8. Pancreatic ducts
Main pancreatic duct
Common bile duct
Hepatopancreatic ampulla (of Vater)
Acinar cells
Pancreatic ductal cells
Exocrine secretion is under vagus nerve
and hormonal control
13. Heavy alcohol drinker
คือบริโภค alcohol มากกว่า 50 gm ต่อวัน
เป็นเวลาอย่างน้อย 5 ปี
Increase secretory function
Induce spasm of the sphincter of Oddi
Induce pancreatic ductal permeability, which
would allow prematurely activated enzymes to
cause damage to the pancreatic parenchyma.
14.
15.
16.
17. autosomal dominant disorder
usually related to mutations of the cationic
trypsinogen gene (PRSS1), causing premature
activation of trypsinogen to trypsin and cause
abnormalities of ductal secretion, both of which
promote acute pancreatitis
35. Symptoms&Signs
•Acute onset of persistent upper abdominal pain, at epigastric and
periumbilical regions
•Nausea and vomiting
•The pain may radiate to the back, chest, flanks, and lower abdomen.
•Patients are usually restless and bend forward (the knee-chest position) in an
effort to relieve the pain
•Physical examination findings are variable but may include fever, hypotension,
severe abdominal tenderness, guarding, respiratory distress, and abdominal
distention.
36. Cullen sign
: Periumbilical ecchymosis associated with both severe necrotizing
pancreatitis and retroperitoneal hemorrhage of various causes.
Severe necrotizing
pancreatitis
37. Grey Turner sign
: An ecchymosis of the flank due to retroperitoneal hemorrhage.
: When present, it usually occurs 3-7 days after the onset of pain and is
indicative of severe pancreatitis.
38.
39. Require 2 out of following 3 features:
1.abdominal pain consistent with acute pancreatitis
(acute onset of a severe constant epigastric pain which often
radiates through to the mid back)
2.The elevation of serum amylase or lipase
(>3 times upper limit of normal).
3.Imaging (usually by contrast enhanced CT scanning)
is only required for the diagnosis of acute pancreatitis when
these diagnostic criteria are not met.
Diagnosis
Revised Atlanta classification 2012 by
international consensus
40. Diagnostic Imaging Modalities
1. CXR
• pleural effusions, atelectasis, or hemidiaphragm elevation
(suggestive of fluid sequestration),
• To exclude free air (pneumoperitoneum)
2. Plain and upright abdominal X-rays
• possible calcifications ( indicating chronic pancreatitis),
• gallstones (though only about 15% of gallstones are radio-
opaque),
• local dynamic ileus (or sign of bowel obstruction),
• “cutoff sign” : the gas in the transverse colon appears to end abruptly.
• “sentinel loop”: a single dilated jejunal loop in the upper abdomen
41.
42. 3. Ultrasound
Features to be detected in acute pancreatitis on
ultrasound are as follow:
• Pancreatic swelling
• Peripancreatic fluid collection
• Extrapancreatic soft tissue edema
• Gallstones or CBD stones (Gallstones pancreatitis)
By the way, U/S may be of limited value in obese patients
or in patients with significant amounts of bowel gas
overlying the pancreas
43. 4. CT scan:
Features to be detected in acute pancreatitis on CT scan
are as follow:
•Pancreatic edema
•Peripancreatic fluid collection
•Extrapancreatic soft tissue edema
•Pancreatic necrosis
: hypodensity area in pancreatic parenchyma
•Air bubble in peripancreatic area
•Gallstones or CBD stones (Gallstones pancreatitis)
The primary purpose of cross sectional imaging is the diagnosis of
local complications, in particular the development and extent of
pancreatic necrosis or the presence of different fluid collections.
45. Classification of acute pancreatitis—2012: revision of the Atlanta classification and definitions by international consensus
1. Classification of the Severity of Acute Pancreatitis
46. Definition of organ failure
Three organ systems should be assessed to define organ failure:
respiratory, cardiovascular and renal.
Organ failure is defined as a score of 2 or more for one of these three
organ systems using the Modified Marshall scoring system
Classification of acute pancreatitis—2012:
revision of the Atlanta classification and definitions by
international consensus
Respiratory
Renal
Cardiovascular
47. Definition of local complications
Local complications are
acute peripancreatic fluid collection,
Pancreatic pseudocyst,
acute necrotic collection
walled-off necrosis
gastric outlet dysfunction,
splenic and portal vein thrombosis,
colonic necrosis
Classification of acute pancreatitis—2012:
revision of the Atlanta classification and definitions by
international consensus
48. 2. Multifactorial severity system
1. Ranson’s criteria
2. APACHE ( Acute Physiologic And Chronic Health Evaluation ) II score
3. BISAP score ( the Bedside Index for Severity in Acute Pancreatitis )
49. 3 or more positive criteria,
the disease is considered
“predicted severe.”
