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Spontaneous resolution of pancreatic pseudocysts
Spontaneous Resolution of Pancreatic Pseudocysts Implications
for Timing of Operative Intervention
E. L. Bradley, Ill, MD, Atlanta, Georgia Luther J. Clements, MD, Atlanta, Georgia
Much of our knowledge concerning the behavior of pancreatic pseudocysts has been derived from many extant surgical series [l-5]. However, operative substantiation of the preoperative diagnosis of pseudocyst has been a necessity for inclusion into these retrospective reports. Under this highly selected circumstance, natural history data derived from such reports may not be representative of the entire spectrum of this disease process. Does spontaneous resolution of a pancreatic pseudocyst ever occur ? Despite opinions pro [1,2,6] and con [3,4,7], in the absence of reliable diagnostic technics, this question has not been resolved. In this and other questions dealing with natural history information, the primary difficulty has been in obtaining a reliable preoperative diagnosis of pseudocyst [4,8,9]. In an earlier study, we have shown that the classical inferential diagnostic methods for pseudocyst are frequently in error and, in particular, that peripancreatitic edema may exactly simulate pseudocyst by all previously employed diagnostic procedures [IO]. Resolution of this edema may create the false impression that a “pseudocyst” has spontaneously resolved. Without operative substantiation of the diagnosis of pseudocyst, the behavior of any retroperitoneal mass in the region of the pancreas may incorrectly be attributed to pseudocyst. The present report is prompted by our observations in a continuing investigation into the uses of diagnostic ultrasound in the management of pancreatitis. From the Departments of Surgery and Radiology, Emory University School of Medicine and Affiliated Hospitals, Atlanta. Georgia. Reprint requests should be addressed to Dr E. L. Bradley, Ill, Department of Surgery, 69 Butler Street, S.E.. Atlanta. Georgia 30303. Presented at the Fifteenth Annual Meeting of the Society for Surgery of the Alimentary Tract, San Francisco, California, May 21 and 22, 1974.
Volume 129, January 1975
Material and Methods For the past eighteen months, each patient admitted to Grady Memorial Hospital with a diagnosis of pancreatitis and either a palpable abdominal mass or marked anterior gastric or duodenal displacement by upper gastrointestinal series has undergone diagnostic ultrasound evaluation. Thirty-eight such patients have presently been identified. Our initial studies were carried out using the Echoline 20 Diagnostic Ultrasonoscope (Smith Kline Instruments, Inc., Palo Alto, California). Currently, ultrasound investigations are being performed with the Echoview System 8-A (Picker Corp., Cleveland, Ohio), capable of A-mode, B-mode, and B-scan presentations with capabilities for storage and instant hard copy output. General operating principles and procedures have been well covered in previous publications [11,12]. When sequential ultrasound studies were performed, transducer location was matched by means of abdominal grid measurements based on osseous reference points. Initially, all studies were performed by one of the authors (ELB). Recent procedures have been carried out by radiology technicians. During the course of our investigations, cystic masses in five patients have spontaneously resolved as serially documented by clinical, radiographic, and ultrasonic means. These patients form the basis of the present report.
Case Reports Case I. The patient (GB), a forty-two year old white male chronic alcoholic, was admitted in May 1973 with abdominal pain, an 8 by 10 cm epigastric mass, and a serum amylase of 1,050 Somogyi units. Past medical history revealed five previous admissions for pancreatitis, but on no previous occasion had an abdominal mass been palpated. Ultrasonography showed the mass to be a 9 cm cyst. (Figure 1.) Marked anterior gastric displace-
23
Bradley and Clements
Comment: Recurrent pancreatit,is in this patient may eventually prove t.o he secondary to cholelithiasis. Recurrence of t,he pseudocyst after spontaneous drainage has not occurred during the short six month f’ollow-up period.
Figure 1. Spontaneous cyst regression. A, lateral upper gastrointestinal series showing marked anterior gastric displacement. B, classic configuration of cystic area by A-mode ultrasound at admission. C, regression of anterior gastric displacement after ten days. 0, solid configuration fourteen days after original scan. ment was noted on upper gastrointestinal series. Over the next twelve days the abdominal mass regressed until it was no longer palpable. Repeated ultrasonography revealed a solid tissue configuration in the region previously demonstrated to be cystic. A significant decrease in the retrogastric mass by upper gastrointestinal series was also noted. No cystoenteric communication was demonstrated. With apparent spontaneous resolution of the pseudocyst, the patient was discharged. He was readmitted in August 1973 with mild right upper quadrant pain and jaundice. No abdominal masses were present. Total bilirubin was 4.2 mg/lOO ml and alkaline phosphatase was 548 mg/lOO ml, with a serum glutamic oxalacetic transaminase of 146. Serum amylase was within normal limits and Australia antigen was negative. Because of the patient’s allergy to iodinated dyes, and because of the likelihood of alcoholic hepatitis, liver biopsy was performed which showed only centrilobular bile stasis. Ultrasonography carried out on this admission showed only solid tissue, and upper gastrointestinal series was interpreted as normal. The jaundice resolved and t,he patient declined exploration for cholelithiasis. He is now being followed up in the outpatient clinic.
