HISTORY TAKING

IDENTIFICATION DATA

Name : Mastura Binti Taqul Arifin

Age : 32 Years old

Gender : Female

Ethnicity : Malay (Muslim)

Residence : Taman Meru Jaya, Klang.

Occupation : Primary School Teacher

Marital status : Married

Informant : Patient

Ward No. : 3 A

Bed No. : 31 A

R/N : HTAR 1460436

Date of admission : 12/6/2014

Date of examination: 16/6/2014

CHIEF COMPLAINTS

Mrs Mastura was presented to the Emergency Department of HTAR with abdominal

pain for 3 days which associated with vomiting and fever for one day prior to

admission.

HISTORY OF PRESENTING ILLNESS

Mrs Mastura was apparently well until she developed abdominal pain at the right

hypochondriac region for three days. The pain was gradually increasing and worsens

on inspiration and after meal. She characterized the pain as burning in nature. The

pain radiates to the back which is below the right shoulder blade. The pain lasted for

one hour and it is more frequent on day time. The pain even affected her daily

activities include her work and she took medical leave for past three days. The pain

is relieved when she lies down. The severity score of the pain was seven out of ten.

Regarding vomiting, the content of the vomitus was food particles and fluids with no

blood or bile. She vomited twice before reaching hospital. The subsequent bout of

vomitus was whitish and scanty in volume. She neither had nausea nor loss of

appetite.

She also complained of low grade fever on the day of admission. The onset of fever

was sudden and associated with chills and rigors. It associated with generalized

itching on the body.

She has clay-coloured stools and dark yellow coloured urine until the day of clerking.

She denied diarrhoea, constipation, loss of appetite, loss of weight, alteration of

bowel habit, bloody stool, painful urination or dysphagia.

SYSTEMIC REVIEW

Respiratory system

She complained of cough. However, she denied shortness of breath, haemoptysis,

wheezing or night sweats.

Cardiovascular system

She denied chest pain, bluish discolouration, ankle oedema, palpitations, syncope,

paroxysmal nocturnal dyspnoea or orthopnoea.

Genitourinary system

She denied pain in urination, urinary incontinence or loin pain. She has normal

frequency and amount of urine. Urine is dark yellow coloured.

Central Nervous system

She has headache. However, she denied of dizziness, syncope, blurry vision or

double vision.

Musculoskeletal system

She denied any muscle pain or joint pain.

HISTORY OF PAST ILLNESS

Medical

She consulted a general practitioner regarding his abdominal pain on the first

day of her illness. She was treated as gastritis and was prescribed with

magnesium carbonate. However, the pain does not relieve. Thus, she came

to Emergency Department of HTAR and was referred to be admitted due to

abnormal blood results for further investigation. This is her first admission to

the hospital. Otherwise, she has no known medical illness such as diabetes

mellitus or hypertension.

Surgical

She has done caesarean section for her first child only at HTAR on 2006.

Trauma/Accidents

No history of trauma or accidents.

Blood transfusion

No history of blood transfusion.

Menstrual history

Her Last Menstrual Period was on 6th June 2014. Her menses is regular with

duration of 6 to 7 days and 28 to 30 days of cycle length.

DRUG HISTORY

She is not on medication and denies taking oral contraceptive pills or traditional

medication.

She has no allergy towards any drug.

DIET HISTORY

Her diet is usually heavy meal with meat or mutton and less fibre intake. She denied

abdominal pain or vomiting with heavy post-meal, taking oily or fatty food.

She has no allergy to any food.

FAMILY HISTORY

Mrs Mastura, 32 years old married to Mr Nazir 42 years old with five children and all

of them are healthy. She is the third child out of four children for her parents. Her

parents died of unknown reason where most probably due to aging. Her father died

at the age of 75 and has no medical illness while her mother died at the age of 68,

who was under dialysis and had diabetes mellitus.

There is no significant history of gallstone disease or biliary disease in her family.

