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Cholelithiasis
Stones in the gallbladder
Risk factors
Over 40
Obesity
Female
Multiparous
S/S
Pain, depending on the severity of gallstones
Fullness, abdominal distention, RUQ pain
Biliary colic – follows a meal rich in fried or fatty foods
Cholecystitis
Acute or chronic inflammation of the gallbladder
Calculous cholecystitis – gallbladder stone obstructs bile outflow
Acalculous cholecystitis – absence of gallstones
Risk for secondary infection and perforation
S/S – RUQ pain, may radiate to the midsternal/right shoulder, nausea, vomiting, and s/s of acute inflammation
Gallbladder disease subjective and objective assessment
Subjective
Pain – Murphy’s Sign
Distention/fullness
N/V
Objective
Fever
Jaundice/pruritic
Stool and urine characteristics
Labs
CBC
PT/INR and PTT
Aspartate aminotransferase (AST)
Alanine aminotransferase (ALT)
Diagnosis of gallbladder disease
Ultrasound (90% accuracy), X-ray
Endoscopic retrograde cholangiopancreatography (ERCP)
Stone removal
ERCP Pre-procedure
Educate patient on the procedure and their role
NPO
Consent
IV
ERCP post-procedure
Monitor patient condition, vital signs, assessing for signs of perforation or infection
Side effects of any meds administered during the procedure (sedatives)
Risk for pancreatitis
Gallbladder disease implementations
Reduce the incidence of acute episodes of pain and cholecystitis by supportive and dietary management
Remove the cause by pharmacological therapy, endoscopic procedures, and surgical intervention
Nutrition and supportive therapies
Nutrition and supportive therapies for gallbladder disease
80% of patients with mild acute gallbladder inflammation achieve remission with bowel rest, IV fluids, nasogastric suction, analgesia, and antibiotics
Surgical intervention after acute symptoms subsides
Advancing diet: low-fat liquids
High protein supplements, skim milk, cooked fruits, rice/tapioca, lean meats, non-gas forming vegetables, bread, coffee, or tea
Avoid eggs, cream, pork, fried foods, cheese, rich dressings, gas-forming vegetables, and alcohol
Fatty foods may exacerbate episodes
Pharmacological interventions for gallbladder disease
Analgesics
Anti-emetics
IV fluids
Ursodeoxycholic acid (UDCA) or Chenodeoxycholic acid (chenodiol or CDCA) PO
Mono-octanoin or methyl tertiary butyl ether
Lithotripsy
Surgery
Ursodeoxycholic acid (UDCA) or Chenodeoxycholic acid (chenodiol or CDCA) PO
Medication used to treat gallbladder disease
Reduces the size or dissolves small gallstones (cholesterol stones)
Prevents more gallstones from occurring
6-12 months of therapy required
Not eligible for patients with frequent symptoms, cystic duct occlusion, or pigment stones
Used if surgery is contraindicated or refused
Mono-octanoin or methyl tertiary butyl ether
Medication used to treat gallbladder disease
Infused through a percutaneous tube directly into the gallbladder or via ERCP
Used to dissolve gallstones
Lithotripsy
Laser pulse or shock wave therapy causing gallbladder stones to fragment
Laparoscopic cholecystectomy
Surgical procedure to treat gallbladder disease
Carbon dioxide to inflate abdomen
Fiberoptic scope with camera
Removed through abdomen incision
May require a Jackson-Pratt drain
Monitor for peritonitis, infection, bile duct injury, or bleeding
Laparoscopic cholecystectomy post-op care
Airway
Breathing (CDB/IS)
Circulation (VS, DVT)
Pain
Nausea/vomiting
Bowel sounds
Incision/drain care
Activity
Low-fat diet
Gallbladder disease surgical implementations
Laparoscopic cholecystectomy
Open cholecystectomy
Transhepatic biliary catheter
Acute pancreatitis
80% caused by cholelithiasis or alcohol abuse
Mild – interstitial (edematous) pancreatitis
Severe – necrotizing pancreatitis
Pathology – autodigestion of the pancreas
Subjective assessment of acute pancreatitis
Alcohol use
Pain: mid-epigastrium, back
N/V
PMH
Objective assessment of acute pancreatitis
Integumentary
Respiratory
GI/GU
VS
CBC, BMP
Hypocalcemia, hyperglycemia
Amylase/lipase
Ultrasound
CT
CT for acute pancreatitis
Check creatine
Teach about warm feeling
Screen for allergies
Contrast? Start IV
Assess for reactions
NPO if ordered
