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Pancreatitis GASTROINTESTINAL: Note # 13^1 of^14
13. PANCREATITIS
I. PATHOPHYSIOLOGY A. A CUTE P ANCREATITIS B. C HRONIC P ANCREATITIS II. CAUSES A. A CUTE P ANCREATITIS B. C HRONIC P ANCREATITIS
III. CLASSIC FINDINGS OF PANCREATIC DISORDERS A. E PIGASTRIC A BDOMINAL P AIN
IV. COMPLICATIONS OF PANCREATIC DISORDERS A. A CUTE P ANCREATITIS B. C HRONIC P ANCREATITIS
V. DIAGNOSTIC APPROACH TO PANCREATIC DISORDERS A. A CUTE P ANCREATITIS B. C HRONIC P ANCREATITIS C. C HRONIC P ANCREATITIS
VI. TREATMENT OF PANCREATIC DISORDERS A. A CUTE PANCREATITIS B. C HRONIC PANCREATITIS
I. Pathophysiology
A. Acute Pancreatitis o Pancreatic Duct or Acinar Cell Injury → Inadvertent activation of pancreatic enzymes → Autodigestion of pancreas → Acute pancreatic inflammation, pancreatic edema, pancreatic necrosis, and possibly pancreatic hemorrhage develops
B. Chronic Pancreatitis o Repeated Pancreatic Duct or Acinar Cell Injury → Repeated inadvertent activation of pancreatic enzymes → Repeated autodigestion of pancreas → Repeated pancreatic inflammation occurs → Results in Fibrosis and Calcification of the pancreatic tissue
GASTROINTESTINAL
Acinar Cell Injury
+ (^) +
+ +
Chronic pancreatitis
II
II
TNF-α IL- 1 IL- 6
Inflammation
Acute pancreatitis
Epigastric pain
+ Edema
+ Necrosis
+ Hemorrhage
Local complications
Repeated bouts of inflammation
SIRS
Effect +
Proteases
Lipases
Amylases
Ductal cells
**+
+**
Acinar cell
Ductal Cell Injury
+^ Autodigestion of pancreas +
Last edited: 3/4/
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FIGURE 1. ↑PAIN LYING SUPINE
II. Causes
A. Pancreatic Duct Injury
1. Acute Pancreatitis
o Gallstone near the hepatopancreatic ampulla → blocks flow of pancreatic enzymes → Inadvertent activation of pancreatic enzymes One of the most common causes o Endoscopic Retrograde Cholangiopancreatography (ERCP) → Pancreatic duct injury when maneuvering throughout the biliary and pancreatic ductal tree → Inadvertent activation of pancreatic enzymes
2. Chronic Pancreatitis
o Cystic Fibrosis → Repeated mucus plugging of pancreatic ducts → Repeatedly blocks flow of pancreatic enzymes → Inadvertent activation of pancreatic enzymes
B. Pancreatic Acinar Cell Injury
1. Acute Pancreatitis
o Alcohol Abuse → Acinar cell injury → Inadvertent activation of pancreatic enzymes One of the most common causes o Hypertriglyceridemia (> 1000) → Acinar cell injury → Inadvertent activation of pancreatic enzymes o Hypercalcemia → Inadvertent activation of pancreatic enzymes o Drugs (e.g. Steroids and Antiretrovirals) → Acinar cell injury → Inadvertent activation of pancreatic enzymes
2. Chronic Pancreatitis
o Chronic Alcohol Abuse → Repeated acinar cell injury → Inadvertent activation of pancreatic enzymes
III. Classic Findings of Pancreatic Disorders
A. Epigastric Abdominal Pain Inflammation of the pancreas causes pain to localize to the anatomical location of the pancreas → Epigastric region, but can also radiate to the back (interscapular region) o Positional Pain Worse with lying flat Better with leaning forward
Acute causes
Gallstone (*)
ERCP
Chronic causes
Cystic fibrosis
Ductal cell injury
F IGURE 2. ↓PAIN LEANING F ORWARD
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4. Acute Pancreatic Fluid Collection (APFC)
Pathophysiology: o Pancreatic inflammation attracts macrophages and neutrophils → ↑Release of IL-1 and TNF-alpha → ↑Pancreatic vessel vasodilation and ↑Capillary permeability → Leakage of fluid into pancreatic tissue spaces Presentation: o Typically, asymptomatic and found incidentally on CT scan < 4 weeks after diagnosis of pancreatitis
5. Pancreatic Pseudocyst
