Current views on the pathogenesis, classification, diagnostic criteria, natural history and surgical treatment of pancreatitis are reviewed

Bank, S

Louw, J.H.

Marks, I.N.

English

AJOL - African Journals Online

1138 S.-A. MEDIESE TYDSKRIF 23 Oktober 19718. Atwell, J. D. (1966): Ibid., 1, 427.9. Okamoto, E. and Ueda, T. (1967): Ibid., 2, 437.10. Ehrenpreis, Th., Norberg, K-A and Wirsen, C. (1968): Ibid., 3, 43.11. Lawson, J. O. N. and Nixon, H. H. (1967): Ibid., 2, 544.12. Tobon, F., Reid, N. C. R. W., Talbert, J. L. and Schuster, M. M.(1968): New Engl. J. Med., 278, 188.13. Santulli, T. V., Kiesewetter, W. B. and Bill, A. H. (1970): J. Pediat.Surg., 5, 281.14. Cremin, B. J. (1971): Clin. Radiol., 12, 239.15. Louw, J. H., Cywes, S. and Cremin, B. J. (1971): S. AfT. J. Surg.,9, 21.16. Cy\ves, S., Louw, J. H., and Cremin, B. J. (1971): Ibid., 9, 31.Some Current Views on Pancreatitis1. N. MARKS, B.sc., M.B., CH.B., F.R.C.P. (EDIN.), S. BANK, M.B., CH.B., M.R.C.P. (LaND.), AND J. H. LOUW,CH.M., F.R.C.S. (ENG.), Gastro-intestinal Service and Department of Surgery, Groote Schuur Hospital, CapeTownSUMMARYCurrent views on the pathogenesis, classification, diag-nostic criteria, natural history and surgical treatment ofpancreatitis are reviewed.5. Afr. Med. l., 45, 1138 (1971).The past decade has seen few dramatic advances in thediagnosis and treatment of pancreatitis. The aetiopathoge-nesis remains uncertain, the diagnosis is still difficult andthe management is seldom straightforward. But there hasbeen a broadening in the understanding of the classifica-tion, diagnostic features, natura:! history and surgicalmanagement of the disease.PATHOGENESISThe cause of acute pancreauus remains elusive, and theaetiology and pathogenesis of the disease is almost ascontroversial now as it was some 50 years ago.McCutcheon,' in an attempt to unify the various aetiolo-gical factors, has reviewed the evidence for reflux of duo-denal contents into the pancreatic duct as the mechanismresponsible for initiating the disease and concludes thatreflux pancreatitis is the common denominator in all casesof pancreatitis. This would appear to be an over-simplifi-cation of the problem, particularly in alcohol-inducedpancreatitis, sinc;e many patients do not give a history ofnausea or vomiting before the onset of p~in. Furthermore,the elegant experimental studies of Davis' suggest thatalcohol-induced pancreatitis is due to factors other thanduodenal reflux into the pancreatic duct.The pathological changes in acute pancreatitis rangefrom slight oedema to extensive haemorrhagic infarction.A vicious circle of increasing vascular damage occurs inacute pancreatitis, and experimental studies by Goodhead'support the view that these changes in pancreatic bloodflow are crucial in determining the outcome of an attack.A decreased blood flow favours the development of acutehaemorrhagic pancreatitis. Low-molecular-weight dextranhas been shown to exert a protective effect in maintaininga normal perfusion rate and has been used, with goodresults, in patients with severe acute pancreatitis. Anotheraspect of the pathogenesis which has a therapeutic bearinghas been recently reviewed by Creutzfeld and Schmidt:These workers have stressed that the morphology of pan-creatitis can best be explained by the intrapancreatic effectof phospholipase A and elastase, and that only smallamounts of trypsin are required for activation of theseenzymes. It will be interesting to note whether this de-emphasis of the dominant role of trypsin in the pathoge-nesis of pancreatitis will herald a decline in the vogue ofthe antitryptic preparation Trasylol in this disease.A challenging breakthrough in the pathogenesis of alco-hol-induced pancreatitis has recently been made by SarJeset at.' These workers were able to reproduce the histologi-cal lesions of calcific pancreatitis in man by means of atwo-year period of ethanol intoxication in the rat. Thechanges in the affected lobules in the experimental animalcomprised protein plugs, some of which were calcified, inthe ducts; acinar cell replacement by dilated ducts; andsclerosis. SarJes et at.' believe that the primary disturbancein calcific pancreatitis is protein precipitation in the ductsleading to duct obstruction and, subsequently, to ductdilatation, acinar cell atrophy and fibrosis.CLASSIFICATIONThe conventional clinical classification has given way tothe aetiological and, more recently, the clinico-pathologicalclassification.The aetiological approach has the great advantage ofaffording an insight into the natural history of the diseaseand of providing a guide as to the advisability or surgeryin a particular patient. Alcohol-induced