Acute Pancreatitis (Hepato-pancreatobiliary).ppt

Pancreatitis

1. Dr. S.V.Bharti
2
nd
year Resident
Dept of General Surgery

2. Introduction
Wt: 75-100 gm
Length:15-20 cm long
Retroperitoneal organ that lies in an oblique position
sloping upward from the c-loop of the duodenum
overlying the body of second lumbar vertabra and to
the splenic hilum.

4. Regions of Pancreas
Head
Uncinate process
Neck
Body
tail

6. Development of Pancreas
Dorsal pancreatic bud: dorsal side of duodenum-body
and tail.
Ventral bud: base of the hepatic duct :-uncinate
process and inferior part of head of pancreas

7. Blood Supply
Head :
Ant. and Post. Sup pancreaticoduodenal artery,
Ant. and Post Inf. Pancreaticoduodenal artery.
Body and tail:
Branches of splenic artery

8. Definition
Acute onset of symptom in previously healthy
individual and the disappearance of those symptoms
as the attack resolves.

9. CLASSIFICATION OF PANCREATITIES

14. Causes
Abuse of alcohol
Biliary tract stone
Drugs
Post ERCP
Post operative
Infection
Trauma
Hypercalcaemia and hyperlipidemia
Idiopathic

15. Pathophysiolgy
Biliry tract stone:
Common pancreaticobiliary channel obstruction
Ductal hypertension(stone induced panc. Duct obst)

16. Alcohol:
Hypertryglyceredemia ,
Oxygen free radical,
Promotes secretion of pancreatic juice ,
Spasm of sphincter of oddi

17. Colocalization theory
Cathepsin B + Trypsinogen

18. Clinical feature
Symptoms
Epigastric pain radiating to back
Nausea +++
Vomiting +
Distension of abdomen
Jaundice

19. General condition:
Restless, anxious, febrile
Tachycardia , tachypnea, hypotension , altered mental
status

20. Per abdominal :
Distended abdomen
Guarding, rigidity ,tenderness and rebound tenderness
more in epigastrium
Decreased bowel sound
Retroperitoneal hemorrhage
2. Respiratory finding: decreased air entry, stony dullness
on percussion.

21. Investigation
Blood examination:
Haemogram : PCV & Hb -Raised
Creatinine and blood urea nitrogen -Raised
Raised blood sugar
Hyperbilirubinemia
S. amylase and urinary amylase level
S.lipase level

22. Imaging
CXR with both dome of diaphragm
Pleural effusion –more on left side
Basal atelactasis
Also done to r/o other cause of upper abd. Pain

23. Abdominal x-ray:
Gas pattern of paralytic ileus
Retroperitoneal gas bubbles
Obliteration of psoas shadow
Sentinal loop
Colon cut off sign
Pancreatic calcification

24. USG abdomen
Gall bladder pathology and CBD stone
Pancreatic enlargement
Peripancreaticfluid collection
CECT
Non enhancement of organ during arterial phase(
indicating necrosis)
Pancraticswelling, edema and fluid collection
Delineates anatomy of CBD and pancreas very well

25. Differential Diagnosis
Small bowel obstruction
Acute cholecystitis
Cholangitis
Mesentric ischemia/infarction
Perforated hollow viscus
Inferior wall MI
Basal pneumonia

26. Prognosis of an attack of Acute
pancreatitis
Ranson criteria
Glassgow criteria
APACHE II
Balthazar scoring system
The Atlanta classification system

27. Ransoncriteria

28. Element Findings Points
Grade of inflammation Normal pancreas 0
Pancreatic enlargement1
Inflammation involving
pancreasand
peripancreaticfat
2
Single fluid collection or
phlegmon
3
Two or more fluid
collections or phlegmon
4
Degreeof pancreatic
necrosis
No necrosis 0
Necrosis of 1/3
rd
of
pancreas
2
Necrosis of 1/2 of pancreas4
Necrosis of >1/2 of
pancreas
6

29. Severity index Mortality complications
0-1 0 % 0 %
2-3 3 % 8 %
4-6 6 % 35 %
7-10 17 % 92 %

30. The Atlanta classification system
Based on clinical, radiological and pathological
findings
It has become the standard tool for defining a severe
attack of acute pancreatitis.
The Atlanta classification defines severe pancreatitis
as a score of 3 or more on Ranson'scriteria, a score of 8
or more on the Acute Physiology And Chronic Health
Evaluation (APACHE) II scoring system, or evidence of
organ failure and intrapancreaticpathology.

