Кт картина калькулезного панкреатита
Калькулезным панкреатитом называется разновидность хронического воспаления поджелудочной железы, при которой в протоке образуются конкременты (камни). Хронический панкреатит часто сочетается с желчнокаменной болезнью и требует радикального лечения. В поджелудочной железе синтезируются ферменты (трипсин, химотрипсин, липаза, протеаза) и гормоны (глюкагон, инсулин), которые участвуют в обменных процессах и пищеварении. Панкреатит приводит к нарушению их выработки. При остром воспалении она усиливается, а при хроническом — снижается.
В поджелудочной железе синтезируются ферменты (трипсин, химотрипсин, липаза, протеаза) и гормоны (глюкагон, инсулин), которые участвуют в обменных процессах и пищеварении.
Основные причины
Главными причинами развития этой патологии являются:
- Желчнокаменная болезнь. Изначально поражается желчный пузырь. На фоне этого повышается давление в протоках, что отражается на состоянии поджелудочной.
- Регулярное употребление спиртных напитков. Этанол и продукты его распада оказывают токсическое воздействие на паренхиму органа.
- Заброс желчи в протоки поджелудочной железы.
При регулярном употребление спиртных напитков, этанол и продукты его распада оказывают токсическое воздействие на паренхиму поджелудочной, что может спровоцировать калькулезный панкреатит.
В качестве предрасполагающих факторов выступают:
- повышенное содержание триглицеридов в крови;
- непроходимость сфинктера Одди;
- рубцовые изменения тканей в области сосочка 12-перстной кишки;
- аутоиммунные нарушения;
- курение;
- муковисцидоз (поражение желез внешней секреции);
- повышение уровня кальция в крови;
- прием лекарств, нарушающих холестериновый обмен (цефалоспоринов, аналогов соматостатина, эстрогенов, фибратов);
- ожирение;
- заболевания кишечника;
- оперативные вмешательства;
- избыток в меню острой и жирной пищи;
- переедание;
- употребление пищи 1-2 раза в день с большими интервалами;
- изменение химического состава желчи.
Одним из фактором риска образования камней в протоке органа при панкреатите является пожилой возраст.
Факторами риска образования камней в протоке органа при панкреатите являются инфекционные заболевания (бактериальные, вирусные, паразитарные) и пожилой возраст.
В меню вводят при панкреатите макароны только из высшего сорта пшеницы.
Симптомы
Признаками заболевания являются:
- Боль. Локализуется слева в подреберье или верхней части живота. Реже бывает опоясывающей. Может протекать по типу желчной колики. Иррадиирует в грудную клетку слева и спину. Сопровождается признаками нарушения процесса переваривания пищи. Усиливается при погрешностях в питании и после употребления спиртных напитков. Чаще всего тупая и ноющая, но может быть колющей и режущей.
- Тошнота.
- Рвота. Бывает неоднократной. Во время рвоты может выделяться желчь.
- Изжога.
- Горькая отрыжка.
- Вздутие живота вследствие повышенного образования газов на фоне нарушения синтеза ферментов.
- Чередование жидкого стула с запором. При хроническом панкреатите стул часто содержит остатки непереваренной пищи и много жиров, от чего он трудно смывается и имеет блеск. При развитии воспаления на фоне желчнокаменной болезни и застое желчи с развитием желтухи фекалии могут обесцвечиваться.
- Снижение аппетита.
- Желтушный оттенок кожи.
- Сухость кожных покровов.
- Красно-синюшные пятна в области живота и груди.
- Болезненность живота в верхней его части.
Иногда при панкреатите отмечается увеличение печени и селезенки.
Диагностика
При наличии жалоб требуются консультация гастроэнтеролога и комплексное обследование органов пищеварительного тракта. Для выявления панкреатита понадобятся:
- УЗИ органов брюшной полости;
- компьютерная томография;
- эндоскопическая ультрасонография (исследование с помощью ультразвуковых волн с применением эндоскопа и датчика);
- ретроградная холангиопанкреатография (контрастное исследование);
- общий и биохимический анализы крови;
- анализ мочи и каловых масс;
- функциональные тесты;
- сцинтиграфия (исследование с применением радиоактивных изотопов);
- опрос пациента;
- пальпация живота;
- перкуссия (простукивание различных участков туловища);
- выслушивание сердца и легких;
- измерение давления, пульса и частоты дыхания.
УЗИ органов брюшной полости используется для выявления калькулезного панкреатита.
При данной форме панкреатита возможны следующие изменения в лабораторных показателях:
- повышение активности эластазы и трипсина в крови;
- повышение концентрации билирубина в крови;
- незначительное повышение СОЭ;
- лейкоцитоз;
- высокое содержание холестерина в крови;
- повышение щелочной фосфатазы.
УЗИ и томография позволяют обнаружить известковые отложения (камни) в просвете поджелудочной железы, протоков и желчного пузыря. Для исключения патологии желудка может проводиться ФЭГДС (осмотр при помощи зонда с камерой).
