1
C LINICA L N U T R I T I O N
I
OBESITY, JEJUNO-ILEAL BYPASS AND DEATH Jejuno-ilealshunts for obesity can result in death years later due to failure of the liver.
Key Words: liver, cirrhosis, anastomosis, diarrhea, ma1n u t r it ion
The intestinal bypass operation for treatment of obesity has passed through several stages from the anastomosis of the jejunum to the colon (associated with many complications including liver disease) t o modifications resulting i n the jejuno-ileal anastomosis with bypass of certain lengths of small intestine. It is now considered by some to be a fairly safe operation. Cirrhosis and death, however, have been reported after jejuno-ileal shunt for A recent report concerned a white woman, 41 years old, 59 inches tall, who had been obese since adolescence. She had a history of heavy drinking but had no documented hepatic complications from alcohol. She weighed 260 pounds when she underwent jejuno-ileal bypass. An end to side anastomosis of 17 cm of jejunum to the terminal 6 cm of ileum was done. The operation bypassed 397 cm of small bowel which was left in the abdomen as a blind loop. Before the operation her lab values for albumin, globulin, bilirubin, SGOT, LDH, and BSP retention were normal. Alkaline phosphatase was mildly elevated. The liver appeared normal a t surgery; it was not biopsied. After discharge, she resumed her previous high calorie, high carbohydrate, low protein diet Five months later, when she was admitted to the hospital for diarrhea, small bowel malabsorption was not present; the diarrhea subsided during hospitalization. Three months later she was admitted again with diarrhea, weighing only 120 38
NUTRITION REVIEWSIVOL. 33. NO. PIFEBRUARY 1975
pounds. She demonstrated pellagra-like skin Iesions, smooth magenta tongue, brittle nails, palmar erythema, spider nevi, hepatomegaly, and edema. Albumin levels were 2.3 gm per 100 ml, prothrombin time elevated, bilirubin 2.4 mg per 100 ml, SGOT 203, LDH 425, and alkaline phosphatase 203 IU (normal level 85 IU). A I iver biopsy demonstrated severe fatty metamorphosis w i t h minimal portal scarring but no hepatocellular necrosis or regenerative nodule formation was noted. Her diarrhea subsided, she gained weight, and liver function improved on the hospital diet. She was considered for reanastomosis of the blind loop but it was not done. Four months later she was admitted with severe protein malnutrition and hypovitaminosis. She was weak, demonstrating gross muscle wasting, cheilosis, tender feet, depigmentation of hair, gross ascites, peripheral edema, and hepatomegaly. Albumin was only 1.5 g per 100 ml, subsequently decreasing to a level of 0.6 g per 100 ml. Prothrombin time remained elevated; it was not corrected by vitamin K. Bilirubin was 4 mg per 100 mi, SGOT 101, alkaline phosphatase 131 IU, potassium concentration had decreased to 2.7 mEq per liter, and blood urea nitrogen was a t a very low level of 2 mg per 100 ml. Phosphorus, calcium, and magnesium were all decreased in concentration. A t the time of admission, she would eat only candy. Nasogastric tube feedings produced diarrhea and volume ranged as high as 4 liters per day. Intravenous total parenteral nutrition produced hepatic coma with hyperammonemia on three separate occa-
sions, despite slow administration of the solution and bowel sterilization. Discontinuation of amino acids in the infusate produced recovery, but she was still considered a poor operative risk for the anastomosis. A fourth episode of hepatic coma associated with gastrointestinal bleeding occurred despite oral antibiotic therapy and low protein intake. She died two months after hospital admission and the premortem l a b o r a t o r y values were: bilirubin, 8.8 mg per 100 ml; alkaline phosphatase, 1 13; LD H, 197; prothrombin time elevated; albumin 0.6 per 100 ml (despite intravenous albumin given in large quantities). Blood cultures one week before death were positive for Candida albicans. Autopsy findings revealed an emaciated woman with marked muscle wasting. She was jaundiced with ascites (2500 ml), splenomegaly, esophageal varices, and a healing gastric ulcer. The liver was enlarged, weighing 1450 g. On cut section, the liver demonstrated a green surface interspersed with light yellow fibrous bands running in all directions. There was no evidence of bile duct obstruction. There