A comprehensive ppt about acute pancreatitis

1. ACUTE PANCREATITIS

2.  INTRODUCTION
 DEFINITION
 INCIDENCE
 AETIOLOGY
 CLINICAL PRESENTATION
 INVESTIGATIONS
 ASSESSEMENT OF SEVERITY
 MANAGEMENT
 COMPLICATION

3.  Pancreatitis- inflammation of the
pancreatic parenchyma.
Acute
Emergency condition
Mild
Severe
Chroni
c
Prolonged and frequently
lifelong disorder resulting
from the development of
fibrosis within the pancreas

4. ACUTE PANCREATITIS
DEFINITION
• Acute condition presenting with
abdominal pain, three fold rise in the
serum amylase or lipase level, and /or
characteristic finding of pancreatic
inflammation on CECT.
• Reversible inflammation of the
pancreas

5.  Divided into mild(interstitial
oedematous pancreatitis) or severe
(necrotising pancreatitis)
 Mild –characterised by interstitial
oedema of the gland and minimal organ
dysfunction.
 Severe – characterised by pancreatic
necrosis, a severe systemic
inflammatory response and often multi-
organ failure

6. Early phase
 Lasts a week
 Characterised by SIRS which –if
severe-can lead to transient or
persistent organ failure
Late phase
 Weeks to months
 Characterised by persistent signs of
inflammation and /or local
complications, like fluid collections and
peripancreatic sepsis.

7. INCIDENCE
 Accounts for 3% of all cases of
abdominal pain among patients
admitted to hospital in the UK
 Hospital admission rate for aucte
pancreatitis is 9.8 per year per
100000 population in UK, world wide it
may range from 5 to 50 per 100000.
 In lndia, 114-200/100,000 population
 May occur at any age, with a peak in
young men and older women

8. AETIOLOGY
 Biliary calculi(50-70%)
 Alcohol abuse(25%)
 Post ERCP
 Abdominal trauma
 Ampullary tumour
 Drugs-corticosteriods, azathioprine,
asparaginase, valproic acid, thiazides,
oestrogen
 Scorpion bite
 Viral infection-mumps, coxsackie B
 Hereditary pancreatitis
 idiopathic

10. CLINICAL PRESENTATION
 Pain- first in epigastrium but may be
localised to either upper quadrant or
felt diffusely throughout the abdomen.
sudden onset, sharp, severe,
continous, radiates to the back,
reduced by leaning forward.
 Nausea, non projectile vomiting,
retching
 Anorexia
 Fever, weakness

11. SIGNS
 Tachypnoea
 Tachycardia
 Hypotension
 Mild icterus( gall stone pancreatitis)

12.  Acute swinging pyrexia( cholangitis)
 Abdominal distension(ileus, ascites)
 Shifting dullness, reduced bowel
sounds
 Rebound tenderness, rigidity

14. DD
 Perforated viscus
 Acute cholecystitis, Biliary colic
 Acute intestinal obstruction
 Esophageal rupture
 Mesenteric vascular obstruction
 Renal colic
 Dissecting aortic aneurysm
 MI
 Basal pneumonia
 Diabetic ketoacidosis

15. INVESTIGATION
 CBC
 S. amylase (3 times normal) and
lipase(more sensitive and specific test
than amylase)
 C-reactive protein
 SE
 RFT
 LFT
 LDH
 Coagulation profile
 ABG analysis

16. OTHERS:-
 CECT

19.  X ray

20.  MRCP and EUS- helps in detecting
stones in the common bile duct and
directly assessing the pancreatic
parenchyma
 ERCP- identification and removal of
stones in CBD in gall stone
pancreatitis

21. ASSESSEMENT OF SEVERITY

24. OTHER SYSTEMS
 APACHE
 SAPS
 SOFA
 MODS
 MODIFIED MARSHALL SCORING
SYSTEM

27. MANAGEMENT
GOALS OF TREATMENT
 Aggressive supportive care
 Decrease inflammation
 Limit superinfection
 Identify and treat complication (of
pancreatitis and its treatment)
 Treat cause if possible

28. CONSERVATIVE MANAGEMENT
 IV access, obtain blood sample, rapid
fluid resuscitation & electrolytes
replacement.
 Gives analgesics (IM pethidine)
 Anti-emetics
 Keep the patient in NPO(until pain
free/2-3 days)
 NGT insertion to relieve vomiting.
 CBD insertion
 Monitor vitals.

