Материал: Advanced Imaging of the Abdomen - Jovitas Skucas

that a thyroidectomy is considered once a diagnosis is confirmed.

One patient with MEN-II also had Hirschsprung’s disease (16); aganglionosis involved the distal 5cm of the rectum. Whether this association is fortuitous is not clear.

von Hippel-Lindau Disease

A relationship probably exists between pancreatic microcystic adenomas and von HippelLindau disease; VHL gene alterations are detected in these tumors both in patients with von Hippel-Lindau disease and in those with sporadic microcystic adenomas. These patients are at increased risk for pancreatic and adrenal neuroendocrine tumors.A not uncommon presentation is with large liver metastases.

Figure 9.5. Traumatic pancreatic rupture (arrow) in a 7–year- old boy. (Courtesy of Algidas Basevicius, M.D., Kaunas Medical University, Kaunas, Lithuania.)

Trauma

A note on definition: surgeons define distal pancreas as that part containing the tail of the pancreas, while proximal means pancreatic head.

A pancreatic injury classification scale, devised by the American Association for the Surgery of Trauma, is outlined in Table 9.1. Other abdominal injuries are common in patients with pancreatic trauma. The exception is with bicycle handlebar injuries, which are a common cause of mechanical pancreatic trauma in children; these tend to produce iso-

Table 9.1. Surgical pancreatic injury scale

* Advanced one grade for multiple injuries, up to grade III. Source: Modified from Moore et al. (17).

lated pancreatic injury and often lead to pseudocysts.

Both clinical and radiologic diagnosis of pancreatic injury is fraught with difficulty. Even in a setting of major pancreatic injury, at times initial physical findings are mild or masked by other trauma. Both CT and ERCP are often necessary to diagnose pancreatic fracture and duct disruption (Fig. 9.5). The most common site for fracture is at the pancreatic head and neck junction.

In many institutions CT is the imaging modality of choice in suspected pancreatic trauma. In both adults and children CT findings of pancreatic trauma can be subtle. At times an adjacent hematoma is the only suggestion of pancreatic injury. A pancreatic laceration, including complete transection, may not be apparent initially with CT. Therefore, with a strong suspicion for pancreatic injury and an unremarkable initial CT, a follow-up study 12 to 24 hours later is often helpful.

A CT finding of fluid (peripancreatic blood) separating the splenic artery or vein from pancreas suggests pancreatic injury. Still, such fluid may also be present in the absence of any pancreatic injury, and thus additional CT findings should be sought.

In general, CT cannot directly detect pancreatic duct injury, although a deep pancreatic laceration suggests duct disruption. Endoscopic

PANCREAS

retrograde cholangiopancreatography is the primary study in evaluating pancreatic duct injury. Nevertheless, to better delineate pancreatic duct injury, one group of Japanese investigators performed repeat CT shortly after completing ERCP, believing that such an approach confirms ERCP findings, detects injuries not identified on ERCP, and excludes injuries in patients with equivocal ERCP (18).

Magnetic resonance pancreatography can detect complete main pancreatic duct disruption, although the literature on this topic is sparse. Current MRCP application is primarily in defining pancreatic ducts not evaluated with ERCP.

Management of children admitted with a diagnosis of pancreatic injury is individualized, keeping in mind that, in the absence of clinical deterioration or major duct injury, a more conservative therapeutic approach has evolved than practiced previously. In children with pancreatic injury a primary consideration of whether to operate or not often depends on the status of the pancreatic duct. Yet even with duct injury the trend is toward more conservative therapy. Anecdotal reports suggest that some transected pancreatic ducts recanalize spontaneously.

Duct disruption in some patients, at times involving a secondary or smaller duct, leads to pseudocyst formation. Classic therapy for traumatic pancreatic pseudocysts is cystogastrostomy or distal pancreatectomy. Children with pancreatic duct disruption and pseudocysts, however, have had successful long-term cyst catheter drainage (19).

