Case Presentation

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Cholelithiasis
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Introduction
Cholelithiasis
Presence of one or more calculi (gallstones) in the

gallbladder

common health problem, affecting about 1 out of every

1,000 people and is the fifth leading cause of hospitalization among adults and accounts for 90% of all gallbladder and duct diseases. occurs, in which case the prognosis depends on its severity and response to antibiotics.

prognosis is usually good with treatment unless infection

Prevalence of cholelithiasis is affected by many factors

including;
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Gallstones
tend to be asymptomatic Diagnosis is usually by ultrasonography. made of cholesterol, calcium bilirubinate, or a mixture of

cholesterol and bilirubin pigment

Migration of gallstones may lead to occlusion of the biliary

and pancreatic ducts, causing pain (biliary colic) and producing acute complications, such as acute cholecystitis, ascending cholangitis, or acute pancreatitis.

Asymptomatic gallstones
In patients with asymptomatic gallstones discovered
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incidentally, the likelihood of developing symptoms or complications is 1-2% per year

In most cases, asymptomatic gallstones do not require any

Biliary colic
Pain termed biliary colic occurs when gallstones fortuitously

impact in the cystic duct during a gallbladder contraction, increasing gallbladder wall tension.
In most cases, the pain resolves over 30 to 90 minutes as

the gallbladder relaxes and the obstruction is relieved.

Episodes of biliary colic are sporadic and unpredictable. The patient localizes the pain to the epigastrium or right

upper quadrant and may describe radiation to the right scapular tip.
From onset, the pain increases steadily over about 10 to 20

minutes and then gradually wanes.

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Predisposing factors
Age - elderly people are prone to gallstone

formation because of weakened immune system and deteriorating body organs.

Diabetic - are prone to gallstone formation

because of impaired protein synthesis and fatty acid storage.

Genetic - family with a history of

cholelithiasis has a high risk of acquiring the disease condition.

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Precipitating factor

 Excess alcohol consumption Oral contraceptives. High fat, low fiber diet. Rapid weight loss. Women who have had many children.(multiparity) Hemolytic disorders such as sickle cell anemia, hereditary

spherocytosis.
Liver cirrhosis. Diabetes. Female gender. Inflammatory bowel disease such as crohns.

Signs and symptoms

5/17/12 Symptoms usually manifest after a stone, which is greater

 Cholangitis- If the common bile duct is blocked for a

period of time, certain bacteria may grow in the stagnant bile producing symptoms of cholangitis.

Jaundice- a yellow pigmentation of the sclerae, skin,

and deeper tissues cause by excessive accumulation of bile pigments in the blood. The accumulation is due to the continuous blockage of bile to the intestines where it is partly excreted as waste.
Pancreatitis- stones blocking the lower end of the

common bile duct where it enters the duodenum may obstruct secretion from the pancreas producing pancreatitis.

Note: Often there are no symptoms.

Additional symptoms that may be associated with 5/17/12 this disease:

 heartburn- because of vomiting gas/flatus, excessive - decrease in peristalsis because of

decrease in water in the intestine.

abdominal indigestion- decrease ability to emulsify fats

,intolerance to fatty foods leading to indigestion

abdominal fullness, gaseous-decrease in peristalsis

because of decrease in water in the intestine.

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Complications of gallbladder stones

Acute cholecystitis
occurs when persistent stone impaction in the cystic duct causes

the gallbladder to become distended and progressively inflamed.

Chronically, gallstones may cause progressive fibrosis of the

gallbladder wall and loss of gallbladder function, termed chronic cholecystitis.

Gallbladder adenocarcinoma
an uncommon cancer that usually develops in the setting of

gallstones and chronic cholecystitis. producing jaundice.

commonly invade the adjacent liver and common bile duct,

Medical Intervention
Dissolution Agents (Cholesterol Stones) Extracorporeal Shock Wave Lithotripsy
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Personal Data
NAME: Mrs. Dimakasuka ADDRESS: Bgy. Calaocan, Santiago City, Isabela BIRTHDAY: January 11, 1968 BIRTHPLACE: Quezon City AGE: 43 years old NATIONALITY: Filipino DIALECTS SPOKEN: Ilokano, Tagalog RELIGION: Roman Catholic EDUCATIONAL ATTAINMENT: High School Graduate OCCUPATION: Vendor DATEOF ADMISSION: June 02, 2011

