NSG210 Hinkle Ch. 44: Management of Patients with Biliary Disorders
Source: Hinkle & Cheever, Brunner & Suddarth’s Medical-Surgical Nursing 15e, Chapter 44, pp. 1416-1444 (textbooks/HINKLE_MS_CH44.pdf, also in textbooks/exam04/). Week 12 (hepatic and biliary); Exam 4 content. Numbering note: the Week 12 syllabus entry “Ch. 44” is the 16th edition hepatic chapter (15e Ch. 43); this 15e biliary chapter (16e Ch. 45) is included because it is in the curated exam04/ folder, and it covers the pancreas (pancreatitis, pancreatic cancer). See nsg210-textbook-chapter-crosswalk. Liver disease is in nsg210-hinkle-ch43-hepatic-disorders.
Learning Outcomes
Identify the structure and function of the biliary tract and pancreas.
Describe the pathophysiology, manifestations, and medical management of cholelithiasis.
Differentiate acute and chronic pancreatitis.
Apply the nursing process to the patient with cholelithiasis, laparoscopic or open cholecystectomy, or acute pancreatitis.
Explain the nutritional and metabolic effects of surgery for pancreatic tumors.
Zollinger-Ellison syndrome: gastric acid hypersecretion and peptic ulcers from a non-beta islet cell tumor (gastrinoma)
I. Anatomy and Physiology
Gallbladder: pear shaped, 7.5 to 10 cm, holds 30 to 50 mL; concentrates bile 5 to 10 times; cystic duct joins CBD. CCK triggers contraction and sphincter of Oddi relaxation when food enters the duodenum.
Exocrine pancreas: pancreatic duct joins CBD at ampulla of Vater; alkaline, bicarbonate-rich secretion neutralizes gastric acid; amylase, trypsin, lipase; secretin stimulates bicarbonate; CCK stimulates enzymes; 1500 to 3000 mL/day. Considerable dysfunction occurs before digestion is impaired.
Endocrine pancreas (islets of Langerhans): beta cells (insulin, lowers glucose), alpha cells (glucagon, raises glucose), delta cells (somatostatin, hypoglycemic effect by blocking GH and glucagon). Blood glucose normally under 100 mg/dL. Glucose-raising hormones: glucagon, epinephrine, adrenocorticosteroids, growth hormone, thyroid hormone.
Older adults: more fibrous and fatty tissue after 70; less amylase, lipase, trypsin, and bicarbonate; impaired fat and calcium absorption.
II. Gallbladder Disorders
A. Cholecystitis
Pain, tenderness, rigidity of RUQ, may radiate to midsternum or right shoulder; nausea, vomiting, inflammatory signs. Empyema if pus fills gallbladder.
Calculous: over 90 percent of acute cholecystitis; stone obstructs outflow, chemical reaction, edema, compromised blood supply, possible gangrene and perforation. Secondary infection in about 50 percent (E. coli, Klebsiella, Streptococcus).
Acalculous: no stones; after major surgery, orthopedic procedures, severe trauma, burns, multiple transfusions; bile stasis and viscosity.
B. Cholelithiasis
Prevalence: 5 to 20 percent of women 20 to 55; 25 to 30 percent of women over 50; about 50 percent of women by 70. Most of 15 million Americans with stones have no pain.
Pigment stones (10 to 25 percent): unconjugated pigment precipitates; risk with cirrhosis, hemolysis, biliary infection; cannot be dissolved, must be removed surgically.
Cholesterol stones (about 75 percent): bile supersaturated with cholesterol; women 2 to 3 times men, usually over 40, multiparous, obese; oral contraceptives, estrogens, clofibrate; age; ileal resection or disease; diabetes.
Risk factors (Chart 44-1): diabetes, frequent weight changes, ileal resection or disease, estrogen, obesity, rapid weight loss, women (multiple pregnancies, Native American or southwestern US Hispanic).
C. Clinical Manifestations
May be silent. Epigastric fullness, distention, vague RUQ pain after fried or fatty meal.
Biliary colic: stone obstructs cystic duct; excruciating RUQ pain radiating to back or right shoulder; nausea, vomiting several hours after a heavy meal; restless; RUQ tenderness on deep inspiration limits inspiratory excursion; fever and palpable mass with acute cholecystitis. If stone stays lodged: abscess, necrosis, perforation, peritonitis.