Infection/Inflammation

Acute Pancreatitis

Classification

Acute pancreatic inflammation does not lend itself to an easy classification. Since 1963, at least four international symposia have debated this subject and proposed classifications. Among the changes adopted has been a shift in emphasis from pancreatic necrosis to presence of organ failure and inclusion of information obtained from various imaging examinations (inciden-

tally, the terms pancreatic necrosis and necrotizing pancreatitis are used synonymously). Some of the terminology has also been redefined. There now is a distinction between an acute fluid collection that occurs early in acute pancreatitis and often regresses spontaneously and a pseudocyst that requires several weeks to form and has a distinct wall. A pancreatic abscess is defined as an intraabdominal collection of pus near the pancreas that contains little if any necrotic tissue. The term infected pseudocyst has been deleted and this entity is now considered a pancreatic abscess.

The terms hemorrhagic pancreatitis and phlegmon have also been deleted, although the wisdom in deleting the term phlegmon has been questioned. The primary reason for deleting phlegmon was its past imprecise usage. For instance, some physicians interpret phlegmon to mean a sterile process while others place it in the infectious category. Nevertheless, the vagueness of this term is useful during initial evaluation of acute pancreatitis prior to imaging studies; contrast-enhanced CT can then subdivide a phlegmon into interstitial versus necrotizing pancreatitis, while percutaneous aspiration can establish a sterile versus infected collection of fluid. It remains to be seen whether phlegmon will continue to be used in a setting of acute pancreatitis.

Etiology

Congenital Anomaly

Aberrant pancreaticobiliary duct insertions are associated with recurrent pancreatitis. Thus a pancreatic duct inserting into a communicating duodenal duplication or diverticulum and cystic duct insertion close to the ampulla have resulted in pancreatitis. Even a communicating duplication results in stasis, and, in time, calculi form within a duplication. The rare intraluminal duodenal diverticulum is also associated with acute pancreatitis.

Some patients with pancreas divisum develop pancreatitis; therapeutic options in this clinical setting are discussed in the Congenital Abnormalities section.

In the absence of more common etiologies for pancreatitis, especially in a younger patient, aberrant pancreaticobiliary duct communica-

tions and termination should be sought. An MRCP should detect any major duct anomalies and related fluid-filled structures suggesting a duplication. The inability to cannulate the main papilla during ERCP should prompt efforts to cannulate the duct of Santorini.

Bile Duct Related

Acute biliary pancreatitis appears to be more severe; more complications develop and mortality is greater in patients who have an intact gallbladder compared to those who had a previous cholecystectomy.

Choledocholithiasis is a common cause of acute pancreatitis. Although not common, gallstone pancreatitis does occur during pregnancy. Presumably a stone impacts at the ampulla of Vater, but most of these obstructions are transient and the stone passes into the duodenum. About 40% of gallstone pancreatitis recurs within 6 months, with recurrence often associated with stones in the gallbladder, and thus the rationale for performing cholecystectomy once pancreatitis is quiescent.

Clinically it is difficult to differentiate between gallstoneand non–gallstone- associated acute pancreatitis. One useful laboratory test is alanine aminotransferase (ALT) level; a greater than threefold elevation above normal has a strong positive predictive value for acute gallstone pancreatitis.

Admission plasma cholecystokinin levels in patients with gallstone pancreatitis are significantly higher than in patients with other causes of acute pancreatitis (20), although cholecystokinin levels do not correlate with serum bilirubin or pancreatic enzyme levels or severity of acute pancreatitis. Plasma cholecystokinin elevation in gallstone pancreatitis appears to be a result of a transient bile flow disturbance by stones or duct wall edema.

Hemobilia, regardless of cause, is associated with acute pancreatitis.

Anecdotal etiologies of acute pancreatitis include a bile duct suture or clip acting as a nidus, debris from a hepatocellular carcinoma rupturing into the bile ducts, and associations with primary sclerosing cholangitis and duodenal Crohn’s disease. A patient with familial adenomatous polyposis with adenomas in the common bile duct developed relapsing acute pancreatitis (21).

ADVANCED IMAGING OF THE ABDOMEN

Ethanol

Ethanol ingestion is the most common cause of acute pancreatitis in the United States.

