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The Diagnosis of Diseases of the Pancreas
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The Diagnosis of Diseases of the Pancreas PAUL V. HARPER, M.D., F.A.C.S.*
THE surgeon encounters diagnostic problems involving the pancreas in both acute and chronic abdominal conditions, and at operation. ACUTE PANCREATITIS
Severe, acute hemorrhagic pancreatitis is one of the most spectacular of abdominal catastrophes. The patient, usually with an antecedent history of biliary disease and often following an alcoholic episode, develops sudden, severe, epigastric pain and tenderness with vomiting. Fever and leukocytosis appear, and a shocklike state supervenes within a few hours after onset. Even with prompt and vigorous treatment, death is often the outcome. The extensive autodigestion and hemorrhage of the pancreas observed at autopsy with resultant massive outpouring of plasma and pancreatic juice into the peritoneal cavity adequately accounts for the clinical findings and rapid downhill course in these cases. Fortunately, most cases of acute pancreatitis do not fall into this severe class. Milder cases of hemorrhagic and edematous pancreatitis form an almost infinite gradation into the chronic relapsing and chronic forms of this disease. It is necessary to distinguish acute pancreatitis from other acute upper abdominal conditions, particularly since patients with acute pancreatitis do not tolerate operation well. The principal conditions which enter into the differential diagnosis are acute cholecystitis, perforated peptic ulcer upper intestinal obstruction, mesenteric thrombosis and myocardial infarction, all of which require distinctly different management than acute pancreatitis. In the case of trauma to the abdomen, acute pancreatitis occurs and must be distinguished from intra-a,bdominal hemorrhage and ruptured or perforated viscus. From the Department of Surgery, The University of Chicago, Chicago.
* Associate Professor, Department of Surgery and The Argonne Cancer Research Hospital, The University of Chicago. 141
t Paul V. Harper Significance of Elevated Serulll Alllylase and Lipase Levels
Since the pioneer work of Elman, the serum amylase determination in pancreatitis has been available as a fairly specific confirmatory laboratory test. l The obligation of the diagnostician would in many instances be largely fulfilled were he only to consider the diagnosis of acute pancreatitis and order a serum amylase determination to be performed. Serum amylase under normal conditions probably originates from a number of different tissues. An increase of the serum amylase level indicates either an increased amount of this enzyme entering the blood stream or a reduced amount leaving via the urine. In renal failure with increasing nonprotein nitrogen levels of the blood, amylase is retained in the blood and the serum amylase rises in a parallel manner to the nonprotein nitrogen to levels of 400 or 500 units (Somogyi), the normal levels being 80 to 250 units. Salivary gland disease (mumps) has sometimes been responsible for elevated serum amylase in the absence of abdominal symptoms, and presumably in the absence of pancreatic involvement; however, by far the most common causes of elevated serum amylase are related to the pancreas. Blockage of the secretory ducts of the pancreas by mechanical means or by inflammation or spasm especially when the gland is actively secreting, results in retention in the gland and absorption into the blood stream of abnormal amounts of amylase. Mechanical blockage may result from biliary stone lodged in the ampulla of Vater or from pancreatic duct ligation in connection with resection. Inflammatory blockage as result of pancreatitis, and spasm of the ampulla from certain drugs such as morphine, will give high serum amylase levels. Escape of pancreatic juice into the peritoneal cavity results in absorption of amylase into the blood stream, resultant high serum amylase. This situation occurs in an acute pancreatitis where evidence of pancreatic digestion of fat can be seen far from the gland in the peritoneal cavity and also in perforated peptic ulcer where the peritoneal cavity is flooded with duodenal juice, containing pancreatic enzymes. Amylase levels as high as 2000 units have been reported in perforated duodenal ulcer where there was no evidence of pancreatic disease at operation. In acute and in chronic relapsing pancreatitis, the serum amylase level increases abruptly with the attack to several times the normal value, persists at this level for 24 to 72 hours and then usually returns to normal levels even though the inflammatory process in the pancreas appears active. While this rise in serum amylase is almost invariably present, in rare cases it may not be observed. The fall to normal level may be due to opening up of temporarily occluded ducts which drain the pancreatic juice into the intestinal tract, thus being a good prognostic sign, or to extensive destruction of the pancreatic acinar tissue by autodigestion. The absorption of pancreatic juice, previously released into the peritoneal cavity, has been shown to result in this same serum amylase pattern. In
