Download - Acute pancreatitis
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ACUTE PANCREATITIS
Dr. Shailendra.V.L.Specialist in AnesthesiologyAl Bukariya general hospital
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PANCREAS
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PANCREATIC FUNCTIONS 500 – 800 ml per day Enzymes: amylase, lipase & protease Hormones: Insulin, glucagon,
somatostatin & pancreatic polypeptide
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HISTOLOGY OF PANCREAS
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AUTO PROTECTION OF PANCREAS Auto-digestion of pancreas is prevented
by packaging of proteases in precursor form:Protease inhibitors:
Pancreatic secretory trypsin inhibitor Serine pprotease inhibitor
Low calcium levels in pancreas decrease trypsin activity
Loss of any of these protective mechanisms leads to zymogen activation, auto digestion and acute pancreatitis
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ACUTE PANCREATITIS Wide clinical spectrum:
Mild (acute edematous pancreatitis)Severe (necrotizing pancreatitis)
Course of the disease:70% of patients have benign course30% of patients develop complications
50% mortality in these patients
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ETIOLOGYI GET SMASHED I – Idiopathic G – Gall stones E – Ethanol (alcohol) T – Trauma S – Steriods M – Mumps, Epstein barr & Cytomegalo virus A – Auto immune disease – SLE S – Scorpion bites H – Hypercalcemia, Hyperlipedemia,
Hypertriglyceremia E – ERCP following procedure 2 % develop D – SAND- steroids, Azothiprine,NSAIDs,Diuretics –
furesomide, thiazides
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DEMOGRAPHIC SIGNIFICANCE Western countries: 85 % cases due to
alcoholism & gall stones Eastern countries: Gall stones Children: Trauma Adoloscents & young adults: mumps
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PATHOGENESIS The pancreas produces a variety of
enzymes,, exocrine such as proteases, and saccharidases. These enzymes contribute to food digestion by breaking down food tissues. In acute pancreatitis, the worst offender among these enzymes is protease trypsinogen which converts to the active trypsin. Trypsin is responsible for auto-digestion of the pancreas which in turn causes the pain and complications of pancreatitis
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PATHOGENESIS Cellular injury & death result in
liberation of bradykinin peptides, vasoactive substances & histamines
Vasodilatation, increased vascular permeability & edema with profound effect on lungs
Systemic inflammatory response syndrome (SIRS) & Acute respiratory distress syndrome (ARDS) as well as multi organ failure occur as result of these cascading effects
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ROLE OF GALL STONES IN A P
Obstruction of pancreatic duct by stone
Ductal hypertension
Breakdown of intracellular compartments
Zymogen activation gives rise to
Auto-digestion initiated
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SIGNS OF ACUTE PANCREATITIS Signs which are less common, and indicate severe
disease, include: Grey-Turner’s sign(hemorrhagic discoloration of the flanks) Cullen’s sign (hemorrhagic discoloration of the umbilicus) Grünwald sign (appearance of ecchymosis around the
umbilicus due to local toxic lesion of the vessels) Körte's sign (pain or resistance in the zone where the
head of pancreas is located (in epigastrium, 6–7 cm above the umbilicus)
Kamenchik's sign (pain with pressure under the xiphoid process)
Mayo-Robson's sign (pain while pressing at the top of the angle lateral to the erector spinae muscles and below the left 12th rib (left costo-vertebral angle (CVA))[2]
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ESSENTIALS OF DIAGNOSIS1. Severe abdominal pain radiating to back2. Nausea & vomitting3. Elevated serum levels of amylase, lipase
1. Elevated amylase is not very specific test as it is raised in bowel perforation, ruptured ectopic, bowel obstruction
2. No definite correlation between severity of disease & serum amylase levels
3. Serum lipase levels elevated on first day and persists longer than amylase level
4. CT scan (most preferred)5. Ultrasound abdomen
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ESSENTIALS OF DIAGNOSIS Leukocytosis: occurs frequently Hyperglycemia: due to decreased insulin
release, increased glucogon release, increased output of adrenal glucocorticoids & catecholamines
Hypocalcemia: due toHypoalbuminemiaHypomagnesemiaBinding of calcium by free acid albumin
complexes Intracellular translocation of calcium
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ESSENTIALS OF DIAGNOSIS Jaundice may or may not be present
Present in only 10% of cases SGOP & SGPT levels transiently raised Markedly increased LDH levels indicate
poor prognosis Hypoxemia paO2 < 60 mm herald the
onset of ARDS
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DIAGNOSIS Diagnosis usually entertained when a