SOCIAL AND PERSONAL HISTORY

Home circumtances:

She lives with her husband and five children currently stay in their own

double-storey terraced house with adequate house amenities.

Smoking, alcohol or illicit drug abuse:

She does not smoke, drink alcohol or take illicit drugs as well as her husband.

Education status:

Her husband works as Secondary school teacher. They both are degree

holders.

Income:

Combined monthly income of them is about RM5500.

SUMMARY

Mrs Mastura, 32 years old, Malay lady was presented with severe burning pain on

right hypochondriac region for 3 days and associated with fever and vomiting for one

day prior to admission. The pain worsens as her inspire and aggravated by fatty

food. The vomitus contained food particles and fever was associated with chills and

rigors.

PHYSICAL EXAMINATION

GENERAL CONDITION

On inspection,

Patient was lying comfortably in supine position supported by one pillow.

She was conscious, oriented and alert to time, place and person.

Large-built and her BMI were 27.0 which ranged to be overweight.

There was a cannula on the dorsum of her right hand and attached to

intravenous infusion of normal saline (0.9% of NaCl).

She was not in respiratory distress or in pain. Her hydration and nutrition

status was adequate. There were no signs of gross deformity.

VITAL SIGNS

a) Blood pressure : 128/80 mmHg (normotensive)

b) Pulse rate : 89 beats per minute (normal)

c) Respiratory rate : 18 breath per minute (normal)

d) Temperature : 36.6°C (afebrile)

PERIPHERAL EXAMINATION

HEAD & NECK

a. Conjunctiva : Mild pallor

b. Sclera : icteric

c. Mouth : Lips were pale, no central cyanosis, good oral hygiene,

no angular stomatitis and no gingivitis

d. Neck : No swelling

e. Lymph node : Not palpable

SKIN

Warm peripheries and yellow discolouration of the skin.

UPPER LIMBS

a. Palms : Dry, warm and pale.

b. Nails : No peripheral cyanosis, no clubbing, no

leukonychia, and no koilonychias

c. Capillary refill time : Less than 2 seconds

LOWER LIMBS

a. No pitting oedema.

b. No varicose veins

BREAST

Both breasts were symmetrical and nipples were everted. Nipples were hyper

pigmented. No fungal infection beneath the breast, no masses, no retraction

of the nipples, no leakage and other abnormalities were noted.

Impression: Normal

SYSTEMIC EXAMINATION

CARDIOVASCULAR SYSTEM

a) Inspection: The chest wall is symmetrical and normal in shape. There

was no scar, no precordial bulging and no visible apex beat.

b) Palpation: The apex beat was located in the 5th intercostal space, at the

mid-clavicular line. There was no thrill and heave. The peripheral

pulses were present with normal rhythm and volume.

c) Auscultation: The first and second heart sounds were normal. There

were no murmurs heard. Increased heart rate was noted.

Impression: Physiologically normal.

RESPIRATION SYSTEM

a) Inspection: The chest moved symmetrically with respiration with no

deformity seen. There was no sign of respiratory distress. There were

no scar, prominent dilated.

b) Palpitation: The chest expansion and vocal fremitus were equal

anteriorly and posteriorly at all three zones of the lungs.

c) Percussion: The lung was resonant bilaterally, anteriorly and

posteriorly. There were normal liver and cardiac dullness.

d) Auscultation: There were vesicular breath sound anteriorly and

posteriorly at all three zones. No added sounds heard.

Impression: Lungs clear.

LOCAL EXAMINATION

ABDOMINAL EXAMINATION

a) Inspection: The abdomen was distended and the flanks are full due to

fat. All quadrants move symmetrically with respiration. Umbilicus is

inverted and centrally located. There was no striae, no surgical scars,

no prominent and dilated veins, no visible peristalsis and no obvious

mass seen.

Cough impulse was negative.

b) Palpitation:

- On superficial palpation, the abdomen was soft and non-tender.

There was no superficial mass present.