Ranson’s criteria
Ranson’s score
0 - 2 : mortality rate nearly 0 %
3 - 5 : mortality rate 10 - 20 %
> 7 : mortality rate > 50 %
50. APACHE ( Acute Physiologic
And Chronic Health Evaluation ) II score
1. Physiologic points :
Temperature
MAP (Mean Arterial Pressure)
Heart rate
Respiratory rate
Oxygenation (PaO2)
Arterial pH
Serum sodium
Serum potassium
Hematocrit
White cell count
Glasgow coma score
1+2+3 = Total Score
2. Age points
3. Chronic health points :
Liver
Cardiovascular
Respiratory
Renal
Immunocompromised
The main advantage of the APACHE II
system is that a score can be derived at any
time during the patient’s hospital course,
while the Ranson’s criteria are only
prognostic during the initial 48 hours.
Score >_ 8 indicate severe pancreatitis
51.
52. Bedside Index for Severity of Acute Pancreatitis
(BISAP)
Although it has the
advantage of simplicity
and can be performed
within the first 24 hours
of admission,
it has performed no better
than other predictors
in comparison studies
54. Unfortunately !!!
these and many other single and combined predictors
of severity have an accuracy of only around 70%.
This means that there is misclassification error of 30%
55. Imaging severity assessment system
CT severity index score (CTSI)
score 0 - 3 : morbidity 3 % mortality 8 % : mild form
score 4 - 6 : morbidity 6 % mortality 35 % : moderate form
score 7 - 10 : morbidity 17 % mortality 92 % : severe form
70. Enteral nutrition should be commenced after
initial fluid resuscitation and within the first
24 hours of admission.
To avoid development of intestinal ileus and
feeding intolerance.
Route: Nasogastric or Nasojejunal
เพื่อวินิจฉัย pancreatic necrosis
เวลาที่เหมาะสมคือช่วงปลายสัปดาร์แรกของโรค
Revised Atlanta classification
1.Interstitial edematous pancreatitis
+/- acute peripancreatic fluid collection
(APFC)
2.Necrotizing pancreatitis ( parenchymal necrosis or peripancreatic
necrosis ) +/- acute necrotic collection (ANC)
ผู้ป่วยที่ควรได้ Antibiotics:
1.Necrosis > 30% of pancreas
2.มี Organ failure
3.ไม่สามารถรับ enteral feeding ได้
Preferred ATB: Carbapenem group
Percutaneous drainage
Endoscopic necrosectomy
76. • Chronic pancreatitis results in interstitial
inflammation w/duct obstruction and dilation
leading to parenchymal loss and fibrosis.
• Loss of both exocrine and endocrine
• Clinicically significant malabsorption occurs
when 90% of pancreas is lost.
Chronic pancreatitisChronic pancreatitis
77. • Presents as mild epigastric abdominal pain,
nausea, vomiting
• Pts. May appear chronically ill, w/sign of
pancreatic insufficiency such as weight loss,
steatorrhea, clubbing, polyuria
• Differentiating acute vs chronic pancreatitis is
difficult b/c primary distinction is based on
disease reversibility
Chronic pancreatitisChronic pancreatitis
78.
79. DIFFERENTIAL DIAGNOSIS
• Pancreatic cancer (most important)
– older age
– absence of a history of alcohol use
– weight loss
– a protracted flare of symptoms
– onset of significant constitutional symptoms
– pancreatic duct stricture greater than 10 mm in length on ERCP
– Markers such as CA 19-9 and CEA
• peptic ulcer disease
• gallstones
• irritable bowel syndrome
• Acute pancreatitis
80. • Tests of function – hormone stimulation
– Secretin/ secretin CCK test
– Fecal elastase
– Fecal chymotrypsin
– Serum trypsinogen (trypsin)
– Fecal fat
– Blood glucose
–Tests of structure
– Endoscopic US
– ERCP
– MRI/MRCP/CT
– Abdominal US
– Plain abdominal film
81. US or CT grading system
• Normal – no abnormality on good quality study
• Equivocal – mild parenchymal duct dilatation (2-4mm)
– gland enlargement <2 fold
• Mild –moderate - + duct dilatation >4mm,
» duct irregularity,
» cavity < 10mm,
» parenchymal heterogenity,
» increased echo of duct wall,
» irregular head and body,
» focal parenchymal necrosis
• Severe - + cavity >10mm,
» intraductal filling defects,
» caliculi/ pancreatic calcification,
» ductal obstruction/stricture,
» severe ductal dilatation or irregularity,
» contiguous organ invasion
82.
83. Complications
• Cobalamin malabsorption
– Excess binding by cobalamin binding proteins other than
intrinsic factor which were degraded by pancreatic
enzymes
• DM – but end organ damages of DM and DKA are rare
• Non DM retinopathy (peripheral) due to Vit A and Zn defc.