patient with possible predisposition to pancreatitis presents with severe & constant abdominal pain, nausea, emesis, fever, tachycardia
Labs reveal leukocytosis, hypocalcemia, hyperglycemia
Diagnosis usually confirmed by finding of threefold or greater elevated level of serum amylase or and lipase
Strong indicators include hemoconcentration Hct > 44% and signs of organ failure
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DIFFERENTAIL DIAGNOSIS1. Perforated viscus – peptic ulcer2. Acute cholecystitis & biliary colic3. Acute intestinal obstruction4. Mesentric vascular obstruction5. Renal colic6. Myocardial infarction7. Diabetic ketoacidosis
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ESTIMATION OF SEVERITY & DETERMINATION OF PROGNOSIS Many scoring systems introduced prior
CT scan days Most are difficult to remember Most accepted score is
Ranson’s early prognostic signsAPACHE II scoring Imirie’s prognostic criteriaSimplified prognostic criteriaGlasgow criteria
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CT SCAN SCORING OF ACUTE PANCREATITIS
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RANSON’S CRITERIA It is a clinical prediction rule for
predicting the severity of acute pancreatitis introduced in 1974
Ranson’s score less than 2 indicated mild disease with good prognosis
Ranson’s score more than 6 correlates with a mortality rate of 20% and complication rate of 80%
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RANSON’S CRITERIAAt 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/LAt 24 hours: Calcium (serum calcium < 2.0 mmol/L (< 8.0 mg/dL) Hemotocrit 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
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INTERPRETATION OF RANSON’S If the score ≥ 3, severe pancreatitis
likely. If the score < 3, severe pancreatitis is
unlikelyOr Score 0 to 2 : 2% mortality Score 3 to 4 : 15% mortality Score 5 to 6 : 40% mortality Score 7 to 8 : 100% mortality
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APACHE – II SCORING APACHE – II scores on admission &
within 48 hours help distinguish mild from severe pancreatitis and predict death
Most patitents whose APACHE –II score are 9 or less during the first 48 hours survive
However patients with APACHE-II scores of 13 or more have a likelihood of dying
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COMPLICATIONS OF ACUTE PANCREATITIS Acute fluid collections:
Detected by CT scan or ultrasound Most acute fluid collections resolve
spontaneoulsy Pseudocyst:
Collection of pancreatic fluid enclosed by a wall of granulation tissue
Intra-abdominal infections: Intestinal flora is the source
E coli, psedomonas, staph, proteus Pancreatic necrosis:
Nonviable area of pancreatic tissue with fat necrosis dignosed by ct scan
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PANCREATIC NECROSIS
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SYSTEMIC EFFECTS OF ACUTE PANCREATITIS Pulmonary:
Pleural effusion Atelectasis Mediastinal abscess Pneumonitis ARDS
Cardiovascular: Hypotension Hypovolemia Sudden death Non specific ST-T changes Pericardial effusion
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SYSTEMIC EFFECTS OF ACUTE PANCREATITIS Hematologic:
DIC Gastro intestinal hemorrhage
Peptic ulcer disease Erosive gastritis Pancreatic necrosis with erosion of vessels Portal vein thrombosis
Renal: Oliguria Azotemia Renal artery or vein thrombosis Acute tubular necrosis
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SYSTEMIC EFFECTS OF ACUTE PANCREATITIS Metabolic:
HyperglycemiaHypertriglyceridemiaHypocalcemiaEncephalopathy
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TREATMENT Early & aggressive resuscitation reduces
mortality rate by reducing incidence of multi system organ failure.1. Fluid resusitation2. Physiologic monitoring3. Inotropic support4. Respiratory support5. Renal support6. Nutrition
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FLUID RESUSITATION Tissue fluid shifts due to release of
vasoactive toxins & retroperitoneal losses
Replacement with crystalloid has no great advantage over colloids
Albumin given when levels < than 3g/L Blood transfused when Hb < than 10g/dl Measurement of CVP is a guide for
replacement
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INOTROPIC SUPPORT Incrementally increased infusion of
Dopamine or Dobutamine is preferred
RESPIRATORY SUPPORTHypoxemia PaO2 < 60mm Hg need early
intubation & ventilationSedation, analgesia & ventilation improve
cardiac performance
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RENAL SUPPORT Acute Tubular Necrosis (ATN) seen in
acute pancreatitis, needing temporary hemodialysis
Prognosis for renal function is good
Nutrition support:Enteral nutrition impossible as gut is restedParentral nutrition is needed
Early TPN not recommended in hemodynamically unstable patient
No specific outcome studies about nutrition regimes
Tuesday, May 2, 2023 37Thank you