a simplified approach to diagnosis and management of acute pancreatitis based on 2013 update from ASG ( American Society of Gastroenterology ).

1. Management of Acute
Pancreatitis
2013 update
by
Ahmed Adel Abdelhakeem
Assistant lecturer
Internal Medicine Department - GIT unit
Asyut university hospital

2. Etiology

3. Etiology (most common)
** GALLSTONES (40 – 70 % )
usually an acute event and resolves when the stone is
removed or passes spontaneously.
** ALCOHOL (25 – 35 % )
- often manifests as a spectrum ranging from discrete
episodes of AP to chronic irreversible silent changes.
- the e diagnosis should not be entertained unless a
person has a history of over 5 years of heavy alcohol
consumption ( > 50 g per day )

4. Etiology ( other causes )
**PRIMARY AND SECONDARY HYPERTRIGLYCERIDEMIA can cause
AP however, these account for only 1 – 4 % of cases ( 36 ). Serum
triglycerides should rise above 1,000 mg / dl to be considered the
cause of AP (should be re-evaluated 1 month after discharge )
**HYPERCALCEMIA
**HYPERPARATHYROIDISM
**DRUGS o(6-mercaptopurine, azathioprine )
**BENIGN OR MALIGNANT mass that obstructs the main pancreatic
duct can result in AP. It has been estimated that 5 – 14 % of patients
with benign or malignant pancreatobiliary tumors present with
apparent IAP .Historically, adenocarcinoma of the pancreas was
considered a disease of old age. However, increasingly patients in
their 40s — and occasionally younger — are presenting with
pancreatic cancer.
This entity should be suspected in any patient > 40 years of age
with idiopathic pancreatitis.

5. Etiology ( IDIOPATHIC AP )
** IAP is defined as pancreatitis with no etiology established
after initial laboratory (including lipid and calcium level) and
imaging tests ( transabdominal U/S and CT in the appropriate
patient).
** Anatomic anomalies of the pancreas occur in 10 – 15 % of
the population, including pancreas divisum and sphincter of
oddi dysfunction
** The role of Genetic testing in AP has yet to be determined
, but may be useful in patients with:
- young patients ( < 30 years old )
- no cause is evident
- family history of pancreatic disease is present

6. DIAGNOSIS
- CLINICAL PRESENTATION
- LABORATORY PARAMETERS
- ABDOMINAL IMAGING

7. DIAGNOSIS
The diagnosis of AP is most often established by the
presence of 2 of the 3 following criteria:
(1) abdominal pain consistent with the disease,
(2) serum amylase and / or lipase greater than three
times the upper limit of normal, and / or
(3) characteristic findings from abdominal imaging.
Contrast-enhanced computed tomography (CECT) and / or
magnetic resonance imaging (MRI) of the pancreas should
be reserved for patients in whom the diagnosis is unclear

8. DIAGNOSIS (Clinical Presentation)
** Patients with AP typically present with epigastric or left
upper quadrant pain.
** The pain is usually described as constant with radiation to
the back, chest, or flanks but this description is nonspecific.
** The intensity of the pain is usually severe, but can be
variable. the intensity and location of the pain do not
correlate with severity. Pain described as dull, colicky, or
located in the lower abdominal region is not consistent with
AP and suggests an alternative etiology.

9. DIAGNOSIS ( Serum Amylase )
** cannot be used reliably for the diagnosis of AP.
** rises within a few hours after the onset of symptoms and
returns to normal values within 3 – 5 days; however, it may
remain within the normal range on admission in as many as
one-fifth of patients.
** most studies show a diagnostic efficacy of greater than
3 – 5 times the upper limit of normal

10. DIAGNOSIS ( Serum Amylase )
may be normal in:
*Alcohol-induced AP
*Hypertriglyceridemia.
Serum amylase concentrations might be high in the
absence of AP in:
*Macroamylasaemia *
glomerular filtration rate
*Diseases of the salivary glands
*Extra pancreatic abdominal diseases associated with
inflammation including : acute appendicitis, cholecystitis,
intestinal obstruction or ischemia, peptic ulcer, and
gynecological diseases.

11. DIAGNOSIS ( Serum Lipase )
** more specific
** remains elevated longer than amylase after disease
presentation
** similar problems with the predictive value remain in
certain patient populations , including :
- Macro lipasemia
- Renal disease , appendicitis , cholecystitis
- Diabetics who appear to have higher median lipase ( 3 – 5
times may be needed )

12. DIAGNOSIS ( Serum Lipase )
Neither serum amylase nor lipase
has any role in prognosis , assessing
severity or follow up.

