GROUP D Mamba-Medinilla

COMMON CAUSES Gallstones Alcohol Intake Hypertriglyceridemia ERCP especially after biliary manometry Blunt abdominal trauma Postoperative operations Drugs (sulfonamides, 6- MP) Sphincter of Oddi dysfunction UNCOMMON CAUSES Vascular causes CT disorders Cancer of the pancreas Hypercalcemia Periampullary diverticulum Pancreas divisum Hereditary pancreatitis Cystic Fibrosis Renal Failure

 Autodigestion theory  Proteolytic enzymes activated in the pancreas rather than in the intestinal lumen Source: p

PROENZYMES  Trypsinogen  Chymotrypsinogen  Proelastase  Phospholipase A ACTIVATING FACTORS  Endotoxins  Exotoxins  Viral infections  Ischemia  Anoxia  Direct trauma  Activated proenzyme, (eg. Trypsin) Source: p

INITIAL PHASE  acinar cell injury due to intrapancreatic digestive enzyme activation  Zymogen activation mediated by lysosomal hydrolases e.g. cathepsin B Source: p

SECOND PHASE  Intrapancreatic inflammation reaction  Due to activation, chemoattraction, and sequestration of neutrophils in the pancreas * This neutrophil sequestration can activate trypsinogen Source: p

THIRD PHASE – Activated proenzymes, (esp. Trypsin) Digest pancreatic and peripancreatic tissues Activate other enzymes (i.e. elastase, phospholipase) – Due to effects of activated proteolytic enzymes and cytokines, released by inflamed pancreas, on distant organs, most notably the lungs May result to SIRS and ARDS Multiorgan failure Source: p

Activated enzymes digest cellular membranes, cause proteolysis, edema, interstitial hemorrhage, vascular damage, coagulation & fat necrosis, parenchymal cell necrosis Liberation of bradykinin peptides, increased vascular permeability, and edema with profound effects on many organs, esp. the lungs SIRS, ARDS, Multiorgan Failure, other distant effects Source: p

 Major symptom  Vary from mild to severe, constant pain  Steady and boring in character  Located in epigastrium and periumbilical radiating to the back  Chest, flank and lower abdomen  Pain more intense on supine, relieved by sitting

 Nausea, vomitting, abdominal distention  Low grade fever, tachycardia, hypotension  Shock  Jaundice  Erythematous skin nodules  In 10-20% of patients- basilar rales, atelectasis, and pleural effusion

 Bowel sounds usually diminished or absent  Palpable enlarged pancreas, or a pseudocyst in the upper abdomen  Cullen’s Sign  Turner’s Sign

 History and PE  Laboratory Tests  Imaging Studies

History  Severe and constant abdominal pain  Nausea, emesis  Fever, tachycardia PE  Abdominal tenderness, muscle rigidity  Diminished bowel sounds  Cullen’s sign, Turner’s sign

 Increased level of serum amylase  Elevated pancreatic isoamylase and lipase levels  Markedly increase levels of peritoneal or pleural fluid amylase [ >1500 nmol/ L (> 5000U/ dl)]  Leukocytosis (15,000-20,000 leukocytes/ microliter)  Hemoconcentration ( Hct > 44%)  Hyperglycemia  Hypocalcemia  Hypertriglyceridemia  Elevated LDH  ECG: ST segment and T wave abnormalities

 Abdominal plain films  Localized ileus, involving the jejunum  Generalized ileus with air- fluid levels  Colon cutt- off sign  Duodenal distention with air fluid levels  Mass, frequently a pseudocyst  Ultrasonography: enlarged pancreas; also evaluates gallbladder

 CT SCAN:  confirms clinical impression of acute pancreatitis even with normal serum amylase  indicates severity and risk of morbidity and mortality

Patients develop an inflammatory mass or a pseudocyst 1 st 2-3 weeks Pancreatic abscess develops After 6 weeks Fauci, et al., Principles of Internal Medicine, 17 th ed. US:Mcgraw Hill

 Key indicators of a severe attack of pancreatitis 1. Associated with organ failure and/or local complication 2. Clinical Manifestations 3. Organ Failure Fauci, et al., Principles of Internal Medicine, 17 th ed. US:Mcgraw Hill

Key indicators of a severe attack of pancreatitis 1. Associated with organ failure and/or local complication 2. Clinical Manifestations – Obesity BMI >30 – Hemoconcentration (Hct >44%) – Age >70 3. Organ Failure – Shock (Systolic BP 130) – Pulmonary insufficiency ( PO2 <60) – Renal failure (Crea >2.0mg%) – GI Bleeding (>500ml/24hr) Fauci, et al., Principles of Internal Medicine, 17 th ed. US:Mcgraw Hill

LOCAL COMPLICATIONS NecrosisSterile, Infected, Organized Pancreatic fluid collectionsPancreatic abscess Pancreatic Pseudocyst pain, rupture, hemorrhage, infection, Obstruction of GIT Pancreatic ascitesDisruption of main pancreatic duct Leaking pseudocyst Involvement of contiguous organs by necrotizing pancreatitis Massive intraperitoneal hemorrhage Thrombosis of blood vessels Bowel infarction Obstructive jaundice Fauci, et al., Principles of Internal Medicine, 17 th ed. US:Mcgraw Hill

 Necrotizing pancreatitis  severe form of acute pancreatitis,  increasing abdominal pain, fever, marked leukocytosis, and bacteremia Cooper, D., et al. (2007) The Washington Manual of Medical Therapeutics 32nd Ed. Lippincott Williams & Wilkins,