24
Case II. The patient (JA), a forty-three year old black woman, was admitted in August 1973 with a three day history of nausea, vomiting, and abdominal pain, denying having had jaundice, chills, or fever. She claimed lifelong abstinence from alcohol and was known to have insulin-dependent diabetes. Physical examination revealed a 6 by 8 cm mass in the left upper quadrant associated with abdominal tenderness, but not rebound. Admission serum amylase was 460 Somogyi units. An upper gastrointestinal series obtained shortly after admission revealed marked anterior displacement of the barium-filled stomach. (Figure 2.) Ultrasonic evaluation shortly thereafter substantiated the clinical impression of a 5 cm pancreatic pseudocyst. Intravenous pyelography gave normal results. As few systemic signs were present, a period of observation was elected. Over the course of the next five days, the abdominal mass appeared to regress. A repeated upper gastrointestinal series and ultrasound evaluation corroborated the clinical impression of spontaneous regression: the diameter of the cyst as measured at one external reference point had decreased from 5 to 3 cm. Accordingly, further observation was continued. Serum amylase at this time was 170 Somogyi units. The abdominal mass was no longer palpable eight days after admission. Repeated ultrasonography at this time showed only solid tissue in the region previously demonstrated to be cystic. Thorough investigation into the cause of the recurrent, pancreatitis has revealed only an abnormal lipoprotein pattern. Further workup is presently in progress.
Comment: Spontaneous regression was suspected clinically, but definitive diagnosis of pseudocyst and substantiation of actual cyst regression were provided by ultrasound. Case III. The patient (LH), a fourteen year old black girl, was initially seen in 1969, at which time a diagnosis of diabetes mellitus was established. Since this time, the patient has had numerous admissions for diabetic ketoacidosis. On several occasions, severely abnormal lipid metabolism (triglycerides 8,000 mg/lOO ml) has been noted and extensively investigated. Although features resembling both lipodystrophy and lipoatrophic diabetes mellitus have been observed, no definitive diagnosis has been established. In addition, she has had multiple episodes of upper abdominal pain associated with diabet.ic ketoacidosis and extensive hypertriglyceridemia and markedly elevated free fatty acids. During three of these episodes, the serum amylase level has been elevated and the clinical diagnosis was pancreatitis. In February 1972, the patient was admitted with abdominal pain, a 6 by 8 cm mass in the left upper quadrant, and an
The American Journal 01 Surgery
Pancreatic Pseudocysts
amylase of 820 Somogyi units. (Figure 3.) Ultrasonography demonstrated the mass to be a 5 cm cystic structure. Marked anterior gastric displacement was noted on upper gastrointestinal series. The mass completely resolved within seven days by clinical radiographic and ultrasonic means. Ultrasonography repeated periodically on subsequent admissions has failed to demonstrate any cystic configuration. Comment: An undiagnosed abnormality of metabolism may prove to be responsible for her recurrent episodes of pancreatitis. Recurrence of the cyst has not been noted during the two year span after spontaneous resolution. Case IV. The patient (WR),* a twenty-eightyear old black male known alcoholic, was admitted in July 1972 with abdominal pain and an epigastric msss. Multiple previous admissions for pancreatitis were noted. A 10 by 15 cm mass in the left upper quadrant was visible on inspection. Admission amylase was 338 Somogyi units. An upper gastrointestinal series and an ultrasound evaluation were performed, confirming the presence of a retrogastric cyst, 9 cm in diameter. (Figure 4.) Intravenous pyelography gave normal results except for some extrinsic displacement of the left kidney. Shortly after admission, the abdominal mass began to resolve and within four days could no longer be palpated. Repeated evaluation by ultrasound showed only solid tissue. A third sonogram was taken eleven days after admission which also showed a solid configuration where the previously demonstrated cyst had been. The serum amylase level became normal, and in view of the patient’s lack of symptoms, he was discharged to the surgical outpatient clinic. The patient was next seen in November 1972, having failed to keep his clinic appointments. He was brought to the emergency room in, a moribund condition and died shortly after admission. His wife stated that the abdominal mass had reappeared two weeks prior to this final admission and that on the day before admission he had complained of a sudden severe continuing abdominal pain. Postmortem examination reveaIed a 12 by 5 by 3 cm pseudocyst with a 4 cm linear rupture situated anteriorly through the transverse mesocolon. Careful dissection of the cyst wall revealed no evidence of recent or suspected sites of cystoenteric communication. Comment: Spontaneous resolution of the pseudocyst was followed by recurrence four months later. In the absence of evidence of previous cystoenteric communication at autopsy, the mechanism of regression of the initial cyst is uncertain.
Case V. The patient (JF), a thirty-five year old black man, known to have chronic alcoholism with multiple previous admissions for pancreatitis, was admitted in *Patient previously reported in detail.
Vokana 128. January 1875
Figure 2. Regression of small cyst. A, anterior gastric dispacement at admission. f3, 4 cm anteroposterlor transsonic echo free zone at high gain at two days. D, soltd configuration at -eight days.
October 1972 with abdominal pain, nausea,.and vomiting. Physical examination showed an 8 by 10 cm mass in the left upper quadrant and little abdominal tenderness. Admission amylase was 1,040 Somogyi units. An upper gastrointestinal series revealed stretching of the gastric mucosa and marked anterior displacement of the stomach. (Figure 5.) Ultrasonography demonstrated the mass to be an 8 cm cystic structure. Intravenous pyelography gave normal results. Over the course of the next six days, the abdominal mass regressed until it was no longer palpable. At this time, the serum amylase level had fallen to 400 units and the patient was alimenting well. A dental abscess developed and the patient required another week of hospitalization. Prior to discharge, ultrasonography revealed only solid tissue in the area previously demonstrated by this technic to have been cystic. He was readmitted one month later with recurrent pancreatitis. At this time, no abdominal mass was palpated and ultrasonography revealed solid tissue in the pancreatic region. Similar ultrasonic findings were noted at three subsequent clinic visits, the last being in October 1973.