13. DIAGNOSIS (Abdominal Imaging)
Abdominal U/S :
- Transabdominal ultrasound should be performed in
all patients with AP.
CECT: Routine use of CECT in patients with AP is
unwarranted , as the diagnosis is apparent in many
patients and most have a mild , uncomplicated
course.

14. DIAGNOSIS (Abdominal Imaging)
- Indications of CECT :
- Patient failing to improve after 48 – 72 hr after
admission ( persistent pain , fever , nausea, unable to
begin oral feeding ).
- Uncertain diagnosis
- Patient > 40 years old ( pancreatic tumor should be
considered as a possible cause ).

15. DIAGNOSIS (ABDOMINAL IMAGING)
MRI : helpful in patients with a contrast allergy and renal
insufficiency where T2-weighted images without
gadolinium contrast can diagnose pancreatic necrosis
MRCP: has the advantage of detecting
choledocholithiasis down to 3 mm diameter and
pancreatic duct disruption if CT is non - conclusive.
EUS : used when a more extensive evaluation for a
suspected underlying pathology is needed after a recurrent
episode of IAP

16. DIAGNOSIS ( Role of ERCP )
- Patients with AP and concurrent acute cholangitis should
undergo ERCP within 24 h of admission
- ERCP is not needed early in most patients with gallstone
pancreatitis who lack laboratory or clinical evidence of ongoing biliary
obstruction
- In the absence of cholangitis and / or jaundice, MRCP or EUS rather
than diagnostic ERCP should be used to screen for choledocholithiasis
if highly suspected.
- Pancreatic duct stents and / or post procedure rectal nonsteroidal
anti-inflammatory drug (NSAID) suppositories ( indomethacin rectal
supp. 100 mg once post procedure ) should be utilized to lower the
risk of severe post-ERCP pancreatitis in high-risk patients.

17. Assessment of severity
Atlanta Revised criteria 2013
Based on : local complications and presence of
organ failure.
BISAP score
Ranson’s criteria

18. Assessment of severity
Atlanta Revised criteria 2013
Mild acute pancreatitis
Absence of organ failure
Absence of local complications
Moderately severe acute pancreatitis
Local complications AND / OR
Transient organ failure ( < 48 h)
exacerbated co - morbidities
Severe acute pancreatitis (15 – 20 %)
Persistent organ failure > 48 h

19. Assessment of severity
- Local complications include : peripancreatic fluid collections and
pancreatic or peripancreatic necrosis (sterile or infected)
- Pancreatic necrosis is defined as diffuse or focal areas of nonviable
pancreatic parenchyma > 3 cm in size or > 30% of the pancreas
- edematous pancreas is defined as interstitial pancreatitis
- CT and / or MRI imaging also cannot reliably determine
severity early in the course of AP, as necrosis usually is not present
on admission and may develop after 24 – 48 h
- different scoring systems are available for assessing severity but
all of them are cumbersome and typically require 48 h to become
accurate.

20. Assessment of severity
Organ failure :

21. Assessment of severity
BISAP score

22. Assessment of severity
Ranson’s criteria:

25. Assessment of severity
Mild disease
Severe disease
- Mild pain
- Normal look
- Normal pulse rate
- Normal temp. or mild fever
- Severe pain
- Toxic look
- Tachycardia
- High grade or subnormal
temp.
- Hypoxia
- Decreased UOP
- Rigid abdomen
- shock
- Normal O2 saturation
- Adequate UOP
- Flat soft abdomen
- Normal BP

26. Assessment of severity
Mild disease
Severe disease
- Mild pain
- Normal look
- Normal pulse rate
- Normal temp. or mild fever
- Severe pain
- Toxic look
- Tachycardia
- High grade or subnormal
temp.
- Hypoxia
- Decreased UOP
- Rigid abdomen
- shock
- Normal O2 saturation
- Adequate UOP
- Flat soft abdomen
- Normal BP

27. Assessment of severity
- Most patients with severe disease present to the emergency room
with no organ failure or pancreatic necrosis; unfortunately, this has
led to many errors in clinical management of this disease.
- These errors include failure to provide adequate hydration, failure
to diagnose and treat cholangitis, and failure to treat early organ
failure.
- For this reason, it is critical for the clinician to recognize the
importance of not falsely labeling a patient with mild disease within
the first 48 h of admission for AP.

