CPC held at Frontier Medical College on Acute Pancreatitis Prepared by Quratulain Nasir,Zeeshan Ghias Khan,Ummair Munawar,Parsa Bashir,Kanwal Shehzadi,Urfa Mir and Zeeshan Ahmed

1. Clinico-pathologicalconference
4TH
Final Year MBBS
Friday, August 21st, 2015
Presentation by
1668- Quratulain Nasir
1696- Zeeshan Ghias
Khan
1686- Urfa Mir
1637- Kanwal Shehzadi
1694- Zeeshan Ahmed
1667- Parsa Basheer

2. Case History
Presented by:
Ummair Munawar
Roll no 1684

3. CASE HISTORY
 Name: Shaista Bibi w/o Abdul Rehman
 Age: 38 Years
 Sex: Female
 Address: Darbar, Mansehra
 MOA: Emergency
 TOA: 5:30 pm
 DOA: 6/08/2015
 Chief Complaints:
Epigastric Pain – 8 hrs
Vomiting- 3 hrs

4. CASE HISTORY
 History Of Present Illness
 Pain:
According to my patient she was alright 8 hours ago before she
suddenly developed severe epigastric pain following a large meal the
night before. The pain was sudden in onset, severe in intesity, sharp in
character and radiates to the back and the tip of the left shoulder.
The Pain is associated with nausea and vomiting. The pain is aggrevated
when she walks and is relieved somewhat when she is sitting and
leaning forward.
 Vomiting:
Vomiting developed a few hours after onset of pain. Frequency is twice
in the past 8 hrs. The vomiting occurred after a light breakfast in the
morning, but also occurs even after patient stopped eating. The
vomitus is greenish-yellow in colour, foul smell. There was no blood in
the vomitus. Associated with pain, and no other associations.

5. CASE HISTORY
 Systemic Inquiry
- Cardiovascular System -Palpitations
- Respiratory System- Laboured Breathing
- Alimentary System- Pain Epigastrium, Vomting
- Urinary System - None
- Nervous System - None
- Skin - None
- Locomotor System - None
- Endocrine - None

6. CASE HISTORY
 Past Medical & Surgical History:
-She is a known patient of gall stones for the past one year,
for which she has not yet been operated for.
She was admitted in the hospital 3 years ago for Typhoid
from which she recovered after receving adequate
treament. The patient has also had 3 previous c-sections
for all 3 of children.
 Family History
- There is no history of Asthma, Tuberculosis, Hypertension
in her immediate family. However, her mother is a known
Diabetic for the past 30 years, and her older brother
suffers from Ischemic Heart Disease

7. CASE HISTORY
 Personal History
- Sleep is disturbed for the past 2 days since she has been
admitted into the hospital
- Diet was normal, until illness and now she has a decreased
appetite. Bowel habits are normal.
 Socioeconomic History
- She is a housewife while husband is a driver. Income is
satisfactory for their needs. She lives in 2 room home in which
there is one bathroom and the water supply is obtained through
well.
 Drug History
- Before illness the patient was not on any long term medication ,
besides taking the occasional panadol for pain.
 Allergic History
- No known allergies

8. EXAMINATION
 General Physical Examination:
General Appearance
Middle-aged, ill –looking woman lying in bed with I/v line passed on hand.
She is conscious
Vitals:
Blood Pressure: 110/60 mmhg
Pulse: 79 bpm
Temperature: 100 Degrees Farenheight
Respiration: 18/min
Pallor
Cyanosis Absent
Jaundice Absent
Clubbing Absent
Kolionychia Absent
Splinter Hemorrhages Absent
Leukonychia Absent
Osler’s Nodes Absent
Herberden’s Nodes Absent
Bouchard’s Nodes Absent
Thyroid- Non tender, Normal Looking
Lymph Nodes – No tender or palpable enlarged lymph nodes
Ankle Edema – Absent

9. CASE HISTORY
 Abdominal Examination
Inspection:
The shape of the abdomen is normal, and symmetric with normal
movements. Visible scar of previous c-sections and some striae.
There were no prominent veins or visible pulsations. The patient
had slight bluish discoloration of left flank (Turner’s Sign)
Palpation:
Upon superficial palpation the patient was very tender, Deep
palpation was not done do to pain experienced by patient
Percussion & Ausculation
No shifting dullness, & fluid thrills. Upon Ausculation bowel
sounds were barely audible and no audible Bruits were heard.