Pathophysiology: o Pancreatic inflammation attracts macrophages and neutrophils → ↑Release of IL-1 and TNF-alpha → ↑Pancreatic vessel vasodilation and ↑Capillary permeability → Leakage of fluid into pancreatic tissue spaces → Walling-Off of Pancreatic Fluid Collection Presentation: o Typically, asymptomatic → However, may develop some symptoms/complications: ↑Epigastric Abdominal Pain:
- ↑Size of pancreatic pseudocyst → ↑Epigastric pain ↑Risk of SBO:
- ↑Size of pancreatic pseudocyst → ↑Compression of small bowel ↑Risk of Pseudocyst Rupture:
- Rupture of pseudocyst into peritoneal cavity → inflammation of the peritoneum → peritonitis ↑Risk of Infected Pseudocyst:
- Hypovolemia → Poor bowel and pancreatic perfusion → Bowel and pancreatic necrosis → Bowel integrity lost → Bacterial translocation → Bacteria invades pseudocyst or necrotic tissue o CT scan finding > 4 weeks after diagnosis of pancreatitis
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IL- 1
TNF-
+ Tissue necrosis
Acute pancreatic
necrosis
(< 4 wks)
Infected
necrosis
WBC
Fever
BV
Walled off
necrosis
(> 4 wks)
BV
Autodigestion
Pancreatic vessels
Necrosis (~ 15 %)
Hemorrhage
6. Acute Pancreatic Necrosis
Pathophysiology: o Pancreatic inflammation attracts macrophages and neutrophils → ↑Release of IL-1 and TNF-alpha → ↑Pancreatic vessel vasodilation, ↑Capillary permeability, and ↑Lipase enzymes lead to pancreatic edema and necrosis (Hypovolemia can worsen this) Presentation: o ↑Epigastric pain, ↑WBC and ↑Fever o CT scan finding < 4 weeks after diagnosis of pancreatitis
7. Walled-Off Necrosis
Pathophysiology: o Pancreatic inflammation attracts macrophages and neutrophils → ↑Release of IL-1 and TNF-alpha → ↑Pancreatic vessel vasodilation, ↑Capillary permeability, and ↑Lipase enzymes lead to pancreatic edema and necrosis (Hypovolemia can worsen this) → The necrotic tissue can also be walled off/encapsulated Presentation: o ↑Epigastric pain, ↑WBC and ↑Fever o CT scan finding > 4 weeks after diagnosis of pancreatitis
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B. Chronic Pancreatitis
1. Global Malabsorption
Pathophysiology: o Chronic Pancreatitis → Exocrine pancreatic Insufficiency → Loss of function in the exocrine portion of the pancreas → ↓Pancreatic proteases, lipases, and amylases are released into the intestinal lumen → Leads to the inability to digest proteins, fats, and carbohydrates in the stool Presentation: o Weight Loss This is due to ↓protein absorption → Leads to muscle wasting o Chronic Diarrhea This is due to ↓carbohydrate absorption → Leads to water being pulled into the bowel lumen → Larger volumes of liquid stool pass through the intestines
- This is often associated with Abdominal pain from bowel distention from increased fluid in the intestinal lumen
- This is often associated with Flatulence from increased gas production as a byproduct of carbohydrate breakdown by bacteria in the intestinal lumen o Steatorrhea: Due to ↓fat absorption → Leads to greasy and foul-smelling stools o Vitamin A, D, E, K Deficiency: Due to ↓Fat absorption → Leads to the inability to assist in the co-absorption of fat-soluble vitamins across the small intestines
- Vitamin A Deficiency: o May present with night blindness
- Vitamin D Deficiency: o May present with hypocalcemia , rickets , or Osteomalacia
- Vitamin E Deficiency : o May present with hemolytic anemia or neuropathy
- Vitamin K Deficiency: o May present with bleeding o Anemia: This is due to ↓B12, Folate, and Iron absorption → Leads to the inability of the bone marrow to mature and produce RBCs → ↓RBCs enter the circulation
- B12 and Folate deficiency → Macrocytic Anemia
- Iron deficiency → Microcytic Anemia
2. Diabetes Mellitus
Pathophysiology: o Chronic Pancreatitis → Endocrine pancreatic Insufficiency → Loss of function in the endocrine portion of the pancreas → ↓Insulin production → Hyperglycemia Presentation: o Polyphagia o Polydipsia o Polyuria