- Upon deep palpation, abdomen was tender at right hypochondriac

region. Liver was palpable with two finger breadths below the costal

margin. The spleen was not palpable and the kidneys were not

ballotable. There was no palpable mass found on the abdomen.

- Murphy’s sign was negative.

c) Percussion: The abdomen was resonance. There was no shifting

dullness and fluid thrill was negative.

d) Auscultation: Normal bowel sound was heard with high pitched gurgling

noise. About 20 bowel sounds per minute was heard.

Impression: Liver is enlarged. Otherwise, physiologically normal.

PER-RECTAL EXAMINATION

Per-rectal examination was unremarkable.

SUMMARY

On examination, patient’s eyes, lips and palms were pallor. Vital signs were normal.

Upon abdominal examination, she has icterus and yellowish discolouration of skin

suggestive of jaundice. Abdomen was distended and tender on right hypochondriac

region, also liver is slightly enlarged. Murphy’s sign was negative.

DIAGNOSIS

PROVISIONAL DIAGNOSIS

Points support Points against

Acute cholecystitis Severe burning and

colicky pain in the right

hypochondriac region of

the abdomen, vomiting,

fever associated with chills

and rigors, jaundice and

tender at right

hypochondriac region of

the abdomen.

Hepatomegaly, cough.

DIFFERENTIAL DIAGNOSIS

Points support Points against

Chronic Cholecystitis Colicky pain in the right

upper quadrant of the

abdomen, vomiting,

jaundice and pain worsens

after meal (fatty food

intolerance).

No repeated acute

cholecystitis or biliary colic

symptoms, no recurrent

flactulence and no feeling

of distension or heartburn.

Ascending cholangitis Severe pain in the right

upper quadrant of

abdomen, fever

associated with chills and

rigors, vomiting and

jaundice.

No ill looking.

Choledocho-lithiasis Colicky pain in the right

upper quadrant of the

abdomen, fever, vomiting.

Pale stools present.

-

FINAL DIAGNOSIS

Acute cholecystitis secondary to choledocholithiasis.

LABORATORY EXAMINATION

Full blood count (15/6/2014)

Objective: To check for signs of anaemia and leucocytes level.

Type of specimen: Whole blood.

Results Normal range

Haemoglobin 13.6 g/dL 13.0-18.0

Haematocrit 41.2% 40.0-54.0

Platelet 235 x 10 /L⁹ 150-400

Total white blood cells 18.3 x 10 /L⁹ 4.0-11.0

Percentage of Neutrophils 73% 40-75

Interpretation: Total white blood cell count and neutrophils were increased which might be due to infection. Haemoglobin and haematocrit levels were normal.

Liver function test (14/6/2014)Objective: To rule out Cholangitis and Choledocho-lithiasis

Type of specimen: Whole blood.

Results Normal range

Total protein 80 g/dL 64-83Albumin 40 g/dL 35-50Globulin 40 g/dL 34-50Albumin/Globulin ratio 1.00 -Total bilirubin 40.3µmol/L 3.4-20.5Alanine Transaminase 22 U/L < 44Alkaline Phosphatase 60 U/L 40-150

Interpretation: Total bilirubin was markedly increased which indicates hyperbilirubinaemia that caused jaundice.

Renal Profile (14/6/2014)Objective: To monitor levels of fluid loss and renal function.

Type of specimen: Whole blood.

Results Normal range

Urea 5.1 mmol/L 3.2-9.2Sodium 132 mmol/L 3.2-9.2Potassium 3.7 mmol/L 3.5-5.1

Chloride 95 mmol/L 98-107Creatinine 96 µmol/L 62-115

Interpretation: Slight decrease in the level of chloride indicates electrolyte

imbalance occurred.

RADIOLOGICAL INVESTIGTIONS

Abdominal X-ray (14/6/2014)

Findings: No visible gallstones or abdominal mass. Faecal loaded was seen

at the left iliac region. There is no sign of intestinal obstruction.