Analgesia: morphine traditionally avoided (sphincter of Oddi spasm) but this is controversial; morphine is preferred for acute pain and all opioids affect the sphincter somewhat.
Jaundice (CBD obstruction) with marked pruritus.
Dark urine; grayish, putty, or clay-colored stools.
Deficiency of fat-soluble vitamins A, D, E, K (bleeding from vitamin K deficiency).
D. Diagnosis (Table 44-1)
Abdominal x-ray: only 10 to 15 percent of stones visible.
Ultrasonography: procedure of choice; rapid, accurate (90 percent), no radiation, usable with jaundice; best after overnight fast.
Cholescintigraphy (HIDA-type radionuclide scan): acute cholecystitis or duct blockage; used when ultrasound inconclusive (acalculous).
Oral cholecystography: if ultrasound unavailable; iodine contrast 10 to 12 hours before; check iodine or seafood allergy.
MRCP: visualizes biliary tree and obstruction.
ERCP: side-viewing endoscope into duodenum, contrast into biliary and pancreatic ducts; also treats CBD stones (sphincterotomy, extraction). NPO several hours before; IV sedation; glucagon or anticholinergics may be given; afterward monitor VS, signs of perforation and infection, respiratory and CNS depression, hypotension, oversedation, vomiting (glucagon).
Percutaneous transhepatic cholangiography (PTC): rarely used; needle through liver into bile duct; coagulation and platelets must be normal; broad-spectrum antibiotics; watch for bleeding, peritonitis, sepsis.
About 80 percent of acute gallbladder inflammation remits with rest, IV fluids, NG suction, analgesia, antibiotics; laparoscopic cholecystectomy follows once acute symptoms subside (usually a few days).
Ursodeoxycholic acid (UDCA) or chenodiol: dissolve small radiolucent cholesterol stones; 6 to 12 months; high recurrence; for those who refuse or cannot have surgery; not for frequent symptoms, cystic duct occlusion, or pigment stones.
Instrument removal: basket through T-tube tract; ERCP with sphincterotomy and basket or balloon (watch for bleeding, perforation, pancreatitis, sepsis).
Intracorporeal lithotripsy (laser or electrohydraulic) and extracorporeal shock wave lithotripsy (ESWL): mostly replaced by laparoscopic surgery.
F. Surgical Management
Preop: chest x-ray, ECG, LFTs; vitamin K if prothrombin low; nutrition support; teach turning and deep breathing; open procedures may need drains and NG tube.
Laparoscopic cholecystectomy: standard of care; 80 to 90 percent of candidates; CO2 pneumoperitoneum; no paralytic ileus; less pain; discharge same day or 1 to 2 days; full activity within 1 week. Conversion to open about 2.2 percent (US) when inflammation makes dissection unsafe. Most serious complication: bile duct injury (bile leak may appear days later). Right shoulder or scapular pain from migrating CO2: heating pad 15 to 20 minutes hourly, sit up, walk. Patient needs help at home for first 24 to 48 hours.
Open cholecystectomy: right subcostal incision; drain if bile leak; T-tube only with complications (retained CBD stone).
Older adults: biliary surgery is the most common operation; may lack typical fever, pain, chills, jaundice; may present with septic shock signs (oliguria, hypotension, mental change, tachycardia, tachypnea).
G. Nursing Process: Surgery for Gallbladder Disease
Preop teaching: stop smoking; avoid aspirin, NSAIDs, OTC and herbal products that alter coagulation; assess respiratory status and nutrition.
Diagnoses: acute pain; impaired gas exchange (high abdominal incision); impaired skin integrity (biliary drainage); impaired nutrition; lack of knowledge. Complications: bleeding, GI symptoms (bile leak, bowel injury).
Postop: low Fowler position; IV fluids; NG suction for open procedures; fluids within hours after laparoscopy; soft diet when bowel sounds return.
Pain: analgesics so the patient can turn, cough, deep breathe, ambulate; splint with pillow or binder.
Respiratory: deep breathe and cough every hour; incentive spirometry; early ambulation (also prevents VTE). Higher risk in older, obese, and lung-disease patients.
Biliary drainage: connect drain immediately; secure tubing with slack; keep bag below waist (common duct level); change dressings; bile is corrosive to skin. Watch for infection, bile leak, obstruction (jaundice, RUQ pain, nausea, vomiting, bile around tube, clay stools, VS change).
