CASE SUMMARY MEDICINE POSTING MBBS PHASE 3B UNIVERSITY MALAYA

Name:

Megat Mohamad Amirul Amzar Megat Hashim

Matric No: MEM080084 Group: 4 (F)

Lecturer: Prof Sanjiv Mahadeva

Patients Details Name: Address: Marital Status: Age: Nationality: IC No: R/N: Date of Admission: Subramaniam A/L Sivalingam Taman Medan, Petaling Jaya, Selangor Married 47 years old Malaysian 650512-10-6357 09878173 28 May 2012

Chief Complaint Mr Subramaniam presented to UMMC with abdominal and bilateral leg swelling three months prior to admission History of Presenting Illness He was previously well until he was diagnosed to have liver disease in 2000. He initially presented to Kelana Jaya Medical Centre with chest pain. The chest pain at that time was burning in nature and persisted for several days. It was localized over the left precordium but possessed no radiation or any other associated symptoms such as sweating or loss of consciousness. It was associated with nausea and vomiting. At that time, he denied of having abdominal pain, changes in bowel output or hematemesis. He also denied of having jaundice or body swelling during that episode. In KJMC he underwent a procedure which he claimed to clean the liver and he was diagnosed to have chronic liver disease based on the biochemical finding. After that, he was well until 4 years later where he presented with the same problem and underwent the same procedure in KJMC. He cannot clarify the exact procedure done and whether it involves an endoscopy or not. After that he went for several follow up to monitor his liver function but receive no other treatment at KJMC Last year, he was referred to UMMC for oesophagoduodenoscopy and claimed to have a rubber banding done. However, he denied of any symptoms suggestive of upper gastrointestinal bleed such as malaena or hematemesis. The procedure was uncomplicated and he was well until current presentation Three months ago, he noticed his leg started to get swollen bilaterally. The leg oedema started in the ankle joints and progressed up to the knee level. He was still able to walk but with difficulty. The leg oedema was associated with abdominal swelling. However

there was no facial or periorbital oedema. He also complained of jaundice which initially only involved the eyes but for the past one week it has progressed to involve his skin. He also complained of reduced effort tolerance but there were no orthopnoea, no paroxysmal nocturnal dsypnoea and no chronic cough. He denies of any pruritus or easy bruising. He claimed to have loss his appetite and weight for about 10kg within these three months. He also claimed to have reduced bowel output but his stool was normal. Three weeks prior to admission, the wife claimed that he was confused as he cannot differentiate dream and reality. It occurred on several occasion but was not continuous. There was no associated memory loss, seizure or loss of consciousness. Both his confusion and his leg oedema worsen until one week prior to admission he came to UMMC for consultation. During consultation he refused to be admitted and was told by the RUKA physician to come again to review his blood test result. On the day of admission, he came to review his blood result and was admitted because of derangement in his blood test result. On assessing the risk factor for chronic liver disease; This patient is a chronic alcoholic where he started to drink 32 years ago. He drank stout and beer about four can per day He have a tattoo which was done last year over his right forearm He denies of intravenous drug usage He denies of sexual promiscuity There were no history of blood transfusion

After being admitted, a peritoneal tapping was done (29 May 2012) and several blood investigation was done but he was unsure of the result. On enquiry of the patient knowledge, he knows that he is having a chronic liver disease and realized this may not be reversible. He is also aware that this is the consequences of his chronic alcoholism but he was still taking alcohol even few days prior to admission. On systemic review, he noticed a lump above his umbilicus two months ago. Currently it is painless and reducible. Its size is about egg size. He denied of any symptoms suggestive of intestinal obstruction. Past Medical and Past Surgical History Previously in 2000, he was diagnosed to have hypertension. He took medication from KJMC for several years but had stop coming for follow up there after his wife stopped working. However, he claimed that his blood pressure was normal every time he come for follow up in UMMC. Apart from that, he had no other chronic illnesses and no other past medical history.

