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With the exception of eight cases of higher gastrectomy required for GEA stenosis following stomal ulcer, nearly all specific late reoperations after biliopancreatic diversion (BPD) consisted of elongations of the common limb (CL) or restorations of intestinal continuity, protein malnutrition (PM) (with or without additional problems) being the condition to be cured in the vast majority of cases.1 As both the reoperations are generally implemented to correct an excess of effect of the original operation, and they entail a permanent modification of intestinal absorption, it is critical to ensure that intestinal adaptation mechanisms have been substantially completed, what requires at least 1 year. If the problems persist and reoperation is then indicated, the risk of reoperating prematurely with resultant overcorrection and undue weight regain is minimal.


The elongation of the CL is indicated whenever a recurrent PM occurs in a BPD subject with normal food intake. In this case, PM is due to insufficient protein intestinal absorption, either absolute (insufficient absorption capacity per unit of intestinal length, too rapid intestinal transit due to excessively little stomach) or relative (insufficient protein content of ingested food, excessive loss of endogenous nitrogen). In both cases the aim of the surgical revision is to increase protein absorption, and this, keeping in mind the physiology of the operation, would not be obtained by elongating the CL along the alimentary one. Since, as said above, protein absorption after BPD substantially depends on the total intestinal length from the GEA to the ileocecal valve (ICV), the elongation of the CL for correction of a recurrent PM must be performed at the expense of the biliopancreatic limb, the length which in our experience has proven effective in all cases being 150 cm, with the result of a total of 400 cm of small bowel in the food stream (Figure 34–1). Similar to what happens with the ad hoc stomach–ad hoc alimentary limb (AHS–AHAL) BPD, this type of revision has a double mechanism of action. In fact, by also increasing fat and starch absorption, it reduces the loss of endogenous nitrogen and the colonic bacteria overgrowth, with the result of a decreased protein requirement and an increased protein absorption in the colon. Incidentally, the fact that mean alimentary protein absorption after elongation is still reduced to ∼ 80%2,3 indicates that (1) colonic protein absorption is fully exploited also after elongation; (2) the amount of protein absorbed in the colon after BPD is probably greater than that absorbed in the small bowel; and (3) increasing the length of small bowel between the GEA and the ICV most probably acts by increasing protein absorption more in the colon than in the small bowel.

Figure 34–1.
Graphic Jump Location

Elongation of the common limb along the biliopancreatic limb.


On the basis of the same rationale, this type of elongation is also indicated in case ...

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