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Acute pancreatitis

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ACUTE PANCREATITIS
Etiology
"I GET SMASHED": I = Idiopathic, G = Gall stones(most common, biliary pancreatitis)
, E=Ethanol, T = Trauma, S = Steroids, M = Mumps, A = Autoimmune and
rheumatological disordes (e.g. Sjôgren syndrome), S = Scorpion
poison, H= Hypercalcemia, Hypertriglyceridemia, E = ERCP, D = Drugs.(steroids
azathioprine sulfonamides furosemide estrogen protease inhibitors NRTIs)
Pathophysiology(video osmosis)
Sequence of events leading to pancreatitis:
1. Intrapancreatic activation of pancreatic enzymes: secondary
to pancreatic ductal outflow obstruction (e.g., gallstones, cystic fibrosis) or
direct injury to pancreatic acinar cells (e.g., alcohol, drugs)
Alcohol can also be responsible for blocked ducts by increasing zymogen
secretion (elevating pancreatic juice’s viscosity) and decreasing of fluid secretion
in the interstitial tissu, that leads to membrane trafficking, fusing of zymogens
and autodigestion
2. Enzymatic autodigestion of pancreatic parenchyma
3. Attraction of inflammatory cells (neutrophils, macrophages) → release of
inflammatory cytokines → pancreatic inflammation (pancreatitis)
Sequelae of pancreatitis (depending on the severity of pancreatitis)
1. Capillary leakage: Release of inflammatory cytokines and vascular injury
by pancreatic enzymes → vasodilation and increased vascular permeability
→ shift of fluid from the intravascular space into the interstitial space (third
space loss) → hypotension, tachycardia → distributive shock
2. Pancreatic necrosis: Uncorrected hypotension and third space loss →
decreased organ perfusion → multiorgan dysfunction (mainly renal)
and pancreatic necrosis
3. Hypocalcemia: Lipase breaks down peripancreatic and mesenteric fat →
release of free fatty acids that bind calcium → hypocalcemia
Disease progression

Mild acute pancreatitis: interstitial edema, no necrosis; no local and
systemic complications, no organ failure

Moderate acute pancreatitis: associated with local
(e.g., necrosis, abscesses, pseudocysts) or systemic complications, such as
temporary organ failure (e.g., kidney failure), which improves within 48 hours

Severe pancreatitis: associated with persistent pancreatic failure (> 48
hours), as well as single or multiple organ failure
Clinical features
Constant, severe epigastric pain

o
Classically radiating towards the back
o
Worse after meals and when supine
o
Improves on leaning forwards
o
Nausea, vomiting
General physical examination

o
Signs of shock: tachycardia, hypotension, oliguria/anuria
o
Possibly jaundice in patients with biliary pancreatitis
Abdominal examination

Abdominal tenderness, distention, guarding
o
As the pancreas is a retroperitoneal organ, abdominal guarding does not
present with the typical hard rigidity seen
in inflammation of intraperitoneal organs. Instead, the abdomen is
distended and elastic on palpation.
o
Ileus with reduced bowel sounds and tympany on percussion
o
Ascites
o
Skin changes (rare)
Circulating pancreatic enzymes cause swelling of the subcutaneous tissue and
localized hemorrhages. These signs, though nonspecific, suggest retroperitoneal
bleeding and are associated with a poor prognosis.

Cullen's sign: periumbilical ecchymosis and discoloration (bluish-red)

Grey Turner's sign: flank ecchymosis with discoloration

Fox's sign: ecchymosis over the inguinal ligament
Diagnostics
Acute pancreatitis is diagnosed based on a typical clinical presentation, with
abdominal pain radiating to the back, and either detection of highly
elevated pancreatic enzymes or characteristic findings on
imaging. Serum hematocrit is an easy test that should be conducted to help quickly
predict disease severity.
Laboratory tests
Tests to confirm clinical diagnosis

↑ Serum pancreatic enzymes
o

Lipase: if ≥ 3 x the upper reference range → highly indicative of
acute pancreatitis