Дифференциальная диагностика проводится с холециститом, гастритом, язвенной болезнью, опухолями, болезнью Крона и язвенным колитом.
Лечение калькулезного панкреатита
Главный метод лечения панкреатита данной формы — хирургический. Схема терапии определяется врачом. Чаще всего требуется госпитализация.
Главный метод лечения калькулезного панкреатита — хирургический.
Медикаментозная терапия
При лечении панкреатита применяются:
- спазмолитики (Но-шпа, Дротаверин, Дюспаталин);
- анальгетики;
- НПВС;
- антибиотики (назначаются для профилактики инфекционных осложнений);
- желчегонные;
- дезинтоксикационные средства.
При остром калькулезном воспалении поджелудочной железы, когда выработка ферментов усилена, могут назначаться ингибиторы протеаз. Нередко применяются препараты, снижающие уровень сахара в крови.
Желчегонные при панкреатите с камнями могут назначаться только при функционирующем желчном пузыре. Они противопоказаны при выраженном нарушении функции поджелудочной железы. К желчегонным относятся: Урдокса, Урсосан и Урсофальк.
Ферменты (Микразим, Пангром, Креон) использовать в острую стадию заболевания нельзя. Данные лекарства назначаются только при ферментативной недостаточности на фоне хронического панкреатита.
Ферменты принимаются во время еды при отсутствии болевого синдрома.
Физиопроцедуры
При панкреатите может проводиться физиотерапия. Наиболее эффективны: диатермия, парафинолечение и УВЧ-терапия. Физиопроцедуры показаны после проведения хирургического вмешательства.
После хирургического лечения калькулезного панкреатите показана физиотерапия.
Диета
В период обострения нужно воздержаться от приема пищи. Лечебное питание допускает питье негазированной воды, киселя, рисового отвара, травяных настоев и отвара шиповника. Через несколько дней назначается лечебный стол №5. Целями подобной диеты являются щажение поджелудочной железы и улучшение отхождения желчи.
Из меню нужно убрать продукты, которые содержат холестерин, пурины, эфирные масла и щавелевую кислоту.
Рацион обогащается продуктами, содержащими витамины, липотропные вещества, пектин и пищевые волокна. Блюда запекают, отваривает или тушат. Нельзя употреблять жареную, копченую, маринованную и соленую пищу.
Режим приема пищи — 5-6 раз в день маленькими порциями с одинаковыми промежутками. Перед употреблением продукты рекомендуется измельчать или протирать. Блюда при панкреатите должны быть комнатной температуры.
При проблемах с поджелудочной больному назначается лечебный стол №5.
При воспалении и камнях в поджелудочном органе разрешены к употреблению:
- вчерашний, подсушенный хлеб;
- сухой бисквит;
- постная рыба;
- морепродукты;
- нежирное мясо (птица, кролик);
- молочные и овощные супы без приправ;
- кисломолочные продукты, включая нежирный творог;
- неострый сыр;
- растительное и сливочное масла;
- крупы;
- белковый омлет;
- овощи;
- сухофрукты;
- некоторые орехи;
- запеченные яблоки;
- овощные соки;
- зеленый чай;
- зелень (петрушка, укроп).
Продукты разрешенные при калькулезном панкреатите.
Запрещены к употреблению при панкреатите:
- кондитерские и изделия из сдобного теста;
- газированные и алкогольные напитки;
- колбасы;
- консервы;
- маринады;
- соления;
- жирные продукты;
- яичный желток;
- майонез;
- чипсы;
- сало;
- наваристые супы;
- грибы;
- сметана;
- ряженка;
- жирный творог;
- сливки;
- субпродукты;
- щавель;
- шпинат;
- редька;
- зеленый лук;
- редис;
- чеснок;
- шоколад;
- крепкий кофе;
- соусы;
- мороженое;
- прохладительные напитки;
- макаронные изделия.
Диеты при панкреатите нужно придерживаться около месяца.
Операция
При обтурации (закупорке) протока поджелудочной железы показано хирургическое вмешательство. Операции бывают эндоскопическими и открытыми. Первые являются наиболее щадящими и менее травматичными. При необходимости требуется наркоз. Могут проводиться следующие вмешательства:
- резекция поджелудочной железы;
- дренирование протоков;
- папиллосфинктеротомия;
- формирование анастомоза;
- удаление нежизнеспособных тканей;
- холецистэктомия (полное удаление желчного пузыря).
Операция является наиболее эффективным методом лечения заболевания.
Народные средства
Дополнением к операции и лекарственной терапии являются народные средства в виде травяных настоев, отваров и настоек.
Дополнением к операции и лекарственной терапии панкреатита являются народные средства в виде травяных настоев, отваров и настоек.
При панкреатите с камнями эффективны:
- свежий картофельный сок;
- отвар овсяных зерен;
- отвар на основе листьев черники и стручков фасоли;
- отвар шиповника.