T-tube: may be elevated above abdomen so bile drains externally only if pressure builds; measure and record drainage every 24 hours; may be clamped 1 hour before and after meals after several days; removed in 7 days to 3 weeks. Observe stool color daily; I&O.
Nutrition: low fat, high carbohydrate and protein right after surgery; fat restriction usually lifted in 4 to 6 weeks as ducts dilate.
Complications: bleeding (VS, incision and drains, abdominal tenderness and rigidity); after laparoscopy report anorexia, vomiting, pain, distention, fever. Teach-back.
Teaching (Chart 44-2, laparoscopic): walk immediately; shower after 1 to 2 days; drive after 3 to 4 days; no lifting over 5 lb for about 1 week; let adhesive strips fall off; resume normal diet, add fat gradually if previously intolerant; surgeon visit 7 to 10 days; call for wound infection signs, fever of 37.7 C (100 F) or more for 2 days, nausea, vomiting, abdominal pain. Report jaundice, dark urine, pale stools, pruritus. One to three stools a day may occur and diminish over weeks to months.
III. Acute Pancreatitis
A. Overview
About 200,000 cases a year; 80 percent from gallstones or sustained alcohol use. Commonly described as autodigestion (mainly trypsin).
Interstitial edematous (most common; edema confined to gland; recovery within 6 months; still at risk for hypovolemic shock, electrolyte imbalance, sepsis) vs necrotizing (parenchymal or peripancreatic necrosis, sterile or infected; hemorrhage, thrombosis; cysts, abscesses, fluid collections; organ failure).
Mechanism: gallstone lodges at ampulla of Vater, obstructing pancreatic flow or causing bile reflux into pancreatic duct, activating enzymes; vasodilation, permeability, necrosis, hemorrhage.
Other causes: infection (mumps), duodenitis, blunt trauma, peptic ulcer, ischemia, hyperlipidemia, hypercalcemia, corticosteroids, thiazide diuretics, oral contraceptives, surgery or instrumentation near the pancreas, tobacco. Idiopathic up to 10 percent; hereditary.
Mortality 2 to 10 percent; 10 to 30 percent have severe necrotizing disease. Older adults: higher mortality and more MODS.
B. Clinical Manifestations
Severe midepigastric pain (major symptom), often 24 to 48 hours after a heavy meal or alcohol; radiates to back; worse after meals; unrelieved by antacids; vomiting does not relieve pain.
Distention, poorly defined mass, decreased peristalsis; guarding; rigid boardlike abdomen = peritonitis; ecchymosis in the flank or around the umbilicus = severe pancreatitis.
Fever, jaundice, confusion, agitation.
Hypotension and shock (protein-rich fluid loss into tissues and peritoneum); tachycardia, cyanosis, cold clammy skin; acute kidney injury common.
Two of three: upper abdominal pain; serum amylase or lipase over three times upper limit of normal; typical imaging (CT, MRI, ultrasound).
Amylase and lipase rise within 24 hours; amylase normal in 48 to 72 hours; lipase stays elevated longer; urinary amylase stays elevated longer than serum.
X-rays (pleural effusion), ultrasound, contrast CT, MRI (size, cysts, abscesses, pseudocysts); Hgb and Hct for bleeding.
Revised Atlanta: mild (no organ failure), moderately severe (transient organ failure or complications), severe (persistent organ failure over 48 hours). APACHE II, Ranson, BISAP; CRP, procalcitonin, BUN.
Ranson criteria (Chart 44-3): on admission: age over 55, WBC over 16,000, glucose over 200, LDH over 350, AST over 250. Within 48 hours: Hct fall over 10 percent, BUN rise over 5 mg/dL, calcium under 8 mg/dL, base deficit over 4, fluid sequestration over 6 L, PO2 under 60. Mortality: 2 or fewer signs 1 percent; 3-4 signs 15 percent; 5-6 signs 40 percent; over 6 signs 100 percent.
D. Medical Management
Withhold oral intake to rest the pancreas; enteral feeding preferred and started early when possible (prevents infection); parenteral if enteral not tolerated.
NG suction for nausea, vomiting, distention, paralytic ileus (not routine to limit secretion).
H2 blockers or PPIs may be given.
