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 theoryProteolytic enzymes activated in the

pancreas rather than in the intestinal lumen

Source: p. 2006-2007

PROENZYMES

Trypsinogen Chymotrypsinogen Proelastase Phospholipase A

ACTIVATING FACTORS

Endotoxins Exotoxins Viral infections Ischemia Anoxia Direct trauma Activated proenzyme,

(eg. Trypsin)

Source: p. 2006-2007

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

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

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

Source: p. 2006-2007

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

Nausea, vomitting, abdominal distention

Low grade fever, tachycardia, hypotension

Shock JaundiceErythematous 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 SignTurner’s Sign

History and PELaboratory Tests Imaging Studies

HistorySevere and constant abdominal pain Nausea, emesisFever, tachycardiaPEAbdominal tenderness, muscle

rigidityDiminished bowel soundsCullen’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

Fauci, et al., 2008. Principles of Internal Medicine, 17th ed. US:Mcgraw Hill

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

• 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

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

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., 2008. Principles of Internal Medicine, 17th 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., 2008. Principles of Internal Medicine, 17th ed. US:Mcgraw Hill

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

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.,

• 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.,

Acute Pancreatitis

Analgesics pain IV fluids & colloids maintain

normal intravascular volumeNo oral alimentation

Usually, subsides spontaneously within 3 to 7 days after treatment

• 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)

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

• 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 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.

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

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

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