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The roentgen manifestations of pancreatitis
The Roentgen
Manifestations
of Pancreatitis
By M. H. POPPEL, M.D.
T
HE ROENTGEN MANIFESTATIONS of pancreatitis,g*12T15particularly in the acute stages, are identical whether due to the common nonspecific form or to uncommon specific diseases such as mumps,S tuberculosis, smallpox, etc. To correlate the roentgen manifestations with the clinical aspects and the pathologic states, the roentgen manifestations are described in three stages: ( 1) acute pancreatitis, including the migrate y form, (2) chronic inactive or residual pancreatitis, and (3) chronic progressive relapsing pancreatitis. ROENTGEN MANIFESTATIONS OF ACUTE PANCREATITIS
In any case of acute pancreatitis, roentgen manifestations may vary in type and degree not only among different patients but even in the same patient from hour to hour or day to day. Occasionally roentgen signs may not be evident at all. New changes are seen when one stage of the disease passes into another, or when a complication arises. For example, sudden perforation of the involved pancreas may alter the entire roentgen picture. For purposes of simplification, the signs of acute pancreatitis will be described according to the areas involved. Roentgen Manifestations Involving the Duodenum The first roentgen evidence may be that of a functional disturbance such as a change in motility (usually an increase), altered peristalsis, retroperistalsis, localized transient areas of spasm, irritability and modification of the mucosal pattern. The valvulae conniventes, which normally have a continuously uniform appearance, may show skip areas free of barium, The duodenal loop may be SOirritable that it is difficult to visualize any barium within it. The bulb, with or without gas, may assume a transverse position or may be elevated, slightly displaced toward the right or simply flattened. The papilla of Vater (Fig. 1) may become enlarged as the result of edema (the papillary sign), often even before pancreatic swelling can be detectedlOy” (Fig. 2). If the inflammation is severe, the edema, as evidenced by enlargement of the folds, spreads from the papilla and involves the contiguous mucosa in all directions. However, the papillary enlargement is always greatest. This papillary edema increases and decreases proportionate to the degree of inflammation When the head of the pancreas becomes sufficiently enlarged and the intense inflammation has abated, widening and displacement of the duodenal loop with pressure on its inner concave border may become apparent. This is denoted by a single large, uniform indentation with displacement of the loop toward the right (Fig. 3). Sometimes the perivaterial pancreatic enlargement produces an impression on the medial duodenum resembling a reversed figure 3. M. H. University Radiolngy, SEMINARS
Professor and Chirman, Department of Radiology, New York University Hospital; Consultant in Cenier; Director of Radiology, Bellevue Hospital, New York, N.Y.
POPPEL,
M.D.:
Medical
IN ROENTGENOLOCY,
Vo~.3,No.3
(Ju~~),l968
227
228
M.
H.
POPPEL
Fig. L-Radiographs of barium-coated specimen of normal descending duodenum.
The anatomic specimen was cut along the greater curvature and laid open so that in A, the frontal view, we are looking directly at the papillae on the medial border of the duodenum. In B, the lateral view, we are seeing the profile. The larger arrows point to the major papilla, which measured 1.8 x 0.8 x 0.8 cm.; the smaller arrows point to the minor papilla.
Fig. 2. - Enlarged papilla in early acute pancreatitis. There is
considerable enlargement of the mucosal folds.
229
Fig. L-Widening &d displacement of the duodenal loop with
pressure on its inner concave border. There is also pressure on the greater curvature of the stomach with marked edema of the gastric folds as well as those of the duodenum.
Duodenal ileus, seen as air distention on the plain film, occurs at a still later stage (Fig. 4). The ileus may be limited to the duodenum, involve the surrounding viscera (stomach, jejunum or midtransverse colon) as well, or be part of a generalized ileus. Air-fluid levels in the duodenum may occur. When barium is ingested, considerable amounts are often retained in the dependent portions of the duodenum. In the late stages of acute pancreatitis the entire duodenal loop may become irregularly distorted and obstruction may supervene.
Roentgen Manifestations Involving the Stomach Early in the course of the disease the stomach may be irritable, as shown by intolerance to barium along the greater curvature. When the pancreas enlarges, there is usually elevation of the stomach and flattening of the greater curvature, associated with a slight forward displacement. A localized impression may be seen on the greater curvature (Fig. 3). In some patients there is an actual increase in distance between the stomach and the transverse colon. The gastric mucosal folds are often edematous. When generalized ileus is present, the stomach will be distended with gas and fluid. It then appears atonic and shows no peristaltic activity.
Roentgen Manifestatiom Znvoltiiug the Pancreatic Area Itself In the early stages, a mass may not be visible. Later, there may be increased density in the pancreatic region. In the presence of a gas-producing infection of the pancreas, gas bubbles (Fig. 5) or one or more large air-fluid levels
M.
230
(Fig. 6) may be visualized. a gas-containing abscess. Roentgen Manifestations
Perforation
H.
POPPEL
into a hollow viscus may also result in
Znvolving the Colon
In the earlier stages of acute pancreatitis, there is spasm and irritability of the midtransverse colon (Fig. ‘7)) later involving the left half, and finally the
Fig. 4.-Duodenal
ileus in acute pancre-
atitis.