was generalized moniliasis, and cerebral atrophy. On microscopic examination sections of the liver revealed cellular necrosis, parenchymal cell loss, cholestasis, and bile duct pro1iferation. Lymphocytic infiltration in portal areas with moderate fatty change was noted. A marked fibrosis of a diffuse nature with bands linking portal triads was present, and regenerative nodule formation was noted. The jejuno-ileal shunt operation, therefore, is associated with pathologic changes which can produce death some time after the ~ p e r a t i o n .Twenty-five ~ months after the bypass operation the liver of the subject of this report passed through stages of fatty metamorphosis t o cirrhosis and death. Although it was thought that the individual was drinking through the first two of the 25 months, it was felt that alcohol was not solely responsible for hepatic changes. She definitely was not taking alcohol during her last three months while she was hospitalized, during which time liver failure developed rapidly. She had consumed a
poor diet which had produced malnutrition and diarrhea during the period after the operation. There are now seven deaths repgrted from liver disease in 63 patients with jejuno-colic anastomosis. Benign steatosis has been shown in a number of reports after jejuno-ileal shunts for obesity but this present case marks only the second case in which definite cirrhosis occurred after the operation, which was linked with death. It appears that the changes in liver which have been reported are a function, in some regard, of the length and type of small bowel bypass and anastomotic site. The 200 cm ileal bypass for the treatment of hypercholesterolemia is not associated with a significant loss of weight or known complication s. Several possibilities for the hepatic injury after jejuncileal bypass are hepatic toxicity of absorbed secondary bile salts such as lithocholic acid, the absence of Iipotrophic factor which is absorbed due to the malnutrition associated with the operation, protein malnutrition, and the blind loop syndrome. Thus there is no doubt that severe liver damage can result from the jejuno-ileal bypass for obesity. Although liver problems in this case were compounded by poor choices of food by the subject, the question arises as t o how many deaths of this type have occurred. Many of the people who have had jejuno-ileal bypass operations have had them taken down and thus, the natural history of liver changes with this disorder cannot be accurately documented. It may be that most obese people have mild to moderate hepatic steatosis prior to operation and that these changes are accentuated and can eventually result in cirrhosis as a result of the surgical procedure. In some people with jejuno-colic shunts, f a t accumulation in the liver was associated with inflammation, leading to cirrhosis and liver failure and occasionally death.3 These changes may be reversed i f anastomosis is taken down and normal intestinal contin u ity restored. NUTRlTiON REVIEWSIVOL. 33, NO. 2/FEBRUARY 1975
39
The case reports and the documented problems associated with liver failure indicate that if there i s a place for the jejunoileal shunt in the treatment of obesity, it should be reserved for massive obesity which cannot be resolved in any other way. Perhaps these individuals should be followed repeatedly with liver biopsies and the shunt taken down when evidence of histological changes suggestive of impending cirrhosis occur. More data are needed on the natural history of people who survive the operation. For instance, do they begin t o gain weight once again if they do not develop liver failure? If the liver is protected by the length of shunt involved operatively, then it may well be that these people will eventually begin to gain weight again if the segment of bypassed gut is decreased. Unfortunately, this type of surgical procedure can be performed by any qualified surgeon and most likely, the procedure is being done more frequently than reported. The possibility of severe changes produced in the liver after a fairly long period of time leading to death, makes this a procedure which must be regulated in some fashion by physicians caring for patients with obesity. A cure for obesity has been estimated to advance life span five years. We do not know the five year or lifetime sur-