10. CASE HISTORY
 Cardiovascular Examination
*No Remarkable Findings
Chest Deformities - Absent
Visible Scars - Absent
Heaves, Thrills -Absent
Heart sounds are normal with no Added sounds, and no Murmurs
 Respiratory Examination
Respiratory Rate is 18/min. Shape of Chest is Normal.
Deformity -Absent
Scars -Absent
Pulsations -Absent
Chest Movements and expansion is Normal.
Trachea is in Midline.
Vocal Fremitus - Absent
Crepitus -Absent
Palpable sounds -Absent
 Central Nervous System Examination
Cranial Nerves are normal, with normal reflexes that present.
No other significant abnormalities found.

11. Diagnosis???

12. Acute Pancreatitis

13. Anatomy And Physiology of
Pancreas
Presented by:
Quratulain Nasir

14. “Anatomy is to
physiology as
geography is to
history; it
describes the
theatre of
events.”
― Jean Fernel

15. Pancreas - Anatomy

16. Anatomy
Pancreas is an elongated,
accessory digestive gland
that lies retroperitoneally
Transversely across the
posterior abdominal wall
posterior to the stomach
between duodenum on the
right and the spleen on the
left.

17. Anatomy
Parts of pancreas
• Head
• Neck
• Body
• Tail

18.  HEAD
• The expanded part of the gland that is
embraced by the C shaped curve of the
duodenum to the right of the superior
mesenteric vessels.
• Firmly attaches to the medial aspect of the
descending and horizontal parts of the
duodenum.
• The head of the pancreas rests posteriorly on
the IVC
• On its way to opening into the descending
part of the duodenum, the bile duct lies in a
groove on the posterosuperior surface of the
head or is embedded in its substance.

19. Anatomy
 NECK
• Short and overlies the superior
mesenteric vessels, which
form a groove in its posterior
aspect.
• The anterior surface of neck,
covered with peritoneum, is
adjacent to the pylorus of the
stomach.

20.  BODY
• Continues from the neck and
lies to the left of the superior
mesenteric vessels,
• Passing over the aorta and L2
vertebra
• The posterior surface of the
body is devoid of peritoneum
and is in contact with the
aorta, SMA, left suprarenal
gland and left kidney and
renal vessels

21.  TAIL
• Lies anterior to the left
kidney, where it is
closely related to the
left kidney,where it is
closely related to the
splenic hilum and the
left colic flexure.
• The tip of the tail is
usually blunted and
turned superiorly

22.  Accessory pancreatic
duct
• Usually (60%) communicates
with the main pancreatic
duct
• Opens into the duodenum at
the summit of the minor
duodenal papilla

23. • Smooth muscle sphincter that control the flow of
bile & pancreatic juice into duodenum :
 - Sphincter of the pancreatic duct
 - Sphincter of the bile duct
 - Sphincter of hepatopancreatic (sphincter of Oddi)

24. Blood Supply - Arterial
 -The pancreatic arteries
derive mainly from the
branches of the splenic
artery
 -The anterior and posterior
superior
pancreaticoduodenal
arteries, branches of the
gastroduodenal artery
 -The anterior and posterior
inferior
pancreaticoduodenal
arteries, branches of the
SMA

25. Venous Drainage
 The pancreatic veins

26. Lymphatics
 The pancreatic lymphatic
vessels follow the blood
vessel. Most of them end
in the pancreaticosplenic
nodes that lie along the
splenic artery, but some
vessels end in the pyloric
lymph nodes.
 Efferent vessels from
these nodes drain to the
superior mesenteric lymph
nodes or to the celiac
lymph nodes via the
hepatic lymph nodes.