pancreatitisaccount for 62 % of pancreatitis in' the Cape Peninsula,and biliary disease, miscellaneous and unknown causes forthe remainder.6The clinico-pathological classification' recognizes acute,acute relapsing, chronic relapsing and chronic varieties.'In the acute varieties, clinical and pathological restitutiontakes place foJJowing the attack, whereas the chronic varie-ties show permanent residual pancreatic damage. The mainshortcoming of this classification is that it is largely depen-dent on histologicaJ confirmation, a problem in centressuch as 'ours where laparotomy is not readily undertaken.and where pancreatic biopsy is viewed with disfavour.Furthermore, the clinico-pathological classification is apathological rather than a clinical classification and doesnot allow separation of those patients in the chronic groups23 October 1971 S.A. MEDICAL JOURNAL 1139who have had clinically acute attacks. In general, gallstonepancreatitis tends to the acute and alcohol-induced to thechronic varieties of the disease.DIAGNOSTIC CRITERIAThere has been a trend toward stricter diagnostic criteriain recent years, and many workers insist on one or moreof the following for diagnosis: laparotomy evidence show-ing haemorrhagic pancreatitis, fat necrosis or histologicalevidence of chronic pancreatitis, a serum amylase in excessof I 000 Somogyi units, radiological calcification of thepancreas or autopsy evidence of the disease. To these maybe added a grossly abnormal pancreatic function test.The serum amylase values in 32 consecutive patientswith laparotomy evidence of acute pancreatitis show thatthe amylase level is not necessarily greater than I 000 unitsand may indeed be normal in a small proportion of thosewith alcohol-induced acute pancreatitis. In addition, theserum amylase level is of no value in distinguishihg haem-orrhagic from oedematous pancreatitis.We believe that a definite, let alone a gross abnormalityin the pancreatic function test offers adequate biochemicalsupport for pancreatic disease. Only 75% of patients withcalcific pancreatitis, the most advanced form of the disease,have grossly abnormal pancreatic function; a definiteabnormal~ty is present in a further 20 % and the test inthe remaining 5 % is normal or borderline.Recognition of these factors have led to consideration ofcriteria other than those outlined above. A suggestivehistory coupled with an abnormal pancreatic function testand a serum amylase value in excess of 300 U is sufficientto warrant a diagnosis of pancreatitis. An abnormal pro-vocative enzyme test, glucose tolerance test or bariummeal suggestive of pancreatic compression is of limitedd;agnostic value, but the combination of one of theseabnormalities with a suggestive history and disturbed pan-creatic function or a raised serum amylase level may beregarded as being in favour of the diagnosis. Pancreaticscanning with "Se has been claimed by some enthusiastsas one of the more important diagnostic aids in pancreaticdisease, but our experience with this technique has notbeen particularly rewarding. It may have a limited placeas a screening procedure for carcinoma or pancreatitis incentres which do not have facilities for the pancreaticfunction test.RadiologyThe radiological features of pancreatitis are well knownbut there are 4 radiological signs that merit attention. Thefirst is the 'target deformity' of the duodenal cap on bariummeal examination which simulates an active ulcer' cratersurrounded by a 'halo' of oedema, and the second is thecharacteristic tapering of the lower third of the commonbile duct on cholangiography. The presence of reflex ileusor the colon cut-off sign on straight X-ray of the abdomenis a recognized feature of acute pancreatitis, but the find-ing of multiple fluid levels in patients with an acuteabdomen should direct attention to the probability of anintestinal obstruction requiring urgent surgery. Hypotonicduodenography is sometimes of value in demonstratinginflammatory or malignant disease of the head of the pan-creas. With regard to the latter it should be stressed thatpainless pancreatic steatorrhoea unassociated with overtdiabetes in the elderly should be regarded as being due tocarcinoma of the pancreas until proved otherwise.Other Clinical FeaturesConsideration should also be given to the diagnosticvalue of other clinical features of pancreatitis. It is nowappreciated that the Cullen's and Grey Turner's signs mayoccur not only with acute haemorrhagic pancreatitis butin other conditions associated with retroperitoneal andindeed intraperitoneal haemorrhage. The latter conditionsmay also cause methaemoglobinaemia, a sign hailed initial-ly as