Despite repeated episodes of panComment: creatitis and continued alcoholism, reformation of the cyst has not as yet been demonstrated by clinical, radiographic, or ultrasonic means. 25
Bradley and Clernents
F&we 3. Pseu&cysf or perlpancreatttk edema? A, note marked dispfacement of body of the stomach on admkskn. B, marked regresskn of gastrk ImpmsMn by extr8g8strk mass seven d8ys iater. ANhough this siltation can exactly be sbnut8ted by per&tncreatftk edems, d&y sonk studks showed regress&n of a cystk mass.
F&ure 4. Large cyst regresston. A, marked ante&w gadrk dtspkcement o/m day slyer &M&on. B, ante-e&r sonk demonstr8tknsofagcmcystbeforeu~r g8strolntesttn8J se&s. c, sottd tissue conllgurstkn four days leter.
F&we 5. Large cyst regress/on. A, marked g&h tmpresskm. B, anteroposte&r sonk demonstratton of an 8 cm cyst. C, sttN&g tmprovement abler twelve days. D, A-mode uttrasound sottd conffguration at fourteen days.
26
The American Journalof SurWry
Pancreatic Pseudocysts
Comments The preoperative diagnosis of pancreatic pseudocyst has classically been made by such indirect, findings as an upper abdominal mass or fullness, usually associated with an elevated serum amylase level in a patient with a history of chronic pancreatitis or pancreatic trauma, and marked displacement of the barium-filled stomach or duodenum on upper gastrointestinal series. The accuracy of this diagnostic triad has been established in retrospective series when the diagnosis of pseudocyst has been substantiated by exploration. Few authors have addressed their attention to the accuracy of this diagnostic triad in a prospective fashion. Folk and Freeark [13] have recognized that severe pancreatitis may clinically and radiologically simulate a pseudocyst by current diagnostic methods, but have believed that exploration, even though unwarranted in this self-limiting condition, may be unavoidable. No doubt other surgeons have explored patients for pseudocyst only to find severe pancreatitis, but the frequency of this error has not been known, as retrospective reports dealing with pseudocyst begin by limiting their discussion to operatively proved cases. That severe pancreatitis may exactly mimic pseudocyst by previous diagnostic procedures may be more widely appreciated than is suggested by examination of the literature. There is a seemingly widespread unpublished dictum that advises withholding exploration in patients with pancreatitis and an abdominal mass for one or two weeks if the clinical condition permits. Perhaps this aphorism is based on the observation that such masses frequently resolve. If some of these spontaneously resolving masses have been peripancreatitic edema, the mistaken impression may have been gained that a pseudocyst has resolved spontaneously. Diagnostic ultrasound is capable of distinguishing between solid and cystic abdominal masses with meaningful clinical accuracy [14-161. Goldberg and Lehman [11] have reported that ultrasound achieved 97 per cent accuracy in distinguishing solid from cystic abdominal masses in a series of 275 patients. Such noninvasive accuracy is impressive and may be particularly suitable for investigations of pancreatic disease. In an earlier study of twenty-five patients with pancreatitis and a pre-existing clinical and radiologic diagnosis of pseudocyst, preoperative diagnostic ultrasound correctly predicted the operative findings of formation of a cyst or solid tissue in twenty-four cases [IO]. In eight operatively confirmed cases in which a solid tissue mass was corVotume129, January1975
rectly predicted by ultrasound despite the clinical and radiographic diagnosis, massive retroperitoneal edema was found. We have termed this condition peripancreatitic edema and have consistently observed it to be self-limiting, undergoing spontaneous resolution. Although the majority resolved within seven to ten days, three patients with peripancreatitic edema had courses of several weeks before clinical resolution occurred. In view of the demonstrated failure rate of at least 30 per cent with the currently used diagnostic procedures in suspected pancreatic pseudocyst, previous claims of spontaneous resolution of a pseudocyst based on these diagnostic methods must be viewed with caution. How many of these cases represented, in fact, resolution of peripancreatitic edema cannot be known. The present report clearly documents the position that spontaneous resolution of retrogastric cystic structures in patients with presumed pancreatic pseudocysts does occur. Since no histologic information is obtainable by the technic of ultrasound, absolute identification of the origin of the retroperitoneal cysts is not possible. However, in the absence of any abnormalities on intravenous pyelography, and given the investigated anatomic location in a group of patients with historical and clinical evidence of active pancreatic disease, the presumption that these cystic structures were in fact pseudocysts does not seem unwarranted. If a pseudocyst does resolve, what is the mechanism? Although largely conjectural, it is interesting to speculate on the route of spontaneous cystic drainage. Since resolution, when it does take place, seems to be complete within a few days, it may be unlikely that anterior transmural absorption is taking place in the absence of peritoneal signs of the development of ascites. Spontaneous rupture of a pancreatic pseudocyst into the gastrointestinal tract has been documented [IT]. However, since communication between the ‘cyst cavity and the gastrointestinal tract was not demonstrated by barium studies, it seems less probable that spontaneous cystoenteric drainage occurred in our patients. Although drainage into the extrapancreatic retroperitoneal tissues is another theoretic possibility, none of these patients experienced back pain coincident with the resolution of the cyst. Ductal obstruction as a major factor in the pathogenesis of pseudocyst is suggested by the usual failure of retrograde operative pancreatography to visualize the coexisting cyst [I 1. However, the absence of cystic duct communication does not delineate the cause of the obstruction. Nakamura, 27
