HPB CYSTIC LESIONS OF THE PANCREAS72 HPBINTERNATIONAL CYSTICLESIONSOFTHEPANCREAS ABSTRACT...

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72 HPB INTERNATIONAL CYSTIC LESIONS OF THE PANCREAS ABSTRACT Warshaw, A. L, Compton, C. C., Lewandrowski, K., Cardenosa, G. and Mueller, P. R. (1990) Cystic tumors of the pancreas. New clinical, radiologic and pathologic observa- tions in 67 patiems. Annals of Surgery, 212, 432-445. Within a 12-year period we treated 67 patients (49 women, 18 men; mean age, 61 years) with cystic neoplasms of the pancreas, including 18 serous cystic adenomas, 15 benign mucinous cystic neoplasms, 27 mucinous cystadenocarcinomas, 3 papillary cystic tu- mors, 2 cystic islet cell tumors, and 2 cases of mucinous ductal ectasia. Mean tumor size was 6cm (2 to 16cm). In 39% the patients had no symptoms, and in 37% the lesions had been misdiagnosed as a pseudocyst. Computed tomography was useful for detection, for distinguishing the microcystic subgroup of serous cystadenoma, and for showing rim calcification (all 7 cases were malignant) but was not reliable for distinguishing neoplasm from pseudocyst, serous from mucinous tumors, or benign from malignant. Arteriogra- phy showed hypervascularity in 4 of 10 serous adenomas, 3 of 11 mucinous carcinomas, and I of I papillar cystic tumors. Endoscopic pancreatography showed no communication with the cyst cavity in 37 of 37 cases of cystic neoplasms but opacified the ectatic ducts in 2 of 2 cases of mucinous ductal ectasia. Stenosis or obstruction of the pancreatic duct indicated cancer. The tumor was resected by distal pancreatectomy in 25 patients, by proximal resection in 29, and by total pancreatectomy in one, with no operative deaths. Forty-four percent of the tumors were malignant. In 10 cases the tumor was unresectable because of local extension or distant metastases, and those patients died at a mean of 4 months. Seventy-five percent of those resected for cure are alive without evident recurrence. Because the epithelial lining of the tumor was partially (5% to 98%) absent in 40% to 72% of cases of the major tumor types, and the mucinous component comprised only about 65% of mucinous cystadenoma lining, misdiagnoses on frozen and even permanent sections were made. Mitoses and histologic solid growth correlated with malignancy. Neuroendorine elements were seen in 87% of benign and 47% of malignant mucinous tumors. It is recommended that the terms macrocystic and microcystic be abandoned in favor of the histologic designations serous and mucinous. Incomplete examination of the cyst wall can be misleading, however. It is suggested that mucinous ductal ectasia be recognized separately from cystic tumors and that all of these lesions be resected, with the possible exception of asymptomatic confirmed serous cystadenomas. KEY WORDS: Pancreatic cystic tumours, Pancreas tumours PAPER DISCUSSION Dr. Warshaw and his colleagues, certainly leading authorities on the subject of cystic neoplasms of the pancreas, have once again produced a paper of great interest. They have succeeded in giving us reliable guidelines on the diagnosis and treatment of this com- plex group of tumours in an article which demonstrates the depth of their experience and knowledge of pancre- atic surgery. Cystic tumours of the pancreas are not as common as pseudocysts but the distinction is vital 1’2. Early adequate treatment of a malignant cystic neoplasm gives the patient a reasonable chance of cure whereas an inadvertent cystenterostomy reduces the prospects substantially.

Transcript of HPB CYSTIC LESIONS OF THE PANCREAS72 HPBINTERNATIONAL CYSTICLESIONSOFTHEPANCREAS ABSTRACT...

  • 72 HPB INTERNATIONAL

    CYSTIC LESIONS OF THE PANCREAS

    ABSTRACT

    Warshaw, A. L, Compton, C. C., Lewandrowski, K., Cardenosa, G. and Mueller, P. R.(1990) Cystic tumors of the pancreas. New clinical, radiologic and pathologic observa-tions in 67 patiems. Annals ofSurgery, 212, 432-445.

