Acute Pancreatitis

XUE Huiping

Acute Pancreatitis

XUE Huiping

Pancreatitis is an inflammatory process in which pancreatic enzymes autodigest the gland.

√The gland can sometimes heal without any impairment of function or any morphologic changes. This process is known as acute pancreatitis. √It can recur intermittently, contributing to the functional and morphologic loss of the gland, the pathological change referred to as chronic pancreatitis.

√Acute pancreatitis refers to an attack involving a previously normal pancrease.√Chronic pancreatis is applied to an attack involving a previously, permanently damaged pancrease.

√Acute pancreatitis is an acute inflammatory process of the pancreas, with variable involvement of other regional tissue or remote organ systems. √ Although pancreatic function and structure usually return to normal, the risk of recurrent attacks is 20 to 50% unless the precipitating cause is removed. √ The disease includes a broad spectrum of pancreatic disease, which varies from mild parenchymal edema to severe hemorrhagic pancreatitis associated with subsequent gangrene and necrosis.

急性胰腺炎（ acute pancreatitis）是指胰酶在胰腺内激活后引起胰腺组织自身消化的急性化学性炎症。

A sensible classification system separates pancreatitis into mild and severe disease based on physiologic findings, laboratory values, and radiologic imaging.

Mild pancreatitis is not associated with organ dysfunction or complications, and recovery is uneventful. Severe pancreatitis is associated with decreased function of the pancreas, local and systemic complications, and a complicated recovery.

√ 轻型急性胰腺炎是指仅有很轻微的脏器功能紊乱，没有明显腹膜炎体征及严重代谢紊乱等临床表现，临床恢复顺利者。该型病理上绝大多数为水肿型胰腺炎，少数也可有胰腺实质坏死。

Severe pancreatitis is defined as a local complication and/or organ failure.

√重症急性胰腺炎是指急性胰腺炎伴有脏器功能障碍，或出现坏死、脓肿或假性囊肿等局部并发症，或两者兼有。该型病理上绝大多数为坏死型胰腺炎，但少数情况下水肿型胰腺炎也可表现为重症胰腺炎。

Local complications are defined as (1) acute fluid collections;(2) pancreatic necrosis;(3) pancreatic abscess;(4) pancreatic pseudosyst

√ The clinical presentation of acute pancreatitis is variable, from episodes of mild abdominal discomfort alone to a severe illness associated with hypotension, metabolic derangements, sepsis, fluid sequenstration, multiple organ failure or even death.

√ It is always accompanied by an increased concentrations of pancreatic enzymes in blood and in urine.

EtiologyEtiology

Approximately 70-80% of patients either Approximately 70-80% of patients either have gallstones or a history of sustained have gallstones or a history of sustained alcohol abuse. alcohol abuse.

√Choledocholithiasis( 胆总管石病 ) and ethanol abuse account for 70 to 80% of all cases.

√ Gallstones may cause pancreatitis by impacting in the ampulla of Vater.

√ The incidence of gallstone-associated pancreatitis parallels that of cholelithiasis( 胆石症 ): it peaks at ages 50 to 70, and women outnumber men by 2 to 1.

Causes of Acute PancreatitisCauses of Acute PancreatitisObstruction:Obstruction:Biliary tract disease: Biliary tract disease: cholelithiasis, tumor, ascarid, stenosis cholelithiasis, tumor, ascarid, stenosis pancreatic duct obstruction: neoplasms, cysts,pancreas pancreatic duct obstruction: neoplasms, cysts,pancreas

divisum annular pancreas divisum annular pancreas

ampullary stenosis, ampullary stenosis, duodenal diverticulum duodenal diverticulum Duodenal obstructionDuodenal obstructionAlcoholAlcoholHyperlipidemiaHyperlipidemiaHypercalcemiaHypercalcemiaHereditaryHereditaryTrauma:external, operative,ERCPTrauma:external, operative,ERCPIschemia:hypotension,cardiopulmonary bypass, Ischemia:hypotension,cardiopulmonary bypass, atheroembolism,vasculitis atheroembolism,vasculitisInfectious causes: parastic bacterial viral fungalInfectious causes: parastic bacterial viral fungalDrugs:steroids,azathioprine 6-mercaptopurine, Drugs:steroids,azathioprine 6-mercaptopurine, IdiopathicIdiopathic

Obstructive Causes• Choledocholithiasis胆总管石病• Ampullary obstruction by tumor or

sphincter of Oddi hypertension• Choledochocele胆总管囊肿• Periampullary duodenal diverticulum(憩室 )• Pancreas divisum : annular(环状的 )

pancreas• Primary or metastatic pancreatic tumor• Parasites in pancreatic duct: Clonorchis(支睾吸虫 ), Ascaris

Drugs

• azathioprine硫唑嘌呤 /6-mercaptopurine6-巯基嘌呤 ;

• valproic acid丙戊酸 ; • estrogens雌激素 ; • metronidazole灭滴灵，甲硝唑 ; • loop diuretics, including thiazides 噻嗪类 ,

furosemide速尿 ; • pentamidine; • sulfonamides, including sulfasalazine; • methyldopa: L-asparaginase; • tetracyclines, etc.

