- Email: [email protected]
Pancreas divisum and pancreatitis
August
CORRESPONDENCE
1986
vessels to respiration, might have improved the sensitivity of ultrasonography in the diagnosis of cirrhosis. Third, descriptive qualities of parenchymal texture (2), e.g., uniformity and average size and population density of echo targets, might have proved useful in the assessment of diffuse parenchymal abnormalities. Finally, we would have considered the irregularity of liver margins as further evidence of cirrhosis, as cases of neoplastic liver disease have been excluded from the series. Before accepting Sandford’s disappointing conclusions, usefulness of ultrasonography in diffuse hepatic disease should be evaluated according to a better definition of technical parameters and a wider and more accurate choice of sonographic features of liver echo-texture and portal hypertension.
525
was uncommon unless the cirrhosis was advanced, when other signs of portal hypertension were usually present. We did not set out to analyze the signs of portal hypertension but, rather, the echo-texture of the parenchyma, and we still stand by our conclusion that ultrasonography has limited use in the evaluation of diffuse parenchymal liver disease. DR. N.L. SANDFORD
Department of Gastroenterology Princess Alexandra Hospital Brisbane, Australia PROFESSORH. BADDELEY Department of Radiology University of Queensland Brisbane, Australia
ANTONIO GIORGIO, M.D. PIETRO AMOROSO,
M.D. PAOLA PIERRI, M.D. Hepato-Biliary Ultrasound Service “D. Cotugno” Hospital for Infectious Naples, Italy
Pancreas Divisum and Pancreatitis Diseases
GIAMPIERO FRANCICA, M.D. ROBERTO MORANTE, M.D. LUIGI CACCIATORE, M.D.
4th Department
of Internal University of Naples 2nd School of Medicine Nuovo PoJicJinico Via Sergio Pansini, 5 80131 Naples, Italy
Medicine
Sandford NL, Walsh P, Matis C, et al. Is ultrasonography useful in the assessment of diffuse parenchymal liver disease? Gastroenterology 1985;89:186-91. Rizzatto G, Sirotti P, Bazzocchi M, et al. Optical analysis of hepatic echo-texture in diffuse liver disease. In: Labb G, Bolondi L, Rizzatto G, eds. Clinical advances in ultrasonography. Milano: Masson Italia Editori, 19836-7. Bolondi L, Gandolfi L, Labb G. Diagnostic ultrasound in gastroenterology. Italy: Piccin/Butterworths, 1984.
Reply. The letter of Dr. Giorgio et al. was read with interest. The main purpose of our study was to correlate the histologic findings with the ultrasound characteristics of brightness, loss of detail of vascular structures, and attenuation of the beam. As the physical characteristics of each patient vary, it is not possible to obtain an image of sufficient clarity to assess these characteristics unless a variable combination and number of transducers is used. We agree that for others to reproduce our findings it would be desirable to have a standard setting on one transducer, but this would limit the information available and make assessment of the overall value of ultrasound difficult to gauge. We do not consider splenomegaly to be a sign of portal hypertension alone; however, in a predominantly alcoholic population, splenomegaly (if present) is much more likely to be due to portal hypertension than to other causes, and as this can be assessed accurately by the Octoson water-delay echoscope, we consider it to be a valid ultrasound sign of portal hypertension. In addition to assessing the size of the main portal vein and its branches and the vessels at the splenic hilum, intraabdominal collateral vessels were sought in all patients, and, if found, portal hypertension was considered present. Variation with respiration was not assessed, as real-time ultrasonography was not analyzed, but we agree that this may affect the sensitivity of the procedure. In the population group studied, irregularity of the liver surface
Dear Sir: Delhaye and colleagues (1) recently reported on the relationship between pancreas divisum and pancreatitis. The authors studied a total of 5357 patients successfully investigated by endoscopic retrograde pancreatography. Pancreas divisum was observed in 5.7% of patients without pancreatitis and in 6.9% of subjects with pancreatitis (chronic and acute). As the difference between both groups was not significant, the authors concluded that their results “do not support the hypothesis that stenosis of the accessory papilla occurs frequently in cases of pancreas divisum, and pancreas divisum should not be regarded as an etiologic factor in pancreatitis but should be considered as a coincidental anatomic variant.” However, the authors failed to comment on one particular finding in their study which challenges the above conclusion. When examining the etiologies of acute pancreatitis (n = 335), patients with alcohol abuse were significantly more likely to have pancreas divisum (15%, p < 0.025) than all other groups. We suggest that alcohol abuse is a risk factor for acute pancreatitis. particularly in patients with pancreas divisum. To study the possible relationship between pancreas divisum and development of pancreatitis, we have performed endoscopic retrograde manometry (2) in the pancreatic duct [duct of Wirsung)
PATIENTS (n-6)
mm lig
Dw
30 1
DS CONTROLSh.8)
t
26 Dw 22-
18-
14-
IO8-
Figure
.
