Presentation regarding acute pancreatitis

1. ACUTE PANCREATITIS
AHMAD IRFAN SYAKIR BIN KAMALUDDIN

2. Outline
• Anatomy
• Physiology
• Pathophysiology
• Causes
• Presentation
• Classification
• Acute pancreatitis
• Diagnosis
• Investigation
• Severity assessment
• Complication
• Management
• Prognosis
• Chronic pancreatitis
• Exocrine Pancreatic Insuffiency

3. ANATOMY

4. • Derived from Greek:
• ‘pan’ (all) and ‘kreas’ (flesh)
• Retroperitonium organ
• Positioned at the level of the transpyloric plane (L1)
• Weighs ~100g and 14-20cm long
• Divided into
• Head
• Body
• Tail

9. • The head
- lies within the curve of the duodenum, body of the second lumbar
vertebra and the vena cava.
• The neck
-aorta and superior mesenteric vessel behind of the neck
-the superior mesenteric vein joins the splenic vein to form the portal
vein.
• The tip of the pancreatic tail extends up to the splenic hilum

10. Duct system
• Main pancreatic duct (Wirsung
duct)
• Accessory duct (Santorini duct)
• Pancreatic duct joins CBD to
form ampulla of Vater

12. Pancreas is
retroperitoneal
organ with
exception of its
tail.

14. Anatomical relations of the pancreas
Anterior Stomach, lesser sac (omental bursa), transverse mesocolon, superior
mesenteric artery
Posterior Aorta, inferior vena cava, right renal artery, right and left renal veins, superior
mesenteric vessels, splenic vein, hepatic portal vein, left kidney, left suprarenal
gland
Superior Splenic artery
Lateral Spleen
Medial Duodenum (descending and horizontal parts)

15. ARTERY

16. VEINS

17. RESECTIONAL ANATOMY OF PANCREAS

23. PHYSIOLOGY

24. Pancrease
Exocrine
(digestion)
Acinar cells & Duct
cells
Endocrine
(glucose homeostasis)
Islet of Langerhans

26. • Exocrine cells (80-
90%)
• acinar tissue
• clumped around a
central lumen –
communicates with
the duct system
• Exocrine glands
produce
• Trypsin, chymotrypsin
– digest protein
• Amylase –digest
carbohydrate
• Lipase –breakdown
fats

27. • Endocrine cells
• Clusters of endocrine cells =
islets of Langerhans
• distributed throughout
pancreas
• Consist of
• B cells (75%) – produce
insulins
• A cells (20%) – produce
glucagon
• D cells –produce somatostatin
• PP cells –produce pancreatic
polypeptide

28. Physiology
• Meal ingested
• Cholecystokinin (CCK) will be released from duodenal mucosa in
response to food
• Secretin will stimulate secretion of large quantities of water solution
of sodium bicarbonate
• Acinar cells produce digestive enzymes
• Packaged into storage vesicles (zymogens)
• Released by exocytosis
• Released via pancreatic ductal cells into pancreatic ducts

30. • Proenzymes travel to duodenum
• Trypsinogen convert into trypsin
• Facilitates conversion of other proenzymes
into their active forms
• Feedback mechanism
• Limits pancreatic enzyme activation
• High trypsin > decreased CCK and
secretin level > limiting further pancreatic
secretion

31. Hunger vs Satiety Hormones
• Ghrelin (hungry hormone)
-released primarily in the stomach
-hormone that increase the appetite, increase when person is under
eating and decrease if person overeating.
-sleep deprivation wan associated in increased ghrelin level.
• Leptin (appetite suppressor)
-made by fat cells
-many obese people have built up resistance against leptin hormone
effect

32. • is inflammation of the gland parenchyma of the pancreas.
• Divided into acute, which is an emergency and chronic which is
prolonged resulting from development of fibrosis In pancreas.
• incidence : 5-30 cases per 100,000
• overall case fatality rate : ~ 5%
• Can occur at any age, with a peak in young men and older women.
PANCREATITIS

33. Pancreatitis
Acute
Mild
Interstitial oedema of
the gland and minimal
organ dysfunction
Severe
Pancreatic necrosis, a
severe systemic
inflammatory response
and often multi-organ
failure
Chronic
Continuing inflammatory
disease of the pancreas
characterised by
irreversible
morphological change
typically causing pain
and/or permanent loss
of function.