При воспалении поджелудочной железы полезны следующие растения:
- семена укропа;
- перечная мята;
- боярышник;
- бессмертник;
- ромашка аптечная;
- корни одуванчика;
- фиалка трехцветная;
- анис;
- чистотел;
- кукурузные рыльца.
При воспалении поджелудочной железы полезен настой полыни горькой, употреблять его следует перед приемом пищи.
Можно приготовить настой полыни горькой. Для этого понадобится 1 ч. л. сушеного растения и 1 стакан кипятка. Данный настой нужно выпить в течение суток, разделив на равные порции. Употребляют его перед приемом пищи.
Осложнения
Наиболее частыми осложнениями панкреатита данного вида являются:
- колика;
- присоединение инфекции;
- возникновение абсцессов;
- панкреонекроз;
- перитонит;
- шоковое состояние;
- желтуха;
- скопление жидкости в паренхиме органа или в брюшной полости;
- полиорганная недостаточность;
- портальная гипертензия;
- внутреннее кровотечение;
- прободение протока или стенки железы камнем;
- флегмона клетчатки;
- энцефалопатия;
- синдром диссеминированного внутрисосудистого свертывания.
Одним из наиболее частых осложнений калькулезного панкреатита является панкреонекроз.
При отсутствии должной помощи возможен летальный исход. Осложнения при панкреатите чаще всего возникают при несоблюдении диеты, невозможности исключить прием алкоголя, отказе от операции и позднем обращении к врачу.
Прогноз
На прогноз при данной патологии влияют следующие факторы:
- правильность и своевременность лечения;
- наличие сопутствующих заболеваний;
- возраст больных.
При хроническом панкреатите и отсутствии терапии прогрессируют дистрофические изменения. Возможны кальцификация и склероз железы. При соблюдении всех рекомендаций гастроэнтеролога прогноз чаще всего благоприятный.
Особенности
Панкреатит с камнями различной этиологии имеет свои особенности.
Наиболее часто диагностируется воспаление железы в сочетании с желчнокаменной болезнью.
Калькулезный панкреатит и холецистит
Калькулезным холециститом и панкреатитом чаще страдают женщины. Камни бывают холестериновыми (выявляются в 80% случаев) и пигментными.
Калькулезным холециститом и панкреатитом чаще страдают женщины.
При сочетании панкреатита с холециститом часто возникает желчная колика. Это острый болевой синдром. Приступ чаще всего возникает в ночное время. Боль усиливается при вдохе и в положении на левом боку. Беспокоят многократная рвота и общее недомогание. Данное состояние требует неотложной помощи.
Источник
Хронический калькулезный панкреатит. Атрофия тела и хвоста поджелудочной железы, множественные кальцинате в паренхиме и крупные камни в просвете расширенного Вирсунгова протока:
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Author: Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR; Chief Editor: John Karani, MBBS, FRCR
Chronic pancreatitis is characterized by progressive pancreatic damage that eventually leads to impairment of both exocrine and endocrine functions of the pancreas. The most common cause of chronic pancreatitis in Western societies is alcohol abuse. Understanding of the pathogenesis of chronic pancreatitis has improved primarily because of advances in the understanding of the mechanisms responsible for development of pancreatic fibrosis after repeated acute attacks of pancreatic necroinflammation. The pancreatic stellate cells are considered to be the key cells in fibrogenesis, particularly when they are activated by toxic factors such as alcohol, its metabolites, or oxidant stress or by cytokines released during pancreatic necroinflammation.[1, 2]
See the images below of chronic pancreatitis.
Chronic pancreatitis. Plain abdominal radiograph shows coarse calcification in the distribution of the pancreas due to chronic calcific pancreatitis.
Chronic pancreatitis. Plain abdominal radiograph shows calcification in the pancreas associated with osteomalacia secondary to malabsorption. Note the pseudofracture in the right 11th rib (arrow).
Chronic pancreatitis. Nonenhanced axial CT scan through the pancreas shows granular calcification in the pancreas, associated with a 4-cm pseudocyst to the right of the head of the pancreas.
Chronic pancreatitis. Transverse sonogram shows an echogenic, enlarged pancreas with multiple small hyperechoic nonshadowing foci in the pancreas.
Research has focused on the genetic factors that may predispose to chronic pancreatitis. Genes regulating trypsinogen activation/inactivation and cystic fibrosis transmembrane conductance regulator function have received particular attention. Mutations in these genes are now increasingly being recognized for their potential “disease modifier” role in distinct forms of chronic pancreatitis, including alcoholic, tropical, and idiopathic pancreatitis.
Imaging plays an important role in the diagnosis and management of chronic pancreatitis. Treatment of uncomplicated chronic pancreatitis is usually symptomatic and directed toward the relief of pain, malabsorption, and diabetes. Minimally invasive therapy and surgery are generally reserved for complications such as pseudocysts, abscess, and malignancy.[3] Acute pancreatitis and chronic pancreatitis are assumed to be different disease processes, and most cases of acute pancreatitis do not result in chronic disease.