PathogenesisPathogenesis1.A complicated pathophysiologic process1.A complicated pathophysiologic process

2.Enzyme autoactivation and self-digestion (key 2.Enzyme autoactivation and self-digestion (key

point)point)

3. Many agents participating in the process3. Many agents participating in the process

4. Complete mechanism remaining unknown4. Complete mechanism remaining unknown

Pancreatic self-protective mechanismPancreatic self-protective mechanism1.mucopolysaccharide on pancreatic duct 1.mucopolysaccharide on pancreatic duct

epithelia epithelia

2.proenzyme2.proenzyme

3.pancreatin inhibitor3.pancreatin inhibitor

4.acinus metabolism activity4.acinus metabolism activity

5. Anti-reflux mechanism: oddi’s sphincter 5. Anti-reflux mechanism: oddi’s sphincter

pancreatic duct sphincter pancreatic duct sphincter

Initiation factor in Earlier periodInitiation factor in Earlier periodInitiation factor in Earlier periodInitiation factor in Earlier period

1. 1. Pancreatic Enzyme Abnormally ActivatedPancreatic Enzyme Abnormally ActivatedBile reflux⑴Bile reflux⑴

Bile Bile common channelcommon channel pancreatic duct pancreatic duct 1.hypertension in pancreatic duct1.hypertension in pancreatic duct 2.premature activation of pancreatic enzymes 2.premature activation of pancreatic enzymes

3.injury to the lining of the pancreatic ducts3.injury to the lining of the pancreatic ducts pancreatic edema or necrosis pancreatic edema or necrosis MODS MODS

⑵ ⑵ Duodenal RefulxDuodenal Refulx

duodenal enterokinase pancreatic ductduodenal enterokinase pancreatic duct

trypsinogen trypsintrypsinogen trypsin

elastasnogen elastaseelastasnogen elastase

phospholipasogen phospholipasephospholipasogen phospholipase

lecithin lysolecthin lecithin lysolecthin

2.Alcohol Toxicity2.Alcohol Toxicitystimulate the pancreas to secrete ⑴stimulate the pancreas to secrete ⑴

pancreatic hypertention tiny pancreatic pancreatic hypertention tiny pancreatic

duct and acinus rupture pancreatic juice duct and acinus rupture pancreatic juice

spillage spillage

spasm of the sphinctor of oddi⑵spasm of the sphinctor of oddi⑵

direct injury to pancreas⑶direct injury to pancreas⑶

3.Pancreatic Microcirculation Disorder3.Pancreatic Microcirculation Disorder

systemic hypotension⑴systemic hypotension⑴hyperlipidemia: triglycerides lipase free ⑵hyperlipidemia: triglycerides lipase free ⑵

acid fatty acids injure pancreatic acid fatty acids injure pancreatic

microcirculationmicrocirculation

artheroembolism⑶artheroembolism⑶vasculitis⑷vasculitis⑷

Aggravatiing factors in later periodAggravatiing factors in later periodInfection: pancreatic abscess⑴Infection: pancreatic abscess⑴

Intestinal bacteria translocation⑵Intestinal bacteria translocation⑵

Cytokine and systemic inflammation ⑶Cytokine and systemic inflammation ⑶

reaction syndromereaction syndrome

TNF IL-1 IL-6 PAF MSOFTNF IL-1 IL-6 PAF MSOF

Free radicals⑷Free radicals⑷

PATHOGENESIS

•Premature activation of zymogens( 酶原 ) and the escape of activated enzymes from acinar cells and pancreatic ducts set the stage for the autodigestive process that represents acute pancreatitis.

PATHOGENESIS

•Proteases(蛋白酶 ) released into the blood are inactivated by circulating inhibitors, including α2-macroglobulin( 巨球蛋白 ). α1-antitrypsin(抗胰蛋白酶 ), and the C1-esterase( 酯酶 ) inhibitor.

• In addition, trypsin(胰蛋白酶 ) activates kallikrein(激肽释放酶 ), a peptidase(肽酶 ), which then cleaves several peptides, including bradykinin(缓激肽 ) and kallidin(胰激肽 ), from their inactive precursors in blood plasma.

PATHOGENESIS

PATHOGENESIS

•These peptides, termed kinins(激肽 ), have various deleterious effects including vasodilatation, increased vascular permeability, pain, and neutrophil(嗜中性粒细胞 ) accumulation.

Two mechanisms may trigger pancreatic

autodigestion•zymogen activation within the pancreatic acinar cell.

•increased pancreatic duct permeability

PATHOGENESIS

• After the acinar cell is triggered, it provokes an intense inflammatory response in the pancreas.

• Weeping of pancreatic juice into the peripancreatic space or microperforations of the pancreatic ductal system can lead to pseudocyst formation.