Fig. 5. - Gasforming infection of the body and
tail of the pancreas. Note multiple small gas above bubbles the ligament of (arrow). Treitz The stomach is displaced upward and medially.
PANCREATITIS
Fig. 6.-Gas abscess of the pancreas with single air-fluid level
above lesser curvature of stomach.
Fig ;. 7‘.-The transverse colon in acute pancreatitis. E:derna, marked irrita-
bility am1 spasrn are seen.
entire transverse colon and splenic flexure. Subsequently, narrowing of the lumen may take place, When the pancreas enlarges or when an abscess presents in the gastrocolic region, depression of the distal transverse colon may be seen. Fistulae between the pancreas and colon may occur (Fig. 8). Should ileus supervene, it may be localized to the transverse colon (Fig. 9) or be of a more generalized distribution. The “colon cut-off” sign in acute pancreatitis indicates adynamic changes in the colon. It consists of an “iso-
232
M.
H.
POPPEL
Fig. GFistula between colon and pancreas visualized by post-
operative pancreatography
lated gaseous distension of the ascending colon and hepatic flexure, with sharp delimitation of the gas shadow just to the left of the splenic flexure.“ls These adynamic changes, which simulate colonic obstruction at the splenic flexure, have also been described by others.19
Roentgen Manifestations Involving the Jeiunum and Ileum In the early stages of acute pancreatitis, spasm and irritability of the upper jejunum occur. As in the duodenum, the mucous membrane may become edematous and present a coarsely feathered appearance. The remaining portion of the jejunum and the ileum may be normal or show functional changes, i.e.,
Fig.
9.-Ileus
of the left side of the transverse
colon in acute pkcreatitis.
2333
PANCREATITIS
Fig. lO.-Small bowel changes in acute pancreatXs 10 days after onset. There is considerable motor dysfunction. The duodenal loop is enlarged.
increased motility, segmentation and evanescent areas of spasm (Fig. 10). Diminished pancreatic secretion may contribute to the functional disturbances. Displacement of the duodenojejunal junction and upper jejunum downward and slightly forward may occur. Small bowel obstruction is quite rare. Localized paralytic ileus, as indicated by gaseous dilatation of the upper jejunum, has been designated as the “sentinel loop. “6 If the ileus becomes generalized, it will involve the lower jejunum and the ileum as well.
Roentgen Manifestations Involving the Biliary Tract Opaque calculi may be seen in the gallbladder, cystic or common duct, or near the ampulla of Vater. The gallbladder is not usually enlarged. In a later stage, a pancreatic abscess or an extrapancreatic collection may rupture into the biliary tract.
Roentgen. Manifestations lnvolving
the General Peritoneal Cavity
Varying amounts of exudate may be present in the peritoneal cavity. This is indicated by a uniformly increased density throughout the abdomen and absence of normal organ outlines because of inflammatory changes in the surrounding fat. The properitoneal fat layer will generally disappear. The stomach, small bowel and colon, including the rectum, will usually exhibit gaseous distention (adynamic ileus) .
234
M.
H.
POPPEL
Irregular, rounded, mottled areas of increased density 1 to 3 cm. in diameter scattered throughout the abdomen have been observed on the plain roentgenogram in a case of acute pancreatitis. Z There were no associated calcifications. At operation and at autopsy it was found that these densities represented intra-abdominal fat necrosis and saponification. Similar changes are occasionally seen in the abdominal wall.?’ Roentgen Manifestations
Involving
the Abdominal
Wall and Other Soft Tissues
In acute pancreatitis, the lateral margin of the left psoas and quadratus lumborum muscles may become indistinct because of local edema or fluid in the peritoneal cavity. This may be associated with bulging of the flanks and of the anterior abdominal wall. Postoperatively a fistulous communication from the pancreatic area to the anterior abdominal wall may result. Soft-tissue calcifications have been described in other areas, such as the thighs and legs, in patients with chronic pancreatitis.315J0 Roentgen Manifestations
Involving
the Left Kidney
Along with indistinctness of the left psoas shadow, the left kidney outline may be obscured. This may result from inflammation of the surrounding fat. Occasionally pressure from an extrapancreatic mass may displace the kidney downward or outward, or there may be pressure on the left renal artery and vein, with subsequent impairment of the function of the left kidney. In such instances, hypertension may ensue. If the extrapancreatic mass is large and firm, it may press upon the left ureter and produce urinary tract dilatation above this level. Roentgen Manifestations
Involving
the Diaphragm
and Chest
In the early stages, both hemidiaphragms may show slight elevation and restriction of motion. Later, complete immobility may occur. The changes are usually more pronounced, appear earlier and persist longer on the left side. Linear, horizontal focal patches of atelectasis may be seen in either lung base. Migratory
AspectP
When the acute inflammation extends beyond the confines of the pancreas, localized, space-occupying inflammatory tumefactions or collections may be visualized at a distance. Sometimes this is the initial phase of the disease, masquerading as a local, perinephritic, subphrenic or pelvic abscess, a fistula, a pleurisy, empyema, mediastinal mass, appendicitis, etc. These collections may be seen in the retroperitoneal areas behind the pancreas (Fig. ll), in the lesser omentum between the stomach and liver, in the lesser peritoneal sac, in the gastrocolic ligament between the stomach and transverse colon, or in the subphrenic regions (Fig. 12). In the latter instance, there is elevation of the diaphragm and subsequently a pleural effusion on the involved side. On CCcasion, the effusion may extend into the interlobar fissure. In one of our cases, a right subphrenic abscess perforated the right hemidiaphragm into the right pleural cavity, producing an empyema. In another, a left subphrenic collection eroded through the diaphragm, displaced the esopha-
PANCREATITIS
2.335
gus, and formed mediastinal, pericardial and left pleural collections (Fig. 13). In still another patient, the inflammatory material lysed the diaphragm in the region of the esophageal hiatus and drained into the mediastinum posteriorly to the level of D 4. A large pseudocyst paralleling the esophagus was demonstrated by pancreatography (Fig. 14).