Chronic pancreatitis can be classified into 3 categories:
Chronic calcifying pancreatitis
Chronic obstructive pancreatitis
Chronic inflammatory pancreatitis
Chronic calcifying pancreatitis
Chronic calcifying pancreatitis is invariably related to alcoholism. The earliest finding is precipitation of proteinaceous material in the pancreatic ducts that forms protein plugs that subsequently calcify. The ducts and lobules are initially involved in a random manner, and they are surrounded by normal parenchymal tissue. However, as the disease progresses, these normal areas become more diffuse. The pancreatic ductal epithelium undergoes atrophy, hyperplasia, and metaplasia at the site of the protein plugs. Many of the small pancreatic ductules dilate, while others are obliterated by fibrosis.
The main pancreatic duct shows a chain-of-lakes appearance due to alternating stenoses and dilatation. In approximately 50% of patients with chronic calcific pancreatitis, the pancreatic parenchyma contains cysts of varying sizes (several millimeters to 5 cm). These cysts are lined by cuboidal epithelium and contain pancreatic enzymes. Peripancreatic fibrosis is usually a late finding that involves the portal and/or splenic veins. Peripancreatic fibrosis causes stenosis or occlusion of retroperitoneal lymph channels. Ascites may complicate chronic calcific pancreatitis as a result of portal hypertension or lymphatic obstruction in 1-2% patients.
Chronic obstructive pancreatitis
In chronic obstructive pancreatitis, the prominent histologic changes are periductal fibrosis and subsequent ductal dilatation. These changes are much more focal than those in the other forms, and in most patients, the changes involve only the portion of the pancreas in which ductal drainage is impaired. Diffuse changes may occur, in which the main pancreatic duct or ampulla is obstructed. Although protein inspissation may occur, histologic changes in the ductal mucosa are less common, and calcification is unusual. Moreover, the pancreatic duct is dilated, and the pancreas is normal in size, atrophic, or focally and/or globally enlarged. A variety of factors are implicated in chronic obstructive pancreatitis; these include ductal obstruction due to ampullary stenosis, inflammatory or neoplastic causes, surgical ductal ligation, and fibrosis due to a pseudocyst as a complication of an episode of acute pancreatitis.
Chronic inflammatory pancreatitis
Chronic inflammatory pancreatitis is rare and can affect elderly persons without a previous history of alcohol excess.
Autoimmune pancreatitis
Autoimmune-related chronic pancreatitis is a distinct clinical entity, which may present with signs of acute or chronic pancreatitis, sometimes associated with cholestatic jaundice. On imaging, it may appear as diffuse (duct destructive) or pseudotumoral lesions. These 2 aspects are probably different clinical forms of chronic autoimmune pancreatitis.[4]
Some autoimmune diseases are associated with chronic autoimmune pancreatitis, but not consistently. One such disease involves a bile disorder that is very similar to primary sclerosing cholangitis but is responsive to corticosteroid treatment. Pancreatitis may be associated with Crohn disease and ulcerative colitis and thus provides justification to investigate patients with idiopathic pancreatitis for underlying inflammatory bowel disease. Chronic autoimmune pancreatitis must always be considered in patients with a pancreatic mass that is atypical for carcinoma on imaging or clinical findings. Corticosteroid therapy for 4 weeks in patients with pancreatic adenocarcinoma is probably less harmful than pancreatectomy (or chemotherapy) in patients with chronic autoimmune pancreatitis.
Diagnosis depends on clinical and radiologic findings. The diagnostic value of serologic markers and, especially, autoantibodies must still be clarified.[4]
Preferred examination
Plain radiographs show pancreatic calcification in 25-59% of patients. This feature is pathognomonic for chronic pancreatitis. Gastrointestinal (GI) tract barium testing still has a place in the management of chronic pancreatitis. First, some patients with chronic pancreatitis present with atypical abdominal complaints, and initially, barium studies may be ordered. Second, complications from chronic pancreatitis may cause obvious changes in the GI tract.
Ultrasonography is the first modality to be used in patients presenting with upper abdominal pain, although the direct diagnosis of chronic pancreatitis is not always possible. Sonography can help in determining the cause of chronic pancreatitis (eg, alcoholic liver disease, calculus disease) and in assessing the complications of the disease (eg, pseudocysts, ascites, splenic/portal venous obstruction).[5, 6]
Magnetic resonance imaging (MRI), particularly MR cholangiopancreatography (MRCP), is a noninvasive technique.[7, 8, 9, 10] MRI provides excellent images that may show the changes in the diseased pancreas and the complications of chronic pancreatitis. The use of secretin with MRCP can demonstrate pancreatic exocrine reserve, as well as a “santorinocele” (ie, a dilated Santorini duct seen in pancreas divisum).
CT is excellent for imaging of the retroperitoneum, and it is useful in differentiating chronic pancreatitis from pancreatic carcinoma.[11] Cholangiopancreatography is the most sensitive imaging modality; it is used to show the ductal anatomy directly and when intervention (eg, stricture dilatation, stent placement) is being considered. Angiography is reserved for patients with suspected complications resulting from chronic pancreatitis.
