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MEDICINE POSTING
YEAR 3 2014
CASE WRITE-UP 2
NAME :
MATRIX NO :
GROUP :
SUPERVISOR :
NB: IF FOUND, PLEASE KINDLY RETURN TO DEANS OFFICE OF UITM SG BULOH
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Presenting Ilness:
Mr. S, a 48 year old Malay gentleman with underlying hypertension and diabetes
mellitus presented to Emergency department of Hospital Sungai Buloh with a
complaint of shortness of breath and bilateral leg swelling since July 2014.
He was previously admitted to Hospital Sungai Buloh with the same presentation
for 3 times. The shortness of breath occurs for about 20 minutes and relieved by
rest. The bilateral leg swelling is up to thigh associated with numbness. He also
complaint of reduced effort tolerance as he can no longer climb up stairs for 1-2
floors, and can only walk less than 100 meters as he is getting tired easily and
shortness of breath.
He did also complaint of chest pain which is localized on the left side of chest
wall, which is sudden in onset, non-radiating, triggered by exertion, lasting for
about 30 minutes and the pain score of 5 was given by the patient by taking 0 is
no pain and 10 is the most painful sensation. He also complaint of dizziness that
lasts for about 5 minutes. However, he denied of any syncope. He is taking 2
tablets of Panadol to relieve the chest pain and dizziness.
He also complaint that he has to sleep with 2 pillows, as he will have shortness of
breath when lying supine and he also complaint paroxysmal nocturnal dyspnea.
Other associated symptoms are sweating, palpitations, nocturia, polyuria,
polydipsia, diarrhoea 10 times a day which is loose watery stool and no black
tarry stool, vomiting 10 times a day with food contents and no hematemesis with
generalized abdominal pain with a fever associated with chills and rigors and
history of taking food outside, loss of appetite and loss of weight.
Systems Findings
General There is no general pain elsewhere.
Cardiovascular System No cyanosis, No syncope or presyncopal
attack
Respiratory System No cough, No hemoptysis
Central Nervous System No headache, No confusion
Gastrointestinal System No nausea
Urinary System No dysuria, No urinary and bowel
incontinence
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Musculoskeletal System No stiffness of joints
Endocrine System No hoarseness of voice, No heat or cold
intolerance
Skin No rashes
He has underlying diabetes mellitus and hypertension for the past 10 years and
not compliance to medication and under Klinik Kesihatan Sungai Buloh follow-up.
He also has hepatitis B since July 2014. He had one surgery done at Hospital
Sungai Buloh in 2012 for carbuncle drainage on his back. He had also a history of
pulmonary tuberculosis 20 years ago and he managed to complete the
treatment. He had no allergies to drugs and foods.
Family History
His mother is having diabetes mellitus while his father had hypertension,
however his father died at the age of 60 because of old age. Otherwise, all family
members were healthy.
Social History
Physical Examination
Vital Signs
Temperature: Afebrile
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Pulse rate: 98 beats per minute
Hands
His palm was warm, moist and pink. Capillary refill time is less than 2
seconds.
No palmar erythema.
No peripheral cyanosis.
There are no nail abnormalities such as nail clubbing, leukonychia and
koilonychia.
There are no stigmata of infective endocarditis such as Oslers node,
Janeway lesion, splinter hemorrhages.
No flapping tremor present.
Eyes
Mouth
Legs
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Scaling of the skin probably due to shrinkage of the oedema following
diuretics.
Systemic Examination
1. Inspection:
The jugular venous pulse is not raised. The chest wall moves
symmetrically with each respiration. There is no chest wall deformity, no
surgical scars, no dilated veins, no skin discolouration, no visible pulsation
of the apex beat noted.
2. Palpation:
The apex beat is at left 5th intercostal space and mid-clavicular line, and
there is no heaves or thrills were palpable
3. Percussion:
Normal cardiac dullness.
4. Auscultation:
Normal heart sound S1 and S2 heard, no added sounds or murmurs.
1. Inspection:
There was no chest wall deformity such as pectus excavatum or pectus
carinatum. Chest wall moved symmetrically with respiration. There was no
surgical scars, no dilated vein and no visible pulsation. No usage of
accessory muscle noted.
