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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%

√ Acute pancreatitis is an acute inflammatory process of the pancreas, with variable involvement of other

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.

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

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

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

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 Pancreatitis Obstruction: Biliary tract disease: cholelithiasis, tumor, ascarid, stenosis pancreatic duct obstruction: neoplasms,
Causes of Acute Pancreatitis
Obstruction:
Biliary tract disease: cholelithiasis, tumor, ascarid, stenosis
pancreatic duct obstruction: neoplasms, cysts,pancreas
divisum annular pancreas
ampullary stenosis,
duodenal diverticulum
Duodenal obstruction
Alcohol
Hyperlipidemia
Hypercalcemia
Hereditary
Trauma:external, operative,ERCP
Ischemia:hypotension,cardiopulmonary bypass,
atheroembolism,vasculitis
Infectious causes: parastic bacterial viral fungal
Drugs:steroids,azathioprine 6-mercaptopurine,
Idiopathic

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.

Pathogenesis 1.A complicated pathophysiologic process 2.Enzyme autoactivation and self-digestion (key point) 3. Many agents participating in
Pathogenesis
1.A complicated pathophysiologic process
2.Enzyme autoactivation and self-digestion
(key
point)
3. Many agents participating in the process
4. Complete mechanism remaining unknown
Pancreatic self-protective mechanism 1.mucopolysaccharide on pancreatic duct epithelia 2.proenzyme 3.pancreatin inhibitor 4.acinus metabolism activity 5. Anti-

Pancreatic self-protective mechanism

1.mucopolysaccharide on pancreatic duct
1.mucopolysaccharide on pancreatic duct
epithelia 2.proenzyme
epithelia
2.proenzyme
Pancreatic self-protective mechanism 1.mucopolysaccharide on pancreatic duct epithelia 2.proenzyme 3.pancreatin inhibitor 4.acinus metabolism activity 5. Anti-

3.pancreatin inhibitor 4.acinus metabolism activity 5. Anti-reflux mechanism: oddi’s sphincter pancreatic duct sphincter

Pancreatic self-protective mechanism 1.mucopolysaccharide on pancreatic duct epithelia 2.proenzyme 3.pancreatin inhibitor 4.acinus metabolism activity 5. Anti-
Initiation factor in Earlier period
Initiation factor in Earlier period
1. Pancreatic Enzyme Abnormally Activated ⑴Bile reflux Bile common channel pancreatic duct 1.hypertension in pancreatic duct
1. Pancreatic Enzyme Abnormally Activated
⑴Bile reflux
Bile
common channel
pancreatic duct
1.hypertension in pancreatic duct
2.premature activation of pancreatic enzymes
3.injury to the lining of the pancreatic ducts
pancreatic edema or necrosis
MODS
⑵ Duodenal Refulx duodenal enterokinase pancreatic duct trypsinogen trypsin elastasnogen elastase
⑵ Duodenal Refulx
duodenal enterokinase
pancreatic duct
trypsinogen
trypsin
elastasnogen
elastase
phospholipasogen phospholipase
phospholipasogen
phospholipase
⑵ Duodenal Refulx duodenal enterokinase pancreatic duct trypsinogen trypsin elastasnogen elastase phospholipasogen phospholipase lecithin lysolecthin
⑵ Duodenal Refulx duodenal enterokinase pancreatic duct trypsinogen trypsin elastasnogen elastase phospholipasogen phospholipase lecithin lysolecthin
lecithin lysolecthin
lecithin
lysolecthin
2.Alcohol Toxicity ⑴stimulate the pancreas to secrete pancreatic hypertention tiny pancreatic duct and acinus rupture pancreatic
2.Alcohol Toxicity
⑴stimulate the pancreas to secrete
pancreatic hypertention
tiny pancreatic
duct and acinus rupture
pancreatic juice