27. Nerve Supply
 The nerves of the pancreas are derived from the vagus and
abdominopelvic splanchnic nerves.

28. Pancreas - Physiology
FUNCTIONS:
 neutralize chyme
 digestive enzymes
 hormones

29. Physiology
 The pancreas produces :
• An exocrine secretion ( pancreatic juice from the acinar
cells) that enter the duodenum through the main and
accessory pancreatic ducts.
• Endocrine secretion (glucagon & insulin) from the pancreatic
islets (of langerhans) that enter blood.

30. Physiology

31. Pancreatic Hormones
Secreted by the Islets of Langerhans
 Alpha Cells – Glucagon ( increases the glucose in blood)
 Beta Cells – Insulin (decreases the glucose in blood)
 Delta cells – Somatostatin (regulates/stops alpha & beta
cells)
 PP cells, or Gamma cells- Pancreatic Peptide

32. Pancreatic Enzymes
 PROTEOLYTIC LIPOLYTIC ENZYMES
ENZYMES Lipase
Trypsinogen Prophospholipase A2
Chymotrypsinogen Carboxylesterase lipase
Proelastase
Procarboxypeptidase A NUCLEASES
Procarboxypeptidase B Deoxyribonuclease (DNAse)
Ribonuclease (RNAse)
 AMYOLYTIC ENZYMES
Amylase OTHERS
Procolipase
Trypsin inhibitor

33. Pancreatic Enzymes

34. Enzyme Secretion
pancreatic duct
duodenum
acinus
microscopic view
of pancreatic acini

35. Enzyme Secretion
pancreatic duct
common bile
duct
ampulla
pancreatic enzymes
TAIL
BODY
HEAD
UNCINATE

36. Control of Pancreatic Secretions

37. Activation Of Enzymes
trypsinogen trypsin
chymotrypsin
elastase
phospholipase
carboxypeptidase
enterokinase
chymotrypsinogen
proelastase
prophospholipase
procarboxypeptidase
duodenal lumen

38. Protective Measures
 COMPARTMENTALIZATION - digestive enzymes are
contained within zymogen granules in acinar cells.
 REMOTE ACTIVATION - digestive enzymes are secreted as
inactive proenzymes within the pancreas.
 PROTEASE INHIBITORS – trypsin inhibitor is secreted
along with the proenzymes to suppress any premature
enzyme activation.
 AUTO “SHUT-OFF” – trypsin destroys trypsin in high
concentrations.

39. Etiology and Pathophysiology
Presented By
Zeeshan Ghias Khan
Roll no 1696

40. Starting with the quote
Doctors are men who prescribe
medicines of which they know
little, to cure diseases of
which they know less, in
human beings of whom they
know nothing. (1760)
 — Francois Marie Arouet Voltaire

41. ACUTE PANCREATITIS
Inflammation of the parenchyma of the pancreas
Due to premature activation of Pancreatic enzymes
Results in autodigestion
Pancreatic function and morphology return to normal after (or
between) attacks

42. Acute Pancreatitis – Etiology
 G: Gallstone.(common)
 E: Ethanol.
 T: Trauma..
 S: Steroid..
 M: Mumps.
 A: Alcoholism (common) or
autoimmune.
 S: Scorpion bites.
 H: Hyperlipidemia.
 E: ERCP.
 D: Drugs: Thiazide,
Azathioprine.

