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;
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”
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
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
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
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
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 collection 3 points
Multiple collections of fluid or gas 4 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.
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
35.
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.
Editor's Notes
It is a retroperitoneal organ and comprises of head body and tail. The aorta and the superior mesenteric vessels lie behind the neck of the gland. Behind the neck of the pancreas the SMV joins the spleenic vein to form the portal vein. The tip extends to the spleenic hilum.
Nascent proteins are synthesized as preproteins and undergo modification in a sequence of steps;
The proteins move from the RER to the Golgi complex;
Where lysosomes and mature zymogen storage granules containing proteases are stored;
And then to the ductal surface of the cell, from which they are extruded by exocytosis;
During this phase, the proteolytic enzymes are in an inactive form, the maintenance of which is important in preventing pancreatitis.
(1) Production of bicarbonate-rich fluid to neutralize gastric fluid in the duodenum – duct cells primarily (CFTR gene = chloride / bicarbonate channel)
(2) Synthesis of digestive enzymes – acinar cells
(3) Insulin production = Islet cells
Accounts for 3% of all cases of abdominal pain among patients admitted to hospital in the UK;
Hospital admission rate is 9.8 per year per 100,000 population in the UK.
This disease can occur at any age, with a peak in young men and older women.
Influenza
MAC
Measles
Mumps, Rubella
Mycoplasma
Rubeola
Viral Hepatitis
Varicella
Gallstones (35%-60%)
Gallstone pancreatitis risk is highest among patients with small GS &lt; 5mm and with microlithiasis
GS pancreatitis risk is also increased in women &gt; 60 yrs
Accounts for 3% of all cases of abdominal pain among patients admitted to hospital in the UK;
Hospital admission rate is 9.8 per year per 100,000 population in the UK.
This disease can occur at any age, with a peak in young men and older women.
After 1 week Septic complications
Biliary obstruction/ Bleeding into
Cullen&apos;s sign
Turners Sign
ABD US: Check pancreatic mucosa, Visualize CBD + GB to rule out stones (Biliary pancreatitis) /If patient is stable PT NEEDS A CT SCAN to rule out other causes
Morphine not ideal but can still be used – it can theoretically worsen symptoms by increasing spasm of the Sphincter of Oddi
Demerol
Hydromorphone
All narcs cause Sphincter of Oddi spasm
PCA is generally preferred in the beginning
Always use the gut if you can to transition off IV pain meds