This document provides information about pancreatitis, including: - Pancreatitis is inflammation of the pancreas that can be acute (presenting as an emergency) or chronic (a prolonged disorder resulting in pancreatic fibrosis). - The two major causes of acute pancreatitis are gallstones and alcohol abuse. Acute pancreatitis presents with severe abdominal pain and elevated pancreatic enzymes. - Severe acute pancreatitis is characterized by pancreatic necrosis, systemic inflammatory response, and often multi-organ failure with a mortality rate of 20-50%. - Chronic pancreatitis is defined as a continuing inflammatory disease of the pancreas causing pain and/or permanent loss of pancreatic function.

1. Pancreatitis
Dr. Mostafa Hegazy

2. Anatomy

3. Pancreatitis is inflammation of the gland
parenchyma of the pancrease.
For clinical purposes, it is useful to divide pancreati-
tis into :
Acute, which presents as an emergency, and
Chronic, which is a prolonged and frequently
lifelong disorder resulting from the development of
fibrosis within the pancreas.
It is probable that acute pancreatitis is but a phase of
chronic pancreatitis.

4. Acute pancreatitis is defined as an acute condition presenting
with abdominal pain and is usually associated with raised
pancreatic enzyme levels in the blood or urine as a result of
pancreatic inflammation. Acute pancreatitis may recur.
The underlying mechanism of injury in pancreatitis is thought
to be premature activation of pancreatic enzymes within the
pancreas, leading to a process of autodigestion.
Anything that injures the acinar cell and impairs the
secretion of zymogen granules, or damages the duct
epithelium and thus delays enzymatic secretion, can trigger
acute pancreatitis.

5. Once cellular injury has been initiated, the inflammatory
process can lead to pancreatic oedema, haemorrhage and,
eventually, necrosis.
As inflammatory mediators are released into the
circulation, systemic complications can arise, such as
haemodynamic instability, bacteraemia (due to
translocation of gut flora), acute respiratory distress
syndrome and pleural effusions, gastrointestinal
haemorrhage, renal failure and disseminated intravascular
coagulation (DIC).

6. Acute pancreatitis may be categorised as mild or severe.
Mild acute pancreatitis is characterised by interstitial
oedema of the gland and minimal organ dysfunction. Eighty
per cent of patients will have a mild attack of pancreatitis, the
mortality from which is around 1%.
Severe acute pancreatitis is characterised by
pancreatic necrosis, a severe systemic inflammatory response
and often multi-organ failure, the mortality varies from 20% to
50%.
About one-third of deaths occur in the early phase of the
attack, from multiple organ failure, while deaths occurring
after the first week of onset are due to septic complications.

7. Chronic pancreatitis is defined as a continuing
inflammatory disease of the pancreas characterised by
irreversible morphological change typically causing pain
and/or permanent loss of function. Many patients with
chronic pancreatitis have exacerbations, but the
condition may be completely painless.

8. Incidence
Acute pancreatitis accounts for 3% of all cases of
abdominal pain among patients admitted to hospital in the
UK.
 The hospital admission rate for acute pancreatitis is 9.8 per
year per 100 000 population in the UK, although worldwide,
the annual incidence may range from 5 to 50 per 100 000.
 The disease may occur at any age, with a peak in young
men and old women.

9. Etiology
The two major causes of acute pancreatitis
 Biliary calculi, which occur in 50–70% of
patients, and
 Alcohol abuse, which accounts for 25% of
cases.

10. Gallstone pancreatitis: is thought to be triggered
by the passage of gallstones down the common bile
duct.
If the biliary and pancreatic ducts join to share a
common channel before ending at the ampulla, then
obstruction of this passage may lead to reflux of bile
or activated pancreatic enzymes into the pancreatic
duct.
Patients who have small gallstones and a wide cystic
duct may be at a higher risk of passing stones.

11. .

12. Alcoholic pancreatitis
The proposed mechanisms for alcoholic
pancreatitis include the effects of diet,
malnutrition, direct toxicity of alcohol,
concomitant tobacco smoking,
hypersecretion, duct obstruction or reflux,
and hyperlipidaemia.

13. Possible causes of acute pancreatitis
 Gallstones
 Alcoholism
 Post ERCP
 Abdominal trauma
 Following biliary, upper gastrointestinal
or cardiothoracic surgery
 Ampullary tumour

14. Drugs (corticosteroids, azathioprine, asparaginase, valproic
acid, thiazides, oestrogens)
Hyperparathyroidism
Hypercalcaemia
Pancreas divisum
Autoimmune pancreatitis
Hereditary pancreatitis
Viral infections (mumps, coxsackie B)
Malnutrition
Scorpion bite
Idiopathic

15. ■ It is essential to establish the aetiology
■ Investigate thoroughly before labelling
it as ‘idiopathic’
■ After the acute episode resolves,
remember further management of the
underlying aetiology
■ If the aetiology is gallstones,
cholecystectomy is desirable during the
same admission

16. Clinical presentation

 Pain is the cardinal symptom.
 It characteristically develops quickly, reaching
maximum intensity within minutes rather than
hours and persists for hours or even days.
 The pain is frequently severe,constant and
refractory to the usual doses of analgesics.