3. ↑ Risk of Pancreatic Cancer
Pathophysiology: o Chronic Pancreatitis → Chronic pancreatic inflammation → ↑Risk of dysplasia Presentation: o Epigastric Pain o Courvoisier’s Sign: Nontender distended gallbladder and Jaundice o Trousseau's Syndrome: Hypercoagulable state → Superficial thrombophlebitis
Exocrine function
Malabsor ption
syndrome
- G G G G Glucose
Diabetes
mellitus
Dysplasia
Pancreatic adenocarcinoma
Pancreatic
cancer
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V. Diagnostic Approach to Pancreatic Disorders
A. Acute Pancreatitis
1. Assess for Evidence of Acute Pancreatitis
a) Obtain Lipase Indications: o High degree of suspicion for Acute Pancreatitis Abnormal Findings: o ↑Lipase (3x upper limit of normal) This is specific for the diagnosis of pancreatitis The presence of epigastric pain and ↑Lipase → Supports the diagnosis of acute pancreatitis
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FIGURE 7. RUQ U/S INDICATING G ALLSTONE F IGURE 8. RUQ U/S INDICATING DUCTAL DILATION
F IGURE 9. S TOOL S AMPLE FOR F ECAL E LASTASE LEVELS F IGURE 10. CT A BDOMEN I NDICATING P ANCREATIC C ALCIFICATION & F IBROSIS
3. Assess for Gallstone-Related Pancreatitis
Obtain RUQ U/S Indications: o Diagnosis of pancreatitis o Presence of Jaundice o Presence of ↑AST, ALT, ALP and Bilirubin Abnormal Findings: o Stone present in the common bile duct o Dilation of the common bile duct
B. Chronic Pancreatitis
1. Assess for Loss of
Pancreatic Function
Obtain Fecal Elastase Indications: o Epigastric pain with normal lipase levels, but the presence of Malabsorption and Diabetes Mellitus with concern for Chronic Pancreatitis Abnormal Findings: o ↓Fecal elastase highly supports Chronic Pancreatitis
2. Assess for Evidence of Pancreatic Fibrosis and
Calcifications
Obtain CT Abdomen Indications: o Epigastric pain with normal lipase levels, but ↓Fecal elastase levels supporting Chronic Pancreatitis Abnormal Findings: o Pancreatic ductal dilation related to strictures from fibrosis mixed with calcification This reveals a “Chain of Lakes” appearance
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VI. Treatment of Pancreatic Disorders
A. Acute pancreatitis
1. Management of Abdominal Pain and Nausea/Vomiting
Treatment: o NPO o NGT decompression if severe Purpose: o NPO By preventing the further intake of food and fluids, the buildup of substances before the swollen pancreas, which is compressing the small intestine, is reduced. This leads to decreased vomiting and bowel dilation, thereby reducing distention and pain. It also allows time for the inflammation in the pancreas to subside o NGT Initiating decompression alleviates the accumulation of fluid and contents ahead of the swollen pancreas, which is pressing on the small bowel. This action reduces vomiting, lessens bowel dilation, minimizes distention, and decreases pain, thereby providing time for the inflammation in the pancreas to subside This may also prevent aspiration of gastric contents, especially in a patient with a decreased level of consciousness, which increases the risk for aspiration PNA Monitoring: o Improvement/Resolution of abdominal pain, nausea and vomiting
2. Management of Gallstone Pancreatitis
Treatment: o ERCP Indications: o RUQ U/S with the diagnosis of Gallstone in Hepatopancreatic Ampulla Purpose: o Decompress the pressure proximal to the hepatopancreatic ampulla obstruction Monitoring: o Improvement/Resolution in abdominal pain, LFTs, and jaundice
TABLE 1. A CUTE P ANCREATITIS OVERVIEW
Endoscopic Retrograde
Cholangiopancreatography
Procedure that is used to remove Gallstones from the Bile Duct
(ERCP)
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4. Utilization of Ranson's Criteria
