Acute Pancreatitis LH

ACUTE PANCREATITIS
LOH LING HUI

SUPERVISED BY DR ANGELINE
Anatomy
• Greek words pan (all) and kreas (flesh)
• Both endocrine and exocrine (digestive) organ
• 12-15cm long J-shaped (like a hockey stick), soft, lobulated,
retroperitoneal organ
• Lies transversely on the posterior abdominal wall behind the
stomach, across the lumbar (L1-2) spine
• Adult gland weighs between 70-110g
1. https://emedicine.medscape.com/article/1948885-overview 2
Embryology
• Endodermal origin – forms from endodermic
foregut
• Begins with the formation of a ventral and a dorsal
pancreatic bud
• Dorsal bud forms the head, neck, body, and tail
• Ventral bud forms the uncinate process
2. https://en.wikipedia.org/wiki/Pancreas 3
Embryology
• Duodenum rotates to the right
• It carries with it the ventral pancreatic bud and
common bile duct (swings posteriorly)
• Upon reaching its final destination, the ventral bud
fuses with the dorsal bud, trapping the superior
mesenteric vessels in between.
3. http://cursoenarm.net/UPTODATE/contents/mobipreview.htm?26/21/26970 4
Embryology
• At this point of fusion, the main ducts of the ventral
and dorsal pancreatic buds fuse, forming the main
(Wirsung) pancreatic duct.
• The duct of the dorsal bud regresses, the proximal
part forming the accessory duct.
3. http://cursoenarm.net/UPTODATE/contents/mobipreview.htm?26/21/26970 5
Anatomy
6
Anatomy
• Head
 Lies in the C-shaped curve of the duodenum
 Uncinate process hooks behind the superior mesenteric
vesesls
 Terminal CBD runs behind the upper half of the head of
pancreas before joining the main pancreatic duct of
Wirsung to form a common channel (ampulla), which
opens at the major papilla on the medial wall of the
second part of the duodenum.
Anatomy
• Neck
 2.5 cm (1 in) long
 Lies in front of the superior mesenteric artery and vein,
splenic vein and portal vein
 Front upper surface supports the pylorus (the base) of
the stomach.
 Grooved by the gastroduodenal artery on the right
Anatomy
• Body
 Largest part of the pancreas
 Lies behind the pylorus, along the transpyloric plane
 Runs obliquely upwards to the left
• Tail
 Reaches the splenic hilum in the splenorenal (lienorenal)
ligament
Blood supply
• The pancreas receives blood
from branches of both the
coeliac artery and superior
mesenteric artery.
• Neck, body and tail of the
pancreas are supplied by the
splenic artery through its
pancreatic branches
• Head of the pancreas is
supplied by the superior and
inferior pancreaticoduodenal
arteries.
Blood supply
• The body and neck of
the pancreas drain into
the splenic vein
• The head drains into
the superior
mesenteric and portal
veins.
Lymphatic drainage
• Head drains into
pancreaticoduodenal lymph
nodes and lymph nodes in the
hepatoduodenal ligament, pre
and postpyloric lymph nodes.
• Body and tail drain into
mesocolic lymph nodes (around
the middle colic artery) and
lymph nodes along the hepatic
and splenic arteries.
• Final drainage occurs into celiac,
superior mesenteric, and para-
aortic and aortocaval lymph
nodes.
Nerve supply
• Parasympathetic
supply from the
posterior vagal trunk
via celiac branch
• Sympathetic supply
from T6-T10 via the
thoracic splanchnic
nerves and the celiac
plexus.
Roles of the pancreas
• The pancreas is a composite gland containing both
exocrine and endocrine components.
Exocrine - external digestive role
• Acini, formed of acinar cells
around a central lumen, are
arranged in lobules.
• Each lobule has its own ductule,
and many ductules join to form
intralobular ducts, which then
form interlobular ducts that
drain into branches of the main
pancreatic duct.
• Two main ducts, the main
pancreatic duct and the
accessory pancreatic duct, drain
pancreatic juice through the
ampulla of Vater into the
duodenum.
Exocrine - external digestive role
• Secretion of the pancreatic juice:
Digestive enzymes are stored in an inactive
form to prevent autodigestion
Upon stimulation, zymogen fuse with cell

