The document provides an in-depth overview of acute pancreatitis, covering anatomy, pathology, symptoms, diagnosis, and treatment. It highlights key aspects such as the roles of exocrine and endocrine functions, mortality rates, and various etiologies for the condition. Diagnosis involves enzyme level assessments and imaging techniques, while treatment primarily consists of supportive measures and surgical interventions as necessary.

1. Acute pancreatitis
Presenter GATERE JORAM
Egerton university
MBCHB IV
10/09/2018

2. ANATOMY & HISTOLOGY OF THE
P A N C R E A S
• 15 cm in length, 60-140 gm, consists of head, body & tail; pancreatic duct empty
into duodenum or common bile duct
• Histologically, consists of 2 components:
• 1) Exocrine: 80-85%, consists of numerous glands (acini) lined by columnar
basophilic cells containing zymogen granules, which form lobules; ductal
system
• Trypsin, chemotrypsin, aminopeptidase, amylase, lipase
• 2) Endocrine: islets of Langerhans, which are invaded by capillaries. Islets
consist of:
• 4 main cell types: B (insulin), A (glucagon), D (somatostatin), PP cells
(pancreatic polypeptide)
• 2 minor cell types: D1 (VIP) & enterochromaffin cells (serotonin)

3. Mortality/Morbidity:
• The overall mortality rate of patients with acute pancreatitis is 10-15%.
• In patients with severe disease, the mortality rate is approximately 30%.
• In the first week of illness, most deaths result from multi organ system
failure. In subsequent weeks, infection plays a more significant role, but
organ failure still constitutes a major cause of mortality.
• Sex:
• In general, acute pancreatitis affects males more often than females.
• The etiology in males is more often related to alcohol; in females, to
biliary tract disease.

4. AUTO PROTECTION
• First, proteins are translated into an inactive form called
pro enzymes.
• The pro enzymes are packaged in a para- crystalline
arrangement with protease inhibitors(zymogens
granules)
• Zymogen granules have an acidic pH and a low calcium
concentration, which are factors that guard against
premature activation

5. Pathology
• :
4 basic alterations:
1) Proteolytic destruction of pancreatic substance
2) Necrosis of blood vessels & interstitial hemorrhage
3) Fat necrosis by lipolytic enzymes
4) Associated acute inflammatory reaction
• Pathologic lesions:
• Acute pancreatic necrosis
• Acute hemorrhagic pancreatitis
• Suppurative peritonitis
• Pancreatic pseudocysts

6. Pathogenesis:
• Autodigestion of pancreatic tissue by inappropriately activated pancreatic enzymes
• Trypsin has a major role:
• Activates other proenzymes (proelastase , prophospholipase )
• Converts prekallikrein to kallikrein (Kinin system)
• Hageman factor is activated
• Mechanisms of pancreatic enzyme activation:
• Pancreatic duct obstruction
• Primary acinar cell injury
• Defective intracellular transport of proenzymes within acinar cells

8. ETIOLOGY
• REMEMBER -I GET SMASHED
• : Although pancreatitis has numerous etiologies, alcohol
dependence and biliary tract disease cause most cases. In 10-30%
of cases, the cause is unknown, and careful evaluation may
identify a rare etiology in 10% of cases.
• Metabolic: alcohol, hyperlipoproteinemia, hypercalcemia, drugs (e.g.
thiazides), genetic
• Mechanical: gallstones, traumatic & perioperative injury
• Vascular: shock, atheroembolism, polyarteritis nodosa
• Infections: Mumps, Coxsackie virus, Mycoplasma
• Idiopathic : 10-20% ; ? Genetic basis
I-idiopathic,G-gallstone(micro harrison),E-ethanol,T-trauma,S-
mumps,A-autoimmune dse,S-scorpion bite,H-
hyperkalemia/hypertryglyceridaemia,E-ercp(endoscopic retrograde
cholangiopancretography),D-drugs(NRTIS,protease inhibitor)

10. SYMPTOMS
• History:
• The cardinal symptom of acute pancreatitis is abdominal pain, which is characteristically
dull, boring, and steady. Most often, it is located in the upper abdomen, usually in the
epigastric region, but it may be perceived more on the left or right side, depending on
which portion of the pancreas is involved.
• The pain radiates to the back in approximately half of cases.
• The duration of pain varies but typically lasts more than a day.
• The pain may be aggravated by eating or lying supine and it may be alleviated by
fasting or lying on the left side with the knees and hips flexed.
• Associated symptoms (eg, anorexia, nausea, vomiting) are common, and some patients
experience diarrhea due to indigestion.
• Avulsion to fatty foods may be reported

