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Pancreatic Cancer
22
KULIYYAH OF MEDICINE DEPARTMENT OF SURGERY CASE WRITE UP 1 CANCER OF HEAD OF PANCREAS Name: Nurul Farhana Binti Mustafa Matric No.: 0816492 Group: C2 Year: 3
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KULIYYAH OF MEDICINE

DEPARTMENT OF SURGERY

CASE WRITE UP 1

CANCER OF HEAD OF PANCREAS

Name: Nurul Farhana Binti Mustafa

Matric No.: 0816492

Group: C2

Year: 3

Supervisor: Prof. Dr. Azmi Mohd Nor

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HISTORY TAKING

Identification Data

Name: Mohd Ramly AzizDate of Birth: 3 November 1964Age: 46 years oldGender: MaleEthnicity: MalayRegistration No.: 659098Ward: Kiambang 5CHospital: Hospital Tuanku Ampuan AfzanHome Address: Lot 10002, Jalan Salleh Aman, Kampung Kelat Rendang, Pekan, Pahang.Referred from: Kuantan Medical CentreDate of Admission: 15 October 2010Date of Clerking: 17 October 2010Date of Discharge: 18 October 2010

Chief complaint:

Abdominal pain for 10 weeks duration and jaundice for 8 weeks duration

History of presenting illness:

Patient is a known case of gastritis which was diagnosed on 2009 and has been treated by medication and currently resolved. He is also a known case of hypertension which was diagnosed at age of 40 years old and currently on antihypertensive medication.

Patient was apparently well until 10 weeks ago when he gradually developed abdominal pain localized at epigastric region. The pain was dull, aching in nature and was intermittent. Each episode of pain was last about 10 minutes with pain free interval about 3 to 4 hours. The pain was radiating to the back. The pain was aggravated by movement and partially relieved by lying down. The pain was not associated with food intake. The pain was moderate in which it does not restrict his daily activities and not waking up patient at night.

2 weeks after the onset of abdominal pain, patient noticed there was yellowish discolouration of sclera and 3 days later, there was also yellowish discolouration of skin spread to the whole body. It was associated with passing out tea-coloured urine and pale, floating stool. There was also generalized skin itchiness that waking up patient at night due to the itchiness. There was increase in flatus and belching. Patient also complained of loss of appetite and cloth became loosen with loss of weight about 15kg within 2 month. There was no fever, nausea, vomit or loose stool. The patient also denied of dysphagia, odynophagia, hematemesis, melena or hamatochezia.

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On further questioning, patient denied history of passing out worms, eating unusual food or travelling. Patient was a chronic smoker since 18 years old until 2 months ago. He smoked 15 to 20 cigarettes per day. There was no chronic consumption of alcohol. Patient also consumed high fat diet.

Patient denied any bruises, bleeding tendency, polyuria, polydipsia and polyphagia.

3 days after onset of yellowish discolouration of sclera, patient went to seek treatment at Klinik Kesihatan Prabu and was given medication (yellow tablet) for itchiness but it did not resolved. 1 week later, patient went to Hospital Pekan and was given appointment with specialist at surgical outpatient department of Hospital Tuanku Ampuan Afzan on 25 November 2010. Increasing worrisome of his condition, patient then went to Kuantan Medical Centre (KMC) instead of waiting for the appointment with specialist in Hospital Tuanku Ampuan Afzan on 2 days prior to admission. At KMC, abdominal ultrasound was done and showed the presence of mass at head of pancreas. He was then referred to Hospital Tuanku Ampuan Afzan 2 days later.

Systemic Review

General: Patient denied having fever. He has los of appetite, loss of weight, generalized skin itchiness and sleep disturbance due to itchiness.

Respiratory: Patient denied of having cough, breathlessness, sputum and haemoptysis.

Cardiovascular: There was no complaint of chest pain, dyspnoea, orthopnoea, cyanosis, palpitations or leg swelling.