vival rates of people with this operation. Many of the individuals who are operated on for the jejuno-ileal shunt must also consider a lifetime of living with chronic diarrhea - it may not be worth it. This case history also reveals the improvement of hepatic coma obtained with a low protein diet. One question arises, not related to this particular case, but t o the general problem of treatment of cirrhosis: Would low protein diets as are currently prescribed for patients with chronic renal disease be helpful? Compensated cirrhotics usually are discharged from hospitals with no diet p1,escription a t all and with a projected l i f e span of one to ten years. Since gastroenterologists have not added nutrition to their sub-specialty, the treatment of cirrhotics with controlled protein diets should be seriously considered by them. 0 ~
~~~
1. Current Status of Jejuno-Ileal Bypass for 0 besity. Nutrition Reviews 32: 333-336, 1974 2. J.C. Mangla, W. Hoy, Y. Kim, and M. Chopek: Cirrhosis and Death after Jejuno-Ileal Shunt for Obesity. Am. J. Dig. Dis. 19: 759-765, 1974 3. D. B. McGill, S. R. Humphreys, A. H. Baggenstoss, and E. R. Dickson: Cirrhosis and Death after Jejuno-Ileal Shunt. Gastroenterology 63: 872-877, 1972
MASSIVE OBESITY AND NEPHROSIS Massive obesity can produce the nephrotic syndrome which disappears after the loss of body weight
K q Words: proteinuria, nephrotic syndrome, weight loss, lung volume, edema
Obesity is associated, perhaps causally, with many disorders; hypertension, joint disease, diabetes mellitus, right heart failure, and hyperlipidemia, for example. It decreases respiratory function and increases surgical risk. A recent report' appears to d e m on s trate that massive obesity can produce the nephrotic syndrome. 40
NUTRITION REVIEWSNOL. 33, NO. PfFEBRUARY 1975
Four cases were studied. The first was a 25-year-old woman who had a negative history for chronic renal disease. There was no familial history of obesity or renal disease and she became obese after contracting poliomyelitis. The only complication of massive obesity on initial examination was bilateral pitting edema of her feet and legs. Several random urine samples showed a 4+ proteinuria.
C LINICA L N U T R I T I O N
I
OBESITY, JEJUNO-ILEAL BYPASS AND DEATH Jejuno-ilealshunts for obesity can result in death years later due to failure of the liver.
Key Words: liver, cirrhosis, anastomosis, diarrhea, ma1n u t r it ion
The intestinal bypass operation for treatment of obesity has passed through several stages from the anastomosis of the jejunum to the colon (associated with many complications including liver disease) t o modifications resulting i n the jejuno-ileal anastomosis with bypass of certain lengths of small intestine. It is now considered by some to be a fairly safe operation. Cirrhosis and death, however, have been reported after jejuno-ileal shunt for A recent report concerned a white woman, 41 years old, 59 inches tall, who had been obese since adolescence. She had a history of heavy drinking but had no documented hepatic complications from alcohol. She weighed 260 pounds when she underwent jejuno-ileal bypass. An end to side anastomosis of 17 cm of jejunum to the terminal 6 cm of ileum was done. The operation bypassed 397 cm of small bowel which was left in the abdomen as a blind loop. Before the operation her lab values for albumin, globulin, bilirubin, SGOT, LDH, and BSP retention were normal. Alkaline phosphatase was mildly elevated. The liver appeared normal a t surgery; it was not biopsied. After discharge, she resumed her previous high calorie, high carbohydrate, low protein diet Five months later, when she was admitted to the hospital for diarrhea, small bowel malabsorption was not present; the diarrhea subsided during hospitalization. Three months later she was admitted again with diarrhea, weighing only 120 38
NUTRITION REVIEWSIVOL. 33. NO. PIFEBRUARY 1975