Fig. ll.-Large fluid collection in the region of the tail of the pancreas with downward tail-like projection. Postoperative pancreatogra-
Fig . l&.-Migratory pancreatitis in the left subphrenic space
236
M. H. POPPEL
Fig. 13.-Migratory pancreatitis with displacement of the esophagus as a result of extension
through the diaphragm. There were also left pleural ancl pericardial effus:ons which contained pancreatic enzymes. Note calcifications in the region of the tail of the pancreas (arrow),
The inflammatory material may also drain downward retroperitoneally to the right lower quadrant, producing a perityphlitis. On the left, the material may collect just beyond the pancreatic tail in the region of the hilum of the spleen or extend down the left gutter retroperitoneally for a variable distance, as far as the left iliac fossa, often forming a cyst (Fig. 11). These collections often communicate with the pancreas by a fistulous tract which can usually be filled during operative or postoperative pancreatography.
Roentgen Manifestations Involving the OsseousSystem Circulating enzymes during an attack of acute pancreatitis may cause bone infarction by producing intramedullary fat necrosis.1J,7.“1 Early infarcts show lytic defects in the shafts of the long bones or in the femoral or humeral heads. As will be discussed later, this may eventually lead to the typical appearance of chronic infarction. ROENTGEN
MANIFESTATIONS
OF CHRONIC
INACTIVE
PANCREATITIS
Unfortunately, even after a number of years, chronic pancreatitis may suddenly become activated into the recurrent or relapsing type. This .is especially true if the patient is an alcoholic. However, in many patients the condition
PANCREATITIS
237
Fig. 14.-Migratory pancreatitis. On postoperative pancreatography, a large collection of contrast medium extends from the tail of the pancreas into the mediastinum.
remains quiescent for long intervals or even permanently. The following are the roentgen manifestations of chronic inactive pancreatitis and are simply those of residual disease. I. Calcareous deposits. These include calcifications in the pancreatic parenchyma (Figs. 13 and 15), calculi in the pancreatic ducts, and calcifications in the wall of a pseudocyst or cyst.14 2. Masses. Localized masses in the pancreas or in the parapancreatic area are attributable to cysts or pseudocysts or to fibrosis. Such masses may result in an increase in the midline retrogastric soft-tissue diameter.ll 3. Adhesions. In pancreatitis of long duration, adhesions to the duodenum or stomach (particularly the antrum and the lesser curvature) may be demonstrated. 4. Pancreatogenic steatorrhea. This results in the nonspecific finding of a disordered motor pattern of the small bowel. In the early stages, there is hypermotility and the barium may reach the ileocecal region within 30 minutes. The jejunal folds may be unusually coarse, and wider, flatter and more separated than normal. They may appear as rounded indentures in the margin of the barium shadow. The lumen in some areas may be narrower due to hypertonicity. These changes are most marked in the midthird of the small bowel. In the more advanced stages, hypomotility is the rule, with gastric retention and slow transit of the barium meal, Large, dilated smooth segments of bowel (hypotonicity) alternate with irregular contracted segments so that there is a marked alteration of continuity of the barium column ( segmentation). Flocculation, stippling or scattering produce a granular appearance to the barium lingering behind in the upper loops. The mucosal folds may be greatly reduced in number or, in well-advanced stages, be obliterated with the mucosa of the bowel taking on a smooth appearance. This is best seen in the jejunum.
238
M.
H.
POPPEL
5. Cholangiographic changes. The lower end of the common duct shows an irregular, undulated, tapered narrowing through its parapancreatic portion, while the suprapancreatic segment is dilated in proportion to the resistance at the narrowed segment (Fig. 16). The undulation is very characteristic, The distal end of the duct is often occluded. A stone may be impacted at the distal end or incarcerated in the dilated duct above the zone of stenosis. Peristalsis in the common duct is altered or absent. 6. Changes in the osseous system. The lytic intramedullary areas of bone necrosis seen in the acute cases may now appear as calcified or ossified medullary infarcts (Fig. 17)) or the femoral or humeral heads may show the “snow cap” appearance of articular bone infarction.“,l”
PANCREATITIS
239
Fig. 17.-Chronic
infarction
of the t ibia.