 Pancreatic fluid collections  Pancreatic abscess ▪ Ill defined collection of pus ▪ persistent fever, leukocystosis, and ileus  Pancreatic pseudocyst ▪ Collections of tissue, fluid, debris, pancreatic enzymes, and blood ▪ persistent pain or hyperamylasemia ▪ Palpable, tender mass in the middle or LUQ of abdomen Fauci, et al., Principles of Internal Medicine, 17 th ed. US:Mcgraw Hill

 Pancreatic ascites  disruption of the main pancreatic duct, often by an internal fistula between the duct and the peritoneal cavity or a leaking presudocyst.  Hyperamylasemia Fauci, et al., Principles of Internal Medicine, 17 th ed. US:Mcgraw Hill

SYSTEMIC COMPLICATIONS PulmonaryPleural effusion, Atelectasis, Mediastinal abscess, Pneumonitis, ARDS CardiovascularHypotension, Hypovolemia, Sudden death, Nonspecific ST-T changes in ECG` Pericardial effusion HematologicDIC GI HemorrhagePUD, Erosive gastritis, Hemorrhagic pancreatic necrosis with erosion into major BV, Portal vein thrombosis, Variceal hemorrhage RenalOliguria, Azotemia, Renal artery and/or vein thrombosis, Acute tubular necrosis MetabolicHyperglycemia, Hypertriglyceridemia, Hypocalcemia, Encephalopathy, Sudden blindness (Purtscher’s retinopathy) Central Nervous SystemPsychosis, Fat emboli Fat necrosisSubcutaneous tissues, Bone Fauci, et al., Principles of Internal Medicine, 17 th ed. US:Mcgraw Hill

 Pulmonary: ARDS  damage to the pulmonary surfactant layer by circulating phospholipase A and free fatty acids  Cardiovascular: Circulatory shock  a combination of volume depletion and hyperdynamic circulatory state with decreased peripheral vascular resistance Goldman, L., et al (2004).Cecil’s Textbook of Medicine 22 nd ed.,

Renal: Acute renal failure – caused by circulatory shock and a selective increase in renal vascular resistance. GI: Hemorrhage – erosion of the splenic or gastroduodenal arteries. – diffuse mucosal bleeding from the antrum and duodenum – perforation of peripancreatic inflammation into any portion of the gastrointestinal tract from esophagus to colon. – Splenic involvement by direct extension of the inflammatory process or, secondarily, by splenic vein thrombosis, which leads to gastric fundic varices. Goldman, L., et al (2004).Cecil’s Textbook of Medicine 22 nd ed.,

Acute Pancreatitis

 Analgesics  pain  IV fluids & colloids  maintain normal intravascular volume  No oral alimentation  Usually, subsides spontaneously within 3 to 7 days after treatment

IV fluids and fasting Clear liquid diet: started on the 3 rd to 6 th day Regular diet: 5 th to 7 th day Reintroduction of oral intake based on: ↓ or resolution of abdominal pain Hungry patient Resolved organ dysfunction (if present)

 IMIPENEM-CILASTATIN  500mg 3x/day for 7 days  Current recommendation in patients with necrotizing acute pancreatitis  Fungicide prophylaxis  Due to increase frequency of intraabdominal Candida infection

Peritoneal Lavage – through percutaneous dialysis catheter Necrosectomy – after confirmation of the presence of infected necrosis Laparotomy + adequate drainage + removal of necrotic tissue – if conventional therapy does not halt the patient’s deterioration

Types of Acute Pancreatitis Treatment / Managment Fulminant Pancreatitis Large amounts of fluids Close attention to complications: Cardiovascular collapse Respiratory insufficiency Pancreatic infection. Gallstone-induced Pancreatitis Papillotomy within first hours of the attack Patient with severe gallstones pancreatitis considered for urgent ERCP.

Types of Acute Pancreatitis Treatment / Managment Hypertriglyceridemi a-Associated Pancreatitis Weight loss to ideal weight A lipid-restricted diet Exercise Avoidance of alcohol Avoidance of drugs that can ↑ serum triglycerides Control of diabetes

PatientAcute Pancreatitis Severe, boring, epigastric pain, sudden onsetPain varies  may be mild discomfort to severe, which is steady and boring Pain radiating to the interscapular area ; His mother had cholecystectomy for gallstones Gallstones continue to be the leading cause in most series ( 30-60%) Pain slightly relieved by sitting with trunk flexed and knees drawn up Obtains pain relief with the trunk flexed and knees drawn up Alcoholic bingeAmount of alcohol ingested, plus other factors, affected susceptibility to developing acute pancreatitis Similar epigastric pain before radiating to the back Epigastric pain that often radiates to the back, chest, flanks and lower abdomen Drinks 5 bottles of beer weeklyAlcohol is the second most leading cause

PatientAcute Pancreatitis PR 105, RR 28/min temp 38 degrees celciusLow grade fever, tachycardia are common BP 130/70 = pre-hypertensive/normotensivehypotension Sclerae icteric+jaudice Abdomen slightly distended, tympanitic, with hypoactive bowel sounds Abdominal distention due to hypomotility and chemical peritonitis are frequent complaints; diminished bowel sounds Tender epigastriumAbdominal tenderness and muscle rigidity are present No massAn enlarged pancreas with organized necrosis or a pesudocyst may be palpable