CHOLELITHIASIS

DEFINITION
• Calculi, or gallstones, usually form in the gallbladder from the solid constituents of bile and vary greatly in size,
shape, and composition.
- Smeltzer, S.C., Bare, B.G. Brunner & suddarth’s Textbook of Mecial-Surgical Nursing !0th Edition.
• Stones on the gallbladder or biliary tree are referred to collectively as cholelithiasis. Most patients have multiple
stones, sometimes several dozen. Most gallstones (80%) are cholesterol gallstones, which form when bile
becomes oversaturated with cholesterol. Pigment gallstones, accounting for the remaining 20% of gallstones are
composed of bilirubin and bile substances other than cholesterol.
- McConnell, T. H., The Nature of Disease Pathology for the Health Professions. 2007
• Gallstones are hard, pebble-like deposits that form inside the gallbladder. Gallstones may be as small as a grain
of sand or as large as a golf ball, depending on how long they have been forming.
- http://www.nlm.nih.gov/medlineplus/ency/article/000273.htm

ANATOMY AND PHYSIOLOGY

Gastroinstestinal Tract
The gastrointestinal tract (GIT) consists of a hollow muscular tube starting from the oral cavity, where food enters
the mouth, continuing through the pharynx, esophagus, stomach and intestines to the rectum and anus, where food is
expelled. There are various accessory organs that assist the tract by secreting enzymes to help break down food into its
component nutrients. Thus the salivary glands, liver, pancreas and gall bladder have important functions in the digestive
system. Food is propelled along the length of the GIT by peristaltic movements of the muscular walls. The primary
purpose of the gastrointestinal tract is to break down food into nutrients, which can be absorbed into the body to provide
energy.

Focus: GALLBLADDER

The gallbladder (or cholecyst, sometimes gall bladder) is a small organ whose function in the body is to harbor bile and
aid in the digestive process.
Anatomy
• The cystic duct connects the gall bladder to the common hepatic duct to form the common bile duct.
• The common bile romero duct then joins the pancreatic duct, and enters through the hepatopancreatic ampulla at
the major duodenal papilla.
• The fundus of the gallbladder is the part farthest from the duct, located by the lower border of the liver. It is at the
same level as the transpyloric plane.
Microscopic anatomy
The different layers of the gallbladder are as follows:
• The gallbladder has a simple columnar epithelial lining characterized by recesses called Aschoff's recesses,
which are pouches inside the lining.
• Under the epithelium there is a layer of connective tissue (lamina propria).
• Beneath the connective tissue is a wall of smooth muscle (muscularis externa) that contracts in response to
cholecystokinin, a peptide hormone secreted by the duodenum.
• There is essentially no submucosa separating the connective tissue from serosa and adventitia.
Size and Location of the Gallbladder
The gallbladder is a hollow, pear-shaped sac from 7 to 10 cm (3-4 inches) long and 3 cm broad at its widest point.
It consists of a fundus, body and neck. It can hold 30 to 50 ml of bile. It lies on the undersurface of the liver’s right lobe
and is attached there by areolar connective tissue.
Structure of the Gallbladder
Serous, muscular, and mucous layers compose the wall of the gallbladder. The mucosal lining is arranged in folds
called rugae, similar in structure to those of the stomach.
Function of the Gallbladder
The gallbladder stores bile that enters it by way of the hepatic and cystic ducts. During this time the gallbladder
concentrates bile fivefold to tenfold. Then later, when digestion occurs in the stomach and intestines, the gallbladder
contracts, ejecting the concentrated bile into the duodenum. Jaundice a yellow discoloration of the skin and mucosa,
results when obstruction of bile flow into the duodenum occurs. Bile is thereby denied its normal exit from the body in the
feces. Instead, it is absorbed into the blood, and an excess of bile pigments with a yellow hue enters the blood and is
deposited in the tissues.
The gallbladder stores about 50 mL (1.7 US fluid ounces / 1.8 Imperial fluid ounces) of bile, which is released
when food containing fat enters the digestive tract, stimulating the secretion of cholecystokinin (CCK). The bile, produced
in the liver, emulsifies fats and neutralizes acids in partly digested food.
After being stored in the gallbladder the bile becomes more concentrated than when it left the liver, increasing its
potency and intensifying its effect on fats. Most digestion occurs in the duodenum.
ETIOLOGY

