MANAGEMENT OF PATIENTS WITH DISORDERS OF THE
ACCESSORY ORGANS
CHOLECYSTITIS AND CHOLELITHIASIS
Cholecystitis
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Acute inflammation of the gall bladder
Forms: Calculous and Acalculous
Calculous Cholecystitis
➔ Most common form of cholecystitis
➔ Bile flow obstruction due to gallbladder stones
➔ Autolysis, edema, blood vessel compression Gangrene
may result
Acalculous Cholecystitis
➔ Bile flow obstruction without gallbladder stones
➔ May occur after a major surgical operation, severe
trauma or burns
➔ Predisposing factors: torsion, cystic duct obstruction, a
primary bacterial infection of the gallbladder, multiple
blood transfusions
➔ Bile stasis and increased viscosity
Cholelithiasis
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Stone formation in the gall bladder
Occurs due to hypercholesterolemia high incidence
among women 4fs (female, fat, fertile, forty)
STATIN use increases bile concentration
Transcribed by Mika Galabin
Risk Factors for Cholelithiasis
➔ Obesity
➔ Women, especially those who have had multiple
pregnancies or who are Native American or U.S.
Southwestern Hispanic ethnicity
➔ Frequent changes in weight
➔ Rapid weight loss (leads to rapid development of
gallstones and high risk of symptomatic disease)
➔ Treatment with high-dose estrogen (ie, in prostate
cancer)
➔ Low-dose estrogen therapy-a small increase in the risk
of gallstones
➔ Ileal rescretion or disease
➔ Cystic fibrosis
➔ Diabetes mellitus
Pathophysiology
➔ Gallstone formation
Pigment stones (unconjugated pigments from
bile)
Cholesterol stones (bile supersaturation)
➔ Inflammatory changes in the gallbladder
Clinical Manifestations
➔ Usually asymptomatic
➔ RUQ pain that radiates to scapular area or right
shoulder
➔ Steatorrhea
➔ Cholecystitis-Charcot’s TRIAD: fever, RUQ pain and
jaundice
Diagnostic Tests
➔ Ultrasound
➔ Abdominal Xray
➔ Cholecyscintigraphy
➔ Cholecystography
➔ ERCP
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Nursing Management
➔ Pain control
➔ Improve respiratory status
➔ Promote skin care and biliary drainage
➔ Low-fat non-gas forming diet/foods
➔ NGT insertion
➔ Antibiotic (after culture) ascending infection
CHRONIC LIVER DISEASE
Cirrhosis: Alcoholic Liver Disease
Progressive destruction of the liver
Causes
➔ Alcoholic liver disease
➔ Biliary cirrhosis - Associated with immune
disorders
Linked with chronic
➔ Postnecrotic cirrhosis hepatitis or long-term exposure to toxic materials
➔ Metabolic - Usually caused by genetic metabolic
storage disorders
➔ Extensive diffuse fibrosis
Interferes with blood supply
Bile may back up.
➔ Loss of lobular organization
➔ Degenerative changes may be asymptomatic
until the disease is well advanced.
➔ Liver biopsy and serologic test to determine the
cause and extent of damage
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Medical-Surgical Management
➔ Intracorporeal lithotripsy
(with the aid of an endoscope stone is directly
pulverized by the hydraulic process)
➔ Laparoscopic Cholecystectomy
Postop: T-tube- 200-500 ml/day
Maintain patency
Prevent bile leakage to peritoneum
Monitor bile drainage (separate recording sheet)
Initial Stage
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FATTY LIVER
Enlargement of the liver
Asymptomatic and reversible with
reduced alcohol intake
Second Stage
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ALCOHOLIC HEPATITIS
Inflammation and cell necrosis
Fibrous tissues
formation—irreversible change
Third Stage
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END-STAGE CIRRHOSIS
Fibrotic tissue replaces normal
tissue.
Little normal function remains.
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Pathophysiology
Transcribed by Mika Galabin
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Live insult, alcohol
ingestion, viral hepatitis,
exposure to toxins
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Hepatocyte Damage
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Liver Inflammation
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Alterations in blood and
lymph flow
Signs and Symptoms
➔
Increased WBC,
Fatigue, N/V, Pain,
Fever, Anorexia
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Liver Necrosis
➔ Decreased ADH and
aldosterone
detoxification
➔
Edema
➔
Decreased
androgen, and
estrogen
➔
Palmar erythema,
testicular atrophy,
spider angiomas,
gynecomastia, loss
of body hair,
menstrual changes
➔
Decreased
metabolism of CHO,
CHON, and fats
➔
Ascites, Edema,
Hypoglycemia, and
Malnutrition,
Steatorrhea
➔
Decreased vitamin K
absorption
➔
Bleeding tendency
➔
Decreased bilirubin
metabolism
➔
Hyperbilirubinemia
= Jaundice
-
Edema, esophageal
varices,
hemorrhoids, caput
meducae, ascites
Splenomegaly=
ANEMIA,
THROMBOCYTOPEN
IA, LEUKOPENIA Bleeding, Delayed
Wound Healing,
Infection
Liver necrosis
➔ Liver fibrosis and
scarring
Portal
hypertension
-
➔
-
-
Liver failure
Inability to
metabolize
ammonia to
urea
-
Increased serum
ammonia, Fetor
hepaticus
Hepatic
encephalopathy
-
Asterixis, Resp.