34. 1. ACUTE PANCREATITIS

35. • An acute condition presenting with abdominal pain and usually
associated with raised pancreatic enzyme levels as a result of
pancreatic inflammation.
• Mechanism of injury
-premature activation of pancreatic enzymes within the pancreas,
leading to process of auto digestion.
a)Acinar cells injury
b)Impair secretion of zymogen
c)Delay of enzymatic secretions

36. CAUSES

41. • Common causes:
• Gallstone 50-70%
• Alcohol 25%
• ‘I GET SMASHED’

42. A) Gallstone

43. b) Alcohol
Intracellular
accumulation
of digestive
enzymes
Increase
ductules
permeability
Increase
protein
content of
pancreatic
juice
Decrease
HCO3 and
trypsin
inhibitor

44. c) Idiopathic (10-30% )
• Sludge and microlithiasis
• Relative deficiency of
phosphatidylcholine in bile
• Causing fast and extensive
cholesterol crystallization

45. d) ERCP
• Mechanical trauma
• Papillary injury
-Spincter of oddi spasm
-Prolonged/repeated attempts at cannulating pancreatic duct
-Multiple contrast injections
-Thermal injury from electrocautery current during sphicterectomy
• Hydrostatic injury
• Over injection of pancreatic duct

46. e) Trauma
• Penetrating injuries –knives, bullet
• Blunt injuries – steering wheels, bicycles

47. f) Steroids
• Corticosteroids might obstruct small pancreatic ductules by leading to
increased viscosity of pancreatic secretions, resulting in pancreatic
changes.
• These changes included reduced basophilia, vacuolization of acini,
peripancreatic fat necrosis, and hyperplasia of the islets of
Langerhans

48. g) Hypercalcaemia
• It is postulated that hypercalcemia leads to accelerated
intrapancreatic conversion of trypsinogen to trypsin, which causes the
pancreatic damage
• Can cause formation of pancreatic calculi and by modifying pancreatic
secretion, may lead to protein plug formation.

49. h) Hyperlipidemia
• TG > 1000mg/dL, a level at which chylomicrons are present
• Chylomicrons are triglyceride-rich lipoprotein particles.
• These are large enough to occlude the pancreatic capillaries leading
to ischemia and subsequent acinar structural alteration and release of
pancreatic lipase.

50. i) Viral pancreatitis
• such as Mumps virus, Coxsakie virus, Hepatitis B virus,
Cytomegalovirus, Epstein-Barr virus and Herpes simplex virus
• Direct destruction of pancreatic acinar cells by inflammation and
edema
• The damaging of pancreatic acinar cells by the virus leads to a leaking
intracellular enzyme or precipitates a process of cell death

51. J) Drugs
• Eg: Sodium valproate, azathioprine, thiazide, frusemide,
metronidazole
• immune-mediated or hypersensitivity reactions
• direct toxic effects
• bradykinin-induced inflammatory reactions

52. PRESENTATION

53. Presentation
• Abdominal pain
• acute onset of persistent severe epigastric pain
• radiates to the back
• relief by sitting or leaning forwards
• Nausea and vomiting
• Retching
• Hiccoughs
• Due to gastric distention or irritation of diaphragm

54. • Risk factors:
• Previous biliary colic
• Binge alcohol consumption
• H/o trauma/MVA
• Family history of HPL
• Recent operative or other invasive procedures