5/17/12 CHIEF COMPLAINT: fever, body weakness, severe abdominal pain,

History of Past Illness She acquired chicken pox and measles when she was young and was already twice hospitalized for the delivery of both her children but aside from that she was never brought to hospital for conditions which are related to her condition now. However during the past 5 months (starting January 2011) the patient has been experiencing pain on her right upper side part of the abdomen which she ignored. And she verbalized that it was a tolerable pain and was easily relieved by rest and sleep. Due to her work, Mrs. Dimakasuka was not able to have a check up or medical examinations done. Two months before the hospitalization, she experienced an intense abdominal pain accompanied by nausea and vomiting but instead of going to the hospital for checkup she just took pain medications. HISTORY of PRESENT ILLNESS

Two days prior to admission the patient again experienced severe abdominal pain while at work accompanied by fever (May 31). By 11 pm of June 2, 2011 she was admitted at CVAH with chief complaints of fever, body weakness, severe abdominal pain, nausea and vomiting He was immediately attended by the nurses by taking his vital signs. Her consent was signed. She was immediately examined by Dr. JJ with orders made and carried out. The patient was inserted with an IVF of D5LRS 1L x 30gtts/min inserted at her left 5/17/12 hand. She had undergone laboratory exams such as, CBC, Urinalysis, HBT

LABORATORY AND DIAGNOSTIC EXAMS

HBTPancreas Ultrasound

Results: Abnormally contracted gallbladder with a lithiasis at the neck. Intrahepatic and extrahepatic ducts are not dilated. Unremarkable liver and pancreas. (-) for ascites
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Analysis and Interpretation of Results

Abnormally contracted gallbladder with a lithiasis at the neck.

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Physical Assessment
June 2, 2011 (upon admission, based on the patient's chart)
Patient Is conscious, coherent but in distress with

steady severe aching pain in the right upper quadrant of the epigastrium radiating to the right shoulder
Vital signs:

BP- 90/60 T- 38 P-80

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June 3,2011 (patient's chart)

Patient is conscious and coherent with

IVF of 1L D5LRS regulated at 30

gtts/min still with (+) jaundice, tolerable

pain in the right upper quadrant of the epigastrium

Vital signs:

BP-100/70 T-37.1 PR-87

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RR-21

Sclera: appears yellowish Lips: pale

:dry
Skin: yellowish in color

:warm to touch
Abdomen: guarding behavior upon palpation

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Anatomy and Physiology

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 The gallbladder stores bile, which is released when food

containing fat enters the digestive tract, stimulating the secretion of cholecystokinin (CCK). The bile 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.
The liver's cells (hepatocytes) excrete bile into canaliculi,

which are intercellular spaces between the liver cells. These drain into the right and left hepatic ducts, after which bile travels via the common hepatic and cystic ducts to the gallbladder. The gallbladder, which has a capacity of 50 milliliters (about 5 tablespoons), concentrates the bile 10 fold by removing water and stores it until a person eats. At this time, bile is discharged from the gallbladder via the cystic duct into the common bile duct and then into the duodenum (the first part of the small intestine), where it begins to dissolve the fat in ingested food.
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 The liver excretes approximately 500 to 1000 milliliters (50

to 100 tablespoons) of bile each day. Most (95%) of the bile that has entered the intestines is resorbed in the last part of the small intestine (known as the terminal ileum), and returned to the liver for reuse. Metabolic functions, such as the maintenance of glucose (blood sugar) levels Synthetic functions, such as the synthesis of serum proteins such as albumin, blood clotting (coagulation) factors, and complement (a mediator of inflammatory responses) Storage functions, such as the storage of sugar (glycogen), fat (triglycerides), iron, copper, and fat soluble vitamins (A, D, E, and K) Catabolic functions, such as the detoxification of drugs

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Pathophysiology

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Predisposing/Non Modifiable
Age

Bile become saturated with cholesterol

Increase Precipitating/Modifiable cholesterol/ intake of fatty foods, low fiber diet

Gender Race

Changes of bile composition

Decreased capacity to dissolve fats

Decreased digestion and absorption of fats

Fat intolerance

buildup of bile constituents

Nausea and vomiting (June, 2008)

Concretion of bile constituents

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Crystalline structures are formed

Indigestion of fats Stimulates the secretion of Cholecystokinin RUQ colicky pain (January, 2011 June 2011,

Stimulates the gallbladder to produce more bile.

Cholelithiasis

Bile stasis become a medium for bacterial growth Infection Endogenous pyrogens

Inflammation obstruction

Release of chemical mediators Reset of hypothalamus

Conjugated bilirubin Escape from liver into the blood stream

Fever 5/17/12