latest Presentation

2. Acute pancreatitis (AP) is an acute inflammatory
process of the pancreas with variable
involvement of other regional tissues or remote
organ systems.

3.  Acute pancreatitis is the most common inpatient principal
gastrointestinal diagnosis
 Incidence of acute pancreatitis also varies in different
countries
 Annual Incidence – 13 to 45 cases per 100,000 persons.
 Hospitalisation rates increase with Age
 88% higher among Blacks
 Males > Females
 Overall, about 20% of patients with acute pancreatitis have a
severe course, and 10% to 30% of those with severe acute
pancreatitis die.

4.  Most Common Causes— (80-90%)
 Gallstones – Leading cause (30-60%)
 Alcohol – 2nd most common (15-30%)
 Post ERCP – 5-10%
 Hypertriglyceridemia (>1000 mg/dl) – 1.3 – 3.8 %.
 Deficiency of APOLIPOPROTEIN C2.
 Drugs – 0.1 – 2%

7. Acute pancreatitis evolves in Three phases :---
1. Initial phase – intra pancreatic digestive enzyme activation
and acinar cell injury. Due to Trypsin activation which is
mediated by lysosomal hydrolases e.g. cathepsin B.
2. Second phase – Activation, chemoattraction and
sequestration of leukocytes and macrophages in the
pancreas - intrapancreatic inflammatory reaction.
3. Third phase- due to the effects of activated proteolytic
enzymes and cytokines released by inflamed organs.

8. Activated proteolytic enzymes esp.
Trypsin
Digestion of pancreatic and peripancreatic
tissue and Activation of other enzymes such
as Elastase and Phospholipase A2
Destruction of cell membrane, edema,
interstitial heamorrhage, vascular damage,
coagulation necrosis, fat necrosis and
parenchymal cell necrosis

9.  Cellular injury and necrosis causes:-
 Release of Bradykinin peptides, vasoactive substances and histamine.
 That produce Vasodilation, Increase vascular permeability and oedema in
Various Organs.
 SIRS – Systemic Inflammatory Response Syndrome,
 ARDS
 Multi-organ failure.
 Genetic Factors : Genes that are linked to intrapancreatic trypsin control
and variants that are associated with susceptibility to pancreatitis:-
 1) PRSS1 – cationic trypsinogen gene
 2) SPINK1 – pancreatic secretory trypsin inhibitor
 3) CFTR – Cystic fibrosis transmembrane conductance regulator gene
 4) CTRC – Chymotrypsin C gene
 5) CASR – calcium sensing receptor

10. CLINICAL FEATURES:
Abdominal pain:- Major symptoms
 Mild discomfort to severe , constant, incapacitating distress.
 steady, boring in character.
 Epigastrium and periumbilical in location.
 Radiate towards back, chest, flanks and lower abdomen
 Nausea, vomiting, abdominal distension .
PHYSICAL EXAMN :- pt.looks distressed and anxious
 Low grade fever, tachycardia, hypotension and shock.
 Erythematous skin nodules (d/t subcutaneous fat necrosis)
 Basilar rales, atelectesis, pleural effusion (Left > right).
 Abdomen tenderness and muscle rigidity,
decreased /absent bowel sounds
palpable upper abdominal mass.

11.  Cullen’s sign : faint blue discoloration in periumbilical region due to
hemoperitoneum.
 Turner’s sign : blue-red-purple or green-brown discoloration of the
flanks due to catabolism of haemoglobin from severe N.P with
hemorrhage.

12. Serum Lipase and Amylase:
 Increased 3 times or more than the upper limit value  Acute pancreatitis
 Lipase preferred over Amylase, more specific
 Levels of amylase fall down after 3-7 days but Lipase remains elevated till 7-
14 days.
 Does not correlate to severity
 Luekocytosis : 15,000 – 20,000 ecocytes/micro L
 Hemoconcentration : Hematocrit value >44% indicates necrosis.
 Pre renal azotemia : BUN >22 mg/dl
 Hyperglycemia
 Hypocalcemia (~25%)
 Hyperbilirubinemia : S. bilirubin >4.0 mg/dl (~10%) , Transient jaundice
 Raised S.ALP and SGOT: transient, may point to gall bladder related d/s or
inflammation in pancreatic head.

