pancreatitis

Report
pancreatitis
ferencz baranyay
surgical resident
royal melbourne hospital
• 23 y/o M BIBA with epigastric pain is your next
patient in the emergency department
• Pt driving along in passenger seat with his mum when began to feel
worsening pain in abdo
• ‘thought I was going to die’, told his mum to stop the car and call an
ambulance…
• After 5 mins of beginning to feel the pain, it hit a crescendo and
stayed until received IV morphine
• Felt pain as stabbing sensation, radiating retrosternally, with slight
nausea and associated shortness of breath
thoughts on diagnoses at this stage?
• No fevers or chills, no unusual bowel or
urinary symptoms, no genital issues.
• Previous night he’d had 14-15 drinks, he is an
overseas cricketer touring Australia
• Noted a history of GORD symptoms on
occasion but is otherwise medically well
examination
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o/e stable afebrile
small area of decreased A/E at lung bases
Abdo inspection NAD
++ epigastric/RUQ tenderness on deep palpation
Murphy’s -ve
No flank tenderness/renal angle tenderness
BS +ve
PR not done and genitals not examined
No peripheral oedema, JVPNE
lab testing
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Ix: lipase 230 (60 is upper limit N)
FBE N EUC N AST 87 GGT 227
Erect CXR NAD
ECG – sinus 96 bpm, no ST/T w abnormalities
FWT: negative
• Pt given lignocaine/mylanta preparation, with PPI
and reported no real benefit.
• Dx?
pancreas anatomy
Made up of head, neck body and tail
Retroperitoneal
Head lies in the ‘C’ of the duodenum
• also overlies IVC, L2 vertebra, medial
aorta and superior mesenteric vessels
Behind the neck splenic veins joins superior
mesenteric vein to form portal vein
Pancreatic duct closely related to common
bile duct
Acute pancreatitis
Spectrum of:
mild
severe
Mild inflammation of pancreas
Extensive pancreatic necrosis
Multi-organ failure
75% cases seen in ED
25% cases seen in ED
Mortality <1%
Mortality 20-30%
pathophysiology
neutrophils
Acinar cell necrosis
Pseudocyst formation
Possible abscess development with
multi-organ failure
macrophages and lymphocytes
trypsinogen
chymotrypsinogen
Proelastase
procarboxypeptidase
trypsin cascade
active elastases
autodigestion of pancreas
causes
Gallstones (35-40%)
ETOH (2nd most frequent cause)
Tumours
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pancreas, ampulla, choledochocele
Scorpion sting
Microbiological – infection
Autoimmnune (SLE, crohn’s)
Surgery/trauma (blunt trauma, cardiac surgery, ERCP)
Hyperlipidaemia (<11mmol, 3rd most freq cause), hypocalcemia, hypothermia
Emboli/ischemia
Drugs (carbamazepine, valproate, frusemide, opiates, estrogens, erythromycin, enalapril, rifampicin)
Cause is unknown in 15-20% of cases.
Clinical presentation acute pancreatitis
History
• Any severe acute pain in the abdomen or back should suggest acute pancreatitis.
• The diagnosis is usually entertained when a patient presents with
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severe and constant abdominal pain (classically in epigastrium, radiating through to back)
nausea
emesis
fever
tachycardia
Examination
• Fever (76%), sinus tachy (65%)
• Dehydration
• Upper abdo tenderness/epigastric tenderness (68%)
in severe pancreatitis…
• Pulmonary signs (effusions, tachypnea secondary to diaphragmatic irritation)
• Cullen’s sign (bluish/red discolouration periumbilical wall
• Grey-turner’s sign (bluish/red discolouration of flanks)
• peritonitis
Cullen’s + Grey Turner’s sign
laboratory testing
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No gold standard for diagnosis
(apart from histopathological
testing of the pancreas)
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Lipase and amylase
– ↑ amylase
• fallopian tubes, ovaries,
testes, adipose tissue,
small bowel, lung, thyroid,
skeletal muscle,
and certain neoplasms.
