FACULTY OF MEDICINE
SURGERY POSTING (3rd ROTATION)
YEAR 5 (19/20)
CASE WRITE UP
NAME : NURULASYIKIN BINTI MOHD ALI
ALFIKRI
STUDENT ID : 2015428728
GROUP : C
SUPERVISOR: DR. YAHYA MOHD ARIPIN
DEMOGRAPHIC DETAILS
Patients initials W
R/N 443515
Hospital Hospital Selayang
Ward 8D
Age 50 years old
Sex Female
Occupation Tailor and RELA worker
Marital status Married
Race Malay
Date of Admission 31/12/2019
Date of Clerking 2/1/2020
Date of Discharge 3/1/2020
CHIEF COMPLAINT
Madam W, 50 years old, Malay woman working as a tailor and RELA worker with
underlying diabetes mellitus type 2 and hepatitis B was electively admitted to Hospital
Selayang for laparoscopic cholecystectomy. She initially presented to the hospital with
right upper quadrant pain for 3 days prior to admission.
HISTORY OF PRESENTING ILLNESS
She was previously well until 1 months ago where she had sudden right upper quadrant
pain which is throbbing pain for 3 days prior to admission. The pain was continuous pain
which radiates to the back and shoulder. The pain was exacerbated with movement and not
relieve by paracetamol, eating or bending forward. The pain was severe as she could not
move and unable to fall asleep at night. She scored the pain as 9/10 upon presentation to
the hospital. It was associated with nausea, vomiting and diarrhoea. She had 3 episodes of
vomiting which the content of the vomitus was food content (1st episode), fluid (2nd
episode) and bile stained vomitus (3rd episode). No blood in the vomitus. Regarding the
diarrhoea, she had more than 4 episodes of diarrhoea which was abnormal for her as she
usually open her bowel once daily. There was no blood and mucus in the stool. She also
has tea coloured urine and pale stool for 2 days prior to admission. She also noticed that
her skin is yellowish. However, there was no pruritus.
Upon further questioning, she has menopause 2 years ago at the age of 48 years old and
she did not consume high fat diet, high protein diet and spicy diet. She has never consumed
alcohol and a non-smoker. She has no recent history of travelling, no history of shared
needle and no history of tattooing. She has no history of eating outside food, no recent
water activity and recent history of jungle trekking. There is no similar complaint in the
family.
Otherwise there is no fever, no loss of appetite, no loss of weight, no chest pain, no
shortness of breath, no UTI or URTI symptoms, no hemoptysis.
SYSTEMIC REVIEW
SYSTEM FINDINGS
General No fever, no loss of appetite or loss of
weight
Central Nervous System No headache, no loss of consciousness, no
seizure, has vision blurry, no hearing
problems, has headache and no altered
sensation.
Ear, Nose and Throat No ear and nasal discharge.
Cardiovascular System No cyanosis, no dyspnoea at rest, no ankle
swelling, no chest pain, no orthopnoea, no
palpitation.
Respiratory System No cough, no chest pain, no hemoptysis,
no shortness of breath.
Gastrointestinal System no difficulty in swallowing, no oral ulcer,
no heartburn
Genitourinary System No dysuria, no incontinence, no nocturia,
no loin pain, no hematuria.
Musculoskeletal System No joint pain, no joint stiffness or swelling.
Skin No rash, no beeding, no bruising.
Endocrine System No heat or cold intolerance, no polydipsia.
PAST MEDICAL, HOSPITALIZATION AND SURGICAL HISTORY
She was diagnosed with type 2 diabetes mellitus 13 years ago and was on
Metformin 500mg BD. She is compliance to her medication and has 6 monthly follow up
at Klinik Kesihatan. Her blood sugar is well controlled as she did self-monitoring blood
glucose. She has had history of 4 hospital admission in 2009 due to gangrenous right foot.
She was diagnosed to have hepatitis B last months and not on any medication. She has
never undergone any surgery before. She has no known allergies to food or drugs.
FAMILY HISTORY
Total siblings in the family is 6, all her siblings are healthy and living. Her father
died at the age of 66 years old due with no known cause while her mother is still living
well and has diabetes. Her father has hepatitis B. Her 2 siblings has undergone
cholecystectomy. No other chronic disease history in the family such as hypertension, heart
disease or asthma. There is no first-degree history of malignancy such as colon cancer,
ovarian or breast cancer.
SOCIAL HISTORY
She is married and blessed with 4 sons. She lives in Bukit Beruntung with her
husband and sons. Her estimated total income is about RM4000. She is a non-smoker, not
an alcoholic drinker and not taking any recreational drugs.