Genitourinary: Patient complained of having tea coloured urine since 8 weeks ago. He also complained of terminal dribbling since the last few years but he was not sure the exact duration. However, he denied of having frequent micturition, dysuria, urgency, urinary incontinence or hematuria.

Haemopoeitic: Patient denied of pallor, bleeding tendency, bone pain or swellings of body.

Musculoskeletal: Patient denied of joint pain, swelling, restricted movement or limb weakness.

Neurological: Patient denied of headache, fit, abnormal movements or speech.

Past medical history

Patient was diagnosed to have gastritis on 2009. He was treated with medications and currently the illness has resolved. He was also diagnosed to have hypertension at age of 40 years old and currently on antihypertensive drug. This is the second hospitalization. The first hospitalization was when the patient in primary school for four days for acute gastroenteritis and he was discharged well. He has history of ureteric calculi 3 years ago which was treated as outpatient by medication and resolved. There was no history of undergoing any surgery or blood transfusion.

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Drug history:

Patient is currently on tablet metoprolol 50mg taken once daily after eating for the past 6 years for hypertension. However, he was not compliance to the drug in which sometimes he forgot to take the drug at least twice a week. He denied of having any allergy to drugs or foods.

Family history:

Patient was the eighth child of nine siblings from a non-consanginuous marriage. Both of his parents and one of his siblings have hypertension. He was married with 6 children and all of them are healthy. There is no history of malignancy or diabetes run in the family. There was no other similar illness in the family.

Social history:

Patient works as security guard at plywood factory for 8 hours per day and 6 days per week in which he sometimes exposed to the plywood dust. His income is about RM800 per month. He was an active smoker since 18 years old until 2 months ago when he quit from smoking. He smoked about 15 cigarettes per day. He does not take alcohol and denied sexual promiscuity and drug abuse. He likes to take food with high calories. He lives in Pekan with his family of 8 people in an isolated, wooden house in village with 4 rooms. The toilet was inside the house. The water supply is from pipe water but he complained that sometimes the water was dirty but the water was always boiled before consuming it. The electrical supply was adequate. The waste disposal was proper in which the rubbish was taken away by garbage lorry.

Physical examination

General inspection:

Patient was conscious, alert and cooperative. He was not in respiratory distress. His hydrational and nutritional status was fair. Patient is jaundiced and scratch marks noted all over the extremities. He was not anemic and not cyanosed. There was a branula attached on the dorsum of left hand with intravenous drip of dextrose 5%.

The vital signs were:

Respiratory rate: 18 breaths per minutePulse rate: 58 beats per minute (regular in rhythm and good volume)Temperature: 37 CBlood pressure: 130/74 mmHg

General examination:

Skin: The skin was yellow-tinged. The hair was normally distributed. There was no petechiae, bruising or any sign of bleeding disorder.

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Hand: There was scratch marks on hand. However, there was no clubbing, leukonychia, peripheral cyanosis, palmar erythema, Dupuytren’s contracture or flapping tremor noted.

Head and neck:

There was no gross facial abnormality. The sclera was jaundiced. The conjunctiva was not pale.

The tongue was moist but there was yellowish discolouration under the tongue. There was no central cyanosis or ulcer. The oral hygiene was good. The throat was normal and the tonsil was not enlarged. The cervical and supraclavicular lymph nodes were not palpable.

Limbs: There was no pedal edema or any joint swelling noted.

Abdominal examination:

On inspection, the abdomen was not distended and move with respiration. Umbilical was centrally located and inverted. There was no herniation, dilated vein, scar or striae.

On superficial palpation, the abdomen was soft and non-tender. On deep palpation, there was no mass noted. Liver and spleen were not palpable. Traube’s space was resonance. Kidney was not ballotable.

On percussion, the abdomen was resonance. Liver dullness was noted from right 5 th

intercostals space at midclavicular line up to subcostal border. Liver span was 9 cm. There was no ascites.