17.  Pain is usually experienced first in the epigastrium but
may be localised to either upper quadrant or felt diffusely
throughout the abdomen.
There is radiation to the back in about 50% of patients,
and some patients may gain relief by sitting or leaning
forwards.
 The suddenness of onset may simulate a perforated
peptic ulcer, while biliary colic or acute cholecystitis can
be mimicked if the pain is maximal in the right upper
quadrant.

18.  Radiation to the chest can simulate myocardial
infarction, pneumonia or pleuritic pain.
 In fact, acute pancreatitis can mimic most causes of
the acute abdomen and should seldom be discounted in
differential diagnosis.

19. Nausea, repeated vomiting and retching are usually marked
accompaniments. The retching may persist despite the
stomach being kept empty by nasogastric aspiration.
Hiccoughs can be troublesome and may be due to gastric
distension or irritation of the diaphragm.

20. On examination, the appearance may be that of a
patient who with profound shock, toxicity and
confusion.
Tachypnoea is common,
Tachycardia is usual,
Hypotension may be present.
The body temperature is often normal or even
subnormal, but frequently rises as inflammation
develops.
Mild icterus can be caused by biliary obstruction in
gallstone pancreatitis, and an acute swinging pyrexia
suggests cholangitis.

21.  Bleeding into the fascial planes can produce bluish
discolouration of the flanks (Grey Turner’s sign) or
umbilicus (Cullen’s sign). Neither sign is
pathognomonic of acute pancreatitis; Cullen’s sign was
first described in association with rupture of an ectopic
pregnancy.
Subcutaneous fat necrosis may produce small, red,
tender nodules on the skin of the legs.
 Abdominal examination may reveal distension due to
ileus or, more rarely, ascites with shifting dullness.

22.  A mass can develop in the epigastrium due to
inflammation.
 There is usually muscle guarding in the upper abdomen,
although marked rigidity is unusual.
A pleural effusion is present in 10–20% of patients.
Pulmonary oedema and pneumonitis are also described and
may give rise to the differential diagnosis of pneumonia or
myocardial infarction.
 The patient may be confused and exhibit the signs of
metabolic derangement together with hypoxaemia.

23. Investigations
 Typically, the diagnosis is made on the basis
of the clinical presentation and an elevated
serum amylase level.
 A serum amylase level three to four times
above normal is indicative of the disease.
 A normal serum amylase level does not
exclude acute pancreatitis, particularly if the
patient has presented a few days later.

24. If the serum lipase level can be checked, it provides a
slightly more sensitive and specific test than amylase.
If there is doubt, and other causes of acute abdomen have
to be excluded, contrast-enhanced CT is probably the best
single imaging investigation.
Investigations in acute pancreatitis should be aimed
at answering three questions:
■ Is a diagnosis of acute pancreatitis correct?
■ How severe is the attack?
■ What is the aetiology?

25. Assessment of severity
Various scoring systems,
 Ranson
 Glasgow scoring systems
 The APACHE II scoring system, used in
intensive care units, can also be applied.

27. Sever attack may be heralded by an initial clinical
impression of a very ill patient and an APACHE II score
above 8. At 48 hours after the onset of symptoms,
Glasgow score of 3 or more, a C-reactive protein level
greater than 150 mg l–1 and a worsening clinical state with
sepsis or persisting organ failure indicate a severe attack.
Severity stratification should be performed in all patients
within 48 hours of diagnosis.
Patients with a body mass index over 30 are at higher risk
of developing complications.

28. Acute Severe Pancreatitis
Pathophysiology
Injury or disruption of pancreatic ducts
leakage of pancreatic enzymes  autodigestion
Breakdown of cell membranes  edema 
vascular damage, hemorrhage, necrosis 
inflammatory mediators  Shock, MODS, …..

29. Imaging
 Plain erect chest and abdominal radiographs are not
diagnostic of acute pancreatitis, but are useful in the
differential diagnosis.
 Non-specific findings in pancreatitis include a generalised or
local ileus (sentinel loop), a colon cut-off sign and a renal
halo sign. Occasionally, calcified gallstones or pancreatic
calcification may be seen
 A chest radiograph may show a pleural effusion and, in
severe cases, a diffuse alveolar interstitial shadowing may
suggest acute respiratory distress syndrome.