PATHOGENESIS

• Subsequent hypoperfusion to the gland can convert mild edematous/interstitial pancreatitis to necrotizing pancreatitis.

• At this point, release of toxic factors into the systemic circulation, such as trypsin, elastase, phospholipase A2, and platelet activating factor or other cytokines, can lead to cardiovascular and pulmonary collapse.

• The necrotic pancreas can become secondarily infected from hematogenous or transperitoneal sources.

重症胰腺炎是一多因素、累及多环节的疾病。首先是几种致病因素引发胰腺腺泡的损伤，释放多种受激活的胰酶及炎症细胞因子，有多种细胞的过度激活和相互作用，产生氧自由基和炎症介质引起胰腺、腹膜和一些主要器官 (肺、脑 )的血管通透性增加，最后导致了重症胰腺炎及其并发症的发生。

PathologyPathology1.Edematous pancreatitis:1.Edematous pancreatitis:**interstitial edemainterstitial edema*inflammatory cell infiltration of the gland *inflammatory cell infiltration of the gland

parenchyma parenchyma

2.Hemorrhagic or necrotizing pancreatitis2.Hemorrhagic or necrotizing pancreatitis*extensive pancreatic and peripancreatic *extensive pancreatic and peripancreatic fat necrosis fat necrosis *parenchymal necrosis*parenchymal necrosis

Overview of the pancreatic gland

• The pancreatic gland contains three major types of cells.

• The duct cells make up about 10% of the pancreas and secrete solutions rich in bicarbonate.

• The acinar cells comprise over 80% of the pancreas and they synthesize and secrete pancreatic enzymes.

Overview of the pancreatic gland

• The islet cells make up about 10% of the pancreas and form the endocrine portion of the pancreas.

• The four major types of islet cells secrete the hormones insulin, glucagon, somatostatin, and pancreatic polypeptide.

Interstitial• The gross architecture of the gland is

preserved, but it is edematous. • Hemorrhage is absent. • Interstitial edema and inflammatory cells

within the parenchyma are prominent. • Disruption of the normal acinar cell

architecture is common and may contribute to characteristically reduced enzyme secretion.

• Interstitial edema and inflammatory cells within the parenchyma

Hemorrhagic• Macroscopically, marked tissue necrosis

and hemorrhage are apparent. • Surrounding areas of fat necrosis are also

prominent. These are chalky白垩的 areas of dead adipose tissue that are found within the peripancreatic tissue and throughout the abdomen.

• Large hematomas血肿 often are located in the retroperitoneal腹膜后的 space.

Hemorrhagic• The microscopic appearance of the

pancreas parallels the gross changes, with marked fat and pancreatic necrosis.

• Vascular inflammation and thrombosis are common.

Fat necrosis• Fat necrosis seen

at surgery is associated with peripancreatic release of lipase, with hydrolysis of triacylglycerols (triglycerides) to toxic fatty acids.

Clinical PresentationClinical Presentation

•Steady, dull, or boring midepigastric pain associated with nausea and vomiting is the classic presentation of acute pancreatitis.

Abdominal pain Abdominal pain • predominant clinical featurepredominant clinical feature• midepigastrium, in the right or left upper midepigastrium, in the right or left upper

quadrants quadrants• The pain reaches peak intensity within 15 minutes to 1 The pain reaches peak intensity within 15 minutes to 1

hour from onset, in contrast to the more abrupt onset of hour from onset, in contrast to the more abrupt onset of pain with a perforated viscus.pain with a perforated viscus.

• a penetrating pain, radiating to the back (a penetrating pain, radiating to the back (It radiates straight to the midline of the lower thoracic vertebral region in about 50% of patients and is usually worse in the supine position.)

Abdominal painAbdominal pain

• rare patients without abdominal pain but rare patients without abdominal pain but with a severe systemic illnesswith a severe systemic illness ( hypotension, ( hypotension, hypoperfusion and depression of mental hypoperfusion and depression of mental status) ---- status) ---- Painless acute pancreatitis is very rare but carries a grave prognosis because the patients frequently present in shock.

Clinical PresentationClinical Presentation

• Nausea and vomitingNausea and vomiting• Abdominal DistentionAbdominal Distention

resulting from a paralytic ileus arising from resulting from a paralytic ileus arising from retroperitoneal irritation or ascites or a retroperitoneal irritation or ascites or a retroperitoneal phlegmonretroperitoneal phlegmon

• JaundiceJaundice distal common bile duct obstruction by gallstones’ distal common bile duct obstruction by gallstones’ compression of the distal CBD by pancreatic head compression of the distal CBD by pancreatic head edema or by other uncommon findingsedema or by other uncommon findings

Abdominal DistentionAbdominal Distention

•Paralytic ileus(麻痹性肠梗阻 ) with abdominal distention may develop during the first few days, signifying extension of the inflammatory process into the small intestinal and colonic(结肠的 ) mesentery(肠系膜 ).

