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Acute pancreatitis
 

Acute pancreatitis

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Acute pancreatitis

Acute pancreatitis
definition of acute pancreatitis
complications of acute pancreatitis

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    Acute pancreatitis Acute pancreatitis Presentation Transcript

    • ACUTE PANCREATITIS DR.RAHUL GARG M.D.MEDICINE(Std.) S.N.M.C.,AGRA DR. RAHUL GARG
    • DEFINITIONS Atlanta Symposium definition of acute pancreatitis : An acute inflammatory process of the pancreas with variable involvement of other regional tissues or remote organ systems. Acute pancreatitis is best defined clinically by a patient presenting with two of the following criteria: (1)Symptoms, such as epigastric pain, consistent with the disease. (2)A serum amylase or lipase greater than three times the upper limit of normal. (3) Radiologic imaging consistent with the diagnosis, usually using CT or MRI.
    • CAUSES OF ACUTE PANCREATITS COMMON CAUSE • • • • • • • Gall Stones ( including microlithiasis ) (40%) Alcohol ( acute and chronic alcoholism (30%) Hypertriglyceridmia ( mainly over >1000 mg/ dl ) ERCP ( Specially after billary manometry) Trauma (specially after blunt trauma ) Post – operative ( abdominal and non abdominal) Drugs (azathioprin, 6 – mp , sulfonamides, estrogen, anti – HIV protease inhibitor , Vaproic acid ,thiazide,erythromycin,acetaminophen) • Annular pancreas,Choledochocele
    • CLINICAL FEATURE  HISTORY  Abdominal pain :  Severity  Character  Site  Radiation  Agg /releaving factor mild tolerable discomfort Severe constant incapacitating distress steady and boring in character located in epigastrium and Periumblical region radiation to back and chest, lower abdomen flanks. pain increases when pt in supine and relieved by sitting with trunk flexed and knee drawn up  Nausea/ vomiting / abdominal distention
    • PHYSICAL EXAMINATION     Hypo or hyperthermia(<98.6or>100.4f) Tachycardia (>90beats/min) Hypotension and shock (BP<90mmhg) Jaundice – infrequentely occure due to edema of the head of pancrease and compression of intrahepatic portion of cbd.  Erythematous skin nodules – due to subcutaneous fact necrosis  In 10 – 20% patients pulmonary findings Basilar rales atelcectesis left sided pleural effusion  Abdominal tenderness and rigidity  Bowel sound diminished and absent  Palpable pancreatic pseudocyst in upper abdomen  In severe necrotizing pancreatitis –  Cullens sing : faint blue discoloration around umlicus  Turner,s sing: blue red purpel or grey brown discoloration of the flanks Sleisenger and Fordtran's Gastrointestinal and Liver Disease ninth edition
    • LABORATORY DIAGNOSIS PANCREATIC ENZYMES  Diagnosis of acute pancreatitis relies on at least a three-fold elevation of amylase or lipase in the blood. • Serum Amylase(30-180 IU/L) • It rises within 6 to 12 hours of onset (half-life, 10 hours). • The serum amylase is usually increased on the first day of symptoms, and it remains elevated for three to five days in uncomplicated attacks. • Sensitivity is greater than 85%, the serum amylase may be normal or minimally elevated in fatal pancreatitis, during a mild attack or an attack superimposed on chronic pancreatitis , or during recovery from acute pancreatitis also in hypertriglyceridemia-associated pancreatitis. • Hyperamylasemia is not specific for pancreatitis because it occurs in many conditions other than acute pancreatitis.
    • • Serum Lipase(0-160 IU/L) • The sensitivity of serum lipase is similar to that of serum amylase and is between 85% and 100%. • Lipase may have greater specificity for pancreatitis than amylase. • Serum lipase always is elevated on the first day of illness and remains elevated longer than does the serum amylase. • Some believe that serum lipase is preferable to that of serum amylase , whereas others find no clear advantage .
    • • Secretin-pancreozymin (CCK) test • Secretin leads to increased output of pancreatic juice and HCO3; CCK leads to increased output of pancreatic enzymes. • Sensitive enough to detect occult disease; involves duodenal intubation and fluoroscopy ,only role in acute on chronic pancreatitis. Other Pancreatic Enzymes • They include PLA2, trypsin/typsinogen, carboxylester lipase, carboxypeptidase A, colipase, elastase, and ribonuclease. • None, alone or in combination, are better than serum amylase or lipase
    • Other blood test• White blood cell count -Increased • Haematocrit->44 show poor prognosis, moniter daily. • Serum Creatinine and serum electrolytes • AST,ALT,alkaline phosphatase, and bilirubin also may increase . • MCV- Alcoholic patients tend to have a higher MCV . • Serum triglyceride levels- increase in acute pancreatitis, but also with alcohol use, uncontrolled diabetes mellitus, or defective triglyceride metabolism
