Материал: Advanced Imaging of the Abdomen - Jovitas Skucas

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creatitis? Using comparable clinical scores at initial diagnosis, studies tend to show that clinical pancreatitis lasts longer in patients who receive contrast as part of a CT study than those who do not, yet most of these studies are retrospective and thus have an inherent bias.

In general, CT provides better detection of peripancreatic inflammation, hemorrhage, and abscesses than US. Dynamic CT aids in defining the extent of necrosis.

The earliest CT finding is diffuse pancreatic enlargement; less often detected is focal enlargement. Computed tomography findings do not always correlate with clinical impression, and even with acute edematous pancreatitis CT can be normal. Also, imaging findings tend to lag behind clinical resolution, especially with phlegmonous pancreatitis when imaging findings can persist for months.

Inflammation evolves into an inflammatory mass, or phlegmon, which upon further damage results in pancreatic necrosis (Fig. 9.7). A

phlegmon usually has a higher CT attenuation than water and is heterogeneous in appearance due to contained blood and debris. Most phlegmons exhibit poor contrast enhancement. Nonenhancing pancreatic tissue on CT is assumed to represent pancreatic necrosis (i.e., dead tissue). Nevertheless, not all nonenhancing tissue represents necrosis. At times follow-up CT reveals enhancement, indicative of viable tissue, in a region that previously did not enhance.

Surrounding tissue inflammation is common and is identified as a hazy peripancreatic thickening of fascial planes. Peripancreatic fat increases in attenuation, and these tissues reveal increased contrast enhancement. Extrapancreatic fluid collections develop with progression in severity, with fluid dissecting along tissue planes to the transverse colon, mesentery, or even spleen and left kidney. Often this fluid is not well defined, has low attenuation, tends to be poorly marginated, and consists of

A

Figure 9.7. Examples of necrotizing pancreatitis. A: CT reveals mild contrast enhancement in the pancreatic head and essentially no enhancement in the body and tail. Fluid surrounds these structures. Pancreatitis resolved only after 8 months. B: CT reveals little enhancement in the pancreatic head and body but mild enhancement in the tail, reflecting extensive necrosis. The portal vein is thrombosed. A nephrogram is evident in the kidneys but no contrast excretion was identified. Vicarious contrast excretion has occurred in the gallbladder. (Courtesy of Patrick Fultz, M.D., University of Rochester.) C: The pancreas in another patient is replaced by a large soft tissue tumor containing gas (arrows). Ascites is also present. (Courtesy of Algidas Basevicius, M.D., Kaunas Medical University, Kaunas, Lithuania.)

B

C

extravasated pancreatic secretions, fat necrosis, edema, and hemorrhage. Colonic wall thickening, often first detected by CT, implies an advanced severity and increased risk for a complicated clinical course (30).

In patients with obliterated perivascular fat planes, a ratio of superior mesenteric artery diameter to superior mesenteric vein diameter is useful in differentiating pancreatitis from pancreatic carcinoma (31); a ratio greater than 1.0 suggests a malignancy.

At times pancreatitis extends to the anterior abdominal wall (Cullen’s sign) or flank (Grey Turner’s sign). Computed tomography findings show that anterior periumbilical extension is not directly related to extensive extraperitoneal inflammation, nor is it related to pseudocyst formation.

Ultrasonography

The role of conventional US in acute pancreatitis is limited. In most patients US can differentiate mild or edematous acute pancreatitis from severe or necrotizing pancreatitis. One established role of US is to detect whether gallstones are present.

In uncomplicated acute pancreatitis endoscopic US often (but not always) shows an enlarged pancreas; the pancreas has either normal echogenicity or is diffusely hypoechoic. Necrotizing pancreatitis presents as a focal hypoechoic tumor with or without interspersed echogenic regions. Endoscopic US can usually differentiate between edematous and necrotizing pancreatitis and will detect peripancreatic fluid, although in some patients it is difficult to detect progression to necrosis using only US criteria.

If needed, US provides guidance for percutaneous interventional procedures.

Magnetic Resonance Imaging

Whether conventional MRI offers any advantage over CT in a setting of acute pancreatitis is debatable. Viable pancreatic tissue can usually be distinguishing from necrosis with either modality. Gas and calcifications are better seen with CT.

