4. History of Presenting
Complaint
• Tummy pain
• S: umbilical region
• O: Original episode, onset of the pain happened that afternoon
• C: gripping
• R: radiates to epigastrium and as high as the 5th intercostal space
• A: No vomiting, nausea, weight loss, fever
• T: constant
• E: Nothing made it better or worse
• S: Between 8 and 10/10
5. What do we want to ask about to
find the cause of the pancreatitis?
• G – gallstones
• E – ethanol
• T - trauma
• S – structural abnormality
• M -mumps
• A – autoimmune (PAN)
• S – Scorpion venom
• H –hyperlipidaemia, hypothermia,
hypercalcaemia
• E – ERCP, emboli
• D –Drugs
(Also pregnancy or idiopathic)
6. How to establish pancreatitis
severity?
• Assess ABC
• P – PaO2
• A – Age >55years
• N – Neutrophils, WCC>15x109/L
• C – Calcium <2mmol/l
• R – renal function; urea >16mmol/L
• E – Enzymes: LDH >600iu; AST>200iu/L
• A- Albumin <32g/L (serum)
• S – sugar blood glucose >10mmol/L
7. Management
• Acute Pancreatitis has a 12% mortality rate
• Import to call a specialist when someone presents
to A&E
• Patient must be nil by mouth
9. Management
• If assessed as severe or symptoms worsen transfer directly
to ITU
• Antibiotics may be useful in severe disease
• Give oxygen is O2 drops
• Suspected abscess or pancreatic necrosis – consideration
for parenteral nutrition with or without laparotomy &
debridement
• Suspected gallstones/worsening jaundice – indication for
ERCP and gallstone removal
• Monitor using repeat CT
11. Anatomy of the pancreas
• Head, uncinate process, neck, body and tail
12. Physiology of the Exocrine
Pancreas
Exocrine
Extracellular Matrix
Blood Vessels and Ducts
Endocrine Pancreas
The Exocrine Pancreas
-Acinar cells – digestive enzyme
secretion
-Centroacinar/ductal cells –
secretion of electrolytes
13. Acute Pancreatitis
• Acute injury of the pancreas resulting in
inflammation
• Severe episodes (10% of cases) carry a 40-50%
mortality rate
• Premature/exaggerated enzyme response within
the pancreas
• Possibly triggered by acute increase in
intracellular calcium
14. Typical Presentation
• Symptoms
• Central abdominal pain
• Epigastric pain
• Pain radiates to back – inflammation to the retroperitoneum
• Pain can be made better by sitting forwards
• Vomiting – common
• Signs
• Tachycardia, fever, jaundice, shock, ileus, rigid abdomen with
or without tenderness,
• Cullen’s sign (peri-umbilical) and Grey Turner’s sign (flank)
• Widespread abdominal tenderness and guarding
• Jaundice/cholangitis – indication of gallstone involvement
15. Predicting the severity of an
attack
• CRP >200ng/L in first 4 days = 80% predictive of a
severe attack
• Obesity – increases the inflammation
• Ranson (gallstone) Glasgow (alcohol) scoring
80% sensitivity (only after 48hours of
presentation)
• Acute Physiology and Chronic Health Evaluation II
(APACHE II) – high sensitivity as early as 24hours
after symptoms
16. Treatment
• Nasogastric Suction – prevents abdominal distention,
vomiting and aspiration pneumonia
• Analgesia: Tramadol/opiates; morphine and diamorphine
cause theoretical contraction of sphincter of Oddi.
• Nasogastric/Nasojejunal feeding
• If in Multi-organ failure – positive pressure ventilation and
renal support required – mortality in this group> 80%
• Gallstones: sphincterectomy and stone extraction
17. Complications
• Early
• Shock
• Hypocalcaemia
• ARDS
• Renal Failure
• DIC (Disseminating Intravascular Coagulation)
• Sepsis – can be managed by percutaneous drainage
• Glucose
• Multiple organ failure
18. Complications
• Late Complications (post 1 week)
• Abscesses
• Bleeding
• Thrombosis
• Fistulae
• Recurrent Oedematous pancreatitis
• Pancreatic necrosis and pseudocyst (fluid in lesser
sac)
• Surgical debridement or minimally invasive
necrosectomy
Pancreatic enzymes are secreted in great excess
Pancreatic secretion is regulated by several peptides that are released from GIT
Bicarbonate concentation increases chloride concentration falls
Maximum output chloride <50mEq/Land bicarbonate concentration on creases to 150mEq/L
pH between 8 and 8.5
Produces secretin in the S cells of the crypt of lieberkuhn
Basal Secretion and post prandial secrection
Postprandial – cephalic phase, gastric phase, intestinal phase
Cephalic – sight/taste of food, vagus mediated, results in enzyme and bicarbonate
Gastric – stomach distension, vagal reflex, gastrin and neural reflex stimulate enzyme secretion
Intestinal – acid entering duodenum, pH<4.5 secretin released
Secretin causes release of bicarbonate
Fatty acid, oligopeptides, and amino acids lead to CCK – increasing secretion of pancreatic enzymes
Ranson’s Criteria (for gallstone related)
On admission
Age > 55 yrs = 1 point
WCC > 16,000 = 1 point
LDH > 600 U/l = 1 point
AST >120 U/l = 1 point
Glucose > 10 mmol/l = 1 point
Within 48 hours
Haematocrit fall >10% = 1 point
Urea rise >0.9 mmol/l = 1 point
Calcium < 2 mmol = 1 point
pO2 < 60 mmHg = 1 point
Base deficit > 4 = 1 point
Fluid sequestration > 6L = 1 point
Score of >=3 prompts review for admission to HDU
Score <3. mortality risk <1%, >3 = 18%, >5 = 40%, >7 = close to 100%
Can not be applied fully for 48 hours
Poor predictorof outcome later in disease
Glasgow Criteria (alcohol related)
Age > 55 years = 1 point
Serum albumin < 32 g/L (3.2 g/dL) = 1 point
Arterial PO2 on room air < 60 mmHg = 1 point
Serum calcium < 2 mmols/L (8 mg/dL) = 1 point
Blood glucose > 10.0 mmols/L (180 mg/dL) = 1 point
Serum LDH > 600 units/L = 1 point
Serum urea nitrogen > 16.1 mmols/L (45 mg/dL) = 1 point and
WBC count > 15 x 10^9/L (15 x 10^3/microlitre) = 1 point.
The score can range from 0 to 8.
If the score is greater than 2, the likelihood of severe pancreatitis is high.
If the score less than 3, severe pancreatitis is unlikely.
