Pancreatitis

Acute pancreatitis-scoring-treatment-anatomy

1. Pancreatitis
By : Darayus P.Gazder

2. Pancreatitis - Objectives
Discuss basic Anatomy, Physiology
Etiology
Clinical Presentation
Diagnosis
Prognosis
Management
Complications

3. Anatomy:

4. Physiology:
In response to a meal, the
pancreas secretes digestive
enzymes in an alkaline (pH 8.4)
bicarbonate-rich fluid.
CCK is released from duodenal
mucosa in response to food
and is responsible for enzyme
release.
Vagal stimulation increases the
volume of secretion.
Protein is synthesized at a
greater rate in the pancreas
than in any other tissue;

5. Pancreatitis:
It is the inflammation of the gland parenchyma of the
pancreas.

6. Acute Pancreatitis:
Acute Pancreatitis: inflammatory process with cascade of
release of inflammatory cytokines(TNF-A, IL2, IL6, PAF)
and pancreatic enzymes (Trypsin, lipases, co-lipases)
initiated by pancreatic injury but which may develop into
full blown MODS or SIRS

7. Mechanism of Injury:
Premature activation of pancreatic enzymes within
the pancreas process of auto digestion.
Anything that injures the acinar cells and impairs the
secretion of zymogen granules, or damages the duct
epithelium and thus delays the enzymatic secretion
can trigger acute pancreatitis.

8. Acute Pancreatitis – Epidemiology
180,000 - >200,000 Hospital Admissions / Year
20% have a severe course
10-30% mortality for this group, which has not
significantly changed during the past few decades
despite improvement in critical care and other
interventions
CAUSES: “I GET SMASHHED”

9. I: Idiopathic
G: Gall stones
E: Ethanol (alcohol)
T: Trauma
S: Steroids
M: Mumps (and other infections) / malignancy
A: Autoimmune
S: Scorpion stings/spider bites
H: Hyperlipidaemia/hypercalcaemia (metabolic
disorders)
E: Post ERCP
D: Drugs: Diuretics, OCPs, Sulfonamides

10. Gallstone Pancreatitis:

11. Etiology
Alcohol (30-40%)
Mechanism not fully understood
Not all alcoholics get pancreatitis (only about 15%)
This suggests a subset of the population predisposed to
pancreatitis, with alcohol acting more as a co-
precipitant
The mechanism includes the effects of diet, malnutrition
and direct toxicity

12. Post ERCP Pancreatitis:

13. Etiology – Idiopathic
Investigate thoroughly before labelling a patient as
“Idiopathic”
Experts suggest that idiopathic pancreatitis should
account for no more than 5-10% of the total cases,
yet the broadly quoted percentage in the literature at
this time in the US is currently 20-25%.

14. Acute Pancreatitis:
MILD:
Interstitial edema of the
gland;
Minimal organ
dysfunction;
80% of the patients will
have mild form of attack;
Mortality rate is around
1%.
SEVERE:
Pancreatic necrosis;
Severe systemic
inflammatory response;
Multi-organ failure;
Mortality is 20-50%
About one-third of
deaths occur in early
phase of the attack from
multiple-organ failure.

15. Clinical Presentation
Clinical
Continuous mid-epigastric / peri-umbilical
abdominal pain  Radiating to back, lower
abdomen or chest
Emesis
Fever
Aggravated by eating
Progressive, Refractory to analgesics
Restless and uncomfortable

16. Clinical Presentation
More Severe cases
Vitals: Tachypnea, Tachycardia, Hypotension
Jaundice
Muscle guarding in upper abdomen
Ascites
Pleural effusions – 10-20% cases
Pulmonary edema, Pneumonitis
Cullen’s sign – bluish peri-umbilical discoloration
Grey Turner’s sign – bluish discoloration of the
flanks

19. Diagnosis – Investigations
CBC
UCE
LFTs: bilirubin increased, mild derangement of others
Amylase raised >1000 u/L
Calcium/ Blood sugar
 ABG
ECG: changes may occur, diminished T waves.
 CXR: Pleural effusions
CT: necrosis, abscess, assessment of severity.