Pain implementations for acute pancreatitis
Parenteral opioids
PCA
Antibiotics
PPI
NG to LIS
Non-pharmacological
Biliary drains and stents
Bed rest
Imbalance nutrition implementations for acute pancreatitis
NPO
TPN
Anti-emetics
Electrolyte replacement – Calcium
Eliminate alcohol/caffeine
Albumin levels
Daily weights
Accu checks/insulin administration
Pancrelipase pancreatic enzyme
Creon
Pancreatic enzyme
Deficient fluid volume implementations for acute pancreatitis
IV fluids
Blood products as needed
Anti-emetics
Daily weights
Albumin infusion
Risk for impaired gas exchange implementations for acute pancreatitis
Positioning – Semi-Fowler’s
C&DB
IS
ABGs
Oxygen as needed
Pancreatic cancer risk factors and diagnosis
RF: smoking, alcohol, diets high in fats/meats, obesity, chemicals/toxins
Metastasis likely due to malignant cells shedding into the peritoneal cavity (lung and liver)
Diagnosis: spiral CT, ERCP with fine-needle biopsy
Usually don’t seek medical attention until later stages
Pancreatic cancer surgical treatment
Pancreatoduodenectomy (Whipple procedure)
Total pancreatectomy)
Nursing care before and after
Nutritional needs
Pain control
Infection/bleeding precautions
Blood glucose control
Vital signs
Causes of liver failure
Viral hepatitis
Drugs and chemicals: Acetaminophen, antidepressants, anticonvulsants, antifungals
Autoimmune
Wilson’s disease – inherited disease; excessive amount of copper
Hemochromatosis – iron overload
Nonalcoholic fatty liver disease
Diagnosis of hepatic disorders
AST, ALT, GGT
Look for underlying cause
Virology testing
Biopsy
Informed consent
Post-procedure
Right-side lying
Monitor VS and for complications
Ultrasound
Clinical manifestations of hepatic disorders
Integumentary – jaundice, pruritus, spider angioma, petechiae
Endocrine – inability to metabolize hormones (estrogen and testosterone)
Hematologic – anemia, thrombocytopenia, coagulation disorders, splenomegaly
Metabolic – electrolyte imbalances (hypokalemia, hyponatremia, hypoalbuminemia)
Cardiovascular – fluid retention, peripheral edema, ascites
GI – changes in bowel, N/V, esophageal/gastric varices, hemorrhoidal varices
Neurological – hepatic encephalopathy, asterixis
Portal HTN
Ascites
Subjective data for hepatic disorders
PMH – family history
Medications – prescribed and OTC, herbal
Pain and weakness
Objective data for hepatic disorders
Vitals
Bleeding – easy bruising, hypotension, blood in emesis or stool
CV – edema
Integumentary – jaundice, ecchymoses, pallor
MSK – atrophy
Respiratory – hypoxia
GI/GU – ascites, palpable liver and spleen
Neurological – AMS, asterixis, hepatic encephalopathy
Labs for hepatic disorders
CBC/BMP
Albumin
Ammonia
Bilirubin
Platelet
PT/INR
LFTs
PT/INR
Prothrombin time/INR: measures the body’s ability to clot
Elevated INR = risk of bleeding: Vitamin K → increases coagulation
Implementations for imbalanced nutrition in hepatic disorders
High-CHO, protein, and calorie diet (UNLESS ammonia levels are high*) – may need to do enteral feeding
Low sodium (500-2000 mg/day)
Vitamin supplements (A, D, E, K)
Implementations for skin integrity in hepatic disorders
Lotions
Medications
Pruritus: hydroxyzine (PO) – antihistamine
Meticulous skin care
Edematous areas are more prone to breakdown
Specialty mattress
Turning schedule
Mobility
Implementations for excess fluid in hepatic disorders
Fluid and sodium restriction
Diuretics
Ascites
Paracentesis
Transjugular intrahepatic portosystemic shunt (TIPS)
Positioning
Electrolyte replacement
Albumin – can be given through an IV
Paracentesis
Procedure to treat ascites
Informed consent
Empty bladder to avoid bladder puncture
Obtain fluid samples for culture
Aseptic technique
Assist with positioning during procedure
Implementations for esophageal or gastric varices
IV fluids – aggressive fluid resuscitation; place a large-bore IV
Blood transfusion
CBC, BMP, clotting factors
Foley catheter (strict I&Os)
Balloon tamponade
Endoscopic sclerotherapy/variceal ligation banding
TIPS procedure
Beta-blockers – used to prevent first episode of bleeding
TIPS procedure
creates a pathway between the portal vein and hepatic vein in the liver to reduce portal HTN and swelling