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SEARCH RESULTS FOR: Acute-Pancreatitis

Acute-Pancreatitis

Acute Pancreatitis: Pathogenesis and Clinical Findings
Authors: Yan Yu Reviewers: Laura Craig Noriyah AlAwadhi Ryan Brenneis Maitreyi Raman* * MD at time of publication
Associated signs due to intra- abdominal hemorrhage from an unknown mechanism (classically associated with pancreatitis, but happens in <1% of cases):
   Note:
It is not enough to just diagnose “acute pancreatitis”. Full management requires determining underlying etiology with further work-up.
Alcohol
↑ Toxic metabolites within pancreas and Spincter of Oddi Spasms
Gallstones
Migration to common bile duct blocks Sphincter of Oddi
           Hypertriglyceridemia
Unknown
mechanism (rare)
Idiopathic
Further investigations:
CBC: Cell counts elevated, due to sever hypovolemia
Serum [Lipase]: Gold Standard Diagnostic Test; rupture of pancreatic cells releases lipase into circulation
Pancreatic secretions back up, ↑ pressure within pancreas
Hypercalcemia (Rare; Ca2+ depositions in bile ducts block outflow of pancreatic secretions)
Since pancreas is retroperitoneal, somatic
nerves in the parietal peritoneum are directly stimulated
Inflammation triggers cytokine release
Inflamed pancreas irritates adjacent intestines, causing ileus
Inflamed, more permeable blood vessels leak fluid into pancreas
• •
Cullen’s sign (bruising in peri-umbilical region) Grey-Turner’s sign (bruises along both flanks)
Sudden, severe epigastric pain (with peritoneal signs), radiates to the center of the back
Fever, nausea/vomiting
(general signs of inflammation)
Diminished bowel sounds Profound dehydration
(flat JVP, hypotension, tachycardia, oliguria) – may happen, not always
      1. Pressure compresses pancreatic blood vessels, causing tissue ischemia.
2. Activation of inactive proteases (zymogens) digesting pancreatic tissue
Necrosis (death) of pancreatic cells
               Inflammation self- perpetuates
    Massive systemic inflammatory response
         2 main complications, usually detected on CT;
may happen, but not always
1. Pancreatic pseudocyst (enlargement of the
pancreas due to fluid accumulation)
2. Pancreatic necrosis/abscesses (death of a part of the pancreas)
  Legend:
 Pathophysiology
 Mechanism
Sign/Symptom/Lab Finding
  Complications
Re-published September 1, 2019 on thecalgaryguide.com

acute-pancreatitis-complications

Acute pancreatitis:
Complications
Inflammation causes vasodilation and vasculature leakage
Mild, (85%):
Interstitial edematous pancreatitis
Local accumulation of fluid in the pancreas
<2 weeks after onset
Acute peripancreatic fluid collection (not encapsulated)
Walled off by fibrous & granulation tissue
>2 weeks after onset
Pancreatic pseudocyst
(completely encapsulated)
Peritoneal irritation à pain
Large cyst can (very rarely) compress surrounding bowel
Acute Pancreatitis
Inflammatory cytokines are released from damaged pancreas
If recurrentàchronic pancreatitis (see relevant slide)
Inflammation damages pancreatic exocrine
cellsàInappropriate release of pancreatic enzymes into surrounding tissue & vasculature àdigesting pancreatic parenchyma
Authors: Nissi Wei, *Yan Yu Reviewers: Dean Percy, Miles Mannas, Varun Suresh, Brandon Hisey, *Kerri Novak, *Sylvain Coderre * MD at time of publication
                     complete resolution (most cases)
Necrotic tissue is vulnerable to
infection (esp. Gram neg GI bacteria)
inflammation & necrosis activate cytokine cascade
Severe, necrosis (15%): Necrotizing pancreatitis
Local infection
Severe pancreatic inflammation shifts body fluid into retroperitoneal spaceàintravascular volume depletion
                 Systemic Inflammatory Response Syndrome (SIRS) (see relevant slide)
Organ failure (may be sole feature on presentation)
Stagnant fluid can more easily become infected
Infection spreads to bloodstream
Cardiac failure Hypovolemic shock Renal failure
Local accumulation of fluid & necrosis in the pancreas
< 4 weeks after onset:
Acute necrotic collection (not encapsulated)
Walled off by fibrous & granulation tissue
> 4 weeks after onset
walled-off necrosis
(completely encapsulated)
When treated with excess fluid resuscitation:
Intra- abdominal hypertension
                Respiratory failure (ARDS)
Disseminated intravascular coagulation (DIC)
          Bowel obstruction Gastric outlet (see relevant slide) obstruction
Infected pancreatic necrosis
  Legend:
 Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
  Complications
Published September 20, 2016, updated September 7, 2020 on www.thecalgaryguide.com

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Akute Pankreatitis: Komplikationen

Akute Pankreatitis:
Komplikationen