7. Enlargement of the liver. When extensive destruction of the pancreas results, there may occur a lipocaic deficiency ( pancreaticohepatic syndrome) with fatty degeneration of the liver. ROENTGEN MANIFESTATIONS OF CHRONIC PROGRESSIVE RELAPSING PANCREATITIS'
In recent years, the pathologists have increasingly emphasized the continuing, chronic progressive and relapsing nature of this disease as well as its varied manifestations. The clinicians also recognize relapsing pancreatitis as a distinct multifaceted entity. It is sometimes difficult to detect, or even suspect, since the clinical picture may be so diverse. This is especially true in the subclinical. phases. Relapsing pancreatitis is most commonly associated with chronic alcoholism. It is a disease of recurring exacerbations interspersed with intervals of relative clinical quiescence. At times, the roentgen picture may demonstrate the residual changes of previous episodes, such as calcareous deposits, cysts, adhesions, etc., plus the changes attributable to the current acute exacerbation. Of particular significance, however, is the papillary sign (Fig. 18).10,17 The hardness, the calcifications and the adhesions of the pancreas do not permit it to enlarge easily, so that the papillary sign is often the earliest roentgen indication of a sudden acute exacerbation. Occasionally, if the pancreas is able to enlarge, previously visible calculi are seen to spread apart (Fig. 19). Very early in the relapse, the papilla becomes enlarged as the result of edema. If the inflammation is severe, the edema spreads from the papilla and involves the contiguous duodenal mucosa in all directions. The papillary enlargement is always greatest. This papillary edema reflects the underlying inflammatory condition, increasing or decreasing almost daily with the degree of pancreatic inflammation. In a case of known chronic pancreatitis it is almost pathognomanic of a relapse.
M.
Fig. swelling papilla
l&-Relapsing indicates is present.
H.
POPPEL
pancreatitis. Calcareous deposits are present. The papillary exacerbation. Edema of the mucosal folds above and below the There is no significant enlargement of the pancreas. REFERENCES
1. Bank, S., Marks, I. N., Farman, J., and Immelman, E. J.: Further observations on calcified medullary bone lesions in chronic pancreatitis. Gastroenterology 51:224, 1966. 2. Baylin, G. J., and Weeks, K. D.: Some roentgen aspects of pancreatic necrosis. Radiology 42:466, 1944. 3. Blauvelt, H.: A case of acute pancreatitis with subcutaneous fat necrosis. Brit. J. Surg. 34:207, 1946. 4. Comfort, M. W., Gambill, E. E., and Baggenstoss, A. H.: Chronic relapsing pancreatitis: A study of twenty-nine cases without associated disease of the biliary or gastro-intestinal tract. Gastroenterology 6:239, 1946. 5. Gerle, R. D., Walker, L. A., Achord, J. L., and Weens, H. S.: Osseous changes in chronic pancreatitis. Radiology 85:330, 1965.
6. Grollman, A. I., Goodman, S., and Fine, A.: Localized paralytic ileus: An early roentgen sign in acute pancreatitis. Surg. Gynec. Obstet. 91:65, 1950. 7. Immelman, E., Krige, H., and Bank, S.: Radiological changes in bone due to intramedullary fat necrosis in pancreatitis: A preliminary report. Clin. Radiol. 14:273, 1963. 8. Poppel, M. H., and Bercow, C.: The roentgen manifestations of pancrcatitis complicating mumps. Amer. J. Roentgen. 61:219, 1949. 9. Poppel, M. H.: Roentgen Manifestations of Pancreatic Disease. Springfield, Ill.: Charles C Thomas, 1951. 10. Poppel, M. H., Jacobson, H. G., and Smith, R. W.: The Roentgen Aspects of the Papilla and Ampulla of Vater. Springfield, Ill., Charles C Thomas, 1953.
241
PANCREATITIS
Fig. lg.-Chronic ing a relapse. and spreading
relapsing pancreatitis. A. Quiescent There is now enlargement of the duodenal of the previously visualized calcifications.
11. Poppel, M. H., Sheinmel, A., and Mednick, E.: The procurement and critical appraisal of the width diameter of the midsoft tissues. Amer. J. line retrogastric Roentgen. 61:56, 1949. 12. Poppel, M. H., and Marshak, R. H.: The roentgen diagnosis of pancreatic disease. Amer. J. Roentgen. 52:307, 1944. 13. Poppel, M. .H., and Robinson, W. T.: The roentgen manifestations of caisson disease. Amer. J. Roentgen. 76:74, 1956. 14. Poppel, M. H., and Levy, A. H.: Pancreatic lithiasis. Radiology 37: 174, 1941. 15. Poppel, M. H.: Lesions of the pancreas. In Clinical Radiology, Vol. I. Philadelphia: F. A. Davis, 1946. 16. Poppel, M. H.: Some migratory aspects of inflammatory colhotions of pancreatic origin. Radiology 72:323, 1959.
stage. B. Same patient durloop, edema of the mucosa
17. Poppel, M. H.: The roentgen festations of relapsing pancreatitis. ology 62:514, 1954.
maniRadi-
18. Price, C. W. R.: The “colon cut-off” sign in acute pancreatitis. Med. J. Aust. 1: 313, 1956. 19. Schwartz, S., and Nadelhaft, J.: Simulation of colonic obstruction at the splenic flexure by pancreatitis: Roentgen features. Amer. J. Roentgen. 78:607, 1957. 20. Swerdlow, A. B., Berman, M. E., Gibbel, M. I., and Valaitis, J.: Subcutaneous fat necrosis associated with acute pancreatitis. J.A.M.A. 173:765, 1960. 21. Weens, H. S., and Walker, L. A.: The radiologic diagnosis of acute cholecystitis and pancreatitis. Rad. Chn. North Amer. 2 ( 1) : 89, 1964.
