Percutaneous pancreatography: case report and presentation of technique.

A case of traumatic pancreatitis with a radiopaque calculus producing pain by obstructing the distal pancreatic duct is presented. Preoperative ductal anatomy was defined by a percutaneous pancreatogram that established the presence of mechanical duct obstruction as the cause of pain, and the potential for operative relief of duct obstruction. A remission from pain resulted from pancreatic duct decompression by a lateral pancreaticojejunostomy. The potential value of percutaneous pancreatography is discussed.

Hepatic artery flow improvement after portacaval shunt: a single hemodynamic clinical correlate.

We have documented a highly significant increment in hepatic arterial flow following a portacaval shunt in patients with cirrhosis of the liver and portal hypertension. In contrast with other hemodynamic variables, the increment in arterial flow was directly related to morbidity, hospital mortality, and long term survival. Patients with increments smaller than 100 ml/min had the worst clinical results. They accounted for all of the hospital mortality, the largest incidence of encephalopathy, and the worst long term cumulative survival rates. The extent of the increment was not related directly to the type of shunt but, rather, to some intrinsic capability of the cirrhotic liver to increase its arterial flow in response to the relief of sinusoidal hypertension produced by the shunt. This capablilty appears related to the degree of entrapment of the hepatic arterioles by the fibrous tissues of cirrhosis. This encasement of arterioles should change the elastic properties of the hepatic arterial bed and we propose to measure these properties by determining the characteristic input impedance of the arterial bed.

Spontaneous reversal of portal blood flow: the case for and against its occurrence in patients with cirrhosis of the liver.

Because of its presumed serious clinical significance, we made an analysis of the evidence for and against the occurrence of spontaneous reversal of portal flow in cirrhosis of the liver. We examined the evidence obtained from manometric studies, radioactive tracer studies, radiologic studies, and actual measurements of magnitude and direction of portal blood flow. Concerning manometric studies, we introduced a physical analysis, based on first principles, which demonstrates that the occluded portal pressures cannot be used to construct a hydraulic gradient for portal flow. Similarly, we examined the weakness of the evidence derived from radioactive tracer and radiologic studies and, in the latter, the drastically opposite results reported by different investigators. Finally, we found that actual measurements of magnitude and direction of portal flow provide impressive evidence against the occurrence of spontaneous reversal of portal flow in cirrhosis. We conclude that unless new and convincing evidence is provided, it may not serve the best interests of medicine and of our patients to continue accepting spontaneous reversal of portal flow in cirrhosis as if it were a proven phenomenon.

The hemodynamics of portal hypertension revisited: determinants and significance of occluded portal pressures.

We bring up to date our series of direct measurements of portal flow and pressure in patients with cirrhosis of the liver. In 153 patients the portal flow averaged 447 plus or minus 350 ml. Hg per minute and the portal pressure 28.5 plus or minus 4 mm. Hg (approximately 387 mm. H2O). Both quantities compare favorably with our previous measurements in smaller groups of patients. In 80 of our patients we had also measurements of pressure on the hepatic and splanchnic sides of a clamp occluding the portal vein. Nine of these patients had an hepatic occluded portal pressure higher than either or both the free portal pressure and the splanchnic occluded portal pressure. Of these nine patients with reversed pressure differences, two had stagnant portal flow and the remaining seven had forward flow into the liver measuring from 80 to 1,116 ml. Hg per minute.

Portal blood flow in cirrhosis of the liver.

Direct measurements of portal flow and pressure in a relatively large number of patients with cirrhosis show a marked reduction in flow associated with a nearly constant plateau of portal pressure. This lack of correlation indicates the complex relationships of resistances in the splanchnic, collateral, and hepatic circuits determining the division of the available splanchnic flow between the portal vein and the collateral pathways. Subtracting the measured portal flow from well-established estimates of total hepatic blood flow in cirrhosis suggests that the hepatic artery contributes more than one-half of the blood perfusing the cirrhotic liver. There was no instance of retrograde portal flow during the preshunt measurements, although such reversal was frequent after side-to-side portacaval anastomosis. Attempting to explain the plateau of portal pressure in the face of an increasing outflow resistance presumably associated with progress of the disease, we postulate that an augmented inflow resistance to the splanchnic chamber reduces splanchnic flow in cirrhosis. End-to-side portacaval anastomosis did not return normal portal flow, although it decreased pressure to accepted control levels. The assumption is that most of the splanchnic blood was flowing through the shunt, leading to a high splanchnic resistance in the immediate postshunt status. If this resistance was previously elevated, as suggested by the plateau of portal pressure, the mechanism responsible for the elevation was not immediately deactivated after the shunt, and the true effect of the operation upon splanchnic flow may not be measurable at such time. Respiratory oscillations were a significant component of portal flow in cirrhosis before and after portacaval anastomosis, indicating the limitations of any steady state analysis of the circulatory derangement in cirrhosis.