    Within a 12-year period we treated 67 patients (49 women, 18 men; mean age, 61 years)with cystic neoplasms of the pancreas, including 18 serous cystic adenomas, 15 benignmucinous cystic neoplasms, 27 mucinous cystadenocarcinomas, 3 papillary cystic tu-mors, 2 cystic islet cell tumors, and 2 cases of mucinous ductal ectasia. Mean tumor sizewas 6cm (2 to 16cm). In 39% the patients had no symptoms, and in 37% the lesions hadbeen misdiagnosed as a pseudocyst. Computed tomography was useful for detection, fordistinguishing the microcystic subgroup of serous cystadenoma, and for showing rimcalcification (all 7 cases were malignant) but was not reliable for distinguishing neoplasmfrom pseudocyst, serous from mucinous tumors, or benign from malignant. Arteriogra-phy showed hypervascularity in 4 of 10 serous adenomas, 3 of 11 mucinous carcinomas,and I of I papillar cystic tumors. Endoscopic pancreatography showed no communicationwith the cyst cavity in 37 of 37 cases of cystic neoplasms but opacified the ectatic ducts in2 of 2 cases of mucinous ductal ectasia. Stenosis or obstruction of the pancreatic ductindicated cancer. The tumor was resected by distal pancreatectomy in 25 patients, byproximal resection in 29, and by total pancreatectomy in one, with no operative deaths.Forty-four percent of the tumors were malignant. In 10 cases the tumor was unresectablebecause of local extension or distant metastases, and those patients died at a mean of4 months. Seventy-five percent of those resected for cure are alive without evidentrecurrence. Because the epithelial lining of the tumor was partially (5% to 98%) absent in40% to 72% of cases of the major tumor types, and the mucinous component comprisedonly about 65% of mucinous cystadenoma lining, misdiagnoses on frozen and evenpermanent sections were made. Mitoses and histologic solid growth correlated withmalignancy. Neuroendorine elements were seen in 87% of benign and 47% of malignantmucinous tumors. It is recommended that the terms macrocystic and microcystic beabandoned in favor of the histologic designations serous and mucinous. Incompleteexamination of the cyst wall can be misleading, however. It is suggested that mucinousductal ectasia be recognized separately from cystic tumors and that all of theselesions be resected, with the possible exception of asymptomatic confirmed serouscystadenomas.

    KEY WORDS: Pancreatic cystic tumours, Pancreas tumours

    PAPER DISCUSSION

    Dr. Warshaw and his colleagues, certainly leadingauthorities on the subject of cystic neoplasms of thepancreas, have once again produced a paper of greatinterest. They have succeeded in giving us reliableguidelines on the diagnosis and treatment of this com-plex group oftumours in an article which demonstrates

    the depth of their experience and knowledge of pancre-atic surgery.

    Cystic tumours of the pancreas are not as commonas pseudocysts but the distinction is vital 1’2. Earlyadequate treatment of a malignant cystic neoplasmgives the patient a reasonable chance of cure whereasan inadvertent cystenterostomy reduces the prospectssubstantially.

  • HPB INTERNATIONAL 73

    A previous publication from Warshaw and Rutledgehad focused on the distinction between neoplastic cysts(benign or malignant) and pseudocysts, based on bothclinical parameters and imaging criteria, and is there-fore essential reading for all clinicians involved in themanagement of patients with pancreatic disease3. Pa-tients with neoplastic cysts usually have no history ofacute or chronic pancreatitis nor of gallstones, alcoholabuse or trauma. Serum amylase is likely to be normalin neoplasia but raised in over half of the patients witha pancreatic pseudocyst. On imaging neoplastic cystsare more likely to be irregular or septate and maycontain solid components. The wall is often calcified,calcification being confined to the cyst wall and notapparent in other parts of the pancreas which would bemore likely in a pseudocyst due to the association withchronic pancreatitis4. Duct abnormalities characteris-tic of chronic pancreatitis may also be present inpatients with pseudocysts where ERCP will identifycyst-duct communication in over 60% of patients.Such a communication would be exceptional in neo-plastic cysts.

