more than six months, strong consideration should be given to reversal of the shunt. for
for morbid obesity have in selected patients since been used 1962 when Lewis and associates1 reported two patients in whom jejunocolic bypasses were undertaken for intrac¬ table morbid obesity. Jejunocolic bypasses have been asso¬ ciated with excessive complications, including irreversible liver disease, and have since been abandoned. The jejuno¬ ileal bypass procedure as described by Payne and DeWind2 and as modified by Scott and Law3 has been described as safe in most reports.-11 In November 1972, McGill and col¬ leagues12 reported a case of postoperative liver failure and death following jejunoileal bypass. Their review of the lit¬ erature did not reveal well-documented cirrhosis following the jejunoileal bypass. They concluded that, on the basis of reports to date, liver failure is uncommon in the patient who has undergone a 35.6 to 10.2-cm (14 to 4-inch) jejuno¬ ileal shunt. Our extensive review of the literature con¬ firms this conclusion. This article reports the development of abnormal liver function test results and biopsy-proven pathologic changes following this procedure with later re¬ versal of liver failure and pathologic findings.
procedures Intestinal bypass experimentally
REPORT OF A CASE
41-year-old woman with a history of obesity since the age of admitted to another facility to be evaluated for morbid obesity. Preoperative evaluation revealed normal liver function test results, sulfobromophthalein test, and liver scan. There was no history of ethyl alcohol intake or previous history of hepatitis. No base-line liver biopsy specimen was obtained. On June 9, 1972, the patient underwent a jejunoileal bypass with 35.6 cm (14 A
12
was
for publication Oct 8, 1974. From the departments of surgery and pathology, Wilford Hall USAF Medical Center, Lackland Air Force Base, Tex. Reprint requests to General Surgery Service, Wilford Hall USAF Medical Center, Lackland Air Force Base, TX 78236 (Dr. Andrassy).
Accepted
inches) of jejunum distal to the ligament of Treitz anastomosed end-to-end to 10.2 cm (4 inches) of ileum proximal to the ileocecal valve. The patient's preoperative weight was 145.5 kg (322 lb). The patient did well postoperatively and had approximately four to eight bowel movements per day. In August 1973, she developed a form of polyarthritis and was hospitalized. Liver function tests revealed an alkaline phosphatase value of 27 King-Armstrong units/100 ml (normal, 17 King-Armstrong units/100 ml) and a serum glutamic oxaloacetic transaminase (SGOT) value of 153 m/i/ml (normal, 48 µ/ ). A liver biopsy examination revealed severe fatty infiltration, marked portal fibrosis with entrapment of hepatocytes, and portal triaditis. Some areas revealed necrosis of hepatocytes with eosinophilic inclusions suggestive of Mallory bodies (Fig 1 and 2). No cause for the polyarthritis was ascer¬ tained, and this spontaneously cleared in the hospital. The patient was transferred to this facility on Sept 19, 1973. Results of a phys¬ ical examination were unremarkable, and the liver was not pal¬ pable. Her weight was now 91.3 kg (202 lb). Liver function tests on admission here revealed an alkaline phosphatase level of 320 in¬ ternational units (IU) (normal, 85 IU). Laboratory studies dis¬ closed the following values: SGOT, 150 µ/ml (normal, 48 µ/ml); lactic dehydrogenase, 210 IU/liter (normal, 90 to 200 IU/liter); creatine phosphokinase (CPK), 25 IU (normal, 10 to 50 IU); and bilirubin, 0.8 mg/100 ml. Electrolytes, blood urea nitrogen, creati¬ nine, calcium, and phosphate values were within normal limits. On Sept 21, 1973, the patient underwent surgery. The previous bypass was taken down and normal anatomy was restored. Post¬ operatively the patient did well and was discharged on the tenth postoperative day. Liver function values rapidly returned toward normal and by November 1973 were all within normal limits. The patient returned in February 1974, at which time liver function tests, a sulfobromophthalein test, and a percutaneous liver biopsy examination were performed. Results of the liver function tests and the sulfobromophthalein test were normal. The liver biopsy examination revealed complete resolution of the fatty infiltrate and no evidence of necrosis of hepatocytes. Mild portal fibrosis re¬ mains (Fig 3 and 4). The patient will continue to be observed in the out-patient clinic. COMMENT Intestinal bypass procedures for severe obesity have been performed with increasing frequency during the past 12 years. The incidence of cirrhosis following the jejunoileal shunt is extremely difficult to document. The majority of patients selected for this procedure have pre¬ operative fatty infiltration. Many have abnormal sulfobro¬ mophthalein test results with otherwise normal liver func¬ tion test results. After bypass, the liver generally becomes further infil¬ trated with fat, but this usually clears spontaneously after several months. The SGOT and alkaline phosphatase ele¬ vations are frequently seen transiently postoperatively. Although a review of the early literature reveals a 5% to 10% incidence of cirrhosis after the jejunocolic shunt, the frequency after jejunoileal shunts is difficult to ascertain. Drenick et al" reported one case of possible early cirrhotic changes, but made no mention of preoperative liver func¬ tion tests or biopsy examination and the liver enzymes did not become abnormal in the case described. Maxwell et al" reported one case of hepatomegaly with fatty degeneration. The alkaline phosphatase value was within normal limits, while the total bilirubin level was 2.4
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Fig 1.—Severe fatty infiltration involving nearly (hematoxylin-eosin, 100).