He had an appendicectomy done ten years ago in Hospital Assuntha. There was no complication after the surgery. Drug History There was no known drug allergy. He was not on any longstanding medication either conventional or traditional medication. Family History Mr Subramaniam is married with three children. His parents died of old age. He has six siblings in which all of them are still alive and healthy. There was no family history of malignancy or congenital liver disorder. He also denies of family history of systemic illnesses such as Wilsons disease, hemochromatosis, diabetes mellitus or hypertension. Social History Mr Subramaniam is a chronic alcoholic which he takes about 28 units of alcohol per week. He is also a smoker since 32 years ago and smoked one pack per day. He lives in Taman Medan with his family. Previously he worked as a lorry driver but had stopped working in April 2011 due to his liver disease. His wife previously worked as an operator in a factory near Taman Medan but had stopped working after an accident in the workplace. Currently she is financing her family with the SOCSO compensation of RM350 per month. Their eldest son is working while the other two is still studying at tertiary education. Summary Mr Subramaniam is a 47 year old Indian gentleman with background history of chronic alcoholic liver disease presented with abdominal and leg oedema associated with jaundice and confusion for three months prior to admission. Physical Examination General Inspection The patient is lying comfortably flat on the bed with hir head supported by a pillow. He was alert, conscious and attentive. There was no gross skeletal deformity and he was not cachexic. He is not in a respiratory distress evidenced by respiratory rate of 14 breaths per minute and no usage of accessory respiratory muscle. However the patient look jaundiced evedince by the yellowish discoloration of the sclera and also the skin. His blood pressure was 130/82 mmHg. Peripheral Examination Examination of the hand revealed finger clubbing grade 3, leuconychia and also palmar erythema. There were no duputryen contracture, no peripheral cyanosis and normal capillary filling time. There was a flapping tremor noted. There was no wasting of the small

muscle of the hands and the patients palm is not pale. The pulse is 91 beats per minute with regular rhythm and good volume. Moving to the face, there was scleral jaundice but no conjuctival pallor. His oral hygiene is fair and his hydrational status is adequate. There was no aphtous ulcer or angular stomatitis presence. Examination of the neck reveals no lymphadenopathy or thyroid swelling. His JVP was not raised. Respiratory Examination On inspection of the chest, there was no surgical scar noted. The chest moved symmetrically with each respiration. There was no chest wall deformity. The trachea was not deviated. The chest expansion was normal and symmetrical. Tactile fremitus was normal and equal note felt at both of the chest wall. Percussion of the chest revealed normal resonant note all over the lung. Cardiac and liver dullness was noted. On auscultation, both inspiratory and expiratory breath sound heard without any added sound. Cardiovascular Examination Apex beat was palpable at midclavicular line of the fourth intercostal space which is normal. There are no palpable thrills and no parasternal heave. On auscultation, both S1 and S2 sound heart with normal intensity at all area. There was no murmur or added heart sound heard. Abdominal Examination The abdomen was distended. There was a McBurneys point scar noted measuring about 8cm which had healed normally. There was a paraumbilical hernia which is non-tender and reducible. The hernia size is about an egg size (4cm x 3cm) and it is normal in temperature and colour. There was no dilated vein noted. On superficial palpation, there was no tenderness or mass noted. On deep palpation, the liver cannot be palpated due to gross abdominal distension but no deep tenderness was noted. Fluid thrill was positive. There was no sacral oedema. There is no significant finding in the genitalia. There was pitting oedema of both lower limbs extending from ankle up to the knee joint. Neurological Examination

All the cranial nerves are intact. Both the lower limbs and upper limbs had normal tone, power, reflex and sensation. Assessment of cerebellar function revealed no abnormalities. Summary The patient has stigmata of chronic liver disease which is finger clubbing, palmar erythema, leuconychia and flapping tremor. Furthermore, there was also evidence of ascites by the gross abdominal distension and positive fluid thrill. There was also a paraumbilical hernia noted which is painless and reducible. Lastly, the patient has bilateral leg swelling up to the knee joint. These findings are consistent with chronic liver disease. Provisional Diagnosis Chronic decompensated alcoholic liver disease with hepatic encephalopathy. This patient presented with ascites and leg oedema with stigmata of chronic liver disease. He also had series of confusion episode indicating hepatic encephalopathy. Furthermore he is also a chronic alcoholic which exceed the safe limit of alcohol intake (21 units/week for male). He took 28 units per week for the past 32 years. The symptoms of confusion, jaundice, ascites and also leg oedema arise from decompensation of his liver function. Differential Diagnosis Chronic heart failure. Ascites and leg oedema can present as a symptom of fluid overload secondary from chronic heart failure. However, Mr Subramaniam had no orthopnoea and paroxysmal nocturnal dyspnoea and there is no evidence of pulmonary oedema based on clinical examination. Furthermore gross ascites rarely is caused by heart problem. Chronic renal failure. As fluid overload can be caused by liver and heart problem, renal failure can also present with similar symptoms. Furthermore encephalopathy may arise due to uremia secondary to renal failure. However, this patient have no urinary symptom and thus making the diagnosis least favourable.