Amylase (nonspecific)

The enzyme levels are not directly proportional to severity or
prognosis!
Tests to assess severity

Hematocrit (Hct)
o

Should be conducted at presentation as well as 12 and 24 hours after
admissions

↑ Hct (due to hemoconcentration) indicates third space fluid loss and
inadequate fluid resuscitation

↓ Hct indicates the rarer acute hemorrhagic pancreatitis
o
WBC count Leukocytosis is an indicator of severe pancreatitis.
o
Blood urea nitrogen
o
↑ CRP
and procalcitonin levels
Procalcitonin levels help determine if a rise in CRP is due to necrosis caused
by bacterial pancreatitis, as procalcitonin typically indicates bacterial
infection, whereas CRP may be elevated in either sterile or
bacterial pancreatitis.
↑ ALT
o
Tests to determine etiology

o
Alkaline phosphatase, bilirubin levels (evidence of gallstone pancreatitis)
o
Serum calcium levels
o
Serum triglyceride levels (fasting)
Determining calcium values is very important: Hypercalcemia may cause pancreatitis,
which may then, in turn, cause hypocalcemia!
Imaging
Ultrasound (most useful initial test): indicated in all patients with
acute pancreatitis

o
Main purpose: detection of gallstones and/or dilatation of the biliary
tract (indicating biliary origin)
o
Signs of pancreatitis

Indistinct pancreatic margins (edematous swelling)

Peripancreatic build-up of fluid
; evidence of ascites in some cases

Evidence of necrosis, abscesses, pancreatic pseudocysts
CT scan: not routinely indicated

Indications
o

At admission: only when the diagnosis is in doubt (e.g., not very highly
elevated pancreatic enzymes, non-specific symptoms)

> 72 hours of symptom onset: if complications such as
necrotizing pancreatitis or pancreatic abscess (e.g.,
persistent fever and leukocytosis, no clinical improvement or evidence
of organ failure > 72 hours of therapy) are suspected
Pancreatic necrosis or abscess takes time to develop and therefore, a CT
scan done on the first day of symptom onset will not delineate
the necrotic and/or infected pancreatric parenchyma and will not alter
the treatment.
o
Findings

Enlargement of
the pancreatic parenchyma with edema; indistinct pancreatic margins
with surrounding fat stranding

Necrotizing pancreatitis: lack of parenchymal enhancement or presence
of air in the pancreatic tissue

Pancreatic abscess: circumscribed fluid collection
Balthazar score :
MRCP and ERCP

o
Indications: suspected biliary or pancreatic duct obstructions
o
MRCP is noninvasive but less sensitive than ERCP
o
ERCP can be combined with sphincterotomy and stone extraction; but
may worsen pancreatitis.
Conventional x-ray

o
Sentinel loop sign: dilatation of a loop of small intestine in the upper
abdomen (duodenum/jejunum)
dilatation of a loop of small intestine due to a functional ileus near an inflamed
process.
o
Colon cut off sign: gaseous distention of the ascending and transverse
colon that abruptly terminates at the splenic flexure
o
Evidence of possible complications: pleural effusions, pancreatic calcium
stones; helps rule out intestinal perforation with free air
Treatment
General measures

Admission to hospital and assessment of disease severity
(consider ICU admission)

Fluid resuscitation: aggressive hydration with crystalloids (e.g., lactated
Ringer's solution , normal saline)

Analgesia: IV opioids (e.g., fentanyl)

Bowel rest (NPO)and IV fluids are recommended until the pain subsides

Nasogastric tube insertion: not routinely recommended; indicated in
patients with vomiting and/or significant abdominal distention

Nutrition
o
Begin enteral feeding (oral/nasogastric/nasojejunal) as soon as
the pain subsides
o
Total parenteral nutrition: only in patients who cannot tolerate enteral
feeds (e.g., those with persistent ileus and abdominal pain)
Drug therapy