spillage spasm of the sphinctor of oddi direct injury to pancreas

2.Alcohol Toxicity ⑴stimulate the pancreas to secrete pancreatic hypertention tiny pancreatic duct and acinus rupture pancreatic
2.Alcohol Toxicity ⑴stimulate the pancreas to secrete pancreatic hypertention tiny pancreatic duct and acinus rupture pancreatic
2.Alcohol Toxicity ⑴stimulate the pancreas to secrete pancreatic hypertention tiny pancreatic duct and acinus rupture pancreatic
3.Pancreatic Microcirculation Disorder ⑴systemic hypotension ⑵hyperlipidemia: triglycerides lipase free acid fatty acids microcirculation ⑶artheroembolism ⑷vasculitis injure
3.Pancreatic Microcirculation Disorder
⑴systemic hypotension
⑵hyperlipidemia: triglycerides lipase free
acid fatty acids
microcirculation
⑶artheroembolism
⑷vasculitis
injure pancreatic
Aggravatiing factors in later period ⑴Infection: pancreatic abscess ⑵Intestinal bacteria translocation ⑶Cytokine and systemic inflammation reaction
Aggravatiing factors in later period
⑴Infection: pancreatic abscess
⑵Intestinal bacteria translocation
⑶Cytokine and systemic inflammation
reaction syndrome
TNF IL-1 IL-6 PAF
MSOF
⑷Free radicals

PATHOGENESIS

Premature activation of zymogens() 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 α 2 -

macroglobulin(巨球蛋白). α 1 -

PATHOGENESIS • Proteases( 蛋白酶 ) released into the blood are inactivated by circulating inhibitors , including

antitrypsin(抗胰蛋白酶), and the C 1 - esterase(酯酶) inhibitor.

PATHOGENESIS • Proteases( 蛋白酶 ) released into the blood are inactivated by circulating inhibitors , including

PATHOGENESIS

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(激肽), from their inactive precursors in blood plasma.

PATHOGENESIS

These peptides, termed kinins(), have various deleterious effects including vasodilatation, increased vascular permeability, pain, and neutrophil(嗜中性粒细 ) 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。

Pathology 1.Edematous pancreatitis:
Pathology
1.Edematous pancreatitis:

*interstitial edema *inflammatory cell infiltration of the gland parenchyma

Pathology 1.Edematous pancreatitis: * interstitial edema *inflammatory cell infiltration of the gland parenchyma 2.Hemorrhagic or necrotizing
Pathology 1.Edematous pancreatitis: * interstitial edema *inflammatory cell infiltration of the gland parenchyma 2.Hemorrhagic or necrotizing
2.Hemorrhagic or necrotizing pancreatitis *extensive pancreatic and peripancreatic fat necrosis *parenchymal necrosis
2.Hemorrhagic or necrotizing pancreatitis
*extensive pancreatic and peripancreatic
fat 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

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.

Fat necrosis • Fat necrosis seen at surgery is associated with peripancreatic release of lipase, with
Clinical Presentation
Clinical 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 feature • midepigastrium, in the right or left upper quadrants •
• predominant clinical feature • midepigastrium, in the right or left upper quadrants • The pain
• predominant clinical feature
• midepigastrium, in the right or left upper
quadrants
• The pain reaches peak intensity within 15
minutes to 1 hour from onset, in contrast to the
more abrupt onset of pain with a perforated
viscus.

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

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

position.)

Abdominal pain
Abdominal pain

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

frequently present in shock.

Clinical Presentation • Nausea and vomiting • Abdominal Distention resulting from a paralytic ileus arising from
Clinical Presentation
• Nausea and vomiting
• Abdominal Distention
resulting from a paralytic ileus arising from
retroperitoneal irritation or ascites or a
retroperitoneal phlegmon
• Jaundice
distal common bile duct obstruction by
gallstones’ compression of the distal CBD by
pancreatic head edema or by other uncommon
findings
Abdominal Distention
Abdominal 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 Pancreatitis • Circulatory Derangements: hypotention, hypovolemia, hypoeffusion ⑴circulating myocardial depressant factor
Clinical Presentation of Sever Pancreatitis
• Circulatory Derangements: hypotention,
hypovolemia, hypoeffusion
⑴circulating myocardial depressant
factor

decreased preload to the heart reduced systemic vascular resistance sepsis-like syndrome hyperdynamic state elevated cardiac output