Predisposing Factors Justification

Age (40 and above) Most internal functions decline as one ages. Inevitably resulting in organ degeneration
which also affects the body's metabolism of lipids.
Gender Gallstones is more frequent on women especially who had have had multiple pregnancies
or who are taking oral contraceptives. Increase level of Estrogen reduces the synthesis of
bile acid in women. Female sex hormones have long been suspected to have a side effect
of gallstone formation by altering respective bile constituents (mainly the FAT metabolism).
Ileal Disease/Resection People who have disease of the terminal ileum or who have undergone resection of the
terminal ileum deplete their bile salt pool and run a greater risk of developing cholesterol
gallstones.
Race Cholesterol stones are common in Northern Europe and in North and South America.
Genetics Most clinicians have an impression that gallbladder disease characterizes some families.
Indeed, the younger sisters of women with gallstone prove to have bile more highly
saturated with cholesterol than the younger sisters of women without gallstones, all of
which suggests that Cholelithiasis does run in families.
Inflammation and Inflammation or infection in the biliary structures may provide a focus for stone formation or
infection of the may alter the solubility of the constituents, fostering the development of a stone.
gallbladder-
Hemolytic Disease and In cirrhosis, at least two fifths of patients have gallstones. One possible mechanism behind
Hepatic Cirrhosis the appearance of pigment softness, so far unproven, is the excretion of unconjugated
bilirubin directly into the bile, something that might happen in patient with hemolysis or in
the cirrhotic with his high incidence of pigment stones, currently estimated at 27 %.
Bile stasis Brown pigment gallstones form when there is stasis of bile (decreased flow), for example,
when there are narrow, obstructed bile ducts.

Precipitating Factors Justification

Faulty Diet Excessive intake of high fat or cholesterol food such as pork meat, animal skin (e.g.
chicharon and chicken skin) can result to an increase in cholesterol level in the body,
making it hard for the liver to make bile enough to metabolized the all cholesterol present.
Excess cholesterol present builds up and increases the cholesterol serum level. Normal
Liver function would then try to compensate and excrete excess cholesterol to the bile plus
the body would reabsorb water from the bile making it more concentrated. Supersaturation
of Cholesterol along with other constituents of the bile (bilirubin, lecithin etc.) builds up
microcrystals. When microcrystals aggregate it would result to Gallstones.
Weight Loss Weight loss is associated with an increased risk of gallstones because weight loss
increases bile cholesterol supersaturation, enhances cholesterol crystal nucleation, and
decreases gallbladder contractility.
Obesity Obesity is a major risk factor for gallstones, especially in women. A large clinical study
showed that being even moderately overweight increases the risk for developing
gallstones. The most likely reason is that obesity tends to reduce the amount of bile salts in
bile, resulting in more cholesterol. Obesity also decreases gallbladder emptying.
Pregnancy Altered physiology of the biliary system during pregnancy may play a role in accelerating
the formation of stones in susceptible women.
Treatment with estrogen/ The contraceptive pill not only promotes thromobphlebitis but points to an endocrine
contraceptives background of gallstones by the risk of gallstones in young women taking the pill. This is
largely as a result of increased cholesterol secretion into the bile and a decrease in
chenodeoxycholic acid content, along with impaired emptying of the gallbladder brought
about by estrogen.
Frequent Starvation and Starvation decreases gallbladder movement causing the bile to become overconcentrated
Prolonged parenteral with cholesterol. The liver also secretes extra cholesterol into bile adding to the
nutrition supersaturation causing stone formation. Also, fasting persons have a diminished bile salt
pool and lithogenic bile.Gallbladder stasis plays a key role in permitting stone formation.
Defective or infrequent gallbladder emptying occurs in the settings of prolonged fasting,
rapid weight loss, pregnancy, and spinal cord injury.
Clofibrate use and other Drugs that lower the serum level of cholesterol, notably clofibrate, are associated with an
Antilipemic drugs increased incidence of gallstones. Clofibrate presumably increases the secretion of
cholesterol into the bile and apparently also decreases bile acid synthesis, so increasing
the cholesterol saturation of the bile. Clinical reflection of these physiologic abnormalities
has been found in the overwhelming association between clofibrate therapy and gallstones.
SYMPTOMATOLOGY