Optical coherence tomography
Optical coherence tomography (OCT) allows high-resolution imaging of tissue microstructures by using a probe inserted into the main pancreatic duct (MPD) through an endoscopic retrograde cholangiopancreatography (ERCP) catheter. Perkins conducted a prospective study to assess the capacity of OCT to differentiate between noncancerous and cancerous lesions in patients with MPD segmental strictures investigated by endoscopic ultrasonography (EUS), with fine-needle aspiration cytology if necessary, and ERCP, followed by brush cytology and OCT scanning.[12]
OCT identified 3-layer architecture in all cases with normal MPD or chronic pancreatitis; in all the neoplastic lesions, the 3-layer architecture was totally subverted, with heterogeneous backscattering of the signal. OCT was 100% accurate in detecting cancer tissue, compared with 66.7% for brush cytology. OCT is therefore feasible with ERCP in cases of MPD segmental stricture and superior to brush cytology in distinguishing noncancerous from cancerous lesions.
Limitations of techniques
On anteroposterior radiographs, the spine may mask small punctate calcifications; therefore, the acquisition of additional oblique or lateral imaging may be indicated.
On sonograms, the pancreas may appear normal even in the presence of advanced disease. In patients who are obese, excessive intraperitoneal gas may obscure the pancreas. Gas overlying the pancreas also can make visualization of the pancreas difficult.
Anatomy
An understanding of pancreatic anatomy is important in delineating the cross-sectional anatomy of the pancreas and the causation of pain in pancreatic disease. The pancreas varies in shape and lies in the anterior pararenal space. The head of the pancreas lies within the curve of the duodenal loop, and the inferior vena cava and right renal vessels lie posteriorly. The common bile duct receives the main pancreatic duct as it passes through the pancreatic head and then drains into the duodenum at the ampulla.
The gastroduodenal artery may be seen anteriorly at the pancreatic head and neck. The head of the pancreas is the most bulbous part of the gland, which then narrows to the neck. The union of the superior mesenteric and splenic veins, which forms the portal vein posteriorly, marks the anatomic position of the pancreatic neck. The pylorus lies anteriorly. The lesser sac lies anterior to the pancreas, whereas the splenic vein runs along its posterosuperior surface. The tail of the pancreas is related to the spleen, left adrenal gland, and upper pole of the left kidney.
Sonograms of the pancreas typically demonstrate a homogeneous echo pattern, and the pancreas is more echogenic than the liver. The pancreatic head measures 2.5-3.5 cm; the body, 1.75-2.5 cm; and the tail, 1.5-3.5 cm. The size of the pancreas varies considerably; therefore, reliance on size alone can lead to diagnostic errors. Generally, the size of the gland decreases with patient age, while echogenicity increases. The pancreas is more echogenic than the liver in 52% of young adults and equally echogenic in 48%. With the use of modern ultrasonographic machines, the main pancreatic duct can be identified in 85% of patients. On sonograms, the normal duct diameter is 1.3 mm ± 0.3. In patients with gallstones, the average diameter is 1.4 mm.
The typical criteria for pancreatic size on CT scans are the following: the head is 23 mm; neck, 19 mm; body, 20 mm; and tail, 15 mm. By using optimal CT techniques, the pancreatic duct can be identified in just more than 50% of the patients. Normally, the pancreatic diameters demonstrated on CT scans vary from 2-4 mm, but the effect of pixel averaging on normal pancreatic duct measurements is significant and can make such measurements unreliable. Errors of 1 or 2 mm may occur.
In most patients, a normal pancreatic duct is seen on images obtained with T2-weighted short-tau inversion recovery MRI sequences and magnetic resonance cholangiopancreatography (MRCP).
Plain radiography
Pancreatic calcifications are a common finding in chronic calcific pancreatitis and are considered pathognomonic for alcoholic chronic pancreatitis. Calcification primarily represents intraductal calculi, either in the main pancreatic duct or in the smaller pancreatic ductal radicles. Calcification is punctate or coarse, and it may have a focal, segmental, or diffuse distribution.
See the radiographic images of chronic pancreatitis below.
Chronic pancreatitis. Plain abdominal radiograph shows coarse calcification in the distribution of the pancreas due to chronic calcific pancreatitis.
Chronic pancreatitis. Plain abdominal radiograph shows calcification in the pancreas associated with osteomalacia secondary to malabsorption. Note the pseudofracture in the right 11th rib (arrow).
Chronic pancreatitis. Upper gastrointestinal tract barium study shows a reverse 3 in the duodenum due to chronic pancreatitis. Pancreatic carcinoma can have a similar appearance.
Chronic pancreatitis. Plain abdominal radiograph shows a common bile duct stent in situ and fairly extensive pancreatic calcification.
Upper GI tract barium series
Even in the age of cross-sectional imaging, upper GI tract barium series may provide information that is critical to the treatment of patients with chronic pancreatitis.
