GROUP D Mamba-Medinilla. COMMON CAUSES Gallstones Alcohol Intake Hypertriglyceridemia ERCP...
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Transcript of GROUP D Mamba-Medinilla. COMMON CAUSES Gallstones Alcohol Intake Hypertriglyceridemia ERCP...
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GROUP D Mamba-Medinilla
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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
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Autodigestion theoryProteolytic enzymes activated in the
pancreas rather than in the intestinal lumen
Source: p. 2006-2007
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PROENZYMES
Trypsinogen Chymotrypsinogen Proelastase Phospholipase A
ACTIVATING FACTORS
Endotoxins Exotoxins Viral infections Ischemia Anoxia Direct trauma Activated proenzyme,
(eg. Trypsin)
Source: p. 2006-2007
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INITIAL PHASE acinar cell injury due to
intrapancreatic digestive enzyme activation
Zymogen activation mediated by lysosomal hydrolases e.g. cathepsin B
Source: p. 2006-2007
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SECOND PHASE Intrapancreatic inflammation reaction Due to activation, chemoattraction,
and sequestration of neutrophils in the pancreas
* This neutrophil sequestration can activate trypsinogen
Source: p. 2006-2007
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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. 2006-2007
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Source: p. 2006-2007
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Major symptomVary from mild to severe, constant
painSteady and boring in characterLocated in epigastrium and
periumbilical radiating to the backChest, flank and lower abdomenPain more intense on supine,
relieved by sitting
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Nausea, vomitting, abdominal distention
Low grade fever, tachycardia, hypotension
Shock JaundiceErythematous skin nodules In 10-20% of patients- basilar rales,
atelectasis, and pleural effusion
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Bowel sounds usually diminished or absent
Palpable enlarged pancreas, or a pseudocyst in the upper abdomen
Cullen’s SignTurner’s Sign
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History and PELaboratory Tests Imaging Studies
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HistorySevere and constant abdominal pain Nausea, emesisFever, tachycardiaPEAbdominal tenderness, muscle
rigidityDiminished bowel soundsCullen’s sign, Turner’s sign
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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
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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
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CT SCAN: confirms clinical impression of acute
pancreatitis even with normal serum amylase
indicates severity and risk of morbidity and mortality
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Fauci, et al., 2008. Principles of Internal Medicine, 17th ed. US:Mcgraw Hill
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Key indicators of a severe attack of pancreatitis1. Associated with organ failure and/or
local complication2. Clinical Manifestations3. Organ Failure
Fauci, et al., 2008. Principles of Internal Medicine, 17th ed. US:Mcgraw Hill
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• Key indicators of a severe attack of pancreatitis1. 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 <90 mmHg/ PR >130)– Pulmonary insufficiency ( PO2 <60)– Renal failure (Crea >2.0mg%)– GI Bleeding (>500ml/24hr)Fauci, et al., 2008. Principles of Internal Medicine, 17th ed. US:Mcgraw Hill
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LOCAL COMPLICATIONS
Necrosis Sterile, Infected, Organized
Pancreatic fluid collections Pancreatic abscessPancreatic Pseudocyst• pain, rupture, hemorrhage, infection,Obstruction of GIT
Pancreatic ascites Disruption of main pancreatic ductLeaking pseudocyst
Involvement of contiguous organs by necrotizing pancreatitis
Massive intraperitoneal hemorrhageThrombosis of blood vesselsBowel infarction
Obstructive jaundice
Fauci, et al., 2008. Principles of Internal Medicine, 17th ed. US:Mcgraw Hill
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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,
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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., 2008. Principles of Internal Medicine, 17th ed. US:Mcgraw Hill
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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., 2008. Principles of Internal Medicine, 17th ed. US:Mcgraw Hill
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SYSTEMIC COMPLICATIONS
Pulmonary Pleural effusion, Atelectasis, Mediastinal abscess, Pneumonitis, ARDS
Cardiovascular Hypotension, Hypovolemia, Sudden death, Nonspecific ST-T changes in ECG`
Pericardial effusion
Hematologic DIC
GI Hemorrhage PUD, Erosive gastritis, Hemorrhagic pancreatic necrosis with erosion into major BV, Portal vein thrombosis, Variceal hemorrhage
Renal Oliguria, Azotemia, Renal artery and/or vein thrombosis, Acute tubular necrosis
Metabolic Hyperglycemia, Hypertriglyceridemia, Hypocalcemia, Encephalopathy, Sudden blindness (Purtscher’s retinopathy)
Central Nervous System Psychosis, Fat emboli
Fat necrosis Subcutaneous tissues, BoneFauci, et al., 2008. Principles of Internal Medicine, 17th ed. US:Mcgraw Hill
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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 22nd ed.,
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• 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 22nd ed.,
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Acute Pancreatitis
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Analgesics pain IV fluids & colloids maintain
normal intravascular volumeNo oral alimentation
Usually, subsides spontaneously within 3 to 7 days after treatment
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• IV fluids and fasting• Clear liquid diet: started on the 3rd to
6th day• Regular diet: 5th to 7th day
• Reintroduction of oral intake based on:• ↓ or resolution of abdominal pain• Hungry patient• Resolved organ dysfunction (if present)
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IMIPENEM-CILASTATIN 500mg 3x/day for 7 days Current recommendation in patients
with necrotizing acute pancreatitisFungicide prophylaxis
Due to increase frequency of intraabdominal Candida infection
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• 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
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Types of Acute Pancreatitis
Treatment / Managment
Fulminant Pancreatitis
Large amounts of fluidsClose attention to complications:
Cardiovascular collapseRespiratory insufficiencyPancreatic infection.
Gallstone-induced Pancreatitis
Papillotomy within first 36-72 hours of the attackPatient with severe gallstones pancreatitis
considered for urgent ERCP.
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Types of Acute Pancreatitis
Treatment / Managment
Hypertriglyceridemia-Associated Pancreatitis
Weight loss to ideal weightA lipid-restricted dietExerciseAvoidance of alcohol Avoidance of drugs that can ↑ serum triglyceridesControl of diabetes
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Patient Acute Pancreatitis
Severe, boring, epigastric pain, sudden onset
Pain 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 binge Amount 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 weekly Alcohol is the second most leading cause
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Patient Acute Pancreatitis
PR 105, RR 28/min temp 38 degrees celcius
Low grade fever, tachycardia are common
BP 130/70 = pre-hypertensive/normotensive
hypotension
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 epigastrium Abdominal tenderness and muscle rigidity are present
No mass An enlarged pancreas with organized necrosis or a pesudocyst may be palpable