Acute pancreatitis 2013 update
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Acute pancreatitis 2013 update

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a simplified approach to diagnosis and management of acute pancreatitis based on 2013 update from ASG ( American Society of Gastroenterology ).

a simplified approach to diagnosis and management of acute pancreatitis based on 2013 update from ASG ( American Society of Gastroenterology ).

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Acute pancreatitis 2013 update Acute pancreatitis 2013 update Presentation Transcript

  • Management of Acute Pancreatitis 2013 update by Ahmed Adel Abdelhakeem Assistant lecturer Internal Medicine Department - GIT unit Asyut university hospital
  • Etiology
  • Etiology (most common) ** GALLSTONES (40 – 70 % ) usually an acute event and resolves when the stone is removed or passes spontaneously. ** ALCOHOL (25 – 35 % ) - often manifests as a spectrum ranging from discrete episodes of AP to chronic irreversible silent changes. - the e diagnosis should not be entertained unless a person has a history of over 5 years of heavy alcohol consumption ( > 50 g per day )
  • Etiology ( other causes ) **PRIMARY AND SECONDARY HYPERTRIGLYCERIDEMIA can cause AP however, these account for only 1 – 4 % of cases ( 36 ). Serum triglycerides should rise above 1,000 mg / dl to be considered the cause of AP (should be re-evaluated 1 month after discharge ) **HYPERCALCEMIA **HYPERPARATHYROIDISM **DRUGS o(6-mercaptopurine, azathioprine ) **BENIGN OR MALIGNANT mass that obstructs the main pancreatic duct can result in AP. It has been estimated that 5 – 14 % of patients with benign or malignant pancreatobiliary tumors present with apparent IAP .Historically, adenocarcinoma of the pancreas was considered a disease of old age. However, increasingly patients in their 40s — and occasionally younger — are presenting with pancreatic cancer. This entity should be suspected in any patient > 40 years of age with idiopathic pancreatitis.
  • Etiology ( IDIOPATHIC AP ) ** IAP is defined as pancreatitis with no etiology established after initial laboratory (including lipid and calcium level) and imaging tests ( transabdominal U/S and CT in the appropriate patient). ** Anatomic anomalies of the pancreas occur in 10 – 15 % of the population, including pancreas divisum and sphincter of oddi dysfunction ** The role of Genetic testing in AP has yet to be determined , but may be useful in patients with: - young patients ( < 30 years old ) - no cause is evident - family history of pancreatic disease is present
  • DIAGNOSIS - CLINICAL PRESENTATION - LABORATORY PARAMETERS - ABDOMINAL IMAGING
  • DIAGNOSIS The diagnosis of AP is most often established by the presence of 2 of the 3 following criteria: (1) abdominal pain consistent with the disease, (2) serum amylase and / or lipase greater than three times the upper limit of normal, and / or (3) characteristic findings from abdominal imaging. Contrast-enhanced computed tomography (CECT) and / or magnetic resonance imaging (MRI) of the pancreas should be reserved for patients in whom the diagnosis is unclear
  • DIAGNOSIS (Clinical Presentation) ** Patients with AP typically present with epigastric or left upper quadrant pain. ** The pain is usually described as constant with radiation to the back, chest, or flanks but this description is nonspecific. ** The intensity of the pain is usually severe, but can be variable. the intensity and location of the pain do not correlate with severity. Pain described as dull, colicky, or located in the lower abdominal region is not consistent with AP and suggests an alternative etiology.
  • DIAGNOSIS ( Serum Amylase ) ** cannot be used reliably for the diagnosis of AP. ** rises within a few hours after the onset of symptoms and returns to normal values within 3 – 5 days; however, it may remain within the normal range on admission in as many as one-fifth of patients. ** most studies show a diagnostic efficacy of greater than 3 – 5 times the upper limit of normal
  • DIAGNOSIS ( Serum Amylase ) may be normal in: *Alcohol-induced AP *Hypertriglyceridemia. Serum amylase concentrations might be high in the absence of AP in: *Macroamylasaemia * glomerular filtration rate *Diseases of the salivary glands *Extra pancreatic abdominal diseases associated with inflammation including : acute appendicitis, cholecystitis, intestinal obstruction or ischemia, peptic ulcer, and gynecological diseases.