Fig 3.—Complete resolution of fatty (hematoxylin-eosin, 100).
shunt
all
hepatocytes
infiltration after takedown of
Fig 2.—Severe fatty infiltration and area of portal fibrosis. Entrap¬ ment of hepatocytes in fibrotic process is notable, as well as portal
triaditis (hematoxylin-eosin,
400).
Fig 4.—Fibrosis along with mild portal triaditis still present. Note bile duct proliferation also (hematoxylin-eosin, 400).
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mg/100 ml. After takedown, the liver decreased in size and his patient did well. McGill et al12 reported a well-documented case of cir¬ rhosis and death 11 months after jejunoileal shunt in a
nonalcoholic woman. The majority of large series, however, report no evi¬ dence of liver disease other than occasional fatty infil¬ tration. "·" Many possible causes for the fatty degenera¬ tion have been proposed, but none as yet proved: (1) hepatitis; (2) rapid lipid mobilization; (3) essential fatty acid deficiency (malnutrition); (4) absorption of hepatotoxic material from the colon or from the "blind" loop (sec¬ ondary to bile acids); (5) protein malabsorption. White and his associates17 recently likened the lesion in small bowel bypass patients to kwashiorkor, and found decreased ab¬ sorption of leucine, lycine, and glycine in their patients. Although the suggestion of possible liver failure is fre¬ quently made, on the basis of reports to date, liver failure after jejunoileal bypass is quite rare. The liver biopsy specimen taken 14 months after the by¬ pass procedure revealed severe fatty infiltration that in¬ volved nearly all the hepatocytes. There was marked por¬ tal fibrosis with entrapment of hepatocytes, as well as a mononuclear portal triaditis. Some areas revealed actual
necrosis of hepatocytes with eosinophilic inclusions sug¬ gestive of Mallory bodies. No specific pseudolobules or regenerative nodules can be identified, and hence these changes fall somewhat short of the criteria for cirrhosis as recently outlined by Smetana.18 These changes have been described by some as "precirrhotic" or "cirrhotic"; however, they are still reversible at this point and hence are not true cirrhosis. This case strongly supports the previously proposed po¬ tential hazard of liver damage after jejunoileal bypass. Anatomical reversal of the procedure led to normal liver function. These patients should be maintained on a high protein, vitamin-supplemented diet and should avoid alco¬ hol. If the initial operative liver dysfunction does not show signs of resolution by the fourth to sixth postoperative month, the shunt should be taken down. Extremely close observation of these patients over the first two years postoperation is absolutely essential for their continued wellbeing. Further documentation of the true incidence of sub¬ stantial liver function abnormality and hepatic failure is needed if use of this procedure is to be continued on an in¬ creasing scale.
References 1. Lewis LA, Turnbull RB Jr, Page IH: "Short-circuiting" of the small intestine. JAMA 182:77-79, 1962. 2. Payne JH, DeWind LT: Surgical treatment of obesity. Am J Surg 118:141-146, 1969. 3. Scott HW, Law DH: Clinical appraisal of jejunoileal shunt in patients with morbid obesity. Am J Surg 117:246-253, 1969. 4. Shibata HR, Mackenzie JR, Huang S: Morphologic changes of the liver following small intestinal bypass for obesity. Arch Surg 103:229-237, 1971. 5. Lewis LA, Turnbull RB Jr, Page IH: Effects of jejunocolic shunt on obesity, serum lipoproteins, lipids and electrolytes. Arch Intern Med 117:4-16, 1966. 6. Scott HW, Dean R, Shull JH, et al: New considerations in use of jejunoileal bypass in patients with morbid obesity. Ann Surg
177:723-735, 1971.