t The Diagnosis of Diseases of the Pancreas
143
some cases of pancreatitis, usually the edematous nonhemorrhagic or chronic relapsing varieties, the serum amylase remains high for many weeks suggesting a partial obstruction of the duct system, since complete chronic obstruction as by tumor usually results in a sclerosing process in the obstructed portion of the gland with disappearance of the acinar tissue and no increase of serum amylase. Serum lipase levels have been used in a similar manner to serum amylase levels with satisfactory results. The high lipase level persists for a longer period of time than the amylase level and the rise is somewhat slower, so that the two tests are to some extent complementary. Serum calcium levels in severe acute pancreatitis are lower, presumably because of the binding of larger amounts of calcium as insoluble calcium soaps in the regions of extensive fat digestion. This is of some prognostic significance. SerUlll Alllylase Deterlllinations in the Differential Diagnosis of an Acute Upper Abdolllinal Crisis
From the above considerations it is evident that in approaching the problem of a patient with acute upper abdominal crisis the results of the serum amylase determinations while all important must be interpreted in the light of the entire clinical situation. In acute cholecystitis with cholelithiasis, temporary blockage of the ampulla by a stone may produce a high serum amylase without significant pancreatitis, and operation should not be withheld if perforation of the gallbladder appears imminent. On the other hand, routine surgery for acute cholecystitis as advocated by some authors should definitely be withheld in the presence of a high serum amylase until it becomes clear whether or not acute pancreatitis actually does exist. As mentioned above, prior administration of morphine or codeine should always be considered in the interpretation of serum amylase levels. The differential diagnosis between acute pancreatitis and perforated peptic ulcer is more critical, because of the sharp difference in the surgical indications in the two conditions. Fortunately, the conservative management of perforated ulcer with gastric aspiration and antibiotics has proved reasonably safe. In the presence of severe upper abdominal symptoms with high serum amylase level without demonstration of gas under the diaphragm, probably the best course is conservative management. In traumatic pancreatitis,2 however, unless damage to other organs can be ruled out with reasonable certainty, abdominal exploration is probably the best course since the incidence of the associated injury to other organs is high and of unpredictable severity. Acute upper intestinal obstruction resembles a clinical picture of acute pancreatitis to some extent. The ileus from the chemical peritonitis can give an x-ray picture similar to that of obstruction. In this situation the
144
Paul V. Harper
amylase determination can be a determining factor and likewise in mesenteric thrombosis. Coronary occlusion may be particularly confusing since electrocardiographic changes may be induced in patients, especially when they have previous coronary insufficiency, by the shock associated with pancreatitis. The following illustrative case demonstrates this point well. CASE 1. The patient was a retired policeman who entered the hospital for checkup for burning epigastric pain and shortness of breath. Physical examination was essentially negative. Gastroduodenal x-rays demonstrated a large hiatus hernia. The electrocardiogram showed extensive myocardial damage. Secretion studies revealed a high gastric acidity. The patient was placed on ulcer management, which controlled his epigastric pain, and sent home. He returned as an emergency case several days later with a severe exacerbation of his epigastric pain. Blood pressure was low and his color was poor. Serum amylase was drawn and was found to be 350 units. Since this was only slightly elevated the diagnosis of pancreatitis was not seriously considered. Electrocardiography showed changes compatible with further coronary occlusion, and on this basis the patient was treated with oxygen, anticoagulants and minimal parenteral fluids. He died 36 hours after admission. An extensive unsuspected acute pancreatitis was found at autopsy.