On auscultation, normal bowel sound was present.

Genital was normal. There was no testicular atrophy.

On per rectal examination, there was no fissure, skin tags or excoriation of the anal skin. The anal tone was normal. There was presence of faecal matter in the bowel but no palpable growth or masses were felt.

Chest:

On inspection, the chest shape was normal and symmetry. The chest moves symmetrically with respiration. There was no scar, use of accessory muscles of respiration or subcostal, substernal and intercostals recession noted. In addition, there was no dilated vein, gynecomastia, bruising or loss of body hair noted.

Cardiovascular:

On palpation, the pulse was normal in volume, regular in rhythm with no bounding pulse. There was no radio-radial or radio-femoral delay noted. All peripheral pulses were palpable. The

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apex beat was palpable at 5th intercostal space at left midclavicular line. There was no parasternal heave or thrill noted.

On auscultation, the first and second heart sounds were present and normal. There was no added sound, murmurs or pericardial rub heard.

Respiratory:

On palpation, trachea was centrally located. Chest expansion was normal and equal on right and left sides. Apex beat was located at 5th intercostal space at left midclavicular line. Vocal fremitus was normal in both lungs.

On percussion, all areas of lung are resonant.

On auscultation, the air entry was equal on both side of lung and vesicular breath sound was heard all over both of the lung. There was no added sound and vocal resonance was normal.

Neurological and musculoskeletal examination:

Patient was conscious, alert and well oriented. There was no muscle weakness of limb or joint swelling noted. The cranial nerves were grossly intact. All reflexes and sensation were normal.

Summary:

Mohd Ramly Aziz, 46 years old, Malay male presented with complaint of abdominal pain for 10 weeks and jaundice for 8 weeks prior to admission. The pain was intermittent, dull in nature, radiating to the back and worsen by movement. It is associated with progressive obstructive jaundice with tea-coloured urine, pale coloured stool and generalized skin itchiness. He also lost of appetite and weight but no fever, nausea or vomiting. He was a chronic smoker and likes to consume high fat diet.

On physical examination, patient was jaundiced all over the body with scratch marks on extremities. There was no other significant finding in other systemic examination.

Provisional diagnosis

Carcinoma of head of pancreas

Diagnosis Supportive points Opposing pointsCarcinoma of head of pancreas

-obstructive, progressive jaundice-tea-coloured urine-pale, floating stool-pruritus-loss of appetite and loss of

-gallbladder not palpable (gallbladder is frequently palpable in patient with obstructive jaundice due to pancreatic cancer)

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weight-abdominal pain at epigastric region-man: men are more commonly affected than women-risk factors: i) tobacco smokingii) high fat diet

Differential diagnosis

1. Periampullary carcinoma2. Choledocholithiasis3. Cholangiocarcinoma4. Viral hepatitis5. Hepatocellular carcinoma6. Acute cholecystitis7. Ascending cholangitis

Diagnosis Supporting points Opposing points1. Periampullary

carcinoma-jaundice-nausea-pruritus-dark coloured urine-pale stool-abdominal pain-loss of appetite and loss of weight

-gallbladder was not distended or palpable-no diarrhea (diarrhea is a common symptom but not universal for periampullary carcinoma)

2. Choledocholithiasis -jaundice-abdominal pain-loss of appetite-nausea

-no fever-pain is not colicky-pain not associated with food intake-no vomit

3. Cholangiocarcinoma -progressive obstructive jaundice-Jaundice was preceded by vague dyspeptic pain-loss of appetite and loss of weight-generalized pruritus

-abdominal pain is not localized (usually in cholangiocarcinoma, there is dull ache pain on right upper quadrant)-courvoisier’s sign was negative, gallbladder not palpable (if cholaniocarcinoma located

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distal to origin of the cystic duct, patient may have a palpable gallbladder.-no hepatomegaly