30. Ultrasound does not establish a diagnosis of acute
pancreatitis. The swollen pancreas may be seen, but
ultrasonography should be performed within 24 hours in all
patients to detect gallstones as a potential cause, rule out
acute cholecystitis as a differential diagnosis and determine
whether the common bile duct is dilated.

31. CT is not necessary for all patients, particularly those
deemed to have a mild attack on prognostic criteria. But
a contrastenhanced CT is indicated in the following
situations:
• if there is diagnostic uncertainty;
• in patients with severe acute pancreatitis, to distinguish
interstitial from necrotising pancreatitis.
In the first 72 hours, CT may underestimate the extent
of necrosis.
The severity of pancreatitis detected on CT may be
staged according to the Balthazar criteria;

32. • in patients with organ failure, signs of sepsis or
progressive clinical deterioration;
• when a localised complication is suspected, such as fluid
collection, pseudocyst or a pseudoaneurysm.
 Cross-sectional MRI can yield similar information to that
obtained by CT.
 EUS and MRCP can help in detecting stones in the
common bile duct and directly assessing the pancreatic
parenchyma.
 ERCP allows the identification and removal of stones in the
common bile duct in gallstone pancreatitis.

33. The presentation is so variable that sometimes even an expe-
rienced clinician can be mistaken, occasionally the diagnosis is
only made at laparotomy. The appearances at laparotomy are
characteristic

34. Key Questions
 What clinical manifestation occurs because the
pancreas lies retroperitoneally in the abdominal
cavity?
 What is the sphincter of Oddi? What common pain
medication causes spasms of this sphinter?
 Which digestive enzymes are secreted by the
pancreas?
 What is the hallmark lab abnormality in pancreatitis?

35. Assessment
Physiological Variable
Diagnostic tests
 Serum amylase
 >200U/L for 24-72 hr – 4x
starts to rise 2-6 hr after onset of pain
Peaks @ 24 hours
Return to normal @ 72 hr
 Serum lipase
used with amylase; rises later than
amylase (48 hours)
return to normal 5-7 days
  WBC’s
  glucose
  lipids
  calcium
  magnesium

36. Ranson-Imrie Scale
On admission or dx
 Age >55 years
 WBC >16K/mm³
 BG >200 mg/dl
 LDH >400 IU/L
 AST >250 IU/L
During first 48 hours
  in HCT by 10%
 FV  or 4000 ml
 Ca < 8 mg/dl
 PO2 < 60 mm Hg
 BUN > 5 mg/dl after IV’s
 Serum albumin < 3.2 gm/dl

37. Diagnostic Tests
 Abdominal and chest films
 CT scan
 Ultrasound
 Aspiration biopsy
 Peritoneal lavage
 Endoscopic Retrograde
Cholangio-pancreatography
(ERCP)

38. Complications
Pulmonary
Coagulation
Immunological
Cardiovascular
Renal

39. Systemic (More common in
the first week)
 Cardiovascular
 Shock
 Arrhythmias
 Pulmonary
 ARDS
 Renal failure
 Haematological
 DIC
 Metabolic
 Hypocalcaemia
 Hyperglycaemia
 Hyperlipidaemia
 Gastrointestinal
 Ileus
 Neurological
 Visual disturbances
 Confusion, irritability
 Encephalopathy
 Miscellaneous
 Subcutaneous fat
necrosis
 Arthralgia

40. Local (Usually develop after the first week)
Acute fluid collection
Sterile pancreatic necrosis
Infected pancreatic necrosis
Pancreatic abscess
Pseudocyst
Pancreatic ascites
Pleural effusion
Portal/splenic vein thrombosis
Pseudoaneurysm

41. Pulmonary
Enzyme induced inflammation
of the diaphragm
Abdominal distention &
 diaphramatic movement
 Pleural Effusion
 Atelectasis
Pancreatic enzymes can injure the lungs directly
Watch for hypoxia – PO 2 < 60 mm Hg

42. Cardiovascular and Coagulation
Complications
  Capillary permeability 
fluid shifts (3rd spacing) 
distributive shock
 Vasodilation d/t
inflammatory mediators 
distributive shock
 Thrombus formation d/t
hypercoaguability  DIC

43. - Cardiovascular Complications
3rd spacing   BP,  HR, vasoconstriction
(compensatory mechanisms) d/t SNS activation
Recall: compensatory mechanisms work for only a
short while before they begin to fail

44. Coagulation
Trypsin activates prothrombin  clotting
Trypsin also activates plasminogen  lysing
This mechanism 
Intravascular & pulmonary clotting 
DIC & pulmonary emboli

45. Renal
Hypovolemia   GFR,  renal perfusion 
development of clots in renal circulation 
Acute tubular necrosis & Acute renal failure

46. Immunological
 GI motility  movement of bacteria outside GI tract
 pancreatic abscesses & necrosis  INFECTION

47. If mild attack of pancreatitis, a conservative approach is
indicated with intravenous fluid administration and frequent,
but non-invasive, observation.
A brief period of fasting may be sensible in a patient who is
nauseated and in pain, but there is little physiological
justification for keeping patients on a prolonged ‘nil by mouth’
regimen.
Antibiotics are not indicated.
Apart from analgesics and anti-emetics, no drugs or
interventions are warranted.
CT scanning is unnecessary unless there is evidence of
deterioration.