CHRONIC PANCREATIC DISEASE
Chronic abdominal pain often related to meals, for which no demonstrable cause may b~ found, not infrequently turns out to be of pancreatic origin, resulting either from tumor or chronic pancreatitis. Clinical diagnosis in this type of patient must almost necessarily be made by exclusion or by therapeutic trial, or in the case of suspected malignant tumor by exploratory laparotomy. Relief of pain by paravertebral block establishes its visceral but not necessarily its pancreatic origin. Antisecretory and antacid drugs suppress the vagal and hormonal pancreatic secretion, diminish or abolish pain of pancreatic origin but may have the same symptomatic effect on pain originating elsewhere in the gastrointestinal tract. The origin of pain in chronic sclerosing pancreatitis is not clear but, in part at least, is probably due to the secretion of acinar tissue into blocked ducts. In its fully developed form, this condition is one of the most severe and distressing of chronic abdominal complaints resulting frequently in drug addiction and suicide. Tests of pancreatic function have been disappointing in evaluating these cases of chronic pancreatic disease. The serum amylase is normal, studies on the pancreatic secretions by duodenal intubation are time-consuming, distressing to the patient and except in the case of positive cytologic findings not very conclusive. A number of tests have been devised3 in which stimulation of the pancreatic secretion by secretin or other secretagogues is accompanied by measurement of the blood amylase clotting factors, etc. While many of these tests do i3how some changes in most cases of chronic pancreatic
The Diagnosis of Diseases of the Pancreas
145
disease, the basic information they supply is insufficient to establish firmly a diagnosis. While the results of single tests of pancreatic function are thus not very conclusive in chronic pancreatic disease, the results of a number of different tests taken together, as in liver disease, may be more helpful. Two cases illustrating some of these points and their attendant difficulties are presented below. CASE II. This patient was a 62 year old salesman who had undergone an exploratory operation 1 year previously in another hospital for painless jaundice and weight loss. At this time a carcinoma of the pancreas was diagnosed without biopsy and a choledochoduodenostomy was performed. Following this procedure, the patient remained fairly well with complete relief of his jaundice without further weight loss. However, beginning a few months after his operation he developed severe progressive epigastric and back pain characteristically made worse by meals. He required large quantities of narcotics daily, and characteristically remained sitting, leaning forward, in order to relieve hie pain even when sleeping. Physical examination was essentially negative and x-ray examination showed no abnormality except for the biliary anastomosis. Secretion studies showed high gastric acidity. Because the patient had had four previous coronary occlusions, exploratory laparotomy was not considered; He was placed on strict medical management with Pro-Banthine and antacids with complete relief of his pain. He required no more narcotics and was able to sleep lying down.
In all probability the diagnosis of cancer made at the previous operation was in error, and the lesion observed was in reality chronic sclerosing pancreatitis. CASE III. This patient was a 58 year old Pullman porter who had for 3 years been having severe recurrent attacks of epigastric pain lasting for several days. These attacks occurred without warning at intervals of several months. Exploration at another hospital was carried out at which time no abnormality was found. Examination on admission was essentially negative. X-ray studies revealed a slight duodenal deformity and secretion studies showed low gastric acidity. Bilateral splanchnic block produced complete, dramatic relief of pain. Serum amylase was never elevated. It was felt that the diagnosis of chronic pancreatitis was most likely and that strict management on antacids and Banthine gave temporary relief. Incapacitating attacks of pain returned however, and a year following his first admission a bilateral extrapleural splanchnicectomy was performed with complete relief. The patient did well for 2 years, his only complaints being referrable to the intercostal pain from his operation. He was then readmitted in emergency with massivtl gastrointestinal hemorrhage from a duodenal ulcer. At operation the pancreas appeared normal.
In retrospect, although the x-ray appearance of the duodenum of this patient was never conclusive for ulcer and the acid secretion was never high, the original diagnosis of pancreatitis was probably incorrect. A duodenal ulcer probably accounted for the findings all along.