28. Assessment of severity
If there is
:
- 100 cases of AP
>>>>>
20 cases will be
severe ( 20 % ) .
- from those 20 cases
be infected ( 4 % ) .
>>>>>
4 cases will

29. Management
- Aggressive hydration
- Antibiotics
- Nutrition
- Role of ERCP
- Role of surgery

30. Management (Aggressive hydration)

31. Management (Aggressive hydration)
-- The use of hematocrit , BUN and creatinine as
surrogate markers for successful hydration has been
widely recommended.
-- Although no firm recommendations regarding
absolute numbers can be made at this time, the goal to
decrease hematocrit ( demonstrating hemodilution ) and
BUN ( increasing renal perfusion ) and maintain a normal
creatinine during the first day of hospitalization is
recommended.

32. Management (Antibiotics)

33. Management (Antibiotics)
- Fever, tachycardia, tachypnea, and leukocytosis associated
with SIRS that may occur early in the course of AP may be
indistinguishable from sepsis syndrome.
- When an infection is suspected, antibiotics should be given
while the source of the infection is being investigated.
- However, once blood and other cultures are found to be
negative and no source of infection is identified, antibiotics
should be discontinued

34. Management (Role of CT FNA)

35. Management (Role of Surgery)

36. Management (Role of Surgery)
cholecystectomy:
*Mild gallstone pancreatitis: should be performed during
hospitalization
*Severe AP: cholecystectomy is typically delayed after
discharge except if necrosectomy will be done.
*No stones / sludge on ultrasound and recurrent pancreatitis :
no role for cholecystectomy.
*In patients with mild AP who cannot undergo surgery, such
as the frail elderly and / or those with severe co morbid
disease, biliary sphincterotomy alone may be an effective way
to reduce further attacks of AP, although attacks of
cholecystitis may still occur

37. Management (Role of Surgery)
Necrosectomy (debridement):
- Early open debridement for sterile necrosis was
abandoned
- Debridement for sterile necrosis is recommended
if associated with:
*Gastric outlet obstruction and / or
*Bile duct obstruction.

38. Management (Role of Surgery)
Minimally invasive Necrosectomy :
Debridement through :
- Laparoscopic ,
- Percutaneous or
- Radiologic
by catheter drain
** Becoming the standard of care for cases of severe
necrotizing pancreatitis requiring debridement.

39. Management (Nutrition)

40. Management (Role of ERCP)

41. Management (Role of ERCP)
PREVENTING POST-ERCP PANCREATITIS (2 – 4
%) :
(1) Guide wire cannulation,
(2) pancreatic duct stents
(3) rectal NSAIDs ( Diclofenac 100 mg or
Indomethacin 100 mg once post procedure )

44. Systemic Complications of AP

45. Local Complications of AP
Pancreatic pseudo cyst
Pancreatic abscess
Necrotizing pancreatitis
Hemorrhagic pancreatitis

46. Pseudo -Cyst
- Localized fluid collection that is rich in amylase and other
pancreatic enzymes and is surrounded by a wall of fibrous tissue
that is not lined by epithelium.
- May remain within pancreatic parenchyma , extend into lesser
sac or retro peritoneum.
- Common clinical problem and complicate the course of chronic
pancreatitis in 30% to 40% of patients

47. Pseudo –Cyst …
Presentation
- Asymptomatic
- Acute complications include : bleeding (usually from splenic
artery pseudoaneurysm), infection, and rupture
- Chronic complications include gastric outlet obstruction,
biliary obstruction and thrombosis of the splenic or portal vein
with development of Gastric Varices secondary to portal
hypertension.

48. Pseudo -Cyst
Differential Diagnosis
- Once pancreatic cyst is identified by an imaging modality, the
most important question is to differentiate pseudo cyst from
other TRUE cystic lesions of the pancreas.
- The main differentiating features are :
1 - History of acute pancreatitis.
2 – amylase level ( very high in pseudo cyst )
3 – Aspiration of cyst content ( CEA , amylase , bacteriology ,
cytology ) usually and preferably done by EUS.

49. Pseudo -Cyst
Treatment
Wait 6 weeks post AP .. Why ?
Some pseudo cysts disappear spontaneously within 6 weeks.
To give sufficient time for a thick pseudo capsule to form.
Options :
- Endoscopic : cystogastrostomy.
- Percutaneous : pig – tail drainage.

52. Pancreatic Abscess
- Occurs as a complication of pseudo cyst if not drained.
- Complicates about 4 % of cases.
- The only reliable sign in CT is the presence of air bubbles within
the cyst that arises mainly from gas forming organism or a
fistula with the stomach, but unfortunately this is present only
in 50 % of cases.
- Diagnostic aspiration may differentiate it from a pseudo cyst if
there is no air bubbles ( physical , bacteriology , cells ).
- It was an indication for surgery in the past but now it could be
drained percutaneously (pig tail).

60. Thank you