Clinical Presentation of Sever PancreatitisClinical Presentation of Sever Pancreatitis

• Circulatory Derangements: Circulatory Derangements: hypotention, hypotention, hypovolemia, hypoeffusion hypovolemia, hypoeffusion

circulating myocardial depressant factor⑴circulating myocardial depressant factor⑴ ⑵ ⑵decreased preload to the heartdecreased preload to the heart

reduced systemic vascular resistance⑶reduced systemic vascular resistance⑶sepsis-like syndrome⑷sepsis-like syndrome⑷

hyperdynamic statehyperdynamic stateelevated cardiac outputelevated cardiac outputlowered systemic vascular resistancelowered systemic vascular resistancelowered arteriovenous oxgen differencelowered arteriovenous oxgen difference

Clinical Presentation of Sever PancreatitisClinical Presentation of Sever Pancreatitis

• left pleural effusionleft pleural effusion

• pulmonary failurepulmonary failure tachypnea, dyspnea and cyanosis tachypnea, dyspnea and cyanosis

• cerebral abnormalitiescerebral abnormalities belligerence, confusion, psychosis and coma belligerence, confusion, psychosis and coma

• Turner sign and Cullen sign Turner sign and Cullen sign a bluish color in the flanks or around the a bluish color in the flanks or around the umbilicus, (representing blood dissecting to those umbilicus, (representing blood dissecting to those areas from the retroperitoneum near the pancreas areas from the retroperitoneum near the pancreas along fascial planes)along fascial planes)

• One to 2 weeks after the onset, large ecchymoses(瘀斑 ) may appear in the flanks侧腹 (Grey Turner’s sign) or the umbilical area (Cullen’s sign);

• One to 2 weeks after the onset, large ecchymoses(瘀斑 ) may appear in the flanks侧腹 (Grey Turner’s sign) or the umbilical area (Cullen’s sign);

• One to 2 weeks after the onset, large ecchymoses(瘀斑 ) may appear in the flanks侧腹 (Grey Turner’s sign) or the umbilical area (Cullen’s sign);

Physical ExaminationPhysical Examination

•Initial physical examination reveals mild fever and tachycardia( 心动过速 );

•Hypotension is present in 30 to 40% of patients.

Physical ExaminationPhysical Examination

• epigastria tenderness, rigidity and rebound epigastria tenderness, rigidity and rebound tenderness (There is marked tenderness to deep tenderness (There is marked tenderness to deep palpation of the upper abdomen, but signs of palpation of the upper abdomen, but signs of peritoneal irritation are frequently absent.)peritoneal irritation are frequently absent.)

• bowel sounds decreased or absent bowel sounds decreased or absent • palpable masspalpable mass

swollen pancreasswollen pancreasPseudocystPseudocystabscessabscess

Laboratory TestLaboratory Test

Serum AmylaseSerum Amylase

• Total serum amylase activity is the test most frequently used to diagnose acute pancreatitis.

• The level rises 6 to 12 hours after onset of symptoms and remains elevated for 3 to 5 days in most cases. (hyperamylasemia hyperamylasemia is observed within 24-48 hrs; gradually return to is observed within 24-48 hrs; gradually return to

normal values during the subsequent 2-5daysnormal values during the subsequent 2-5days)

Serum AmylaseSerum Amylase

• Values more than 3 times the upper limit of normal are highly specific for acute pancreatitis but are found in only 80 to 90% of cases.

• The magnitude of the rise in serum amylase does not correlate with the severity of the attack, nor does prolonged hyperamylasemia indicate developing complications.

• the absence of hyperamylasemia can’t exclude the diagnosis of acute pancreatitis (extensive pancreatic necrosis)

Disorders Associated with hyperamylasemiaDisorders Associated with hyperamylasemiaIntra-Abdominal Extra-AbdominalIntra-Abdominal Extra-AbdominalPancreatic disordersPancreatic disorders Salivary gland disordersSalivary gland disordersacute pancreatitis mumpsacute pancreatitis mumpschronic pancreatitis parotitischronic pancreatitis parotitistrauma traumatrauma traumacarcinoma calculicarcinoma calculipseudocyst irradiation sialoadenitispseudocyst irradiation sialoadenitispancreatic ascites impaired amylase excretionpancreatic ascites impaired amylase excretionabscess renal failureabscess renal failureNonpancreatic disordersNonpancreatic disorders mecroamylasemia mecroamylasemiabiliary tract disease biliary tract disease MiscellaneusMiscellaneusintestinal obstruction pneumoniaintestinal obstruction pneumoniamesenteric infarction pancreatic pleural effusionmesenteric infarction pancreatic pleural effusionperforated peptic ulcer mediastinal pseudocystperforated peptic ulcer mediastinal pseudocystperitonitis cerebral traumaperitonitis cerebral traumaafferen loop syndrome severe burnsafferen loop syndrome severe burnsacute appendicitis diabetic reto acidosisacute appendicitis diabetic reto acidosiseuptured ectopic pregnancy pregnancyeuptured ectopic pregnancy pregnancysalpingitis drugssalpingitis drugsruptured aortic aneurysm bisal buminemia ruptured aortic aneurysm bisal buminemia