Clinical Presentation of Sever Pancreatitis • Circulatory Derangements: hypotention, hypovolemia, hypoeffusion ⑴circulating myocardial depressant factor ⑵
lowered systemic vascular resistance
lowered systemic vascular resistance

lowered arteriovenous oxgen difference

Clinical Presentation of Sever Pancreatitis • left pleural effusion • pulmonary failure tachypnea, dyspnea and cyanosis
Clinical Presentation of Sever Pancreatitis
• left pleural effusion
• pulmonary failure
tachypnea, dyspnea and cyanosis
• cerebral abnormalities
belligerence, confusion, psychosis and coma
• Turner sign and Cullen sign
a bluish color in the flanks or around the
umbilicus, (representing blood dissecting to
those areas from the retroperitoneum near the
pancreas along fascial planes)
• One to 2 weeks after the onset, large ecchymoses( 瘀斑 ) may appear in the

One to 2 weeks after the onset, large ecchymoses(瘀斑) may appear in the flanks侧 腹 (Grey Turners sign) or the umbilical area (Cullens sign);

• One to 2 weeks after the onset, large ecchymoses( 瘀斑 ) may appear in the

One to 2 weeks after the onset, large ecchymoses(瘀斑) may appear in the flanks侧 腹 (Grey Turners sign) or the umbilical area (Cullens sign);

One to 2 weeks after the onset, large ecchymoses(瘀斑) may appear in the flanks(Grey Turners sign) or the umbilical area (Cullens sign);

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

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

Hypotension is present in 30 to 40% of patients.

Physical Examination • epigastria tenderness, rigidity and rebound tenderness (There is marked tenderness to deep palpation
Physical Examination
• epigastria tenderness, rigidity and rebound
tenderness (There is marked tenderness to deep
palpation of the upper abdomen, but signs of
peritoneal irritation are frequently absent.)
• bowel sounds decreased or absent
• palpable mass
swollen pancreas
Pseudocyst
abscess
Laboratory Test
Laboratory Test
Serum Amylase
Serum 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 is

observed within 24-48 hrs; gradually return to normal values during the subsequent 2-5days)
observed within 24-48 hrs; gradually return to normal
values during the subsequent 2-5days)
Serum Amylase
Serum 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 cant exclude the diagnosis of acute pancreatitis (extensive

pancreatic necrosis)

Disorders Associated with hyperamylasemia Intra-Abdominal Extra-Abdominal Pancreatic disorders Salivary gland disorders acute pancreatitis mumps chronic pancreatitis
Disorders Associated with hyperamylasemia
Intra-Abdominal
Extra-Abdominal
Pancreatic disorders
Salivary gland disorders
acute pancreatitis
mumps
chronic pancreatitis
parotitis
trauma
trauma
calculi
irradiation sialoadenitis

carcinoma pseudocyst pancreatic ascites abscess

Disorders Associated with hyperamylasemia Intra-Abdominal Extra-Abdominal Pancreatic disorders Salivary gland disorders acute pancreatitis mumps chronic pancreatitis
impaired amylase excretion renal failure
impaired amylase excretion
renal failure
Nonpancreatic disorders mecroamylasemia Miscellaneus
Nonpancreatic disorders
mecroamylasemia
Miscellaneus

biliary tract disease intestinal obstruction mesenteric infarction perforated peptic ulcer peritonitis

pneumonia pancreatic pleural effusion mediastinal pseudocyst cerebral trauma

Disorders Associated with hyperamylasemia Intra-Abdominal Extra-Abdominal Pancreatic disorders Salivary gland disorders acute pancreatitis mumps chronic pancreatitis
Disorders Associated with hyperamylasemia Intra-Abdominal Extra-Abdominal Pancreatic disorders Salivary gland disorders acute pancreatitis mumps chronic pancreatitis
afferen loop syndrome severe burns
afferen loop syndrome
severe burns
Disorders Associated with hyperamylasemia Intra-Abdominal Extra-Abdominal Pancreatic disorders Salivary gland disorders acute pancreatitis mumps chronic pancreatitis

acute appendicitis euptured ectopic pregnancy salpingitis ruptured aortic aneurysm

diabetic reto acidosis pregnancy drugs bisal buminemia

Disorders Associated with hyperamylasemia Intra-Abdominal Extra-Abdominal Pancreatic disorders Salivary gland disorders acute pancreatitis mumps chronic pancreatitis
Urinary Amylase • a sensitive index of the pancreatitis • elevations persist for a longer period
Urinary Amylase
• a sensitive index of the pancreatitis
• elevations persist for a longer period than
serum amylase
• some other diseases also manifest
hyperamylasuria
• a normal urinary amylase can’t preclude
the 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612小时即升高,4872小时逐渐