  • DIAGNOSIS ( Serum Lipase ) ** more specific ** remains elevated longer than amylase after disease presentation ** similar problems with the predictive value remain in certain patient populations , including : - Macro lipasemia - Renal disease , appendicitis , cholecystitis - Diabetics who appear to have higher median lipase ( 3 – 5 times may be needed )
  • DIAGNOSIS ( Serum Lipase ) Neither serum amylase nor lipase has any role in prognosis , assessing severity or follow up.
  • DIAGNOSIS (Abdominal Imaging) Abdominal U/S : - Transabdominal ultrasound should be performed in all patients with AP. CECT: Routine use of CECT in patients with AP is unwarranted , as the diagnosis is apparent in many patients and most have a mild , uncomplicated course.
  • DIAGNOSIS (Abdominal Imaging) - Indications of CECT : - Patient failing to improve after 48 – 72 hr after admission ( persistent pain , fever , nausea, unable to begin oral feeding ). - Uncertain diagnosis - Patient > 40 years old ( pancreatic tumor should be considered as a possible cause ).
  • DIAGNOSIS (ABDOMINAL IMAGING) MRI : helpful in patients with a contrast allergy and renal insufficiency where T2-weighted images without gadolinium contrast can diagnose pancreatic necrosis MRCP: has the advantage of detecting choledocholithiasis down to 3 mm diameter and pancreatic duct disruption if CT is non - conclusive. EUS : used when a more extensive evaluation for a suspected underlying pathology is needed after a recurrent episode of IAP
  • DIAGNOSIS ( Role of ERCP ) - Patients with AP and concurrent acute cholangitis should undergo ERCP within 24 h of admission - ERCP is not needed early in most patients with gallstone pancreatitis who lack laboratory or clinical evidence of ongoing biliary obstruction - In the absence of cholangitis and / or jaundice, MRCP or EUS rather than diagnostic ERCP should be used to screen for choledocholithiasis if highly suspected. - Pancreatic duct stents and / or post procedure rectal nonsteroidal anti-inflammatory drug (NSAID) suppositories ( indomethacin rectal supp. 100 mg once post procedure ) should be utilized to lower the risk of severe post-ERCP pancreatitis in high-risk patients.
  • Assessment of severity Atlanta Revised criteria 2013 Based on : local complications and presence of organ failure. BISAP score Ranson’s criteria
  • Assessment of severity Atlanta Revised criteria 2013 Mild acute pancreatitis Absence of organ failure Absence of local complications Moderately severe acute pancreatitis Local complications AND / OR Transient organ failure ( < 48 h) exacerbated co - morbidities Severe acute pancreatitis (15 – 20 %) Persistent organ failure > 48 h
  • Assessment of severity - Local complications include : peripancreatic fluid collections and pancreatic or peripancreatic necrosis (sterile or infected) - Pancreatic necrosis is defined as diffuse or focal areas of nonviable pancreatic parenchyma > 3 cm in size or > 30% of the pancreas - edematous pancreas is defined as interstitial pancreatitis - CT and / or MRI imaging also cannot reliably determine severity early in the course of AP, as necrosis usually is not present on admission and may develop after 24 – 48 h - different scoring systems are available for assessing severity but all of them are cumbersome and typically require 48 h to become accurate.
  • Assessment of severity Organ failure :
  • Assessment of severity BISAP score
  • Assessment of severity Ranson’s criteria:
  • Assessment of severity Mild disease Severe disease - Mild pain - Normal look - Normal pulse rate - Normal temp. or mild fever - Severe pain - Toxic look - Tachycardia - High grade or subnormal temp. - Hypoxia - Decreased UOP - Rigid abdomen - shock - Normal O2 saturation - Adequate UOP - Flat soft abdomen - Normal BP
  • Assessment of severity Mild disease Severe disease - Mild pain - Normal look - Normal pulse rate - Normal temp. or mild fever - Severe pain - Toxic look - Tachycardia - High grade or subnormal temp. - Hypoxia - Decreased UOP - Rigid abdomen - shock - Normal O2 saturation - Adequate UOP - Flat soft abdomen - Normal BP
  • Assessment of severity - Most patients with severe disease present to the emergency room with no organ failure or pancreatic necrosis; unfortunately, this has led to many errors in clinical management of this disease. - These errors include failure to provide adequate hydration, failure to diagnose and treat cholangitis, and failure to treat early organ failure. - For this reason, it is critical for the clinician to recognize the importance of not falsely labeling a patient with mild disease within the first 48 h of admission for AP.