SIGNS AND SYMPTOMS JUSTIFICATION

Jaundice results from an abnormally high accumulation of bilirubin in the blood as a result of
Jaundice which there is a yellowish discoloration to the skin and deep tissues. Jaundice becomes
evident when the serum bilirubin level rises above 2.0 to 2.5 mg/dL.

Bilirubin together with cholesterol is normally absorbed in the intestines and is usually
excreted within the feces. The bile gives the stool its brown to black color. Obstruction in the
Pale Stool
bile flow lessens and may hinder the absorption of bile in the intestines making the stool pale
in color.

Normally urine are not dark in color, excess bilirubin are excreted by the kidneys as a
Dark Urine
compensatory mechanism to balance the bile level in the body.

Pruritus or generalized Prutitus is the most common presenting symptom in persons with cholestasis, probably
itching related to an elevation in plasma bile acids

Due to the gallstones and microcrystals present inside the gall bladder, the gallbladder can't
contract properly which creates pain in the epigastric area (right side of the abdominal area),
often with reffered pain, above the waist , the right shoulder and the right scapula or the
Pain
midscapular region.
-A gallstone produces visceral pain by obstructing the cystic duct or ampulla of Vater,
resulting in distention of the gallbladder or biliary tree

Epigastric Distress Less or absence of bile acid in the doudenum means less or no digestion of fats.
• Nausea &
Vomiting
• Fullness
• Indigestion

Increased bilirubin in the When gallstones obstruct the bile going to the intestine, bilirubin tends to return the body’s
blood circulation.

Obstruction of bile flow also interferes with absorption of the fat-soluble vitamins A, D, E & K.
Vitamin deficiencies Therefore the patient may exhibit deficiencies of these vitamins if biliary obstruction has
been prolonged
 SCHEMATIC DIAGRAM

Precipitating Factors:
Predisposing Factors: Obesity/ Overweight
Advanced Age Pregnancy/ Contraception
Gender Frequent Starvation, total
Ileal Resection/Disease parenteral nutrition
Race Clofibrate Use
Genetics Diet/
Weight loss

(Cholesterol Stones)

Decreased Increased levels of fat in

level of Bile the blood stream
Acids

↑ Synthesis of cholesterol
in the liver

↑ Excretion of cholesterol
to the bile

Ratio of bile salts & lecithin with

cholesterol is no longer within the
area of solubility

Cholesterol concentration >

solubility capacity of the bile

No formation of mixed miccelles

 Lithogenic bile/ supersaturated bile
(creamy)

Mucoprecipitates of organic& inorganic

calcium salts become nucleation sites

Nucleation and production of

cholesterol monohydrate crystals

Large Cholesterol Stones

Extrusion of stones from

Gallbladder

Impaction at cystic and bile duct

Bile not excreted to doudenum

Distention of biliary tree and
fundus of gallbladder
Backflow of bile and goes to the
circulation

Forceful
contractions
of gallbladder

↑ levels of bilirubin/bile pigments ↓ conversion of Fat not emulsified

in the circulation bilirubin to
Spasm of urobilinogen in the
smooth intestines No absorption of fat in
muscle in the the intestines
ducts