4. Viral hepatitis -nausea-anorexia-jaundice-dark urine (tea-coloured urine)-pale stool

-Abdominal pain not localized at right upper quadrant-No risk for infected with viral hepatitis: i) history of blood transfusionii) intravenous drug abuseiii) multiple sexual partneriv) good sanitation

5. Hepatocellular carcinoma

-abdominal pain-jaundice-loss of appetite and loss of weight

-no hepatomegaly-no ascites

6. Acute cholecystitis -abdominal pain and radiating to the back-pale-coloured stool-jaundice-nausea

-no fever-abdominal pain not localized to right upper quadrant and not severe-pain was not associated with food intake-no vomit-gallbladder not palpable-negative murphy’s sign

7. Ascending cholangitis -jaundice-abdominal pain

-no fever-pain was not localized at right hypochondrium region

Investigation

1. Full blood count:It is done to look for evidence of anemia by looking at the hemoglobin level. If the patient has hemolytic anemia, hemolysis will lead to increase bilirubin production resulting in jaundice. It is also done to look for evidence of infection by looking at total white blood cell count. Increase in neutrophil count suggests bacterial infection while increase in lymphocyte count suggests viral infection.

Result Unit Reference rangeHemoglobin 14.0 g/dL 13.0 – 17.0Total red blood cell 4.80 1012/L 4.50 – 6.50PCV 41.6 % 40.0 – 50.0MCV 86.7 fL 83.0 – 101.0

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MCH 29.2 PG 27.0 – 32.0MCHC 33.7 g/dL 31.5 – 34.5Platelet 198 109/L 150 – 400Total white blood cell 5.63 109/L 4.0 – 10.0WBC differential count: Neutrophil Lymphocyte Monocyte Eosinophil Basophil

50.331.47.59.61.2

%%%%%

45.0 – 75.024.0 – 45.02.0 – 10.01.0 – 6.00 – 1.0

Comment: The total white blood cell was normal in this patient. This makes infection or acute cholecystitis (inflammation) as a cause of jaundice unlikely. However, eosinophil and basophil count were raised.

2. Liver Function Test

It was done to confirm types of jaundice in this patient either prehepatic, hepatic or posthepatic jaundice based on types of bilirubin and liver enzymes. In prehepatic jaundice, the indirect bilirubin is markedly, normal direct bilirubin and normal liver enzymes. In hepatic jaundice, the indirect and direct bilirubin can both be elevated with increase in aminotransferase enzyme more than alkaline phosphatase. In posthepatic or obstructive jaundice, the direct bilirubin is markedly elevated with marked elevation of alkaline phosphatase. It was also done to assess for function of liver by looking at albumin level.

Result Unit Reference rangeTotal bilirubin 304.9 µmol/L 5.0 – 21.0Direct bilirubin 130.8 µmol/L 0.0 – 3.4Indirect bilirubin 174.1 µmol/L 0.0 – 12.0Total protein 60.8 g/L 66 – 83Albumin 34.4 g/L 35 – 52Globulin 26.4 g/L 20 – 35Albumin/Globulin ratio

1.3 1.0 – 2.2

ALP 228 U/L <129ALT 63 U/L 0 – 45AST 37 U/L 0 – 35

Comment: Total bilirubin was high with elevation in both direct and indirect bilirubin. Alkaline phosphatase was markedly elevated while alanine aminotransferase and aspartate aminotransferase were mildly elevated. The result confirmed of obstructive jaundice. The albumin level was low. This showed decrease function of liver.

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3. Random Blood SugarIt is done to look for presence of hyperglycemia due to diabetes mellitus as a result of complication of pancreatic carcinoma.

Result: 7.8 mmol/L Reference range: 6.5 – 10.0

Comment: The random blood sugar level was normal. This excludes presence of diabetes mellitus.

