Shamsurin CWU Awerz

You might also like

Download as doc, pdf, or txt
Download as doc, pdf, or txt
You are on page 1of 10

HISTORY TAKING

Patient’s Demography

Patient’s Initial: SS

Age: 31 years old

Sex: Male

Race: Malay

Occupation: Health Inspector

Hometown: Jerantut, Pahang

Current Medical Illness:

1. Congenital Ventricular Septal Defect without corrective surgery done


2. Hypertension
3. Gout

Date of admission: 23rd of August 2008

Chief Complaints

He complained of shortness of breath and cough one day prior to admission.

History of Presenting Illness

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

Genitourinary symptoms: No urinary symptoms such as dysuria,


hematuria, polyuria, nocturia, urinary incontinence or urgency.

Gastrointestinal symptoms: No gastrointestinal symptoms such as change


in bowel habit, nausea or vomiting.

Past Medical History

He has congenital ventricular septal defect and being followed-up at


Institut Jantung Negara (IJN) until he was 15-years old. No corrective surgery
was done at that time. On 2004, he was diagnosed by IJN to have dilated
cardiomyopathy. He is now on medication and being followed-up by IJN every
three month.

He also has hypertension, diagnosed on 2003. He was on medication but


not compliant because the medication cause him difficult to work.

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.

He does not have diabetes mellitus or asthma.

Drug History

1. Carvedilol 12.5mg two times daily


2. Digoxin 0.125mg once daily
3. Spironolactone 12.5mg twice per day
4. Lasix 40mg once daily
5. Allopurinol
6. Painkiller for the gout.
7. Steroid-base cream for the rashes at his buttock and thigh. He has
been using it for the past two months.

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.

His vitals were:

Pulse rate: 112 beats/min

Blood pressure: 160/100 mmHg

Respiratory rate: 20 breaths/min

Temperature: 38.6 oC

SpO2: 98% on room air

On examination of the hand, it was warm in temperature. There were


whitish tophi deposit at interphalangeal and metacarpophalangeal joints, wrist
joints and elbow. The movements of hand joints were restricted.

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.

On examination of the neck, the patient has dorsocervical hump. Jugular


venous pulse was not seen and there was no palpable lymph node.

On examination of the lower limbs, there was pitting oedema up to the


shin. There were also similar whitish deposits on the toes and heels of the foot
but compared to the hand, these deposits were tender.

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.

On ascultation, S1 and S2 were present and normal. There was


pansystolic murmur at tricuspid area. There was no added heart sound.

Respiratory System

On inspection of the chest, there was no deformity of the chest shape.


There was no usage of the accessory respiratory muscles.

On palpation, trachea was not deviated. Chest expansion was symmetrical


but which measured 3cm. Tactile vocal fremitus was equal on both side.

On percussion, the lung was resonance without any area of dullness or


hyper resonance.

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.

On palpation, the abdomen was soft and non-tender. There was no


palpable mass and no organomegaly. Liver span was 10cm. Shifting dullness was
present but fluid thrill was negative.

On ascultation, bowel sound was present and normal.

Musculoskeletal System

There were whitish tophi deposits at the metacarpophalangeal and


interphalangeal joints, wrist joints and elbow joints. It was non-tender. The
movement of hands was restricted. There were similar whitish tophi deposits on
the toes and heels of the foot and they were tender. Movements of the toes were
also restricted. On further examination, similar tophi deposits also present at the
helixes of the ears.

Nervous System

Central and peripheral nervous systems were grossly intact.

SUMMARY

A 31 year-old Malay male, with history of congenital ventricular septal


defect, dilated cardiomyopathy, hypertension and gout, complained of shortness
of breath associated with productive cough, and orthopnea but no chest pain. On
examination, he has Cushingoid appearance, there was precordial bulging, apex
beat was at 6th intercostal space at anterior axillary line, there were of palpable
P2 and pansystolic murmur at tricuspid area and bilateral basal crepitation.