Pain: parenteral opioids (morphine, fentanyl, hydromorphone; PCA or bolus); WHO ladder with NSAIDs (caution with bleeding risk); high-dose opioids worsen ileus.
ICU: correct fluid, blood loss, low albumin; hemodynamic and ABG monitoring; antibiotics only if infection (prophylactic not recommended); insulin for hyperglycemia, target 140 to 200 mg/dL in critically ill (avoid under 140); antiemetics.
Respiratory: elevated diaphragm, infiltrates, effusions, atelectasis; hypoxemia common even with normal x-ray; oxygen to mechanical ventilation.
Biliary drains and pancreatic duct stents via endoscopy.
Surgery: diagnostic laparotomy, drainage, resection or debridement of infected necrosis; open incision irrigated and repacked every 2 to 3 days; multiple sump drains.
Postacute: low-fat, low-protein oral feedings gradually; no caffeine or alcohol; stop thiazides, steroids, oral contraceptives if implicated; follow-up imaging or ERCP.
E. Nursing Management (Chart 44-4)
Pain: frequent assessment with pain scale; opioids; NPO; bed rest (reduces metabolism and secretions); NG drainage; report unrelieved or increasing pain (may be pancreatic hemorrhage); reposition every 2 hours; nonpharmacologic methods. Simple repeated explanations (patient often confused).
NG tube comfort: water-soluble lubricant at nares, oral hygiene, alcohol-free gargles.
Breathing: semi-Fowler position; reposition frequently; pulse oximetry and ABGs; cough, deep breathe, incentive spirometry every hour; oxygen; antibiotics; hypothermia blanket for fever.
Nutrition: daily weights, labs; glucose every 4 to 6 hours with enteral or parenteral nutrition; between attacks the text calls for a high-protein, low-fat diet, while Chart 44-4 lists high-carbohydrate, low-fat, low-protein (textbook inconsistency; low fat is consistent); avoid heavy meals, alcohol, excess coffee, spicy foods.
Skin: turn every 2 hours; protect skin from drainage; WOC nurse; specialty beds.
Fluid and electrolytes: skin turgor, mucous membranes, daily weight, I&O including NG output, girth if ascites; IV fluids and blood products; emergency medications at hand; report falling BP and urine output (shock, AKI); urine output goal at least 0.5 mL/kg/h; keep IV calcium gluconate or chloride available (tetany); watch low calcium and magnesium.
Pancreatic necrosis: major cause of death (hemorrhage, septic shock, MODS); step-up approach: percutaneous or endoscopic catheter drainage first, then minimally invasive debridement, surgery only if these fail; targeted antibiotics; no prophylactic antibiotics.
Teaching: weakness for weeks to months; repeat education; avoid high-fat foods, heavy meals, alcohol; signs to report; diet changes for gallstone cause; AA referral for alcohol cause; teach-back.
IV. Chronic Pancreatitis
Progressive destruction with fibrosis; obstruction of pancreatic duct, CBD, duodenum. About 90 percent of exocrine function lost before symptoms.
Alcohol causes 70 to 80 percent in Western societies (protein plugs, calculi, direct toxicity); malnutrition worldwide; smoking. Incidence 50 times greater with alcoholism. Usually ages 40 to 60.
Recurring severe upper abdominal and back pain with vomiting; opioids may not relieve; opioid dependence risk; some have painless disease; pain may “burn out.”
Weight loss in over 80 percent (anorexia, fear of eating). Malabsorption late (10 percent function left): steatorrhea. Calcification and duct stones.
Diagnosis: CT first (calcifications, duct changes); MRCP; ultrasound; EUS; ERCP; glucose tolerance test (diabetes); fecal fat for steatorrhea; amylase may rise in exacerbations.
Nonsurgical: endoscopic stone removal, stenting, cyst drainage; WHO ladder, nonopioids first; antioxidants, antidepressants; EUS-guided celiac nerve block; yoga, mindfulness. No treatment relieves pain if drinking continues.
Diabetes from islet dysfunction: diet, insulin, or oral agents; warn of severe hypoglycemia with alcohol. Pancreatic enzyme replacement for malabsorption and steatorrhea.
Surgery: pancreaticojejunostomy (Roux-en-Y; over 85 percent pain relief within 6 months, may recur); sphincter revision, cyst drainage, stent, resection, Whipple, Beger or Frey operations; gallstone cause: CBD exploration, cholecystectomy, sphincterotomy, T-tube. About two thirds managed endoscopically or laparoscopically.
