1. Acute Pancreatitis
XUE Huiping

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

3. √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.

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

5. √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。

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

7. 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.

8. √ 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。

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

10. √ 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。

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

12. √ 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.

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

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

15. √ Gallstones may cause
pancreatitis by impacting in the
ampulla of Vater.
√ The incidence of gallstoneassociated pancreatitis parallels
that of cholelithiasis( 胆石症 ): it
peaks at ages 50 to 70, and women
outnumber men by 2 to 1.

16. 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

17. 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

18. 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.

19. 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

20. Pancreatic self-protective mechanism
1.mucopolysaccharide on pancreatic duct
epithelia
2.proenzyme
3.pancreatin inhibitor
4.acinus metabolism activity
5. Anti-reflux mechanism: oddi’s sphincter
pancreatic duct sphincter

21. Initiation factor in Earlier period

22. 1. Pancreatic Enzyme Abnormally Activated
⑴ Bile 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

23. ⑵ Duodenal Refulx
duodenal enterokinase
pancreatic duct
trypsinogen
trypsin
elastasnogen
elastase
phospholipasogen
phospholipase
lecithin
lysolecthin

24. 2.Alcohol Toxicity
⑴ stimulate the pancreas to secrete
pancreatic hypertention
tiny pancreatic
duct and acinus rupture
pancreatic juice
spillage
⑵ spasm of the sphinctor of oddi
⑶ direct injury to pancreas

25. 3.Pancreatic Microcirculation Disorder
⑴ systemic hypotension
⑵ hyperlipidemia: triglycerides lipase free
acid fatty acids
injure pancreatic
microcirculation
⑶ artheroembolism
⑷ vasculitis

26. Aggravatiing factors in later period
⑴ Infection: pancreatic abscess
⑵ Intestinal bacteria translocation
⑶ Cytokine and systemic inflammation
reaction syndrome
TNF IL-1 IL-6 PAF
⑷ Free radicals
MSOF

27. 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.

28. PATHOGENESIS
• Proteases( 蛋白酶 ) released into the
blood are inactivated by circulating
inhibitors, including α 2macroglobulin( 巨球蛋白 ). α1antitrypsin( 抗胰蛋白酶 ), and the
C1-esterase( 酯酶 ) inhibitor.

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

30. 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.

31. Two mechanisms may
trigger pancreatic autodigestion
• zymogen activation within the
pancreatic acinar cell.
• increased pancreatic duct
permeability

32. 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.

33. 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.

35. 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。

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

37. 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.

38. 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.

40. 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.

41. • Interstitial edema and inflammatory cells
within the parenchyma

42. 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.

43. Hemorrhagic
• The microscopic appearance of the
pancreas parallels the gross changes,
with marked fat and pancreatic
necrosis.
• Vascular inflammation and
thrombosis are common.

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

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

48. Abdominal 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
position.)

49. 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.

50. 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

51. 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 ).

52. Clinical Presentation of Sever Pancreatitis
• Circulatory Derangements: hypotention,
hypovolemia, hypoeffusion
⑴ circulating myocardial depressant
factor
⑵ decreased preload to the heart
⑶ reduced systemic vascular resistance
⑷ sepsis-like syndrome
hyperdynamic state
elevated cardiac output
lowered systemic vascular resistance
lowered arteriovenous oxgen difference

53. 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)

54. • 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);

55. • 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);

56. • 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);

57. Physical Examination
• Initial physical examination
reveals mild fever and
tachycardia( 心动过速 );
• Hypotension is present in 30 to
40% of patients.

58. 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

59. Laboratory Test

60. 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)

61. 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 can’t exclude
the diagnosis of acute pancreatitis (extensive
pancreatic necrosis)

62. Disorders Associated with hyperamylasemia
Intra-Abdominal
Pancreatic disorders
acute pancreatitis
chronic pancreatitis
trauma
carcinoma
pseudocyst
pancreatic ascites
abscess
Nonpancreatic disorders
biliary tract disease
intestinal obstruction
mesenteric infarction
perforated peptic ulcer
peritonitis
afferen loop syndrome
acute appendicitis
euptured ectopic pregnancy
salpingitis
ruptured aortic aneurysm
Extra-Abdominal
Salivary gland disorders
mumps
parotitis
trauma
calculi
irradiation sialoadenitis
impaired amylase excretion
renal failure
mecroamylasemia
Miscellaneus
pneumonia
pancreatic pleural effusion
mediastinal pseudocyst
cerebral trauma
severe burns
diabetic reto acidosis
pregnancy
drugs
bisal buminemia

63. 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

64. • 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.

