Gallium-67 scintigraphy in acute pancreatitis

Acute pancreatitis is a serious surgical problem with a high incidence of mortality. Both ultrasound and X-ray CT have problems in identifying the extent and severity of the disease and the response to therapy. ⁶⁷Ga-citrate has been used in 21 patients with clinically diagnosed acute pancreatitis:9 patients had X-ray CT and 15 had US examination. Gallium scans were more sensitive than X-ray CT and US in detecting the extent and severity of acute pancreatitis. In addition, gallium was helpful to monitor the response to therapy when the scan was repeated at various intervals in three patients. A subtraction technique using ^99mTc-tin colloid and ⁶⁷Ga-citrate was helpful to mask the liver uptake of gallium and clearly identify the extent of acute pancreatitis.     

Gallium-67 scintigraphy in acute pancreatitis

Acute pancreatitis is a serious surgical problem with a high incidence of mortality. Both ultrasound and X-ray CT have problems in identifying the extent and severity of the disease and the response to therapy. 67Ga-citrate has been used in 21 patients with clinically diagnosed acute pancreatitis: 9 patients had X-ray CT and 15 had US examination. Gallium scans were more sensitive than X-ray CT and US in detecting the extent and severity of acute pancreatitis. In addition, gallium was helpful to monitor the response to therapy when the scan was repeated at various intervals in three patients. A subtraction technique using 99mTc-tin colloid and 67Ga-citrate was helpful to mask the liver uptake of gallium and clearly identify the extent of acute pancreatitis.     

Biliary complications of pancreatitis

The biliary complications of pancreatitis include cholestasis, secondary biliary cirrhosis, cholangitis, and pseudocyst or fistula affecting the hepatobiliary system. Of these, the most relevant for radiologists is cholestasis caused by biliary duct stenosis in an inflamed pancreatic head. Radiologic assessment of these complications is based on judicious use of ultrasound, computed tomography, and direct cholangiography. The typical imaging finding of common bile duct stenosis due to chronic pancreatitis is gradual tapered narrowing of the intrapancreatic common bile duct, which can be portrayed by carefully accomplished computed tomography, and ultrasound as well as cholangiography. When combined with clinical assessment, imaging tests can help determine strategies for treatment, which include traditional operations as well as transhepatic, endoscopic, or percutaneous interventions.     

Biliary pleural fistula detected by hepatobiliary scintigraphy

A biliary pleural fistula is a rare complication secondary to trauma, infection, malignancy, biliary disease, malignancies, or percutaneous procedures. Its presence may be suggested by the development of a right pleural effusion in a patient with such history and can be confirmed with a hepatobiliary scan or endoscopic retrograde cholangiopancreatography. Patients are treated with antibiotics and the fistula usually spontaneously closes. If after 2 weeks the fistula persists, percutaneous drainage, sphincterotomy, or biliary stent placement can be performed to promote healing of the fistula. In complicated cases, open thoracic surgery or video-assisted thoracic surgery may be required.     

Biliary scintigraphy. The "hot rim" sign

A new cholescintigraphic finding, the "hot rim" sign, is reported in a case of acute cholecystitis. Local inflammation in the gallbladder fossa may be the cause of this phenomenon.     

Hepatobiliary scintigraphy in acute cholecystitis

Hepatobiliary scintigraphy is a mature imaging technique for evaluation of patients with acute cholecystitis (AC). It is effective in calculous and acalculous forms of AC. The test is used in contemporary medical practice as the arbiter when the findings from screening abdominal ultrasound do not fit a clinical picture. It is also performed in severely ill patients who have AC suspected on other testing, but whose frail condition and high operative risk demand the highest level of certainty. This review, therefore, examines all technique variations of hepatobiliary scintigraphy, offering an approach that may best fit a variety of clinical situations and philosophies on AC.     

Acute pancreatitis: Secondary findings on hepatobiliary scintigraphy

Review of hepatobiliary scintigrams in patients with serologically documented pancreatitis revealed scintigraphic abnormalities in 19 of 21 studies (90%) in 19 patients. Abnormalities included duodenal loop widening (14/21 or 65%) and duodenogastric reflux (10/21 or 48%). Total biliary obstruction was seen in five studies, thereby precluding evaluation of the gastrointestinal phase in these patients. Excluding these, duodenal loop widening and duodenogastric reflux were seen in 88% and 63% of patients respectively. We evaluated three patients in whom initial scans showed obstruction, but repeat examination showed resolution of obstruction following passage of common duct stone, with duodenal loop widening and duodenogastric reflux suggestive of acute pancreatitis. Duodenal loop widening as demonstrated by hepatobiliary scintigraphy is a sign of pancreatic enlargement in acute pancreatitis, whereas duodenogastric reflux appears to be an indirect manifestation of an adjacent inflammatory process.     

