Summary about bowel pancreatitis including Hx, examinations, ddx & Tx

1. Pancreatitis
1- Acute pancreatitis
Is an inflammatory condition of the pancreas most commonly caused by gallstones, alcohol use
Etiology
• Biliary pancreatitis (∼ 40% gallstones)
• Alcohol Use (∼ 20%)
• Idiopathic (∼ 25%)
• Hypertriglyceridemia (TGs> 1,000 mg/dL)
• Hypercalcemia
• Post-ERCP
• Drug-induced pancreatitis
Steroids
Loop and thiazide diuretics
Estrogen
• Viral infections
• Trauma (especially in children)
• Autoimmune Disorders
A diagnostic and/or therapeutic
procedure in which a side-viewing
endoscope is inserted into the
duodenum and contrast is injected
into the bile ducts.
Pathophysiology
1- Obstruction Pancreatic ductat (Gallstones, Cystic fibrosis, Direct injury to panc. acinar cells)
2- Intra-pancreatic activation of pancreatic enzymes
3- Increased proteolytic and lipolytic enzyme activity → destruction of pancreatic parenchyma
4- Attraction of inflammatory cells (neutrophils, macrophages) → release of inflammatory
Cytokines → pancreatic inflammation (pancreatitis)
Clinical features
1- Constant, severe epigastric pain
• Radiating towards the back
• Increase after meals and when supine
• Improves on leaning forwards
2- Nausea, vomiting
3- Fever
Symptoms:
Examination
1- General
• Signs of shock (Tachycardia, Hypotension, Oliguria/Anuria)
• Possibly jaundice (Biliary Pancreatitis)
2- Abdominal examination
• Cullen sign (peri-umbilical ecchymosis and discoloration (bluish-red))
• Grey Turner sign (flank ecchymosis with discoloration)
Cullen Sign = Peri-umbilical , Grey Turner Sign = Flank
s
Ws
S
W
↳ -
-
-
-
-
-
-
⑮
is
to
↳
-
↑
I
I
I
↑
-
S
-
A
S
-
s
s
s
W
-
-
W
W
W
-
-
⑮
sjo
-
-
-
S
I S
-
-
&
↳
n
-
-
d
-
-
/
/ >
- /
-
-
It
is
i
-
-
E
S
-
iI
↑ 2
2
W
W
S
S

2. Diagnostics
• Characteristic abdominal pain
• Serum pancreatic enzymes (↑ Lipase or Amylase ≥ 3×Upper Limit Normal)
• Cross-sectional Imaging (CT With Contrast)
Two of the three following criteria
Approach
1- Laboratory Studies
• serum lipase and/or amylase levels
• CBC
• BMP (Basic Metabolic Panel)
• LDH
• Serum Calcium
2- Imaging
• U/S (Pancreatitis Visible In 20% of Cases, Gallstone)
• CT With Contrast
• MRCP
• ERCP
Treatment
1- General Management For All Patient With Acute Pancreatitis
• IV fluid therapy
• Analgesics
◦ NSAIDS
◦ Opioids (hydromorphone, morphine)
• Nutrition
◦ Early oral feeding
◦ Enteral tube (nasogastric or nasojejunal)
◦ IV nutrition
2- Management of the underlying cause
A- Biliary pancreatitis
• Therapeutic ERCP
◦ Biliary pancreatitis associated with cholangitis or persistent CBD obstruction
• Cholecystectomy
◦ All patients with biliary pancreatitis to prevent recurrence
mijind
-
-
⑮sin
Brigitte
-
-