恢复正常,尿淀粉酶约在发病后1224小时升高,要

持续35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

含量可以相当高

淀粉酶-肌酐肾廓清率比值(ACR

ACCR正常比值为3.85.3%,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

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 Lipase
Serum Lipase
• a more accurate indicator of acute pancreatitis • lipase is solely of pancreatic origin •
• a more accurate indicator of acute pancreatitis
• lipase is solely of pancreatic origin
• The serum lipase levels tend to remain elevated longer
than the amylase levels during the healing phase of
pancreatitis.
• some other diseases also manifest elevated serum lipase
Serum Lipase • a more accurate indicator of acute pancreatitis • lipase is solely of pancreatic

perforated peptic ulcer acute cholecystitis

Serum Lipase • a more accurate indicator of acute pancreatitis • lipase is solely of pancreatic
intestinal ischemia
intestinal ischemia

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

Serum Lipase • a more accurate indicator of acute pancreatitis • lipase is solely of pancreatic
Hypocalcemia • the consequence of dilutional hypoalbuminemia • calcium desposition in areas of fat necrosis •
Hypocalcemia
• the consequence of dilutional
hypoalbuminemia
• calcium desposition in areas of fat necrosis
• resistance of skeletal bone to parathyroid
hormone stimulation
• The ionized calcium concentration remains
normal, and symptoms of tetany(手足抽搐) are
extremely rare.
Other laboratory Test √Elevated white cell count > 10000 cells per mm 3 Leukocytosis (白细胞增多)
Other laboratory Test
√Elevated white cell count > 10000 cells per mm 3
Leukocytosis (白细胞增多)
√ Hyperglycemia
√ Hyperglycemia

Mild azotemia氮质血症: related to fluid sequestration

Other laboratory Test √Elevated white cell count > 10000 cells per mm 3 Leukocytosis (白细胞增多) √

Abnormalities of liver function test

Other laboratory Test √Elevated white cell count > 10000 cells per mm 3 Leukocytosis (白细胞增多) √

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(氨酶) (ALT) and alkaline phosphatase values suggest gallstone-associated pancreatitis.

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

Imaging Tests 1. A plain Abdominal Film * not specific * dilatation of an isolated loop
Imaging Tests
1. A plain Abdominal Film
* not specific
* dilatation of an isolated loop of intestine
adjacent to the pancreas
* calcification in the pancreas
* left pleural effusions
Plain films should be obtained routinely to rule out the
presence of free air caused by perforation of a viscus.
2. Ultrasound Examination * no trauma * pancreatic and peripancreatic edema of fluid collection * pseudosyst
2. Ultrasound Examination
* no trauma
* pancreatic and peripancreatic
edema of fluid collection
* pseudosyst
* dilation of pancreatic duct
* GB stone and CBD stone
• Ultrasound examination showing two large pancreatic pseudocysts. Both cysts are indicated by the large white

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

3. CT Scans * confirm diagnosis of pancreatitis
3.
CT Scans
* confirm diagnosis of pancreatitis
* confirm diagnosis of complications such
* confirm diagnosis of complications such
3. CT Scans * confirm diagnosis of pancreatitis * confirm diagnosis of complications such as abscess

as abscess or pseudocyst * reveal extension of inflammation and necrosis * imply prognosis * a needle aspiration under CT guide

3. CT Scans * confirm diagnosis of pancreatitis * confirm diagnosis of complications such as abscess
3. CT Scans * confirm diagnosis of pancreatitis * confirm diagnosis of complications such as abscess
3. CT Scans * confirm diagnosis of pancreatitis * confirm diagnosis of complications such as abscess