Endoscopic Retrograde

Cholangiopancreatography Induced

Endoscopic retrograde cholangiopancreatography is a not uncommon cause of subclinical or mild pancreatitis. Of more importance is that ERCP is an occasional precursor to acute necrotizing pancreatitis, especially if a sphincterotomy is performed. Among 72 consecutive patients with acute necrotizing pancreatitis requiring surgery at the Mayo Clinic, ERCP was implicated in 8% (22); of note is that on admission these post-ERCP patients had higher Acute Physiology and Chronic Health Evaluation (APACHE II) scores, more extensive pancreatic necrosis, and a higher rate of infected necrosis, and they required earlier necrosectomy and developed more enteric fistulas than similar non–ERCP-induced acute necrotizing pancreatitis patients. These post-ERCP patients had a lower mortality rate, but they were significantly younger; nevertheless, all survivors suffered long-term morbidity. The authors postulated that infection introduced during ERCP may account for some of the increased severity of pancreatitis in these patients.

A relationship appears to exist between common bile duct diameter and the subsequent risk of sphincterotomy-induced pancreatitis, with pancreatitis developing more often in patients with a nondilated bile duct.

Infection

Infectious organisms linked to pancreatitis include viral (mumps, measles, Coxsackie, hepatitis B, cytomegalovirus, varicella-zoster virus, herpes simplex virus), bacterial (mycoplasma, legionella, leptospira, salmonella), fungal (aspergillosis), and occasional parasitic infestations (toxoplasmosis, cryptosporidiosis, ascariasis) (23). Even a scorpion bite has been implicated. Acute fatal necrotizing pancreatitis has developed after liver transplantation for fulminant hepatitis B virus infection, presumably due to the hepatitis B virus.

An ascaris roundworm migrating into the pancreatic duct after sphincterotomy and pan-

PANCREAS

creatic stent placement led to acute pancreatitis (24). These worms can be removed with a Dormia basket.

Intrabiliary rupture of a hydatid cyst and the subsequent spill of cyst contents into the bile ducts is a cause of acute pancreatitis; CT and US identify both the liver infection and bile duct debris.

Neoplasm

Pancreatic carcinomas are commonly associated with surrounding pancreatitis, although symptoms related to the cancer tend to predominate.

An occasional papilla of Vater carcinoid or a pancreatic islet cell tumor produces a pancreatic duct stricture and a clinical picture consistent with acute pancreatitis.

Drug Related

Steroids, diuretics, some antibiotics, and even cimetidine are some of the medications implicated in acute pancreatitis. Yet drug-associated pancreatitis is uncommon. Organophosphate insecticide toxicity is a rare cause of pancreatitis. Intranasal snorted heroin is associated with pancreatitis (25).

Vascular

Pancreatic ischemia is not common but does result in pancreatitis. Thus patients undergoing thoracoabdominal aortic aneurysm repair and descending thoracic aorta cross-clamping are subject to pancreatic ischemia and pancreatitis.

Cholesterol crystal embolization to the pancreas has led to necrotizing pancreatitis. Such embolization probably is more common than reported in patients with atherosclerotic vascular disease.

Other Etiologies

Rarer conditions associated with pancreatitis include the vasculitides, hyperlipidemia, ulcerative colitis, chronic renal failure, a peri-Vaterian diverticulum or neoplasm, and even a choledochal cyst. Acute pancreatitis in long-distance runners is more common in women. A rare cause of acute pancreatitis is pancreatic volvulus associated with a hiatal hernia (26).A patient

with duodenal obstruction distal to the papilla occasionally presents with acute pancreatitis; more distal small bowel obstruction is not associated with pancreatitis. Thus an obstructing duodenal carcinoma distal to the papilla of Vater or even an afferent loop obstruction after a gastrectomy and Billroth II gastrojejunostomy has led to acute pancreatitis. Hypercalcemia due to hyperparathyroidism is a known cause of acute pancreatitis. Hypercalcemia secondary to a malignancy, on the other hand, seldom causes acute pancreatitis.

Clinical

Acute injury to the exocrine pancreas and resultant inflammation is the hallmark of acute pancreatitis. Usually the entire pancreas is involved. The pancreas becomes edematous and inflamed, with these changes then spreading to surrounding structures. Pancreatic enzyme release leads to tissue necrosis and hemorrhage. Pancreatic ascites is uncommon in necrotizing pancreatitis.