• Pleural, peritoneal and pericardial effusions with high
amylase
• GI bleeding – PUD, gastritis, pseudocyst, varies (SV
thrombosis)
• Cholestasis, icterus, cholangitis, biliary cirrhosis
• Fistula – internal or external
• Subcutaneous fat necrosis – tender red nodules on the shins
• Pseudocyst, obstruction
• Pancreatic carcinoma – 4% life time risk
•
84. Chronic Pancreatitis
• Nonoperative management
– Control of abdominal pain
• Can be a problem (drug dependency)
• In some patients total abstinence from alcohol relieves
the pain
• Dietary changes are also recommended
– Treatment of endocrine insufficiency
– Treatment of exocrine insufficiency
85. Chronic Pancreatitis
• Operative management
– Ampullary procedures
• Designed to eliminate pancreatitis by preventing bile reflux into
the pancreatic duct (results have not been favorable)
– Ductal drainage procedures
• Designed to decompress the pancreatic duct in a retrograde
manner
– Pancreaticojejunostomy (success rates of 60-90%)
– Ablative procedures (last step)
• Pancreatectomy (total or subtotal)
– Most obtain adequate pain relief however these procedures can
cause IDDM
This is derived from branches of the coeliac and superior mesenteric arteries.
The head and uncinate process receive
superior pancreaticoduodenal branches from the gastroduodenal artery (a branch of the hepatic artery)
inferior pancreaticoduodenal branches from the superior mesenteric artery
The remainder of the gland is supplied by branches from the splenic artery.
The venous drainage of the pancreas passes into the portal system.
Superior and inferior pancreaticoduodenal veins from the head of the gland pass respectively into the portal vein and the superior mesenteric vein.
Veins from the remainder of the gland terminate in the splenic vein.
The lymphatic drainage from the pancreas is diffuse and widespread and this contributes to the fact that pancreatic cancer often presents
with positive lymph nodes and a high incidence of local recurrence after resection.
The pancreas is innervated by the sympathetic and parasympathetic nervous systems.
The parasympathetic system stimulates endocrine and exocrine secretion and
the sympathetic system inhibits secretion.
The pancreas also has a rich supply of afferent sensory fibers, which are responsible for the intense pain associated with advanced pancreatic cancer, and acute and chronic pancreatitis. These somatic fibers travel superiorly to the celiac ganglia. Interruption of
these somatic fibers can stop transmission of pain sensation.
1. The acinar cells of the exocrine pancreas secrete a number of enzymes that are necessary for digestion of proteins, starches, and fats.
2. The pancreatic ductal cells secrete fluid with a high bicarbonate content that serves to neutralize the acid entering the duodenum from the stomach.
Pancreatic secretion is under neural (vagus nerve) and hormonal (secretin and CCK) control, and the exocrine secretions empty primarily into the main pancreatic duct, which joins the common bile duct at the hepatopancreatic ampulla (of Vater).
A smaller accessory pancreatic duct also empties into the second part of the duodenum above the major duodenal papilla.
The endocrine pancreas is represented by clusters of islet cells (of Langerhans), a heterogeneous population of cells responsible for the elaboration and secretion primarily of insulin, glucagon, somatostatin, and several lesser hormones.
An understanding of embryology is required to appreciate the common variations in pancreatic duct anatomy.
The pancreas is formed by the fusion of a ventral and dorsal bud.
The duct from the smaller ventral bud, which arises from the hepatic diverticulum, connects directly to the common bile duct. The duct from the larger dorsal bud, which arises from the duodenum, drains directly into the duodenum.
The duct of the ventral anlage becomes the duct of Wirsung, and the duct from the dorsal anlage becomes the duct of Santorini.
With gut rotation, the ventral anlage rotates to the right and around the posterior side of the duodenum to fuse with the dorsal bud.
The ventral anlage becomes the inferior portion of the pancreatic head and the uncinate process, although the dorsal anlage becomes the body and tail of the pancreas.
The ducts from each anlage usually fuse together in the pancreatic head such that most of the pancreas drains through the duct of Wirsung, or main pancreatic duct, into the common channel formed from the bile duct and pancreatic duct.
The length of the common channel is variable. In about one third of patients
the two ducts remain distinct to the end of the papilla, the two ducts merge at
the end of the papilla in another one third, and in the remaining one-third a true
common channel is present for a distance of several millimeters.
Commonly, the duct from the dorsal anlage, the duct of Santorini, persists as the lesser pancreatic duct, and sometimes drains directly into the duodenum through the lesser papilla just proximal to the major papilla.
In approximately 30 percent of patients, the duct of Santorini ends as a blind accessory duct and does not
empty into the duodenum.
In 10 percent of patients, the ducts of Wirsung and Santorini fail to fuse. This results in the majority of the pancreas draining
through the duct of Santorini and the lesser papilla, although the inferior portion of the pancreatic head and uncinate process drains through the duct of Wirsung and major papilla.
This normal anatomic variant, which occurs in one out of 10 patients, is referred to as pancreas divisum. In a minority of these
patients, the minor papilla can be inadequate to handle the flow of pancreatic
juices from the majority of the gland. This relative outflow obstruction can result in pancreatitis and is sometimes treated by sphincteroplasty of the minor papilla.