13.  Hypertriglyceridemia (~5 - 10 %)- S.amylase level may be spuriously normal
 Hypoxemia ( 5- 10%) : PaO2 <60 mmHg  ARDS
 ECG : occassionally abnormal with ST segment and T wave abnormalities
simulating MI.
 IMAGING :
 USG abdomen: – initial diagnostic imaging.
:- most useful to evaluate for gallstone diseases and pancreatic head.
 CECT abdomen – Revised Atlanta criteria
* Show morphologic features of acute pancreatitis on CT as follows:-
1. Interstitial pancreatitis
2. Necrotizing pancreatitis
3. Acute pancreatic fluid collection
4. Pancreatic pseudocyst
5. Acute necrotic collection (ANC)
6. Walled off necrosis (WON)

15.  Established by 2 of the 3 following criteria :
 1. Typical abdomen pain in epigastrium that may radiate to
back.
 2. three times or more elevation in S. lipase and / or S.
Amylase.
 3. confirmatory findings of acute pancreatitis in cross
sectional abdomen imaging.

16.  Perforated viscus – esp. peptic ulcer
 Acute Cholecystitis and Biliary colic.
 Acute intestinal obstruction.
 Acute Mesenteric vascular occlusion.
 Renal colic.
 Inferior wall MI.
 Aortic dissection.
 Connective Tissue disorders with vasculitis.
 Pneumonia.
 Diabetic ketoacidosis.

17.  Two phases have been defined :-
1. Early (<2 weeks):
Defined by clinical parameters rather than morphological changes. Most
patients exhibit SIRS and thus predisposed to organ failure.
 Three organ system should be assessed – Respiratory, Cardiovascular and
Renal system.
 Organ failure is defined as score of 2 or more for one of these organ system
using Modified Marshal Scoring system.
 Persistant Organ failure (>48 hrs) is the most imp clinical finding in
regard to severity of Acute pancreatitis episodes.

18.  2. Late (>2 weeks):-
 Protracted course of illness and may require imaging to evaluate for
local complications.
 Patients may require supportive measures like renal dialysis,
Ventilatory support, supplemental nutrition via naso-jejunal or
Parentral route.
 Development of Necrotizing Pancreatitis on CT imaging.
 May require Operative, endoscopy or percutaneous intervention.

19. 1) Mild acute pancreatitis – without local complications or Organ failure
seen after Interstitial acute pancreatitis. Usually self limiting .
2) Moderately severe acute pancreatitis –
Transient organ failure (< 48 hrs) or
Local or Systemic complications
in the absence of persistent organ failure
3) Severe Acute Pancreatitis –
Persistent organ failure ( >48 hrs)
CT or MRI should be obtained to assess for necrosis and complications

20. BISAP Score
( Bedside Index of Severity in Acute
Pancreatits )
B – BUN >25 mg/dl
I – Impaired mental status GCS <15
S - SIRS 2 or more out of 4
A - Age >60 yrs
P – Plueral effusion
Modified Marshall Score for Organ
Failure.
• CVS:- SBP<90 mmHg, HR >130
• Pulmonary:- Pa O2 <60 mm Hg
• Renal :- S.creatinine >2.0 mg %

23.  Criteria:-
1. Arterial Oxygen Partial Pressure < 60 mmHg (8.0 kPa)
2. Age > 55 years
3. White Blood Cell Count >15 x10^3/mm3
4. Serum Calcium <8.0 mg/dl (2.0 mmol/L)
5. Blood Urea Nitrogen 44 mg/dl (16 mmol/L)
6. Blood Glucose >180 mg/dl (10 mmol/L)
7. Serum Albumin <3.2 g/dl (32 g/L)
8. Lactate Dehydrogenase > (600 IU/L)
 Severe Pancreatitis: More than 3 criteria present within first 48 hours
of presentation

29.  2 types – interstitial or necrotising based on pancreatic
perfusion.
 CT is best evaluated 3-5 days into hospitalisation when patients
not responding to supportive care.
 Interstital pancreatitis- 90-95% . Characterised by diffuse gland
enlargement , homogenous contrast enhancement and mild
inflammatory Changes.
 Necrotizing pancreatitis – 5-10% which is c/b lack of pancreatic
parenchymal enhancement by iv contrast and presence of
peripancreatic necrosis.