lo.9 i 1.9
i
??SEM
. iz
r:.
1
23.7t 1.3
DS
10.0~1.0
4
10.5 t 0.9
1. Pressure in the ducts of Wirsung (DW) and in the duct of Santorini (DS) in patients with pancreas divisum (n = 6) and in controls (n = 8).
526
CORRESPONDENCE
and in the duct of Santorini of patients with normal pancreatic duct anatomy (n = 8) and in patients with pancreas divisum (n = 6) (3). In patients presenting with pancreas divisum and suffering from relapsing upper abdominal pain accompanied by elevation of the pancreatic enzymes but without morphologic evidence of pancreatic destruction, the pressure obtained after cannulation of the accessory papilla was significantly higher (23.7 -+ 1.3 mmHg vs. 10.8 f 1.9 mmHg) than that obtained in the duct drained through the papilla of Vater. In the controls with normal pancreatic anatomy no difference was observed between the two ducts (10.5 -+ 0.9 mmHg vs. 10.0 ? 1.0 mmHg) (Figure 1). We conclude from this observation that patients with pancreas divisum may develop chronic stasis of pancreatic fluid. Whether this fact induces pancreatitis is still unclear. Additional factors, such as alcohol intake, causing increased viscosity of pancreatic saliver may increase the risk of pancreatitis. Keeping our results, which are mentioned above, and the statistical data of Delhaye and coworkers (1) in mind, we consider pancreas divisum to add to the risk factors for development of pancreatitis, particularly in patients with chronic alcohol intake. MARTIN STARITZ, M.D. THOMAS HfJTTEROTH, M.D. KARL-HERMANN
MEYER ZUM BtJSCHENFELDE, M.D.
First Medical Department University of Mainz Langenbeckstrasse 1 D 6500 Mainz, Federal Republic of Germany
Delhaye M, Engelholm L, Cremer M. Pancreas divisum: congenital anatomic variant or anomaly? Gastroenterology 1985; 89:951-8. Staritz M, Poralla T, Meyer zum Biischenfelde K-H. Effect of glyceryltrinitrate on the sphincter of Oddi motility and baseline pressure. Gut 1985;26:194-7. Staritz M, Hiitteroth T, Meyer zum Biischenfelde K-H. Pancreas divisum: Prldisposition zur chronischen Pankreatitis durch chronischen Sekretstau? Dtsch Med Wochenschr 1986 (in press). Reply. Concerning the higher incidence of pancreas divisum (PD) among patients with acute alcoholic pancreatitis (15%) than among patients with acute nonalcoholic pancreatitis (5.8%) (l), we would like to provide some related comments. It is generally accepted that acute alcoholic pancreatitis is merely an acute episode during the course of chronic pancreatitis (2). Indeed, many authors (3-5) consider that the diagnosis of chronic pancreatitis could be made if the patients were followed up during an average of 5 yr after the first acute painful attack. Symptoms of acute pancreatitis should develop only after functional and histologic changes of chronic pancreatitis have been established (5). Another argument for considering acute and chronic alcoholic pancreatitis as belonging to the same pathological subgroup is based on the diagnostic criteria of chronic pancreatitis we have used (1). Indeed, we have considered that ductal abnormalities at pancreatography (duct strictures and/or dilatations, pruning of branches, calcifications or protein plugs and cysts) are highly suggestive of chronic pancreatitis. The demonstration of these typical morphologic lesions of the pancreatic ducts in cases of PD requires the opacification of both ventral and dorsal pancreatic ducts. However, opacification of both ducts was achieved in only 2 of 9 cases of “acute alcoholic pancreatitis.” If the ventral pancreas was considered absent in 3 other cases of acute alcoholic pancreatitis with only dorsal pancreatography, then there re-
GASTROENTEROLOGY Vol. 91. No.