Acidosis, Sleep
Alteration, Dec LOC
Hepatic coma
-
Death
Jaundice
➔ Jaundice is a symptom where the skin and eyes
become yellow
➔ Yellowing is associated with the accumulation of
bilirubin in the skin, most often caused by liver and
gallbladder disorders.
➔ Increased Bilirubin Direct >.1-.3mg/dl indirect >.2- .7
mg/dl
➔ A symptom of a disease
➔ Yellow pigmentation of the skin
➔ Due to accumulation of bilirubin pigment
➔ Usually observed first in the sclera (interest)
➔ Kernicterus (brain) fatal
Clinical Manifestations
➔ Deep orange, foamy urine
➔ Dark tea-colored urine
➔ Clay-colored stool
➔ Severe itchiness-bile salts
➔ Steatorrhea
Jaundice Management
➔ Control pruritus
➔ Calamine lotion
➔ Baking soda
➔ NaHCO3
➔ Antihistamine
➔ Soothing baths
➔ Drug
Cholestyramine = it binds bile salts in the intestine
and eliminated via feces.
➔ Look for the cause and manage it
Portal Hypertension
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Caused by portal vein obstruction
Clinical Manifestations
➔ Esophageal varices
➔ Umbilical varices (caput medusae)
➔ Hemorrhoids
➔ Fluid extravasation
➔ Ascites and edema
➔ ^ Collateral circulation
➔ Spider angioma (dilated vessels w/d red center)
➔ Palmar erythema (inc Estrogen)
➔ Esophageal varices
Ascites
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Accumulation of free fluids in the peritoneum
Assessment: P.E reveals fluid wave, shifting dullness
Increased amount of fluid between abdominal structures
Effects of Advanced Cirrhosis
Pathophysiology
➔ Cirrhosis with portal hypertension
➔ Splanchnic arterial vasodilation
➔ Decrease in circulating arterial blood volume
➔ Activation of renin-angiotensin and sympathetic
nervous systems and antidiuretic hormone
➔ Kidney retains sodium and water
➔ Hypervolemia
➔ Persistent activation or systems for retention of sodium
and water; ascites and edema formation
➔ Continued arterial underfilling; cycle repeats
Transcribed by Mika Galabin
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Medical Management
Supportive:
➔ Modify diet
➔ Bed rest
➔ Albumin
➔ Diuretic Therapy
➔ Surgery
Paracentesis - assessed for cell count,specific
gravity, protein, microorganismS
➔ Indicated for respiratory and abdominal distress
Empty bladder before procedure
Monitor BP
Remove 1-1.5L of fluid
Medical Management
➔ Iced normal saline lavage
➔ Transfusion with FWB
➔ Vit. K
➔ Sengstaken Blakemore tube (3 lumens)
➔ Injection sclerotherapy
➔ Surgery
➔ Ligation of esophageal varices
➔ Surgery for portal HPN
Nursing Considerations
➔ Monitor nutrition
➔ Modify diet
➔ Restrict sodium (200-500mg/day)
➔ Restrict fluids (1000-1500 ml/day)
➔ High calorie diet
➔ Prevent increasing edema
➔ Administer diuretics as ordered
➔ Monitor I and O
➔ Measure abdominal girth
➔ Adminster salt poor albumin to replace vascular volume
(dextran70,Haemaccel)
Esophageal Varices
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Dilatation of the veins of esophagus
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Resulting in distension,hypertrophy,increase fragility
Assessment
➔ Anorexia,N & V, hematemesis, fatigue, weakness
➔ Splenomegaly,ascites,caput medusae,peripheral edema
Pathophysiology
➔ Portal hypertension (caused by resistance to portal flow
and increased portal venous flow)
➔ Development of pressure gradient of 12 mmHg or
greater between portal vein and inferior vena cava
(portal pressure gradient)
➔ Venous collaterals develop from high portal system
pressure to systemic veins in esophageal plexus,
hemorrhoidal plexus and retroperitoneal veins
➔ Abnormal varicoid vessels from in any of above locations
may
rupture
causing
life-threatening
➔ Vessels
hemorrhage.