55. Physical examination:
• Appearance: well or gravely ill –profound shock, toxicity, confusion
• Tachypnoea, tachycardia, hypotension
• Mild icterus
• Pleural effusion, pulmonary edema
• Abdominal tenderness, distention, guarding
• Ascites

56. • Severe necrotizing pancreatitis
• Cullen sign
• Grey Turner sign
• Erythematous skin nodules
• due to focal subcutaneous fat
necrosis
• <1cm, on extensor skin surface
• polyarthritis

57. CLASSIFICATION

59. DIAGNOSIS

60. Diagnosis
• Requires at least 2 features:
1. Characteristic abdominal pain
2. Biochemical evidence of pancreatitis
• Amylase or lipase >3x above reference range
3. Characteristic imaging findings

61. • Amylase
• Not specific, Short half life
• Rises within few hours of pancreatic
damage
• Declines over the next 4-8 days
• Lipase
• More sensitive and specific to
pancrease
• Longer half-life, remains high for 12
days
• Does not indicate whether the disease is
mild, moderate or severe

63. Investigation Findings
FBC • Leucocytosis
• Hemoconcentration due to fluid sequestration
• Low Hct due to dehydration or hemorrhage
RP, e • electrolyte imbalance secondary to third spacing of fluids
• Hypocalcaemia due to saponification of fats in retroperitoneum
• Hypercalcaemia causing pancreatitis
• TRO renal failure
LFT • ALP, TB, AST, ALT
• ALT>150U/L –suggests gallstone pancreatitis
CRP • Indication of prognosis
• Higher level correlates with a propensity towards organ failure
FLP Hyperlipidaemia as the cause
LDH Higher in severe pancreatitis
ABG To monitor oxygenation and acid-base status
IgG4 Autoimmune pancreatitis

64. IMAGING

65. Investigation Findings
AXR • Sentinel loop –localized ileus of small intestine
• Colon cut-off sign –spasm of the descending
colon
• Gallstone, pancreatic calcification
CXR • Pleural effusion
• Hemidiaphragm elevation
• Basal atelectasis
• Pulmonary edema –suggestive of ARDS
• Air under diaphragm
- TRO Perforated viscus

66. Colon cut-off sign
• gaseous distension in proximal colon
+ abrupt termination of gas in the
colon,
+ decompression of distal colon
• The spread of inflammatory
exudates along the phrenicocolic
ligament including the transverse
mesocolon is the reason for the
constriction of the colon in the area
of the left flexure

67. Sentinel loop sign
• is a short segment of adynamic ileus close
to an intra-abdominal inflammatory
process
• may aid in localizing the source of
inflammation
• upper abdomen – pancreatitis
• right lower quadrant - appendicitis

69. • Calcification within pancreas

70. Investigation Findings
USG Abdomen Detect gallstones
Identify area of necrosis –hypoechoic regions
EUS
(Endoscopic
ultrasound)
Visualize pancrease and biliary tract
Detect microlithiasis and periampullary lesions

73. Transverse ultrasound demonstrates
diffuse enlargement of the pancreas ,
which appears abnormally hypoechoic

77. Investigation Findings
MRCP • Non invasive image of biliary and pancreatic ducts
ERCP • Pancreatitis secondary to chelodecholithiasis
• Biliary pancreatitis with worsening jaundice and clinical
deterioration despite max support therapy
CT • Pancreatic tumour
• Severe pancreatitis
• To assess complications
• Prognosis –Balthazar

78. CT scan
• Indications:
• Diagnostic uncertainty
• Severe pancreatitis – to distinguish interstitial from
necrotizing pancreatitis (Balthazar criteria)
• Organ failure, signs of sepsis or progressive clinical
deterioration
• Localised complication is suspected – fluid collection,
pseudocyst, pseudoaneurysm

79. (A) Localised oedema around the pancreas
(B) Extensive fluid collections around the pancreas

80. Axial CECT in a patient after
ERCP with placement of a
stent >
demonstrates enlargement
of the pancreas, edema
with loss of normal fatty
lobulation, and
peripancreatic fat stranding
and fluid, compatible with
acute edematous
pancreatitis.

