AhmedMokhtar326574
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Aug 06, 2024
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About This Presentation
updated guidelines of mangement of acute pancreatitis 2024 and data concern anatomy and physiology of pancreas
Size: 12.07 MB
Language: en
Added: Aug 06, 2024
Slides: 74 pages
Slide Content
Acute pancreatitis Dr Ahmed Mokhtar Ass. Lecturer of Gastroenterology, MFM
Anatomy of the pancreas The pancreas lies in the abdomen, retroperitoneally . In adults, it is about 12–15 cm long , lobulated , and salmon-colored in appearance. Anatomically, the pancreas is divided into a head, neck, body, and tail . The pancreas is an organ of the digestive system and endocrine system .
Duct system
Ventral pancreatic bud (VP) arises from hepatic diverticulum, and dorsal pancreatic bud (DP) arises from dorsal mesogastrium (A). During 7th gestational week, expansion of duodenum causes ventral pancreatic bud to rotate and pass behind duodenum from right to left and fuse with dorsal pancreatic bud (B-D). Ventral bud forms posterior head and uncinate process, whereas dorsal bud forms anterior head, body, and tail. Finally, ventral and dorsal pancreatic ducts fuse, and pancreas predominantly is drained through ventral duct, which joins common bile duct at level of major papilla and dorsal duct drains at level of minor papilla. Normal embryologic development of pancreas
Variations in configuration of pancreatic duct (A) Bifid configuration with dominant duct of Wirsung drainage, (B) bifid configuration with dominant duct of Santorini drainage without divisum , (C) rudimentary non-draining duct of Santorini (D) pancreas divisum , (E) ansa pancreatica
Annular pancreas Annular pancreas arises as a failed result of normal rotation of the ventral bud of the pancreas, causing it to elongate and encircle the second portion of the duodenum. Commonly, annular pancreas presents in the neonatal period and is manifest as duodenal atresia.
Acute pancreatitis (AP) Itis one of the principal gastrointestinal disorders that cause abdominal pain , associated with raised pancreatic enzymes , in the blood or urine because of pancreatic inflammation and autodigestion.
Epidemiology of acute pancreatitis 3% of all cases of abdominal pain . Hospital admission rate 9.8 per 100 000 population annually. It may occur at any age, with a peak incidence in young men and old women.
Etiology The most common etiologies of AP are: - gallstones (40-70%) alcohol (25-35%). Other causes are almost rare or idiopathic.
Gallstone pancreatitis This is caused by a gallstone blocking CBD reflux of bile into pancreatic duct and impaired flow of normal pancreatic juice premature activation of pancreatic enzymes within the duct system.
Acute pancreatitis (classification)
Acute pancreatitis (History taking) To assess: Pain Causes complications
Acute pancreatitis (Physical examination) General Fever Abdominal ….
Acute pancreatitis (Investigations)
Other blood tests
Role of imaging in acute pancreatitis
1- Ultrasound
2- ERCP
ERCP: Gallstones
3- Plain abdominal x-ray
Sentinel loop sign
Colon cut-off sign
4- CT scan
CT anatomy pancreatic level
Local complications of AP
CT severity index
Assessment of AP severity
Ranson’s score
Glasgow score
APACHE II score (Acute physiology and chronic health evaluation)
AP Management
Mild AP
Severe AP
Severe AP (cont.)
American College of Gastroenterology Guidelines: Management of Acute Pancreatitis
1- Diagnosis and Initial Assessment
Ultrasound Transabdominal ultrasound for patients with acute pancreatitis (AP) to evaluate for biliary pancreatitis. a report US if the initial examination is inconclusive.
Reserve CT for uncertain diagnosis failure to improve in 48-72 hours.
Risk factors for severe disease :
Etiology
In absence of gallstones or ETOH use Evaluate serum triglyceride level (>1000 mg/dL more suggestive) N.B. The most common etiologies of AP are - gallstones (40-70%) - alcohol (25-35%)
Pancreatic tumor Concern for pancreatic tumor is highest for those: - aged 40+ with no clear etiology of AP
Cholecystectomy is recommended in those with 2nd episode of AP with no cause.
Management
1- Fluids
Monitor patient closely the first 6-12 hours while checking vitals, BUN/HCT to assess fluid needs. ( LR preferred) Moderately aggressive hydration is most important the first 6-12 hours. Moderately aggressive hydration is of little benefit after 24-48 hours ….. continue to monitor the patient closely during this time.
2- Antibiotics
No antibiotics unless concern for infection. If infected necrosis is suspected (typically after 10-14 days), use antibiotics that can penetrate: (1) Carbapenems (2) Quinolones (3) Cephalosporins (4) Metronidazole
3- Feeding
In mild disease: Early oral feeding with low fat solid diet (within 24-48 hours) as tolerated. Avoid parenteral nutrition if possible.
In moderately severe or severe disease: Consider NG for enteral feeding (NG>NJ preferred) Add small peptide-based medium chain TG oil for tolerance. Continuous feeding > cyclic or bolus
4- Procedures and Surgery
ERCP ERCP within 24 hours if complicated by cholangitis. Consider rectal indomethacin, pancreatic duct stent, and hydration to avoid post ERCP pancreatitis
Cholecystectomy It is preferably before discharge in mild acute biliary pancreatitis
In stable pancreatic necrosis: Wait 4-6 weeks for surgical, radiological, and/ or endoscopic interventions.