    • RADIAOLIGICAL – Chest X- ray / X – ray abdomen errect  See for pulmonary complication pleural effusion  Rule out other diagnosis,specially – a perforation USG- Specially for diagnosis of gall stone Helical CT Scan (Contrast Enhanced ,After 48 -72hrs of onset)  Helpful to know severity and prognosis  Allows estimation of presence and extend of pancreatic necrosis.  Conferm the cinical impression of acute pancreatitis in face of normal s. Amylase.  Severe allergy and renal impairment(s.crt>2mg/dl) are contraindication for contrast use.  EUS and/or MRCP are better than CT for choledocolithiasis.
    • Markers of Severity within 24 Hours • BMI>30 • SIRS [temperature >38° or <36°C (>100.4° or 96.8°F), Pulse >90, Tachypnea >24, WBC >12,000] • Hemoconcentration (Hct >44%) • BISAP • (B) Blood urea nitrogen (BUN) >22 mg% • (I) Impaired mental status • (S) SIRS: 2/4 present • (A) Age >60 years • (P) Pleural effusion • Organ Failure
    • Atlanta Criteria for Severe Acute Pancreatitis Organ Failure a. Shock: systolic blood pressure <90 mm Hg b. Pulmonary insufficiency: Pao2 ≤60 mm Hg c. Renal failure: serum creatinine >2 mg/dL d. Gastrointestinal bleeding: >500 mL/24 hr Local Complications a. Necrosis b. Abscess c. Pseudocyst
    • -- Ranson's Prognostic Criteria NON-GALLSTONE PANCREATITIS At Admission Age >55 yr White blood cells >16,000/mm3 Blood glucose >200 mg/dL Serum lactate dehydrogenase >350 IU/L Serum aspartate aminotransferase >250 IU/L During Initial 48 hr Hematocrit decrease of >10 % Blood urea nitrogen increase of >5 mg/dL Serum calcium <8 mg/dL Arterial po2 <60 mm Hg Serum base deficit >4 mEq/L Fluid sequestration >6 L GALLSTONE PANCREATITIS Age >70 yr >18,000/mm3 >220 mg/dL >400 IU/L >250 IU/L >10% >2 mg/dL <8 mg/dL NA >5 mEq/L >4 L
    • SEVERITY INDEX IN ACUTE PANCREATITIS Grade of Acute pancreatitis Points A NORMAL PANCREAS 0 B PANCREATIC ENLARGMENT ALONE FOCAL OR DIFFUSE WITH CONTOUR IRREGULARITIES AND INHOMOGENOUS ATTENUATION 1 C B+PERIPANCREATIC INFLAMMATION 2 D C+ONE PERIPANCREATIC FLUID COLLECTION 3 E D+TWO OR MORE PERIPANCREATIC OR RETROPERITONEAL FLUID COLLECTION OR GAS COLLECTION 4 DEGREE OF PANCREATIC NECROSIS 1 NO – NECROSIS 0 2 NECROSIS OF <33% PANCREASE 2 3 NECROSIS OF 33%-50% OF PANCREASE 4 4 NECROSIS OF > 50% OF PANCREASE 6 CT SEVERITY INDEX ( CT SI )BALTHAZAR SCORE+NECROSIS SCORE CT GRADE + NECROSIS GRADE (0 - 4) + ( 0 – 6 )  ( 0 – 10 )
    • Contrast-enhanced computed tomography shows diffuse swelling of the pancreas (P) with peripancreatic inflammatory changes (arrows). The pancreas was well perfused without evidence of necrosis. G, gallbladder.
    • Acute pancreatic necrosis. Contrast-enhanced c t demonstrates focal areas of decreased perfusion in the pancreatic parenchyma (arrows) with surrounding peripancreatic inflammation. The necrosis was estimated to involve less than 30% of the pancreas. G, gallbladder
    • MANAGEMENT; • Patients with acute pancreatitis require adequate intravenous hydration and adequate analgesia to eliminate or markedly reduce pain. • The patient is usually on npo until any nausea and vomiting have subsided. • Opiate dosing is monitored carefully and adjusted on a daily basis according to ongoing needs. • Nasogastric intubation is not used routinely because it is not beneficial in mild pancreatitis. • It is used only to treat gastric or intestinal ileus or intractable nausea and vomiting. • Similarly, proton pump inhibitors or H2-receptor blocking agents are not beneficial and not used. Sleisenger and Fordtran's Gastrointestinal and Liver Disease ninth edition
    • • The patient should be carefully monitored for any signs of early organ failure such as hypotension, vital signs and urinary output. • Tachypnea should not be assumed to be due to abdominal pain; monitoring oxygen saturation and, if needed, blood gases is advised and oxygen supplementation is mandatory if there is hypoxemia. • Any patient who exhibits signs of early organ dysfunction should be immediately transferred to intensive care monitoring.
    • FLUID RESUSCITATION; • The goal is to decrease the hematocrit. • Laboratory and clinical studies with intravenous dextran to promote hemodilution have suggested efficacy in preventing severe disease. • One of the markers of severity of pancreatitis defined by Ranson and colleagues is intravascular losses (“fluid sequestration”). • Requirements of a 70-kg person during the first 48 hours, is should be at least 250 to 300 mL/hour for 48 hours. • The rate of volume replacement is more important during the first 24 hours, when a rising hematocrit has been shown to correlate closely with severe disease.
    • • Maintaining adequate intravascular volume in patients with severe disease may require 5 to 10 L of fluid such as isotonic saline daily for the first several days (200 to 400 mL/hour). • In a patient with unclear cardiac output, a Swan-Ganz catheter can be useful . Sleisenger and Fordtran's Gastrointestinal and Liver Disease ninth edition