Manifestations
of Pancreatitis
By M. H. POPPEL, M.D.
T
HE ROENTGEN MANIFESTATIONS of pancreatitis,g*12T15particularly in the acute stages, are identical whether due to the common nonspecific form or to uncommon specific diseases such as mumps,S tuberculosis, smallpox, etc. To correlate the roentgen manifestations with the clinical aspects and the pathologic states, the roentgen manifestations are described in three stages: ( 1) acute pancreatitis, including the migrate y form, (2) chronic inactive or residual pancreatitis, and (3) chronic progressive relapsing pancreatitis. ROENTGEN MANIFESTATIONS OF ACUTE PANCREATITIS
In any case of acute pancreatitis, roentgen manifestations may vary in type and degree not only among different patients but even in the same patient from hour to hour or day to day. Occasionally roentgen signs may not be evident at all. New changes are seen when one stage of the disease passes into another, or when a complication arises. For example, sudden perforation of the involved pancreas may alter the entire roentgen picture. For purposes of simplification, the signs of acute pancreatitis will be described according to the areas involved. Roentgen Manifestations Involving the Duodenum The first roentgen evidence may be that of a functional disturbance such as a change in motility (usually an increase), altered peristalsis, retroperistalsis, localized transient areas of spasm, irritability and modification of the mucosal pattern. The valvulae conniventes, which normally have a continuously uniform appearance, may show skip areas free of barium, The duodenal loop may be SOirritable that it is difficult to visualize any barium within it. The bulb, with or without gas, may assume a transverse position or may be elevated, slightly displaced toward the right or simply flattened. The papilla of Vater (Fig. 1) may become enlarged as the result of edema (the papillary sign), often even before pancreatic swelling can be detectedlOy” (Fig. 2). If the inflammation is severe, the edema, as evidenced by enlargement of the folds, spreads from the papilla and involves the contiguous mucosa in all directions. However, the papillary enlargement is always greatest. This papillary edema increases and decreases proportionate to the degree of inflammation When the head of the pancreas becomes sufficiently enlarged and the intense inflammation has abated, widening and displacement of the duodenal loop with pressure on its inner concave border may become apparent. This is denoted by a single large, uniform indentation with displacement of the loop toward the right (Fig. 3). Sometimes the perivaterial pancreatic enlargement produces an impression on the medial duodenum resembling a reversed figure 3. M. H. University Radiolngy, SEMINARS
Professor and Chirman, Department of Radiology, New York University Hospital; Consultant in Cenier; Director of Radiology, Bellevue Hospital, New York, N.Y.
POPPEL,
M.D.:
Medical
IN ROENTGENOLOCY,
Vo~.3,No.3
(Ju~~),l968
227
228
M.
H.
POPPEL
Fig. L-Radiographs of barium-coated specimen of normal descending duodenum.
The anatomic specimen was cut along the greater curvature and laid open so that in A, the frontal view, we are looking directly at the papillae on the medial border of the duodenum. In B, the lateral view, we are seeing the profile. The larger arrows point to the major papilla, which measured 1.8 x 0.8 x 0.8 cm.; the smaller arrows point to the minor papilla.
Fig. 2. - Enlarged papilla in early acute pancreatitis. There is
considerable enlargement of the mucosal folds.
229
Fig. L-Widening &d displacement of the duodenal loop with
pressure on its inner concave border. There is also pressure on the greater curvature of the stomach with marked edema of the gastric folds as well as those of the duodenum.
Duodenal ileus, seen as air distention on the plain film, occurs at a still later stage (Fig. 4). The ileus may be limited to the duodenum, involve the surrounding viscera (stomach, jejunum or midtransverse colon) as well, or be part of a generalized ileus. Air-fluid levels in the duodenum may occur. When barium is ingested, considerable amounts are often retained in the dependent portions of the duodenum. In the late stages of acute pancreatitis the entire duodenal loop may become irregularly distorted and obstruction may supervene.
Roentgen Manifestations Involving the Stomach Early in the course of the disease the stomach may be irritable, as shown by intolerance to barium along the greater curvature. When the pancreas enlarges, there is usually elevation of the stomach and flattening of the greater curvature, associated with a slight forward displacement. A localized impression may be seen on the greater curvature (Fig. 3). In some patients there is an actual increase in distance between the stomach and the transverse colon. The gastric mucosal folds are often edematous. When generalized ileus is present, the stomach will be distended with gas and fluid. It then appears atonic and shows no peristaltic activity.
Roentgen Manifestatiom Znvoltiiug the Pancreatic Area Itself In the early stages, a mass may not be visible. Later, there may be increased density in the pancreatic region. In the presence of a gas-producing infection of the pancreas, gas bubbles (Fig. 5) or one or more large air-fluid levels
M.
230
(Fig. 6) may be visualized. a gas-containing abscess. Roentgen Manifestations
Perforation
H.
POPPEL
into a hollow viscus may also result in
Znvolving the Colon
In the earlier stages of acute pancreatitis, there is spasm and irritability of the midtransverse colon (Fig. ‘7)) later involving the left half, and finally the
Fig. 4.-Duodenal
ileus in acute pancre-
atitis.
Fig. 5. - Gasforming infection of the body and
tail of the pancreas. Note multiple small gas above bubbles the ligament of (arrow). Treitz The stomach is displaced upward and medially.