43. Acute Pancreatitis - Etiology
 ***Other:
 Iodiopathic.
 Hypercalcemia.
 Hypothermia.
 Genetic disorders:
acute intermittent
porphyria

44. Etiology
EtOH
35%
Idiopathic
10%
Other
10%
Gallstones
45%

45. Acute Pancreatitis Pathophysiology
Pancreatic Ducts
become obstructed
Hypersecretion of the exocrine
enzymes of pancreas
These enzymes enter the bile duct,
where they are activated and with
bile back up into the pancreatic duct
Pancreatitis

46. Acute Pancreatitis Pathophysiology
 Trypsinogen- (a proteolytic enzyme)
 Normally released into the small intestine, where
it is activated to trypsin
 In AP, it is activated to trypsin in the pancreas
causing autodigestion of pancreas

47. Acute Pancreatitis Pathophysiology
 Trypsinogen
 Activated to trypsin by enterokinase
 Inhibitors usually inactivate trypsin
 Enzyme can digest the pancreas and can activate other proteolytic
enzymes
 Elastase
 Activated by trypsin
 Plays a major role in autodigestion
 Causes hemorrhage by producing dissolution of the elastic fibers of
blood vessels
 Phospholipase A
 Plays a major role in autodigestion
 Activated by trypsin and bile acids
 Causes fat necrosis

48. Trypsin Edema, Liquefactive necrosis,
hemorrhage
Elastase Hemorrhage
Phospholipase A Fat necrosis
Kallikrein Edema, vascular permeability,
smooth muscle contraction, shock
Lipase Fat necrosis

49. Acute Pancreatitis Pathophysiology
autodigestion of pancreatic tissue
release of
enzymes into
the circulation
activation
of white
blood cells
local
complications
local
vascular
insufficiency
premature enzyme activation
distant
organ failure

50.  STAGE 1: Pancreatic Injury
 Edema
 Inflammation
 STAGE 2: Local Effects
 Retroperitoneal edema
 Ileus
 STAGE 3: Systemic Complications
 Hypotension/shock
 Metabolic disturbances
 Sepsis/organ failure
SEVERITY
Mild
Severe

52. Progression of Disease
 Autodigestion
Acute Inflammation of Pancreas
Necrosis of Pancreas
Digestion of vascular walls
Thrombus and Hemorrhage
Death

53. Acute Pancreatitis Time Course
0 12 24 36 48 60 72 84 96
hours from pain onset
ER presentation organ failurecytokine release

54. Sign/Symptoms and D/D’s
Presented by
Parsa Bashir

57. Acute Pancreatitis
Signs and Symptoms
1.Pain
Is a cardinal symptom
A.Onset
Sudden
B.site
Pain is experient first in epigastium but may be localized to either
Left upper quadrant or felt diffusely throughout abdomen
C.Radiation
Pain radiates to back

58. D.Progression
Develops quickly,reaching maximum intensity with in
minutes rather than hours and persists for hours or even
days
E.Intensity and Nature
Pain and severe and constant
F.Aggrevating Factors
Fatty meals and ling recumbent

59. G.Relieving factors
Sitting or leaning forward
2.Nausea and Vomiting
Repeated vomiting
3.Hiccoughs
Can be troublesome
May be due to gastric distention
Or irritation of diaphragm

60. Signs
General Appearance
May be normal Or patient may look gravely ill
1. Profound shock toxicity and confusion
2. Tachypnea
3. Tachycardia
4. Hypotention
5. Body Temp
6. Normal or may be subnormal but frequently rises as
inflammation develops
7. Jaundice

61. Abdominal Examination
May reveal any distention due to ileus and Ascites that is
shifting dullness
A mass can develop in epigastrium due to inflammation
The most important signs
Turner’s sign
There is bluish discoloration of flank
Cullen’s sign
Bluish discoloration around umbilicus
Fox’s sign
Small tender red nodules on leg

62. Auscultation
Bowel sounds reduced or absent
Pleural effusion,Pulmunory edema pneumonitis may be
present

63.  GREY TURNER1 SIGN CULLEN2 SIGN FOX3 SIGN
1. Named after British surgeon George Grey Turner(1877-1951)
2. Named for Thomas Stephen Cullen (1869-1953), Canadian
gynecologist who first described the sign in ruptured ectopic
pregnancy in 1916
3.Named after George Henry Fox(1846-1937), American
dermatologist