pounds. She demonstrated pellagra-like skin Iesions, smooth magenta tongue, brittle nails, palmar erythema, spider nevi, hepatomegaly, and edema. Albumin levels were 2.3 gm per 100 ml, prothrombin time elevated, bilirubin 2.4 mg per 100 ml, SGOT 203, LDH 425, and alkaline phosphatase 203 IU (normal level 85 IU). A I iver biopsy demonstrated severe fatty metamorphosis w i t h minimal portal scarring but no hepatocellular necrosis or regenerative nodule formation was noted. Her diarrhea subsided, she gained weight, and liver function improved on the hospital diet. She was considered for reanastomosis of the blind loop but it was not done. Four months later she was admitted with severe protein malnutrition and hypovitaminosis. She was weak, demonstrating gross muscle wasting, cheilosis, tender feet, depigmentation of hair, gross ascites, peripheral edema, and hepatomegaly. Albumin was only 1.5 g per 100 ml, subsequently decreasing to a level of 0.6 g per 100 ml. Prothrombin time remained elevated; it was not corrected by vitamin K. Bilirubin was 4 mg per 100 mi, SGOT 101, alkaline phosphatase 131 IU, potassium concentration had decreased to 2.7 mEq per liter, and blood urea nitrogen was a t a very low level of 2 mg per 100 ml. Phosphorus, calcium, and magnesium were all decreased in concentration. A t the time of admission, she would eat only candy. Nasogastric tube feedings produced diarrhea and volume ranged as high as 4 liters per day. Intravenous total parenteral nutrition produced hepatic coma with hyperammonemia on three separate occa-
sions, despite slow administration of the solution and bowel sterilization. Discontinuation of amino acids in the infusate produced recovery, but she was still considered a poor operative risk for the anastomosis. A fourth episode of hepatic coma associated with gastrointestinal bleeding occurred despite oral antibiotic therapy and low protein intake. She died two months after hospital admission and the premortem l a b o r a t o r y values were: bilirubin, 8.8 mg per 100 ml; alkaline phosphatase, 1 13; LD H, 197; prothrombin time elevated; albumin 0.6 per 100 ml (despite intravenous albumin given in large quantities). Blood cultures one week before death were positive for Candida albicans. Autopsy findings revealed an emaciated woman with marked muscle wasting. She was jaundiced with ascites (2500 ml), splenomegaly, esophageal varices, and a healing gastric ulcer. The liver was enlarged, weighing 1450 g. On cut section, the liver demonstrated a green surface interspersed with light yellow fibrous bands running in all directions. There was no evidence of bile duct obstruction. There was generalized moniliasis, and cerebral atrophy. On microscopic examination sections of the liver revealed cellular necrosis, parenchymal cell loss, cholestasis, and bile duct pro1iferation. Lymphocytic infiltration in portal areas with moderate fatty change was noted. A marked fibrosis of a diffuse nature with bands linking portal triads was present, and regenerative nodule formation was noted. The jejuno-ileal shunt operation, therefore, is associated with pathologic changes which can produce death some time after the ~ p e r a t i o n .Twenty-five ~ months after the bypass operation the liver of the subject of this report passed through stages of fatty metamorphosis t o cirrhosis and death. Although it was thought that the individual was drinking through the first two of the 25 months, it was felt that alcohol was not solely responsible for hepatic changes. She definitely was not taking alcohol during her last three months while she was hospitalized, during which time liver failure developed rapidly. She had consumed a
poor diet which had produced malnutrition and diarrhea during the period after the operation. There are now seven deaths repgrted from liver disease in 63 patients with jejuno-colic anastomosis. Benign steatosis has been shown in a number of reports after jejuno-ileal shunts for obesity but this present case marks only the second case in which definite cirrhosis occurred after the operation, which was linked with death. It appears that the changes in liver which have been reported are a function, in some regard, of the length and type of small bowel bypass and anastomotic site. The 200 cm ileal bypass for the treatment of hypercholesterolemia is not associated with a significant loss of weight or known complication s. Several possibilities for the hepatic injury after jejuncileal bypass are hepatic toxicity of absorbed secondary bile salts such as lithocholic acid, the absence of Iipotrophic factor which is absorbed due to the malnutrition associated with the operation, protein malnutrition, and the blind loop syndrome. Thus there is no doubt that severe liver damage can result from the jejuno-ileal bypass for obesity. Although liver