48. Severe attack of pancreatitis, a more aggressive approach is
required,
Patients should be admitted to an intensive care or high-
dependency unit
Adequate analgesia should be administered.
Aggressive fluid resuscitation guided by frequent measurement
of vital signs, urine output and central venous pressure.
Supplemental oxygen administered and serial arterial blood
gas analysis performed.
The haematocrit, clotting profile, blood glucose and serum
levels of calcium and magnesium should be closely monitored.

49. A nasogastric tube is not essential but may be of value in
patients with vomiting.
Specific treatments such as aprotinin,somatostatin
analogues, platelet-activating factor inhibitors and
selective gut decontamination have failed to improve
outcome in numerous clinical trials and should not be given.
There are no data to support a practice of ‘resting’ the
pancreas and feeding only by the parenteral or nasojejunal
routes.
If nutritional support is felt to be necessary, enteral nutrition
(e.g. feeding via a nasogastric tube) is should be used

50. There is some evidence to support the use of
prophylactic antibiotics (intravenous cefuroxime, or
imipenem, or ciprofloxacin plus metronidazole) in
patients with severe acute pancreatitis for the
prevention of local and other septic complications.
The duration of antibiotic prophylaxis should not exceed
14 days.
Additional antibiotic use should be guided by
microbiological cultures.

51. If gallstones are the cause of an attack of predicted or proven
severe pancreatitis, or if the patient has jaundice, cholangitis
or a dilated common bile duct, urgent ERCP should be carried
out within 72 hours of the onset of symptoms.
There is evidence that sphincterotomy and clearance of the
bile duct can reduce the incidence of infective complications in
these patients.
In patients with cholangitis, sphincterotomy should be carried
out or a biliary stent placed to drain the duct.

52. Early management of severe acute pancreatitis
Admission to HDU/ICU
Analgesia
Aggressive fluid rehydration
Oxygenation
Invasive monitoring of vital signs, central venous pressure,
urine output, blood gases
Frequent monitoring of haematological and biochemical
parameters (including liver and renal function, clotting,
serum calcium, blood
glucose)

53. Nasogastric drainage
Antibiotic prophylaxis can be considered (imipenem,
cefuroxime)
CT scan essential if organ failure, clinical deterioration or signs
of sepsis develop
ERCP within 72 hours for severe gallstone pancreatitis or signs
of cholangitis
Supportive therapy for organ failure if it develops (inotropes,
ventilatory support, haemofiltration, etc.)
If nutritional support is required, consider enteral
(nasogastric) feeding

54. Collaborative Management –
Pain
“Rest” the pancreas & GI tract
 NPO
 NG tube to suction
 parenteral vs. enteral nutrition
 drug therapy
Manage Pain
 morphine
 H2 antagonists

PPI’s
Acute Pain r/t inflammation of pancreas and surrounding
tissue, obstuction of biliary tree & interruption of blood
supply to pancreatic tissue

55. Nutritional management
When can the client
resume eating?

56. Collaborative Management
Hemodynamic stability
Fluid volume replacement
 crystalloid, colloid or blood products
 Hemodynamic monitoring (CVP or PA)
 Monitor peripheral circulation, UOP
Risk for fluid imbalance r/t vomiting &  intake, fever &
diaphoresis, fluid shifts, N/G suction
Vasoactive drugs – dopamine
  BP via vasoconstriction in high doses
  renal perfusion in lower doses

57. Collaborative Management
Respiratory Care
 Supplemental O2 @ 4l/NC
 Positioning for adequate ventilation
 Cough, deep breathe, IS with pain control
 Monitor ABG’s, respiratory effort & breath sounds
Ineffective Breathing Pattern r/t abdominal distention,
ascites, pain or respiratory compromise

58. Collaborative Management
Maintain Metabolic Balance
Monitor labs for alterations, report significant alterations.
Risk for Fluid Imbalance r/t (same as previous dx)
  K,  Ca   dysrhythmias
  Ca  neurologic changes
  FBS  hyperosmolar diuresis, electrolyte shifts
  BUN, Creatinine indicates renal damage from  perfusion
 Amylase, lipase for return to normal

59. Collaborative Management-
Alcohol Withdrawal Syndrome
Monitor for withdrawal from alcohol
 Clinical manifestations of hyperactive sympathetic
nervous system
  body temperature & VS
 Diaphoresis
 Anxiety/Aggitation
 Tremors/Shakiness

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