SUMMARY OF HISTORY
Madam W, 50 years old female with underlying Hepatitis B and diabetes mellitus
was electively admitted to Hospital Selayang for laparoscopic cholecystectomy. She
initially presented to the hospital with right upper quadrant pain for 3 days prior to
admission, vomiting and diarrhoea for 2 days prior to admission associated with jaundice,
pale stool and tea coloured urine.
PHYSICAL EXAMINATION
1. GENERAL EXAMINATION
Madam W, was lying comfortably in a 45° position supported by one pillow. She was not
in pain and not in respiratory distress. She looks conscious, alert and well orientated to
time, place and person. Her hydration and nutritional status were adequate.
Anthropometry results:
a) Weight: 62 kg
b) Height: 150 cm
c) BMI: 27 kg/m2
Vital signs :
a) Blood pressure : 118/56 mmHg
b) Pulse rate : 76 beats per minutes with normal volume and regular rhythm
c) Respiratory rate : 16 breath per minutes
d) Temperature : 37°C
e) Pain score : 0/10
Interpretation : she is pre-obese and all her vital signs were normal.
Hand examination
There were no abnormalities noted such as clubbing, koilonychias, leukonychias and
peripheral cyanosis. Capillary refill time was less than 2 seconds. Hand is warm and moist,
not pale, no palmar erythema and no flapping tremor. No muscle wasting.
Eye examination
There were no sclera jaundice and no conjunctival pallor. No sunken eyes.
Mouth examination
Her hydrational status was good by evidence of moist lips and mucous membrane. Her
tongue was moist and not coated. No central cyanosis seen. She had good oral hygiene.
Neck examination
No palpable lymph node and there was no thyroid enlargement.
Chest examination
No evidence of surgical scar, chest deformity and spider naevi noted.
Lower limb examination
Her lower limb is symmetry. No calf tenderness and no pedal edema on both leg.\
2. ABDOMINAL EXAMINATION
Inspection Abdomen appears to be symmetrical and moves with
respiration with the umbilicus located centrally. There is no
presence of dilated veins or visible pulsation. No surgical
scar noted.
Palpation The abdomen was soft and non-tender. There is no
hepatomegaly and splenomegaly. The kidneys are non-
ballotable. No mass palpable.
Percussion Liver span is 13cm.No shifting dullness heard on percussion.
Auscultation Normal bowel sounds are heard and no renal and aortic
bruits.
Interpretation: unremarkable findings.
3. RESPIRATORY EXAMINATION
Inspection The chest wall moved symmetrically with respiration. The
chest shape was normal with no chest wall deformity. The
patient was not in respiratory distress.
Palpation No tracheal deviation. Vocal resonance and tactile vocal
fremitus equal bilaterally
Percussion No abnormality is detected and the lobes were resonance on
percussion both anteriorly and posteriorly.
Auscultation Vesicular breath sounds were heard with equal air entry both
sides. No abnormality is detected.
Interpretation: unremarkable with equal air entry on both lungs and normal breath sounds
heard.
4. CARDIOVASCULAR EXAMINATION
Inspection The chest wall moves with respiration. Chest is symmetrical
in shape and no deformity is seen. There was no surgical
scar, dilated vein and visible pulsation seen
Palpation The apex beat was palpable at left 5th intercostal space within
the midclavicular line. No heaves or thrills palpable.
Auscultation S1 and S2 heart sounds with dual rhythm were heard with no
murmur.
Interpretation: unremarkable with dual rhythm and no murmur.
5. CENTRAL NERVOUS SYSTEM EXAMINATION
Mental status She was alert, conscious and well oriented
to time, place and person. Her memory
function was intact. She looks calm and not
in state of confusion.
Cranial nerves All the 12 cranial nerves were intact.
Muscle tone Normal muscle tone for all 4 limbs.
Muscle power Power for all for limbs were 5/5.
Sensory system Sensation of pain, light, touch, temperature,
vibration and proprioception for both upper
and lower limbs were intact and equal
bilaterally.
Reflex Reflex were normal bilaterally.
Interpretation: no abnormalities detected.
CLINICAL SUMMARY
Madam W, 50 years old female with underlying Hepatitis B and diabetes mellitus
was electively admitted to Hospital Selayang for laparoscopic cholecystectomy. She
initially presented to the hospital with right upper quadrant pain for 3 days prior to
admission, vomiting and diarrhoea for 2 days prior to admission associated with jaundice,
pale stool and tea coloured urine. The physical examinations were unremarkable.