1 Paul V. Harper
146 OPERATIVE DIAGNOSIS
When surgical exploration is elected to rule out carcinoma of the pancreas, or when a mass is encountered in the pancreas at operation, the surgeon is faced with what is often the most difficult of operative diagnoses. Although radical excision of carcinoma of the pancreas is not so widely advocated as a few years ago, one at least owes the patient a correct diagnosis following his laparotomy. Carcinoma of the pancreas originates in the duct system, consequently causes obstruction to a portion of the gland drained by the involved ducts. The obstructed portion of the gland, as mentioned above, becomes sclerotic and the acinar tissue disappears, leaving islands of duct epithelium surrounded by dense scar tissue. On biopsy and frozen section, tissue of this sort is often extremely difficult to distinguish from adenocarcinoma. The carcinoma is buried deep in the sclerotic degenerated pancreatic tissue from which it cannot be distinguished grossly.4 For these reasons, biopsies of pancreatic masses are often inconclusive. Most surgeons are somewhat reluctant to biopsy the pancreas, because of the troublesome bleeding which results and also because of the danger of precipitating an acute pancreatitis or creating a pancreatic fistula. Both these latter complications should be greatly reduced by suppressing the pancreatic secretion by proper medication for several days after operation. The danger remains, however, of spreading and implanting tumor cells in the course of the biopsy. While many of these difficulties may be obviated by using the technique of multiple needle biopsy, 6 and biopsy of suspicious peripancreatic tissues, diagnosis by this means is certainly not satisfactory, and the results when negative of no great value. If curative resection is to be attempted it must be in small early tumors, in which frequently the diagnosis of malignancy cannot be proved prior to resection. The following two cases illustrate well the problems which are encountered in this type of situation: CASE IV. The patient was a 63 year old farmer who was well until 1 month prior to admission, at which time he developed painless jaundice, which fluctuated somewhat from week to week. Examination on admission revealed nothing remarkable, beyond the jaundice. The gallbladder was not tender or palpable, and there was occult blood in the stools. X-ray revealed no gastrointestinal abnormality. On exploration, a 3X 4X 5 cm., hard, discrete mass was felt in the head of the pancreas, the common duct was dilated, and the gallbladder was diseased and shrunken. After considerable consultation, it was decided to carry out a resection without biopsy, from which the patient recovered well. Examination of the specimen revealed only a localized area of pancreatitis. The ampulla was dilated and lacerated and apparently it had been blocked by a large gallstone. This was evidently the source of the bleeding. CASE V. This 59 year old printer entered the hospital with painless jaundice, anorexia, and weight loss for 8 weeks. Physical examination disclosed an enlarged
1 The Diagnosis of Diseases of the Pancreas
147
liver and jaundice. At exploration the pancreas was hard and indurated throughout its entire length. The common bile duct was dilated. Several biopsies of the pancreas showed only pancreatitis. On opening of the duodenum, a papillary growth in the ampulla was found, and it was impossible to probe the pancreatic ducts for more than a centimeter. It was felt that the papillary growth was probably the cause of the obstruction and a pancreatoduodenectomy was performed, from which the patient recovered well. Examination of the specimen immediately after operation gave no evidence of tumor and several additional frozen sections, taken from the specimen, showed only pancreatitis. Final sections, however, revealed a benign papilloma of the ampulla of Vater and a diffuse involvement of the pancreatic duct system with carcinoma.
REFERENCES 1. Malinowski, T. S.: The Clinical Value of Serum Amylase Determination. J.A.M.A.