29.  Somatostatin or Octreotide (pancreatic
secretions inhibitors)
 Respiratory support- Oxygen
supplementation, or venti mask
 ICU admission in severe acute
pancreatitis

31. ROLES OF ANTIBIOTOCS
 Shows no decrease in mortality in
severe acute pancreatitis
 Antibiotics are justified if:-
-Gas in retroperitoneal space
-needle aspiration of necrotic material
confirms infection
-sepsis
-CRP>120mg/L
-organ dysfunction
-APACHE II score >6

32. OPERATIVE MANAGEMENT
 Surgery has no immediate role
 Aggressive surgical pancreatic
debridement(Necrosectomy) should
be undertaken soon after confirmation
of the presence of infected necrosis.
 Pseudocyst: Cystogastrostomy,
Cystoduodenostomy, Roux-en –Y,
Cystojejunostomy

33. COMPLICATIONS

34. LOCAL COMPLICATION
Acute fluid collection:
 Occurs early in the course of mild
pancreatitis without necrosis
 Located adjacent to the pancreas.
 Has no encapsulated wall and is confined
within normal fascial planes.
 Fluid is sterile and resolves, so no
intervention requires
 Large collection requires percutaneous
aspiration under ultrasound or CT guided.
Trans gastric drainage under EUS

35. Sterile and infected pancreatic
necrosis
 Diffuse or focal area of non viable
parenchyma associated with
peripancreatic fat.
 Identified by an absence parenchymal
enhancement on CECT.

37.  They are sterile to begin with, but can
become subsequently infected, due to
the gut bacterial translocation.
 Sterile necrotic material should not be
drained or interfered with.
 If the patient shows features of sepsis
then a pancreatic necrosis should be
considered.

38. Management :- surgical-
Necrosectomy with
 Closed continuous lavage
 Closed drainage
 Open packing
 Closure and relaparotomy

39. Pseudocyst:
 Collection of amylase rich fluid
enclosed in a well defined wall of
fibrous or granulation tissue.
 Formation requires 4 or more weeks.
 Investigation: ultrasound or CT scan
 EUS and cystic guided aspiration is
done and look for CEA level, Amylase
level and cytology.
 ERCP and MRCP

40.  Management:
- percutaneous drainage
- endoscopic drainage
- surgical drainage

42.  Pancreatic abscess:
 Circumscribed intra abdominal
collection of pus, usually in proximity
to pancreas.
 It may be ANC or WON that has
become infected.
 Management: Percutaneous drainage

43.  Pancreatic ascites:
 Is a c/c generalised, peritoneal, enzyme
rich effusion usually associated with
pancreatic duct disruption
 Paracentesis will reveal turbid fluid with
a high amylase level
 Management: Adequate drainage with
wide bored drain
 ERCP stenting can be done

44.  Pancreatic effusion:
 Is an encapsulated collection of fluid in
the pleural cavity.
 Percutaneous drainage under image
guidance is done.

45.  Portal or splenic vein thrombosis:
 Identified by CT
 Marked rise of platelet count is suspicious.
 Usually conservative
 Patient should be screened for pro-
coagulant tendencies
 If varices present endoscopic banding or
injections should done.
 Use of aspirin and other antiplatelet drugs
should stop

46. OUTCOMES AND FOLLOW UP
OF ACUTE PANCREATITIS
 Mortality- 10-15% over the past 20yrs.
 Failure to remove a predisposing
factor will leads to the second attack.
 Idiopathic groups who suffer repeated
attacks may prove to have biliary
microlithiasis.
 In gallstone pancreatitis- remove
gallbladder and stone

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