a) Purpose: o Helps in determining the severity of pancreatitis and guide therapy
b) Parameters: On admission (Remember mnemonic GA LAW): o Glucose > 200 mg/dL: Hyperglycemia can result from the stress response and is indicative of metabolic derangements o Age (> 55 years): Older age is associated with a higher risk of severe pancreatitis. The mechanism behind this criterion is likely related to the decreased physiological reserve and potential for more complications in elderly patients o Lactate Dehydrogenase (LDH) level > 350 IU/L: Released from damaged tissues and cells, reflecting tissue injury and inflammation o AST > 250 IU/L: Indicates more severe pancreatitis. AST is an enzyme found in the liver and other tissues, and elevated levels can be a sign of tissue damage and inflammation o WBC Count >16,000/mm 3 : Indicates systemic inflammation and suggests a more severe form of acute pancreatitis
At 48 hrs (Remember mnemonic C- HOBB): o Calcium Level < 8 mg/dL: This can occur due to calcium binding to fatty acids released during fat necrosis in the pancreas o Hct Drop of > 10%: Suggests bleeding from retroperitoneal hemorrhage, which can be a complication of severe pancreatitis o Oxygen (PaO2) < 60 mmHg: Suggests respiratory dysfunction such as ARDs, which may necessitate oxygen therapy or mechanical ventilation in severe cases o BUN Increase > 5 mg/dL after 48 hours: Indicates renal dysfunction secondary to hypovolemia, which can be a sign of severe pancreatitis o Base Deficit (Arterial pH < 7.35 or Base Deficit > 4 mEq/L): Metabolic acidosis related to lactic acidosis, as indicated by a low arterial pH or elevated base deficit within the first 48 hours, is a marker of severe pancreatitis. It reflects impaired tissue perfusion and oxygenation
c) Interpretation: Mild Acute Pancreatitis ( 0-2 Ranson's Criteria): o Patients with mild acute pancreatitis typically have a lower risk of complications. o Treatment primarily involves supportive care, including fasting from oral intake, intravenous fluids for hydration, and pain management. o Monitoring for signs of improvement or deterioration is essential.
Moderate Acute Pancreatitis ( 3-4 Ranson's Criteria): o Patients with moderate acute pancreatitis are at a higher risk of complications. o They may require more aggressive fluid resuscitation and close monitoring for signs of organ dysfunction, infection, or pancreatic necrosis. Enteral nutritional support may be considered.
Severe Acute Pancreatitis ( ≥ 5 Ranson's Criteria): o Patients with severe acute pancreatitis are at high risk of developing complications such as pancreatic necrosis, organ failure, and infection. o They often require admission to an intensive care unit (ICU) for aggressive management. o Treatment may involve intensive fluid resuscitation, nutritional support (possibly through enteral or parenteral routes), antibiotics if infection is suspected, and consideration of interventional procedures or surgery for complications like infected necrosis.
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B. Chronic pancreatitis
1. Management of Abdominal pain
Treatment: o Treatment of underlying cause (e.g. alcohol abstinence) In the interim manage pain via the following escalation in therapy:
- Opiates
- Nerve blocks
- Surgical resection Monitoring: o Improvement in abdominal pain
2. Management of Malabsorption
Treatment: o Pancreatic Enzyme Replacement Indications: o Diagnosis of chronic pancreatitis that is causing EPI Purpose: o Provide exogenous pancreatic enzymes to ensure any nutrients being ingested are properly digested and subsequently absorbed Monitoring: o Improvement in steatorrhea, weight gain, and resolution of complications (e.g., anemia, vitamin deficiency, etc.) ensures the efficacy of therapy
