Contrast medlum worsens pancreatitis

human disease in many ways.$ It is precisely because the data in humans have not been obtained or ace unobtainable that the appcoximation of an animal model is necessary. We do not claim that the pace at which pancceatitis develops in out experimental model is identical with the human disease, and it may in fact be telescoped into a mote rapidly evolving pcocess. Histological studies in out model show that necrosis is already present by 6 hours and continues to develop for up to 48 hours after induction3 Therefore, we chose to administer the contcast medium at 7 hours to be able to detect an adverse effect before irreversible development of necrosis. Out data ace statistically sound, and the fact that there ace 6 to 18 animals in each group does not invalidate the power of the obsecvations. All animals in each induction group were randomly allocated after induction to receive either saline or any of the two test compounds, and when comparing each of the subgroups after candomitation but before giving contcast medium (to insure that they were really comparable), we found no differences in clinical parameters oc tcypsinogen activation peptides. The editorial misses the point that no adverse effect of the contrast occurred in either mild oc moderate pancceatitis, but occurred dramatically in severe pancceatitis, the vecy subpopulation in which CECT is considered desirable. Furthermore, it was seen in both subgroups (ionic and non-ionic) receiving contcast in comparison with saline-treated controls. Thus, we find this acgument particularly unfounded. We made no conclusions on the cause of death of the tats but suggested that it could be related to the amount of necrosis. Dts. Balthazac and Fceeny ace wrong in affirming that the cats with modecate pancceatitis had no necrosis. These indeed have necrosis, although to a lesser degree than those with severe pancceatitis; the overall moctality in this group is less than in that of the severe group. Finally, at the time this study was submitted for publication, we had no evidence as to the possible mechanism for the increased pancceatic injury caused by contrast medium. We have since shown that pancreatic perfusion, as measured by reflectance spectroscopy, is impaired in severe experimental pancteatitis and that administration of contrast medium further decreases perfusion in these conditions. Once again, the adverse effect of contcast medium was found only in the severe pancceatitis group and not in mild or moderate disease.’ Still another study, this one using intcavital microscopy, has shown similar findings, in this case shutdown of pancreatic capillary flow after administration of contcast medium.’ Thus, we can affirm that in severe experimental pancceatitis in the cat, early administration of contrast media significantly increases mortality, pancreatic necrosis, and tcypsinogen activation and that the responsible mechanism is probably related to decreased pancreatic perfusion. We accept that CECT is a useful tool in the management ofpatients with neccotizing pancceatitis, and it was never out intent to disqualify its use. Out concern and suggestion is that it perhaps should not be used early in acute pancceatitis. Its principal utility is in identifying necrotic areas in need of debcidement at a later point in the coucse of the disease. Delaying the use of CECT will also reduce its ovecuse by focusing its use on those patients with severe disease because most patients with mild oc moderate disease will have resolved promptly.