In uncomplicated pancreatitis MRI shows a normal or diffusely enlarged pancreas. With more severe involvement the pancreas becomes

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hypointense on fat-suppressed T1-weighted images and is hypointense to normal liver. Decreased enhancement is evident on immediate postgadolinium images. Similar to CT, nonenhancing pancreatic tissue is assumed to represent pancreatic necrosis.

Magnetic resonance cholangiopancreatography is useful for the initial assessment of acute pancreatitis and offers a viable alternative to diagnostic ERCP in these sick patients; therapeutic ERCP can then be performed in those with a correctable abnormality detected by MRCP.

An MRCP is especially valuable in children with acute pancreatitis. Necrosis, pseudocysts, common bile duct dilation, and anomalous pancreaticobiliary ducts can be detected.

Scintigraphy

Leukocyte infiltration of the pancreas is detected by technetium-99m (Tc-99m)– hexamethylpropyleneamine oxime (hexametazime) (HMPAO) leukocyte scintigraphy. In early acute pancreatitis, positive leukocyte scintigraphy suggests a severe course, but the test is also occasionally positive in mild acute pancreatitis. Later in the course of acute pancreatitis, positive Tc-99m-HMPAO leukocyte scintigraphy suggests a superimposed infection, but here also a positive test is not synonymous with infection and is also found with milder inflammation.

Therapy

In Japan, infusion of protease inhibitors is one therapeutic modality used in acute pancreatitis (32); it is not often employed in Europe or North America.

Gallstone Pancreatitis

The evidence suggests that morbidity and mortality are decreased in patients with gallstone pancreatitis if ERCP with stone extraction is performed early in the course. An ERCP not only confirms the diagnosis, but also sphincterotomy and, if possible, extraction of any incriminating stones can be performed. This is a controversial topic; acute pancreatitis can be exacerbated by ERCP. Injection of contrast into the pancreatic duct in experimental animals

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makes acute pancreatitis worse; whether such data can be extrapolated to humans is unknown.

Currently a laparoscopic surgical approach is preferred but timing is controversial. Patients with mild gallstone pancreatitis can safely undergo an operation within the first week or so, but early surgery in severe biliary pancreatitis is associated with increased mortality and morbidity. On the other hand, a prolonged time interval between onset of biliary pancreatitis and subsequent surgery risks a recurrence of pancreatitis.

A prophylactic sphincterotomy can be performed as an alternative to cholecystectomy in patients with gallstone pancreatitis who are at increased surgical risk, such as with severe cardiopulmonary, hepatic, and renal disease. Sphincterotomy decreases the risk of a new episode of acute pancreatitis, although a cholecystectomy is eventually performed in most patients with gallstone-induced pancreatitis.

Necrotizing Pancreatitis

Necrotizing pancreatitis can be defined as necrosis of pancreatic glandular tissue, surrounding fat, interstitial tissue, and associated with regions of hemorrhage. Pancreatitis due to almost any etiology can evolve into pancreatic necrosis, although in many centers pancreatitis due to a biliary etiology predominates.

Infection of necrotic pancreatic tissue is generally considered an indication for surgical debridement. Infection is most often bacterial, especially coliform in origin, but an occasional fungal infection is encountered. Mortality in severe infected pancreatic necrosis is often due to multiorgan failure.

A fluid collection can be defined as not drainable if imaging identifies solid necrotic debris >1cm in diameter. In general, MRI appears to predict drainability better than CT or US.

Endoscopic drainage therapy is feasible in patients with extensive pancreatic necrosis. Resolution can be achieved nonoperatively in some patients by endoscopic drainage via stents and the placement of an intrapancreatic nasobiliary lavage catheter.

Another option is CTor US-guided percutaneous catheter drainage and transcatheter debridement of infected pancreatic necrosis as

the primary means of therapy. Debris is removed during multiple sessions using a combination of large-bore suction catheters, stone baskets, and large amounts of lavage fluid. Results of such drainage are mixed.

Surgeons continue to debate the merits of early versus delayed surgery in severe necrotizing pancreatitis. Some studies suggest no difference in mortality rates between early and delayed surgery (33), but other find delayed necrosectomy superior.