membrane and exocytose
Trypsinogen is converted to trypsin by

enterokinase in duodenum
Tyrpsin then converts other inactive enzymes

into their active forms and are secreted
Ductal cells secrete bicarbonate in exchange for

chloride ions
Endocrine – internal hormone role
• The endocrine cells of pancreas reside in
the islets of Langerhans (2% of pancreas
parenchyma)
• Consists of:
 Insulin from beta cells (75%)
 Glucagon from alpha cells (20%)
 Somatostatin from delta cells
 Pancreatic polypeptide from F cells
Acute pancreatitis
• Acute pancreatitis is an inflammatory
illness of the pancreas of various
severity.
• 2012 Revised Atlanta Classification of
acute pancreatitis
• Classification based on duration:
• Early (first week)
– Clinical parameters and SIRS
• Late (after the first week)
– Morphologic criteria based on CT findings
combined with clinical parameters
4. Klingensmith M.E. et al, The Washington Manual of Surgery 7th Edition. Wolters Kluwer. 2016; 388 - 404
18
Acute pancreatitis
• Mild acute pancreatitis
– No organ failure, local or systemic
complications
• Moderately severe acute pancreatitis
– Organ failure that resolves within 48 h
and/or
– Local or systemic complications without
persistent organ failure
• Severe acute pancreatitis
– Persistent organ failure > 48 h
5. Greenberg JA, Hsu J, Bawazeer M, Marshall J, Friedrich JO, Nathens A, et al. Clinical practice guideline:
management of acute pancreatitis. Canadian Journal of Surgery. 2016;59(2):128-40. 19
Acute pancreatitis
• Morphological classification:
• Interstitial edematous acute pancreatitis
(80%)
Acute inflammation of the pancreatic
parenchyma and peripancreatic tissues
Self limiting, milder, transient clinical
manifestations
• Necrotising acute pancreatitis (20%)
Inflammation and pancreatic parenchymal
necrosis
Higher morbidity and mortality
4. Klingensmith M.E. et al, The Washington Manual of Surgery 7th Edition. Wolters Kluwer. 2016; 388 - 404
20
Epidemiology in Malaysia
• Worldwide, the incidence of acute pancreatitis
ranges between 5 and 80 per 100,000 population,
with the highest incidence recorded in the United
States and Finland. [6]
• Females outnumbered males by a ratio of more
than 3:1 [7]
• Incidence peaks in the 40–60 years age group [8]
• The common factors associated with acute
pancreatitis were alcohol intake in males and
biliary disease in females. [8]
• 8.4% fell into the category of severe pancreatitis [6]
• Overall mortality rate was 2.1% [7]
6. https://emedicine.medscape.com/article/181364-overview#a5
7. Raj SM, Lopez D, Thambidorai CR, Kandasamy P, Toufeeq Khan TF, Mohamad H, et al. Acute pancreatitis in north-
eastern peninsular Malaysia: an unusual demographic and aetiological pattern. Singapore medical journal.
1995;36(4):371-4. 21
8. P T, G H. Comparative study of acute pancreatitis in different ethnic populations in a Malaysian public hospital2008.
Pathophysiology
22
Etiology
23
History
• Abdominal pain
– Usually epigastric, sudden in
onset, dull in nature, radiating to
the back, relieved by bending
forward
• Nausea, vomiting, anorexia
• Fever
• Jaundice
• History of previous biliary colic,
binge alcohol consumption, ECRP,
family history of
hypertriglyceridemia/
autoimmune disease
4. Klingensmith M.E. et al, The Washington Manual of Surgery 7th Edition. Wolters Kluwer. 2016; 388 – 404
6. https://emedicine.medscape.com/article/181364-overview#a5 24
Clinical Presentation
• Tachycardia, hypotension
(hypovolemia)
• Abdominal tenderness, guarding,
distension, silent abdomen
• Febrile
• Jaundice
• Severe systemic effects
– Hypoxemia, renal failure,
hypocalcemia, hyperglycemia,
respiratory failure
• Gray-Turner sign (flank ecchymosis
– reddish brown)
• Cullen sign (periumbilical
ecchymosis - bluish)
• Fox sign (thigh ecchymosis – bluish)
• Purtscher retinopathy (temporary
or permanent blindness) *rare*
6. https://emedicine.medscape.com/article/181364-overview#a5 25
Diagnosis
The diagnosis of acute pancreatitis is made
by fulfilling two of the following three
criteria:
• Abdominal pain (acute onset of a
persistent, severe, epigastric pain often
radiating to the back)
• Lipase/amylase elevation >3 times the
upper limit of normal
• Characteristic imaging features on
contrast-enhanced CT, MRI, or
ultrasound
9. https://gi.org/guideline/acute-pancreatitis/ 26
Blood investigations
Blood test Abnormality Explanation
WBC ↑ Inflammation or infection
Serum amylase ↑ >3 fold Release of enzymes during acute pancreatitis