4. Prothrombin time and activated Partial Thromboplastin Time (PT/APTT)

This test is done to look for presence of clotting derangement. Obstructive jaundice suggests obstruction to bile flow into duodenum. Bile is needed for absorption of lipid soluble vitamin such as vitamin K. When there is decrease bile flow to intestine, vitamin K will be less absorbed. Vitamin K is important for carboxylation of clotting factor. Thus, deficiency of vitamin K can lead to derangement of coagulation characterized by prolong prothrombin time or activated partial thrombin time.

PT: 14.5 seconds N: 10.8 – 12.8

APTT: 21.2 seconds N: 22.1 – 34.1

INR: 1.3

Comment: The PT and APTT results were normal. Thus, there was no clotting derangement in this patient.

4. Renal profile

It was done to assess the function of kidney. In obstructive jaundice due to pathology in the liver, hepatorenal syndrome may develop characterized by progressively rising serum creatinine and diminished urine volume.

Result Unit Reference rangeUrea 5.2 mmol/L 3.20 – 7.30Na+ 138 mmol/L 136 – 146K+ 4.0 mmol/L 3.5 – 5.1Cl- 106 mmol/L 98 – 106Creatinine 91 µmol/L 59 – 104Uric acid 345 µmol/L 208.3 – 428.4

Comment: The results are normal.

5. Tumour marker CA19-9

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CA19-9 is a high molecular weight carbohydrate rich glycoprotein. It is elevated in most individuals with carcinoma of pancreas (80%). It is useful in prediction of unresectability of the tumour. If the level of CA19-9 is more than 200 kU/L, the tumour is unresectable.

Result: Not available

6. Urine full examination microscopic examination (UFEME)

It is done to look for glycosuria due to diabetes mellitus as a complication of pancreatic carcinoma. Urinalysis can help to determine the type of jaundice in this patient by looking at presence of bilirubin and urobilinogen. The presence of elevation of bilirubin in urine without elevated urobilinogen indicates obstructive jaundice while presence of high urobilinogen without bilirubin in urine indicates prehepatic jaundice such as hemolytic anemia.

This test is not done in this patient.

7. Ultrasound of abdomen

Ultrasound is done to look for masses in the pancreas and liver and for dilated bile ducts and stones in the gallbladder.

This test is not done during the admission since it is already done in Kuantan Medical Centre.

Result:

Liver: normal in size and echo-texture, no focal mass or cystBiliary tree: mildly dilated intrahepatic duct, common bile duct is dilated (1.7cm)Gallbladder: distended with normal wall thickness. No stone or mass or sludge.Pancreas: the uncinated process is enlarged with mass formation (3.6 x 4.1 x 5.0 cm). The rest of pancreas is within normal limit. Pancreatic duct is prominent.Spleen: normal with no focal mass or cyst.Kidney: normal in size (R” 11.2cm, L: 11.4 cm). No focal mass, cyst, stone or hydronephrosis.Bladder: underfilled

No ascitesNo lymphadenopathyNo paraaortic lymphadenopathyImpression: No liver abnormality.

No gallstone.Pancreatic malignancy (malignancy of uncinated process).Biliary tree obstruction secondary to pancreatic malignancy.No renal stone or renal disease.

8. Oesophagogastroduodenoscopy (OGDS)

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OGDS is done to visualize any tumour at duodenum or ampulla of Vater and biopsy it. It can confirm the diagnosis of periampullary carcinoma.

Result: Normal with no mass seen.

Comment: The result rules out periampullary carcinoma.

9. CT scan

CT scan is done to show the extent of the tumour and the presence liver metastases. It can also demonstrate vascular tumour invasion of the superior mesenteric and portal veins. The extent of primary or metastases shown on imaging may be such that the tumour is inoperable.

CT scan is not done yet for this patient.

Final diagnosis

Cancer of head of pancreas

Symptoms and signs of obstructive jaundice present in this patient such as jaundice, dark coloured urine, pale stool and pruritus with scratch mark. Loss of appetite and loss of weight are suggestive for malignancy. Malignancy that can present with obstructive jaundice is likely to be either cancer of head of pancreas or periampullary cancer. This is supported by results of liver function test and imaging study. The ultrasound done previously in Kuantan Medical Centre showed enlarged uncinate process of pancreas compressing the bile duct suggestive of cancer of head of pancreas.

