Acute pancreatitis

Tuesday, May 2, 2023 1

ACUTE PANCREATITIS

Dr. Shailendra.V.L.Specialist in AnesthesiologyAl Bukariya general hospital


PANCREAS


PANCREATIC FUNCTIONS 500 – 800 ml per day Enzymes: amylase, lipase & protease Hormones: Insulin, glucagon,

somatostatin & pancreatic polypeptide


HISTOLOGY OF PANCREAS


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


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


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


DEMOGRAPHIC SIGNIFICANCE Western countries: 85 % cases due to

alcoholism & gall stones Eastern countries: Gall stones Children: Trauma Adoloscents & young adults: mumps


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


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


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


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]


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


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


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


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


DIFFERENTAIL DIAGNOSIS1. Perforated viscus – peptic ulcer2. Acute cholecystitis & biliary colic3. Acute intestinal obstruction4. Mesentric vascular obstruction5. Renal colic6. Myocardial infarction7. Diabetic ketoacidosis


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


CT SCAN SCORING OF ACUTE PANCREATITIS


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%


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


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


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


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


PANCREATIC NECROSIS


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


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


SYSTEMIC EFFECTS OF ACUTE PANCREATITIS Metabolic:

HyperglycemiaHypertriglyceridemiaHypocalcemiaEncephalopathy


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


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


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


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

Acute pancreatitis

Healthcare

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