PROVISIONAL DIAGNOSIS
Diagnosis Point to support
Acute pancreatitis secondary to 1. Epigastric pain
choledocholithiasis 2. Pain radiates to back and tip of shoulder
3. Billous vomiting
4. Tea coloured urine
5. Pale stool
6. Jaundice
DIFFERENTIAL DIAGNOSIS
Diagnosis Point to support Point to against
Obstructive jaundice 1. Abdominal pain 1. Pain radiates to the
secondary to 2. Billous vomiting back
chledocholithiasis 3. Tea coloured
urine
4. Pale stool
5. Jaundice
Carcinoma of head of 1. Epigastric pain 1. Has been diagnosed
pancrease 2. Pain radiates to back with diabetes
and tip of shoulder mellitus 13 years
3. Billous vomiting ago
4. Tea coloured urine 2. blood sugar was
5. Pale stool well controlled with
6. Jaundice T. Metformin.
Acute on chronic hepatitis 1. Upper abdominal 1. No fever
pain 2. No swelling
2. Pain radiates to back
3. Vomiting 3. No bleeding
4. Jaundice tendency
5. Underlying hepatitis 4. No sign of chronic
B liver disease
INVESTIGATIONS
1. Full blood count (31/12/2019)
Blood count Results Normal range Interpretation
White Blood Cell 4 – 11 x 10^9 /L Normal
8.26
(WBC)
Red Blood Cell 2-10 x10^12 /L Normal
4.08 x10^12/L
(RBC)
Hemoglobin 12.2 11.5 – 16 g/dL Normal
Hematocrit 45.0 40.0 – 54.0% Normal
Mean Cell Volume 83-101 fl Normal
90.5 fl
(MCV)
Mean Cell 27-32 pg Normal
30.5 pg
Haemoglobin (MCH)
Mean Cell Normal
Haemoglobin 33-36 g/dL
33.7 g/dL
Concentration
(MCHC)
Platelet 231 110 – 450 x 10^9/L Normal
Differential WBC
Neutrophil 58.3% 40-75% Normal
Lymphocyte 32.9% 20-45% Normal
Monocyte 6.5% 0-8% Normal
Eosinophil 0.8% 0-5% Normal
Basophil 1.5% 0-2% Normal
Absolute neutrophil 3.6 x 10^9/L 2.0 – 7.0 x 10^9/L Normal
Absolute lymphocyte 1.0 – 3.6 x 10^9/L Normal
1.2 x 10^9/L
10^9/L
Absolute monocyte 0.2 x 10^9/L 0.2 – 1.0 x 10^9/L Normal
Absolute eosinophil 0.02 x 10^9/L 0.02 – 0.5 x 10^9/L Normal
Absolute basophil 0.02 x 10^9/L 0.02 – 0.1 x 10^9/L Normal
Interpretation: full blood count shows normal blood result.
1. Renal profile (31/12/2019)
Result Normal range Interpretation
Urea 2.6 mmol/L 1.7 – 6.4 mmol/L Normal
Sodium 136 mmol/L 136 – 145 Normal
mmol/L
Potassium 3.7 mmol/L 3.5 – 5.10 Normal
mmol/L
Creatinine 64 umol/L 50 – 98 umol/L Normal
Interpretation: normal renal profile
2. Liver function test (31/12/2019)
Result Normal range Interpretation
Total protein 44.0 g/L 35.0 – 50.0 g/L Normal
Total bilirubin 101.0 umol/L 3.4 – 20.5 High
umol/L
Alanine 442 U/L 20.0 – 65.0 U/L High
transaminase
(ALT)
Alkaline 212 U/L 40 – 150 U/L High
phosphatase
(ALP)
Albumin 44.0 g/L 35 – 50 g/L Normal
Interpretation: liver function test suggestive og liver injury and obstructive
jaundice.
3. Serum amylase
Result: 1132.6
Impression: acute pancreatitis
4. HPB system ultrasound scan
Result:
• Liver has slight increase in echogenicity however margins are regular. Liver span
measures 13.3cm. No obvious focal liver lesion.
• No biliary tree dilatation.
• Portal vein is patent with normal hepatopetal flow.
• Gallbladder is distended with minimal sludge within. There are few calculi seen,
collectively measuring 1.3cm. No pericholecystic fluid noted. The gallbladder wall
measures 1.3cm.
• Visualized part of pancreas is normal.
• Spleen measures 9.0cm. No focal lesion seen.
• No ascites
Impression: cholelithiasis with minimal sludge within and features of fatty liver disease
5. Endoscopic ultrasound
Result:
• Pancreas appears heterogenous and edematous.