Esophageal involvement rarely occurs in chronic pancreatitis, and obstruction is usually the result of mediastinal extension of a pseudocyst. Pancreatic enlargement or a pseudocyst may compress the stomach. Peripancreatic fibrosis may involve the antrum of the stomach or duodenum, resulting in stenosis. The anatomic proximity of the pancreatic head and stomach antrum is constant, and enlargement of the pancreatic head usually causes effacement of the antrum; this has been termed the pad sign. Chronic pancreatitis may cause gastric nodularity and thickening of the mucosal folds; these findings are most prominent on the posterior aspect.
Gastric varices secondary to splenic venous thrombosis may have similar findings. The C loop of the duodenum may be widened because of mass effect from an enlarged pancreatic head, or it may be present as an inverted 3 sign due to traction on the medial wall of the duodenum. In the duodenum, mucosal changes occur, such as spiculation, flattening, or slight nodularity of the mucosal folds of the medial border of the duodenum or concentric narrowing due to periduodenal fibrosis.
Small-bowel changes infrequently occur in chronic pancreatitis. Displacement and stretching may occur as a result of pseudocysts. Small-bowel changes may occur as a result of exudation of pancreatic enzymes during the early stages of chronic pancreatitis, when the pancreatic secretory function is still intact. The enzymes may affect the mesenteric vessels at their roots, causing small-bowel ischemia, fibrotic stricture, and malabsorption pattern. As a result of the close anatomic relationship between the transverse colon and the pancreas, the pancreatic enzymes have direct access to the colon.
Changes in the colon include thickening of the haustral folds due to mucosal edema and luminal narrowing. These changes are usually confined to the inferior haustral row of the transverse colon and the splenic flexure. Rarely, fistula formation may occur. All 3 of these colon findings are best appreciated on barium enema examination.
Endoscopic retrograde cholangiopancreatography
Earliest changes are observed in side branches of the pancreatic duct, including dilatation without stenosis, dilatation with downstream stenosis, intraluminal mucosal irregularity, and intraluminal filling defects due to protein plugs or calculi. The number of opacified side branches may be reduced in a focal or diffuse manner because of ductal occlusion. (See the image below.)
Chronic pancreatitis. Endoscopic retrograde cholangiopancreatogram shows a dilated common bile duct (CBD) associated with a stricture of the lower CBD (not well shown on this image) and a dilated ectatic tortuous pancreatic duct. A stent was subsequently placed across the CBD stricture.
In late stages of the disease, changes in the main pancreatic duct are prominent and are similar to those in the side branches, such as ductal dilatation with or without stenosis, short segmental narrowing or long strictures, and intraluminal filling defects due to protein plugs or calculi.
The pancreatic duct may show beading or a chain-of-lakes or string-of-pearls appearance because of alternating stenosis and dilatation of the pancreatic duct.
Small (1-2 cm), round or oval, irregular or well-delineated pancreatic parenchymal cavities may be observed.
Occasionally, contrast material may fill large pseudocysts via fistulous communications. Prolonged emptying of contrast material may be observed.
Common bile duct changes are common in chronic pancreatitis. The most common finding is a long, smooth narrowing of the duct, with gradual tapering of the distal segment due to periductal fibrosis.
In 25% patients with chronic pancreatitis, alternating stenosis and dilation may cause the common bile duct to have an hourglass appearance.
Degree of confidence
The sensitivity of plain abdominal radiography in the detection of pancreatic calcification is approximately 80%, which is higher than that of sonography but lower than that of CT. When seen, pancreatic calcification is pathognomonic for chronic pancreatitis. Barium study findings can be specific for GI tract changes secondary to chronic pancreatitis in the appropriate clinical setting.
ERCP is the most sensitive and specific technique for chronic pancreatitis, although it is invasive and may cause an acute episode of pancreatitis and ascending cholangitis.
False positives/negatives
On anteroposterior radiographs, the spine may mask small punctate calcifications; therefore, the acquisition of additional oblique or lateral images may be indicated. Bowel contents may obscure pancreatic calcification, and calcification in the pancreas and pancreatic bed is not specific for chronic pancreatitis. Causes of pancreatic calcification include acute pancreatitis, cavernous lymphangioma, hemangioma, cystic fibrosis, pancreatic hematoma/infarction, cystadenoma and/or cystadenocarcinoma, islet tumors, metastasis, pseudocysts, and kwashiorkor. Calcification in a vascular atheroma, an aortic aneurysm, or branches of the aorta can occasionally be confused with pancreatic calcification on plain abdominal radiographs.
Gastric displacement seen on barium examination is not specific for chronic pancreatitis and may be due to pancreatic carcinoma, a variety of peripancreatic masses (including adrenal gland or renal masses), aortic aneurysms, exophytic gastric or duodenal tumors, lymphoma and other retroperitoneal tumors, mesenteric cysts, splenic masses, or enlargement of the left lobe of the liver. In some patients, nodular mucosal changes on the medial border of the duodenum may be prominent and may mimic pancreatic carcinoma. Thickened gastric mucosal folds are not specific for chronic pancreatitis; similar thickening can occur with pancreatic carcinoma, lymphoma, gastric carcinoma, gastric sarcoidosis, and Ménétrier disease.