31. Definition of severe acute pancreatitis based on
the Atlanta criteria
Severity criteria
Ranson score > 3
APACHE II score > 8 Systemic
complications or organ dysfunction
Respiratory Pa O
2< 60 mmHg (8 kPa)
Renal Serum creatinine > 177 µmol/l (2 mg/dl) after resuscitation
Cardiovascular Systolic blood pressure < 90 mmHg (after resuscitation)
Coagulation system Platelet count < 100 ×10
9
/l or fibrinogen level < 1 g/l
Gastrointestinal haemorrhage > 500 ml per 24 h
Metabolic disturbance Corrected serum calcium < 1·85 mmol/l (7·5 mg/dl) Serum lactate levels > 5 mmol/l
Local complications
Acute fluid collections Occur early in the natural history of acute pancreatitis and lack a fibrous capsule
Pseudocyst Occurs at least 4 weeks after the onset of symptoms and has a fibrous capsule
Pancreatic abscess A localized collection of pus containing little or no necrotic pancreatic material
Pancreatic necrosis Pathological features: diffuse or focal area of non-viable pancreas that may be associated
with peripancreatic fat necrosis CT features: an area of non-enhancing pancreas measuring > 3 cm in
diameter or 30% of pancreatic tissue

32. Management
General supportive ( npo,ng tube,urinary
catheterisation)
Pain: Meperidine and its analogue
Fluid and electrolyte
Antibiotics
PPI
Nutritional support

33. Early complication and their
management
CVS:
Respiratory System:
Renal system:
GIT:

34. Role of early endoscopy and stone
extraction
Mild : Rarely beneficial
Severe: 3 studies
i) early stone clearance reduced severity and
morbidity of biliarypancreatitis
ii) reduced the incidence of infectious
complication
iii) increased incidence of complications
But at present most preferred –Endoscopic intervention
in severe biliarypancreatitis if presented within 48 hrs
after the onset of symptoms.

35. Role and timing of cholecystectomyin
patient with gallstone pancreatitis
Some form of definitive treatment before discharge
1.GB derived problem like cholecystitisor biliarycolic:
cholecystectomy
2.Stone in CBD( problem relating only to ductalstone)
do not necessarily require cholecystectomy
T/t: endoscopic clearance of stone + endoscopic
sphincterotomy.
25-30% develop GB symptom in 3-5 yrs.

36. Late complication
Acute fluid collection
Pancreatic and peripancreatic necrosis
Pancreatic pseudocyst
Pancreatic abscess and pancreatic necrosis

37. Treatment
Diagnosis : CECT-non enhancement of organ
indicates necrosis or CT guided aspiration of fluid
Management:
1. acute fluid collection
> 50 % regress spontaneously remaining may get walled
off and become pseudocystor necrosed, if infected CT
guided aspiration under antibiotic coverage.

38. 2. Sterile or infected necrosis.
a. sterile: aggressive debridement-
Decreases mortality and speed up recovery
Operation makes the situation worse
b. Infected necrosis:
Conventional and unconventional approach

39. Conventional approach Unconventional approach
Debridement with
reoperation when clinically
indicated or planned interval
Debridement with open or
closed packing and
reoperation when clinically
indicated or at planned
interval
Debridement with
continuous lavage
Antibiotics alone
Antibiotics with
percutaneous drainage
Antibiotics with endoscopic
drainage
Antibiotics with surgical
drainage but not
debridement
Antibiotics with debridement
through minimally invasive
surgery

40. Pancreatic pseudocyst
> 6cm in diameter
Symptomatic: tender,massefffectto adjacent
organ,obstructivejaundice,haemosuccuspancreaticus
t/t: symptomatic pseudocyst: drainage
cystogastrostomy
cystoduodenostomy
Roux en y jejunostomy
Pseudocystin tail: distal pancreatectomy
Head:transpapillarydrainage

41. Management of pancreatic ascites
Pancreatic juice in peritoneal cavity either through
duct disruption or from a leakage of pseudocyst
Diagnosis :high amylase level in asciticfluid
Treatment : initial ; decrease pancreatic secretion by
limiting enteralfeeding, NG tube insertion,
antisecretoryhormone somatostatin
If still persist: endoscopic pancreatic sphincterotomy
with or without placement of pancreatic duct stent.

42. Management of pancreatitis
induced false aneurysms
Pancreatic pseudocystcan erode into pancreatic or
peripancreaticvascular structure
If communicate with ductalsystem: bleeding into
pancreatic duct-haemosuccuspancreaticus
Bleeding into free peritoneal cavity: haemoperitoneum
T/t: therapeutic angiographic embolization; false
aneurysms in distal pancreas: distal pancreatectomy

43. Pancreticoenteral fistula
Pancreaticopleural fistula
Pancreatitis induced splenic vein thrombosis and
Sinistral Varices