Bradley and Ciements
Sarles, and Payan [18] have demonstrated plugs of precipitated protein in the pancreatic ductal system of patients with chronic pancreatitis. If nontraumatic pseudocysts can arise from proximal duct obstruction, then protein precipitation as one cause of duct obstruction may occasionally permit drainage of a pseudocyst through the pancreatic ductal system itself, if this protein plug becomes resolved or dislodged. Clearly, pseudocysts arising from fibrotic duct obstruction could not be expected to resolve under a similar mechanism. Admittedly, without objective support and primarily by exclusion, it must be considered that the spontaneous resolution of pancreatic pseudocysts documented in this report may have been the result of internal drainage through the pancreatic ductal system after clearance of a temporary obstruction of the duct. Since we have shown that previous natural history information for pancreatic pseudocysts based on prevailing diagnostic procedures is subject to question, do these studies have meaning for operative therapy, particularly with regard to the timing of surgical intervention? Although we have demonstrated that resolution of a cyst can occur, comments on the likelihood that any given cyst may resolve spontaneously or on the frequency of cystic resolution in general are precocious. Free intraperitoneal rupture of a pancreatic pseudocyst is said to occur in approximately 5 per cent of cases and is attended by a prohibitive mortality [ 171. Th is realization has prompted many surgeons to advocate immediate drainage when the diagnosis is made [2,4,19]. Since this controversy cannot be resolved on the basis of existing information, we have adopted a policy of immediate exploration in all patients with regional sepsis and a diagnosis of pseudocyst supported by ultrasound. Most other patients with an ultrasonic diagnosis of pseudocyst are managed supportively for four to six weeks, allowing for maturation of the fibrous cyst capsule. Based on serial ultrasound studies in this latter group, exploration is undertaken earlier if the cyst is increasing in size and is postponed indefinitely if resolution occurs. We would encourage more widespread use of this noninvasive procedure since definitive diagnosis may be made and unnecessary exploration avoided. Whether such a serialized ultrasound technic will also facilitate the timing of surgical intervention necessitates further study.
28
Summary Approximately half the clinical diagnoses of pancreatic pseudocysts will be erroneous if made during the acute phase of coexisting pancreatitis. Since self-limiting peripancreatitic edema may clinically simulate pseudocyst, previous natural history information is subject to question. Occasional spontaneous resolution of a pseudocyst has been confirmed in five patients using serial ultrasound studies. It appears that although most pseudocysts maintain dimensional stability, a few may exhibit relatively rapid changes in volume. The pathophysiologic and surgical implications of these observations are discussed. References 1. Anderson MC: Management of pancreatic pseudocysts. Am J Surg 123: 209, 1972. 2. Harbrecht PJ: Cystic disease of the pancreas. Am J Surg 124: 607, 1972. 3. Kaiser GC, King RD. Kilman JW, et al: Pancreatic pseudocysts: an eVaiUatiOn of surgical management. Arch Surg 89: 275, 1964. 4. Thomford NR, Jesseph JE: Pseudocyst of the pancreas: a review of fifty cases. Am J Surg 118: 86, 1969. 5. Warren KW, Athanassiades S, Frederick P, et al: Surgical treatment of pancreatic cysts: review of 183 cases. Ann Surg 163: 886, 1966. 6. Caravati CM, Ashworth JS, Frederick P: Pancreatic pseudocysts: a medical evaluation. JAMA 197: 572, 1966. 7. Becker W, Pratt HS, Ganji H: Pseudocyst of the pancreas. Surg Gynecol Obstet 127: 744, 1968. 8. Balfour JF: Pancreatic pseudocysts: complications and their relation to the timing of treatment. Surg C/in North Am 50: 395, 1970. 9. Cerilli J, Faris TD: Pancreatic pseudocysts: delayed versus immediate treatment. Surgery 61: 541, 1967. 10. Bradley EL Ill, Clements JL Jr: Implications of diagnostic ultrasound in the surgical management of pancreatic pseudocysts. Am J Surg 127: 163, 1974. 11. Goldberg BB. Lehman JS: Some observations on the practical uses of A-mode ultrasound. Am J Roentgenol Radium Ther Nucl Med 107: 198. 1969. 12. Holm HH. Mortensen T: Ultrasonic scanning in diagnosis of abdominal diseases. Acta Chir Stand 34: 333, 1968. 13. Folk FA, Freeark RJ: Reoperations for pancreatic pseudocyst. Arch Surg 100: 430, 1970. 14. Filly RA, Freimanis AK: Echographic diagnosis of pancreatic lesions: ultrasound scanning techniques and diagnostic findings. Radio/ogy 96: 575, 1970. 15. Ostrum BJ, Goldberg BB, lsard HJ: A-mode ultrasound differentiation of soft-tissue masses. Radiology 88: 745. 1967. 16. Stuber JL, Templeton AW, Bishop K: Sonographic diagnosis of pancreatic lesions. Am J Roenfgenol Radium Ther Nucl Med 116: 406, 1972. 17. Hanna W: Rupture of pancreatic cysts: report of a case and review of the literature. Br J Surg 47: 495, 1960. 18. Nakamura K, Sarles H, Payan H: Three-dimensional reconstruction of the pancreatic ducts in chronic pancreatitis. Gastroenterology 62: 942, 1972. 19. Baker RJ: Acute surgical diseases of the pancreas. surg C/in North Am 52: 239, 1972.
