INTRODUCTION

The gallbladder is a small pear-shaped organ which aids in the digestive process. Its function is

to store and concentrate bile - a digestive liquid continually secreted by the liver. The bile in turn

emulsifies fats and neutralizes acids in partly digested food. Despite its importance in the digestion of fat,

many people are unaware of their gallbladder. Fortunately enough, the gallbladder is an organ that

people can live without. Perhaps, this fact contributes to the laxity of the majority. The gallbladder tends to

be taken for granted – ignored of the proper care and conditioning. Lifestyle together with heredity, sex,

race and age are just some factors that leave a room for gallbladder complications to occur.

This study is about cholecystitis. The most common cause of cholecystitis is gallstones (90% of

the cases). The bile becomes concentrated in the gallbladder. This later causes irritation and is probably

the leading cause of inflammation. Cholecystitis affects women more often than men and is more likely to

occur after age 40. People who have a history of gallstones are at increased risk for cholecystitis. In the

international level, cholecystitis has an increased prevalence among people of Scandinavian descent,

Pima Indians, and Hispanic populations, whereas cholelithiasis is less common among individuals from

sub-Saharan Africa and Asia. It affected 20.5 million people (1988- 1994) with a mortality record of 1,077

deaths in 2002. Hospitalizations total up to 636,000 in the same year and over 500,000 have undergone

cholecystectomies.

Cholelithiasis is the presence of one or more calculi (gallstones) in the gallbladder. In developed

countries, about 10% of adults and 20% of people > 65 yr have gallstones. Gallstones tend to be

asymptomatic. The most common symptom is biliary colic; gallstones do not cause dyspepsia or fatty

food intolerance. More serious complications include cholecystitis; biliary tract obstruction (from stones in

the bile ducts orcholedocholithiasis), sometimes with infection (cholangitis); and gallstone pancreatitis.

Diagnosis is usually by ultrasonography. If cholelithiasis causes symptoms or complications,

cholecystectomy is necessary. About 80% of people with gallstones are asymptomatic. The remainder

have symptoms ranging from biliary-type pain (biliary colic) to cholecystitis to life-threatening cholangitis.

Biliary colic is the most common symptom

(http://www.merck.com/mmpe/sec03/ch030/ch030b.html ).
Clinical Features
History: Gallstones usually remain asymptomatic throughout the patient’s life.
The most common presenting symptom is intermittent pain below the right ribcage; pain
might radiate to the back

Nausea, with or without vomiting, might be present.

•

Certain foods, especially those with high fat content, can provoke symptoms. The
patient might experience episodes of acute abdominal pain, called biliary colic.
Physical: Physical examination frequently is normal.
•

Discomfort might be elicited on deep palpation of the right upper quadrant of the
abdomen.
•

Murphy sign (pain on palpation of the right upper quadrant when the patient
inhales) might indicate acute cholecystitis. Other signs of cholecystitis include
fever and tachycardia.
•

Physical exam might indicate complications of cholelithiasis.

o

Passage of gallstones from the gallbladder into the common bile duct can
result in a complete or partial obstruction of the common bile duct.
Frequently, this manifests as jaundice. In all races, jaundice is detected
most reliably by examination of the sclera in natural for yellow
discoloration.
o

Pancreatitis, another complication of gallstone disease, presents with more diffuse abdominal pain, including
pain in the epigastrium and left upper quadrant of the abdomen.
o

Severe hemorrhagic pancreatitis occurs in 15% patients and carries a

high mortality because of multisystem organ failure. In a few patients, the
hemorrhagic pancreatic process and retroperitoneal bleeding induce
discoloration around the umbilicus (Cullen sign) or the flank (Grey-Turner
sign).
o

Charcot triad (right upper quadrant pain, fever, and jaundice) is

associated with common bile duct obstruction and cholangitis. Additional
symptoms, such as alterations in the mental status and hypotension,
indicate Raynaud pentad, a harbinger of worsening, ascending
cholangitis.

Mortality and morbidity are related directly to the complications of the disease and its

surgical treatment. Approximately 10% patients with gallstones have common bile duct
stones as well. The natural history of common bile duct stones is not completely known.
Gallstones can cause obstruction of the common bile duct, causing jaundice.
Cholangitis, a potentially life-threatening infection, can follow biliary obstruction.
Obstruction of the neck of the gallbladder causes bile stasis, which can lead to
inflammation and edema of the gallbladder wall. Sequelae of this condition include acute
cholecystitis secondary to compromised lymphatic, venous, and, ultimately, arterial
supply to the gallbladder. The latter can lead to gangrene or abscess formation
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CHOLELITHIASIS
DEFINITION
•
Calculi, or gallstones, usually form in the gallbladder from the solid constituents of bile and vary greatly in
size,
shape, and composition.
- S m e l t z e r , S . C . , B a r e , B . G . B r u n n e r & s u d d a r t h ’ s T e x t b o o k
o f M e c i a l - S u r g i c a l N u r s i n g ! 0 t h E d i t i o n .
•

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.
- M c C o n n e l l , T . H . , T h e N a t u r e o f D i s e a s e P a t h o l o g y f o r t h e
H e a l t h P r o f e s s i o n s . 2 0 0 7
•
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.
- h t t p : / / w w w . n l m . n i h . g o v / m e d l i n e p l u s / e n
c y / a r t i c l e / 0 0 0 2 7 3 . h t m
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 smallorgan whose function in the body is to
harborbile 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 byrecesses 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
infection of the
gallbladder-
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.
Hemolytic Disease and
Hepatic Cirrhosis
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 %.
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/
contraceptives
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.
Frequent Starvation and
Prolonged parenteral
nutrition
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.
Clofibrate use and other
Antilipemic drugs
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.
SYMPTOMATOLOGY
SIGNS AND SYMPTOMS
JUSTIFICATION
Jaundice
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.
Pale Stool
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.
Dark Urine
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.
Pruritus or generalized
itching
Prutitus is the most common presenting symptom in persons with cholestasis, probably
related to an elevation in plasma bile acids
Pain
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
Epigastric Distress
•
Nausea &
Vomiting
•
Fullness
•
Indigestion
Less or absence of bile acid in the doudenum means less or no digestion of fats.
Increased bilirubin in the
blood
When gallstones obstruct the bile going to the intestine, bilirubin tends to return the body’s
circulation.
Vitamin deficiencies
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
(Cholesterol Stones)
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
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
Lar
g
e Cholesterol Stones
Extrusion of stones from
Gallbladder
Im
p
action at c
y
stic and bile duct
Distention of biliary tree and
fundus of gallbladder
Forceful
contractions
of gallbladder
Spasm of
smooth
muscle in the
ducts
PAIN
Bile not excreted to doudenum
Backflow of bile and goes to the
circulation
↑ levels of bilirubin/bile pigments
in the circulation
•
Nausea
and
Vomiting
•
Fullnes
•
Indigestion
•
Vit. ADEK
↑ Renal secretion of
bilirubin
Dark urine
Nucleation and production of
cholesterol monohydrate crystals↓ conversion of
bilirubin to
urobilinogen in the
intestines
↓ excretion of
urobilinogen in stool
Grayish stool
Fat not emulsified
No absorption of fat in
the intestines
•
Obstructiv
e Jaundice
•
Pruritus
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], andpara -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

Cholelithiasis brief discussion

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