Clinical Pancreatology for Practising Gastroenterologists and Surgeons. Группа авторов. Читать онлайн. Newlib. NEWLIB.NET

Автор: Группа авторов
Издательство: John Wiley & Sons Limited
Серия:
Жанр произведения: Медицина
Год издания: 0
isbn: 9781119570141
Скачать книгу
of which splenic vein thrombosis is most prevalent, seen in 10–40% of cases [16,17]. Thrombosis can be seen on noncontrast images, as blood clots are hyperintense compared with blood. Post‐contrast images have even greater diagnostic accuracy as they show nonenhancing filling defects in vessels.

      Pseudoaneurysm develops from vessel wall erosion caused by severe inflammation and pancreatic enzymes. The most common arteries involved are the splenic (40%), pancreaticoduodenal (20%), and rarely gastric and hepatic arteries [18,19]. In the setting of severe acute pancreatitis, reviewing radiologists should vigilantly inspect arteries for possible pseudoaneurysm or bleeding. Post‐contrast dynamic sequences depict pseudoaneurysm as a bulging structure arising from a vessel wall. Hemorrhage will be depicted as high‐density areas on T1‐weighted pre‐contrast images and active bleeding can be seen on post‐contrast images as extravasation of contrast from a vessel.

Photos depict a 61-year-old male referred from an off-site institution due to abdominal pain for a month. His CT examination suggested acute pancreatitis and portal vein thrombosis. (a) Axial T2-weighted image demonstrates an organized complex collection with fistulization to the portal vein. (b) Coronal MRCP image demonstrates fistulization of the collections and entire portal system filled with pancreatic fluid. (c) Post-contrast T1-weighted image demonstrates the walled-off necrosis that replaced the pancreatic parenchyma.

      Sources: (a, c) courtesy of J.E. Domínguez‐Muñoz; (b) Morgan [14]. Reproduced with permission of Elsevier.

      1 1 Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis – 2012: revision of the Atlanta classification and definitions by international consensus. Gut 2013; 62(1):102–111.

      2 2 Tkacz JN, Anderson SA, Soto J. MR imaging in gastrointestinal emergencies. Radiographics 2009; 29:1767–1780.

      3 3 Bamrungchart S, Tantaway EM, Midia EC, et al. Free breathing three‐dimensional gradient echo‐sequence with radial data sampling (radial 3D‐GRE) examination of the pancreas: comparison with standard 3D‐GRE volumetric interpolated breath hold examination (VIBE). J Magn Reson Imaging 2013; 38:1572–1577.

      4 4 Arvanitakis M, Delhaye M, De Maertelaere V, et al. Computed tomography and magnetic resonance imaging in the assessment of acute pancreatitis. Gastroenterology 2004; 126(3):715–723.

      5 5 Manfredi R, Mucelli RP. Secretin‐enhanced MR imaging of the pancreas. Radiology 2016; 279:29–43.

      6 6 Pamuklar E, Semelka RC. MR imaging of pancreas. Magn Reson Imaging Clin North Am 2005; 13(2):313–330.

      7 7 Sandrasegaran K, Tahir B, Barad U, et al. The value of secretin‐enhanced MRCP in patients with recurrent acute pancreatitis. AJR Am J Roentgenol 2017; 208(2):315–321.

      8 8 Zhang XM, Feng ZS, Zhao QH, et al. Acute interstitial edematous pancreatitis: findings on non‐enhanced MR imaging. World J Gastroenterol 2006; 12(36):5859–5865.

      9 9 Balthazar EJ. Acute pancreatitis: assessment of severity with clinical and CT evaluation. Radiology 2002; 223:603–613.

      10 10 Balthazar EJ, Robinson DL, Megibow AJ, Ranson JH. Acute pancreatitis: value of CT in establishing prognosis. Radiology 1990; 174(2):331–336.

      11 11 Balci NC, Bieneman BK, Bilgin M, et al. Magnetic resonance imaging in pancreatitis. Top Magn Reson Imaging 2009; 20:23–30.

      12 12 Sahni VA, Mortelé KJ. The bloody pancreas: MDCT and MRI features of hypervascular and hemorrhagic pancreatic conditions. AJR Am J Roentgenol 2009; 192:923–935.

      13 13 Drake LM, Anis M, Lawrence C. Accuracy of magnetic resonance cholangiopancreatography in identifying pancreatic duct disruption. J Clin Gastroenterol 2012; 46:696–699.

      14 14 Morgan DE. Imaging of acute pancreatitis and its complications. Clin Gastroenterol Hepatol 2008; 6(10):1077–1085.

      15 15 Foster BR, Jensen KK. Revised Atlanta Classification of acute pancreatitis: a pictorial essay. Radiographics 2016; 36(3):675–687.

      16 16 Kamal A, Singh VK, Akshintala VS, et al. CT and MRI assessment of symptomatic organized pancreatic fluid collections and pancreatic duct disruption: an inter reader variability study using the revised Atlanta classification 2012. Abdom Imaging 2015; 40:1608–1616.

      17 17 Mortelé KJ, Mergo PJ, Taylor HM, et al. Peripancreatic vascular abnormalities complicating acute pancreatitis: contrast enhanced helical CT findings. Eur J Radiol 2004; 52:67–72.

      18 18 Mallick IH, Winslet MC. Vascular complications of pancreatitis. JOP 2004; 5(5):328–337.

      19 19 Boudghene F, L’Hermine C, Bigot JM. Arterial complications of pancreatitis: diagnostic and therapeutic aspects in 104 cases. J Vasc Interv Radiol 1993; 4:551–558.

       Thiruvengadam Muniraj1 and Santhi Swaroop Vege2

       1 Section of Digestive Disease, Yale University School of Medicine, New Haven, CT, USA

       2 Mayo Clinic, Rochester, MN, USA

      Acute pancreatitis (AP) is among the most common gastrointestinal causes of hospital admission in the United States, with nearly 250 000 hospitalizations annually at a cost of US$2.6 billion [1]. The incidence of AP is increasing and despite advancement in medical therapies the overall mortality continues to be under 2% [1–3]. Currently, there are no pharmacological therapies existing to treat acute pancreatitis. This chapter focuses on early management of AP in the emergency room within the first few hours of presentation. This includes prompt accurate diagnosis, evaluation for possible etiology, and role of prophylactic antibiotics, urgent endoscopic retrograde cholangiopancreatography (ERCP), nutrition and fluid resuscitation, all very critical for patient outcomes.

      Acute abdominal pain is one of the common complaints among patients presenting to the emergency room. Making an accurate diagnosis and starting appropriate treatment could be challenging. The diagnosis of AP is established by the presence of at least two of the following features: (i) typical abdominal pain; (ii) elevated amylase or lipase greater than three times the upper limit of normal; and/or (iii) characteristic findings on cross‐sectional imaging [4]. In general, patients with AP present with typical mid‐epigastric and/or upper abdominal pain, which sometimes radiates to the back. The intensity of abdominal pain does not correlate with the severity of the disease [5]. However, the presence of two or more systemic inflammatory response syndrome (SIRS) criteria within the first 24 hours may be associated with severe AP [6]. Physical examination findings often include tenderness in the upper abdomen. Late‐stage findings, such as skin discoloration around the umbilicus (Cullen sign) and flank (Grey Turner sign) from retroperitoneal hemorrhage, are uncommon and seen in less than 1% of patients [7]. When considering the diagnosis of AP, emergency room clinicians should order basic laboratory tests including complete blood count, lipase, amylase, liver function tests, blood urea nitrogen, creatinine,