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.
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.
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.
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
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
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
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.
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.
39.
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.
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.
44.
45.
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
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)
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.
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
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