diagnostic of acute pancreatitis.' Hyperlipaemia orsubcutaneous metastatic fat necrosis in patients with ab-dominal pain may alert one to the diagnosis of pancreatitis.Diagnostic labels applied to patients before recognitionof the true nature of their disease are legion and under-line the importance of an awareness of the possibility ofpancreatitis in all cases of abdominal pain. A word ofcaution is necessary, however, regarding the possible over-diagnosis of pancreatitis. This is particularly important inpatients presenting with an 'acute abdomen' in whom thereis any doubt about the diagnosis. Confirmation of thediagnosis by laparotomy is far safer than temporizing witha possible perforation or bowel strangulation.NATURAL mSTORYDifferences between the natural histories of alcohol-in-duced and gallstone pancreatitis have been studied in somedetail during the past decade and most workers are nowagreed to their being separate and distinct disease entities.Alcohol-Induced PancreatitisEssentially a disease of the young or middle-aged males,it tends to develop some 5 - 15 years after the commence-ment of alcohol overindulgence. The majority of ourpatients are moderately heavy drinkers rather than 'chronicalcoholics' in the accepted sense of the term, and the clueto the alcohol aetiology is provided mainly by the charac-teristic time re!ationship between a night's overindulgenceand the onset of pain some 24 to 48 hours later. Typically,the attack starts on the 'afternoon after the night before'.The pain is frequently gradual in onset and mild tomoderate in severity, and the attack usually settles within4 - 5 days; acute, fulminating attacks occur in less than10% of patients. An elevated ESR and white blood count,transient glycosuria and slight jaundice are useful diagnos-tic leads but the serum amylase is usually slightly ratherthan markedly raised. There is a marked tendency to re-current attacks and, not infrequently, progression todiabetes, pancreatic calcification and steatorrhoea someyears after the first attack. Complete alcohol withdrawalis the only effective' measure in reducing the liability tofurther attacks and progressive pancreatic damage, andsurgery is of value only in the management of complica-tions such as cyst and abscess formation and common-duct obstruction.1140 S.-A. MEDIESE TYDSKRIF 23 Oktober 1971Gallstone PancreatitisThis tends to occur in middle-aged or elderly patientsand is usually a more severe disease than the alcohol-induced variety. It often presents as an acute abdominalemergency but less severe attacks sometimes manifest asacute cholecystitis associated with a raised serum amylaselevel or laparotomy evidence of an oedematous pancreas.Despite the relapsing nature of the untreated disease, pan-creatic insufficiency is rare and cyst formation unusual.The diagnosis of acute pancreatitis is readily established byserum amylase determinations or laparotomy findings butthe gallstone aetiology is not always apparent. The latterwas overlooked in a number of patients subjected toemergency laparotomy and subsequent cholecystographyand the diagnosis was sometimes made only after repeatedoral and intravenous cholecystography and biliary drainageand microscopy. Further attacks are almost invariablyprevented by removal of the stones and diseased gall-bladder, preferably as an elective procedure.SURGICAL TREATMENTThe role of surgery in pancreatitis has become moreclearly defined. In general, surgeons have become moreaggressive with regard to laparotomy in establishing adiagnosis of pancreatitis in patients in whom doubt existsregarding the nature of an acute abdomen" and rathermore cautious with regard to the surgery of chronicpancreatitis. Surgical intervention is, of course, indicatedin gallstone pancreatitis and in the management of localcomplications such as persistent obstructive jaundice, cystformation, duodenal stenosis, and segmental portal hyper-tension due to splenic vein compression.Surn;ery in Chronic PancreatitisRecurrent attacks of pain, lasting a few days at a time,are usually due to acute exacerbations of the pancreatitisand are treated in much the same way as attacks ofacute pancreatitis. The prognosis of these exacerbations isalways good, and the attacks tend to become milder withprogressive destruction of the pancreatic parenchyma.Surgeons have been tempted in the past to perform avariety of procedures on such patients in the hope of re-ducing the frequency and severity of attacks-to no avail.Snhincterotomy, biliary surgery and distal pancreatectomywith pancreatico!!:astrostomy. deSPite certain theoretical ad-vanta.ges. have failed to stand the test of time and arenow re!!:arded