classical presentation on ACUTE PANCREATITIS LECTURE @ SOMALI NATIONAL UNIVERSITY INTERNAL MEDICINE DEPARTMENT

1. Acute Pancreatitis
Prepared & Presented by
Dr.Abdirazaq Ali Yusuf
(Dr.Cazaam),
Internalmedicinedepartment
@Somali National University

2. General
Acute pancreatitis is an acute inflammatory condition of the pancreas
that may extend to local and distant extrapancreatic tissues.
The clinical diagnosis of acute pancreatitis is based on the presence
of two of the following three features:
1) serum amylase and lipase levels elevated three times the upper limit
of normal;
2) Epigastric abdominal pain (often radiating to the back); and
3) typical imaging features on computed tomography (CT) or magnetic
resonance imaging (MRI).
Acute pancreatitis accounts for more than 200, 000 hospital admissions
each year in the US.

3. Etiology
The majority (80%) of cases of acute pancreatitis are caused by
gallstones or alcohol

4. Differential Diagnosis
1. Peptic ulcer disease
2. Gastritis/gastropathy
3. Intestinal perforation
4. Acute cholecystitis
5. Mesenteric ischemia
6. Small intestinal obstruction
7. Ruptured abdominal aortic aneurysm
8. Acute hepatitis

5. Pathophysiology
Normal mechanisms that protect the pancreas include:
the activation of pancreatic proenzymes occurs outside of the
pancreas within the duodenal lumen;
 enterokinase, the enzyme responsible for activating pancreatic
proenzymes, is located only in the duodenum;
 trypsin inhibitor (SPINK1) partially blocks the activity of trypsin.
Mechanisms of injury in acute pancreatitis (Figure 18.1 ) include:
1. activation of pancreatic proenzymes into active forms occurs
within the pancreatic acinar cells, thereby leading to
autodigestion of pancreatic tissue;
2. failure of normal protective mechanisms to inactivate trypsin
such as SPINK1 dysfunction;
3. microcirculatory injury and damage to the vascular endothelium
in the pancreas lead to the activation of the complement system,
release of proinfl ammatory mediators, and translocation of
bacteria into the systemic circulation

6. Clinical Features
1. Typical symptoms:
a. pain – 90 – 95% of patients with acute pancreatitis present with
abdominal pain that is usually localized to the epigastrium or right
upper quadrant and often radiates to the back. The pain may be
worse after eating;
b. nausea and vomiting – in 90% of patients;
c. fever and chills may occur but do not necessarily indicate infection;
d. anorexia and decreased appetite may also be seen.

7. Physical examination:
2. common findings include tachycardia, fever, epigastric or right upper
quadrant tenderness, localized guarding and rebound tenderness
in the epigastrium, and decreased bowel sounds;
3. findings associated with severe pancreatitis include hypotension,
jaundice, tachypnea, and a palpable mass (which may indicate a
pseudocyst); pancreatic necrosis may track along the falciform ligament
and into the retroperitoneum and can be seen as ecchymoses
in the periumbilical region (Cullen ’ s sign) and fl anks (Grey - Turner ’ s
sign).

9. Complications
Local:
 pancreatic: pseudocyst, ascites, fistula, fluid collection, abscess,
necrosis (sterile and infected);
Organisms most frequently seen in infected pancreatic
necrosis include Escherichia coli , Klebsiella spp., Pseudomonas
spp., Enterococcus spp., and rarely Candida albicans .
nonpancreatic: ileus, bile duct obstruction, gastric outlet
obstruction, duodenal ulcer, splenic vein thrombosis.

10. Physical Examination
 Systemic:
1. cardiovascular: hypotension, tachycardia, shock;
2. pulmonary: pleural effusion, pulmonary edema, acute
respiratory distress syndrome (ARDS);
3. renal: decreased urine output, acute renal failure;
4. hematologic: vascular thrombosis, disseminated intravascular
coagulation;
5. metabolic: metabolic acidosis, hyperglycemia, hypocalcemia;
6. infectious: sepsis, bacteremia, fungemia.