• Common bile duct and pancreatic duct are not dilated.
• Subscentimetric portal lymph nodes.
• Vessels intact.
Impression: recent pancreatitis with no common bile duct obstruction
FINAL DIAGNOSIS: acute pancreatitis secondary to choledocholithiasis
PLAN OF MANAGEMENT
o Admitted for laparoscopic cholecystectomy
o Vital signs monitoring
o Continue T. Metformin 500mg BD
o Nil by mouth
o Intravenous drip 3 pints normal saline with 2 pints dextrose 5% per 24 hours
o Intravenous Tramal 50 mg
o Intravenous Maxalon 10 mg
DISCHARGE SUMMARY
Patient to be discharged with medication and to come again in 6 weeks.
DISCUSSION
Jaundice and asymptomatic hyperbilirubinemia are common clinical problems that
can be caused by a variety of disorders, including bilirubin overproduction, impaired
bilirubin conjugation, biliary obstruction, and hepatic inflammation. Below are the causes
of conjugated hyperbilirubinemia:
Defect of canalicular organic anion transport
Dubin-Johnson syndrome
Defect of sinusoidal reuptake of conjugated bilirubin
Rotor syndrome
Extrahepatic cholestasis (biliary obstruction)
Choledocholithiasis
Intrinsic and extrinsic tumors (eg, cholangiocarcinoma, pancreatic cancer)
Primary sclerosing cholangitis
AIDS cholangiopathy
Acute and chronic pancreatitis
Strictures after invasive procedures
Certain parasitic infections (eg, Ascaris lumbricoides, liver flukes)
Intrahepatic cholestasis
Viral hepatitis
Alcoholic hepatitis
Nonalcoholic steatohepatitis
Chronic hepatitis
Primary biliary cholangitis
Drugs and toxins (eg, alkylated steroids, chlorpromazine, herbal medications
[eg, Jamaican bush tea], arsenic)
Sepsis and hypoperfusion states
Infiltrative diseases (eg, amyloidosis, lymphoma, sarcoidosis, tuberculosis)
Total parenteral nutrition
Postoperative cholestasis
Following organ transplantation
Hepatic crisis in sickle cell disease
Pregnancy
End-stage liver disease
As mentioned in the history, the causes of obstructive jaundice in this case might
be due to extrahepatic biliary obstruction which is choledocholithiasis. However, there no
sign of obstruction in the biliary tree which contradict the diagnosis of choledocholithiasis.
This may be due to the stone has pass through the biliary tree. That is why the obstructive
jaundice in this patient had resolved.
The diagnostic approach to the jaundiced patient begins with a careful history,
physical examination, and initial laboratory studies. A differential diagnosis is formulated
based on those results and additional testing is performed to narrow the diagnostic
possibilities.
Although the evaluation is usually not urgent, jaundice can reflect a medical
emergency in a few situations. These include massive hemolysis (eg, due to Clostridium
perfringens sepsis or falciparum malaria), ascending cholangitis, and fulminant hepatic
failure. Expedient diagnosis and appropriate therapy can be life-saving in these settings.
History and physical examination — Multiple clues to the etiology of a patients'
hyperbilirubinemia can be obtained from the history, which should seek the following
information:
●Use of medications, herbal medications, dietary supplements, and recreational drugs
●Use of alcohol
●Hepatitis risk factors (eg, travel, possible parenteral exposures)
●History of abdominal operations, including gallbladder surgery
●History of inherited disorders, including liver diseases and hemolytic disorders
●HIV status
●Exposure to toxic substances
●Associated symptoms
Associated symptoms often help narrow the differential diagnosis. As examples:
●A history of fever, particularly when associated with chills or right upper quadrant pain
and/or a history of prior biliary surgery, is suggestive of acute cholangitis.
●Symptoms such as anorexia, malaise, and myalgias may suggest viral hepatitis.
●Right upper quadrant pain suggests extrahepatic biliary obstruction.
●Acholic stool (also termed clay colored stool) refers to stool without the yellow-brown
color, which is normally derived mainly from the bilirubin breakdown products, urobilin
and stercobilin.
Although rare, it can also be seen in the acute cholestatic phase of viral hepatitis
and in prolonged near-complete common bile duct obstruction from cancer of the
pancreatic head or the duodenal ampulla.
The physical examination may reveal a Courvoisier sign (a palpable gallbladder,
caused by obstruction distal to the takeoff of the cystic duct by malignancy) or signs of
chronic liver failure/portal hypertension such as ascites, splenomegaly, spider angiomata,
and gynecomastia. Certain findings suggest specific diseases, such as hyperpigmentation
in hemochromatosis, Kayser-Fleischer rings in Wilson disease, and xanthomas in primary
biliary cholangitis.