Nursing Considerations
➔ Promote comfort
➔ Monitor for further bleeding and signs of shock
➔ Health teaching
Minimizing esophageal irritation ( avoid ASA,
alcohol)
Avoid increased abdominal, thoracic pressure
Report signs of hemorrhage
➔ Monitor pt with Sengstaken Blakemore tube
a. Facilitate placement of tube
b. Prevent dislodgment by positioning (semi-fowlers)
c.
Keep scissors at the bedside at all times
d. Monitor Respiratory status: if distress occurs cut
the tube to deflate and remove the tube
e.
Care of nares to avoid cracking
f.
Label each lumen, maintain the prescribed
amount of pressure of the esophageal balloon, and
deflate as ordered to avoid necrosis
Hepatic Encephalopathy
Liver unable to convert ammonia to urea causing
neurologic symptoms
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Aggravated by GI bleeding
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Diagnostics test: Serum ammonia Level
Assessment
➔ Change of mental function (irritability, insomnia, slight
tremor slurred speech, Babinski reflex, hyperactive
reflexes)
➔ Progressive disease (asterixis,d disorientation, apraxia,
tremors, fetor hepaticus)
➔ Late manifestation of the disease (Coma, absent
reflexes)
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Transcribed by Mika Galabin
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Nursing Considerations
➔ Conduct neurologic assessment, report deterioration
➔ Restrict protein in Diet. High CHO, Vit. K
➔ Administer enemas, cathartics intestinal antibiotics, and
lactulose
➔ Protect pt from injury
hepatotoxic
drugs
(acetaminophen,
➔ Avoid
phenothiazines)
➔ Bed rest
Drugs
➔ Neomycin (bacterial flora responsible for NH4
production)
➔ Lactulose (promote excretion of NH4 and cause osmosis
decreasing stool transit time)
ACUTE PANCREATITIS
Inflammation of the pancreas
➔ Results in autodigestion of the tissue
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May be acute or chronic
➔ Acute form considered a medical emergency
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Pancreas lacks a fibrous capsule
➔ Destruction may progress into tissue surrounding
the pancreas
➔ Substances released by necrotic tissue lead to
widespread inflammation
Hypovolemia and circulatory collapse may
follow.
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Chemical peritonitis results in bacterial peritonitis.
➔ Septicemia may result.
➔ Adult respiratory distress syndrome and acute renal
failure are possible complications.
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Causes
➔ Gallstones
➔ Alcohol abuse
➔ Sudden onset may follow the intake of a large meal
or a large amount of alcohol
Clinical Manifestations
➔ Abdominal pain (constant mid epigastric, periumbilical
that may radiate to back or flank and substernal with
DOB aggravated by eating)
➔ Client assumes the fetal position to relieve pressure
(celiac plexus nerve)
➔ Involuntary abdominal guarding
➔ Down or absent bowel sound
➔ Turner’s sign-bluish discoloration of the flank
(ecchymoses)
➔ Cullen’s sign-periumbilical bluish discoloration
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Signs of Shock
Caused by o hypovolemia
➔ Low-grade fever until infection develops
Body temperature may then rise significantly.
➔ Abdominal distention and decreased bowel sounds
Decreased peristalsis and paralytic ileus
Diagnostic Tests
➔ Serum amylase levels—first rise, then fall after 48 hours
➔ Serum lipid levels are elevated.
➔ Hypocalcemia
➔ Leukocytosis
Treatment
➔ Oral intake is stopped.
➔ Treatment of shock and electrolyte imbalances
➔ Analgesics for pain relief
Pathophysiology of Acute Pancreatitis
➔
Medical Management
➔ Drug
Analgesics (Demerol)
Smooth
muscle
relaxants
(papaverine,
nitroglycirine)- relieve pain
Anticholinergic (atropine)-decrease pancreatic
stimulation
Antacids decrease pancreatic stimulation
H2 antagonists, vasodilators
Transcribed by Mika Galabin
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➔ Diet modification - NPO - Peritoneal lavage
Nursing Considerations
➔ Administer analgesics and other meds
➔ Do not give Morphine
➔ Withold food/fluid to decrease pancreatic stimulation in
acute case
➔ NGT
position(Knee
chest,
fetal)
➔ Nonpharmacologic;
Relaxation techniques, restful environment
➔ Diet High protein, CHO; low fat
➔ Small frequent feeding
➔ Avoid caffeine, alcohol
➔ WOF signs of complications:
Nausea and Vomiting
Abdominal distension
Persistent weight loss
Severe epigastric pain or back pain
Irritability
Confusion
Fever
Transcribed by Mika Galabin
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