3. 2- Chronic pancreatitis
Is characterized by progressive inflammation that results in irreversible damage to
the structure and function of the pancreas.
• Chronic heavy alcohol use
• Pancreatic ductal obstruction (e.g., due to trauma, stones)
• Tobacco use
• Idiopathic pancreatitis
• Hereditary pancreatitis (PRSS1 gene mutation)
• Autoimmune pancreatitis
• Systemic disease (Cystic fibrosis)
Etiology
Clinical features
1- Epigastric abdominal pain
• Pain radiates to the back
• Relieved on bending forward
• Exacerbated after eating
2- Nausea & Vomiting
3- Features of pancreatic insufficiency (after 90% of pancreatic parenchyma is destruction)
• Steatorrhea (exocrine enzyme deficiency)
Diarrhea
▪
Deficiency of fat-soluble vitamins (A, D, E, and K)
• Malabsorption and weight loss
• Pancreatic diabetes (endocrine hormone deficiency)
‫ا‬
‫ﻳ‬
‫ﺪ‬
َ
‫ك‬
EDAK
Diagnostics
1- Hx.
• Characteristic abdominal pain
• Signs of:
Exocrine pancreatic insufficiency (Steatorrhea, Weight Loss)
Endocrine pancreatic insufficiency (Diabetes)
2- Imaging studies
• CT with & without contrast
◦ Can exclude gastrointestinal malignancies (e.g., pancreatic carcinoma)
◦ Findings (Pancreatic ductal dilations & Calcifications on plain CT)
• MRI/MRCP
• ERCP
3- Laboratory testing
• Serum Lipase (specific) & Serum amylase (nonspecific) are often normal
4- Pancreatic function tests
• Fecal elastase-1 (FE-1)
5- Genetic testing (PRSS1 Gene Mutations)
• Indications include:
◦ Family history of chronic pancreatitis
◦ Young patients with idiopathic pancreatitis
·insii-
-
-
-
ens
-
·nonsi
y
-

4. Treatment
1- Treatment Of Pain
• Start with nonopioid oral analgesics (NSAIDs if contraindicated Use Limit opioid)
2- Stopped nicotine and alcohol for all patients
3- Interventional therapy
• Endoscopic (if pain not relief with pharmacotherapy)
• Surgical (if pain not relief with pharmacotherapy or endoscopic)
Complications
• Recurrent acute pancreatitis
• Exocrine pancreatic insufficiency
• Endocrine pancreatic insufficiency
• Splenic vein thrombosis
• Pancreatic pseudocysts
• Pancreatic abscess
• Portal vein thrombosis
• Pancreatic cancer (especially in patients with hereditary pancreatitis)
·mons
·mons
·ess
I
&
↓
hh...
⑪
Exhle...