Urinary AmylaseUrinary Amylase

• a sensitive index of the pancreatitisa sensitive index of the pancreatitis

• elevations persist for a longer period than elevations persist for a longer period than serum amylase serum amylase

• some other diseases also manifest some other diseases also manifest hyperamylasuriahyperamylasuria

• a normal urinary amylase can’t preclude a normal urinary amylase can’t preclude the pancreatitisthe pancreatitis

•Separation of total serum amylase into its pancreatic (P) and salivary (S) isoenzymes and measurements of urinary amylase output add little to the diagnostic information.

• The amylase-creatinine clearance ratio (ACR) (the ratio of amylase concentration in urine over plasma, divided by the corresponding values for creatinine) is useful in diagnosing asymptomatic macroamylasemia, in which aggregates of circulating amylase escape glomerular filtration and the ACR is abnormally low.

淀粉酶 这一古老的检查方法虽已应用了半个多世纪，但对胰腺炎的诊断仍不失为良好而简便可行的手段。由于胰酶在胰管内逆流入血或渗出液重吸收入血，则在急性胰腺炎时血、尿的淀粉酶有所升高。血淀粉酶正常值，温氏单位＜ 256单位，苏氏单位＜ 500单位。急性胰腺炎（轻型）发作后 6 ～ 12小时即升高， 48 ～72小时逐渐恢复正常，尿淀粉酶约在发病后 12 ～ 24小时升高，要持续 3 ～ 5天。但急性重型胰腺炎升高的时间要提前。临床上对淀粉酶值的变化要作全面的分析，再结合临床其他症状才能做出正确的判断。

淀粉酶• 血淀粉酶值正常：有两种情况，其一表明病已痊愈，血淀粉酶值恢复正常，同时全身情况良好，无腹部体征。其二在重症急性胰腺炎的初检或治疗中，淀粉酶也可不升高，说明病情会进行性加重恶化。因为胰腺腺泡大量坏死、崩溃，已不能分泌淀粉酶，即所谓的“枯竭”现象。这一现象在急性重症胰腺炎中时有发生，应予以高度重视。

淀粉酶 血淀粉酶升高：有时病人出现腹痛，并伴血淀粉酶升高，但临床的症状、体征并不支持胰腺炎，这时就应考虑到血清淀粉酶检测往往是非特异性的。临床常见的一些急腹症也可伴有血淀粉酶升高，如胆囊炎、胆石症、胆道梗阻、肠梗阻、消化性溃疡病穿孔、肠系膜血栓形成以及使用吗啡后。胆石症时可能是由于排石对Oddi括约肌的刺激，使之痉挛，血淀粉酶一过性升高。消化性溃疡穿孔（特别是十二指肠球部穿孔）时，含有大量胰液的肠内容物进入腹腔后，淀粉酶被腹膜吸收则血淀粉酶值升高。肠梗阻后，肠腔内肠液淤积，淀粉酶通过受损的肠壁渗入腹腔而被吸收。因此，对血淀粉酶的升高必须结合临床进行判断，决不可因单纯血淀粉酶升高而诊断为胰腺炎。

淀粉酶

巨淀粉酶血症：是一罕见病症，其原因不明，可能是由于病人血中的淀粉酶与大分子物质形成复合物，从而不能通过肾小球滤过，将其贮存在血中。特点是血淀粉酶虽高，但尿淀粉酶正常或偏低。血淀粉酶升高可持续数月乃至数年。

淀粉酶

重症胰腺炎往往伴有腹腔大量炎性腹水，应做腹腔穿刺测定腹水淀粉酶，穿刺物多为血性混浊的液体，其淀粉酶含量可以相当高。

淀粉酶 -肌酐肾廓清率比值（ ACR）

• ACCR的正常比值为 3.8 ～ 5.3%，若比值＞5 ～ 6%则提示急性胰腺炎。

• ACCR在急性胰腺炎以外的疾患亦可升高（如慢性肾衰、糖尿病酸中毒、烧伤、严重肝衰等），因此只有在排除以上诸疾患时，才有价值。

• ACCR一方面可用来确诊急性胰腺炎，另一方面亦可用来排除非胰腺炎的高淀粉酶血症。 ACCR的计算公式是：

（尿淀粉酶 /血清淀粉酶） ×（血清肌酐 /尿肌酐） ×100

Serum LipaseSerum Lipase• a more accurate indicator of acute pancreatitisa more accurate indicator of acute pancreatitis• lipase is solely of pancreatic originlipase is solely of pancreatic origin• The serum lipase levels tend to remain elevated longer The serum lipase levels tend to remain elevated longer

than the amylase levels during the healing phase of than the amylase levels during the healing phase of pancreatitis.pancreatitis.