The American Journal of Surgery
for Timing of Operative Intervention
E. L. Bradley, Ill, MD, Atlanta, Georgia Luther J. Clements, MD, Atlanta, Georgia
Much of our knowledge concerning the behavior of pancreatic pseudocysts has been derived from many extant surgical series [l-5]. However, operative substantiation of the preoperative diagnosis of pseudocyst has been a necessity for inclusion into these retrospective reports. Under this highly selected circumstance, natural history data derived from such reports may not be representative of the entire spectrum of this disease process. Does spontaneous resolution of a pancreatic pseudocyst ever occur ? Despite opinions pro [1,2,6] and con [3,4,7], in the absence of reliable diagnostic technics, this question has not been resolved. In this and other questions dealing with natural history information, the primary difficulty has been in obtaining a reliable preoperative diagnosis of pseudocyst [4,8,9]. In an earlier study, we have shown that the classical inferential diagnostic methods for pseudocyst are frequently in error and, in particular, that peripancreatitic edema may exactly simulate pseudocyst by all previously employed diagnostic procedures [IO]. Resolution of this edema may create the false impression that a “pseudocyst” has spontaneously resolved. Without operative substantiation of the diagnosis of pseudocyst, the behavior of any retroperitoneal mass in the region of the pancreas may incorrectly be attributed to pseudocyst. The present report is prompted by our observations in a continuing investigation into the uses of diagnostic ultrasound in the management of pancreatitis. From the Departments of Surgery and Radiology, Emory University School of Medicine and Affiliated Hospitals, Atlanta. Georgia. Reprint requests should be addressed to Dr E. L. Bradley, Ill, Department of Surgery, 69 Butler Street, S.E.. Atlanta. Georgia 30303. Presented at the Fifteenth Annual Meeting of the Society for Surgery of the Alimentary Tract, San Francisco, California, May 21 and 22, 1974.
Volume 129, January 1975
Material and Methods For the past eighteen months, each patient admitted to Grady Memorial Hospital with a diagnosis of pancreatitis and either a palpable abdominal mass or marked anterior gastric or duodenal displacement by upper gastrointestinal series has undergone diagnostic ultrasound evaluation. Thirty-eight such patients have presently been identified. Our initial studies were carried out using the Echoline 20 Diagnostic Ultrasonoscope (Smith Kline Instruments, Inc., Palo Alto, California). Currently, ultrasound investigations are being performed with the Echoview System 8-A (Picker Corp., Cleveland, Ohio), capable of A-mode, B-mode, and B-scan presentations with capabilities for storage and instant hard copy output. General operating principles and procedures have been well covered in previous publications [11,12]. When sequential ultrasound studies were performed, transducer location was matched by means of abdominal grid measurements based on osseous reference points. Initially, all studies were performed by one of the authors (ELB). Recent procedures have been carried out by radiology technicians. During the course of our investigations, cystic masses in five patients have spontaneously resolved as serially documented by clinical, radiographic, and ultrasonic means. These patients form the basis of the present report.
Case Reports Case I. The patient (GB), a forty-two year old white male chronic alcoholic, was admitted in May 1973 with abdominal pain, an 8 by 10 cm epigastric mass, and a serum amylase of 1,050 Somogyi units. Past medical history revealed five previous admissions for pancreatitis, but on no previous occasion had an abdominal mass been palpated. Ultrasonography showed the mass to be a 9 cm cyst. (Figure 1.) Marked anterior gastric displace-
23
Bradley and Clements
Comment: Recurrent pancreatit,is in this patient may eventually prove t.o he secondary to cholelithiasis. Recurrence of t,he pseudocyst after spontaneous drainage has not occurred during the short six month f’ollow-up period.
Figure 1. Spontaneous cyst regression. A, lateral upper gastrointestinal series showing marked anterior gastric displacement. B, classic configuration of cystic area by A-mode ultrasound at admission. C, regression of anterior gastric displacement after ten days. 0, solid configuration fourteen days after original scan. ment was noted on upper gastrointestinal series. Over the next twelve days the abdominal mass regressed until it was no longer palpable. Repeated ultrasonography revealed a solid tissue configuration in the region previously demonstrated to be cystic. A significant decrease in the retrogastric mass by upper gastrointestinal series was also noted. No cystoenteric communication was demonstrated. With apparent spontaneous resolution of the pseudocyst, the patient was discharged. He was readmitted in August 1973 with mild right upper quadrant pain and jaundice. No abdominal masses were present. Total bilirubin was 4.2 mg/lOO ml and alkaline phosphatase was 548 mg/lOO ml, with a serum glutamic oxalacetic transaminase of 146. Serum amylase was within normal limits and Australia antigen was negative. Because of the patient’s allergy to iodinated dyes, and because of the likelihood of alcoholic hepatitis, liver biopsy was performed which showed only centrilobular bile stasis. Ultrasonography carried out on this admission showed only solid tissue, and upper gastrointestinal series was interpreted as normal. The jaundice resolved and t,he patient declined exploration for cholelithiasis. He is now being followed up in the outpatient clinic.