PANCREATITIS
Fig. 6.-Gas abscess of the pancreas with single air-fluid level
above lesser curvature of stomach.
Fig ;. 7‘.-The transverse colon in acute pancreatitis. E:derna, marked irrita-
bility am1 spasrn are seen.
entire transverse colon and splenic flexure. Subsequently, narrowing of the lumen may take place, When the pancreas enlarges or when an abscess presents in the gastrocolic region, depression of the distal transverse colon may be seen. Fistulae between the pancreas and colon may occur (Fig. 8). Should ileus supervene, it may be localized to the transverse colon (Fig. 9) or be of a more generalized distribution. The “colon cut-off” sign in acute pancreatitis indicates adynamic changes in the colon. It consists of an “iso-
232
M.
H.
POPPEL
Fig. GFistula between colon and pancreas visualized by post-
operative pancreatography
lated gaseous distension of the ascending colon and hepatic flexure, with sharp delimitation of the gas shadow just to the left of the splenic flexure.“ls These adynamic changes, which simulate colonic obstruction at the splenic flexure, have also been described by others.19
Roentgen Manifestations Involving the Jeiunum and Ileum In the early stages of acute pancreatitis, spasm and irritability of the upper jejunum occur. As in the duodenum, the mucous membrane may become edematous and present a coarsely feathered appearance. The remaining portion of the jejunum and the ileum may be normal or show functional changes, i.e.,
Fig.
9.-Ileus
of the left side of the transverse
colon in acute pkcreatitis.
2333
PANCREATITIS
Fig. lO.-Small bowel changes in acute pancreatXs 10 days after onset. There is considerable motor dysfunction. The duodenal loop is enlarged.
increased motility, segmentation and evanescent areas of spasm (Fig. 10). Diminished pancreatic secretion may contribute to the functional disturbances. Displacement of the duodenojejunal junction and upper jejunum downward and slightly forward may occur. Small bowel obstruction is quite rare. Localized paralytic ileus, as indicated by gaseous dilatation of the upper jejunum, has been designated as the “sentinel loop. “6 If the ileus becomes generalized, it will involve the lower jejunum and the ileum as well.
Roentgen Manifestations Involving the Biliary Tract Opaque calculi may be seen in the gallbladder, cystic or common duct, or near the ampulla of Vater. The gallbladder is not usually enlarged. In a later stage, a pancreatic abscess or an extrapancreatic collection may rupture into the biliary tract.
Roentgen. Manifestations lnvolving
the General Peritoneal Cavity
Varying amounts of exudate may be present in the peritoneal cavity. This is indicated by a uniformly increased density throughout the abdomen and absence of normal organ outlines because of inflammatory changes in the surrounding fat. The properitoneal fat layer will generally disappear. The stomach, small bowel and colon, including the rectum, will usually exhibit gaseous distention (adynamic ileus) .
234
M.
H.
POPPEL
Irregular, rounded, mottled areas of increased density 1 to 3 cm. in diameter scattered throughout the abdomen have been observed on the plain roentgenogram in a case of acute pancreatitis. Z There were no associated calcifications. At operation and at autopsy it was found that these densities represented intra-abdominal fat necrosis and saponification. Similar changes are occasionally seen in the abdominal wall.?’ Roentgen Manifestations
Involving
the Abdominal
Wall and Other Soft Tissues
In acute pancreatitis, the lateral margin of the left psoas and quadratus lumborum muscles may become indistinct because of local edema or fluid in the peritoneal cavity. This may be associated with bulging of the flanks and of the anterior abdominal wall. Postoperatively a fistulous communication from the pancreatic area to the anterior abdominal wall may result. Soft-tissue calcifications have been described in other areas, such as the thighs and legs, in patients with chronic pancreatitis.315J0 Roentgen Manifestations
Involving
the Left Kidney
Along with indistinctness of the left psoas shadow, the left kidney outline may be obscured. This may result from inflammation of the surrounding fat. Occasionally pressure from an extrapancreatic mass may displace the kidney downward or outward, or there may be pressure on the left renal artery and vein, with subsequent impairment of the function of the left kidney. In such instances, hypertension may ensue. If the extrapancreatic mass is large and firm, it may press upon the left ureter and produce urinary tract dilatation above this level. Roentgen Manifestations
Involving
the Diaphragm
and Chest
In the early stages, both hemidiaphragms may show slight elevation and restriction of motion. Later, complete immobility may occur. The changes are usually more pronounced, appear earlier and persist longer on the left side. Linear, horizontal focal patches of atelectasis may be seen in either lung base. Migratory
AspectP
When the acute inflammation extends beyond the confines of the pancreas, localized, space-occupying inflammatory tumefactions or collections may be visualized at a distance. Sometimes this is the initial phase of the disease, masquerading as a local, perinephritic, subphrenic or pelvic abscess, a fistula, a pleurisy, empyema, mediastinal mass, appendicitis, etc. These collections may be seen in the retroperitoneal areas behind the pancreas (Fig. ll), in the lesser omentum between the stomach and liver, in the lesser peritoneal sac, in the gastrocolic ligament between the stomach and transverse colon, or in the subphrenic regions (Fig. 12). In the latter instance, there is elevation of the diaphragm and subsequently a pleural effusion on the involved side. On CCcasion, the effusion may extend into the interlobar fissure. In one of our cases, a right subphrenic abscess perforated the right hemidiaphragm into the right pleural cavity, producing an empyema. In another, a left subphrenic collection eroded through the diaphragm, displaced the esopha-
PANCREATITIS
2.335
gus, and formed mediastinal, pericardial and left pleural collections (Fig. 13). In still another patient, the inflammatory material lysed the diaphragm in the region of the esophageal hiatus and drained into the mediastinum posteriorly to the level of D 4. A large pseudocyst paralleling the esophagus was demonstrated by pancreatography (Fig. 14).