64. Differential Diagnosis
 Choledocholithiasis
 Perforated ulcer
 Mesenteric ischemia
 Intestinal obstruction
 Ectopic pregnancy

65. Investigations
Presented by
Urfa Mir
Roll no 1686

67. Acute Pancreatitis
Diagnostic Studies
 History and physical examination
 Laboratory tests
 Serum amylase- 23-85 U/L rasied upto 450 U/L
 Serum lipase – 0-160 U/L raised upto 400 U/L
 Blood glucose 200 mg/dL
 Serum calcium below 8 mg/dL
 Triglycerides raised
 Albumin 32 g/dL decreased to 3.2 g/dL
 LDH increased upto 350 IU/L
 Trypsin most senstive blood test but not widely
used

69. Acute Pancreatitis
Diagnostic Studies
1. Flat plate of abdomen
2. Abdominal/endoscopic ultrasound
3. Endoscopic retrograde
cholangiopancreatography (ERCP)
4. Chest x-ray
5. CT of pancreas
6. Magnetic resonance
cholangiopancreatography (MRCP)

70. Diagnostic Studies
 Serum amylase;
 It stays 48-72h then become normal.
 Serum lipase; (diagnostic test)
 It elevated for 7-14 days.
 Other:
-WBC (15000-30000). -LDH>500 U/dl
-Glucose. - Albumin.
-Ca in serum. - AST.Bilurbin,Alkaline Ph.
- ABG show Hypoxia.

71.  Xray of Abdomen:
-gall stones.
-Sentinel loop: air filled SI in the LUQ.
-Colon cut off sign: gas-filled seg of transverous colon
abruptly ending at the area of pancreatic inflammation.
 Xray Chest
It shows pulmunory complications eg pleural effusions
And interstitial inflammation but sometimes it is normal

72. Sentinel Loop
•
- localized ileus from nearby inflammation

73. Colon cutoff sign

74. U/S:
It shows dilatation of pancreatic ducts
Gland Atrophy or Enlargement
Gall stones in pancreatic duct
1. Biliary obstruction.
2. Pseudocyst.

75. Pseudocyst on US

76. Gallstones on US

77. CT: Gold Standard
(is the dignostic even with normal amylase).
 -enlarged pancreas.
 -Psudocyst.
 -Abscess & hemorrhage.
 -Presence of gas bubbles in CT scan indicate
pancreatic abscess.
It shows calcifications of the gland parenchyma and
ducts
Dilatation of the ducts are parenchymal atrophy

78. CT – Normal Pancreas
Spleen
L
Kidne
y
R
Kidney
A
Stomach
Liver
V

79. Pancreatitis on CT
Mild pancreatitis severe pancreatitis
Pseudocyst abscess
Pancreatic necrosis

80. Scoring System and
Complications
Presented by
Kanwal Shehzadi
Roll no 1637

82. Severity Scoring System
 In order to know who will develop severe and
 Acute pancreatitis various scoring systems have
 Been introduced like
 Ransons
 Glasgow Scoring system
 Acute Physiology and Chronic Health Evaluation(APACHE)
 APACHE II

83.  Scoring system to predict the severity of the acute
pancreatitis.. in both systems diseases calssified as
severe when 3 or more factors are present

84.  Scoring systems
  3 Ranson criteria
  8 APACHE II points
 Glasgow scoring
 Glasgow scoring >3


 Severe symptoms CRP level >15mg/l
After
48 hours

85.  Organ failure
 shock (SBP < 90 mmHg)
 pulmonary edema / ARDS (PaO2 < 60 mmHg)
 renal failure (Cr > 2.0 mg/dl)
 Local complications
 fluid collections  pseudocysts
 necrosis (mortality 15% if sterile, 30-35% if
infected)
 abscess