11. Assessment of Severity
Several scoring systems have been developed to predict severity, in
order to identify severe, acute pancreatitis and predict pancreatic
necrosis, mortality, and the need for prompt aggressive fluid resuscitation and
intensive patient monitoring.
1. Ranson ’ s criteria: measured at admission and at 48 hours (Tables
18.1 and 18.2 ).
2. Acute Physiology And Chronic Health Evaluation (APACHE)
III:
 used to predict mortality in critically ill patients admitted to the intensive care
unit;
 can be measured at any time during the hospital admission;
 cumbersome method; some parameters may not be relevant to prognosis in
acute pancreatitis.

13. Assessment of Severity
CT severity index (Balthazar score):
 CT severity index utilizes the presence and degree of pancreatic
necrosis and the presence or absence of peripancreatic fluid
collections on CT to predict morbidity and mortality;
 the limitations of the CT severity index include variability in
radiologists’ interpretation of CT findings and lack of correlation of
the score with the presence of organ failure, extrapancreatic
complications, or peripancreatic vascular complications.
Atlanta classifi cation:
developed to allow comparison among all aforementioned scoring
systems (Ranson ’ s, APACHE, and CT severity index); however, it
only defines mild and severe acute pancreatitis.

14. Assessment of Severity
BISAP scoring system:
 simple five - point scoring system that includes: Blood urea nitrogen (> 25 mg/dL),
Impaired mental status, Systemic inflammatory response (SIRS), Age ( > 65), Presence
of pleural effusion (also called the Bedside Index of the Severity of A cute
Pancreatitis);
 BISAP is used to identify patients within the first 24 hours of admission at increased
risk of in - hospital mortality.
Other indicators of severity or pancreatic necrosis: blood urea nitrogen, hematocrit
value, C - reactive protein (CRP), serum interleukin - 6, urinary trypsinogen activation
peptide level.
HAPS score:
 Harmless Acute Pancreatitis Score;
 absence of rebound abdominal tenderness, a normal hematocrit value, and a normal
serum creatinine level predict a nonsevere course with 98% accuracy.

15. investigation
Laboratory Tests
a. Pancreas specific: the diagnosis of acute pancreatitis relies on elevations of serum
amylase and lipase levels greater than three times the upper limit of normal. See
Tables 18.3 and 18.4 .
b. Amylase tends to rise earlier, within hours, and can remain elevated for 3 – 5 days.
c. Lipase is more specific for pancreatic disease (especially when related to alcohol),
and may remain elevated for longer periods than amylase.
d. The degree of pancreatic enzyme elevation or trend over time does not correlate with
the patient ’ s prognosis.
Others:
a. Liver biochemical tests:
 elevations of the serum bilirubin and alkaline phosphatase levels are often seen with
gallstone pancreatitis;
 greater than threefold elevation of the serum alanine aminotransferase (ALT) level is
highly specific but not sensitive for gallstone pancreatitis;

16. investigation
elevation of the serum aspartate aminotransferase (AST) level
greater than the serum ALT level may indicate acute pancreatitis
due to alcohol consumption.
b. The white blood cell (WBC) count is commonly elevated; however, an
elevated WBC count does not necessarily indicate infection.
c. Hyper - or hypoglycemia, hypocalcemia, and renal insufficiency are of
prognostic significance.
d. Serum triglyceride levels should be checked and if elevated
> 1000 mg/dL may indicate hypertriglyceridemia as the cause of
pancreatitis.
e. CRP>150mg/L at 36h after admission is a predictor of severe
pancreatitis.

18. Imaging Modalities
and abdominal radiographs:No psoas shadow increase
retroperitoneal fl uid), sentinel loop’ of proximal jejunum from
ileus (solitary air-filled dilatation)
Erect chest x-ray : helps exclude other causes (eg perforation).
Ultrasonography: to rule out gallstones (if gallstones + AST).
Contrast-enhanced CT scan: shows pancreas more clearly than
ultrasonography and can determine what percentage of the gland is
enhancing and what percentage is necrotic
MRCP/ERCP: (if LFTS worsen) to assess the presence of a
CBD stone

19. Diagnosis
NB: Two of the Above criteria is diagnostic

20. Treatment
Prevention
Preventive strategies include cessation of alcohol and smoking and
discontinuation of potentially causative medications.
Conservative and Supportive Care
1. The majority (80%) of cases will resolve with supportive measures.
2. Aggressive fluid resuscitation with Ringer ’ s lactate or normal saline
250 – 300 mL/hr intravenously for the first 48 hours is the mainstay
of management of acute pancreatitis.
3. Patients should be given nothing by mouth.
4. Nasogastric suction should be considered in patients who have
protracted vomiting.
5. Electrolyte abnormalities should be corrected.
6. Analgesics and anti - emetics should be given as needed.