2. Palpation:
Trachea was centrally located. Chest expansion was symmetrical on both
sides of the lungs. Vocal fremitus reduced on right lower zone of the right
lungs but normal on the left lungs.
3. Percussion:
There is loss of resonance on right lower zone of the right lungs but normal
on the left lungs.
4. Auscultation:
Vesicular breath sounds was reduced on right lower zone of the right
lungs. There was no added sounds heard.Vocal resonance is reduced on
the right lower zone of the right lungs.
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Interpretation: There is loss of resonance, reduced air entry, vocal
fremitus and vocal resonance on the right lower zone of the left lungs.
1. Inspection:
The abdomen is symmetrical, flat and moves with each respiration. The
umbilicus is inverted and centrally located. There are no surgical scars, no
dilated veins, no skin discolouration, no visible peristalsis, no visible
pulsation.
2. Palpation:
The abdomen was soft and non-tender. No abdominal mass detected. The
liver, spleen, and kidney was not palpable. There was no fluid thrills and
shifting dullness noted.
3. Percussion:
The lower border of the liver is at right lower costal margin and upper
border is at 6th intercostal space.
4. Auscultation:
There was normal bowel sounds, no renal bruits heard.
Summary
Provisional Diagnosis
Points to support:
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He has hypertension for 10 years as hypertension can cause heart failure.
Shortness of breath.
Orthopnea.
Paroxysmal nocturnal dyspnea.
Bilateral pitting oedema up to knee level.
Differential Diagnosis
Investigations
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White blood cell 12.09 X 10^9/L 4-11 X 10^9/L
Hemoglobin 7.5 g/dL 12.0 18.0 g/dL
Hematocrit 23.8% 36 56%
Mean cell volume 75.3 f 78-100 fl
Mean cell hemoglobin 23.7 pg 27-32 pg
Mean cell hemoglobin 31.5 g/dL 31-37 g/dL
concentration
Red cell distribution width 16.6% 11.6-14.6%
Platelet 117 X 10^9/L 150-400 X 10^9/L
Percentage of neutrophil 87.1% 40-75%
Percentage of lymphocyte 8.3% 20-45%
Percentage of monocyte 4.5% 2-10%
Percentage of eosinophil 0.0% 1-6%
Percentage of basophil 0.1% 0-1%
Absolute neutrophil 10.54 X 10^9/L 2-7.5 X 10^9/L
Absolute lymphocyte 1.00 X 10^9/L 1.3-3.5 X 10^9/L
Absolute monocyte 0.54 X 10^9/L 0.2-0.8 X 10^9/L
Absolute eosinophil 0.00 X 10^9/L 0.04-0.44 X 10^9/L
Absolute basophil 0.01 X 10^9/L <0.01 X 10^9/L
Mean Platelet Volume 9.2 fL 7.5- 11.5 fL
Indication: To assess the nutritional status from the albumin level or any liver
damage or to act as a baseline before starting any intervention to the patient.
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3. Renal Function Test
4. Cardiac Markers
Indication:To check for any rise in cardiac enzymes that suggest of myocardial
cell damage.
5. HbA1c Test
Indication: To check for the level of HbA1c as this patient have Diabetes
Mellitus for the past 10 years and to check whether the patient is compliance or
not to medication for the past 1 month.
Interpretation: HbA1c level for this patient is 5.2 most probably is low
because the hemoglobin concentration in this patient also reduced.
6. Electrocardiogram(ECG)
Indication:To check if there is any electrocardiogram waves changes such as ST
elevation, ST depression, T wave inversion, pathological Q waves.
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Interpretation: Sinus Tachycardia with no ischaemic changes.
7. Chest X-ray
8. Echocardiogram
Indication:To assess the function of the heart such as the valve, the chamber
sizes, and the ejection fraction.
Final Diagnosis
Management
General measures
Strict bed rest which is sit up right as the paying is shortness of breath
when lying down supine.
Daily weight monitoring to see how much weight is loss following the
administration of diuretics.
Restriction of fluid 800ml/day
Vital sign monitoring
Specific measures
Flagyl 400mg TDS
Frusemide 80mg
Bisoprolol 2.5mg
Atorvastatin 40mg
Perindopril 2mg
Aspirin 75mg
Indur SR 60mg
Omeprazole capsule 60mg
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Discharge Summary
Discussion
Firstly we should understand or discuss a about the cause of heart failure in this
patient. As we know, there are a lot of etiological causes of heart failure.