Fig. ll.-Large fluid collection in the region of the tail of the pancreas with downward tail-like projection. Postoperative pancreatogra-
Fig . l&.-Migratory pancreatitis in the left subphrenic space
236
M. H. POPPEL
Fig. 13.-Migratory pancreatitis with displacement of the esophagus as a result of extension
through the diaphragm. There were also left pleural ancl pericardial effus:ons which contained pancreatic enzymes. Note calcifications in the region of the tail of the pancreas (arrow),
The inflammatory material may also drain downward retroperitoneally to the right lower quadrant, producing a perityphlitis. On the left, the material may collect just beyond the pancreatic tail in the region of the hilum of the spleen or extend down the left gutter retroperitoneally for a variable distance, as far as the left iliac fossa, often forming a cyst (Fig. 11). These collections often communicate with the pancreas by a fistulous tract which can usually be filled during operative or postoperative pancreatography.
Roentgen Manifestations Involving the OsseousSystem Circulating enzymes during an attack of acute pancreatitis may cause bone infarction by producing intramedullary fat necrosis.1J,7.“1 Early infarcts show lytic defects in the shafts of the long bones or in the femoral or humeral heads. As will be discussed later, this may eventually lead to the typical appearance of chronic infarction. ROENTGEN
MANIFESTATIONS
OF CHRONIC
INACTIVE
PANCREATITIS
Unfortunately, even after a number of years, chronic pancreatitis may suddenly become activated into the recurrent or relapsing type. This .is especially true if the patient is an alcoholic. However, in many patients the condition
PANCREATITIS
237
Fig. 14.-Migratory pancreatitis. On postoperative pancreatography, a large collection of contrast medium extends from the tail of the pancreas into the mediastinum.
remains quiescent for long intervals or even permanently. The following are the roentgen manifestations of chronic inactive pancreatitis and are simply those of residual disease. I. Calcareous deposits. These include calcifications in the pancreatic parenchyma (Figs. 13 and 15), calculi in the pancreatic ducts, and calcifications in the wall of a pseudocyst or cyst.14 2. Masses. Localized masses in the pancreas or in the parapancreatic area are attributable to cysts or pseudocysts or to fibrosis. Such masses may result in an increase in the midline retrogastric soft-tissue diameter.ll 3. Adhesions. In pancreatitis of long duration, adhesions to the duodenum or stomach (particularly the antrum and the lesser curvature) may be demonstrated. 4. Pancreatogenic steatorrhea. This results in the nonspecific finding of a disordered motor pattern of the small bowel. In the early stages, there is hypermotility and the barium may reach the ileocecal region within 30 minutes. The jejunal folds may be unusually coarse, and wider, flatter and more separated than normal. They may appear as rounded indentures in the margin of the barium shadow. The lumen in some areas may be narrower due to hypertonicity. These changes are most marked in the midthird of the small bowel. In the more advanced stages, hypomotility is the rule, with gastric retention and slow transit of the barium meal, Large, dilated smooth segments of bowel (hypotonicity) alternate with irregular contracted segments so that there is a marked alteration of continuity of the barium column ( segmentation). Flocculation, stippling or scattering produce a granular appearance to the barium lingering behind in the upper loops. The mucosal folds may be greatly reduced in number or, in well-advanced stages, be obliterated with the mucosa of the bowel taking on a smooth appearance. This is best seen in the jejunum.
238
M.
H.
POPPEL
5. Cholangiographic changes. The lower end of the common duct shows an irregular, undulated, tapered narrowing through its parapancreatic portion, while the suprapancreatic segment is dilated in proportion to the resistance at the narrowed segment (Fig. 16). The undulation is very characteristic, The distal end of the duct is often occluded. A stone may be impacted at the distal end or incarcerated in the dilated duct above the zone of stenosis. Peristalsis in the common duct is altered or absent. 6. Changes in the osseous system. The lytic intramedullary areas of bone necrosis seen in the acute cases may now appear as calcified or ossified medullary infarcts (Fig. 17)) or the femoral or humeral heads may show the “snow cap” appearance of articular bone infarction.“,l”
PANCREATITIS
239
Fig. 17.-Chronic
infarction
of the t ibia.