22. Management
Immediate resuscitation and
assessment
• Analgesia
• Oral or, if not tolerated, nasogastric or
nasojejunal feeding
• NG tube (controversial)
• IV fluids
• Oxygen
• Catheterisation
• Sliding-scale insulin regimen if
necessary
Systemic management
All patients with severe pancreatitis should be
managed on an HDU or ICU to support and
monitor the
various systems:
• The cardiovascular system may need CVP
monitoring, and inotropes in severe cases
• Renal failure may necessitate dialysis
• Respiratory failure may lead to the need for
ventilation
• Metabolic problems may indicate intravenous
calcium gluconate or intramuscular magnesium
• Enteral or total parenteral nutrition (TPN)
may be needed

23. Oral diet should be initiated by day 3 if the patient ’ s pain is improved and the patient ’
s appetite returns.
Start with clear liquids and advance to a low - fat diet.
If the patient ’ s symptoms do not improve within 72 hours, parenteral or enteral feeding
should be initiated.
Total parenteral nutrition (TPN):
a. has been used traditionally;
b. does not stimulate pancreatic secretion;
c. has been shown to decrease mortality;
d. however, TPN is expensive and is associated with complications such as line
infections, thrombophlebitis, electrolyte disturbances, and liver dysfunction (including
cholestasis).
 Enteral nutrition through a nasogastric or nasojejunal feeding tube:
a. may stimulate pancreatic secretion;
b. is less expensive than TPN;
c. maintains intestinal integrity and prevents intestinal atrophy;
d. reduces the rate of infections and shortens length of hospitalization.
Nutrition

24. Antibiotics
The routine use of prophylactic antibiotics is not recommended for mild acute
pancreatitis, and its use is controversial in severe acute pancreatitis. Routine
use of antibiotics does not affect the rate of infection or mortality. Use of antibiotics
also increases the risk of fungal infections and infections with resistant organisms.
Antibiotics are recommended in the following situations:
 persistent fever or leukocytosis while the source is being identified;
 pancreatic necrosis, both sterile ( ≥ 30% of pancreas) and infected (Figure 18.4 ),
although the use of antibiotics in sterile necrosis is controversial;
 bacteremia;
 infected pancreatic pseudocyst;
 an abscess or infected peripancreatic fl uid collection
Antibiotics that have good pancreatic penetration include imipenem,meropenem,
cefepime, and moxifl oxacin.

26. Gallstones and Bile Duct Stones
Indications for ERCP:
 severe acute gallstone pancreatitis in a hemodynamically stable patient;
cholangitis;
 recurrent idiopathic pancreatitis to rule out microlithiasis, sphincter of
Oddi dysfunction, or pancreas divisum;
 if required during pregnancy, it is safest to do ERCP during the second
trimester.
• Indication for cholecystectomy:
 Gallstones: recurrent pancreatitis occurs in about 30% of patients with
gallstone pancreatitis; therefore, cholecystectomy is recommended.
 Cholecystectomy should be performed during the hospitalization for acute
pancreatitis, if possible, or within 2 – 4 weeks of discharge.

27. Pancreatic Pseudocys
Observation: it usually takes 4 – 6 weeks for a pseudocyst to mature.
Therefore, immediate intervention is usually not necessary.
Indications for drainage of a pseudocyst include worsening abdominal
pain, infected pseudocyst, gastric outlet or bile duct obstruction, associated
leak, and ascites.
Drainage of the pseudocyst may be performed percutaneously,
endoscopically,
or surgically.

28. Pancreatic Ascites
Patients should be placed on TPN.
Octreotide administered intravenously has been shown to be beneficial.
Antibiotics may be used, but the benefit is unclear.
Diuretics are not helpful.
Drainage options include:
I. endscopic stent placement into the pancreatic duct to bridge the leak or relieve duct
obstruction;
II. percutaneous drainage;
III. surgical drainage.
Pancreatic Necrosis
All patients with sterile pancreatic necrosis ( > 30%) and infected pancreatic necrosis
should be placed on antibiotics (see earlier).
Further treatment with endoscopic or surgical debridement depends
on whether the pancreatic necrosis is sterile or infected

29. The End