86. Ranson Criteria
AT ADMISSION
1. Age > 55 years
2. WBC > 16,000
3. Glucose > 200
4. LDH > 350 IU/L
5. AST > 250 IU/L
WITHIN 48 HOURS
1. HCT drop > 10
2. BUN > 5
3. Arterial PO2 < 60 mm Hg
4. Base deficit > 4 mEq/L
5. Serum Ca < 8
6. Fluid sequestration > 6L
Number
Mortality
<2
1%
3-4
16%
5-6
40%
7-8
100%

87. Glasgow Criteria
1. WBC > 15,000
2. Glucose > 180
3. BUN > 16
4. Arterial PO2 < 60 mm Hg
5. Ca < 8
6. Albumin < 3.2
7. LDH > 600 U/L
8. AST or ALT > 200 U/L

88. Complications
 Local Complications

95. Systemic
A. Pulmonary: pleural effusions, atelectasis,
hypoxemia, ARDS.
B. Cardiovascular: myocardial depression,
hemorrhage, hypovolemia.
C.Metabolic:Hypocalcemia,hyperglycemia,Hyperli
pidemia,coagulopathy
D. GI Hemorrhage
E. Renal
F. Hematologic
G. CNS

96. Acute Pancreatitis
Complications
 Main systemic complications are?
 Pulmonary
 Cardiovascular
 Electrolyte imbalance – Hypocalcemia

97. Management and Treatement
Presented by
Zeeshan Ahmed
Roll no 1694

98. Acute Pancreatitis
Goals of Care
 Relief of pain
 Prevention or alleviation of shock
 Decrease respiratory failure
 ↓ of pancreatic secretions
 Maintain Fluid/electrolyte balance

99. Treatment and Nursing Care
1. Pain management
 IV morphine
 Antispasmodic agent
 Bentyl
 Pro-Banthine
 Spasmolytics – Nitroglycerine
 Positioning – sitting up and leaning forward
Why is it important to relieve pain?

100. Treatment
2. Prevention of Shock – hemodynamic
stability
* Administer Blood, Plasma expanders,
Albumin
* RL solution

101. Treatment and Nursing Care
3. Suppress pancreatic enzymes
* NPO
* NG suction
* Antacids, H2 receptor antagonists,
antispasmotics
4. Decrease respiratory distress
* Oxygen; check O2 saturation levels
* Semi-fowlers position, knees flexed,
position changes
* incentive spirometer
5. Antibiotics

102. Treatment and Nursing Care
 6. Correction of electrolyte imbalance
hypocalcemia
 7. Maintain Hydration / Nutrition

103. Treatment and Nursing Care
 Surgical therapy – if
related to gallstones
 ERCP
 Endoscopic
sphincterotomy
 Laparoscopic
cholecystectomy

104. Treatment of Mild Pancreatitis
 Pancreatic rest
 Supportive care
 fluid resuscitation – watch BP and urine output
 pain control
 NG tubes and H2 blockers or PPIs are usually not helpful
 Refeeding (usually 3 to 7 days)
 bowel sounds present
 patient is hungry
 nearly pain-free (off IV narcotics)
 amylase & lipase not very useful here

105. Treatment of Severe Pancreatitis
 Pancreatic rest & supportive care
1. fluid resuscitation* – may require 5-10 liters/day
2. careful pulmonary & renal monitoring – ICU
3. maintain hematocrit of 26-30%
4. pain control
5. correct electrolyte derangements (K+, Ca++, Mg++)
 Rule-out necrosis
1. contrasted CT scan at 48-72 hours
2. prophylactic antibiotics if present
3. surgical debridement if infected
 Nutritional support
1. may be NPO for weeks
2. TPN vs. enteral support (TEN)

106.  Follow up care
 Dietary teaching
 High-carbohydrate, low-fat
diet
 Abstinence from alcohol,
 Patient/family teaching
* Signs of infection, high blood
glucose, steatorrhea
Treatment - Home Care

108. Thank you !