– ↑ lipase
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more specific, but still in small
intestine
Rule out all valid differentials
From Tintinalli’s Emergency Medicine 18th edition
differentials for upper abdo pain and
tenderness
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perforated viscus, especially peptic
ulcer
– Erect CXR
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acute cholecystitis and biliary colic
– LFTs, liver/biliary ultrasound, ERCP
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acute intestinal obstruction
– Abdo XR
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mesenteric vascular occlusion
– CT angiogram of intestinal vessels
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renal colic
– Urinanalysis, hourly urine output,
serum creatinine, CT ureters
• myocardial infarction
– ECG, troponin
• dissecting aortic aneurysm
– CT angiogram
• connective tissue disorders with
vasculitis
– ESR
• Pneumonia
– CXR
• diabetic ketoacidosis
– serum glucose, ABG
Assessing severity
...many severity scores
Ranson’s criteria
At admission
• age in years > 55 years
• white blood cell count > 16000 cells/mm3
• blood glucose > 10 mmol/L (> 200 mg/dL)
• serum AST > 250 IU/L
• serum LDH > 350 IU/L
At 48 hours
• Calcium (serum calcium < 2.0 mmol/L (<
8.0 mg/dL)
• Hematocrit fall > 10%
• Oxygen (hypoxemia PO2 < 60 mmHg)
• BUN increased by 1.8 or more mmol/L (5 or
more mg/dL) after IV fluid hydration
• Base deficit (negative base excess) > 4 mEq/L
• Sequestration of fluids > 6 L
Score 0 to 2 : 2% mortality
Score 3 to 4 : 15% mortality
Score 5 to 6 : 40% mortality
Score 7 to 8 : 100% mortality
Radiology of acute pancreatitis
U/S 
useful for biliary pathology, 70-80% sensitive for pancreatitis
CT more useful for judging severity and regional effects
Try to wait >12 hours as early CT is usually unhelpful
treating acute pancreatitis
mild to moderate pancreatitis:
• usually requires treatment with IV fluids and fasting.
• clear liquid diet is frequently started on the third to sixth day
• regular diet by the fifth to seventh day
• The decision to reintroduce oral intake is usually based on the following criteria:
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a decrease in or resolution of abdominal pain;
the patient is hungry; and
Organ dysfunction, if present, has resolved
(don’t use lipase or amylase! Not indicative of resolution if normal levels)
Antibiotics – controversial, but currently recommended
unremitting fulminant pancreatitis:
• usually requires inordinate amounts of fluid
• close attention to complications
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cardiovascular collapse, respiratory insufficiency, and pancreatic infection, as well as possible
surgical debridement or drainage.
Chronic pancreatitis
• Inflammatory disease of
pancreas
• irreversible morphological
changes in the pancreatic
duct, acinar cell destruction
and fibrosis
• Four clinical manifestations
include abdominal pain,
steatorrhoea, diabetes, and
calcification of pancreas
Etiology of chronic pancreatitis
• Mostly due to ETOH in the Western World
– Increases viscosity of pancreatic juice
– Decreased local secretion of ‘lithostatin’ which usu
makes calcium salts soluable
• Precipitation of calcium within gland
– Direct toxic effect on acinar cells
– Cytokines recruit stellate cells, causing fibrosis
• Other unusual causes such as cystic fibrosis,
severe malnutrition, hereditary or idiopathic
Investigations
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AXR
U/S
CT abdo
Secretin test
complications of chronic pancreatitis
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Narcotic addiction
Gastrointestinal bleeding
Impaired glucose tolerance
Jaundice
Gastroparesis
Cholangitis and/or biliary cirrhosis
Effusions with high amylase content
Pancreatic cancer
Medical treatment of chronic pancreatitis
• Enzyme replacement (lipase, protease,
somatostatin)
• Often require insulin
• Behaviour modification
• Analgesia, often difficult
Surgical treatment
• Pseudocyst drainage
Surgical treatment
• Pseudocyst drainage
Surgical treatment
• Whipple’s procedure
Chronic pancreatitis
Head of pancreas Ca
Duodenal Ca
Cholangiocarcinoma
Ampullary Ca
In summary
• In the patient with an acute abdomen, all
possible differentials should be considered
• Diagnosis of acute pancreatitis should rule out
other differentials, can be life threatening, and
should be carefully managed
• Management of chronic pancreatitis requires
consideration of medical and surgical
therapies

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