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Fluids & Electrolytes
STEPHANIE SMITH, 42, ARRIVES at the ED complaining of severe abdominal pain. Alert and oriented, she tells you that the pain started about 18 hours ago and that she feels nauseated and has vomited four times. You take her vital signs: BP, 92/60 mm Hg; heart rate, 132; respirations, 24; oral temperature, 100.2[degrees] F (37.9[degrees] C); and SpO2, 94% on room air. She rates her pain as an 8 on a pain intensity rating scale of 0 (no pain) to 10 (worst pain imaginable).
On physical assessment, she has dry mucous membranes and bowel sounds are diminished throughout. Her abdomen is tender with muscular guarding, especially in the right upper quadrant and epigastric regions.
You attach Ms. Smith to a cardiac monitor, which shows sinus tachycardia, and administer supplemental oxygen at 2 L/minute via nasal cannula. After establishing I.V. access and notifying the ED physician, you start an infusion of 0.9% sodium chloride solution run wide open and send blood specimens for a complete blood cell count, electrolytes, liver function studies, coagulation studies, and amylase and lipase levels.
Ms. Smith has had several episodes of cholelithiasis in the past 2 years, but hasn't had a cholecystectomy. She says this episode is a little different-the pain is now epigastric in addition to affecting the right upper quadrant as in the past. She has no other significant medical history, takes no medications, doesn't smoke, and denies substance abuse. She drinks two to three alcoholic beverages per month.
The ED physician examines Ms. Smith and orders a right upper quadrant ultrasound and an abdominal computed tomography (CT) scan with intravascular contrast.
Ms. Smith's history of cholelithiasis and clinical condition lead you to suspect gallstone pancreatitis.
About 40% of cases of acute pancreatitis are caused by biliary tract disease, most commonly by choledocholithiasis. Although the exact mechanism of pancreatitis isn't known, researchers think that inappropriate activation of proteases triggers autodigestion of the pancreas. When the biliary tract is obstructed by gallstones, pancreatic duct obstruction or biliary reflux appears to activate pancreatic enzymes. In severe pancreatitis, third-space fluid shifts can lead to hypovolemic shock, acute lung injury, and acute tubular necrosis.
Ms. Smith's ultrasound shows gallstones but no choledocholithiasis or dilated common bile duct. The CT scan shows diffuse pancreatic enlargement. Her lab results are within normal limits except for an elevated white blood cell (WBC) count (14,000/mm3 compared with a normal range of 4,500 to 10,500/mm3), amylase of 500 units/L (normal range is 25 to 125 units/L), and lipase of 560 units/L (normal range is 10 to 140 units/L).
Your first priority is to support Ms. Smith's BP. Continue to give fluid boluses as ordered, and strictly monitor intake and output, watching for signs and symptoms of acute renal failure. Also monitor for respiratory compromise. Administer I.V. hydromorphone as prescribed and monitor her pain levels to determine response to treatment. Ms. Smith is admitted to the telemetry unit for close observation. Because of the possibility of choledocholithiasis, she may need endoscopic retrograde cholangiopancreatography (ERCP).
Ms. Smith's electrolytes, WBCs, amylase, and lipase will be closely monitored. An increase in the number of WBCs might indicate the inflammation associated with pancreatitis or pancreatic infection, a severe complication of pancreatitis. Ms. Smith is also kept N.P.O. for several days to rest the pancreas, and then may resume a high-carbohydrate and low-fat diet. If her pancreatic enzyme levels remain elevated or her pain persists, she may need enteral feeding through a nasojejunal tube.
Before discharge, teach Ms. Smith about a low-fat and low-calcium diet, and make an appointment for her to consult with surgeons about a cholecystectomy. Ms. Smith is discharged home after 5 days and will undergo a cholecystectomy later.
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