20. Diagnosis – Amylase
Elevates within HOURS and can remain elevated for
4-5 days
Normal 30-110 U/L
High specificity when using levels >3x normal
Many false positives
Most specific = pancreatic isoamylase (fractionated
amylase)
It can also be elevated in: 1) Torsion of inrta-abdominal viscus
2) Upper GI perforation 3) Mesenteric infarction 4) Ectopic
pregnancy 5) Retroperitoneal hematoma 6) Salivary gland
inflammation

21. Diagnosis – Lipase
The preferred test for diagnosis
Begins to increase 4-8H after onset of
symptoms and peaks at 24H
Normal: 7-60U/L
Remains elevated for days
Sensitivity 86-100% and Specificity 60-99%
>3X normal S&S ~100%

22. Diagnosis
Elevated ALT > 3x normal (in a non-alcoholic) has
a positive predictive value of 95% for GS
pancreatitis

23. Ultrasound Scan: Pancreatitis

24. Diagnosis – Imaging
CT
Excellent pancreas imaging
Recommended in all patients with persisting organ
failure, sepsis or deterioration in clinical status (6-
10 days after admission)
Search for necrosis – will be present at least 4
days after onset of symptoms; if ordered too early
it will underestimate severity
Follow-up months after presentation as clinically
warranted for CT severity index of >3

25. Diagnosis - Imaging
ERCP / EUS
Diagnostic and Therapeutic
Can see and treat:
Ductal dilatation
Strictures
Filling defects / GS
Masses / Biopsy
In patients with severe acute gallstone pancreatitis
and signs of ongoing biliary obstruction and
cholangitis an urgent ERCP is required

26. Prognosis – Ranson’s (Severe > 3)
 “WALLS FO CHUB”
Ranson’s Score
5 on Admission
WBC > 16000
Age > 55 y
LFT ALT > 250
LDH > 350
Sugar :”Glucose” >200
6 after 48 hours from presentation
Fluid Sequestration > 6L
PaO2 < 60
Calcium < 8
Hct > 10% decrease
BUN > 5
Base Deficit > 4

27. 3 or more= +ve Criteria= SEVERE ATTACK

28. Prognosis – CT Severity Index
CT Grade
Normal 0 points
Focal or diffuse enlargement 1 point
Intrinsic change or fat stranding 2 points
Single ill-defined fluid collection3 points
Multiple collections of fluid or gas4 points
Necrosis Score
None 0 points
1/3 of pancreas 2 points
1/2 of pancreas 4 points
> 1/2 of pancrease 6 points
Severe = Score > 6 (CT Grade + Necrosis)
CTSI 0-3= Mortality 3%, Morbidity 8%
CTSI 4-6= Mortality 6%, Morbidity 35%
CTSI 7-10= Mortality 17%, Morbidity 92%

29. Management of Mild pancreatitis:
Conservative approach is indicated with IV fluid
administration and catheterization.
We can keep the patient on NPO.
Analgesics and Anti-emetics are given.
Antibiotics are not indicated.
No drugs or interventions are warranted.
CT scan, only when there is sign of deterioration

30. Management of Severe pancreatitis:
Admission to HDU/ICU.
Analgesia.
NPO
Aggressive fluid rehydration.
Oxygenation.
Invasive monitoring of vital signs, CVP, urine output, ABGs.
Frequent monitoring of haematological and biochemical
parameters (including liver and renal function, clotting, serum
calcium, blood glucose)
Octreotide is used to reduce pancreatic secretions
Nasogastric drainage.
Antibiotic prophylaxis: IV cefuroxime, or imipenem, or
ciprofloxacin plus metronidazole.
CT scan.
ERCP within 72hrs of severe gallstone pancreatits.

31. Management – Necrosis
Its mostly sterile but can get infected from gut
bacteria. Contrast enhanced CT scan: Failure to
enhance
Necrosis associated Infection generally requires
debridement. Surgical debridement and
Necrosectomy supplemented by either open or
closed drainage.

32. Systemic
Complications
CVS
Neurological
ARDS
Renal
Failure
DIC
Metabolic
GI ileus

34. Complications – Long Term
Chronic Pancreatitis
Abdominal Pain
Steatorrhea, Malnutrition
Exocrine insufficiency (pancreas has a 90%
reserve for the secretion of digestive
enzymes)
DM, i.e.Endocrine Insufficiency, Pancreatic
carcinoma

36. Surgical Treatment
Mass in the head of the pancreas:
Pancreatoduodenectomy or a Beger procedure
(duodenum-preserving resection of the pancreatic
head) is appropriate;
If the duct is markedly dilated, then a longitudinal
pancreatojejunostomy or Frey procedure can be
of value.
 In rare patient with disease limited to the tail will be
cured by a distal pancreatectomy;
With intractable pain a total pancreatectomy is
also formed.