Major hemorrhage is a complication after surgical management of pancreatic necrosis; most often such bleeding is controlled surgically, although in selected patients angiographic therapy is useful.

Prognosis

Several studies have found no differences in clinical course and outcome when patients with acute pancreatitis are subdivided by etiology into the categories (1) alcohol, (2) gallstones, and (3) other, except that pancreatic pseudocysts develop significantly more often in alcoholics than in patients with other etiologies. Another exception to the above is with ERCPinduced acute pancreatitis (see Endoscopic Retrograde Cholangiopancreatography Induced, above). Tissue necrosis and pancreatic failure determine the mortality and morbidity of acute pancreatitis. The overall mortality rate in patients with acute necrotizing pancreatitis increases in those with infection (33).

A number of indexes have been developed to predict the severity and outcome of acute pancreatitis. Clinically, the severity of acute pancreatitis is evaluated using the Ranson prognostic factors, Glasgow, or Hong Kong criteria or the APACHE II score, while imaging relies on contrast-enhanced CT criteria or the Hill classification.

A consecutive series of patients with acute pancreatitis was used to predict the severity acute pancreatitis; the Hong Kong criteria achieved a sensitivity of 52% and specificity of 80%, the Ranson criteria values were 79% and 56%, and the Glasgow score was 83% and 60%, but the best prediction was provided by the APACHE II score (24 hours postadmission), with a sensitivity of 79% and specificity of 82% (34). While a correlation exists between clinical and imaging classifications at the two extremes

of disease, in general the clinical APACHE II score and contrast-enhanced CT criteria do not yield similar results in many of these patients; the APACHE II score appears superior to CT criteria as an indicator of disease severity.

The overall mortality in patients with severe acute pancreatitis is almost 50%.

Focal Pancreatitis

At times acute pancreatitis involves only a portion of the pancreas, with such focal pancreatitis then evolving into chronic changes limited to a segment of the pancreas. A separate description here of focal pancreatitis is not meant to imply that it is a separate disease entity; rather, its importance lies in its mimicry of pancreatic cancer.

An annular pancreas, with pancreatitis limited to the annular portion, has already been discussed. Some descending duodenal stenoses are secondary to focal pancreatitis in the annular segment.

A history of acute or chronic pancreatitis is often lacking in those with focal pancreatitis. Most often focal pancreatitis involves the pancreatic head. Computed tomography shows focal pancreatitis to be hypodense and US reveals hypoechoic tumors. It tends to be hypervascular at angiography.

Groove Pancreatitis

One form of segmental chronic pancreatitis is called “groove pancreatitis.” The groove is located between the pancreatic head, the duodenum, and the common bile duct. Why focal pancreatitis should develop preferentially in this location is puzzling, although this region of the pancreas is drained by the duct of Santorini, and obstruction of this duct or aberrant ducts may play a role. Relation of this entity to focal annular pancreatitis is conjecture.

A typical appearance is a tumor simulating a pancreatic head carcinoma; differentiation between the two entities is difficult at best, and some of these patients undergo resection. Some develop a duodenal stricture.

Magnetic resonance imaging in five patients revealed a sheet-like tumor between the pancreatic head and duodenum (35); these tumors were hypointense relative to the pancreas on T1-

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and isoto slightly hyperintense on T2-weighted images and had delayed contrast enhancement. Histology revealed fibrosis.

Inflammatory Pseudotumor

A number of pancreatic inflammatory pseudotumors have been described. Whether these should be considered a type of focal pancreatitis or as a separate entity is not clear.

Computed tomography detects an inflammatory pseudotumor of the pancreas simply as a large tumor; histology shows a mixed infiltrate of spindle cells, lymphocytes, histiocytes, and plasma cells.

Chronic Pancreatitis

Even repeat bouts of acute pancreatitis do not necessarily lead to chronic pancreatitis. In fact, clinical evidence suggests that chronic pancreatitis is a de novo condition and that acute and chronic pancreatitis should be considered separate diseases.

The most common cause of chronic pancreatitis in North America and Europe is alcohol related.

Classification

No universally acceptable classification of chronic pancreatitis exists. The diagnostic criteria of chronic pancreatitis using ERCP criteria were proposed by the Japan Pancreas Society in 1995 and are used by some. The Marseilles classification defines chronic pancreatitis as continued inflammation of the pancreas associated with irreversible damage. The pancreas may be involved focally or diffusely, and there is loss of both exocrine and endocrine function. Abdominal pain is a constant feature in the vast majority of patients.

