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Shamsurin CWU Awerz
Shamsurin CWU Awerz
Shamsurin CWU Awerz
Patient’s Demography
Patient’s Initial: SS
Sex: Male
Race: Malay
Chief Complaints
The shortness of breath started suddenly while he was lifting heavy boxes.
Therefore it was graded as Grade I according to NY classification of heart failure.
It was constant in nature. The shortness of breath worsens by lying flat.
The shortness of breath was associated with productive cough. The sputum was
bloodstained and amount was approximately 10ml. It also has sudden onset and
constant in nature. The cough was aggravated by cold temperature. His sleep
was affected by the cough.
He denies any previous contact with Tuberculosis patient, fever, chest pain,
palpitation, rigor, night sweat, nausea or vomiting, loss of appetite and weight
loss or recent history of immobilization.
He did not take Lasix for two days before the attack because the medication
causes him difficult to work.
He first went to Klinik Kita before he was refered to Hospital Ampang. He first
managed at Emergency Department before being admitted to the ward.
Systemic Review
He also has gout since six years ago. However, it worsened one year ago
after he took Gamat-based traditional medicine, Gamogen. He was admitted to
Hospital Jerantut for treatment.
Drug History
Family History
His father died at the age of 55, with hypertension. His father has strong
history of gout. His mother is alive at the age of 60 and has hypertension and
gout. His brother also has gout and his sister has valve defect.
Social History
He is married with three children who are all healthy. He works as Health
Inspector in Jerantut, Pahang. He lives in a terrace house in Jerantut but
currently stays at a hostel in Kuala Lumpur for a year to finish his assignment.
His room is at second floor.
He is non-smoker, non-drinker and do not have history of sexual
promiscuity.
PHYSICAL EXAMINATION
General Examination
The patient was conscious, alert and well oriented in time, place and
person. He was lying propped up on one pillow and looking comfortable. He was
coughing from time to time. He has truncal obesity.
Temperature: 38.6 oC
The hand was not pale or cyanotic. There was no clubbing, muscle
wasting, Janeway lesion, Osler’s node or splinter hemorrhage. There was also no
flapping tremor. Pulse was difficult to assess due to the tophi deposits at the
wrist joint. The pulse rate was taken using pulse oxymeter. It was 140 beats/min.
On examination of the head, the face was puffy with acne on the cheeks.
There were no conjunctivae pallour or jaundice. There was no central cyanosis
and the hydration was fair.
Specific Examination
Cardiovascular System
On inspection of the chest, there was precordial bulge and apex beat was
obsevable at 6th intercostal space at anterior axillary line. There were dilated
veins but no scars.
On palpation, apex beat was at 6 th intercostal space at anterior axillary
line. There was palpable P2 but parasternal heave and thrills were absent.
Respiratory System
On ascultation, there was bilateral basal crepitus. Air entry was normal.
Vocal resonance was equal on both sides.
Abdominal Examination
On inspection, the abdomen was distended and there were purple striae
and dilated veins. Umbilicus was centrally located and hernial orifices were
intact.
Musculoskeletal System
Nervous System
SUMMARY
DIAGNOSIS
2. Eisemenger’s syndrome
INVESTIGATION
Blood investigation
Cardiac enzymes
Lipid Profile
Serum Cortisol
Urates
Radiology
Chest X-ray
Echocardiogram
FBC
Hb=12.9 g/dL
Heamatocrit=44.3%
Platelet=329 k/uL
This test is to look for any evidence of infection, which is shown by increase in white
cell count as the patient was presented with fever. This is evidenced by the
temperature of 38.6oC. The result shows increase in white cell count and therefore
source of infection should be pinpoint.
Chest X-Ray
This test is done to look for the sign of heart failure and also evidence of infection
that maybe the cause of exacerbation of the heart failure.
There is haziness on both lower zone of the lung. There is also blunting of the
costophrenic angles. Prominent pulmonary vessels at the hilar and upper lobes
are seen. Besides that, there is evidence of cardiomegaly.
Echocardiogram
There is left ventricle and left atrium dilatation. Left ventricular function is poor.
There is also global hypokinetic. Ejection fraction is 20%.
Blood Glucose
Lipid Profile
Cholesterol=3.38mmol/L
These tests were done to screen if the patient has undiagnosed metabolic syndrome.
Blood glucose and lipid profile are normal.
Cardiac Enzymes
RP
Urea=5.87 mmol/L
Na+=136 mmol/L
K+=4.2 mmol/L
Cl-=106mmol/L
Creatinine=108 umol/L
This test was done to determine the renal function as heart failure can lead to renal
failure. This is due to hypoperfusion to the kidney, as the heart cannot pump blood
sufficiently. This is important to ensure drugs, which are excreted by the kidney
unchanged, will not accumulate in the body. However, the test shows no evidence of
kidney function impairment.
LFT
Albumin/Globulin ratio=0.47
These tests were done to check the function of liver which can be impaired due to
congestion, secondary to heart failure. This is important to ensure that drugs that
is metabolized by the liver to be administered with cautious to prevent
accumulation in the body. The test showed a decrease in albumin and increase in
ALP.
PT & INR
PT=14.0 sec
INR=1.22 sec
APTT
APTT=43.6 sec
PT, INR and APTT are monitored to ensure that the patient is not haemophilic as
warfarin will be administered. INR is important to determine the dosage of
warfarin administered to prevent complication. Warfarin is given as the
hemodynamic within the heart chambers are not normal anymore and this may
cause thrombus formation. This test shows coagulation is normal.
Serum Cortisol
Cortisol=461 umol/L
The patient was presented with Cushingoid features. Therefore, cortisol level was
investigated. The test shows normal serum cortisol level.
Urates
Urates=693umol/L
The patient also came with gout. Urates level was investigated and the test showed
high level of urates in the serum.
MANAGEMENT
2. Intravenous frusemide 80mg three times daily for 1 day then 40 mg three
times daily for 1 day then 40 mg twice daily.
4. Withold carvedilol.
8. Warfarin
9. Colcichine
DIAGNOSIS
2. Gout
DISCUSSION
Glusoce level, lipid profile and renal function are normal and therefore these
factors are unlikely to cause hypertension. Other cause of hypertension besides
renal disease and metabolic syndrome are endocrine diseases such as Cushing’s
and Conn’s syndromes, pheochromocytoma, acromegaly and
hyperparathyroidism.
Absent of similar attack before suggests that the failure was stable. However, the
acute exacerbation most probably due to pneumonia which was evidenced by
the fever, increase in white cells count and chest x-ray that shows areas of
consolidation. Pneumonia in this patient was treated as community-acquired
pneumonia with augmentin.
The patient was also presented moon face, dorsocervical hump and purple striae.
These features most probably due to drug induced Cushingoid syndrome.
According to the history, the patient used steroid-based cream for the rashes at
his buttock and thigh. Besides that, he also took gamat-based traditional
medicine, which may contain steroid. Besides the features, immunosuppression
may ensue and infection is more prone to occur. It is made worse by non-
compliance of the patient with the medication that precipitate the attack.
Besides above condition, the patient also presented with gout. As he was in acute
gout where the joints were very tender, he was given colchicine instead of
allopurinol. Allopurinol will further aggravate the gout. It was only given after
the inflammation has settled down. Painkiller is also given to the patient to
relieve the pain.