Published on August 19, 2018
slide 1: Pancreatitis An acute inflammation process of the pancreas with associated escape of the pancreatic enzyme into surrounding tissue. The primary etiologic factors are alcoholism biliary tract disease. May be a complication of viral or bacterial disease peptic ulcer trauma. slide 2: Pancreatitis Inflammatory Destructive Self-perpetuating ‘third space’ fluid loss Rapidly progressing Can progress to haemorrhagic or necrotising pancreatitis slide 3: Get Smashed allstones thanol rauma teroids umps utoimmune eg PAN corpion venom Trinidadian - Tityus trinitatis yperlipidaemia / hypercalcaemia / hypothermia RCP rugs azathioprines •G •E •T •S •M •A •S •H •E •D slide 4: Differential Diagnosis •Pancreatitis •Acute cholecystitis •Ascending cholangitis •Perforated viscus •Intestinal obstruction •Ruptured AAA •Diverticulitis •Bowel Ischaemia •MI •Severe pneumonia •Appendicitis •Caecal perforation •Ruptured ectopic slide 5: Investigation Bloods FBC U+Es CRP Glucose Amylase Calcium Arterial Blood Gases Abdominal Xray •USS •CT slide 6: Prognostic scoring systems Atlanta classification Ranson Score Glasgow Score Modified Glascow slide 7: Atlanta Classification ACUTE PANCREATITIS Acute pancreatitis is an acute inflammatory process of the pancreas with variable involvement of other regional tissues or remote organ systems. SEVERE ACUTE PANCREATITIS Severe acute pancreatitis is associated with organ failure and/or local complications such as necrosis with infection pseudocyst or abscess. Most often this is an expression of the development of pancreatic necrosis although patients with oedematous pancreatitis may manifest clinical features of a severe attack. slide 8: MILD ACUTE PANCREATITIS Mild acute pancreatitis is associated with minimal organ dysfunction and an uneventful recovery. The predominant pathological feature is interstitial oedema of the gland. ACUTE FLUID COLLECTIONS Acute fluid collections occur early in the course of acute pancreatitis are located in or near the pancreas and always lack a wall of granulation of fibrous tissue. PANCREATIC NECROSIS AND INFECTED NECROSIS Pancreatic necrosis is a diffuse or focal areas of non- viable pancreatic parenchyma which is typically associated with peripancreatic fat necrosis. The onset of infection results in infected necrosis which is associated with a trebling of the mortality risk slide 9: ACUTE PSEUDOCYST An acute pseudocyst is a collection of pancreatic juice enclosed in a wall of fibrous or granulation tissue that arises following an attack of acute pancreatitis. Formation of a pseudocyst requires four or more weeks from the onset of acute pancreatitis. PANCREATIC ABSCESS A pancreatic abscess is a circumscribed intra-abdominal collection of pus usually in proximity to the pancreas containing little or no pancreatic necrosis which arises as a consequence of acute pancreatitis. SPECIALIST UNIT A specialist unit is one in which multidisciplinary expertise is available on- site. Full intensive care facilities are mandatory together with recourse to ERCP at any stage on an emergency basis. Expert radiological input for dynamic scanning percutaneous procedures and angiography is essential. A surgeon with pancreatico-biliary expertise should supervise management. slide 10: Glasgow Scoring system for severity Age yr. 55 White blood cell count 15 × 10 9 /L Glucose 10 mmol/l Urea 16 mmol/l PaO2mm Hg 60 mm Hg Calcium 2 mmol/l Albumin 3.2 g/l Lactate dehydrogenase 600 units/L Asparate/alanine aminotransferase 100 units/L slide 11: Modified Glasgow Score Age 55 years pO2 60mmHg WCC 15x109/litre Ca2+ uncorr. 2.0 mmol/L LDH 600 IU glucose 10 mmol/L urea 16 mmol/L albumin 3.2g/L Minimum score: 0 Maximum score: 8 If score3: severe pancreatitis unlikely If score3:severe pancreatitis likely slide 12: Ranson’s Criteria Ransons Criteria on Admission : age greater than 55 years a white blood cell count of 16000/µL blood glucose 11 mmol/L 200 mg/dL serum LDH 350 IU/L serum AST 250 IU/L Ransons Criteria after 48 hours of admission : fall in hematocrit by more than 10 percent fluid sequestration of 6 L hypocalcemia serum calcium 2.0 mmol/L 8.0 mg/dL hypoxemia PO2 60 mmHg increase in BUN to 1.98 mmol/L 5 mg/dL after IV fluid hydration base deficit of 4 mmol/L Score 0-2: 2 mortality Score 3-4: 15 mortality Score 5-6: 40 mortality Score 7-8: 100 mortality slide 13: Recent international consensus conference redefined severe acute pancreatitis from critical care perspective as: Systemic organ dysfunction irrespective of local complications eg peripancreatic fluid collection necrosis abscess pseudocyst slide 14: Modified Glasgow criteria WCC 15.0 x 10 9 /L Glucose 10 mmol /L LDH 600iu/L AST 200iu/L Urea 16mmol/L Serum Ca 2+ 2mmol/L Serum albumin 32g/L P a O 2 8.0kPa Greater poorer prognosis slide 15: Overview : Bradley reported the criteria for severe acute pancreatitis developed at the International Symposium on Acute Pancreatitis held in Atlanta Georgia. Criteria for severe acute pancreatitis - one or more of the following: 1 Ranson score on admission 3 or during the first 48 hours 2 APACHE II score 8 at any time during course 3 presence of one or more organ failures 4 presence of one or