65. • 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.

66. 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。

67. 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。

68. 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。

69. 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。

70. 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。

71. 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

72. Serum Lipase
•
•
•
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
perforated peptic ulcer
acute cholecystitis
intestinal ischemia
• The combination of serum amylase and lipase
determinations is more accurate than either test alone).

73. 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.

74. Other laboratory Test
√Elevated white cell count > 10000 cells per mm
3
Leukocytosis ( 白细胞增多 )
√ Hyperglycemia
√ Mild azotemia 氮质血症 : related to fluid sequestration
√ Abnormalities of liver function test

75. • 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.

76. • Elevated alanine( 丙胺酸 )
aminotransferase( 转氨酶 ) (ALT) and alkaline
phosphatase values suggest gallstoneassociated 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.

77. 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.

78. 2. Ultrasound Examination
* no trauma
* pancreatic and peripancreatic
edema of fluid collection
* pseudosyst
* dilation of pancreatic duct
* GB stone and CBD stone

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

80. 3. CT Scans
* confirm diagnosis of pancreatitis
* confirm diagnosis of complications such
as abscess or pseudocyst
* reveal extension of inflammation and
necrosis
* imply prognosis
* a needle aspiration under CT guide

81. • 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.

82. Computed Tomographic Findings in Acute pancreatitis
pancreatic changes
nonspecific findings
parenchymal enlargement
diffuse
focal
parenchymal edema
necrosis
peripancreatic changes
blurring of fat planes
thickening of fascial planes
presence of fluid collections
bowel distention
pleural effusion
mesenteric edema

83. This CT scan shows poor perfusion of the pancreas.

84. 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.

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

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

87. •
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

88. •
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.

89. 4. Diagnostic Paracentesis 穿刺术
1. not an ideal test
* an invasive procedure
* complications
* lack of complete specificity of peritoneal
fluid enzyme elevations
2. Help diagnosis
* elevations in peritoneal fluid amylase and lipase

90. Edematous pancreatitis
nercotizing pancreatitis
abdominal pain
+
vomiting and nausea +
fever
low
jaundice
(-)-(+)
psychiatric symptom no
signs of peritonitis
+
cullen’s sign
no
Grey Turner’s sign
no
hemorrhagic ascites no
WBC
<16000/mm3
blood glucose
normal→ ↑
serum calcium
normal
amylase
↑
PaO2
normal
Bun.Cr
no
ARDS
no
DIC
no
ARF
no
mortality
low
+++
++
high
++ - +++
yes
++ - +++
yes
yes
yes
>16000/mm3
> 11.1mmol/L
> 2.0 mmol/L
↑ ↑ ↑ or (-)
< 8.0 kpa
yes
yes
yes
yes
high

91. Differential Diagnosis
1.Intestinal perforation
2.Peptic ulcer
3.Cholecystitis
4.acute intestinal obstruction
5.renal colic
6.myocardial ischemia
7.acute gastroenteritis

92. Treatment

93. 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.

94. 2. Nasogastric Suction
√ reduce vomiting and abdominal
distension
√ reduce pancreatic exocrine secretion by
reducing secretion release

95. 3. Intravenous fluid therapy and electrolyte
replacement
* 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

96. 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

97. 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。

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

99. 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
。

100. 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

101. 7.
Pancreatic Exocrine Secretion Suppression
1.nasogastric suction
2.histamine(H2)-receptor antagonists
3.antacids
4.anticholinergics
5.glucagon
6.somatostatin, octreotide and sandostatin
生长抑素
施他宁 (250µ g 静推， 3000 µ g 静滴 24h)
善宁 (0.1mg 静推 , 0.6mg 静滴 24h)
7.proglumide (cck-receptor antagonists)
antagonists

102. 8. Pancreatic enzyme inhibitor
* aprotinin
* gabexate
* camostat

103. Surgical Treatment

104. Operative indication
1. secondary pancreatic infection
2. correction of associated biliary tract
disease
3. progressive clinical deterioration
Surgery is contraindicated in
uncomplicated acute pancreatitis.

105. 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

106. 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

107. Thanks for
Your Attention