7. Enlargement of the liver. When extensive destruction of the pancreas results, there may occur a lipocaic deficiency ( pancreaticohepatic syndrome) with fatty degeneration of the liver. ROENTGEN MANIFESTATIONS OF CHRONIC PROGRESSIVE RELAPSING PANCREATITIS'
In recent years, the pathologists have increasingly emphasized the continuing, chronic progressive and relapsing nature of this disease as well as its varied manifestations. The clinicians also recognize relapsing pancreatitis as a distinct multifaceted entity. It is sometimes difficult to detect, or even suspect, since the clinical picture may be so diverse. This is especially true in the subclinical. phases. Relapsing pancreatitis is most commonly associated with chronic alcoholism. It is a disease of recurring exacerbations interspersed with intervals of relative clinical quiescence. At times, the roentgen picture may demonstrate the residual changes of previous episodes, such as calcareous deposits, cysts, adhesions, etc., plus the changes attributable to the current acute exacerbation. Of particular significance, however, is the papillary sign (Fig. 18).10,17 The hardness, the calcifications and the adhesions of the pancreas do not permit it to enlarge easily, so that the papillary sign is often the earliest roentgen indication of a sudden acute exacerbation. Occasionally, if the pancreas is able to enlarge, previously visible calculi are seen to spread apart (Fig. 19). Very early in the relapse, the papilla becomes enlarged as the result of edema. If the inflammation is severe, the edema spreads from the papilla and involves the contiguous duodenal mucosa in all directions. The papillary enlargement is always greatest. This papillary edema reflects the underlying inflammatory condition, increasing or decreasing almost daily with the degree of pancreatic inflammation. In a case of known chronic pancreatitis it is almost pathognomanic of a relapse.
M.
Fig. swelling papilla
l&-Relapsing indicates is present.
H.
POPPEL
pancreatitis. Calcareous deposits are present. The papillary exacerbation. Edema of the mucosal folds above and below the There is no significant enlargement of the pancreas. REFERENCES
1. Bank, S., Marks, I. N., Farman, J., and Immelman, E. J.: Further observations on calcified medullary bone lesions in chronic pancreatitis. Gastroenterology 51:224, 1966. 2. Baylin, G. J., and Weeks, K. D.: Some roentgen aspects of pancreatic necrosis. Radiology 42:466, 1944. 3. Blauvelt, H.: A case of acute pancreatitis with subcutaneous fat necrosis. Brit. J. Surg. 34:207, 1946. 4. Comfort, M. W., Gambill, E. E., and Baggenstoss, A. H.: Chronic relapsing pancreatitis: A study of twenty-nine cases without associated disease of the biliary or gastro-intestinal tract. Gastroenterology 6:239, 1946. 5. Gerle, R. D., Walker, L. A., Achord, J. L., and Weens, H. S.: Osseous changes in chronic pancreatitis. Radiology 85:330, 1965.
6. Grollman, A. I., Goodman, S., and Fine, A.: Localized paralytic ileus: An early roentgen sign in acute pancreatitis. Surg. Gynec. Obstet. 91:65, 1950. 7. Immelman, E., Krige, H., and Bank, S.: Radiological changes in bone due to intramedullary fat necrosis in pancreatitis: A preliminary report. Clin. Radiol. 14:273, 1963. 8. Poppel, M. H., and Bercow, C.: The roentgen manifestations of pancrcatitis complicating mumps. Amer. J. Roentgen. 61:219, 1949. 9. Poppel, M. H.: Roentgen Manifestations of Pancreatic Disease. Springfield, Ill.: Charles C Thomas, 1951. 10. Poppel, M. H., Jacobson, H. G., and Smith, R. W.: The Roentgen Aspects of the Papilla and Ampulla of Vater. Springfield, Ill., Charles C Thomas, 1953.
241
PANCREATITIS
Fig. lg.-Chronic ing a relapse. and spreading
relapsing pancreatitis. A. Quiescent There is now enlargement of the duodenal of the previously visualized calcifications.
11. Poppel, M. H., Sheinmel, A., and Mednick, E.: The procurement and critical appraisal of the width diameter of the midsoft tissues. Amer. J. line retrogastric Roentgen. 61:56, 1949. 12. Poppel, M. H., and Marshak, R. H.: The roentgen diagnosis of pancreatic disease. Amer. J. Roentgen. 52:307, 1944. 13. Poppel, M. .H., and Robinson, W. T.: The roentgen manifestations of caisson disease. Amer. J. Roentgen. 76:74, 1956. 14. Poppel, M. H., and Levy, A. H.: Pancreatic lithiasis. Radiology 37: 174, 1941. 15. Poppel, M. H.: Lesions of the pancreas. In Clinical Radiology, Vol. I. Philadelphia: F. A. Davis, 1946. 16. Poppel, M. H.: Some migratory aspects of inflammatory colhotions of pancreatic origin. Radiology 72:323, 1959.
stage. B. Same patient durloop, edema of the mucosa
17. Poppel, M. H.: The roentgen festations of relapsing pancreatitis. ology 62:514, 1954.
maniRadi-
18. Price, C. W. R.: The “colon cut-off” sign in acute pancreatitis. Med. J. Aust. 1: 313, 1956. 19. Schwartz, S., and Nadelhaft, J.: Simulation of colonic obstruction at the splenic flexure by pancreatitis: Roentgen features. Amer. J. Roentgen. 78:607, 1957. 20. Swerdlow, A. B., Berman, M. E., Gibbel, M. I., and Valaitis, J.: Subcutaneous fat necrosis associated with acute pancreatitis. J.A.M.A. 173:765, 1960. 21. Weens, H. S., and Walker, L. A.: The radiologic diagnosis of acute cholecystitis and pancreatitis. Rad. Chn. North Amer. 2 ( 1) : 89, 1964.