82. SEVERITY ASSESSMENT

83. Assessment of severity
•Ranson criteria
•Glasgow criteria
•APACHE II score

84. >10mmol/L
<2.0 mmol/L
If the score ≥ 3, severe pancreatitis likely.
If the score < 3, severe pancreatitis is unlikely

85. If the score ≥ 3, severe
pancreatitis likely.
If the score < 3, severe
pancreatitis is unlikely

86. Measure the severity of disease for adult patients admitted to intensive care units

87. MANAGEMENTS

88. Principles management of pancreatitis
1. Initial assessment and risk stratification
• Assess hemodynamic status
• Begin resuscitation as needed
• Risk assessment
• to stratify patients into higher- and lower-risk categories
• to assist triage, such as admission to an intensive care setting
• Patients with organ failure
• Admit to intensive care unit or intermediary care setting whenever possible

89. 2. Airway and Breathing support
• Maintain spO2 >95%
• Oxygen supplemental
3. Rest the pancreas
• KNBM
• NG tube
• Beneficial in severe pancreatitis, intractable vomiting, severe ileus and severe
abdominal distention
• Fluid resuscitation
• Prevent hypovolaemia and organ hypoperfusion
4. Analgesics and Antiemetics

90. 4. Blood products in acute pancreatitis
• hemorrhagic pancreatitis – transfuse to HCT level of 30%
• If coagulopathic and bleeding – transfuse FFP and platelets
5. Correct electrolyte abnormalities
• Hypocalcaemia
• Hypokalaemia
• Hypomagnesemia

91. Nutrition
• Mild AP
• oral feedings can be started immediately if there is no nausea and vomiting,
and abdominal pain has resolved.
• initiation of feeding with a low-fat solid diet appears as safe as a clear liquid
diet.
• Severe AP
• enteral nutrition is recommended to prevent infectious complications.
• Parenteral nutrition should be avoided unless the enteral route is not
available, not tolerated, or not meeting caloric requirements.

92. Antibiotics
• prophylactic antibiotics in severe acute pancreatitis is not
recommended
• antibiotics in sterile necrosis to prevent the development of infected
necrosis is not recommended
• Infected necrosis should be considered in patients with
• pancreatic or extrapancreatic necrosis
• who deteriorate or fail to improve after 7–10 days of hospitalization.
• antibiotics known to penetrate pancreatic necrosis
• carbapenems, quinolones, and metronidazole

93. • Treat U/L causes
• Gallstones – early lap cholecystectomy
• Urgent ERCP
• Within 72H
• In pt with gallstones, causing jaundice, cholangitis or dilated CBD
• Reduce incidence of infective complication

94. COMPLICATIONS

97. IEP in a 43-year-old man. Axial contrast-
enhanced CT image shows peripancreatic
inflammation (black arrow) and a
homogeneous fluid-attenuation
collection in the left anterior pararenal
space (white arrow), a finding that is
consistent with APFC.

98. Figure 1 Drawings illustrate pancreatic necrosis (a), peripancreatic necrosis (b), and combined pancreatic-
peripancreatic necrosis (c).

99. Figure 4b Pancreatic necrosis in a 65-year-old man. (a) Axial contrast material–enhanced CT image obtained 2
days after the onset of acute abdominal pain shows peripancreatic fluid and stranding (arrows) and normal-
appearing pancreatic parenchyma. (b) Axial contrast-enhanced CT image obtained 5 days later owing to the
patient’s worsening clinical condition reveals an ill-defined hypoattenuating region in the body of the pancreas
(*), a finding that suggests pancreatic necrosis. Peripancreatic fluid and stranding (arrows) are also seen.