Investigation Blood biochemistry which was taken on three occasion (last follow up in 2011, during consultation in RUKA and during admission). Value 22/7/2011 24/5/2012 28/5/2012 Blood urea and serum electrolyte 136 132 3.5 4.8 94 95 3.1 3.8 Normal value 136-145 mmol/L 3.6-5.2 mmol/L 100-108 mmol/L 2.5-6.4 mmol/L

Parameter Date Sodium Potassium Chloride Urea

Creatinine Total protein Albumin Total bilirubin Conjugated bilirubin Alkaline phosphatase ALT AST y-GT Amylase

76 21 (L) 48 (H) 25 (H) 129 28 75 (H) 70 -

94 94 Liver Function Test 80 75 23 (L) 18 (L) 150 (H) 113 (H) 75 (H) 47 (H) 108 78

62-115 mol/L 60-85 g/L 35-50 g/L 3-17 mol/L 0-3 mol/L 50-136 IU/L

32 34 7-56 IU/L 5-35 IU/L 83 (H) 119 (H) 72 53 8-78 IU/L 67 25-115 IU/L Full Blood Count Haemoglobin 14.0 15.1 13.9 13.8-17.2 g/dL Haematocit 0.39 0.42 0.38 0.37-0.47 WBC 7.2 10.5 7.1 4-11 x109/L Platelet 150-400 x109/L 90 (L) 60 (L) 83 (L) 1. Abnormalities within liver function test which are low albumin level and increased bilirubin level indicates that this patients liver is failing. The AST:ALT ratio is more than 2 indicates that this patient is having alcoholic liver hepatitis instead of viral cause. 2. The y-GT was normal despite the patient claimed to drink alcohol a few days prior to admission. This probably means his alcohol intake is low. 3. The platelet count was low which could indicate this patient is having a portal hypertension leading to hypersplenism and hence reducing the platelet count. 4. His renal function was normal which can be used to rule out hepatorenal syndrome and hence his encephalopathy was purely from liver disfunction. 5. However, no coagulation profile was done. This should be done in order to get the information for grading of the liver cirrhosis (Child-Pugh criteria needs prothrombin time). Ultrasound of abdomen 1 June 2012 o Indication: alcoholic liver disease with increasing abdominal distension to rule out liver abscess o Findings: Comparison made with previous US dated 4/7/2011 Ascites noted Liver is coarse in echotexture with irregular margin suggestive of liver cirrhosis No biliary duct abnormalities seen. Portal vein is of normal calibre Cholelithiasis measuring 0.7cm seen with gallbladder wall thickened measuring 1.0cm. Pericholecystic fluid noted Spleen, both kidney and pancreas is normal in size Urinary bladder unidentified

o Impression: Acute calculus cholecystitis Liver cirrhosis with ascites Management 1. His ascites was drained on the second day of admission. His neutrophils count was less than 250/mm3 indicating no spontaneous bacterial peritonitis. Upon the drainage he was also infused with IV albumin to cater for the loss of albumin during the peritoneal tapping. Each 2L of peritoneal fluid tapped, 1 bottle of albumin will be infused. 2. IV antibiotic (Rocephin and Augmentin) was given as prophylaxis for spontaneous bacterial peritonitis. 3. Potassium sparing diuretics, T. Spironolactone 50mg OD was given to lessen the fluid overload. This treatment is appropriate in patient with liver cirrhosis with ascites especially those with portal hypertension. This is because portal hypertension will cause activation of Renin-Angiotensin-Aldosterone axis. Hence spironolactone as an aldosterone antagonist will cease the activation. 4. Oral Lactulose was given 50ml 2 times per day was given as a treatment for hepatic encephalopathy. Lactulose and Lactilol are disaccharides that are not absorbed from the digestive tract. They are thought to improve the generation of ammonia by bacteria, render the ammonia inabsorbable by converting it to ammonium (NH4), and increase transit of bowel content through the gut (1). 5. T. Thiamine 100mg OD was also given due to the chronic alcoholism. Chronic alcoholism may induce thiamine deficiency and may affect the brain. 6. He was referred to the psychiatric clinic for further management of his chronic alcohol dependant. 7. He was also scheduled for another OGDS 2 weeks from the day of his discharge (4 June 2012). Discussion As the region economy grows, alcohol consumption has also increase and has become a major risk factor of liver disease and mortality in Asia. Increased alcohol consumption, combined with poor regulation and policies, pre-existing multiple health risk factors (hepatitis C, hepatitis B and malnutrition) and easier availability of alcohol, was described as a perfect storm by Dr. Marylin O. Arguillas, of Davao Doctors Hospital, Davao City, the Philippines (2). Ultimately the alcohol consumption will lead to cirrhosis and cirrhosis itself has killed 150,000 people a year and 38 to 40 per cent of that is due to alcoholic cirrhosis (1). However, not all alcohol consumers develop alcoholic liver disease. Only 5 to 15 per cent of alcohol consumer suffered from alcoholic liver disease (1). This was postulated to be related to the genetic susceptibility and more importantly frequency and amount of consumption (2).