2
mained 4 cases in which only the pancreatic ventral duct could be opacified without obtaining any information about the morphologic pattern of the pancreatic dorsal duct. It is possible that some of these 4 patients presented unnoticed pancreatic ductal abnormalities and that they have been misclassified into the subgroup of acute alcoholic pancreatitis. Moreover, this underestimation of the diagnosis of chronic changes will generally parallel the failure rate of dorsal pancreatography. Therefore, to avoid the bias of opacification failure of both pancreatic ducts, it is more consistent to collect into the same pathological subgroup the cases of alcoholic pancreatitis without ductal abnormalities (acute) and the cases of chronic alcoholic pancreatitis. The prevalence of PD in alcoholic pancreatitis (acute and chronic) (8.6%) is then not statistically different from that in nonalcoholic pancreatitis (5.4%). In addition, we were very interested in their experience with endoscopic retrograde manometry performed in both the ventral and dorsal pancreatic duct in cases of PD and fused pancreas. First of all, all manometries were obtained using a triple-lumen catheter having a diameter of 1.7 mm (6). It is therefore obvious that the accessory papilla was not stenotic in these 6 patients having a PD and suffering from relapsing acute pancreatitis. Indeed, the size of the dorsal duct orifice evaluated by calibration with fine lacrima probes during operation by Warshaw et al. (7) was judged to be stenotic if it was
Medicosurgical Department Radiology Erasme Hospital Free University of Brussels Brussels, Belgium 1. Delhaye M, Engelholm
of Gastroenterology
L, Cremer M. Pancreas
and
divisum:
con-
CORRESPONDENCE
1986
vessels to respiration, might have improved the sensitivity of ultrasonography in the diagnosis of cirrhosis. Third, descriptive qualities of parenchymal texture (2), e.g., uniformity and average size and population density of echo targets, might have proved useful in the assessment of diffuse parenchymal abnormalities. Finally, we would have considered the irregularity of liver margins as further evidence of cirrhosis, as cases of neoplastic liver disease have been excluded from the series. Before accepting Sandford’s disappointing conclusions, usefulness of ultrasonography in diffuse hepatic disease should be evaluated according to a better definition of technical parameters and a wider and more accurate choice of sonographic features of liver echo-texture and portal hypertension.
525
was uncommon unless the cirrhosis was advanced, when other signs of portal hypertension were usually present. We did not set out to analyze the signs of portal hypertension but, rather, the echo-texture of the parenchyma, and we still stand by our conclusion that ultrasonography has limited use in the evaluation of diffuse parenchymal liver disease. DR. N.L. SANDFORD
Department of Gastroenterology Princess Alexandra Hospital Brisbane, Australia PROFESSORH. BADDELEY Department of Radiology University of Queensland Brisbane, Australia
ANTONIO GIORGIO, M.D. PIETRO AMOROSO,
M.D. PAOLA PIERRI, M.D. Hepato-Biliary Ultrasound Service “D. Cotugno” Hospital for Infectious Naples, Italy
Pancreas Divisum and Pancreatitis Diseases
GIAMPIERO FRANCICA, M.D. ROBERTO MORANTE, M.D. LUIGI CACCIATORE, M.D.
4th Department
of Internal University of Naples 2nd School of Medicine Nuovo PoJicJinico Via Sergio Pansini, 5 80131 Naples, Italy
Medicine
Sandford NL, Walsh P, Matis C, et al. Is ultrasonography useful in the assessment of diffuse parenchymal liver disease? Gastroenterology 1985;89:186-91. Rizzatto G, Sirotti P, Bazzocchi M, et al. Optical analysis of hepatic echo-texture in diffuse liver disease. In: Labb G, Bolondi L, Rizzatto G, eds. Clinical advances in ultrasonography. Milano: Masson Italia Editori, 19836-7. Bolondi L, Gandolfi L, Labb G. Diagnostic ultrasound in gastroenterology. Italy: Piccin/Butterworths, 1984.