  • Assessment of severity If there is : - 100 cases of AP >>>>> 20 cases will be severe ( 20 % ) . - from those 20 cases be infected ( 4 % ) . >>>>> 4 cases will
  • Management - Aggressive hydration - Antibiotics - Nutrition - Role of ERCP - Role of surgery
  • Management (Aggressive hydration)
  • Management (Aggressive hydration) -- The use of hematocrit , BUN and creatinine as surrogate markers for successful hydration has been widely recommended. -- Although no firm recommendations regarding absolute numbers can be made at this time, the goal to decrease hematocrit ( demonstrating hemodilution ) and BUN ( increasing renal perfusion ) and maintain a normal creatinine during the first day of hospitalization is recommended.
  • Management (Antibiotics)
  • Management (Antibiotics) - Fever, tachycardia, tachypnea, and leukocytosis associated with SIRS that may occur early in the course of AP may be indistinguishable from sepsis syndrome. - When an infection is suspected, antibiotics should be given while the source of the infection is being investigated. - However, once blood and other cultures are found to be negative and no source of infection is identified, antibiotics should be discontinued
  • Management (Role of CT FNA)
  • Management (Role of Surgery)
  • Management (Role of Surgery) cholecystectomy: *Mild gallstone pancreatitis: should be performed during hospitalization *Severe AP: cholecystectomy is typically delayed after discharge except if necrosectomy will be done. *No stones / sludge on ultrasound and recurrent pancreatitis : no role for cholecystectomy. *In patients with mild AP who cannot undergo surgery, such as the frail elderly and / or those with severe co morbid disease, biliary sphincterotomy alone may be an effective way to reduce further attacks of AP, although attacks of cholecystitis may still occur
  • Management (Role of Surgery) Necrosectomy (debridement): - Early open debridement for sterile necrosis was abandoned - Debridement for sterile necrosis is recommended if associated with: *Gastric outlet obstruction and / or *Bile duct obstruction.
  • Management (Role of Surgery) Minimally invasive Necrosectomy : Debridement through : - Laparoscopic , - Percutaneous or - Radiologic by catheter drain ** Becoming the standard of care for cases of severe necrotizing pancreatitis requiring debridement.
  • Management (Nutrition)
  • Management (Role of ERCP)
  • Management (Role of ERCP) PREVENTING POST-ERCP PANCREATITIS (2 – 4 %) : (1) Guide wire cannulation, (2) pancreatic duct stents (3) rectal NSAIDs ( Diclofenac 100 mg or Indomethacin 100 mg once post procedure )
  • Systemic Complications of AP
  • Local Complications of AP Pancreatic pseudo cyst Pancreatic abscess Necrotizing pancreatitis Hemorrhagic pancreatitis
  • Pseudo -Cyst - Localized fluid collection that is rich in amylase and other pancreatic enzymes and is surrounded by a wall of fibrous tissue that is not lined by epithelium. - May remain within pancreatic parenchyma , extend into lesser sac or retro peritoneum. - Common clinical problem and complicate the course of chronic pancreatitis in 30% to 40% of patients
  • Pseudo –Cyst … Presentation - Asymptomatic - Acute complications include : bleeding (usually from splenic artery pseudoaneurysm), infection, and rupture - Chronic complications include gastric outlet obstruction, biliary obstruction and thrombosis of the splenic or portal vein with development of Gastric Varices secondary to portal hypertension.
  • Pseudo -Cyst Differential Diagnosis - Once pancreatic cyst is identified by an imaging modality, the most important question is to differentiate pseudo cyst from other TRUE cystic lesions of the pancreas. - The main differentiating features are : 1 - History of acute pancreatitis. 2 – amylase level ( very high in pseudo cyst ) 3 – Aspiration of cyst content ( CEA , amylase , bacteriology , cytology ) usually and preferably done by EUS.
  • Pseudo -Cyst Treatment Wait 6 weeks post AP .. Why ? Some pseudo cysts disappear spontaneously within 6 weeks. To give sufficient time for a thick pseudo capsule to form. Options : - Endoscopic : cystogastrostomy. - Percutaneous : pig – tail drainage.
  • Pancreatic Abscess - Occurs as a complication of pseudo cyst if not drained. - Complicates about 4 % of cases. - The only reliable sign in CT is the presence of air bubbles within the cyst that arises mainly from gas forming organism or a fistula with the stomach, but unfortunately this is present only in 50 % of cases. - Diagnostic aspiration may differentiate it from a pseudo cyst if there is no air bubbles ( physical , bacteriology , cells ). - It was an indication for surgery in the past but now it could be drained percutaneously (pig tail).
  • Thank you