100. Figure 21a Axial contrast-enhanced CT image acquired 4 weeks after the onset of disease in the same
patient as in Figure 20a shows a well-defined, homogeneous peripancreatic collection around the tail
of the pancreas (arrows), a finding that is compatible with a pseudocyst.

101. Local complications
• Acute fluid collection
• Sterile and infected pancreatic necrosis
• Pancreatic abscess
• Pancreatic ascites
• Pancreatic effusion
• Haemorrhage
• Portal or splenic vein thrombosis
• pseudocyst

102. Systemic Complication
• Occurs within days of onset
• Disseminated intravascular coagulation (DIC)
• Acute respiratory distress syndrome (ARDS)
• Hypocalcaemia
• Fat necrosis from released lipases
• results in the release of free fatty acids
• react with serum calcium to form chalky deposits in fatty tissue
• Hyperglycaemia
• Secondary to destruction of islets of Langerhans
• subsequent disturbances to insulin metabolism

103. Surgery in Acute Pancreatitis
• Mild AP + cholelithiasis
• cholecystectomy should be performed before discharge
• to prevent a recurrence of AP
• necrotizing biliary AP
• cholecystectomy is to be deferred until active inflammation subsides and fluid
collections resolve or stabilize
• to prevent infection
• Asymptomatic pseudocysts + pancreatic and/or extrapancreatic necrosis
• do not warrant intervention regardless of size, location, and/or extension

104. • stable patients + infected necrosis
• surgical, radiologic, or endoscopic drainage should be delayed (>4 weeks)
• to allow liquefication of the contents and the development of a fibrous wall
around the necrosis (walled-off necrosis)
• symptomatic patients + infected necrosis
• minimally invasive methods of necrosectomy are preferred to open
necrosectomy

105. Prognosis
• Overall mortality 10-15%
• Patients with biliary pancreatitis have higher mortality than alcoholic
pancreatitis
• In patients with severe disease (organ failure) mortality is ~ 30%

106. CHRONIC PANCREATITIS

107. • Chronic pancreatitis is a progressive Inflammatory disease in
which there is irreversible destruction of pancreatic tissues.
• Characterized by severe pain and in later stage, exocrine and
endocrine pancreatic insufficiency.
• Etiology:
-high alcohol consumption
-pancreatic duct obstruction
-congenital abnormalities
-autoimmune pancreatitis
-others

108. • Clinical features
-pain at epigastric and right subcostal region
-nausea and vomiting
-weight loss
-loss of exocrine function leads to steatorrhea
-loss of endocrine function and development of diabetes
• Investigations
-pancreatic calcification on AXR
-features in CT, MRI, ECRP, EUS

109. A) Medical treatments
• Treat the addiction
-stop alcohol and tobacco
• Alleviate abdominal pains
-eliminate obstructive factors
• Nutritional and pharmacological measures
-diet low in fat and high in protein and carbohydates
-pancreatic enzyme supplementation with meals
-correct malabsorptions of fat soluble vitamins
• Treat diabetes mellitus
Treatments

110. b) Endoscopics or Surgical interventions
-relieve obstruction of the pancreatic duct, bile duct or the
duodenum, or in dealing with complications.
• Endoscopic pancreatic spincterotomy
-for papillary stenosis, high spicter pressure, pancreatic ductal
pressure
• Pancreatoduodenectomy (Beger procedure)
-mass in the head of pancrease
• Longitudinal pancreatojejunostomy (Frey procedure)
-if duct is markedly dilated

112. • Deficiency of the exocrine pancreatic enzyme, resulting in
the inability to digest food properly, or maldigestion.
• Amylase, lipase, protease
• Management
-lifestyle modifications: ex- avoiding fatty foods, limitation of
alcohol intake, consumption of well-balanced diet
-vitamin supplementation (A, D, E, K)
-Pancreatic Enzyme Replacement Theraphy (PERT)
Exocrine Pancreatic Insuffiency