5. Overview of acute and chronic pancreatitis
Acute pancreatitis Chronic pancreatitis
Characteristics
• Acute inflammation
• Potentially reversible damage
• Progressive inflammation
• Irreversible damage with impairment of exocrine and endocrine
function
Etiology
Most common
causes
• Biliary pancreatitis (mostly caused by gallstones)
• Alcohol-induced
• Idiopathic
• Chronic heavy alcohol use (60–70%, esp. men)
• Idiopathic (20–30%)
• Pancreatic ductal obstruction (< 10%)
• Tobacco use
Less common
causes
• Severe hypertriglyceridemia (> 1,000 mg/dL)
• Hypercalcemia
• Post-ERCP
• Drugs (e.g., loop and thiazide diuretics)
• Viral infections (e.g., mumps)
• Trauma (especially in children)
• Autoimmune and rheumatological disorders
• Scorpion stings
• Hereditary pancreatitis
• Cystic fibrosis
• Severe hypertriglyceridemia (levels > 1,000 mg/dL)
• Pancreas divisum
Pathophysiology
• Damage to pancreatic acinar cells (e.g., alcohol), outflow obstruction of pancreatic enzymes or premature activation of trypsinogen to trypsin → intrapancreatic
activation of pancreatic enzymes(e.g., amylase and lipase) → destruction of pancreatic parenchyma (autodigestion)
• Attraction of inflammatory cells (neutrophils, macrophages) → release of inflammatory cytokines → pancreatic inflammation (pancreatitis)
• Possible consequences of pancreatitis
◦ Capillary leakage → hypotension, tachycardia → distributive shock
◦ Pancreatic necrosis
◦ Hypocalcemia: lipase breaks down peripancreatic and mesenteric fat → release of free
fatty acids that bind calcium → hypocalcemia (fatty saponification)
• Fibrosis: exposure to toxins and/or inflammatory mediators (e.g.,
alcohol, cytokines) → activation of pancreatic stellate cells
Course • Sudden onset • Recurrent, progressive episodes
Clinical
features
Main
symptoms
• Constant, severe epigastric pain (classically radiating towards the back)
• Nausea, vomiting
• Fever
• Weakness
• Epigastric abdominal pain (main symptom)
◦ Radiating towards the back
◦ Relieves on bending forward, exacerbates after eating
• Cramping abdominal pain, bloating, diarrhea, constipation,
flatulence
• Nausea
Further
symptoms
• Signs of shock: tachycardia, hypotension, oliguria/anuria
• Abdominal tenderness, distention
• Cullen sign
• Grey Turner sign
• Fox sign
• Pleural effusion and/or ARDS
• Steatorrhea (exocrine pancreatic insufficiency): can lead to a
deficiency of fat-soluble vitamins
• Malabsorption and weight loss
• Pancreatic diabetes (endocrine pancreatic insufficiency)
• Usually manifest late, when > 90% of the pancreatic parenchyma is
destroyed
Diagnostics
Laboratory
studies
• ↑ Lipase (specific)
• ↑ Amylase (nonspecific)
• ↓ Calcium
• Hct (to assess severity)
• Lipase and amylase (often normal)
• ↓ Fecal elastase-1 (confirms that steatorrhea is due to pancreatic
lipase insufficiency)
Imaging
• Ultrasound
◦ Pancreatic edema
◦ Peripancreatic fluid
◦ Hemorrhage, necrosis, abscesses, pancreatic pseudocysts
◦ In biliary pancreatitis: evidence of cholelithiasis or biliary sludge
• CT scan
◦ Enlargement of the pancreatic parenchyma with edema
◦ Indistinct pancreatic margins with surrounding fat stranding
• X-ray
◦ Sentinel loop sign
◦ Colon cut off sign
• MRCP/ERCP (in case of biliary or pancreatic duct obstruction)
• Abdominal CT (best initial imaging modality)
◦ Ductal dilations, stenosis, and calcifications (more sensitive than
x-ray)
◦ Chain-of-lakes appearance of the main pancreatic duct
◦ Pancreatic atrophy
• ERCP
◦ Ductal stones (visible as filling defects)
◦ Chain-of-lakes or string-of-pearls appearance
• Abdominal ultrasound
◦ Pancreatic edema
◦ Pancreatic calcifications
Treatment
• Analgesics: NSAIDs, opioids (fentanyl or hydromorphone) for severe pain
• General measures
◦ Discontinuation of aggravating agents
◦ Fluid resuscitation: aggressive hydration with crystalloids
◦ Enteral feeding (oral/nasogastric/nasojejunal)
◦ O2 administration
◦ Antibiotics: only in patients with evidence of infected necrosis
• Procedures: ERCP/cholecystectomy may be considered for biliary pancreatitis
• General measures
◦ Avoidance of aggravating substances (e.g., alcohol, nicotine)
◦ Pancreatic enzyme replacement (with meals)
• Further pain management
◦ Celiac ganglion block
◦ Endoscopic papillotomy with ductal dilation, stent placement, and
removal of stones
• Surgery (for suspected pancreatic cancer or intractable pain)
Complications
• Localized
◦ Bacterial superinfection of necrotic tissue
◦ Pancreatic pseudocysts
◦ Pancreatic abscess
◦ Fistula formation
◦ Organ dysfunction(e.g., acute lung injury/ARDS, renal failure, shock)
◦ Hypocalcemia (due to saponification)
◦ Blood vessel erosion with bleeding
• Systemic
◦ SIRS, sepsis, DIC
◦ Pneumonia, respiratory failure, ARDS
◦ Shock
◦ Prerenal failure due to volume depletion
◦ Hypocalcemia
◦ Pleural effusion
• Chronic pain
• Opiate addiction
• Pancreatic insufficiency
◦ Exocrine insufficiency: maldigestion, steatorrhea, malabsorption
◦ Endocrine insufficiency: pancreatic diabetes
• Pancreatic pseudocysts
• Splenic vein thrombosis
• Pancreatic abscess
• Portal vein thrombosis
• Pancreatic cancer
Prognosis
• Mortality
◦ In patients without organ failure: < 1%
◦ In patients with organ failure: ∼ 30% [7]
• Dependent on alcohol use, smoking, and presence of end-stage liver
disease
EDAK