Info
🌱 來自: Huppert’s Notes
Pancreas🚧 施工中
Pancreas
Acute pancreatitis
• Etiology: Premature activation of pancreatic digestive enzymes causes autodigestion of pancreatic tissue
• Causes: GET SMASHED – Gallstones (40%), EtOH (30%), Trauma, Scorpion, Mumps, Autoimmune, Steroids, Hypertriglyceridemia (>1000 mg/dL)/Hypercalcemia, ERCP (post-procedure), Drugs (sulfonamides, thiazides, lisinopril, furosemide, antiretrovirals)
• Clinical features:
- Symptoms: Epigastric pain that radiates to the back, often worse after eating. Also fever, nausea/vomiting
- Classic signs: Hemorrhagic: 1) Grey Turner (flank ecchymosis), 2) Cullen (periumbilical ecchymosis), 3) Fox (nontraumatic ecchymosis over the inguinal ligament)
• Diagnosis: Need two of three criteria: 1) Typical pancreatic abdominal pain, 2) Elevation in lipase or amylase >3× ULN, 3) Imaging findings of acute pancreatitis.
• Prognosis: Multiple scoring systems exist, including the following:
- BISAP: 5-point score to predict mortality (BUN >25 mg/dL, GCS <15, SIRS, age >60 yr, pleural effusion)
- Ranson’s criteria: Uses age, admission labs, and labs at 48 hours to predict mortality
• Treatment:
- Make patient NPO, administer early aggressive IVF (5–10 cc/kg, Lactated Ringer’s preferred), replete electrolytes, provide pain control
- Gallstone pancreatitis: Early ERCP, followed by cholecystectomy after recovery
• Complications:
- Pancreatic necrosis: If suspect sterile fluid collection, monitor closely, antibiotics controversial. If infection suspected, give IV antibiotics and pursue surgical debridement.
- Pancreatic pseudocyst: Fluid collection 2–3 weeks after acute pancreatitis. Risk rupture, infection, obstruction. Treatment: Observation if minimal symptoms/no pseudoaneurysm. If symptomatic or rapidly enlarging, drain percutaneously, endoscopically, or surgically.
- Other complications of acute pancreatitis: ARDS, pancreatic ascites, pleural effusions, ascending cholangitis, ileus, renal failure, hemorrhagic pancreatitis, abdominal compartment syndrome.
Chronic pancreatitis
• Etiology: Persistent inflammation of the pancreas with fibrotic tissue replacing pancreatic parenchyma, leading to endocrine/exocrine dysfunction. Heavy alcohol consumption is the most common cause (>80%); gallstones usually don’t cause chronic pancreatitis. Consider the diagnosis of cystic fibrosis in young patients without a history of heavy alcohol use.
• Clinical features: Chronic intermittent abdominal pain, diabetes, steatorrhea (fat in the stool due to lack of pancreatic enzymes)
• Diagnosis: CT abd/pelvis or MRCP – calcifications, dilated main pancreatic duct. ERCP is the gold standard but it is not routinely performed. Labs are not helpful and lipase/amylase are often normal!
• Treatment:
- Nonoperative: Alcohol and smoking cessation, pain control, pancreatic enzyme supplementation, frequent small low-fat meals
- Operative: Pancreatojejunostomy (pancreatic duct drainage to decompress the dilated duct), total pancreatectomy with auto-islet cell transplant, or denervation (celiac plexus block)
Autoimmune pancreatitis (AIP)
• Subtypes:
- Type 1 (“lymphoplasmacytic sclerosing pancreatitis”): IgG4-related autoimmune pancreatitis. Most patients have another concurrent IgG4-related condition, such as sclerosing cholangitis or lymphadenopathy. Often presents as a pancreatic mass or as painless jaundice; can be mistaken for pancreatic cancer.
- Type 2 (“idiopathic duct–centric chronic pancreatitis”): Much more rare than type 1. IgG4 may be elevated or normal. Sometimes associated with IBD.
• Clinical features: Abdominal pain, pancreatic mass or enlargement with obstructive jaundice, extrapancreatic manifestations (e.g., IBD, IgG-4 associated cholangitis, lung nodules, Sjogren’s)
• Diagnosis: HISORt criteria (Histology, Imaging, Serology [IgG4 >2× ULN], Other organ involvement, Response to steroids therapy). “Sausage-like pancreas” is buzzword for CT findings for AIP.
• Treatment: Steroids