Typical clinical findings of acute pancreatitis are well known, but unusual presentations abound. At times acute pancreatitis initially is painless, with the patient presenting in shock or coma. Pancreatitis can mask an underlying pancreatic carcinoma. A patient with acute pancreatitis presented with symptoms referable to the scrotum (27); surgical exploration revealed fat necrosis of tunica vaginalis and spermatic cord.

A biliary etiology is most common in patients over the age of 65 years developing acute pancreatitis, and it is more likely to be necrotizing. Age in itself is not a risk factor for complications, but a relationship exists between coexistent diseases such as hypertension, diabetes, and renal failure and subsequent complications. Overall mortality is greater in the elderly.

Encephalopathy due to liver disease is well known. Less commonly encountered is encephalopathy associated with acute pancreatitis.

Traditional laboratory tests of acute pancreatitis consist of serum amylase and lipase levels. These enzyme levels do not correlate with disease severity and in some patients with acute pancreatitis are normal; a better test appears to be serum phospholipase A2 activity, which correlates with the severity of acute pancreatitis and remains high during the severe episode

Figure 9.6. Jaundice due to pancreatitis after laparoscopic cholecystectomy. Postoperative ERCP was unsuccessful. Percutaneous transhepatic cholangiography reveals marked duct dilatation to the level of the superior pancreatic margin. Only a thin channel is evident in the intrapancreatic portion of the common bile duct (arrow). (Courtesy of David Waldman, M.D., University of Rochester.)

(28). In patients with acute pancreatitis, endotoxin in blood and peritoneal fluid is related to subsequent morbidity and mortality, suggesting that the presence of endotoxin identifies patients at high risk early in the course of acute pancreatitis (29). C-reactive protein level is a relatively accurate predictor of pancreatic necrosis.

Clinically, differential diagnoses for acute pancreatitis include bowel ischemia, perforated ulcer, and other intraabdominal catastrophes. Acute pancreatitis can be a difficult diagnosis, especially in a postoperative patient who becomes jaundiced, and more common etiologies for jaundice are generally considered (Fig. 9.6).

Imaging

Serial imaging is useful not only to follow disease progression, but also to detect complications. Once a diagnosis of acute pancreatitis is established, among other questions, imaging should address the following:

2.Is the disease evolving into pancreatic necrosis?

3.Is infection superimposed on pancreatic necrosis?

4.Are other sequelae developing, such as a pseudocyst?

The answers to these questions influence not only further diagnostic testing but also the choice of therapeutic modalities to be employed.

Although pancreatic necrosis can be suspected clinically, it is better identified by imaging and, at times, at surgery. Superimposed infection of necrotic tissue can also be suspected clinically, but the diagnosis is confirmed by imaging-guided percutaneous aspiration and bacteriologic sampling.

Imaging studies tend to be normal in mild pancreatitis. Generally the first abnormal finding is diffuse pancreatic enlargement. When focal, the pancreatic head is most often involved. The pancreatic outline becomes irregular. Further progression leads to necrosis, hemorrhage, and peripancreatic fluid.

Gas within the pancreas is not common in pancreatitis. Rarely, gas is seen in both pancreatic parenchyma and ducts. In general, intrapancreatic gas suggests an underlying abscess. Nevertheless, pancreatic and peripancreatic gas is found in other conditions, such as after recent laparoscopic cholecystectomy.

Pleural effusion is not an early sign of pancreatitis; generally clinical or other CT findings of severe pancreatitis occur first. The presence of a pleural effusion on admission is indicative of severe disease and has a negative prognostic value. Likewise, pancreatic necrosis is more common in patients with pulmonary infiltrates, and these patients also have a higher mortality rate.

Acute exacerbation in a setting of chronic pancreatitis may have few imaging findings. At times the presence of peripancreatic inflammation is the only finding in a patient with clinically severe acute exacerbation, although superimposed changes of chronic pancreatitis are often found.

Computed Tomography

1.Is the etiology due to gallstone disease or aberrant ducts?

Does administration of IV contrast media, such as during CT, worsen the outcome in acute pan-