Widening of the duodenal loop is reported as a normal variant, but a similar abnormality is reported with aortic aneurysm; choledochal cysts; duodenal hematoma; retroperitoneal lymphadenopathy; retroperitoneal tumors; parasitic disease; and neoplasms of the stomach, colon, and kidney.
Small-bowel changes in chronic pancreatitis may mimic other causes of intestinal ischemia, Crohn disease, and malabsorption. Colonic changes may mimic vascular ischemia, Crohn disease, and primary colonic carcinoma.
Although ERCP findings can be specific in patients with chronic pancreatitis, they may be confused with those of pancreatic carcinoma in 10% of patients. Such confusion may arise with focal forms of chronic pancreatitis, pancreatic carcinoma extending through the entire pancreas, and coexisting chronic pancreatitis and pancreatic carcinoma.
Intraductal papillary mucinous neoplasm (IPMN) may have imaging findings identical to those of chronic pancreatitis, such as main duct and side-chain dilatation. ERCP can be used to differentiate main duct IPMN from chronic pancreatitis, because the former often shows mucin bulging from the ampulla.
Computed Tomography
CT features of chronic pancreatitis that can be visualized on CT scans include dilatation of the main pancreatic duct; calcifications; changes in size, shape, and contour; pseudocysts; and bile duct changes.[13, 14]
See the CT images of chronic pancreatitis below .
Chronic pancreatitis. Nonenhanced axial CT scan through the pancreas shows granular calcification in the pancreas.
Chronic pancreatitis. Enhanced axial CT scan through the pancreas shows a low-attenuating mass at the junction of the head and body of the pancreas due to focal chronic noncalcific pancreatitis.
Chronic pancreatitis. Enhanced axial CT scan through the pancreas (in the same patient as in the previous image) shows a mildly dilated pancreatic duct.
Chronic pancreatitis. Nonenhanced axial CT scan through the pancreas shows granular calcification in the pancreas, associated with a 4-cm pseudocyst to the right of the head of the pancreas.
Chronic pancreatitis. Nonenhanced axial CT scan through the pancreas shows a reverse 3 in the Gastrografin-filled duodenum. Note the patchy attenuation in the head of the pancreas. A contrast-enhanced study was not performed because the patient was allergic to intravenous iodinated contrast material.
Chronic pancreatitis. Nonenhanced axial CT scan through the pancreas shows an enlarged pancreas associated with punctate calcification.
Main pancreatic duct dilatation can be demonstrated, with the width of the main pancreatic duct exceeding 5 mm in the head and 2 mm in the body and tail. CT is the most sensitive and specific modality for depicting pancreatic calcifications, which may be tiny and punctate or larger and coarse. Focal enlargement or atrophy of the pancreas is readily demonstrated on CT scans. Focal enlargement associated with calcification or ductal dilatation in a mass is suggestive of chronic pancreatitis.
Obliteration of the peripancreatic fat, which results in poor definition and an ill-defined pancreatic contour, is usually seen in acute exacerbations of chronic pancreatitis. Obliteration of the fat sleeve around the superior mesenteric artery has been described in both chronic pancreatitis and pancreatic carcinoma.
Obstruction of the common bile duct may be visualized as a gradual tapering of the ductal lumen. By contrast, a pancreatic carcinoma usually results in an abrupt transition of the common bile duct. Vascular complications of chronic pancreatitis are best depicted by contrast-enhanced CT scans. In images of pseudoaneurysms, high-attenuation masses are seen during the arterial phase. Portal and/or splenic vein thrombosis and associated collateral venous channels are better delineated during the portal venous phase of contrast enhancement.
Degree of confidence
Currently, CT is regarded as the imaging modality of choice for the initial evaluation of suggested chronic pancreatitis. The diagnostic features of pancreatic enlargement, pancreatic calcifications, pancreatic ductal dilatation, thickening of the peripancreatic fascia, and bile duct involvement are depicted well on CT scans.
CT is more sensitive than plain radiography and ultrasonography in the depiction of pancreatic calcification. Moreover, CT depicts calcification in the pancreas, and confusion with nonpancreatic calcification is less likely. The accuracy of CT is 59-95%; the wide variation is due to the wide discrepancy in the criteria used for diagnosis and in the quality of CT scanners. CT helps in the diagnosis of atrophy of the pancreas, providing better results than ultrasonography.
Pancreatic pseudocysts and complications associated with pseudocysts, including various organ involvements, infection, hemorrhage with pseudoaneurysm formation, rupture with fistula formation, and gastrointestinal or biliary obstruction, are well depicted on CT. Detection of these complications are important, as they may necessitate prompt intervention or surgery.[13, 15]
False positives/negatives
Chronic pancreatitis and pancreatic carcinoma share many CT features, and occasionally, differentiation may be impossible. Obliteration of the fat sleeve around the superior mesenteric artery has been described in both chronic pancreatitis and pancreatic carcinoma.