• some other diseases also manifest elevated serum lipase some other diseases also manifest elevated serum lipase perforated peptic ulcerperforated peptic ulceracute cholecystitisacute cholecystitisintestinal ischemiaintestinal ischemia

• The combination of serum amylase and lipase The combination of serum amylase and lipase determinations is more accurate than either test alone).determinations is more accurate than either test alone).

HypocalcemiaHypocalcemia

• the consequence of dilutional the consequence of dilutional hypoalbuminemiahypoalbuminemia

• calcium desposition in areas of fat necrosiscalcium desposition in areas of fat necrosis• resistance of skeletal bone to parathyroid resistance of skeletal bone to parathyroid

hormone stimulation hormone stimulation• The ionized calcium concentration remains The ionized calcium concentration remains

normal, and symptoms of tetany(normal, and symptoms of tetany( 手足抽搐手足抽搐 ) ) are extremely rare.are extremely rare.

Other laboratory TestOther laboratory Test

√√Elevated white cell count > 10000 cells per mmElevated white cell count > 10000 cells per mm3 3

Leukocytosis (Leukocytosis ( 白细胞增多白细胞增多 ) )

√√ Hyperglycemia Hyperglycemia

√√ Mild azotemia Mild azotemia 氮质血症氮质血症 : related to fluid sequestration: related to fluid sequestration

√√ Abnormalities of liver function test Abnormalities of liver function test

•Serum triglyceride levels should be obtained in all patients because of their etiologic implications and to help interpret unexpectedly normal serum amylase and lipase levels.

• Elevated alanine(丙胺酸 ) aminotransferase(转氨酶 ) (ALT) and alkaline phosphatase values suggest gallstone-associated pancreatitis.

• The serum aspartate( 天 (门 )冬氨酸 ) aminotransferase (AST) is elevated in approximately 50% of patients, owing to alcoholic liver disease or to the pancreatic inflammation itself.

Imaging TestsImaging Tests1. A plain Abdominal Film 1. A plain Abdominal Film

* not specific* not specific

* dilatation of an isolated loop of intestine * dilatation of an isolated loop of intestine

adjacent to the pancreas adjacent to the pancreas

* calcification in the pancreas* calcification in the pancreas

* left pleural effusions* left pleural effusions

Plain films should be obtained routinely to rule out the Plain films should be obtained routinely to rule out the

presence of free air caused by perforation of a viscus.presence of free air caused by perforation of a viscus.

2. Ultrasound Examination2. Ultrasound Examination* no trauma* no trauma

* pancreatic and peripancreatic * pancreatic and peripancreatic

edema of fluid collection edema of fluid collection

* pseudosyst* pseudosyst

* dilation of pancreatic duct* dilation of pancreatic duct

* GB stone and CBD stone* GB stone and CBD stone

• Ultrasound examination showing two large pancreatic pseudocysts. Both cysts are indicated by the large white arrows.

3. CT Scans3. CT Scans* confirm diagnosis of pancreatitis* confirm diagnosis of pancreatitis

* confirm diagnosis of complications such * confirm diagnosis of complications such

as abscess or pseudocyst as abscess or pseudocyst

* reveal extension of inflammation and * reveal extension of inflammation and

necrosis necrosis

* imply prognosis* imply prognosis

* a needle aspiration under CT guide* a needle aspiration under CT guide

• With rapid intravenous bolus injection of contrast material, a dynamic CT scan will reveal extension of peripancreatic inflammation, involvement of adjacent organs, venous thrombosis, and fluid collections.

• Most importantly, pancreatic necrosis can be identified and quantitated by the lack of contrast medium enhancement after the bolus injection.

• The abdominal CT scan may be normal, however, in about 10% of patients with early, mild pancreatitis.

Computed Tomographic Findings in Acute pancreatitisComputed Tomographic Findings in Acute pancreatitis

pancreatic changes nonspecific findingspancreatic changes nonspecific findings

parenchymal enlargementparenchymal enlargement bowel distention bowel distention

diffuse pleural effusion diffuse pleural effusion

focal mesenteric edema focal mesenteric edema

parenchymal edemaparenchymal edema

necrosisnecrosis

peripancreatic changesperipancreatic changesblurring of fat planesblurring of fat planes

thickening of fascial planesthickening of fascial planes

presence of fluid collectionspresence of fluid collections

This CT scan shows poor perfusion of the pancreas.

Abdominal Ultrasonography (US) and

Computed Tomography (CT)• US is the method of choice for detecting

cholelithiasis(胆石症 ) and for determining the diameter of the extrahepatic and intrahepatic bile ducts.

• Dilatation of these ducts suggests recent or persisting impaction of a stone in the distal common bile duct or the ampulla of Vater.

• When the clinical diagnosis is made, the CT scan is far superior to US for assessing the extent and local complications of pancreatitis.

• Two pancreatic pseudocysts (arrows). Computed tomography following the intravenous administration of contrast material demonstrates four sharply marginated, fluid-filled collections.