    • RESPIRATORY CARE; • Hypoxemia (oxygen saturation <90%) requires supplemental oxygen. • Current guidelines recommend the initial routine use of nasal cannula oxygen to all patients with acute pancreatitis. • ARDS is the most serious respiratory complication of acute pancreatitis. • It generally occurs between the second and seventh day of illness (but can be present on admission) . • Chest radiography may show multilobar alveolar infiltrates. • Treatment is endotracheal intubation with positive endexpiratory pressure ventilation, often with low tidal volumes to protect the lungs from volutrauma. • No specific treatment will prevent or resolve ARDS.
    • • Cardiac complications of severe acute pancreatitis include congestive heart failure, myocardial infarction, cardiac dysrhythmia, and cardiogenic shock. • If hypotension persists even with appropriate fluid resuscitation, intravenous dopamine may help maintain the systemic blood pressure. • Dopamine does not impair the microcirculation of the pancreas as do other vasoconstrictors.
    • METABOLIC COMPLICATION; • Hyperglycemia may present but usually normalizes as the inflammatory process subsides. • Blood sugars fluctuate, and insulin should be administered cautiously. • Reduced serum ionized calcium may occur and cause neuromuscular irritability. • If hypomagnesemia coexists, magnesium replacement should restore serum calcium to normal. • Once the serum magnesium is normal, signs or symptoms of neuromuscular irritability may require administering intravenous calcium gluconate as long as the serum potassium is normal and digitalis is not being given.
    • Prophylactic Antibiotics; • The majority of organisms detected were gram-negative aerobic or anaerobic species (Escherichia coli, Enterobacter aerogenes, Pseudomonas aeruginosa, Proteus species, Klebsiella pneumoniae, Citrobacter freundii, and Bacteroides species), with occasional gram positives and rare fungi . • Imipenem, fluoroquinolones (ciprofloxacin, ofloxacin, pefloxacin), and metronidazole are the drugs that achieved the highest inhibitory concentrations in pancreatic tissue, whereas aminoglycosides did not. • Recently there is no current recommendation of prophylactic antibiotic.
    • ENDOSCOPY AND NUTRITION • Endoscopic early removal of a possibly impacted gallstone in improving the outcome of gallstone pancreatitis remains a controversial issue. • Severe acute gallstone pancreatitis with ascending cholangitis (jaundice and fever) is an indication for urgent ERCP . • Studies demonstrate that enteral nutrition is cheaper and safer and is preferable in patients with severe acute pancreatitis. • It is still unclear, however, when nutrition should be initiated and for how long it needs to be continued.
    •  Clear fluid diet should be given on 3rd - 6th day and regular diet from 5th - 7th day.  The decision to reintroduce oral intake is done by the following criteria     Resolution of abdominal pain The patient is hungry Organ dysfunction if recent has improved In sever pancreatitis in which much longer restriction of oral feed needed parenteral neutriton must be maintained by lipid infusion.
    • OTHER DRUGS; • Gabexate mesylate is pancreatic protease inhibitor in acute pancreatitis found no effect on the 90-day mortality rate, but a reduced incidence of complication. • The antisecretory hormone somatostatin or its synthetic analog octreotide(1microgm/kg slow iv 6-8 hrly) have failed to show evidence of efficacy . • The use of anti-inflammatory cytokines has lexipafant have not shown clear efficacy.
    • ROLE OF SURGERY; • Cholecystectomy should be performed as soon as the patient has recovered and the acute inflammatory process has subsided. • A second potential role for surgery in pancreatitis is to debride pancreatic necrosis (necrosectomy) .
    • COMPLICATION;LOCAL • Necrosis – Sterile / infected • Pancreatic fluid collection – Pancreatic abscess – Pancreatic pseudocyst – Pancreatic ascitis • Involvement of contiguous organ by necrotising pancreatitis – Massive intraperitioneal haemorrhage – Thrombosis of blood vessels • Obstructive jaundice
    • SYSTEMIC  Pulmonary     Pleural effusion Atelectasis Pneumonitis ARDS  Cardiovascular  Hypotension / hypervolemia  Sudden death  Pericardial effusion  Hematological  DIC  GI haemorrhage     Peptic ulcer disease Erosive gastritis Hemorrhagic pancreatitis erosion in blood vessel Portal vein thrombosis
    • SYSTEMIC  Renal  Oliguria  Azotemia  Renal artery / vein thrombosis  Metabolic     Hyperglycemia Hypertriglyceridemia Hypocalcemia Purtscher’s retinopathy ( due to occulsion of post retinal artery by aggregated granulocyte)  CNS  Psychosis  Fat emboli  Fat necrosis  Subcutaneous tissue - erythematous nodule
    • THANK YOU…