24
Case II. The patient (JA), a forty-three year old black woman, was admitted in August 1973 with a three day history of nausea, vomiting, and abdominal pain, denying having had jaundice, chills, or fever. She claimed lifelong abstinence from alcohol and was known to have insulin-dependent diabetes. Physical examination revealed a 6 by 8 cm mass in the left upper quadrant associated with abdominal tenderness, but not rebound. Admission serum amylase was 460 Somogyi units. An upper gastrointestinal series obtained shortly after admission revealed marked anterior displacement of the barium-filled stomach. (Figure 2.) Ultrasonic evaluation shortly thereafter substantiated the clinical impression of a 5 cm pancreatic pseudocyst. Intravenous pyelography gave normal results. As few systemic signs were present, a period of observation was elected. Over the course of the next five days, the abdominal mass appeared to regress. A repeated upper gastrointestinal series and ultrasound evaluation corroborated the clinical impression of spontaneous regression: the diameter of the cyst as measured at one external reference point had decreased from 5 to 3 cm. Accordingly, further observation was continued. Serum amylase at this time was 170 Somogyi units. The abdominal mass was no longer palpable eight days after admission. Repeated ultrasonography at this time showed only solid tissue in the region previously demonstrated to be cystic. Thorough investigation into the cause of the recurrent, pancreatitis has revealed only an abnormal lipoprotein pattern. Further workup is presently in progress.
Comment: Spontaneous regression was suspected clinically, but definitive diagnosis of pseudocyst and substantiation of actual cyst regression were provided by ultrasound. Case III. The patient (LH), a fourteen year old black girl, was initially seen in 1969, at which time a diagnosis of diabetes mellitus was established. Since this time, the patient has had numerous admissions for diabetic ketoacidosis. On several occasions, severely abnormal lipid metabolism (triglycerides 8,000 mg/lOO ml) has been noted and extensively investigated. Although features resembling both lipodystrophy and lipoatrophic diabetes mellitus have been observed, no definitive diagnosis has been established. In addition, she has had multiple episodes of upper abdominal pain associated with diabet.ic ketoacidosis and extensive hypertriglyceridemia and markedly elevated free fatty acids. During three of these episodes, the serum amylase level has been elevated and the clinical diagnosis was pancreatitis. In February 1972, the patient was admitted with abdominal pain, a 6 by 8 cm mass in the left upper quadrant, and an
The American Journal 01 Surgery
Pancreatic Pseudocysts
amylase of 820 Somogyi units. (Figure 3.) Ultrasonography demonstrated the mass to be a 5 cm cystic structure. Marked anterior gastric displacement was noted on upper gastrointestinal series. The mass completely resolved within seven days by clinical radiographic and ultrasonic means. Ultrasonography repeated periodically on subsequent admissions has failed to demonstrate any cystic configuration. Comment: An undiagnosed abnormality of metabolism may prove to be responsible for her recurrent episodes of pancreatitis. Recurrence of the cyst has not been noted during the two year span after spontaneous resolution. Case IV. The patient (WR),* a twenty-eightyear old black male known alcoholic, was admitted in July 1972 with abdominal pain and an epigastric msss. Multiple previous admissions for pancreatitis were noted. A 10 by 15 cm mass in the left upper quadrant was visible on inspection. Admission amylase was 338 Somogyi units. An upper gastrointestinal series and an ultrasound evaluation were performed, confirming the presence of a retrogastric cyst, 9 cm in diameter. (Figure 4.) Intravenous pyelography gave normal results except for some extrinsic displacement of the left kidney. Shortly after admission, the abdominal mass began to resolve and within four days could no longer be palpated. Repeated evaluation by ultrasound showed only solid tissue. A third sonogram was taken eleven days after admission which also showed a solid configuration where the previously demonstrated cyst had been. The serum amylase level became normal, and in view of the patient’s lack of symptoms, he was discharged to the surgical outpatient clinic. The patient was next seen in November 1972, having failed to keep his clinic appointments. He was brought to the emergency room in, a moribund condition and died shortly after admission. His wife stated that the abdominal mass had reappeared two weeks prior to this final admission and that on the day before admission he had complained of a sudden severe continuing abdominal pain. Postmortem examination reveaIed a 12 by 5 by 3 cm pseudocyst with a 4 cm linear rupture situated anteriorly through the transverse mesocolon. Careful dissection of the cyst wall revealed no evidence of recent or suspected sites of cystoenteric communication. Comment: Spontaneous resolution of the pseudocyst was followed by recurrence four months later. In the absence of evidence of previous cystoenteric communication at autopsy, the mechanism of regression of the initial cyst is uncertain.
Case V. The patient (JF), a thirty-five year old black man, known to have chronic alcoholism with multiple previous admissions for pancreatitis, was admitted in *Patient previously reported in detail.
Vokana 128. January 1875
Figure 2. Regression of small cyst. A, anterior gastric dispacement at admission. f3, 4 cm anteroposterlor transsonic echo free zone at high gain at two days. D, soltd configuration at -eight days.
October 1972 with abdominal pain, nausea,.and vomiting. Physical examination showed an 8 by 10 cm mass in the left upper quadrant and little abdominal tenderness. Admission amylase was 1,040 Somogyi units. An upper gastrointestinal series revealed stretching of the gastric mucosa and marked anterior displacement of the stomach. (Figure 5.) Ultrasonography demonstrated the mass to be an 8 cm cystic structure. Intravenous pyelography gave normal results. Over the course of the next six days, the abdominal mass regressed until it was no longer palpable. At this time, the serum amylase level had fallen to 400 units and the patient was alimenting well. A dental abscess developed and the patient required another week of hospitalization. Prior to discharge, ultrasonography revealed only solid tissue in the area previously demonstrated by this technic to have been cystic. He was readmitted one month later with recurrent pancreatitis. At this time, no abdominal mass was palpated and ultrasonography revealed solid tissue in the pancreatic region. Similar ultrasonic findings were noted at three subsequent clinic visits, the last being in October 1973.