149: 1380, 1952. 2. Mathewson, C. and Halter, B. L.: Traumatic Pancreatitis with and without Associated Injuries. Am. J. Surg. 83: 409, 1952. 3. Shingleton, W. W., Anlyan, W. G. and Hart, D.: The Diagnosis of Pancreatic Disorders by Certain Laboratory Procedures. Ann. Surg. 136: 578, 1952. 4. Bowden,IL.: The Fallability of Pancreatic Biopsy. Ann. Surg. 139: 403, 1954. 5. Kirtland, H. B.: A Safe Method of Pancreatic Biopsy. Am. J. Surg. 82: 451, 1951. 950 E. 59th Street Chicago 37, Illinois
The Diagnosis of Diseases of the Pancreas PAUL V. HARPER, M.D., F.A.C.S.*
THE surgeon encounters diagnostic problems involving the pancreas in both acute and chronic abdominal conditions, and at operation. ACUTE PANCREATITIS
Severe, acute hemorrhagic pancreatitis is one of the most spectacular of abdominal catastrophes. The patient, usually with an antecedent history of biliary disease and often following an alcoholic episode, develops sudden, severe, epigastric pain and tenderness with vomiting. Fever and leukocytosis appear, and a shocklike state supervenes within a few hours after onset. Even with prompt and vigorous treatment, death is often the outcome. The extensive autodigestion and hemorrhage of the pancreas observed at autopsy with resultant massive outpouring of plasma and pancreatic juice into the peritoneal cavity adequately accounts for the clinical findings and rapid downhill course in these cases. Fortunately, most cases of acute pancreatitis do not fall into this severe class. Milder cases of hemorrhagic and edematous pancreatitis form an almost infinite gradation into the chronic relapsing and chronic forms of this disease. It is necessary to distinguish acute pancreatitis from other acute upper abdominal conditions, particularly since patients with acute pancreatitis do not tolerate operation well. The principal conditions which enter into the differential diagnosis are acute cholecystitis, perforated peptic ulcer upper intestinal obstruction, mesenteric thrombosis and myocardial infarction, all of which require distinctly different management than acute pancreatitis. In the case of trauma to the abdomen, acute pancreatitis occurs and must be distinguished from intra-a,bdominal hemorrhage and ruptured or perforated viscus. From the Department of Surgery, The University of Chicago, Chicago.
* Associate Professor, Department of Surgery and The Argonne Cancer Research Hospital, The University of Chicago. 141
t Paul V. Harper Significance of Elevated Serulll Alllylase and Lipase Levels
Since the pioneer work of Elman, the serum amylase determination in pancreatitis has been available as a fairly specific confirmatory laboratory test. l The obligation of the diagnostician would in many instances be largely fulfilled were he only to consider the diagnosis of acute pancreatitis and order a serum amylase determination to be performed. Serum amylase under normal conditions probably originates from a number of different tissues. An increase of the serum amylase level indicates either an increased amount of this enzyme entering the blood stream or a reduced amount leaving via the urine. In renal failure with increasing nonprotein nitrogen levels of the blood, amylase is retained in the blood and the serum amylase rises in a parallel manner to the nonprotein nitrogen to levels of 400 or 500 units (Somogyi), the normal levels being 80 to 250 units. Salivary gland disease (mumps) has sometimes been responsible for elevated serum amylase in the absence of abdominal symptoms, and presumably in the absence of pancreatic involvement; however, by far the most common causes of elevated serum amylase are related to the pancreas. Blockage of the secretory ducts of the pancreas by mechanical means or by inflammation or spasm especially when the gland is actively secreting, results in retention in the gland and absorption into the blood stream of abnormal amounts of amylase. Mechanical blockage may result from biliary stone lodged in the ampulla of Vater or from pancreatic duct ligation in connection with resection. Inflammatory blockage as result of pancreatitis, and spasm of the ampulla from certain drugs such as morphine, will give high serum amylase levels. Escape of pancreatic juice into the peritoneal cavity results in absorption of amylase into the blood stream, resultant high serum amylase. This situation occurs in an acute pancreatitis where evidence of pancreatic digestion of fat can be seen far from the gland in the peritoneal cavity and also in perforated peptic ulcer where the peritoneal cavity is flooded with duodenal juice, containing pancreatic enzymes. Amylase levels as high as 2000 units have been reported in perforated duodenal ulcer where there was no evidence of pancreatic disease at operation. In acute and in chronic relapsing pancreatitis, the serum amylase level increases abruptly with the attack to several times the normal value, persists at this level for 24 to 72 hours and then usually returns to normal levels even though the inflammatory process in the pancreas appears active. While this rise in serum amylase is almost invariably present, in rare cases it may not be observed. The fall to normal level may be due to opening up of temporarily occluded ducts which drain the pancreatic juice into the intestinal tract, thus being a good prognostic sign, or to extensive destruction of the pancreatic acinar tissue by autodigestion. The absorption of pancreatic juice, previously released into the peritoneal cavity, has been shown to result in this same serum amylase pattern. In