as being little better than the outlawedvalTotomy for the control of recurrent attacks.Persistent pain. Surgical exploration is important inpatients with persistent pain following an acute or sub-acute attack. in patients with persistent pain desnite medi-cal treatment and alcohol withdrawal and in patients witha comnlication such as a Cyst or nersistent obstructivejaundice with or without common bile-duct stones." Theoneration is undertaken to exclude a cyst or intrapancreaticabscess, pancreatic or bile duct obstruction. pancreaticcarcinoma or incidental disl"ase. A cvst should -be treatedbv means of a suitable internal draina!!:e procedure, butfurther invl"sti!!:ative procl"dures are usually indicated ifno cyst is apparent. An operative cholangiogram and trans-duodenal and, if necessary, transpancreatic or retrogradepancreatogram should be carried out to allow selection ofan operative procedure on the basis of the character andsite of the obstructing lesion or lesions.Cholecystenterostomy or choledochoenterostomy may beadequate in patients with a dilated duct with symptomscompatible with cholangitis rather than pancreatitis. Thereis little indication for a definitive procedure if the pancrea-tic duct is normal, but retrograde pancreaticogastrstomyor pancreaticojejunostomy should be carried out if singleor multiple areas of obstruction are demonstrated. If thepancreatic duct is palpably dilated and filled with stones,it may be opened directly and anastomosed to a loop ofjejunum (puestow's operation). The problem, however, iscomplicated by the fact that these seemingly rational de-compressing procedures yield rather disappointing long-term results. This has led to the wider use of ablative pro-cedures, at least in patients with advanced pancreatic in-sufficiency. Intractable pain in patients with the latter maywarrant subtotal pancreatectomy, and the 95 % distal pan-createctomy recommended by Fry and Child'· is the currentfavourite.However, the possible advantages of ablative proceduresand, in particular, radical pancreatectomy should beweighed against the risk of further deterioration in steat-orrhoea and diabetes. Patients with adequate pancreaticfunctio"n should not be subjected to radical pancreatectomyand in them one of the drainage procedures should beadopted as a primary operation. Persistent pain in patientswithout evidence of duct dilatation and with adequatepancreatic function poses a real problem in management,and in such cases one may be tempted to consider sym-pathectomy or coeliac ganglionectomy.'" Not all workerswould agree with this, however, and some other ill-advisedprocedure would probably be carried out. The decision iseasier in patients with calcific disease and advanced pan-creatic insufficiency, but it should be mentioned that afew workers remain enthusiastic about the Puestow ope-ration carried out with a generous pancreaticojejunostomyof 10 cm or longer" or with a mucosa-to-mucosa typeanastomosis.'"Persistent pain of relatively short duration. The findingof a hard and indurated pancreas in elderly patients witha short history raises the possibility of cancer. Opinionsdiffer as to the advisability of pancreatic biopsy but mostworkers are loath to carry it out because of the highdiagnostic error and appreciable morbidity of the proce~dure.REFERE CES1. McCutcheon. A. D. (1968): Gut, 9, 296. ..2. Davis, A. F. (1971): Paper presented at the Pancreauc SympoSIUm,Canberra, 1970.3. Goodhead, B. (1969): Ann. Rov. Coil. Sun!. Enlll.. 45. 80.4. Creutzfeld, W. and Schmidt, H. (1970): Scand. J. Gastroent., 5,suon!. 6. 47. F5. Sarles, H.. Lebreuil, G., Tasso. F., Fi~arella. C., Clemente. .,Decaux, M. A .. Fago"de, B. and Payan, H. (1971): Gut. 12. 377.6. Marks, T. N., Banks, S. and Louw, J. H. (1968): Progr. Gastroent., I,412. . . M G'7. Sarles, H., Sarles. J-C .. Carnatte. R:. Muratore, R", Glam, ., Ulen,C., Pastor, J. and Le Roy, F. (196,): Gut, 6, 54'. .8. Bank, S., Barhezat, G. 0., Marks, T. N. and Sllber, W. (1968): Bnt.Med.- 1., 2, 86.9. Trapnell, J. E. (1966): Ann. Rov. CoIL Sur<~. Engl.. 38. 765.10. Fry. W. J. and Ch;ld, C. G., (1965): A"n. Surg., 162. 543.11. White, T. T. (1966): Pancreatitis. p. 201. London: Edward Arnold:12. Idem in Riis. AnthonisC'1 a"d Baden, cds. (1970): Advance Abstracts.4th Worlrl Co"gress of Ga<lroenterology. Cooenhagen 12 - 18 July1970, p. 218. Cooenha~en: Danish Gastroenterolo~ical Association.13. Sileo, W. (1971): Paper presented at the Pancreatic SympOSIUm, Can-berra, 1970.

Some current views on pancreatitis

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Some current views on pancreatitis

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