7. Salmon PA: The results of small intestine bypass operations for the treatment of obesity. Surg Gynecol Obstet 132:965-979, 1971. 8. Dano P, Jarnum S, Nielsen OV: Intestinal shunt operation in obesity. Scand J Gastroenterol 8:457-464, 1973. 9. Schwartz MZ, Varco RL, Buchwald H: Preoperative preparation, operative technique, and postoperative care of patients undergoing jejunoileal bypass for massive exogenous obesity. J Surg Res 14:147-150, 1973.
10. Scott HW, Law DH, Sandstead HH, et al: Jejunoileal shunt in surgical treatment of morbid obesity. Ann Surg 171:770-782, 1970. 11. Corso PJ, Joseph WL: Intestinal bypass in morbid obesity. Surg Gynecol Obstet 138:1-5, 1974. 12. McGill DB, Humphreys SR, Baggenstoss AH, et al: Cirrhosis and death after jejunoileal shunt. Gastroenterology 63:872\x=req-\ 877, 1972. 13. Drenick EJ, Simmons F, Murphy JF: Effect on hepatic morphology of treatment of obesity by fasting, reducing diets and small-bowel bypass. N Engl J Med 282:829-834, 1970. 14. Maxwell JG, Richards RC, Albo DJ: Fatty degeneration of the liver after intestinal bypass for obesity. Am J Surg 116:648\x=req-\ 652, 1968. 15. Brown RG, O'Leary JP, Woodward ER: Hepatic effects of jejunoileal bypass for morbid obesity. Am J Surg 127:53-58,1974. 16. Buchwald H, Lober PH, Varco RL: Liver biopsy findings in 77 consecutive patients undergoing jejunoileal bypass for morbid obesity. Am J Surg 127:48-52, 1974. 17. White JJ, Moxley RT, Pozefsky T, et al: Transient kwashiorkor: A cause of fatty liver following small bowel bypass.
Surgery 75:829-840, 1974. 18. Smetana HF: Cirrhosis of the liver: Principles of classification, histogenesis, and pathogenesis. Pathol Annu 7:107-144,1972.
Downloaded From: http://archsurg.jamanetwork.com/ by a University of Manitoba User on 06/04/2015
for morbid obesity have in selected patients since been used 1962 when Lewis and associates1 reported two patients in whom jejunocolic bypasses were undertaken for intrac¬ table morbid obesity. Jejunocolic bypasses have been asso¬ ciated with excessive complications, including irreversible liver disease, and have since been abandoned. The jejuno¬ ileal bypass procedure as described by Payne and DeWind2 and as modified by Scott and Law3 has been described as safe in most reports.-11 In November 1972, McGill and col¬ leagues12 reported a case of postoperative liver failure and death following jejunoileal bypass. Their review of the lit¬ erature did not reveal well-documented cirrhosis following the jejunoileal bypass. They concluded that, on the basis of reports to date, liver failure is uncommon in the patient who has undergone a 35.6 to 10.2-cm (14 to 4-inch) jejuno¬ ileal shunt. Our extensive review of the literature con¬ firms this conclusion. This article reports the development of abnormal liver function test results and biopsy-proven pathologic changes following this procedure with later re¬ versal of liver failure and pathologic findings.
procedures Intestinal bypass experimentally
REPORT OF A CASE
41-year-old woman with a history of obesity since the age of admitted to another facility to be evaluated for morbid obesity. Preoperative evaluation revealed normal liver function test results, sulfobromophthalein test, and liver scan. There was no history of ethyl alcohol intake or previous history of hepatitis. No base-line liver biopsy specimen was obtained. On June 9, 1972, the patient underwent a jejunoileal bypass with 35.6 cm (14 A
12
was
for publication Oct 8, 1974. From the departments of surgery and pathology, Wilford Hall USAF Medical Center, Lackland Air Force Base, Tex. Reprint requests to General Surgery Service, Wilford Hall USAF Medical Center, Lackland Air Force Base, TX 78236 (Dr. Andrassy).