Progression in ward

Patient was referred from Kuantan Medical Centre (KMC) to Hospital Tuanku Ampuan Afzan for further management for findings in the ultrasonography of abdomen done in KMC. The ultrasound showed enlarged uncinated process of pancreas with mass formation and the pancreatic duct was prominent with impression of biliary tree obstruction secondary to pancreatic malignancy (malignancy of uncinated process). On admission at the hospital, patient was alert and conscious. The vital signs were:

Pulse rate: 60 beats per minute (regular in rhythm and good volume)Respiratory rate: 17 breaths per minuteTemperature: 37 CBlood pressure: 126/80 mmHg

On examination, patient was jaundiced of sclera and extremities. The hydration and nutritional status were good. Examination of mouth revealed yellowish discolouration under the tongue. Limb examination showed scratch marks all over the limb. Abdominal examination revealed soft, non-tender abdomen without organomegaly or mass palpable.

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He was given intravenous drip of dextrose 5% on admission. He was allowed orally as he tolerated. Patient was under observation with continuous intravenous drip of dextrose 5% from day 1 until day 4 of admission.

On day 4 of admission, oesophagogastroduodenoscpe (OGDS) was done. The finding from OGDS was normal with no mass seen. Chest x-ray was also done after the OGDS to rule out pneumothorax secondary to OGDS. The chest x-ray showed no evidence of pneumothorax or cardiomegaly. Electrocardiography was also done and revealed no ischemic changes.

On evening of day 4 of admission, patient was discharged with given another appointment for CT scan and further management. On discharged, patient was stable.

Discussion

Adenocarcinoma derived from ductal cells of exocrine pancreas make up more than 90% of pancreatic cancers. 70% of tumors arise in head of gland and 30% in the body or tail. The tumors tend to form a well differentiated ductular pattern but the sheets of cells between the ducts often appear more anaplastic. It is a highly malignant tumor in which it metastasizes early to local lymph nodes, peritoneum and liver.

Carcinoma of pancreas presents at a mean age of 65 and extremely rare under the age of 50. However, Mohd. Ramly was only 46 years old during presentation. Risk factors for carcinoma of pancreas include cigarette smoking and previous resectional gastric surgery. Cigarette smoking increases 2 to 3 times the risk and presenting 15 years earlier. Since the patient was a chronic smoker for 28 years, this increases his risk of getting carcinoma of pancreas and explains the earlier presentation of illness at the age of 46 years old.

Pancreatic cancer arises as a consequence of inherited and acquired mutations in cancer-associated genes. The more common molecular alterations in pancreatic carcinogenesis affect K-RAS, p16, SMAD4 and p53. The p16 gene is the most frequently inactivated tumor suppressor gene in pancreatic cancer.

The common presenting features of pancreatic carcinoma are substantial weight loss, abdominal pain and obstructive jaundice which is often without pain. This patient was presented with abdominal pain localized at epigastric region and followed 2 weeks later by progressive obstructive jaundice symptoms associated with tea-coloured urine, pale stool and generalized pruritus.

The pain of pancreatic carcinoma is severe and continuous. It tends to be nocturnal and poorly relieved by analgesics but may be alleviated by leaning forward from sitting position. This severe pain is usually represents locally advanced disease with extension of tumor beyond the pancreas and involvement of retroperitoneal nerves. However, this patient did not suffer from such severe pain. There are often ill-defined dyspeptic symptoms like anorexia, nausea or

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sporadic vomiting. This patient also has loss of appetite and loss of weight. Weight loss is often dramatic even without liver metastases and is much greater than can be explained by anorexic alone.

The obstructive jaundice in cancer of head of pancreas is caused by compression of the common bile duct in its course through the head of pancreas. This can lead to dilatation of proximal bile duct system including the gallbladder causing it become palpable.