within few - Can also be due to other causes such as
hours of renal failure, intestinal obstruction,
onset, sialadenitis and malignancy
return to - Persistent elevations >10days:
normal over complications
3-5 days
Serum lipase ↑ >3 fold More sensitive for pancreatic disease (95%)
- Remains elevated for a longer period
Urea, creatinine ↑ AKI secondary to hypovolemic shock or direct
effect of enzymes
4. Klingensmith M.E. et al, The Washington Manual of Surgery 7th Edition. Wolters Kluwer. 2016; 388 – 404 27
Blood investigations
Blood test Abnormality Explanation
Albumin ↓ Increased capillary permeability
ALP, ALT ↑ Concomitant biliary or gallstone disease
Acute phase ↑ Markers of severity

proteins (CRP,
TNF-a, IL-6)
Serum calcium ↓ Fat saponification
Triglycerides ↑ Cause of acute pancreatitis
ABG Acidosis, Shock, ARDS

hypoxia
LDH, AST ↑
Radiological investigations
Ultrasound
• Pancreas not visualised in 40% due to overlying bowel gas
and body hiatus. [4]
• Ultrasonography should be performed in all patients at
baseline to evaluate the biliary tract to determine if the
patient has gallstones and/or a stone in the common bile
duct. [5]
• Ultrasonography can also identify gallbladder wall
thickening and edema, gallbladder sludge, pericholecystic
fluid and a sonographic Murphy sign, consistent with
acute cholecystitis.
• When these signs are present, the positive predictive
value of ultrasonography in the diagnosis of acute
cholecystitis is greater than 90%, and additional studies
are rarely needed.
29
management of acute pancreatitis. Canadian Journal of Surgery. 2016;59(2):128-40.
Ultrasound
9. http://wuxifhff.com/ultrasound-abdomen-anatomy/ultrasound-abdomen-anatomy-with-full-of-ultrasound-abdomen-
30
anatomy/
Ultrasound
9. http://wuxifhff.com/ultrasound-abdomen-anatomy/ultrasound-abdomen-anatomy-with-full-of-ultrasound-abdomen-
31
anatomy/
Computed tomography (CT)
• Gold standard (sensitivity 90%, specificity 100%)
• Should be performed selectively when:
1) a patient presents with substantial abdominal pain and a
broad differential diagnosis that includes acute pancreatitis
2) in patients with suspected local complications of acute
pancreatitis (e.g., peritonitis, signs of shock, suggestive
ultrasound findings)
3) Patients with clinical deterioration or failed to improve with
medical management
• Computed tomography for the assessment of local
complications is most useful 48–72 hours after the onset of
symptoms rather than at the time of admission.
• Unless contraindicated (e.g., renal dysfunction), intravenous
contrast should be given in order to assess for pancreatic
necrosis once patients are adequately fluid resuscitated and
normovolemia is restored.
32
CT findings include:
• Parenchymal enlargement and edema
• Necrosis
• Blurring of fat planes
• Peripancreatic fluid collections
• Bowel distention
• Mesenteric edema
• Left pleural effusion and atelectasis
33
Acute pancreatitis
34
Necrotising pancreatitis
35
Necrotising pancreatitis
36
Magnetic resonance imaging (MRI)
• Sensitivity 83%, specificity 91%
• Safe, non invasive
• Useful substitute for CT scan in patients
allergic to contrast or in acute renal failure
• Magnetic resonance
cholangiopancreatography (MRCP) superior
than normal MRI scan in visualising:
– Cholelithiasis
– Choledocholithiasis
– Anomalies of pancreatic and common bile ducts
37
Magnetic resonance cholnagiopancreatography (MRCP)
38
Endoscopic Retrograde Cholangiopancreatography (ERCP)
• Indications:
 Patients with suspected biliary pancreatitis
and possible cholangitis who are not clinically
improving within 24H after admission
 Endoscopic sphincterotomy and stone extraction
 Patients with no identifiable cause to rule out
occult CBD stones, strictures or neoplasm
 Suspected pancreatic ductal disruption eg.
traumatic pancreatitis
• In unstable patients with severe acute
gallstone pancreatitis, bile duct obstruction or
cholangitis, placement of a percutaneous
transhepatic gallbladder drainage tube
should be considered if ERCP is not safely
feasible.
• Pancreatic duct stents and/or postprocedure
rectal NSAID suppositories should be utilized
to prevent severe post-ERCP pancreatitis in
high-risk patients
5. Greenberg JA, Hsu J, Bawazeer M, Marshall J, Friedrich JO, Nathens A, et al. Clinical practice guideline: management of acute 39
pancreatitis. Canadian Journal of Surgery. 2016;59(2):128-40.
Endoscopic Retrograde
Cholangiopancreatography (ERCP)
40
Prognosis
• Predicting risk of developing severe outcomes is
crucial due to high mortality in fulminant acute
pancreatitis and benefits of early aggressive
supportive care
• Parameters in predicting prognosis and severity
of acute pancreatitis:
 Ranson’s scoring
 BISAP scoring
 Glasgow scoring
 CT Severity Index (CTSI)
 Acute Physiology and Chronic Health Evaluation
(APACHE II)
 Multiple Organ Dysfunction Score (MODS) and
Sequential Organ Failure Assessment (SOFA)
Ranson’s scoring
• Assessing prognosis in early acute pancreatitis
on admission and initial 48H
• Limitation:
– Cannot be completed until 48 hours following
admission, which may lead to missing an early
therapeutic window and increased mortality
• Interpretation of severity:
 Score ≥ 3: severe pancreatitis likely
• Interpretation for mortality:
 0-2 criteria: <1%
 3-4 criteria: 15%
 5-6 criteria: 50%
 >6 criteria: 70-90%
42
Ranson’s scoring
On Admission
G
Blood glucose >200mg/dL or >11 mmol/L
A Age > 55 years
L Serum lactate dehydrogenase >350 IU/L
A Aspartate aminotransferase >250 IU/L
W White blood cell count > 16,000/µL
Initial 48 hours
C Serum calcium <8 mg/dL or 2.0 mmol/L
H Hematocrit decrease > 10%
O Arterial PO2 <60mmHg
B Blood urea nitrogen elevation >5 mg/dL

