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 Age (40 and above) Gender Justification Most
internal functions decline as one ages. Inevitably resulting in organ degeneration
which also affects the body's metabolism of lipids. 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). 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. Cholesterol stones are common in
Northern Europe and in North and South America. 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 or infection in the biliary
structures may provide a focus for stone formation or may alter the solubility of
the constituents, fostering the development of a stone. In cirrhosis, at least two
fifths of patients have gallstones. One possible mechanism behind 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 %. Brown pigment gallstones form when there is stasis of bile (decreased flow),
for example, when there are narrow, obstructed bile ducts. Justification 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 is associated
with an increased risk of gallstones because weight loss increases bile
cholesterol supersaturation, enhances cholesterol crystal nucleation, and
decreases gallbladder contractility. 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.
Altered physiology of the biliary system during pregnancy may play a role in
accelerating the formation of stones in susceptible women. The contraceptive pill
not only promotes thromobphlebitis but points to an endocrine 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. Starvation decreases gallbladder movement
causing the bile to become overconcentrated with cholesterol. The liver also
secretes extra cholesterol into bile adding to the 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. Drugs that lower the serum
level of cholesterol, notably clofibrate, are associated with an 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.
Ileal Disease/Resection Race Genetics

Inflammation and infection of the gallbladderHemolytic Disease and Hepatic

Cirrhosis Bile stasis Precipitating Factors Faulty Diet

Weight Loss Obesity

Pregnancy Treatment with estrogen/ contraceptives

Frequent Starvation and Prolonged parenteral nutrition

Clofibrate use and other Antilipemic drugs

SYMPTOMATOLOGY SIGNS AND SYMPTOMS Jaundice JUSTIFICATION Jaundice results from an
abnormally high accumulation of bilirubin in the blood as a result of 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 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 compensatory mechanism to
balance the bile level in the body. Prutitus is the most common presenting symptom
in persons with cholestasis, probably 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 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 Less or absence of bile
acid in the doudenum means less or no digestion of fats.

Pale Stool

Dark Urine Pruritus or generalized itching

Pain

Epigastric Distress • Nausea & Vomiting • Fullness • Indigestion Increased

bilirubin in the blood Vitamin deficiencies

When gallstones obstruct the bile going to the intestine, bilirubin tends to
return the body’s circulation. Obstruction of bile flow also interferes with
absorption of the fat-soluble vitamins A, D, E & K. Therefore the patient may
exhibit deficiencies of these vitamins if biliary obstruction has been prolonged
SCHEMATIC DIAGRAM

Predisposing Factors: Advanced Age Gender Ileal Resection/Disease Race Genetics

Precipitating Factors: Obesity/ Overweight Pregnancy/ Contraception Frequent

Starvation, total parenteral nutrition Clofibrate Use Diet/ Weight loss

(Cholesterol Stones)

Decreased level of Bile Acids

Increased levels of fat in the blood stream

↑ 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

Distention of biliary tree and fundus of gallbladder

Bile not excreted to doudenum Backflow of bile and goes to the circulation

Forceful contractions of gallbladder

↑ levels of bilirubin/bile pigments in the circulation

Spasm of smooth muscle in the ducts

↓ conversion of bilirubin to urobilinogen in the intestines

Fat not emulsified

No absorption of fat in the intestines

PAIN • •

↑ Renal secretion of bilirubin

↓ excretion of urobilinogen in stool

• • • •

Obstructiv e Jaundice Pruritus

Grayish stool
Dark urine

Nausea and Vomiting Fullnes Indigestion 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 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 cholesterolprecipitating 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. when 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