V. Pancreatic Cysts (Pseudocysts)
Amylase-rich fluid collections walled by fibrous granulation tissue (no epithelial lining), 4 to 6 weeks after acute pancreatitis; most common pancreatic “cyst.”
Diagnosis: ultrasound, CT, ERCP. Large ones displace stomach or colon; drain into GI tract or through skin.
External drainage is profuse and enzyme rich, destructive to skin: skin ointment, continuous suction, keep suction tube in place, WOC nurse.
VI. Cancer of the Pancreas
Fourth leading cause of cancer death in men, fifth in women; rare before 45; peaks in 70s-80s; highest in African American men. Risks: smoking (pack-years), heavy alcohol, diabetes, chronic and hereditary pancreatitis, obesity, industrial chemicals, high-fat or high-meat diet.
About 70 percent in the head. Only 7 percent diagnosed early; 80 to 85 percent unresectable at detection; 5-year survival about 7 percent.
Classic signs: pain, jaundice, or both in over 80 percent, plus weight loss (often late). Rapid profound weight loss; vague boring mid-back pain, worse at night and supine, relieved by sitting up and leaning forward; ascites; new diabetes (glucosuria, hyperglycemia) may be an early sign; meals worsen epigastric pain before jaundice and pruritus.
Diagnosis: spiral CT (85 to 90 percent accurate), MRI/MRCP, EUS with fine-needle aspiration, ERCP; percutaneous biopsy for unresectable tumors (risk of seeding); tumor markers (CA 19-9, CEA, DU-PAN-2) track progression but are not specific.
Treatment: usually palliative; gemcitabine is standard for metastatic disease (with erlotinib or nab-paclitaxel); 5-FU, leucovorin, irinotecan; capecitabine or 5-FU as radiosensitizers; intraoperative radiation; biliary stent for jaundice.
Nursing: pain control (liberal opioids, PCA); nutrition; skin care for jaundice, pruritus, weight loss; specialty mattress; symptom clusters (affective, GI, gustatory, discomfort; fatigue, poor sleep and appetite, weight loss most common); end-of-life preferences, hospice.
A. Tumors of the Head of the Pancreas
60 to 80 percent of pancreatic tumors; obstruct CBD: jaundice, clay stools, dark urine, malabsorption of nutrients and fat-soluble vitamins, pain, pruritus, anorexia, weight loss, malaise. (Gallstone jaundice is usually intermittent.)
Preop: high-protein diet with pancreatic enzymes, hydration, vitamin K, treat anemia, enteral or parenteral nutrition, blood products; percutaneous biliary drainage to relieve jaundice.
Whipple procedure (pancreaticoduodenectomy): removes gallbladder, part of stomach, duodenum, proximal jejunum, head of pancreas, distal CBD; remaining pancreas and stomach joined to jejunum. Pylorus-preserving variant. Total pancreatectomy if no extension. Cholecystojejunostomy if unresectable.
Postop complications: hemorrhage, vascular collapse, hepatorenal failure. ICU; NG suction and parenteral nutrition; watch for malabsorption and diabetes; emotional support.
Teaching: pain, drains, incision, parenteral nutrition, lifelong pancreatic enzyme replacement, low-fat diet, vitamin supplements, signs of complications; possible rehab or long-term care; hospice.
B. Islet Cell Tumors and Hyperinsulinism
Neuroendocrine tumors (NETs): insulinomas (hypersecretion of insulin) and nonfunctioning islet cell cancer.
Insulinoma: hypoglycemia (weakness, confusion, seizures) relieved immediately by oral or IV glucose; 5-hour glucose tolerance test; surgical removal; partial pancreatectomy for hyperplasia. Preop watch for hypoglycemia, glucose ready; postop monitor glucose.
Hyperinsulinism: hunger, nervousness, sweating, headache, faintness, seizures, unconsciousness; glucose may fall below 30 mg/dL; surgery is the only successful treatment; about 15 percent later develop diabetes.
C. Ulcerogenic Tumors (Zollinger-Ellison)
Gastrin-secreting islet tumors cause severe acid hypersecretion and ulcers in stomach, duodenum, jejunum; nausea, vomiting, diarrhea, burning upper abdominal pain.