    In this earlier publication Warshaw and Rutledgesuggested that for diagnostic certainty aspiration ofthecyst should be performed for amylase estimation andcytological examination. However, in the more recentarticle Dr. Warshaw has veered away from aspirationbecause of the risk of seeding of malignant cells in theneedle track. We agree completely with this approachas we have found needle track seeding to be a realproblem, particularly when biopsy is used for resect-able malignant liver tumours5. To confuse the issuefurther aspiration of a neoplastic cyst may yield nega-tive cytology and may even give an elevated amylaselevel5’6. We therefore prefer to rely upon those previ-ously mentioned criteria to make a diagnosis and toprovide a therapeutic strategy but would certainly notundertake percutaneous cyst aspiration if malignancywere a possible diagnosis.We also share the reservations of the authors on the

    subject of biopsy of the cyst wall at the time of surgery.Absence of an epithelial lining must not be used toconfirm the diagnosis of a pseudocyst since the epi-thelial lining is missing in many cases of cystic neo-plasm. Frozen and even permanent section may fail toidentify malignancy. If negative intraoperative histol-ogy is so unreliable, why should we then open a cyst totake a biopsy instead of resecting it in its entirety if weare doubtful as to its aetiology? A cyst-enterostomyshould never be carried out in a patient where theremay be a possibility that the lesion is neoplastic. Thetreatment of choice is resection! This may mean that

    rarely (one out of 68 patients in the experience ofWarshaw and colleagues) patients with pseudocystswill undergo an inadvertent pancreatic resection.However, this is not such a disaster since resection isa reasonable treatment for large pseudocysts2, and pre-ferable to leaving behind a possibly curable tumour orcreating needle track seeding. We do not feel that thisis too radical an approach when Warshaw et al.,ourselves and others have shown that the mortalityrate for pancreatectomy in the 1990s can be as low as0_40/o 7-o"

    Within the group of cystic pancreatic neoplasms is itpossible to distinguish benign from malignant lesionsby preoperative imaging? Warshaw and colleagueshave shown that CT and ultrasound are good tech-niques for detecting neoplastic cysts but rarely reliablefor the prediction, or exclusion, of malignancy. Forexample, multiple small loculations are supposed toindicate a benign lesion but were found in only 50%of serous cystadenomas. A central scar with sunburstcalcification is exclusively found in serous cys-tadenomas but was present in two cases only (11%).Nevertheless it may occasionally be used to ’confirm’the diagnosis ofa benign lesion in a surgically high riskpatient. In turn a peripheral rim of calcification on CTscan may indicate malignancy as all seven tumours inwhich it was seen turned out to be malignant. Thisshould not be confused with pancreatic calcificationseen in patients with pseudocysts secondary to chronicpancreatitis. Angiography was not found to be a usefuldiscri-minator, neither was size useful. Both benignand malignant cysts varied in size from 2 to 16 cm andwere unilocular or multilocular.

    There are reports in the literature that cystadenocar-cinomas have an extremely high cure rate. Dr. War-shaw and colleagues, in this large series of patients,have a resectability rate of "only" 63% and corre-sponding overall cure rate of48%. This compares withour own figure of curative resection for cystadenocar-cinomas ofapproximately 60%. Although not a "high"cure rate, 48% is superior to results in selected sub-groups of resectable periampullary cancer, and is verymuch better than the outcome of ductal adenocar-cinoma of the pancreas. Nowadays when aggressivesurgical resection of solid pancreatic cancer is becom-ing accepted as a reasonable therapeutic option itwould be a great shame if cystic neoplasms, with theirmuch better prognosis, were to be left undertreatedwith surgical conservativism and scepticism. Aspointed out by Warshaw, we advocate that thesepatients should always undergo experienced surgicalexploration with a view to pancreatic resection.