t The Diagnosis of Diseases of the Pancreas
143
some cases of pancreatitis, usually the edematous nonhemorrhagic or chronic relapsing varieties, the serum amylase remains high for many weeks suggesting a partial obstruction of the duct system, since complete chronic obstruction as by tumor usually results in a sclerosing process in the obstructed portion of the gland with disappearance of the acinar tissue and no increase of serum amylase. Serum lipase levels have been used in a similar manner to serum amylase levels with satisfactory results. The high lipase level persists for a longer period of time than the amylase level and the rise is somewhat slower, so that the two tests are to some extent complementary. Serum calcium levels in severe acute pancreatitis are lower, presumably because of the binding of larger amounts of calcium as insoluble calcium soaps in the regions of extensive fat digestion. This is of some prognostic significance. SerUlll Alllylase Deterlllinations in the Differential Diagnosis of an Acute Upper Abdolllinal Crisis
From the above considerations it is evident that in approaching the problem of a patient with acute upper abdominal crisis the results of the serum amylase determinations while all important must be interpreted in the light of the entire clinical situation. In acute cholecystitis with cholelithiasis, temporary blockage of the ampulla by a stone may produce a high serum amylase without significant pancreatitis, and operation should not be withheld if perforation of the gallbladder appears imminent. On the other hand, routine surgery for acute cholecystitis as advocated by some authors should definitely be withheld in the presence of a high serum amylase until it becomes clear whether or not acute pancreatitis actually does exist. As mentioned above, prior administration of morphine or codeine should always be considered in the interpretation of serum amylase levels. The differential diagnosis between acute pancreatitis and perforated peptic ulcer is more critical, because of the sharp difference in the surgical indications in the two conditions. Fortunately, the conservative management of perforated ulcer with gastric aspiration and antibiotics has proved reasonably safe. In the presence of severe upper abdominal symptoms with high serum amylase level without demonstration of gas under the diaphragm, probably the best course is conservative management. In traumatic pancreatitis,2 however, unless damage to other organs can be ruled out with reasonable certainty, abdominal exploration is probably the best course since the incidence of the associated injury to other organs is high and of unpredictable severity. Acute upper intestinal obstruction resembles a clinical picture of acute pancreatitis to some extent. The ileus from the chemical peritonitis can give an x-ray picture similar to that of obstruction. In this situation the
144
Paul V. Harper
amylase determination can be a determining factor and likewise in mesenteric thrombosis. Coronary occlusion may be particularly confusing since electrocardiographic changes may be induced in patients, especially when they have previous coronary insufficiency, by the shock associated with pancreatitis. The following illustrative case demonstrates this point well. CASE 1. The patient was a retired policeman who entered the hospital for checkup for burning epigastric pain and shortness of breath. Physical examination was essentially negative. Gastroduodenal x-rays demonstrated a large hiatus hernia. The electrocardiogram showed extensive myocardial damage. Secretion studies revealed a high gastric acidity. The patient was placed on ulcer management, which controlled his epigastric pain, and sent home. He returned as an emergency case several days later with a severe exacerbation of his epigastric pain. Blood pressure was low and his color was poor. Serum amylase was drawn and was found to be 350 units. Since this was only slightly elevated the diagnosis of pancreatitis was not seriously considered. Electrocardiography showed changes compatible with further coronary occlusion, and on this basis the patient was treated with oxygen, anticoagulants and minimal parenteral fluids. He died 36 hours after admission. An extensive unsuspected acute pancreatitis was found at autopsy.