more local complications slide 16: Organ failures include: 1 shock systolic blood pressure less than 90 mm Hg 2 pulmonary insufficiency PaO2 60 mm Hg on room air 3 renal failure serum creatinine 2 mg/dL after fluid replacement 4 gastrointestinal bleeding with 500 mL estimated loss within 24 hours 5 DIC thrombocytopenia and hypofibrinogenemia and fibrin split products 6 severe hypocalemia 7.5 mg/dL slide 17: Local complications Local complications include: 1 pancreatic necrosis 2 pancreatic abscess 3 pancreatic pseudocyst slide 18: Management First 24 hours Symptomatic: Fluid Depleted third space losses IV access Aggressive fluid resiscitation Strict input/output balance Catheter helps with input/output NG tube for vomiting/ileus Analgesia – Morphine/Pethidine slide 19: Treatment Subsequent days Initally observations hourly Daily FBC U+Es Ca 2+ Glucose amylase ABGs HDU/ITU Antibiotics May reduce septic complications Do not forget alcohol withdrawal therapy if due to excess alcohol Chlordiazepoxide 20mg qds PO Pabrinex IV slide 21: Complications Early Shock ARDS Renal failure DIC Hypocalcaemia Hyperglycaemia slide 22: Pancreatitis:Assessment Pain: Steady severe in nature located in the epigastric or umbilical region may radiate to the back. Worsened by lying supine may be lessened by flexed knee curved-back position. Vomiting Varies in severity but is usually protracted worsened by ingestion of food or fluid. Does not relieve the pain. Usually accompanied by nausea. slide 23: Assessment contd. Fever: Rarely exceeds 39 C. Abdominal Finding: Rigidity tenderness guarding distended decreased or absent peristalsis and paralytic ileus.Fatty stools-steatorrhea Laboratory Finding: Elevation of white count- 20000-50000. Elevated serum lipase and amylase5 to 40 times glucose bilirubin alkaline phosphatase. Urine amylase elevated.Abnormal low serum CA Na Mg.-due to dehydration. Binding of Ca in areas of fat necrosis. slide 24: Ranson’s criteria Admission criteria Criteria during initial 48 hours Age: 55 yrs. Or older Hct: decrease or more than 10 WBC: 16000/mm3 or higher BUN:increase greater than 5 mg/dl. LDH: 350 IU/L or higher Glucose 200 mg/dl. CA: falls to less than 8 mg/dl. PaO2 60 mm Hg AST: 250 U/L or higher Fluid sequestration greater than 6 liter. slide 25: Nursing Interventions Alleviate pain anxiety. Anxiety increases pancreatic secretions. Demerol-then morphine. Reduce pancreatic stimulus- NPO NGT to remove gastric secretions. Drugs to reduce pancreatic secretions- anticholinergics-suppress vagal stimulation NaHco-reverse metabolic acidosis.Regular insulin to treat hyperglycemia. Prevent or treat infection-with abx. Aggressive respiratory care- monitor ABG. Reduce body metabolism- bedrest cool quiet environment. Provide client and family instruction-avoid alcohol coffeeheavy meals and spicy food. slide 26: Evaluation and Management: Subjective Acute onset steady intense epigastric abdominal pain radiating to the back with nausea and vomiting may be relieved with leaning forward Medical history: chronic alcoholism gallstones slide 27: Evaluation and Management: Objective Mild: Restlessness low-grade fever tachycardia mild epigastric tenderness Severe: Same as mild + marked tenderness with guarding and abdom.distensionabsent bowel sounds systemic signs of hypotension shock jaundice and pulmonary findings e.g. rales pul.edema Lab. results: ↑ serum and/or urinary levels of pancreatic enzymes i.e. amylaselipase C- reactive protein or trypsinogen activation peptide consider L.F.T Calcium TG albumin CBC ABG glucose Imaging: U.S.G contrast-enhanced CT or MRI with ↑ serum creatinineand MRCP or ERCP if high suspicion of CBD stones slide 28: Differential Diagnosis Acute or chronic alcohol consumption gallstone disease peptic ulcer disease perforated ulcer early appendicitis bowel obstruction mesenteric ischemia medicationshypertriglyceridemia hypercalcemia infection post-traumatic injury pregnancy pulmonaryrenal or cardiovascular disorders slide 29: Assessment of Severity Ranson’s APACHE II CT Index Mild pan ≤ 3 8 7 Severe pan 3 ≥ 8 ≥ 7 slide 30: Management of mild pancreatitis • Aggressive rehydration i.e. dextrose in normal saline at 1 L per hour until adequate urine output • Pain relief morphine • Enteral nutritional support once pain improves and laboratory results normalize • Monitor hemodynamic and laboratory/serum parameters slide 31: Management of severe pancreatitis • Consider intensive care unit admission • Eliminate oral intake for first 48 hours • Aggressive volume replacement • Nutritional support enteral preferred • Consider emergent ERCP with suspected gallstones and obstructive jaundice • Pain relief morphine • Identify if pancreatic or peripancreatic necrosis is present • Consider antibiotics if possible infection • Consider consultation with gastroenterology surgery and/or interventional radiology subspecialists slide 33: Major complications Cardiovascular: hypotension/shock from hypovolemia. Hematologic:Anemia from blood loss DIC leukocytosis from gen.inflammation or secondary infections. Respiratory:atelectasis pneumonia pleural effusion ARDS GI: bleeding Renal: oliguria acute tubular necrosis Metabolic:hyperglycemia hypocalcemia.