Ultrasound of Hepatobiliary System

Findings:

The liver has normal homogenous parenchymal echo texture with raised echo

pattern. There was no focal lesion within the parenchyma. There was no

biliary tree dilatation. The portal vein and common bile duct were normal in

calibre.

However, the gallbladder wall was thickened and blurred in outline. Multiple

stones of various sizes were seen in the gallbladder. The largest stone was

measured about 2.5cm in diameter. There was associated pericholecystic

fluid denoting underlying inflammation of the gallbladder.

The visualised pancreas and the spleen were normal.

TREATMENT AND MANAGEMENT PLAN

On 15/6/2014, the patient was given intravenous fluid drip 5 pints and antibiotics (Ciprofloxacin 400mg twice daiy, IV). Subcutaneous Pethidine 1mg/kg was given for pain relief.

On 16/6/2014, the patient was taken for surgery. Open cholecystectomy was performed. Histopathology of the gallbladder confirmed acute cholecystitis secondary to gallstones. Open cholecystectomy revealed perforated gallbladder empyema with pus collection. There were impacted cholesterol stones seen at Hartmann’s pouch with sludge.

Until 18/6/2014, the patient was monitoring for any post-operative complications. The patient was discharged in the evening of the day.

DISCUSSION

Introduction:

Acute cholecystitis predominantly occurs as a complication of gallstone disease and

typically develops in patients with a history of symptomatic gallstones.  Acute

cholecystitis refers to a syndrome of right upper quadrant pain, fever, and

leukocytosis associated with gallbladder inflammation that is usually related to

gallstone disease.

Choledocholithiasis is the presence of at least one gallstone in the common bile

duct. The stone may be made up of bile pigments or calcium and cholesterol salts.

Anatomy and physiology of biliary system:

Gallstones are formed in the biliary system. The biliary system is concerned with the

production, storage and secretion into the gut of bile and it is comprised of the liver,

the gallbladder, and the biliary tract.

The liver is located in the right upper quadrant of the abdomen. The liver has

many functions: synthesis, storage and breakdown of glycogen, synthesis of

clotting factors, storage of blood, manufacture and breakdown of hormones,

synthesis of bile salts needed for absorption of fat-soluble vitamins and lipids

and removal of cholesterol, metabolism, detoxification and removal of

endogenous and exogenous compounds, metabolism and removal of drugs,

and bile formation. The basic unit of the liver is the hepatocyte (hepato is a

prefix that refers to the liver). The hepatocyte can be thought of as having two

distinct ends: the basolateral membrane that faces the blood vessels of the

liver and the apical membrane that faces the bile canaliculi (Latin for canal).

The canaliculi collect the bile that is secreted by the hepatocytes, directs it

into the terminal bile ducts and from there the bile flows into the hepatic ducts,

into the common bile duct and into the gallbladder where it is stored before it

is released into the small intestine.

The gallbladder is a small, muscular sac that is nestled into the liver. Its

primary function is to concentrate and store bile. The gall bladder is

connected to the common bile duct (at about the same place that the hepatic

ducts join the common bile duct) by the cystic duct. Bile is stored in the

gallbladder until it is needed for the digestion of fat in the gut. Fat entering the

small intestine causes the release of a hormone called cholecystokinin from

the intestinal mucosa. Cholecystokinin is absorbed into the blood stream,

reaches the gallbladder and stimulates it to contract and empty bile into the

small intestine (cholecystokinin also relaxes the sphincter of Oddi, the

sphincter at the junction of the bile duct and the small intestine). The

gallbladder also acts to determine the final composition of bile by absorbing

water, sodium chloride and other electrolytes and leaving behind bile that is

concentrated with bile salts, cholesterol and bilirubin.

The biliary tract is the system of channels through which bile flows. It consists

of the bile canaliculi, terminal bile ducts, right and left hepatic ducts in the

liver; the cystic duct that goes from the gallbladder to the common bile duct;

and the common bile duct that carries bile (along with pancreatic secretions;

before the common bile duct enters the small intestine, there is an

anastamosis with the pancreatic duct) through the sphincter of Oddi into the

small intestine.