The next part of the discussion is about acute pancreatitis. Acute pancreatitis is
characterized by an acute inflammatory process happens in pancreatic gland associated
with acinar cell injury involving local and systemic response. Severity of this condition
may be categorized from mild to severe. Mild pancreatitis might be limited to interstitial
edema with minimal loss of gland function. Differ from mild, severe pancreatitis might
involve peri-pancreatic necrosis with other possible complications which can be an
emergency situation.
The incidence of acute pancreatitis in Western population ranges from 242 per
million to 750 per million. In Malaysia, there is limited data to analyse the pattern of this
condition in the population. A study done by Kandasam P et al in 2002, the racial
breakdown of acute pancreatitis was Malays (28.6%), Chinese (14.3%), Indians (56.4%)
and Orang Asli (0.8%). However, there is no etiological factor discovered in comparing
those three big races. It is more likely to occur in women than men with an increasing
incidence in young and middle age group.
Acute pancreatitis aetiology has been well-established. It is known that there are
multiple causes that can induce inflammation to the pancreatic tissue. The most common
cause of acute pancreatitis in adult is gallstone followed by alcohol consumption. In a study
done by Tonsi Alfredo F et al, in 2009 found that pancreatitis is more common among
women as cholelithiasis is comparatively more common among them. Apart from that,
viral hepatitis can be one of the causes however the pathophysiology is remains unclear.
Referring back to the case, this patient has cholelithiasis with possible
choledocholithiasis that cause the obstructive jaundice signs manifested by this patient.
Although there was no calculus seen in the duct, it is possible that the tiny calculi had
passed through the duct and enter the small bowel. It is hypothesized in that manner as
there was no signs of obstruction due to other factors such as stricture or abnormal growth
tissue in the biliary duct. The visualized pancreatic tissue might be oedematous however
there was no abnormal lesion in the pancreatic head and ampulla of Vater that can cause
obstruction to the bile flow.
The pathophysiology of gallstone pancreatitis occurs when the tiny stone might
have been stuck and blocked the secretion of pancreatic enzymes into the small bowel.
Subsequently, the reflux of bile into the pancreatic tissue and delay in secretion of the
enzyme can induce inflammation in respond to the abnormal flow. The condition can be
worsened with the activation and retention of pancreatic enzyme in the cell because of the
blockage which lead auto digestion of its own cell. This might further damage the acinar
cell leads acute pancreatitis and dysfunction of the gland. Sequel of this condition can lead
to haemorrhage which can be manifested as Grey Turner sign – flank discoloration due to
retroperitoneal bleeding in patient with pancreatic necrosis – and Cullen’s sign –
periumbilicul discoloration due to bleeding – abscess, pseudo cyst, necrosis and systemic
complications including multiorgan failure or septic shock.
This patient also has underlying viral hepatitis B which has been diagnosed a month
ago and family history of hepatitis B.
The relationship between viral hepatitis and acute pancreatitis is recognized for
more than 60 years. Among the case reported, hepatitis B is one of the causes that can
exacerbate inflammation to the pancreas parenchyma. A study by Geokas et al. found that
6% of patient with acute pancreatitis has the role of the virus in the pathology of the injury
to the pancreas. Another study done by Jain et al. in 2007, found an incidence of 5.65% of
pancreatitis from 124 patients with acute viral hepatitis.
The mechanisms in the development of injury to the pancreas parenchyma due to
hepatitis viral infection are unknown and might be due to many factors involved. There are
several hypotheses proposed by researchers, caused by direct cytopathic effect on acinar
pancreatic cell by the viruses, immune-mediated aggression against infected pancreatic
cells. These hypotheses are supported with multiple studies demonstrating the presence of
surface and core antigens of hepatitis B virus within pancreatic parenchyma including its
secretion. However, there is no direct evidence of the pathway of viruses to the pancreatic
tissue.
Acute pancreatitis is common in gallstone patient and might complicate with acute
hepatitis which considered as uncommon. There are association of acute pancreatitis with
acute hepatitis even though no direct evidence showing pathway of viruses reach the
pancreas.
(1269 words)
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NAME OF STUDENT: NURULASYIKIN BINTI MOHD ALI ALFIKRI
MATRIC NO: 2015428728
SUPERVISOR’S COMMENTS ON CASE WRITE-UP
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MARKS:
NAME OF SUPERVISOR: DR. YAHYA MOHD ARIPIN
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