Despite repeated episodes of panComment: creatitis and continued alcoholism, reformation of the cyst has not as yet been demonstrated by clinical, radiographic, or ultrasonic means. 25
Bradley and Clernents
F&we 3. Pseu&cysf or perlpancreatttk edema? A, note marked dispfacement of body of the stomach on admkskn. B, marked regresskn of gastrk ImpmsMn by extr8g8strk mass seven d8ys iater. ANhough this siltation can exactly be sbnut8ted by per&tncreatftk edems, d&y sonk studks showed regress&n of a cystk mass.
F&ure 4. Large cyst regresston. A, marked ante&w gadrk dtspkcement o/m day slyer &M&on. B, ante-e&r sonk demonstr8tknsofagcmcystbeforeu~r g8strolntesttn8J se&s. c, sottd tissue conllgurstkn four days leter.
F&we 5. Large cyst regress/on. A, marked g&h tmpresskm. B, anteroposte&r sonk demonstratton of an 8 cm cyst. C, sttN&g tmprovement abler twelve days. D, A-mode uttrasound sottd conffguration at fourteen days.
26
The American Journalof SurWry
Pancreatic Pseudocysts
Comments The preoperative diagnosis of pancreatic pseudocyst has classically been made by such indirect, findings as an upper abdominal mass or fullness, usually associated with an elevated serum amylase level in a patient with a history of chronic pancreatitis or pancreatic trauma, and marked displacement of the barium-filled stomach or duodenum on upper gastrointestinal series. The accuracy of this diagnostic triad has been established in retrospective series when the diagnosis of pseudocyst has been substantiated by exploration. Few authors have addressed their attention to the accuracy of this diagnostic triad in a prospective fashion. Folk and Freeark [13] have recognized that severe pancreatitis may clinically and radiologically simulate a pseudocyst by current diagnostic methods, but have believed that exploration, even though unwarranted in this self-limiting condition, may be unavoidable. No doubt other surgeons have explored patients for pseudocyst only to find severe pancreatitis, but the frequency of this error has not been known, as retrospective reports dealing with pseudocyst begin by limiting their discussion to operatively proved cases. That severe pancreatitis may exactly mimic pseudocyst by previous diagnostic procedures may be more widely appreciated than is suggested by examination of the literature. There is a seemingly widespread unpublished dictum that advises withholding exploration in patients with pancreatitis and an abdominal mass for one or two weeks if the clinical condition permits. Perhaps this aphorism is based on the observation that such masses frequently resolve. If some of these spontaneously resolving masses have been peripancreatitic edema, the mistaken impression may have been gained that a pseudocyst has resolved spontaneously. Diagnostic ultrasound is capable of distinguishing between solid and cystic abdominal masses with meaningful clinical accuracy [14-161. Goldberg and Lehman [11] have reported that ultrasound achieved 97 per cent accuracy in distinguishing solid from cystic abdominal masses in a series of 275 patients. Such noninvasive accuracy is impressive and may be particularly suitable for investigations of pancreatic disease. In an earlier study of twenty-five patients with pancreatitis and a pre-existing clinical and radiologic diagnosis of pseudocyst, preoperative diagnostic ultrasound correctly predicted the operative findings of formation of a cyst or solid tissue in twenty-four cases [IO]. In eight operatively confirmed cases in which a solid tissue mass was corVotume129, January1975
rectly predicted by ultrasound despite the clinical and radiographic diagnosis, massive retroperitoneal edema was found. We have termed this condition peripancreatitic edema and have consistently observed it to be self-limiting, undergoing spontaneous resolution. Although the majority resolved within seven to ten days, three patients with peripancreatitic edema had courses of several weeks before clinical resolution occurred. In view of the demonstrated failure rate of at least 30 per cent with the currently used diagnostic procedures in suspected pancreatic pseudocyst, previous claims of spontaneous resolution of a pseudocyst based on these diagnostic methods must be viewed with caution. How many of these cases represented, in fact, resolution of peripancreatitic edema cannot be known. The present report clearly documents the position that spontaneous resolution of retrogastric cystic structures in patients with presumed pancreatic pseudocysts does occur. Since no histologic information is obtainable by the technic of ultrasound, absolute identification of the origin of the retroperitoneal cysts is not possible. However, in the absence of any abnormalities on intravenous pyelography, and given the investigated anatomic location in a group of patients with historical and clinical evidence of active pancreatic disease, the presumption that these cystic structures were in fact pseudocysts does not seem unwarranted. If a pseudocyst does resolve, what is the mechanism? Although largely conjectural, it is interesting to speculate on the route of spontaneous cystic drainage. Since resolution, when it does take place, seems to be complete within a few days, it may be unlikely that anterior transmural absorption is taking place in the absence of peritoneal signs of the development of ascites. Spontaneous rupture of a pancreatic pseudocyst into the gastrointestinal tract has been documented [IT]. However, since communication between the ‘cyst cavity and the gastrointestinal tract was not demonstrated by barium studies, it seems less probable that spontaneous cystoenteric drainage occurred in our patients. Although drainage into the extrapancreatic retroperitoneal tissues is another theoretic possibility, none of these patients experienced back pain coincident with the resolution of the cyst. Ductal obstruction as a major factor in the pathogenesis of pseudocyst is suggested by the usual failure of retrograde operative pancreatography to visualize the coexisting cyst [I 1. However, the absence of cystic duct communication does not delineate the cause of the obstruction. Nakamura, 27