DIAGNOSIS

1. Heart failure secondary to dilated cardiomyopathy.

2. Eisemenger’s syndrome

INVESTIGATION

These are investigations that have been done on this patient

Blood investigation

Full blood count (FBC)

Cardiac enzymes

Renal profile (RP)

Liver function test (LFT)

Prothrombin time and International Normalise Ratio (PT & INR)

Activated Partial Thrombin Time (APTT)

Direct and Indirect Bilirubin

Blood Glucose Level

Lipid Profile

Serum Cortisol

Urates

Radiology

Chest X-ray

Echocardiogram

FBC

Hb=12.9 g/dL
Heamatocrit=44.3%

Platelet=329 k/uL

White cell count=13 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%.

Echocardiogram is the definitive investigation to confirm of heart failure. The


findings suggest that the patient have heart failure which maybe secondary to
dilated cardiomyopathy.

Blood Glucose

Blood Glucose=4.90 mmol/L

Lipid Profile

Cholesterol=3.38mmol/L

High Density Lipoprotein (HDL)=1.12mmol/L

Low Density Lipoprotein (LDL)=1.71mmol/L

LDL/HDL ratio= 1.52

These tests were done to screen if the patient has undiagnosed metabolic syndrome.
Blood glucose and lipid profile are normal.
Cardiac Enzymes

Creatinine Kinase (CK)=73 U/L

Aspartate Transaminase (AST)=27 U/L

Lactate dehydrogenase (LDH)=687 U/L

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

Alanine aminotransferase (ALT)=18umol/L


Albumin=25 g/L

Albumin/Globulin ratio=0.47

Alkaline phosphatase (ALP)=149U/L

Direct & Indirect Bilirubin

Direct Bilirubin=14.30 umol/L

Indirect Bilirubin=13.60 umol/L

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

The patient was given:

1. Intravenous augmentin 1.2g stat and three times daily.

2. Intravenous frusemide 80mg three times daily for 1 day then 40 mg three
times daily for 1 day then 40 mg twice daily.

3. Fluid restriction 1L per day.

4. Withold carvedilol.

5. Combivent nebulizer stat and 6 hourly.


6. Continue spironolactone 25 mg twice daily.

7. Digoxin 0.125mg once daily

8. Warfarin

9. Colcichine

The patient was referred to Rheumatology Department of Hospital Selayang for


his gout. He was also referred to IJN for assessment to undergo pacemaker
resynchronization procedure.

DIAGNOSIS

1. Acute heart failure secondary to pneumonia.

2. Gout

DISCUSSION

Heart failure in this patient is the complication of dilated cardiomyopathy which


was diagnosed in 2004. Dilated cardiomyopathy which he is having most
probably secondary to hypertension. However, patient at this age is unlikely to
develop essential hypertension and therefore underlying causes must be
investigated.

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.

Dilated cardiomyopathy is a disease of cardiac muscle characterized by


dilatation and impaired systolic function of right or left ventricle. In this patient
echocardiogram shows dilatation and decrease in left ventricular function.

Dilated cardiomyopthy is commonly cause congestive heart failure. Therefore, it


is presented with signs and symptoms of left and/or right heart failure. This
patient was presented with shortness of breath, orthopnea and paroxysmal
nocturnal dyspneoa. Chest X-ray shows the evidence of pulmonary oedema,
pleural effusion, prominent upper lobe vessels, and cardiomegaly, which is very
suggestive of heart failure. Echocardiogram further confirmed the diagnosis
where the ejection fraction is 20% only with evidence of dilated cardiomyopathy.

As stated in investigation section, renal and liver impairment are the


complication of heart failure. Therefore, investigations were done to monitor the
function of these organs. Some drugs are metabolized and excreted via these
organs and therefore, their functions must be assess before administration of the
drugs to prevent side effects and this case is digoxin.
Besides that, dilated cardiomyopathy will cause hemodynamic disruption within
the heart chambers and this increase the risk of thrombus formation. The
complications of thrombi formation are stroke, pulmonary embolism a
Therefore, warfarin administration is considered to prevent this from happening.
PT, INR, APTT was investigated to ensure that the patient is not haemophilic.

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.

If the disease is refractory to pharmacological treatment, definitive cardiac


transplant should be a choice. However, as the outcome of the transplantation is
not good where 5-year survival is 75%, pacemaker resynchronization will be
another alternative.

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.

You might also like