CHRONIC PANCREATIC DISEASE
Chronic abdominal pain often related to meals, for which no demonstrable cause may b~ found, not infrequently turns out to be of pancreatic origin, resulting either from tumor or chronic pancreatitis. Clinical diagnosis in this type of patient must almost necessarily be made by exclusion or by therapeutic trial, or in the case of suspected malignant tumor by exploratory laparotomy. Relief of pain by paravertebral block establishes its visceral but not necessarily its pancreatic origin. Antisecretory and antacid drugs suppress the vagal and hormonal pancreatic secretion, diminish or abolish pain of pancreatic origin but may have the same symptomatic effect on pain originating elsewhere in the gastrointestinal tract. The origin of pain in chronic sclerosing pancreatitis is not clear but, in part at least, is probably due to the secretion of acinar tissue into blocked ducts. In its fully developed form, this condition is one of the most severe and distressing of chronic abdominal complaints resulting frequently in drug addiction and suicide. Tests of pancreatic function have been disappointing in evaluating these cases of chronic pancreatic disease. The serum amylase is normal, studies on the pancreatic secretions by duodenal intubation are time-consuming, distressing to the patient and except in the case of positive cytologic findings not very conclusive. A number of tests have been devised3 in which stimulation of the pancreatic secretion by secretin or other secretagogues is accompanied by measurement of the blood amylase clotting factors, etc. While many of these tests do i3how some changes in most cases of chronic pancreatic
The Diagnosis of Diseases of the Pancreas
145
disease, the basic information they supply is insufficient to establish firmly a diagnosis. While the results of single tests of pancreatic function are thus not very conclusive in chronic pancreatic disease, the results of a number of different tests taken together, as in liver disease, may be more helpful. Two cases illustrating some of these points and their attendant difficulties are presented below. CASE II. This patient was a 62 year old salesman who had undergone an exploratory operation 1 year previously in another hospital for painless jaundice and weight loss. At this time a carcinoma of the pancreas was diagnosed without biopsy and a choledochoduodenostomy was performed. Following this procedure, the patient remained fairly well with complete relief of his jaundice without further weight loss. However, beginning a few months after his operation he developed severe progressive epigastric and back pain characteristically made worse by meals. He required large quantities of narcotics daily, and characteristically remained sitting, leaning forward, in order to relieve hie pain even when sleeping. Physical examination was essentially negative and x-ray examination showed no abnormality except for the biliary anastomosis. Secretion studies showed high gastric acidity. Because the patient had had four previous coronary occlusions, exploratory laparotomy was not considered; He was placed on strict medical management with Pro-Banthine and antacids with complete relief of his pain. He required no more narcotics and was able to sleep lying down.
In all probability the diagnosis of cancer made at the previous operation was in error, and the lesion observed was in reality chronic sclerosing pancreatitis. CASE III. This patient was a 58 year old Pullman porter who had for 3 years been having severe recurrent attacks of epigastric pain lasting for several days. These attacks occurred without warning at intervals of several months. Exploration at another hospital was carried out at which time no abnormality was found. Examination on admission was essentially negative. X-ray studies revealed a slight duodenal deformity and secretion studies showed low gastric acidity. Bilateral splanchnic block produced complete, dramatic relief of pain. Serum amylase was never elevated. It was felt that the diagnosis of chronic pancreatitis was most likely and that strict management on antacids and Banthine gave temporary relief. Incapacitating attacks of pain returned however, and a year following his first admission a bilateral extrapleural splanchnicectomy was performed with complete relief. The patient did well for 2 years, his only complaints being referrable to the intercostal pain from his operation. He was then readmitted in emergency with massivtl gastrointestinal hemorrhage from a duodenal ulcer. At operation the pancreas appeared normal.
In retrospect, although the x-ray appearance of the duodenum of this patient was never conclusive for ulcer and the acid secretion was never high, the original diagnosis of pancreatitis was probably incorrect. A duodenal ulcer probably accounted for the findings all along.