32.  Fluid resuscitation and Monitoring response to therapy:-
• Most imp – aggressive intravenous fluid resuscitation.
• Patients is made NPO to rest the pancreas and given iv/im narcotic
analgesics e.g. Tramadol 50 mg im TDS for abdomen pain and supplemental
O2 via nasal cannula
• RL or NS bolus at 15 – 20 ml/kg (1050 – 1400 ml)
• Followed by 2-3 ml/kg/hr (200-250 ml/hr) so as to maintain U.O:-
>0.5ml/kg/hr.
• Bedside vitals monitoring.
• RL preferred over NS as it decreases systemic inflammation.
• Targeted Resuscitation Strategy :- measurement of Hematocrite and BUN
every 8-12 hrly. Decrease in BUN and Hematocrite indicate adequate fluid
resuscitation.
• If rise in BUN and Hematocrite – treated with a repeat volume challenge
with 2 L crystalloid bolus f/b fluid rate increase by 1.5 mg/kg/hr.

34.  Gallstone pancreatitis-
Pt with evidence of Ascending cholangitis (↑TLC & liver enzymes) should
undergo ERCP within 24 – 48 hrs of admission.
Cholecystectomy should be considered during admission or after 4-6 wks of
discharge.
Alternative for non surgical candidate can be Endoscopic biliary
sphincterotomy before discharge.
 Hypertriglyceridemia-
S. TG >1000 mg/dl. Initial therapy – Insulin, Heparin or Plasmapheresis
Control of diabetes, Administatn of lipid-lowering agents, weight loss and
avoidance of drugs that increase lipid levels

35. Management of Local Complications :-
NECROSIS –
• percutaneous aspiration of necrosis f/b Gram
stain and culture if signs of ongoing infection
present.
• No role of prophylactic antibiotic in
necrotizing pancreatitis.
• Start broad spectrum antibiotic in septic pts.
• Pancreatic debridement should be considered
for infected necrosis.
• Percutaneous or endoscopic transgastric
drainage f/b open necrosectomy if reqd.

36.  Low incidence. Most acute fluid collection resolve over time.
 <10 % have persistent fluid collection after 6 wks that would meet
the definition of Psuedocyst.
 Only symptomatic collection should be dained w/ surgery or
endoscopic or percutaneous route.
PANCREATIC DUCT DISRUPTION:-
• may present w/ symptoms of increasing abdomen pain or SOB in setting of
an enlarging fluid collection.
• Dx can be confirmed by ERCP or MRCP.
• Placement of a bridging Pancreating stent for 6 wks- effective in >90%
cases.

37.  May include Splenic vein thrombosis with gastric varices and Psuedoanuerysm
 Gastric varices bleed in <5% cases.
 Ruptured Psuedoanuerysm id life threatning and can be diagnosed & treated with
Mesentric angiography and Embolisation.
Extrapancreatic infections:-
• Hospital acquired infection seen in 20% of pt.
• Monitor for pneumonia, UTI and line infection
FOLLOW UP CARE:-
Assess for development of :-
diabetes,
exocrine insufficiency,
Recurrent cholangitis
Infected fluid collection

38. 1. Pulmonary
1. Pleural effusion
2. Atelectesis
3. Mediastinal fluid
4. Pneumonitis
5. ARDS
6. Hypoxemia
2. Cardiovascular
*Hypotension.
*Hypovolemia.
*Non specific ST and T
changes simulating MI.
*Pericardial effusion.

39. 3. Hematologic
*DIC
4. Gastrointestinal haemorrhage
*Peptic ulcer d/s
*erosive gastritis
*Haemorrhagic pancreatic necrosis
*Portal vein thrombosis
*splenic vein thrombosis
*gastric varices
5. Renal
*Oliguria <300 ml/d
*Azotemia
*Renal artery/ renal vein thrombosis
*Acute tubular necrosis
6. Metabolic:-
*Hyperglycemis.
*Hypertriglyceridemia.
*Hypocalcemia.
*encephalopathy
*Sudden blindness (Purtscher’s
retinopathy)
7. CNS:-
*Psychosis.
*Fat embolism.
8. Fat necrosis:-
*subcutaneous erythematous nodules
bone.