↓ excretion of
↑ Renal secretion of urobilinogen in stool • Nausea
PAIN
bilirubin and
Vomiting
Grayish stool • Fullnes
• Obstructiv
e Jaundice Dark urine • Indigestion
• Pruritus • Vit. ADEK
DIAGNOSTIC TESTS

Laboratory Studies
• The workup of cholelithiasis in pediatric patients is similar to that in adults. The goal is to demonstrate evidence of
gall bladder or biliary tract disease.
• Liver function test (LFT) and CBC results are typically within reference ranges. Abnormalities suggest infection or
obstruction, or both.
• All laboratory results in simple cholelithiasis should be within reference ranges. They are of use in identifying a
more complex disease process, including biliary obstruction and cholecystitis.

Imaging Studies
• Use of kidney-ureter-bladder (KUB) plain radiography in these patients is often fruitless because many stones are
not visible. However, it may be beneficial in identifying small-bowel obstruction or free air under the diaphragm.
• Ultrasonography of the right upper quadrant (RUQ) is the study of choice for these patients. Ultrasonography can
be used to identify the location of the stone, gallbladder wall thickening, and pericholecystic fluid, and a
sonographic Murphy sign aids in diagnosis of the disease process.
• Radionuclide scanning, such as scanning with iminodiacetic acid (IDA) derivatives (eg, hepatoiminodiacetic acid
[HIDA], diisopropyl iminodiacetic acid [DISIDA], and para -isopropyliminodiacetic acid [PIPIDA] scanning), are also
used to assess gall bladder function, its ability to harbor and concentrate bile, and perhaps more importantly, its
motility response to cholecystokinin or a fatty meal by quantifying the ejection fraction.
• In children with suspected hepatobiliary complications, magnetic resonance cholangiopancreatography (MRCP) or
endoscopic retrograde cholangiopancreatography (ERCP) can help delineate the anatomy of the extrahepatic and
intrahepatic biliary tract, identify the presence of ductal stones, and provide a therapeutic mode of removing a
stone or decompressing the biliary tract. ERCP in the pediatric population has been associated with the same
frequency of success and complications as in adults. As a noninvasive alternative, the MRCP has demonstrated
promise in the evaluation of choledocholithiasis but is less available at many institutions.
TREATMENT

Medical Care
• One option for nonsurgical management of gallstone disease is the use of ursodeoxycholic acid. One study
demonstrated a 56% reduction in biliary pain after 3 months of therapy and a mean dissolution of gallstones in
59% of cases after 12 months of treatment with 10 mg/kg/d of ursodeoxycholic acid. The primary disadvantage
with this approach is the incidence of recurrent gallstones, approximately 25% within 5 years. The nonsurgical
option is currently only indicated for patients either unfit or unwilling to undergo surgical intervention and has not
been recommended in the pediatric population.
• Extracorporeal shock-wave lithotripsy- repeated shock waves directed at the gallbladder or common bile duct to
fragment the stones
• Intracorporeal shock-wave lithotripsy- fragmentation by ultrasound, pulsed laser, or hydraulic lithotripsy applied
through an endoscope directly to the stones

Surgical Care
• Laparoscopic cholecystectomies are now being routinely performed through a small incision or puncture made
through the abdominal wall in the umbilicus. Laparoscopic cholecystectomy with intraoperative cholangiography
has demonstrated promise as an alternative to ERCP in patients with obstructive common bile duct stones
(choledocholithiasis).
• Cholecystectomy – gallbladder removal after the ligation oaf the cystic duct and artery
• Choledochostomy- incision into the common duct for stone removal
• Cholecystostomy- gallbladder is opened and the stone, bile, or purulent drainage is removed

Diet
A decrease in the consumption of fatty foods and controlled reduction in weight

Activity
Leitzmann et al have demonstrated in a prospective cohort study that symptomatic gallstones in men were reduced by
approximately 20% with increased exercise. This reduction may be extrapolated to the pediatric population.
MEDICATIONS

Gallstone solubilizers
These agents are indicated for the treatment of radiolucent noncalcified gallbladder stones.