Pseudotumoral enlargement around focal pancreatitis with extensive fibrous tissue proliferation usually fails to enhance after the administration of contrast material. This characteristic makes the differential diagnosis of pancreatic carcinoma difficult.
In most patients, a normal pancreatic duct is seen on images obtained with T2-weighted short-tau inversion recovery MRI sequences and magnetic resonance cholangiopancreatography (MRCP). MRCP may depict the characteristic beaded appearance of the pancreatic duct in chronic pancreatitis. Pancreatic duct calculi are depicted as round filling defects. In chronic pancreatitis, fat-suppressed T1-weighted images usually show a loss of signal intensity. This loss is explained by the fact that pancreatic fibrosis decreases the proteinaceous fluid content of the pancreas, resulting in loss of pancreatic signal intensity. Fibrosis is associated with decreased vascularity, which causes decreased pancreatic gadolinium enhancement.
See the magnetic resonance images of chronic pancreatitis below.
Chronic pancreatitis. Transaxial T2-weighted MRI scan through the tail of the pancreas shows a dilated tortuous pancreatic duct (arrow).
Chronic pancreatitis. Magnetic resonance cholangiopancreatogram obtained 24 hours after the placement of a common bile duct stent shows good biliary drainage through the stent. Note the dilated tortuous pancreatic stricture and a downstream stricture in the head of the pancreas (left).
Small punctate pancreatic calcification is difficult to detect by using MRI, but larger calcifications may be seen as foci of a signal void. As a result of its ability to depict fluid, T2-weighted MRI may demonstrate pancreatic and common bile duct irregularities and pseudocysts associated with chronic pancreatitis.
Parenchymal gadolinium enhancement is a useful technique in evaluating focal areas of inflammation. Compared with normal pancreatic segments, inflamed areas have decreased enhancement in the arterial phase and increased enhancement in the equilibrium phase.
Currently, the diagnosis of early chronic pancreatitis is difficult. With future improvement in spatial resolution and with the use of secretin-enhanced pancreatography, the detection of subtle changes of the side branches may allow the earlier noninvasive diagnosis of chronic pancreatitis. Secretin-enhanced pancreatography also has the potential to depict the anatomic relationships of pancreatic ducts and pseudocysts and to aid in the evaluation of pancreatic exocrine function.
Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans.
NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble moving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness.
Degree of confidence
Because of the introduction of faster imaging sequences and phased-array coils, the accuracy of MRCP has improved considerably, although some concern remains regarding the resolution of smaller pancreatic ducts.
Secretin-enhanced MRCP improves the detection of diseased pancreatic ducts when no abnormality can be shown in physiologic conditions. It also provides additional functional information regarding pancreatic exocrine function. As experience grows, MRI imaging, particularly MRCP, may be increasingly used in assessing and screening for chronic pancreatitis.
False positives/negatives
Standard good-quality protocols are important with MRCP; otherwise, poor examination technique may create false lesions, which may increase the frequency of unnecessary ERCP examinations.
Ultrasonography may be useful in depicting the anatomy of the pancreas. Primary findings on abdominal ultrasonography include changes in the size, shape contour, and echotexture of the pancreas (see the images below). Irregular pancreatic contour is seen in 45-60% of patients, focal enlargement is detected in 12-32%, and diffuse enlargement occurs in 27-45%. Peripancreatic fascial thickening and blurring of the pancreatic margins are seen in approximately 15% of patients.[16, 17, 18]
Chronic pancreatitis. Transverse sonogram shows an echogenic, enlarged pancreas with multiple small hyperechoic nonshadowing foci in the pancreas.
Chronic pancreatitis. Longitudinal sonogram through the head of the pancreas (in the same patient as in the previous image) shows an echogenic pancreas with multiple, small, hyperechoic, nonshadowing foci.
Chronic pancreatitis. A 52-year-old woman known to have chronic pancreatitis presented with moderate left upper quadrant pain. Transverse sonogram through the pancreas shows a 4.37-cm pseudocyst in the tail of the pancreas (arrow).
Chronic pancreatitis. Longitudinal sonogram (in the same patient as in the previous image) shows a pseudocyst at the splenic hilum. Doppler sonogram (not shown) showed no signal in the splenic vein.
In early disease, the pancreas may be enlarged and hypoechoic, with ductal dilatation. Later, the pancreas becomes heterogeneous, with areas of increased echogenicity and focal or diffuse enlargement. Pseudocysts may occur, and focal hypoechoic inflammatory masses may mimic pancreatic neoplasia. Calculi and calcification in the gland result in densely echogenic foci, which may show shadow. The pancreatic and common bile ducts may be dilated.
In late stages of the disease, the pancreas becomes atrophic and fibrotic, and it shrinks. These changes result in a small, echogenic pancreas with a heterogeneous echotexture. The pancreatic duct remains dilated and has a beaded appearance because of multipl