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stimulation of the renin-angiotensin-aldosterone system, leading to arteriolar
vasoconstriction to increase afterload and salt and water retention. The decrease
in renal perfusion explained the reduce urine output in some patient. Activation
of the sympathetic nervous system also occurs and may initially maintain cardiac
output through an increase in myocardial contractility, heart rate and venous
return. However prolonged stimulation leads to cardiac myocytes apoptosis,
hypertrophy and focal myocardial necrosis which characterized by less
contractility. These changes produce further fall in cardiac output which then
create a vicious cycle of stimulation.
Minor criteria:
Bilateral ankle edema
Nocturnal cough
Dyspnea on ordinary exertion
Hepatomegaly
Pleural effusion
Decrease in vital capacity by one third from maximum recorded
Tachycardia (heart rate>120 beats/min)
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Abdominal symptoms. Anorexia and nausea associated with abdominal
pain and fullness frequent complaints and may be related to congested
liver and portal venous system.
Cerebral symptoms. Occurs when heart failure accompany with cerebral
artherosclerosis which reduce perfusion to the brain then causing
confusion.
Pulmonary rales, crepitant rales and dullness to percussionover the lung
base are common in patients with heart failure because of pulmonary
edema.
Cardiac edema. Frequently occurs in the sacral region of patient who are
bed-ridden and pitting edema of extremities and face.
Hydrothorax and ascites caused by pleural effusion in congestive heart
failure.
Congestive hepatomegaly.
Jaundice is the late finding in heart failure which is associated with
elevations of both direct and indirect bilirubin due to hepatocellular
hypoxia associated with lobular atrophy. Hepatic enzymes are frequently
elevated.
Cardiac cachexia. Severe chronic heart failure cause cardiac cachexia by
cause increase circulating tumour necrosis factor, elevation of metabolic
rate (increase respiratory rate), anorexia, nausea and vomiting due to liver
congestion or digitalis intoxication.
Other manifestations such as cold, pale and diaphoretic extremities
because of reduce blood flow.
From all of the above manifestations, Mr. S manifested shortness of breath, and
reduced effort tolerance. His shortness of breath can be explained by the flow
chart below:
Investigations:
We can investigate heart failure by doing ECG, which may give clues to the
etiology of heart failure such as left ventricle hypertrophy and evidence of
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previous MI. Besides, chest x-ray also can reveal cardiomegaly and shows
characteristics changes in pulmonary edema, such as distension of upper lobe
pulmonary veins (bat wings appearance), Kerley B lines, hazy hilar opacification
and pleural effusion.
Management:
Management of heart failure patient we can divide it into two types of therapy;
drug therapy and non-drug therapies. For drug therapy, we can give ABCD,
which includes ACE inhibitors, Angiotensin receptor blockers, B-blockers,
Calcium channel blocker (for diastolic heart failure), Digoxin, and vasodilators
while for non-drug we can use cardiac resynchronization therapy, implantation of
cardiac defibrillators, revascularization with coronary artery bypass grafting or
percutaneous coronary intervention, cardiac transplantation and ventricular
assists devices.
There are many factors that increases the risk of getting a heart failure such as
smoking, hypertension, obesity, dyslipidemia to name a few. Therefore, lifestyle
changes or even by taking medication can reduced the risk of getting a heart
failure.
Stop smoking
Keep blood pressure at a healthy level
Keep the cholesterol level under control
Maintain a healthy weight
Eat healthily by taking food that has low fat content
Exercise regularly
References
1. Kumar PJ, Clark ML. Kumar and Clark's Clinical Medicine. W.B. Saunders
Company; 2012.
2. Longmore M, Wilkinson I, Baldwin A et al. Oxford Handbook of Clinical
Medicine. Oxford University Press; 2014.
3. Kumar V, Abbas AK, Aster JC. Robbins Basic Pathology. Saunders; 2013.
4. Clark AL, Goode KM. Do patients with chronic heart failure have chest
pain?. Int J Cardiol. 2013;167(1):185-9.
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SUPERVISORS COMMENTS ON CASE WRITE UP
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