problems in this case were compounded by poor choices of food by the subject, the question arises as t o how many deaths of this type have occurred. Many of the people who have had jejuno-ileal bypass operations have had them taken down and thus, the natural history of liver changes with this disorder cannot be accurately documented. It may be that most obese people have mild to moderate hepatic steatosis prior to operation and that these changes are accentuated and can eventually result in cirrhosis as a result of the surgical procedure. In some people with jejuno-colic shunts, f a t accumulation in the liver was associated with inflammation, leading to cirrhosis and liver failure and occasionally death.3 These changes may be reversed i f anastomosis is taken down and normal intestinal contin u ity restored. NUTRlTiON REVIEWSIVOL. 33, NO. 2/FEBRUARY 1975
39
The case reports and the documented problems associated with liver failure indicate that if there i s a place for the jejunoileal shunt in the treatment of obesity, it should be reserved for massive obesity which cannot be resolved in any other way. Perhaps these individuals should be followed repeatedly with liver biopsies and the shunt taken down when evidence of histological changes suggestive of impending cirrhosis occur. More data are needed on the natural history of people who survive the operation. For instance, do they begin t o gain weight once again if they do not develop liver failure? If the liver is protected by the length of shunt involved operatively, then it may well be that these people will eventually begin to gain weight again if the segment of bypassed gut is decreased. Unfortunately, this type of surgical procedure can be performed by any qualified surgeon and most likely, the procedure is being done more frequently than reported. The possibility of severe changes produced in the liver after a fairly long period of time leading to death, makes this a procedure which must be regulated in some fashion by physicians caring for patients with obesity. A cure for obesity has been estimated to advance life span five years. We do not know the five year or lifetime sur-
vival rates of people with this operation. Many of the individuals who are operated on for the jejuno-ileal shunt must also consider a lifetime of living with chronic diarrhea - it may not be worth it. This case history also reveals the improvement of hepatic coma obtained with a low protein diet. One question arises, not related to this particular case, but t o the general problem of treatment of cirrhosis: Would low protein diets as are currently prescribed for patients with chronic renal disease be helpful? Compensated cirrhotics usually are discharged from hospitals with no diet p1,escription a t all and with a projected l i f e span of one to ten years. Since gastroenterologists have not added nutrition to their sub-specialty, the treatment of cirrhotics with controlled protein diets should be seriously considered by them. 0 ~
~~~
1. Current Status of Jejuno-Ileal Bypass for 0 besity. Nutrition Reviews 32: 333-336, 1974 2. J.C. Mangla, W. Hoy, Y. Kim, and M. Chopek: Cirrhosis and Death after Jejuno-Ileal Shunt for Obesity. Am. J. Dig. Dis. 19: 759-765, 1974 3. D. B. McGill, S. R. Humphreys, A. H. Baggenstoss, and E. R. Dickson: Cirrhosis and Death after Jejuno-Ileal Shunt. Gastroenterology 63: 872-877, 1972
MASSIVE OBESITY AND NEPHROSIS Massive obesity can produce the nephrotic syndrome which disappears after the loss of body weight
K q Words: proteinuria, nephrotic syndrome, weight loss, lung volume, edema
Obesity is associated, perhaps causally, with many disorders; hypertension, joint disease, diabetes mellitus, right heart failure, and hyperlipidemia, for example. It decreases respiratory function and increases surgical risk. A recent report' appears to d e m on s trate that massive obesity can produce the nephrotic syndrome. 40
NUTRITION REVIEWSNOL. 33, NO. PfFEBRUARY 1975
Four cases were studied. The first was a 25-year-old woman who had a negative history for chronic renal disease. There was no familial history of obesity or renal disease and she became obese after contracting poliomyelitis. The only complication of massive obesity on initial examination was bilateral pitting edema of her feet and legs. Several random urine samples showed a 4+ proteinuria.