11. Physical exam:
• Distressed anxious patient
• Low grade fever
• Tachycardia
• Shock-(i)due to exudation of blood and plasma proteins into
retroperitoneal space. (ii)kininins- vasodilation, increased vascular
permeability (iii)systemic effects of lipolytic enzymes released into
circulation
• Jaundice-infrequent-edema of head of pancreas
• Erythematous skin nodules-subcut fat necrosis
• 10-20 %→ pulmonary findings-rales, atelectasis, pleural effusions
• Decreased bowel sounds
• Pancreatic pseudocyst-palpable in upper abdomen
• Cullens sign-faint blue discolouration around umblicus due to
hemoperitoneum
• Turner”s sign → blue-red-purple discolouration or green brown
discolouration in the flanks-Tissue catabolism of hemoglobin-Latter 2
rare. If present-necrotising pancreatitis

12. Diagnosis of acute pancreatitis
Amylase and lipase-elevations of 3 times above reference range
considered diagnostic
Amylase not specific for pancreatic dis-can occur in small intestine
obstruction, mesenteric ischaemia, tubo-ovarian disease, renal insufficiency,
parotitis
Serum T ½ of amylase is short-elevations return to ref range
within a few days.
Lipase-longer half life more specific to the pancreas. Note-levels of
the two do not correlate with prognosis
REF-Lipase-56-239
-Amylase-0-260U/L(under 18 years)
-35-115U/L(over 18years)

13. ….Diagnosis
Liver enzymes-ALP, total bil, AST, Alanine aminotransferase-
search for gall stone pancreatitis if elevated
Alanine aminotransferase >150U/L-gallstone pancreatitis
Calcium levels-hypercalcemia as aetiolgy or saponification if
hypocalcemia- correlates well with severity of disease. Levels
lower than 7 mg/dL (when serum albumin is normal) are
associated with tetany and an unfavorable prognosis.
Cholesterol, TGs, if elevated search for aetiology
(Hyperlipidimia) -fasting triglyceride levels above 1000
mg/dL.
Baseline TGs can be lower in acute pancreatitis

14. ….Diagnosis…
C.B.C –Hct >47 proposed as a sensitive measure of more
severe disease, however this has subsequently been shown
to have value only as a negative predictor of severe disease
i.e. lack of severe hemoconcentration rules out severe
disease
Leukocytosis-inflammation or infection
CRP-higher levels-organ failure. CRP not specific.
BGAs if patient is dyspnoic
Trypsin and its precursor trypsinogen 2 in both urine and
peritoneal fluid-not widely used

15. ….DIAGNOSIS
Imaging-Radiologic findings are inconstant and non-
specific. CXR, K.U.B- exclude other diagnosis
CT scan may confirm impression of acute pancreatitis
and severity (esp. Contrast Enhanced CT-CECT) .
Abdominal ultrasonography-detects gall stones-
Sensitivity in acute pancreatitis 70-80 %
MRCP-emerging role.T2 weighted images provide a
non invasive image of the biliary and pancreatic
ducts
Endoscopic ultrasonography-more details than
transcutaneous U/S-Principal role –evaluating
microlithiasis, biliary sludge, periampulary lesions

16. Diagnostic procedures
ERCP- evaluates biliary and pancreatic ductal
system. Should be used with caution in pts with
acute pancreatitis.Never to be used as a first line
tool in this disease.
Used in suspected choledocholithiasis and biliary
pancreatitis with worsening jaundice
CT-guided needle aspiration-diff sterile from
infected necrosis. Evaluate specimen for culture
and sensitivity and gram stain

17. complications

18. Factors affecting survival

19. ASSESSMENT OF SEVERITY
• Ranson's criteria- are generally used in assessing the severity
of acute alcoholic pancreatitis on presentation (pancreatitis
due to other causes is assessed by similar criteria).
1. When three or more of the following are present on
admission, a severe course complicated by pancreatic
necrosis can be predicted with a sensitivity of 60–80%:
• Age over 55 years.
• White blood cell count over 16,000/mcL.
• Blood glucose over 200 mg/dL.
• Serum LDH over 350 units/L.
• AST over 250 units/L.

20. 2. Development of the following in the first 48 hours
indicates a worsening prognosis:
• Hematocrit drop of more than ten percentage points.
• BUN rise greater than 5 mg/dL.
• Arterial Po2 of less than 60 mm Hg.
• Serum calcium of less than 8 mg/dL.
• Base deficit over 4 mEq/L.
• Estimated fluid sequestration of more than 6 L.