113. • Basis of treatment of EPI
• Typical indication are progressive weight loss and
steatorrhea.
• The Pancreatic Enzyme Products (PEPs) use for PERT are
extract of porcine pancreas that contain all 3 pancreatic
enzymes (amylase, lipase, protease)
- Creon, Zenpap, Pancreaze, Ultresa Viokace, Pertzye
Pancreatic Enzyme Replacement Theraphy (PERT)

114. NON-ALCOHOLIC FATTY PANCREAS DISEASE (NAFPD)

115. • Fat accumulation in the pancreas, defined as fatty pancreas, is usually an
incidental finding during transabdominal ultrasound examination.
• Fatty pancreas without any significant alcohol consumption is defined as non-
alcoholic fatty pancreas disease
• Its clinical impact is still largely unknown, hypothetically the disease progression
could lead to chronic pancreatitis and possibly pancreatic cancer development.
• Metabolic problems such as diabetes, central obesity, fatty liver, and
dyslipidaemia have been considered important risk factors related to non-
alcoholic fatty pancreas disease and pancreatic cancer
ABSTRACT

116. Endoscopic ultrasound image showing bright
hyperechoic of pancreas parenchyma.

117. The risk induction factors of steatopancreatitis include:
(a) Congenital diseases (Shwachman-Diamond
syndrome, Johanson-Blizzard syndrome, cystic
fibrosis, heterozygous carboxyl-ester lipase mutation)
(b) Alcohol abuse
(c) Infections (viral infection with Reovirus)
(d) Hemochromatosis
(e) Medicines (rosiglitazone, corticosteroids, octreotide,
gemcitabine)
(f) Malnutrition
(g) NAFLD, chronic hepatitis B

118. CAN YOU LIVE WITHOUT THE PANCREAS?
By Professor Hemant Kocher
MBBS, MS, MD, FRCS
Professor of Liver and Pancreas Surgery

119. “Total removal of the pancreas requires very
careful medical treatment and close
monitoring by a specialist. With medications,
many such patients can achieve good quality
of life and sometimes normal function and
work. There are no long-term studies on
patients who have no pancreas left, but from
experience patients go on to have normal life
expectancy with careful medical
supervision.”

120. References:
• American Gastroenterological Association Institute Guideline on Initial
Management of Acute Pancreatitis
https://www.gastrojournal.org/article/S0016-5085(18)30076-
3/fulltext#secsectitle0025
• Acute Pancreatitis Medication
https://emedicine.medscape.com/article/181364-medication#showall
• Bailey & Love
• RadioGraphics. Necrotizing Pancreatitis: Diagnosis, Imaging, and
Intervention
https://pubs.rsna.org/doi/full/10.1148/rg.345130012
• https://epomedicine.com/clinical-cases/acute-pancreatitis-case-
discussion/

121. References:
• https://www.cureus.com/articles/36219-steroid-induced-
pancreatitis-a-challenging-diagnosis
• https://www.ijem.in/article.asp?issn=2230-
8210;year=2013;volume=17;issue=5;spage=799;epage=805;aulast=K
ota
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4919820/#:~:text=It
%20is%20postulated%20that%20hypercalcemia,6%2C%207%2C%208
%5D.

122. References:
https://www.topdoctors.co.uk/medical-articles/can-you-live-
without-the-pancreas#
https://www.emjreviews.com/gastroenterology/article/non-alcoholic-fatty-
pancreas-disease-pancreatic-cancer-and-impact-of-endoscopic-ultrasound-
examination-on-screening-and-
surveillance/#:~:text=Fat%20accumulation%20in%20the%20pancreas,non
%2Dalcoholic%20fatty%20pancreas%20disease.
Anatomy and Histology of the Pancreas
Daniel Longnecker, MD
Department of Pathology, Geisel School of Medicine at
Dartmouth, Lebanon, NH
https://www.slideshare.net/HappyKagathara/3-cmeasa-
ahmedabad-january-2015

123. THANK YOU