Base deficit >4 mEq/L
B
Estimated fluid sequestration >6L
S
43
Bedside Index for Severity in Acute
Pancreatitis (BISAP) scoring
• Advantage:
 Only requires parameters from point of
admission
 Lower sensitivity but a higher specificity in
predicting organ failure
• Interpretation of mortality:
– 0: 0.1%
– 1: 0.4%
– 2: 1.6%
– 3: 3.6%
– 4: 7.4%
– 5: 9.5%
11. https://www.ahcmedia.com/articles/62466-pancreatitis 44
Bedside Index for Severity in Acute
Pancreatitis (BISAP) scoring
<3: Low
risk of
mortality
≥3: High
risk of
mortality
11. https://www.ahcmedia.com/articles/62466-pancreatitis 45
Glasgow scoring
• Valid for both gallstone and alcohol

induced pancreatitis
• Limitations:
– Requiring a 48 hours delay before can be
appropriately applied
• Interpretation:
– Scores ≥ 3: severe pancreatitis (suggest
admission to ICU)
Glasgow scoring
Parameters Readings
PaO2 <60mmHg or <8kpa
Age >55 years
Neutrophils WBC >15,000
Calcium <2 mmol/L
Renal function Urea > 16mmol/L
Enzymes AST/ALT > 200IU/L, LDH >600IU/L
Albumin <32 g/L
Sugar Glucose >10mmol/L
Modified CT Severity Index (CTSI)
• Used to predict severity and course of