Jaundice occurs when systemic retention of bilirubin leads to elevated serum level above 2.0 mg/dL. Bilirubin is the end product of heme degradation. Heme oxygenase oxidizes heme to biliverdin, which is then reduced to bilirubin by biliverdin reductase. Bilirubin bound to serum albumin and conjugated by the liver into bilirubin glucuronides. Most bilirubin glucuronides are deconjugated by gut bacteria and degraded to colourless urobilinogens and pigmented bilirubin which imparts the brown colour to normal feces. Some urobilinogen is reabsorbed, passing to the liver and re-excreted in the bile. A small amount of urobilinogen escapes into the systemic circulation and excreted in urine colouring it yellow. Jaundice occurs when there is either excessive bilirubin production (hemolytic anemia), reduced hepatic uptake, impaired conjugation, decreased hepatocellular excretion (hepatocellular damage) or impaired bile flow.

A failure to secrete bile results in failure to solubilize dietary lipids and fat soluble vitamins resulting in malabsorption. Malabsorption of vitamin K leads to decreased hepatic synthesis of clotting factors. Thus, the patient’s coagulation profile should be checked. Buildup of bile acids leads to their deposition in the skin causing intense itching evidenced by scratch marks on patient’s limb. In obstructive jaundice, there is less urobilin to darken the stool resulting in pale coloured stool while conjugated bilirubin is excreted in the urine turning it dark.

This patient was presented with jaundice for 2 months duration. The investigation done on this patient should be with the aim of finding the cause of obstructive jaundice. Jaundice is confirmed to be obstructive jaundice by looking at the level of bilirubin, liver enzymes and urobilinogen and bilirubin in urine in the presence of the symptoms of obstructive jaundice. The liver function test done in this patient was confirmative for obstructive jaundice. The result shows elevated level of plasma bilirubin predominantly in the conjugated form with marked elevation of plasma alkaline phosphatase. The transaminases are mildly elevated. The liver function test result was suggestive for extrahepatic cause of obstructive jaundice. When biliary obstruction in intrahepatic such as cholangiocarcinoma, there may be mixed biochemical picture with evidence of hepatocyte damage. Infective hepatitis should be excluded by serological screening for hepatitis B and C but the test was not done on this patient. Coagulation studies were performed because of likely defects in clotting as there will be malabsorption of vitamin K due to obstructed bile flow.

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Ultrasound may reveal the cause of obstructive jaundice to be a tumour in the head of pancreas or enlarged lymph nodes in the porta hepatis. CT scan can show the extent of the tumour and the presence and volume of liver metastases.

Most patient with pancreatic cancer present at an incurable stage because of local invasion or metastases. Only about 15% have apparently localized disease with a potential for cure by resection. This patient is yet to be assessed for staging of pancreatic carcinoma due to unavailability of CT scan. However, where resection of the pancreatic head is indicated, whipple’s operation (pancreatico-duodenectomy) is done. When there is obvious widespread disease, adequate analgesia is fundamental and severe pain can be relieved by permanent blockade of the celiac ganglion. Plastic or metal biliary stent can be inserted into the compressed bile duct by ERCP (endoscopic retrograde cholangiopancreaticogram) to relieve the obstructive jaundice.

Sources:

1. Burkitt, H.G., Quick, C. R.G, Reed, J.B. (2007). Essential Surgery Problems, Diagnosis & Management. 4th edition.

2. Garden, O.J., Bradbury, A.W., Forsythe, J., Haddock, G. (2002). Principles and Practice of Surgery. 4th edition.

3. Kumar, V., Abbas, A.K., Fausto, N., Mitchell, R.N. (2007). Robbins Basic Pathology. 8th

edition.4. McPhee, S.J., Ganong, W.F. (2006). Pathophysiology of Disease: An Introduction to

clinical Medicine. 5th edition.


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