The pathology arises when alcohol or ethanol enters the body circulation. Most tissues of the body, including the skeletal muscles, contain the necessary enzymes for the oxidative or nonoxidative metabolism of ethanol. However, the major site of ethanol metabolism is the liver. Within the liver, 3 enzyme systemsthe cytosolic alcohol dehydrogenase (ADH) system, microsomal ethanol-oxidizing system (MEOS), and peroxisomal catalase system can oxidize ethanol. The product of all 3 enzymatic reactions is acetaldehyde, which is then further metabolized to acetate by acetaldehyde dehydrogenase (ALDH). Acetaldehyde is a reactive metabolite that can produce injury in a variety of ways (3). Liver failure may be asymptomatic for many years until decompensation occurs. During the asymptomatic period, only biochemical blood test could reveal derangement regarding the liver function. In Mr Subramaniam, during his episode of admission to KJMC in 2000, his liver was probably in the early stage of failure. His admission during that also probably due to cholelithiasis because he presented with pain (although it is chest pain, it could be a referred pain from the abdomen) and the procedure he described is consistent with cholelithiasis. However, he insisted that his liver failure was also diagnosed at that time and he had to come for monthly follow up until he was referred to UMMC for OGDS. Despite having monthly follow up, he did not stop consuming alcohol and hence his liver continued to fail and ultimately he had decompensation of his liver failure. He then suffered from symptom of jaundice, ascites secondary to portal hypertension and recently he developed neurological symptom indicating hepatic encephalopathy. Currently he is at least in stage 2 of hepatic encephalopathy as he suffered from occasional mild confusion and he had asterixis during physical examination. Based on his biochemical blood investigation result and his presentation (bilirubin, albumin, ascites and encephalopathy) he is at least in Child C criteria (the exact score cannot be determined as there is no prothrombin time done). This indicates that his liver cirrhosis is severe and he has high risk of developing oesophageal varices and upper GI bleed. Hence he was scheduled for another OGDS and he may need rubber banding done. Mr Subramaniam was also currently under psychiatric review and follow up as he is having problem with his alcohol dependency. During the clerking, I asked the four CAGE (cut down, angry, guilty and eye opener) questions (4) and he answered yes for the entire question. This indicates him as a severe alcoholic and he need help in changing the habit. His drinking habit also exceeds the maximum safe limit proposed by UK guideline (21 units per week for men) and this has been on-going for 32 years. Initially, the prognosis for Mr Subramaniam is still good (50% of 5 years survival rate) as long as he stop his drinking habits. However since he had developed hepatic encephalopathy, his prognosis became poorer. The most common cause of death in cirrhosis is sepsis (5) which can either arise from nosocomial infection or spontaneous bacterial peritonitis. Other causes of death are hepatic encephalopathy, shock secondary to upper GI bleed and renal failure secondary to hepatorenal syndrome (6).

Reference 1. Hepatic Encephalopathy (June 2012). Retrieved on June 7, 2012 from http://en.wikipedia.org/wiki/Hepatic_encephalopathy#Lactulose.2Flactitol 2. Deaths due to alcohol on the rise in Asia (April 2008). Retrieved on June 7, 2012 from http://www.liver.org.my/resource_education_disease_alcoholic.asp 3. Sandeep M et al. Alcoholic Hepatitis. Medscape Medical Journal (Nov 2011). Retrieved on June 7, 2012 from http://emedicine.medscape.com/article/170539overview#a0156 4. Nicholas J Talley, Simon O Connor. Clinical Examination 6th Edition; 2010 Elsevier (7) 5. In patient Cause of Death in Cirrhosis Shift to Sepsis (July 2005). Retrieved on June 7, 2012 from https://docs.google.com/viewer?a=v&q=cache:_ck0RCid_hcJ:www.internalmedicine news.com/fileadmin/content_pdf/fpn/archive_pdf/vol38iss14/70905_main.pdf+most+ common+cause+of+death+in+cirrhosis&hl=en&gl=my&pid=bl&srcid=ADGEESjRq NR7x1z-jHYehfP6o8lC0aCNT3Q5tYs0fsS9vF008lUbTltGsSP5GCHFCyeIj118yJ3nOLQXEQVXMn3NnvUo_B3axLavPTj2fa_fhtYD0J2rrZq9dRw OFK5P-0Ahz1eSQy0&sig=AHIEtbSI4Px4NJAEK-Hdo9fIzApG93cAwg 6. Cirrhosis of the Liver at the National Digestive Diseases Information Clearinghouse (NDDIC). NIH Publication No. 04-1134, December 2003