Sonography in acute pancreatitis

Noninvasive imaging of the pancreas with sonography and computed tomography has proven to be a major diagnostic advance. This article focuses on the unique contribution of sonography in acute pancreatitis, emphasizing patient selection, scanning technique, and newer sonographic observations regarding extrapancreatic spread of acute pancreatitis. The limitations of sonographic imaging in acute pancreatitis are reviewed and compared with computed tomography.     

Acute pancreatitis: secondary findings on hepatobiliary scintigraphy

Review of hepatobiliary scintigrams in patients with serologically documented pancreatitis revealed scintigraphic abnormalities in 19 of 21 studies (90%) in 19 patients. Abnormalities included duodenal loop widening (14/21 or 65%) and duodenogastric reflux (10/21 or 48%). Total biliary obstruction was seen in five studies, thereby precluding evaluation of the gastrointestinal phase in these patients. Excluding these, duodenal loop widening and duodenogastric reflux were seen in 88% and 63% of patients respectively. We evaluated three patients in whom initial scans showed obstruction, but repeat examination showed resolution of obstruction following passage of common duct stone, with duodenal loop widening and duodenogastric reflux suggestive of acute pancreatitis. Duodenal loop widening as demonstrated by hepatobiliary scintigraphy is a sign of pancreatic enlargement in acute pancreatitis, whereas duodenogastric reflux appears to be an indirect manifestation of an adjacent inflammatory process.     

Biliary tract dilatation in chronic pancreatitis: CT and sonographic findings

The authors retrospectively evaluated 44 patients with chronic pancreatitis to determine (a) what features on computed tomographic and sonographic scans were associated with biliary tract dilatation, (b) how these findings and biliary tract dilatation changed at follow-up, and (c) the correlation between the degree of biliary tract dilatation and the laboratory and histologic findings when available. Twenty-four patients had biliary tract dilatation; of this group 88% had pancreatic calcifications and 75% had a focal mass in the pancreatic head. Sixteen of the 24 patients underwent follow-up studies; in 12 there was no change in the degree of biliary tract dilatation or appearance of the pancreas. The levels of serum alkaline phosphatase and bilirubin were elevated in most of the 24 patients; at follow-up, however, there was no consistent relationship between these values and radiologic findings. Biopsy is recommended for those patients in whom the serum alkaline phosphatase level remains persistently elevated. Four of seven such patients in this study underwent biliary-enteric bypass procedures due to pathologic evidence of cholestasis.     

Lisinopril-induced acute pancreatitis

Drugs are an uncommon but well-recognised cause of acute pancreatitis and new agents of drug-induced pancreatitis continue to be reported. We describe only the 10th reported case of lisinopril-induced pancreatitis in a young female patient.     