Etiology

Many of the etiologies causing acute pancreatitis are also responsible for chronic pancreatitis. Nevertheless, some conditions lead primarily to chronic inflammation (Table 9.2). Aside from cystic fibrosis and hereditary pancreatitis (see Congenital Abnormalities), chronic pancreatitis is rare in children and adolescents. Some families with familial hyperlipidemia, cystic fibrosis,

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Table 9.2. Conditions associated with chronic pancreatitis

Mostly in young patients Hereditary (familial) pancreatitis a1-Antitrypsin deficiency Familial hyperlipidemia

Cystic fibrosis

Familial hyperparathyroidism Congenital syphilis

Idiopathic fibrosing pancreatitis of childhood

Chronic calcific pancreatitis

Tropical calcific pancreatitis

Pancreatitis in severe protein malnutrition

Infection

Viral

Tuberculous pancreatitis

Amebic pancreatitis

Schistosomiasis

Autoimmune pancreatitis

Idiopathic

Associated with Sjögren’s syndrome

Associated with sarcoidosis

Sequelae of pancreatic trauma

Associated with ulcerative colitis

and hyperparathyroidism have a higher than normal prevalence of chronic pancreatitis. a1- Antitrypsin deficiency is typically associated with pulmonary disease; in rare instances it may be associated with chronic pancreatitis.

Chronic pancreatitis has been associated with ulcerative colitis; the several reported patients suggest a possible nonfortuitous relationship between these two entities. The prevalence of chronic pancreatitis is low in primary sclerosing cholangitis, and the occasional synchronous finding is probably by chance. Some cirrhotic patients have ERCP findings consistent with chronic pancreatitis. These changes are found even in nonalcoholic cirrhotic patients.

Clinical

Idiopathic Fibrosing (Autoimmune)

A syndrome of idiopathic fibrosing pancreatitis, also called chronic relapsing pancreatitis of childhood, is a rare form of chronic pancreatitis, often developing in children and young adults. Etiology is unknown, although an

autoimmune basis is postulated. Its relationship to autoimmune hepatitis, a well-established entity, is not clear.

Pain is a common feature. These patients have developed obstructive jaundice, but pancreatic insufficiency is not a prominent feature in this entity.

A curious form of chronic pancreatitis is centered on the pancreatic ducts, called autoimmune pancreatitis, sclerotic pancreatitis and lymphoplasmacytic pancreatitis. Whether these represent the same entity is conjecture. Imaging reveals either a focal pancreatic tumor or the entire pancreas is enlarged and is hypoechoic with US. Pancreatography in patients with autoimmune pancreatitis reveals an irregular and narrowed main pancreatic duct; some patients develop pancreatic duct obstruction. Neither pancreatic duct dilation nor calcifications develop (36). A focal pancreatic tumor, often with pancreatic duct obstruction, is not an uncommon presentation, and surgery for suspected pancreatic cancer is performed. Retroperitoneal fibrosis develops in an occasional patient (37). Resection, often for suspected pancreatic cancer, reveals pancreatic fibrosis and, at times, an eosinophilic infiltrate. Fibrosis, of course, is not limited to this condition and is common in chronic calcifying pancreatitis. Disease often recurs in the remnant pancreas. Their pancreatitis tends to respond to steroid therapy.

An autoimmune mechanism appears to be involved in Sjögren’s syndrome, and the first sign of Sjögren’s syndrome can be evidence of chronic pancreatitis. A not untypical scenario is the patient with a narrowed distal common bile duct believed to be neoplastic in origin, but resection reveals inflammation and fibrosis.

Chronic Obstructive

Duct obstruction with little or no evidence of stones is classified an a separate etiology for chronic pancreatitis. Yet this term is also a descriptive one representing a stage in evolution of chronic pancreatitis due to a number of etiologies, including secondary to inflammation of sphincter of Oddi, acute pancreatitis, or even a malignant tumor. Some patients diagnosed with chronic obstructive pancreatitis do develop ductal stones and, similarly, of those with chronic calcifying pancreatitis not all