Accepted
inches) of jejunum distal to the ligament of Treitz anastomosed end-to-end to 10.2 cm (4 inches) of ileum proximal to the ileocecal valve. The patient's preoperative weight was 145.5 kg (322 lb). The patient did well postoperatively and had approximately four to eight bowel movements per day. In August 1973, she developed a form of polyarthritis and was hospitalized. Liver function tests revealed an alkaline phosphatase value of 27 King-Armstrong units/100 ml (normal, 17 King-Armstrong units/100 ml) and a serum glutamic oxaloacetic transaminase (SGOT) value of 153 m/i/ml (normal, 48 µ/ ). A liver biopsy examination revealed severe fatty infiltration, marked portal fibrosis with entrapment of hepatocytes, and portal triaditis. Some areas revealed necrosis of hepatocytes with eosinophilic inclusions suggestive of Mallory bodies (Fig 1 and 2). No cause for the polyarthritis was ascer¬ tained, and this spontaneously cleared in the hospital. The patient was transferred to this facility on Sept 19, 1973. Results of a phys¬ ical examination were unremarkable, and the liver was not pal¬ pable. Her weight was now 91.3 kg (202 lb). Liver function tests on admission here revealed an alkaline phosphatase level of 320 in¬ ternational units (IU) (normal, 85 IU). Laboratory studies dis¬ closed the following values: SGOT, 150 µ/ml (normal, 48 µ/ml); lactic dehydrogenase, 210 IU/liter (normal, 90 to 200 IU/liter); creatine phosphokinase (CPK), 25 IU (normal, 10 to 50 IU); and bilirubin, 0.8 mg/100 ml. Electrolytes, blood urea nitrogen, creati¬ nine, calcium, and phosphate values were within normal limits. On Sept 21, 1973, the patient underwent surgery. The previous bypass was taken down and normal anatomy was restored. Post¬ operatively the patient did well and was discharged on the tenth postoperative day. Liver function values rapidly returned toward normal and by November 1973 were all within normal limits. The patient returned in February 1974, at which time liver function tests, a sulfobromophthalein test, and a percutaneous liver biopsy examination were performed. Results of the liver function tests and the sulfobromophthalein test were normal. The liver biopsy examination revealed complete resolution of the fatty infiltrate and no evidence of necrosis of hepatocytes. Mild portal fibrosis re¬ mains (Fig 3 and 4). The patient will continue to be observed in the out-patient clinic. COMMENT Intestinal bypass procedures for severe obesity have been performed with increasing frequency during the past 12 years. The incidence of cirrhosis following the jejunoileal shunt is extremely difficult to document. The majority of patients selected for this procedure have pre¬ operative fatty infiltration. Many have abnormal sulfobro¬ mophthalein test results with otherwise normal liver func¬ tion test results. After bypass, the liver generally becomes further infil¬ trated with fat, but this usually clears spontaneously after several months. The SGOT and alkaline phosphatase ele¬ vations are frequently seen transiently postoperatively. Although a review of the early literature reveals a 5% to 10% incidence of cirrhosis after the jejunocolic shunt, the frequency after jejunoileal shunts is difficult to ascertain. Drenick et al" reported one case of possible early cirrhotic changes, but made no mention of preoperative liver func¬ tion tests or biopsy examination and the liver enzymes did not become abnormal in the case described. Maxwell et al" reported one case of hepatomegaly with fatty degeneration. The alkaline phosphatase value was within normal limits, while the total bilirubin level was 2.4
Downloaded From: http://archsurg.jamanetwork.com/ by a University of Manitoba User on 06/04/2015
Fig 1.—Severe fatty infiltration involving nearly (hematoxylin-eosin, 100).
Fig 3.—Complete resolution of fatty (hematoxylin-eosin, 100).
shunt
all
hepatocytes
infiltration after takedown of
Fig 2.—Severe fatty infiltration and area of portal fibrosis. Entrap¬ ment of hepatocytes in fibrotic process is notable, as well as portal
triaditis (hematoxylin-eosin,
400).
Fig 4.—Fibrosis along with mild portal triaditis still present. Note bile duct proliferation also (hematoxylin-eosin, 400).
