pancreatitis

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pancreatitis

• ferencz baranyay
• surgical resident
• royal melbourne hospital

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• 23 y/o M BIBA with epigastric pain is your next
  patient in the emergency department

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• 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?

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• No fevers or chills, no unusual bowel or urinary
  symptoms, no genital issues.
• Previous night hed had 14-15 drinks, he is an
  overseas cricketer touring Australia
• Noted a history of GORD symptoms on occasion but
  is otherwise medically well

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examination

• o/e stable afebrile
• small area of decreased A/E at lung bases
• Abdo inspection NAD
• epigastric/RUQ tenderness on deep palpation
• Murphys -ve
• No flank tenderness/renal angle tenderness
• BS ve
• PR not done and genitals not examined
• No peripheral oedema, JVPNE

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lab testing

• 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?

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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

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Acute pancreatitis

• Spectrum of

mild
severe
Extensive pancreatic necrosis Multi-organ failure
Mild inflammation of pancreas
75 cases seen in ED
25 cases seen in ED
Mortality 20-30
Mortality lt1
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pathophysiology
neutrophils
Acinar cell necrosis Pseudocyst
formation Possible abscess development with
multi-organ failure
macrophages and lymphocytes
trypsinogen chymotrypsinogen Proelastase procarbo
xypeptidase
active elastases
autodigestion of pancreas
trypsin cascade
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causes

• Gallstones (35-40)
• ETOH (2nd most frequent cause)
• Tumours
• pancreas, ampulla, choledochocele
• Scorpion sting
• Microbiological infection
• Autoimmnune (SLE, crohns)
• Surgery/trauma (blunt trauma, cardiac surgery,
  ERCP)
• Hyperlipidaemia (lt11mmol, 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.

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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
• 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)
• Cullens sign (bluish/red discolouration
  periumbilical wall
• Grey-turners sign (bluish/red discolouration of
  flanks)
• peritonitis

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Cullens Grey Turners sign
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laboratory testing

• No gold standard for diagnosis (apart from
  histopathological testing of the pancreas)
• Lipase and amylase
• ? amylase
• fallopian tubes, ovaries,
• testes, adipose tissue,
• small bowel, lung, thyroid,
• skeletal muscle,
• and certain neoplasms.
• ? lipase
• more specific, but still in small intestine
• Rule out all valid differentials

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differentials for upper abdo pain and tenderness

• perforated viscus, especially peptic ulcer
• Erect CXR
• acute cholecystitis and biliary colic
• LFTs, liver/biliary ultrasound, ERCP
• acute intestinal obstruction
• Abdo XR
• mesenteric vascular occlusion
• CT angiogram of intestinal vessels
• 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

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Assessing severity
...many severity scores

• Score 0 to 2  2 mortality
• Score 3 to 4  15 mortality
• Score 5 to 6  40 mortality
• Score 7 to 8  100 mortality

• Ransons criteria
• At admission
• age in years gt 55 years
• white blood cell count gt 16000 cells/mm3
• blood glucose gt 10 mmol/L (gt 200 mg/dL)
• serum AST gt 250 IU/L
• serum LDH gt 350 IU/L
• At 48 hours
• Calcium (serum calcium lt 2.0 mmol/L (lt 8.0 mg/dL)
• Hematocrit fall gt 10
• Oxygen (hypoxemia PO2 lt 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) gt 4 mEq/L
• Sequestration of fluids gt 6 L

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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
gt12 hours as early CT is usually unhelpful
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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
• a decrease in or resolution of abdominal pain
• the patient is hungry and
• Organ dysfunction, if present, has resolved
• (dont 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
• cardiovascular collapse, respiratory
  insufficiency, and pancreatic infection, as well
  as possible surgical debridement or drainage.

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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

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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

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Investigations

• AXR
• U/S
• CT abdo
• Secretin test

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complications of chronic pancreatitis

• Narcotic addiction
• Gastrointestinal bleeding
• Impaired glucose tolerance
• Jaundice
• Gastroparesis
• Cholangitis and/or biliary cirrhosis
• Effusions with high amylase content
• Pancreatic cancer

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Medical treatment of chronic pancreatitis

• Enzyme replacement (lipase, protease,
  somatostatin)
• Often require insulin
• Behaviour modification
• Analgesia, often difficult

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Surgical treatment

• Pseudocyst drainage

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Surgical treatment

• Pseudocyst drainage

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Surgical treatment

• Whipples procedure

Chronic pancreatitis Head of pancreas
Ca Duodenal Ca Cholangiocarcinoma Ampullary Ca
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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