1. Ursodiol (Actigall, Ursodamor, Ursofalk, Ursogal)

Also called ursodeoxycholic acid. Indicated for radiolucent noncalcified gallbladder stones <20 mm in diameter
when conditions preclude cholecystectomy.
Suppresses hepatic cholesterol synthesis and secretion and also inhibits intestinal absorption. It appears to have
little inhibitory effect on synthesis and secretion into bile of endogenous bile acids and does not appear to affect secretion
of phospholipids into bile. After repeated doses, reaches steady-state bile concentrations in about 3 wk.
Cholesterol is insoluble in aqueous media, but it can be solubilized in at least 2 different ways in the presence of
dihydroxy bile acids. In addition to solubilizing cholesterol in micelles, ursodiol acts by dispersing cholesterol as liquid
crystals in aqueous media. The overall effect of ursodiol is to increase the concentration level at which saturation of
cholesterol occurs.
The various actions of ursodiol combine to change the bile of patients with gallstones from cholesterol-
precipitating to cholesterol-solubilizing bile, thus resulting in bile conducive to cholesterol stones dissolution.
Although not approved by the FDA, ursodiol has been used in combination with chenodeoxycholic acid and in
conjunction with extracorporeal shock-wave lithotripsy for the dissolution of gallstones.
Available in 250-mg and 300-mg caps. An extemporaneous liquid formulation may be compounded for pediatric use.

Anti-inflammatory agents
These agents decrease inflammatory responses and systemically interfere with events leading to inflammation.

1. Diclofenac (Voltaren, Cataflam)

Designated chemically as 2-[(2,6-dichlorophenyl) amino] benzene acetic acid, monosodium salt, with an empirical
formula of C14 H10 Cl2 NO2 NA. One of a series of phenylacetic acids that has demonstrated anti-inflammatory and
analgesic properties in pharmacological studies. Believed to inhibit the enzyme cyclooxygenase, which is essential in the
biosynthesis of prostaglandins. Can cause hepatotoxicity; hence, liver enzymes should be monitored in the first 8 wk of
treatment.
Rapidly absorbed; metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation.
Delayed-release, enteric-coated form is diclofenac sodium, and immediate release form is diclofenac potassium. Has
relatively low risk for bleeding GI ulcers.

2. Indomethacin (Indocin)
Rapidly absorbed. Metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation. Inhibits
prostaglandin synthesis.

Source: http://emedicine.medscape.com/article/927522-treatment
http://emedicine.medscape.com/article/927522-diagnosis
Nursing Management

Nsg. Diagnoses:

1. Acute pain related to inflammation and distortion of tissues

2. Imbalanced nutrition: less than body requirements related to inability to ingest or absorb adequate nutrients
3. Deficient knowledge regarding pathophysiology, therepy choices, and self care needs related to lack of
information, misinterpretation
4. Self-Care Deficit: bathing/hygiene and dressing/ grooming related to weakness
5. Activity Intolerance related to generalized weakness and pain
6. Anxiety related to change in health status
Nursing Interventions
• Administer pain relievers as prescribed by the physician to promote comfort.
• Advice the client to have a nutritious diet and avoid excessive fats
• Post-op: remind the patient to cough hourly to prevent atelectasis
• Post op: instruct the patient to use a pillow to splint incision.
• To prevent bleeding, assess periodically for increased tenderness or rigidity of the abdomen and report it to the
 physician; instruct the patient and family to report change in color of stools
• Monitor VS closely, inspect incision for bleeding
• When administering medications, teach the patient about its actions and possible side effects that are to be
expected
• Instruct the patient to report immediately in case symptoms of jaundice, dark urine, pale stools, pruritus, or signs of
infection
• Provide written and verbal instructions to the patent and family about managing pain and about signs and
symptoms of intra-abdominal complications that should be reported such as loss of appetite, vomiting, temp
elevation
• Emphasize the importance of keeping follow-up appointments