Imaging acute pancreatitis

Acute pancreatitis is a common condition (thought to be increasing in incidence worldwide), which has a highly variable clinical course. The radiologist plays a key role in the management of such patients, from diagnosis and staging to identification and treatment of complications, as well as in determining the underlying aetiology. The aim of this article is (i) to familiarise the reader with the pathophysiology of acute pancreatitis, the appearances of the various stages of pancreatitis, the evidence for the use of staging classifications and the associated complications and (ii) to review current thoughts on optimising therapy.The International Symposium on Acute Pancreatitis (AP) in Atlanta defined AP as inflammation of the pancreas with variable secondary involvement of remote organs [1]. The incidence ranges from 5 to 80 per 100 000, with the highest incidence occurring in the USA and Finland [2]. In the UK, the incidence of AP requiring hospital admission has doubled in the past three decades, from 4.9 per 100 000 (1963–1974) to 9.8 per 100 000 (1987–1998) [3]. The severity of AP is highly variable; it can range from mild and self-limiting to fulminant. The latter occurs in 20–30% of all cases of AP and is associated with a protracted clinical course, often complicated by sepsis, multiorgan failure and a mortality rate of up to 50% [1]. It is widely accepted that these two subgroups are separate entities; mild pancreatitis (also known as oedematous AP) rarely progresses to the fulminant necrotising subtype. Clearly, the prognosis and management for these two subgroups of AP are very different. In mild oedematous AP, management is primarily supportive, whereas necrotising AP usually requires care in an intensive unit setting with a combination of surgical and radiological interventions.The commonest aetiological factors for AP are cholelithiasis and alcohol; the former is more prevalent in southern Europe, whereas alcohol-induced pancreatitis is more common in northern Europe. Alcohol is also known to be associated with a higher incidence of acute fulminant pancreatitis [4]. Other less common causes for AP include iatrogenic causes such as endoscopic retrograde cholangiopancreatography (ERCP), abdominal surgery, trauma, congenital pancreatic divisum, hyperlipidaemia, hypercalcaemia and various infections.The initial diagnosis for AP is made clinically from signs and symptoms of an acute abdomen and an elevation of pancreatic enzymes, such as amylase and lipase, in the blood or urine. Once the diagnosis is confirmed, it is usually evident clinically within the first 48–72 h as to whether the condition will be mild or fulminant [5]. Mild pancreatitis is characterised by minimal or absent systemic organ dysfunction and tends to abate by the third day. In contrast, fulminant pancreatitis demonstrates progressive clinical symptoms and signs with associated metabolic and multiorgan dysfunction. Since the 1980s, many clinical scoring systems, such as Ranson''s criteria [6] and the APACHE II (Acute Physiology and Chronic Health Evaluation) score [7], have been used to provide an objective assessment of the severity of pancreatitis.     

Bone scintigraphy in acute intraosseous disc herniation

A 57-year-old woman initially presented with the acute onset of low back pain after gardening. Plain film at that time was reported as showing Scheurmann's disease of the lumbar spine. The pain resolved slowly, but recurred acutely after minimal trauma 5 months later. Bone scintigraphy revealed increased uptake in L4 and L5 around the disc space, thought to be suspicious for discitis. Other blood tests revealed a high alkaline phosphatase level with an elevated bone component. The erythrocyte sedimentation rate and leukocyte count were not elevated. Magnetic resonance imaging (MRI) showed an acute disc herniation of the L4/L5 disc into the lower body of L4 with considerable bone marrow edema. Follow-up imaging showed substantial resolution of marrow edema 18 months later. Acute disc herniation has rarely been reported in the scintigraphic literature and should be kept in mind in such circumstances, particularly in older patients.     

Cross-sectional imaging in acute pancreatitis

Acute pancreatitis is a common disease with potentially serious outcomes. Multiple imaging modalities can be used to evaluate the disease process and its associated complications. Familiarity with the pathogenesis of this disease, indications for imaging, imaging protocols, staging systems, and the strengths and weaknesses of various modalities will help the radiologist optimize patient care.     

Transient splenomegaly in acute pancreatitis

Serial changes in splenic volume of 25 patients (18 men and seven women; 53.4 +/- 20.8 years old, range 25-83) with acute pancreatitis who underwent CT examinations were retrospectively studied. Abdominal CT was performed within 3 days after the onset and there was at least one follow-up CT examination after this time. The percentage changes of splenic volume in the first (4-30 days) and second (31-100 days) follow-up CT were calculated. Splenic volume increased in the first follow-up CT (mean +/- SD: 197.8 +/- 121.0 cm3) compared with the initial CT (124.8 +/- 70.0; p < 0.0001), and then decreased in the second follow-up CT (179.7 +/- 100.7; p < 0.002). The average splenic volume increased 65.5 +/- 88.7% (range -10.4-377.4%) between the initial and first follow-up CT examinations. Five of 25 cases (20%) in whom size of spleen increased more than twice had severe acute pancreatitis (p < 0.05), complicated pseudocyst requiring surgical drainage (p < 0.05), pleural effusion (p < 0.01), splenic vein thrombosis or compression (p < 0.05) and longer hospital stay (p < 0.02) compared with patients with a smaller increase in splenic volume. In conclusion, transient splenomegaly was commonly seen in acute pancreatitis, especially in severe or complicated cases. Congestive splenomegaly caused by obstruction or stenosis of the splenic vein and non-specified acute splenitis were suspected of contributing to the transient splenomegaly.