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 pancreatitis pancreatic changes parenchymal enlargement nonspecific findings bowel distention diffuse pleural
Computed Tomographic Findings in Acute pancreatitis
pancreatic changes
parenchymal enlargement
nonspecific findings
bowel distention
diffuse
pleural effusion
focal
mesenteric edema

parenchymal edema necrosis peripancreatic changes

Computed Tomographic Findings in Acute pancreatitis pancreatic changes parenchymal enlargement nonspecific findings bowel distention diffuse pleural
blurring of fat planes
blurring of fat planes
thickening of fascial planes presence of fluid collections
thickening of fascial planes
presence of fluid collections
This CT scan shows poor perfusion of the pancreas.
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

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

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

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 ,

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 Paracentesis穿刺术 1. not an ideal test * an invasive procedure * complications
4. Diagnostic Paracentesis穿刺术
1. not an ideal test
* an invasive procedure
* complications
* lack of complete specificity of peritoneal
* lack of complete specificity of peritoneal
4. Diagnostic Paracentesis穿刺术 1. not an ideal test * an invasive procedure * complications * lack

fluid enzyme elevations 2. Help diagnosis * elevations in peritoneal fluid amylase and lipase

Edematous pancreatitis nercotizing pancreatitis abdominal pain vomiting and nausea fever jaundice + + low (-)-(+) +++
Edematous pancreatitis
nercotizing pancreatitis
abdominal pain
vomiting and nausea
fever
jaundice
+
+
low
(-)-(+)
+++
++
high
++ - +++
psychiatric symptom
no
yes
signs of peritonitis
+
++ - +++
cullen’s sign
no
Grey Turner’s sign
no
hemorrhagic ascites
WBC
blood glucose
serum calcium
amylase
PaO
Bun.Cr
no
<16000/mm 3
normal→ ↑
normal
yes
yes
yes
>16000/mm 3
> 11.1mmol/L
> 2.0 mmol/L
↑ ↑ ↑ or (-)
normal
< 8.0 kpa
2
no
yes
ARDS
no
yes
DIC
no
yes
ARF
no
yes
mortality
low
high
Differential Diagnosis
Differential Diagnosis
Differential Diagnosis 1.Intestinal perforation 2.Peptic ulcer 3.Cholecystitis 4.acute intestinal obstruction 5.renal colic 6.myocardial ischemia 7.acute gastroenteritis

1.Intestinal perforation 2.Peptic ulcer

3.Cholecystitis
3.Cholecystitis
4.acute intestinal obstruction 5.renal colic 6.myocardial ischemia 7.acute gastroenteritis
4.acute intestinal obstruction
5.renal colic
6.myocardial ischemia
7.acute gastroenteritis
Treatment
Treatment
Nonoperative Management 1. Dietary Control √ Oral intake is initially prohibited; √ Oral intake can be
Nonoperative Management
1. Dietary Control
√ Oral intake is initially prohibited;
√ Oral intake can be resumed during the
first week of treatment when abdominal
pain and tenderness have improved, ileus
has resolved and hyperamylasemia is
normalizing.
2. Nasogastric Suction √ reduce vomiting and abdominal
2. Nasogastric Suction
√ reduce vomiting and abdominal
distension
distension
√ reduce pancreatic exocrine secretion by
√ reduce pancreatic exocrine secretion by
reducing secretion release
reducing secretion release

3. Intravenous fluid therapy and electrolyte replacement

3. Intravenous fluid therapy and electrolyte replacement * hypokalemia, hypochoremia, hypocalcaemia and hypomagnesemia should be corrected
* hypokalemia, hypochoremia, hypocalcaemia and hypomagnesemia should be corrected * Causes of hypovolemia: ⑴ paralytic ileus
* hypokalemia, hypochoremia, hypocalcaemia
and hypomagnesemia should be corrected
* Causes of hypovolemia:
⑴ paralytic ileus
⑵ vomiting
⑶ extensive exudation in abdominal cavity and
peripancreatic region
Generous fluid resuscitation is very
important
* mild hyperglycemia: insulin treatment
* mild hyperglycemia: insulin treatment
4. Nutritional Support * fasting for a long time * persistent pain, ileus or the occurrence
4. Nutritional Support
* fasting for a long time
* persistent pain, ileus or the occurrence of
a complication such as pseudocyst,
phlegmon or abscess
* enteral alimentation is better than that
through 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34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. Antibiotics