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    References1. Layer, P. and Grandt, D. (1993) Diagnosis of pancreatic

    pseudocysts. In: Beger, H. J., Biichler, M. and Malfertheiner, P.(ed), Standards in pancreatic surgery. Springer-Verlag, Heidel-berg-Berlin. 520-525

    2. Grace, P. A. and Williamson, R. C. N. (1993) Modern manage-ment of pancreatic pseudocysts. Br. J. Sur7., 80, 573-581

    3. Warshaw, A. L. and Rutledge, P. L. (1987) Cystic tumours mis-taken for pancreatic pseudocysts. Ann. Suro., 205, 393-398

    4. Mullins, R.J., Mallangoni, M.A. and Bergamini, T. M. et al.(1988) Controversies in the management of pancreaticpseudocyst. Am. J. Sur7., 155, 165-172

    5. Scheele, J. and Altendorf-Hofmann, A. (1990) Needle trackseeding from tumor biopsy on the liver. HepatoTastroenterol, 37,335-337

    6. Railey, D.J., Barkin, J.J. and Livi, J. (1991) Aspiration ofcystadeno carcinoma mimicking pancreatic pseudocyst. Pan-creas, 6, 491-492

    7. Sachs, J. R., Deren, J.J., Sohn, M. and Nausbaun, M. (1989)Mucinous cystadenoma: pitfalls of differential diagnosis. Am. J.Gastroenterol., 84, 811-816

    8. Geer, R. J. and Brannan, M. F. (1993) Prognostic indicators forsurvival after resection of pancreatic adenocarcinoma. Am. J.Surt., 163, 68-73

    9. Gall, F. (1990) Das duktale Pankreaskarzinom. LangenbecksArch Chir (Suppl II), 375, 129-133

    10. Cameron, J.L., Pitt, H.A. and Yeo, C.J., et al. (1993) Onehundred and forty-five consecutive pancreaticoduodenectomieswithout mortality. Ann. Suro., 217, 430-438

    Johannes Scheele, Richard M. Charnleyand Franz P. Gall

    Department of SurgeryUniversity Hospital Erlangen

    F. R. G.

    HAS PROPRANOLOL RENDERED SCLEROTHERAPY OBSOLETEFOR POOR RISK ALCOHOLIC CIRRHOTIC PATIENTS?

    ABSTRACT

    Ink, 0., Martin, T., Poynard, T., Reville, M., Anciaux, M.-L, Lenoir, C., Marill, J.-L.,Labadie, H., Masliah, C., Perrin, D., Chaput, J.-C., Vetter, D., Eugene, C., Lebodic, L.,Licht, H. and Etienne, J.-P. (1992) Does elective sclerotherapy improve the efficacy oflong-term propranolol jbr prevention of recurrent bleeding in patients with severecirrhosis? A prospective multicenter, randomized trial. Hepatology; 16:912-919

    We conducted a prospective, multicenter, randomized trial to compare the efficacy ofsclerotherapy plus propranolol with that of propranoloi alone in the prevention ofrecurrent gastroesophageal bleeding in severely cirrhotic patients. For 2 yr (1987 to 1988)131 patients (96% of whom were alcoholic) with Child-Pugh class B or C cirrhosis (56%were class B and 44% were class C) were randomly assigned to one of our two treatmentgroups after cessation of variceal bleeding, without hernostatic sclerosis, and wereobserved for at least 2 yr. Treatment observance was good in 89% of cases; alcoholwithdrawal was observed in 62% of cases. Sclerotherapy was performed weekly with 1%polidocanol, and variceal obliteration was obtained in 83% ofcases, in a mean number offour sessions. "lhe cumulative percentages (expressed as mean __+ S.D.) of recurrentbleeding at 2 yr were 42%

    ___6% for propranolol plus sclerotherapy and 59% +_ 6% for

    propranolol alone (a nonsignificant difference). Twenty-eight patients from the prop-ranolol group but only 12 patients from the propranoloi-plus-sclerotherapy group hadrecurrent bleeding from esophageal variceal rupture (p < 0.01). The total number of bloodunits per patient with recurrent bleeding was slightly but not significantly more importantin the propranolol group (8 __+ 7) than in the propranoloi-plus-sclerotherapy group (5

    ___5;

    p--0.09). There were no statistical differences in the cumulative survival rate at 2 yr(propranolol plus sclerotherapy, 74% __+ 6% and propranolol alone, 64% __+ 6%) or in thenumber of patients who died of repeat bleeding (propranolol plus sclerotherapy,13% __+ 4% and propranolol alone, 17% + 5%). Among the surviving patients, cirrhosis

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