Analgesics: fentanyl or hydromorphone; consider pump administration
(patient controlled analgesia = PCA)

Antibiotics
o
Prophylactic antibiotic therapy is not recommended.
o
Antibiotics should only be used in patients with evidence of
infected necrosis.
Fenofibrates: in hyperlipidemia-induced acute pancreatitis

Procedures/surgery
Biliary pancreatitis

o
Urgent ERCP and sphincterotomy (within 24 hours): in patients with
evidence of choledocholithiasis and/or cholangitis; followed
by cholecystectomy
o
Cholecystectomy (preferably during same admission once the patient is
stabilized; or within 6 weeks): in all patients with biliary pancreatitis
The most important therapeutic measure is adequate fluid replacement (minimum
of 3–4 liters of crystalloids per day)!
Cours du prof : Pancreatite A B C cholecystectomie au cours de la meme
hospitalisation, Pancreatite D ou E chirurgie reportée à 2 ou 3 mois après
refroidissement
"PANCREAS" - Perfusion (fluid replacement), Analgesia, Nutrition, Clinical
(observation), Radiology (imaging), ERCP (endoscopic stone extraction), Antibiotics,
Surgery (surgical intervention, if necessary).
Complications
Localized
Bacterial superinfection of necrotic tissue → fever

o
Diagnosis: CT-guided percutaneous drainage + culture of the aspirate
o
Treatment: surgical debridement, antibiotics
o
High mortality rate; multiple organ failure in ∼ 50% of cases

Pancreatic pseudocysts

Pancreatic abscess
o
Walled-off infected necrotic tissue or pancreatic pseudocyst; typically
develops > 4 weeks after an attack of acute pancreatitis
o
Abdominal CT: visible contrast-enhanced abscess capsule with evidence of
fluid (pus)
o
Ultrasound: complex cystic, fluid collection with irregular walls and
septations
o
Treatment: cannulation and drainage; necrosectomy if other measures are
not effective

Pleural effusion

Abdominal compartment syndrome

Blood vessel erosion with bleeding
Systemic

SIRS, sepsis, DIC

Pneumonia, respiratory failure, ARDS

Shock

Prerenal failure due to volume depletion

Hypocalcemia

Pleural effusion, pancreatic ascites

Paralytic ileus
Prognosis
Mortality

o
In patients without organ failure: < 1%
o
In patients with organ failure: ∼ 30%
o
Higher mortality in patients with biliary pancreatitis than in patients with
alcoholic pancreatitis
Important predictors of severity

o
Age > 55
o
Gastrointestinal bleeding
o
Abnormal hematocrit within 48 hours

Acute hemorrhagic pancreatitis: ↓ Hct

Third space fluid loss: ↑ Hct
o
Hypocalcemia and/or hyperglycemia
o
Inflammatory markers: ↑↑ CRP, ↑ IL-6, ↑ IL-8
o
Evidence of shock and/or organ failure

↑ AST, ↑ ALT

↑ BUN, creatinine

↑ LDH

ABG: pO2 < 60 mmHg, metabolic acidosis with a base deficit > 4
mmol/L
o
CT findings: pancreatic edema, peripancreatic fluid collection,
and/or necrosis of > 33% of the pancreas
Amylase and lipase, which are used for the diagnosis of pancreatitis, cannot be used to
predict the prognosis!

Numerous scoring systems exist (e.g, Ranson criteria) for assessing the
severity and predicting the prognosis of acute pancreatitis
1. Cite 11 étiologies
2. Physiopathologie : Events leading to pancreatitis, sequelae of
pancreatitis, disease progression
3. Clinical features, physical examination, abdominal examination(4)
4. Laboratory findings : tests to confirm the dg, tests to assess severity,
tests to determine etiology
5. Imaging : Ultrasound’s findinds, CT :when to perform, findings,
Balthazar score, MRCP ERCP, X-ray
6. Treatment : General measures, drug therapy, surgery
7. Complications : localized, systemic
8. Prognosis : predictors of severity
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