5. Antibiotics * prophylaxis * prevent intestinal bacteria translocation * Treat suppurative 化脓性的 complication

* prophylaxis * prevent intestinal bacteria translocation * Treat suppurative化脓性的 complication

5. Antibiotics * prophylaxis * prevent intestinal bacteria translocation * Treat suppurative 化脓性的 complication
5. Antibiotics * prophylaxis * prevent intestinal bacteria translocation * Treat suppurative 化脓性的 complication

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 mg3/日,

2周。

其余抗生素均不能进入胰腺坏死组织,故而无效。

6. Analgesia * Meperidine (哌替啶, 度冷丁) is the preferred drug; * Morphine (吗啡) should be avoided:
6. Analgesia
* Meperidine (哌替啶, 度冷丁) is the
preferred drug;
* Morphine (吗啡) should be avoided:
causing spasm of the sphincter of oddi
7.
7.
Pancreatic Exocrine Secretion Suppression 1.nasogastric suction 2.histamine(H2)-receptor antagonists 3.antacids 4.anticholinergics
Pancreatic Exocrine Secretion Suppression
1.nasogastric suction
2.histamine(H2)-receptor antagonists
3.antacids
4.anticholinergics
5.glucagon
5.glucagon
7. Pancreatic Exocrine Secretion Suppression 1.nasogastric suction 2.histamine(H2)-receptor antagonists 3.antacids 4.anticholinergics 5.glucagon 6.somatostatin, octreotide and sandostatin

6.somatostatin, octreotide and sandostatin 生长抑素 施他宁 (250g 静推,3000 g 静滴24h) 善宁 (0.1mg 静推, 0.6mg 静滴24h) 7.proglumide (cck-receptor antagonists)

7. Pancreatic Exocrine Secretion Suppression 1.nasogastric suction 2.histamine(H2)-receptor antagonists 3.antacids 4.anticholinergics 5.glucagon 6.somatostatin, octreotide and sandostatin
7. Pancreatic Exocrine Secretion Suppression 1.nasogastric suction 2.histamine(H2)-receptor antagonists 3.antacids 4.anticholinergics 5.glucagon 6.somatostatin, octreotide and sandostatin
8. Pancreatic enzyme inhibitor * aprotinin * gabexate * camostat
8. Pancreatic enzyme inhibitor
* aprotinin
* gabexate
* camostat
Surgical Treatment
Surgical Treatment
Operative indication 1. secondary pancreatic infection 2. correction of associated biliary tract disease
Operative indication
1. secondary pancreatic infection
2. correction of associated biliary tract
disease
3. progressive clinical deterioration
3. progressive clinical deterioration

Surgery is contraindicated in uncomplicated acute pancreatitis.

Operative indication 1. secondary pancreatic infection 2. correction of associated biliary tract disease 3. progressive clinical
Surgical Procedure 1. peritoneal lavage: remove toxins and various metabolites 2. pancreatic drainage 3. debridement of
Surgical Procedure
1. peritoneal lavage: remove toxins and
various
metabolites
2.
pancreatic drainage
3.
debridement of necrotic tissue
4.
biliary procedure:
endoscopic sphincterotomy
cholecystectomy
remove the CBD stone
Complications Systemic complications ARDS Renal failure Cardiovascular failure MOSF Local complications pancreatic abscess pancreatic psuedocysts pancreatic
Complications
Systemic complications
ARDS
Renal failure
Cardiovascular failure
MOSF
Local complications
pancreatic abscess
pancreatic psuedocysts
pancreatic phlegmon
pancreatic ascites
pleural effusion
pancreatic fistula
intestinal
fistula
Thanks for Your Attention

Thanks for

Your Attention
Your Attention