• Large arrow indicates inflamed pancreas.Small arrow denotes areas of peripancreatic inflammation extending toward the hilum of the spleen.

• A large pseudocyst (open arrows), which is being percutaneously drained (closed arrow). Pseudocysts that develop in chronic pancreatitis are most commonly caused by duct obstruction, with the formation of a "retention" cyst in the upstream duct or side branch. Unlike the pseudocysts associated with acute pancreatitis, these pseudocysts do not contain activated enzymes, and are usually not a reflection of a necrotizing inflammatory process. These pseudocysts are less likely to produce complications than those associated with acute necrotizing pancreatitis, but they are paradoxically also less likely to resolve. Many of these pseudocysts remain asymptomatic, but they may be complicated by infection, rupture or leak, bleeding, or obstruction of a neighboring hollow viscus (eg, duodenum, bile duct, colon, or ureter, among others). Pseudocysts may also worsen chronic pain or even initiate a wasting syndrome.Recent clinical experience suggests that in patients with pseudocysts smaller than 6 cm, if there is a mature pseudocyst wall on radiographic imaging that does not resemble a cystic neoplasm, minimal symptoms, and no evidence of active alcohol abuse, the risk of complications is extremely small (< 10%). These patients may be safely observed with little risk of serious complication

• Computed tomogram of a patient with pancreatic abscess. The pancreas is diffusely involved, and its margins are difficult to define because of the massive peripancreatic inflammation, which is reflected in the streaking seen in this scan. Toward the tail of the pancreas, numerous small and large bubbles are noted (arrows) in the peripancreatic inflammatory mass. Bubbles, caused by gas-forming microorganisms, indicate that the pancreatic abscess is infected.

4. Diagnostic Paracentesis4. Diagnostic Paracentesis 穿刺术穿刺术1. not an ideal test1. not an ideal test

* an invasive procedure* an invasive procedure

* complications* complications

* lack of complete specificity of peritoneal * lack of complete specificity of peritoneal

fluid enzyme elevations fluid enzyme elevations

2. Help diagnosis2. Help diagnosis

* elevations in peritoneal fluid amylase and lipase* elevations in peritoneal fluid amylase and lipase

Edematous pancreatitis nercotizing pancreatitisEdematous pancreatitis nercotizing pancreatitis

abdominal pain + +++abdominal pain + +++vomiting and nausea + ++vomiting and nausea + ++fever low highfever low highjaundice (-)-(+) ++ - +++jaundice (-)-(+) ++ - +++psychiatric symptom no yespsychiatric symptom no yessigns of peritonitis + ++ - +++ signs of peritonitis + ++ - +++ cullen’s sign no yescullen’s sign no yesGrey Turner’s sign no yesGrey Turner’s sign no yeshemorrhagic ascites no yeshemorrhagic ascites no yesWBC <16000/mmWBC <16000/mm3 3 >16000/mm >16000/mm3 3

blood glucose normal→ blood glucose normal→ ↑↑ > > 11.1mmol/L11.1mmol/Lserum calciumserum calcium normal > normal > 2.0 mmol/L 2.0 mmol/L amylase amylase ↑↑ ↑ ↑ ↑↑ ↑ ↑ oror (-) (-)PaPaOO2 2 normal < 8.0 kpanormal < 8.0 kpaBun.Cr no yesBun.Cr no yesARDS no yesARDS no yesDIC no yesDIC no yesARF no yesARF no yesmortality low highmortality low high

Differential DiagnosisDifferential Diagnosis1.Intestinal perforation1.Intestinal perforation

2.Peptic ulcer2.Peptic ulcer

3.Cholecystitis3.Cholecystitis

4.acute intestinal obstruction4.acute intestinal obstruction

5.renal colic5.renal colic

6.myocardial ischemia6.myocardial ischemia

7.acute gastroenteritis7.acute gastroenteritis

TreatmentTreatment

Nonoperative ManagementNonoperative Management1. Dietary Control1. Dietary Control

√√ Oral intake is initially prohibited;Oral intake is initially prohibited;

√√ Oral intake can be resumed during the Oral intake can be resumed during the

first week of treatment when abdominal first week of treatment when abdominal

pain and tenderness have improved, ileus pain and tenderness have improved, ileus

has resolved and hyperamylasemia is has resolved and hyperamylasemia is

normalizing.normalizing.