disease based on imaging
characteristics
• Interpretation:
0-3 points: Mild (interstitial pancreatitis)
4-6 points: Moderate (exudative
pancreatitis)
7-10 points: Severe (necrotising
pancreatitis)
Modified CT Severity Index (CTSI)
Acute Physiology and Chronic Health
Evaluation II
• Assess disease severity in ICU patients >16 years
old (not specific to acute pancreatitis)
• Advantage:
 Calculated within the first 24 hours and daily
thereafter allowing continual assessment
• Limitations:
 Limited ability to distinguish between interstitial and
necrotizing acute pancreatitis
 Cumbersome and difficult to calculate
• Interpretation:
 Score <8: <4%
 Score ≥8: 11-18%
 Scoring increase during first 48H: Mild
 Scoring decrease during first 48H: Severe
5. Greenberg JA, Hsu J, Bawazeer M, Marshall J, Friedrich JO, Nathens A, et al. Clinical practice guideline: 50
Acute Physiology and Chronic Health
Evaluation II
• Rectal temperature
• Mean arterial pressure
• Heart rate
• Respiratory rate
• A-a gradient or PaO2
• Arterial pH or HCO3-
• Sodium
• Potassium
• Creatinine
• Haematocrit
• WBC
• Glasgow coma scale
• Age
• Comorbidity
Prognosis
• Multiple organ dysfunction score

(MODS)
• Sequential organ failure assessment
(SOFA)
Local Complications
Interstitial Necrotising
Early Acute Acute necrotic

(<4 weeks) peripancreatic collection
collection
Late Pseudocyst Walled-off

(>4 weeks) necrosis
53
Local Complications
54
Local Complications
• Acute peripancreatic collection
55
Local Complications
• Pseudocyst
56
Local Complications
• Acute necrotic collection
57
Local Complications
Infected pancreatic necrosis
58
Local Complications
• Walled-off necrosis
59
Local Complications
Vascular complications:
• Rare complication, most common in necrotising
• Haemorrhage:
– resulting from erosion of blood vessels and tissue
necrosis
• Pseudoaneurysm:
– autodigestion of arterial walls by pancreatic enzymes
results in pulsatile mass that is lined by fibrous tissue
and maintains communication with parent artery
• Splenic vein thrombosis
• Portal vein thrombosis
60
Systemic Complications
• Respiratory: Pao2/FiO2 ≤ 300

• Cardiac: systolic blood pressure < 90
mm Hg (off inotropic support), not
fluid responsive, or pH < 7.3
• Renal: serum creatinine ≥ 170 mmol/L
61
Management
• Supportive care
• Interventional and surgical
• Treatment of gallstone pancreatitis
62
Initial assessment and risk stratification
• Assess hemodynamic status

immediately upon presentation
• Begin resuscitative measures as
needed
• Risk assessment
• Patients with organ failure should be
admitted to an intensive care unit or
intermediary care setting whenever
possible
63
Supportive Care
Volume resuscitation
• Early aggressive intravenous hydration is
most beneficial the first 12–24 H
• Large volume (250-500 ml per hour of
isotonic crystalloid solution)
• Goal of aggressive hydration: decrease BUN
• Monitor urinary output with CBD
(>0.5ml/kg/hr)
• Frequent monitoring of electrolytes
64
Supportive Care
Gastric rest with nutritional support
• Nasogastric decompression
– Decrease neurohormonal stimulation of
pancreatic secretion
• Early nutritional support
– Catabolic
– Started once nausea, vomiting, abdominal pain
resolved
 Initiation of feeding with a low-fat solid diet
• Severe acute pancreatitis
• Early enteral feeding preferred
 Lower rates of infection
 Lower rates of surgical intervention
 Shorter length of stay
65
Supportive Care
Analgesics
• Pain relief
66
Supportive Care
Respiratory and acid base monitoring