Bradley and Ciements
Sarles, and Payan [18] have demonstrated plugs of precipitated protein in the pancreatic ductal system of patients with chronic pancreatitis. If nontraumatic pseudocysts can arise from proximal duct obstruction, then protein precipitation as one cause of duct obstruction may occasionally permit drainage of a pseudocyst through the pancreatic ductal system itself, if this protein plug becomes resolved or dislodged. Clearly, pseudocysts arising from fibrotic duct obstruction could not be expected to resolve under a similar mechanism. Admittedly, without objective support and primarily by exclusion, it must be considered that the spontaneous resolution of pancreatic pseudocysts documented in this report may have been the result of internal drainage through the pancreatic ductal system after clearance of a temporary obstruction of the duct. Since we have shown that previous natural history information for pancreatic pseudocysts based on prevailing diagnostic procedures is subject to question, do these studies have meaning for operative therapy, particularly with regard to the timing of surgical intervention? Although we have demonstrated that resolution of a cyst can occur, comments on the likelihood that any given cyst may resolve spontaneously or on the frequency of cystic resolution in general are precocious. Free intraperitoneal rupture of a pancreatic pseudocyst is said to occur in approximately 5 per cent of cases and is attended by a prohibitive mortality [ 171. Th is realization has prompted many surgeons to advocate immediate drainage when the diagnosis is made [2,4,19]. Since this controversy cannot be resolved on the basis of existing information, we have adopted a policy of immediate exploration in all patients with regional sepsis and a diagnosis of pseudocyst supported by ultrasound. Most other patients with an ultrasonic diagnosis of pseudocyst are managed supportively for four to six weeks, allowing for maturation of the fibrous cyst capsule. Based on serial ultrasound studies in this latter group, exploration is undertaken earlier if the cyst is increasing in size and is postponed indefinitely if resolution occurs. We would encourage more widespread use of this noninvasive procedure since definitive diagnosis may be made and unnecessary exploration avoided. Whether such a serialized ultrasound technic will also facilitate the timing of surgical intervention necessitates further study.
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Summary Approximately half the clinical diagnoses of pancreatic pseudocysts will be erroneous if made during the acute phase of coexisting pancreatitis. Since self-limiting peripancreatitic edema may clinically simulate pseudocyst, previous natural history information is subject to question. Occasional spontaneous resolution of a pseudocyst has been confirmed in five patients using serial ultrasound studies. It appears that although most pseudocysts maintain dimensional stability, a few may exhibit relatively rapid changes in volume. The pathophysiologic and surgical implications of these observations are discussed. References 1. Anderson MC: Management of pancreatic pseudocysts. Am J Surg 123: 209, 1972. 2. Harbrecht PJ: Cystic disease of the pancreas. Am J Surg 124: 607, 1972. 3. Kaiser GC, King RD. Kilman JW, et al: Pancreatic pseudocysts: an eVaiUatiOn of surgical management. Arch Surg 89: 275, 1964. 4. Thomford NR, Jesseph JE: Pseudocyst of the pancreas: a review of fifty cases. Am J Surg 118: 86, 1969. 5. Warren KW, Athanassiades S, Frederick P, et al: Surgical treatment of pancreatic cysts: review of 183 cases. Ann Surg 163: 886, 1966. 6. Caravati CM, Ashworth JS, Frederick P: Pancreatic pseudocysts: a medical evaluation. JAMA 197: 572, 1966. 7. Becker W, Pratt HS, Ganji H: Pseudocyst of the pancreas. Surg Gynecol Obstet 127: 744, 1968. 8. Balfour JF: Pancreatic pseudocysts: complications and their relation to the timing of treatment. Surg C/in North Am 50: 395, 1970. 9. Cerilli J, Faris TD: Pancreatic pseudocysts: delayed versus immediate treatment. Surgery 61: 541, 1967. 10. Bradley EL Ill, Clements JL Jr: Implications of diagnostic ultrasound in the surgical management of pancreatic pseudocysts. Am J Surg 127: 163, 1974. 11. Goldberg BB. Lehman JS: Some observations on the practical uses of A-mode ultrasound. Am J Roentgenol Radium Ther Nucl Med 107: 198. 1969. 12. Holm HH. Mortensen T: Ultrasonic scanning in diagnosis of abdominal diseases. Acta Chir Stand 34: 333, 1968. 13. Folk FA, Freeark RJ: Reoperations for pancreatic pseudocyst. Arch Surg 100: 430, 1970. 14. Filly RA, Freimanis AK: Echographic diagnosis of pancreatic lesions: ultrasound scanning techniques and diagnostic findings. Radio/ogy 96: 575, 1970. 15. Ostrum BJ, Goldberg BB, lsard HJ: A-mode ultrasound differentiation of soft-tissue masses. Radiology 88: 745. 1967. 16. Stuber JL, Templeton AW, Bishop K: Sonographic diagnosis of pancreatic lesions. Am J Roenfgenol Radium Ther Nucl Med 116: 406, 1972. 17. Hanna W: Rupture of pancreatic cysts: report of a case and review of the literature. Br J Surg 47: 495, 1960. 18. Nakamura K, Sarles H, Payan H: Three-dimensional reconstruction of the pancreatic ducts in chronic pancreatitis. Gastroenterology 62: 942, 1972. 19. Baker RJ: Acute surgical diseases of the pancreas. surg C/in North Am 52: 239, 1972.
The American Journal of Surgery