2. Nasogastric Suction2. Nasogastric Suction

√√ reduce vomiting and abdominal reduce vomiting and abdominal

distensiondistension

√√ reduce pancreatic exocrine secretion by reduce pancreatic exocrine secretion by

reducing secretion releasereducing secretion release

3. Intravenous fluid therapy and electrolyte3. Intravenous fluid therapy and electrolyte replacement replacement* hypokalemia, hypochoremia, hypocalcaemia* hypokalemia, hypochoremia, hypocalcaemia and hypomagnesemia should be corrected and hypomagnesemia should be corrected* Causes of hypovolemia:* Causes of hypovolemia:

paralytic ileus⑴ paralytic ileus⑴ vomiting⑵ vomiting⑵ extensive exudation in abdominal cavity and ⑶ extensive exudation in abdominal cavity and ⑶

peripancreatic region peripancreatic region GeGenerous nerous fluid resuscitation is very fluid resuscitation is very important important* mild hyperglycemia: insulin treatment* mild hyperglycemia: insulin treatment

4. Nutritional Support4. Nutritional Support* fasting for a long time* fasting for a long time

* persistent pain, ileus or the occurrence of * persistent pain, ileus or the occurrence of

a complication such as pseudocyst, a complication such as pseudocyst,

phlegmon or abscess phlegmon or abscess

* enteral alimentation is better than that * enteral alimentation is better than that

through the parenteral routethrough the parenteral route

营养支持• 非重症急性胰腺炎患者不需要空肠营养或静脉营养，一般在病程的 4天内即能进食。

• 重症急性胰腺炎病人应给予全胃肠外营养或肠内营养。给予早期肠内营养。病程的第 3 或 4天，经内镜或在 X线引导下给病人置入鼻空肠管，并给予半量要素饮食。浓度大致为 4.184 J/ml，如能耐受，逐渐增量至全能营养配方。

5. Antibiotics5. Antibiotics* prophylaxis* prophylaxis

* prevent intestinal bacteria * prevent intestinal bacteria

translocation translocation

* Treat suppurative* Treat suppurative 化脓性的化脓性的

complicationcomplication

预防性使用抗生素• 并发感染仍然是重症急性胰腺炎死亡的重要原因，因此，有胰腺坏死存在就应考虑预防感染。

• 抗生素的选择应考虑其抗菌谱与感染病原菌的配对并能有效穿透至胰腺实质中。

• 环丙沙星能透入胰腺坏死组织，甲硝唑虽分子量小、通透性高，但只透入坏死液体，因此两者合用为宜胰腺坏死者。

• 对于确有推荐使用亚胺培南（泰能） 500 mg ， 3/日，共 2周。

• 其余抗生素均不能进入胰腺坏死组织，故而无效。

6. Analgesia6. Analgesia

* Meperidine (* Meperidine ( 哌替啶哌替啶 , , 度冷丁度冷丁 ) is the ) is the

preferred drug;preferred drug;

* Morphine (* Morphine ( 吗啡吗啡 ) should be avoided: ) should be avoided:

causing spasm of the sphincter of oddicausing spasm of the sphincter of oddi

7.7. Pancreatic Exocrine Secretion SuppressionPancreatic Exocrine Secretion Suppression

1.nasogastric suction1.nasogastric suction

2.histamine(H2)-receptor antagonists2.histamine(H2)-receptor antagonists

3.antacids3.antacids

4.anticholinergics4.anticholinergics

5.glucagon5.glucagon

6.somatostatin, octreotide and sandostatin6.somatostatin, octreotide and sandostatin

生长抑素生长抑素 施他宁施他宁 (250(250g g 静推，静推， 3000 3000 g g 静滴静滴 24h)24h)

善宁善宁 (0.1mg (0.1mg 静推静推 , 0.6mg , 0.6mg 静滴静滴 24h)24h)

7.proglumide (cck-receptor antagonists7.proglumide (cck-receptor antagonists)

8. Pancreatic enzyme inhibitor8. Pancreatic enzyme inhibitor

* aprotinin* aprotinin

* gabexate* gabexate

* camostat* camostat

Surgical TreatmentSurgical Treatment

Operative indicationOperative indication1. secondary pancreatic infection1. secondary pancreatic infection

2. correction of associated biliary tract 2. correction of associated biliary tract

diseasedisease

3. progressive clinical deterioration3. progressive clinical deterioration

SSurgery is contraindicated in urgery is contraindicated in

uncomplicated acute pancreatitis.uncomplicated acute pancreatitis.

Surgical ProcedureSurgical Procedure1. peritoneal lavage: remove toxins and 1. peritoneal lavage: remove toxins and

various metabolitesvarious metabolites

2. pancreatic drainage2. pancreatic drainage

3. debridement of necrotic tissue3. debridement of necrotic tissue

4. biliary procedure:4. biliary procedure: endoscopic sphincterotomyendoscopic sphincterotomy

cholecystectomy cholecystectomy

remove the CBD stone remove the CBD stone

ComplicationsComplicationsSystemic complicationsSystemic complications ARDSARDS Renal failure Renal failure Cardiovascular failure Cardiovascular failure MOSF MOSFLocal complicationsLocal complications pancreatic abscesspancreatic abscess pancreatic psuedocysts pancreatic psuedocysts pancreatic phlegmon pancreatic phlegmon pancreatic ascites pancreatic ascites pleural effusion pleural effusion pancreatic fistula pancreatic fistula intestinal fistula intestinal fistula

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