Reply. The letter of Dr. Giorgio et al. was read with interest. The main purpose of our study was to correlate the histologic findings with the ultrasound characteristics of brightness, loss of detail of vascular structures, and attenuation of the beam. As the physical characteristics of each patient vary, it is not possible to obtain an image of sufficient clarity to assess these characteristics unless a variable combination and number of transducers is used. We agree that for others to reproduce our findings it would be desirable to have a standard setting on one transducer, but this would limit the information available and make assessment of the overall value of ultrasound difficult to gauge. We do not consider splenomegaly to be a sign of portal hypertension alone; however, in a predominantly alcoholic population, splenomegaly (if present) is much more likely to be due to portal hypertension than to other causes, and as this can be assessed accurately by the Octoson water-delay echoscope, we consider it to be a valid ultrasound sign of portal hypertension. In addition to assessing the size of the main portal vein and its branches and the vessels at the splenic hilum, intraabdominal collateral vessels were sought in all patients, and, if found, portal hypertension was considered present. Variation with respiration was not assessed, as real-time ultrasonography was not analyzed, but we agree that this may affect the sensitivity of the procedure. In the population group studied, irregularity of the liver surface
Dear Sir: Delhaye and colleagues (1) recently reported on the relationship between pancreas divisum and pancreatitis. The authors studied a total of 5357 patients successfully investigated by endoscopic retrograde pancreatography. Pancreas divisum was observed in 5.7% of patients without pancreatitis and in 6.9% of subjects with pancreatitis (chronic and acute). As the difference between both groups was not significant, the authors concluded that their results “do not support the hypothesis that stenosis of the accessory papilla occurs frequently in cases of pancreas divisum, and pancreas divisum should not be regarded as an etiologic factor in pancreatitis but should be considered as a coincidental anatomic variant.” However, the authors failed to comment on one particular finding in their study which challenges the above conclusion. When examining the etiologies of acute pancreatitis (n = 335), patients with alcohol abuse were significantly more likely to have pancreas divisum (15%, p < 0.025) than all other groups. We suggest that alcohol abuse is a risk factor for acute pancreatitis. particularly in patients with pancreas divisum. To study the possible relationship between pancreas divisum and development of pancreatitis, we have performed endoscopic retrograde manometry (2) in the pancreatic duct [duct of Wirsung)
PATIENTS (n-6)
mm lig
Dw
30 1
DS CONTROLSh.8)
t
26 Dw 22-
18-
14-
IO8-
Figure
.
lo.9 i 1.9
i
??SEM
. iz
r:.
1
23.7t 1.3
DS
10.0~1.0
4
10.5 t 0.9
1. Pressure in the ducts of Wirsung (DW) and in the duct of Santorini (DS) in patients with pancreas divisum (n = 6) and in controls (n = 8).
526
CORRESPONDENCE
and in the duct of Santorini of patients with normal pancreatic duct anatomy (n = 8) and in patients with pancreas divisum (n = 6) (3). In patients presenting with pancreas divisum and suffering from relapsing upper abdominal pain accompanied by elevation of the pancreatic enzymes but without morphologic evidence of pancreatic destruction, the pressure obtained after cannulation of the accessory papilla was significantly higher (23.7 -+ 1.3 mmHg vs. 10.8 f 1.9 mmHg) than that obtained in the duct drained through the papilla of Vater. In the controls with normal pancreatic anatomy no difference was observed between the two ducts (10.5 -+ 0.9 mmHg vs. 10.0 ? 1.0 mmHg) (Figure 1). We conclude from this observation that patients with pancreas divisum may develop chronic stasis of pancreatic fluid. Whether this fact induces pancreatitis is still unclear. Additional factors, such as alcohol intake, causing increased viscosity of pancreatic saliver may increase the risk of pancreatitis. Keeping our results, which are mentioned above, and the statistical data of Delhaye and coworkers (1) in mind, we consider pancreas divisum to add to the risk factors for development of pancreatitis, particularly in patients with chronic alcohol intake. MARTIN STARITZ, M.D. THOMAS HfJTTEROTH, M.D. KARL-HERMANN
MEYER ZUM BtJSCHENFELDE, M.D.