21. Severity index in acute pancreatitis

22. TREATMEMT OF ACUTE
PANCREATITIS
• 85 -90 % of patients the disease is self limited, subsides in 3 to 7 days
of rx
• Conventional measures
• (i) analgesics- meperidine, up to 100–150 mg intramuscularly every 3–4
hours as necessary
• (ii) IV fluids and colloids
• (iii) no oral intake
• (iv) NG suction to decrease gastrin release and prevent gastric contents from
entering duodenum.
Anticholinergics-no therapeutic advantage
• Antibiotics-used but RCTs have shown no benefit in mild to
moderate severity disease
Current evidence- prophylactic antibiotics in necrotizing acute
pancreatitis-decreases sepsis and mortality

23. ….TREATMENT…
• Surgery-infected pancreatic necrosis.
Data support delaying surgical debridement of
necrotic tissue for at least 2 weeks for viable
pancreatic tissue to become evident
Patients with severe gall stone induced pancreatitis
may improve if papillotomy is done within 36
to 72 hours
Studies show that only those pts with gall stone
pancreatitis who are in the very severe group
should be considered for ERCP

24. …TREATMENT…
• Hypertryglyceridemia associated
acute pancreatitis-
• (i)wt loss
• (ii)Lipid restricted diet
• (iii)exercise
• (iv)avoid alcohol and drugs e.g. vitamin
A, thiazides, beta blockers
• (v) control DM

25. INFECTED PANCREATIC NECROSIS
• Diffuse infection of acutely inflamed, necrotic
pancreas occurs in the first 1 to 2 weeks of
onset of acute pancreatitis
• Treated by surgical debridement.
• Mostly gram negative bacteria of gut origin.
• Early diagnosis-CT guided needle aspiration
• Imipenem-cilastatin 500 mg TID for 2 weeks-
prophylactic

26. Pancreatic abscess
• Ill defined collection of pus, evolves over
longer period 4 to 6 weeks
• Life threatening but lower rate of surgical
mortality
• Treated surgically or in selected cases
percutaneous drainage

27. PANCREATIC PSEUDOCYST
• Collection of tissue, fluid, debris, pancreatic
enzymes, and blood. Develops over 1-4 weeks.
Forms in 15% of patients
• Wall consists of necrotic tissue, granulation tissue,
fibrous tissue
• Preceded by pancreatitis in 90% of cases, trauma in
10% of cases
• May be two or more.
• 85% located in body or tail.15% head

28. …Pseudocyst…
• Abdominal pain with or without radiation to
the back.
• Palpable tender mass in the middle or left upper
abdomen
• Serum amylase elevated in 75% of patients at
some point during illness
• Sonography reliable in detecting pseudocysts.
Serial u/s indicates resolution or not
• CT complements U/S in diagnosis
• Recent studies show non interventional,
expectant management is the best course in pts
with minimal symptoms with no alcohol use

29. Pseudocyst….
• Complications-pain caused by expansion, rupture,
hemorrhage, abscess
• Increase in size, localized bruit over mass, sudden
drop in Hb/Hct-possibility of hemorrhage from
pseudocyst
• U/S or CT guided repeated needle aspiration/
catheter drainage-success rate 45-75 % success rate

30. Pseudoaneurysm-
• In 10% of pts. Reflects distribution of pseudocyst
and fluid collections.
• Splenic artery most commonly involved, followed by
inferior and superior pancreatico duodenal arteries
• Thin cut CT usually reveals a contrast enhanced
lesion within or adjacent to suspected pseudocyst.
Arteriography is necessary to confirm diagnosis

31. Spiral CT- Pseudoaneurysm(small arrow)
within pseudocyst and duct

32. CT- Lobulated pseudocyst

34. Acute pancreatitis with
necrosis:
Lack of enhancement of the
body and most of the tail

35. THANK YOU let meet in surgery
References:
HARRISON’S PRINCIPLES OF INTERNAL
MEDICINE.
ROBBINS AND COTRAN PATHOLOGICAL BASIS OF
DISEASES 9TH EDITION
William F. Ganong
eMedicine

36. • I-idiopathic
• G-gallstones-the bigger it is the lesser it cause and vice versa
• E-ethanol
• T-trauma
• S-mumps
• M-auto immune dise
• S-scorpion bite
• H-hyperkalemia/hypertryglyceridaemia
• E-ercp(endoscopic retrograde cholangiopancreatography)
• D-drugs-NRTI and protease inhibitors