Downloaded From: http://archsurg.jamanetwork.com/ by a University of Manitoba User on 06/04/2015
mg/100 ml. After takedown, the liver decreased in size and his patient did well. McGill et al12 reported a well-documented case of cir¬ rhosis and death 11 months after jejunoileal shunt in a
nonalcoholic woman. The majority of large series, however, report no evi¬ dence of liver disease other than occasional fatty infil¬ tration. "·" Many possible causes for the fatty degenera¬ tion have been proposed, but none as yet proved: (1) hepatitis; (2) rapid lipid mobilization; (3) essential fatty acid deficiency (malnutrition); (4) absorption of hepatotoxic material from the colon or from the "blind" loop (sec¬ ondary to bile acids); (5) protein malabsorption. White and his associates17 recently likened the lesion in small bowel bypass patients to kwashiorkor, and found decreased ab¬ sorption of leucine, lycine, and glycine in their patients. Although the suggestion of possible liver failure is fre¬ quently made, on the basis of reports to date, liver failure after jejunoileal bypass is quite rare. The liver biopsy specimen taken 14 months after the by¬ pass procedure revealed severe fatty infiltration that in¬ volved nearly all the hepatocytes. There was marked por¬ tal fibrosis with entrapment of hepatocytes, as well as a mononuclear portal triaditis. Some areas revealed actual
necrosis of hepatocytes with eosinophilic inclusions sug¬ gestive of Mallory bodies. No specific pseudolobules or regenerative nodules can be identified, and hence these changes fall somewhat short of the criteria for cirrhosis as recently outlined by Smetana.18 These changes have been described by some as "precirrhotic" or "cirrhotic"; however, they are still reversible at this point and hence are not true cirrhosis. This case strongly supports the previously proposed po¬ tential hazard of liver damage after jejunoileal bypass. Anatomical reversal of the procedure led to normal liver function. These patients should be maintained on a high protein, vitamin-supplemented diet and should avoid alco¬ hol. If the initial operative liver dysfunction does not show signs of resolution by the fourth to sixth postoperative month, the shunt should be taken down. Extremely close observation of these patients over the first two years postoperation is absolutely essential for their continued wellbeing. Further documentation of the true incidence of sub¬ stantial liver function abnormality and hepatic failure is needed if use of this procedure is to be continued on an in¬ creasing scale.
References 1. Lewis LA, Turnbull RB Jr, Page IH: "Short-circuiting" of the small intestine. JAMA 182:77-79, 1962. 2. Payne JH, DeWind LT: Surgical treatment of obesity. Am J Surg 118:141-146, 1969. 3. Scott HW, Law DH: Clinical appraisal of jejunoileal shunt in patients with morbid obesity. Am J Surg 117:246-253, 1969. 4. Shibata HR, Mackenzie JR, Huang S: Morphologic changes of the liver following small intestinal bypass for obesity. Arch Surg 103:229-237, 1971. 5. Lewis LA, Turnbull RB Jr, Page IH: Effects of jejunocolic shunt on obesity, serum lipoproteins, lipids and electrolytes. Arch Intern Med 117:4-16, 1966. 6. Scott HW, Dean R, Shull JH, et al: New considerations in use of jejunoileal bypass in patients with morbid obesity. Ann Surg
177:723-735, 1971.
7. Salmon PA: The results of small intestine bypass operations for the treatment of obesity. Surg Gynecol Obstet 132:965-979, 1971. 8. Dano P, Jarnum S, Nielsen OV: Intestinal shunt operation in obesity. Scand J Gastroenterol 8:457-464, 1973. 9. Schwartz MZ, Varco RL, Buchwald H: Preoperative preparation, operative technique, and postoperative care of patients undergoing jejunoileal bypass for massive exogenous obesity. J Surg Res 14:147-150, 1973.
10. Scott HW, Law DH, Sandstead HH, et al: Jejunoileal shunt in surgical treatment of morbid obesity. Ann Surg 171:770-782, 1970. 11. Corso PJ, Joseph WL: Intestinal bypass in morbid obesity. Surg Gynecol Obstet 138:1-5, 1974. 12. McGill DB, Humphreys SR, Baggenstoss AH, et al: Cirrhosis and death after jejunoileal shunt. Gastroenterology 63:872\x=req-\ 877, 1972. 13. Drenick EJ, Simmons F, Murphy JF: Effect on hepatic morphology of treatment of obesity by fasting, reducing diets and small-bowel bypass. N Engl J Med 282:829-834, 1970. 14. Maxwell JG, Richards RC, Albo DJ: Fatty degeneration of the liver after intestinal bypass for obesity. Am J Surg 116:648\x=req-\ 652, 1968. 15. Brown RG, O'Leary JP, Woodward ER: Hepatic effects of jejunoileal bypass for morbid obesity. Am J Surg 127:53-58,1974. 16. Buchwald H, Lober PH, Varco RL: Liver biopsy findings in 77 consecutive patients undergoing jejunoileal bypass for morbid obesity. Am J Surg 127:48-52, 1974. 17. White JJ, Moxley RT, Pozefsky T, et al: Transient kwashiorkor: A cause of fatty liver following small bowel bypass.
Surgery 75:829-840, 1974. 18. Smetana HF: Cirrhosis of the liver: Principles of classification, histogenesis, and pathogenesis. Pathol Annu 7:107-144,1972.
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