First Medical Department University of Mainz Langenbeckstrasse 1 D 6500 Mainz, Federal Republic of Germany
Delhaye M, Engelholm L, Cremer M. Pancreas divisum: congenital anatomic variant or anomaly? Gastroenterology 1985; 89:951-8. Staritz M, Poralla T, Meyer zum Biischenfelde K-H. Effect of glyceryltrinitrate on the sphincter of Oddi motility and baseline pressure. Gut 1985;26:194-7. Staritz M, Hiitteroth T, Meyer zum Biischenfelde K-H. Pancreas divisum: Prldisposition zur chronischen Pankreatitis durch chronischen Sekretstau? Dtsch Med Wochenschr 1986 (in press). Reply. Concerning the higher incidence of pancreas divisum (PD) among patients with acute alcoholic pancreatitis (15%) than among patients with acute nonalcoholic pancreatitis (5.8%) (l), we would like to provide some related comments. It is generally accepted that acute alcoholic pancreatitis is merely an acute episode during the course of chronic pancreatitis (2). Indeed, many authors (3-5) consider that the diagnosis of chronic pancreatitis could be made if the patients were followed up during an average of 5 yr after the first acute painful attack. Symptoms of acute pancreatitis should develop only after functional and histologic changes of chronic pancreatitis have been established (5). Another argument for considering acute and chronic alcoholic pancreatitis as belonging to the same pathological subgroup is based on the diagnostic criteria of chronic pancreatitis we have used (1). Indeed, we have considered that ductal abnormalities at pancreatography (duct strictures and/or dilatations, pruning of branches, calcifications or protein plugs and cysts) are highly suggestive of chronic pancreatitis. The demonstration of these typical morphologic lesions of the pancreatic ducts in cases of PD requires the opacification of both ventral and dorsal pancreatic ducts. However, opacification of both ducts was achieved in only 2 of 9 cases of “acute alcoholic pancreatitis.” If the ventral pancreas was considered absent in 3 other cases of acute alcoholic pancreatitis with only dorsal pancreatography, then there re-
GASTROENTEROLOGY Vol. 91. No.
2
mained 4 cases in which only the pancreatic ventral duct could be opacified without obtaining any information about the morphologic pattern of the pancreatic dorsal duct. It is possible that some of these 4 patients presented unnoticed pancreatic ductal abnormalities and that they have been misclassified into the subgroup of acute alcoholic pancreatitis. Moreover, this underestimation of the diagnosis of chronic changes will generally parallel the failure rate of dorsal pancreatography. Therefore, to avoid the bias of opacification failure of both pancreatic ducts, it is more consistent to collect into the same pathological subgroup the cases of alcoholic pancreatitis without ductal abnormalities (acute) and the cases of chronic alcoholic pancreatitis. The prevalence of PD in alcoholic pancreatitis (acute and chronic) (8.6%) is then not statistically different from that in nonalcoholic pancreatitis (5.4%). In addition, we were very interested in their experience with endoscopic retrograde manometry performed in both the ventral and dorsal pancreatic duct in cases of PD and fused pancreas. First of all, all manometries were obtained using a triple-lumen catheter having a diameter of 1.7 mm (6). It is therefore obvious that the accessory papilla was not stenotic in these 6 patients having a PD and suffering from relapsing acute pancreatitis. Indeed, the size of the dorsal duct orifice evaluated by calibration with fine lacrima probes during operation by Warshaw et al. (7) was judged to be stenotic if it was
Medicosurgical Department Radiology Erasme Hospital Free University of Brussels Brussels, Belgium 1. Delhaye M, Engelholm
of Gastroenterology
L, Cremer M. Pancreas
and
divisum:
con-