1 Paul V. Harper
146 OPERATIVE DIAGNOSIS
When surgical exploration is elected to rule out carcinoma of the pancreas, or when a mass is encountered in the pancreas at operation, the surgeon is faced with what is often the most difficult of operative diagnoses. Although radical excision of carcinoma of the pancreas is not so widely advocated as a few years ago, one at least owes the patient a correct diagnosis following his laparotomy. Carcinoma of the pancreas originates in the duct system, consequently causes obstruction to a portion of the gland drained by the involved ducts. The obstructed portion of the gland, as mentioned above, becomes sclerotic and the acinar tissue disappears, leaving islands of duct epithelium surrounded by dense scar tissue. On biopsy and frozen section, tissue of this sort is often extremely difficult to distinguish from adenocarcinoma. The carcinoma is buried deep in the sclerotic degenerated pancreatic tissue from which it cannot be distinguished grossly.4 For these reasons, biopsies of pancreatic masses are often inconclusive. Most surgeons are somewhat reluctant to biopsy the pancreas, because of the troublesome bleeding which results and also because of the danger of precipitating an acute pancreatitis or creating a pancreatic fistula. Both these latter complications should be greatly reduced by suppressing the pancreatic secretion by proper medication for several days after operation. The danger remains, however, of spreading and implanting tumor cells in the course of the biopsy. While many of these difficulties may be obviated by using the technique of multiple needle biopsy, 6 and biopsy of suspicious peripancreatic tissues, diagnosis by this means is certainly not satisfactory, and the results when negative of no great value. If curative resection is to be attempted it must be in small early tumors, in which frequently the diagnosis of malignancy cannot be proved prior to resection. The following two cases illustrate well the problems which are encountered in this type of situation: CASE IV. The patient was a 63 year old farmer who was well until 1 month prior to admission, at which time he developed painless jaundice, which fluctuated somewhat from week to week. Examination on admission revealed nothing remarkable, beyond the jaundice. The gallbladder was not tender or palpable, and there was occult blood in the stools. X-ray revealed no gastrointestinal abnormality. On exploration, a 3X 4X 5 cm., hard, discrete mass was felt in the head of the pancreas, the common duct was dilated, and the gallbladder was diseased and shrunken. After considerable consultation, it was decided to carry out a resection without biopsy, from which the patient recovered well. Examination of the specimen revealed only a localized area of pancreatitis. The ampulla was dilated and lacerated and apparently it had been blocked by a large gallstone. This was evidently the source of the bleeding. CASE V. This 59 year old printer entered the hospital with painless jaundice, anorexia, and weight loss for 8 weeks. Physical examination disclosed an enlarged
1 The Diagnosis of Diseases of the Pancreas
147
liver and jaundice. At exploration the pancreas was hard and indurated throughout its entire length. The common bile duct was dilated. Several biopsies of the pancreas showed only pancreatitis. On opening of the duodenum, a papillary growth in the ampulla was found, and it was impossible to probe the pancreatic ducts for more than a centimeter. It was felt that the papillary growth was probably the cause of the obstruction and a pancreatoduodenectomy was performed, from which the patient recovered well. Examination of the specimen immediately after operation gave no evidence of tumor and several additional frozen sections, taken from the specimen, showed only pancreatitis. Final sections, however, revealed a benign papilloma of the ampulla of Vater and a diffuse involvement of the pancreatic duct system with carcinoma.
REFERENCES 1. Malinowski, T. S.: The Clinical Value of Serum Amylase Determination. J.A.M.A.
149: 1380, 1952. 2. Mathewson, C. and Halter, B. L.: Traumatic Pancreatitis with and without Associated Injuries. Am. J. Surg. 83: 409, 1952. 3. Shingleton, W. W., Anlyan, W. G. and Hart, D.: The Diagnosis of Pancreatic Disorders by Certain Laboratory Procedures. Ann. Surg. 136: 578, 1952. 4. Bowden,IL.: The Fallability of Pancreatic Biopsy. Ann. Surg. 139: 403, 1954. 5. Kirtland, H. B.: A Safe Method of Pancreatic Biopsy. Am. J. Surg. 82: 451, 1951. 950 E. 59th Street Chicago 37, Illinois