Predetermined risk factors:

The predetermined risk factors are certain medical conditions, gender, ethnicity,

inherited susceptibility, and age.

Age: For women, the risk of developing gallstones after the age of 15

increases by approximately 1% a year; for men, the risk increases

approximately 0.5% per year. Cholelithiasis is almost unknown in children.

Gender: Gallstones are more common in women. Young women have a much

higher risk than young men; in later decades, the risk for men increases but

never equals that of women. Pregnant women have a higher risk than women

who are not pregnant. This, along with the gender difference, is thought to be

caused by estrogen and progesterone; progesterone may cause pooling of

the bile in the gallbladder and estrogen increases the concentration of

cholesterol in bile.

Genetics: There is no doubt that a predisposition to forming gallstones can be

inherited It has been estimated that this genetic susceptibility accounts for

approximately 30% of the population’s risk for developing gallstones.

Ethnicity: Gallstones are common in Europe, North America, and South

America, but are uncommon in Asia and Africa.

Medical conditions: Medical conditions that increase the risk for developing

gallstones include cirrhosis, Crohn’s disease, irritable bowel syndrome,

hemolytic anemias, cystic fibrosis, B12 or folic acid deficiency, and spinal cord

injury.

Modified risk factors:

Obesity: Obesity is a well-established risk factor for the development of

choledocolitiasis, especially for women. People who are obese have

increased concentration of cholesterol in their bile.

Diet: There is some evidence that diet – particularly a diet high in fat -

may increase the risk of developing gallstones, but there is no conclusive

proof that diet can increase or decrease the risk for developing

choledocolitiasis. Although most gallstones are comprised of cholesterol, high

serum cholesterol has not been associated with an increased risk for

gallstone disease.

Rapid weight loss: A low calorie diet and rapid weight loss (causing a release

of cholesterol from the tissues and increasing the cholesterol concentration of

the bile) is a major risk factor for choledocolitiasis bariatric surgery is, as well.

Drugs: Ceftriaxone (a cephalosporin antibiotic), octreotide (used for treating

acromegaly, complications of carcinoid syndrome, and certain cancers),

clofibrate (used for lowering serum cholesterol and triglycerides) and

estrogens may increase the risk of developing gallstones. Total parenteral

nutrition increases this risk, as well.

Sedentary lifestyle: A sedentary lifestyle may increase the risk for developing

gallstones.

Signs and Symptoms:

Most people who have gallstones have no complaints and are not aware they have

the disease.

Signs and symptoms are caused by inflammation, or obstruction if a stone moves

into the common bile duct or the cystic duct; the gallbladder contracts to release bile,

and the blockage caused by the stone causes the pain.The patient usually

experiences a steady, often severe pain in the right upper quadrant or the epigastric

area. The pain is referred to as biliary colic. It may radiate to the right shoulder or the

back (this is called Collin’s sign). It often starts within an hour after a meal and

typically lasts from 1 to 5 hours. Nausea and vomiting are common; a fever indicates

a complication, e.g., cholecystitis, cholangitis, or pancreatitis.

Diagnosing Choledocholithiasis:

Treatment of Choledocholithiasis:

REFERENCE

1. Bailey & Love’s Short Practice of Surgery, 26th edition, edited by Norman S.

Williams, Christopher J.K Bulstrode by CRC press on 2013; 1097-1117.

2. Friedman GD. Natural history of asymptomatic and symptomatic gallstones. Am

J Surg 1993; 165:399.

3. Fidler J, Paulson EK, Layfield L. CT evaluation of acute cholecystitis: findings

and usefulness in diagnosis. AJR Am J Roentgenol 1996; 166:1085.

4. http://mmspf.msdonline.com.br/ebooks/SchiffsDiseasesoftheLiver/

sid597458.html

5. http://www.nlm.nih.gov/medlineplus/ency/article/003815.htm