• Pulmonary complications occurs up to
50%
• Necessary in severe pancreatitis
• Watchout for hypoxemia and fluid
overload secondary to aggressive fluid
resuscitation
67
Supportive Care
Antibiotics
• Routine use of antibiotics is not
recommended
Some randomised trials demonstrate
significantly lower rates of septic
complications in patients receiving
antibiotics
Meta-analysis demonstrated no
difference in mortality, infected
necrosis, or overall infections with
antibiotic therapy
68
Supportive Care
Antibiotics
• Indications
Extrapancreatic infections (eg. cholangitis)
Catheter-acquired infections
Bacteremia
Urinary tract infection
Pneumonia
• When infection is suspected, treat with
broad-spectrum antibiotics that cover
– Gram-negative bacteria
– Common hospital-acquired pathogens
(depending on length of hospitalization)
69
Supportive Care
Antibiotics
• Infected necrosis should be considered
in patients with pancreatic or
extrapancreatic necrosis who
deteriorate or fail to improve after 7–
10 days of hospitalization.
• Treatment:
CT-guided fine needle aspiration (FNA)
Empiric use of antibiotics such as
carbapenems, quinolones, and
metronidazole
70
Interventional and surgical
Indications:
• Clinical deterioration
• Sepsis
• Hypotension
• Necrotising pancreatitis
 Debridement (18-20 days after onset of attack
to allow sequestration of necrosis)
 Cholecystectomy (deferred until active
inflammation subsides and fluid collections
resolve or stabilize)
• Gastrointestinal obstruction due to
collections
 Percutaneous or endoscopic drainage
 Necrosectomy by endoscopic or minimally
invasive or open surgery 71
72
73
Treatment of gallstone pancreatitis
 Laparoscopic cholecystectomy with operative
cholangiogram on the index admission or soon
thereafter in healthy patients.
 Delay has resulted in the occurrence of a second
attack, which may be more severe.
• Severe gallstone pancreatitis
 Cholecystectomy should be performed when
general and local conditions permit
 Operative cholangiography is needed to rule out
persistent choledocholithiasis
• Patients unfit for surgery
 Endoscopic sphincterotomy may protect against
further attacks of pancreatitis.
74
References
1. https://emedicine.medscape.com/article/1948885-overview
2. https://en.wikipedia.org/wiki/Pancreas
3. http://cursoenarm.net/UPTODATE/contents/mobipreview.htm?26/21/26970
4. Klingensmith M.E. et al, The Washington Manual of Surgery 7th Edition. Wolters Kluwer.
2016; 388 – 404
5. Greenberg JA, Hsu J, Bawazeer M, Marshall J, Friedrich JO, Nathens A, et al. Clinical
practice guideline: management of acute pancreatitis. Canadian Journal of Surgery.
2016;59(2):128-40.
6. https://emedicine.medscape.com/article/181364-overview#a5
7. Raj SM, Lopez D, Thambidorai CR, Kandasamy P, Toufeeq Khan TF, Mohamad H, et al.
Acute pancreatitis in north-eastern peninsular Malaysia: an unusual demographic and
aetiological pattern. Singapore medical journal. 1995;36(4):371-4.
8. P T, G H. Comparative study of acute pancreatitis in different ethnic populations in a
Malaysian public hospital2008.
9. http://wuxifhff.com/ultrasound-abdomen-anatomy/ultrasound-abdomen-anatomy-
with-full-of-ultrasound-abdomen-anatomy/
10. Chen L, Lu G, Zhou Q, Zhan Q. Evaluation of the BISAP Score in Predicting Severity and
Prognoses of Acute Pancreatitis in Chinese Patients. International Surgery. 2013;98(1):6-
12.
11. https://www.ahcmedia.com/articles/62466-pancreatitis
12. https://gi.org/guideline/acute-pancreatitis/
75
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76

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ACUTE PANCREATITIS

LOH LING HUI

Upon stimulation, zymogen fuse with cell

Trypsinogen is converted to trypsin by

Tyrpsin then converts other inactive enzymes

Ductal cells secrete bicarbonate in exchange for

WBC ↑ Inflammation or infection

Serum amylase ↑ >3 fold Release of enzymes during acute pancreatitis

Albumin ↓ Increased capillary permeability

ALP, ALT ↑ Concomitant biliary or gallstone disease

Acute phase ↑ Markers of severity

Triglycerides ↑ Cause of acute pancreatitis

ABG Acidosis, Shock, ARDS

Magnetic resonance cholnagiopancreatography (MRCP)

B Blood urea nitrogen elevation >5 mg/dL

• Valid for both gallstone and alcohol

PaO2 <60mmHg or <8kpa

Age >55 years

Neutrophils WBC >15,000

Calcium <2 mmol/L

Renal function Urea > 16mmol/L

Enzymes AST/ALT > 200IU/L, LDH >600IU/L

Albumin <32 g/L

Sugar Glucose >10mmol/L

• Used to predict severity and course of

• Multiple organ dysfunction score

Early Acute Acute necrotic

Late Pseudocyst Walled-off

• Acute peripancreatic collection

• Acute necrotic collection

• Respiratory: Pao2/FiO2 ≤ 300

• Assess hemodynamic status

Respiratory and acid base monitoring

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