ACUTE EXACERBATION OF BRONCHIAL

ASTHMA
Patient Data

Name: Salleh Bin Amirudin

Age: 29 year-old
Sex: Male
Race: Malay
Occupation: Guard officer
Marital Status: Married with one child
Address: Triang 3
Date of Admission: 12/09/2009
Date of Clerking: 14/09/2009
Presenting Complaint

Patient with a known case of asthma since childhood, presented to emergency department
of Temerloh Hospital, with shortness of breath, which was started 2 days ago prior to
admission.

History of Presenting Complaint

Patient was apparently well until 2 days ago where he had sudden onset of
shortness of breath in which was continuous at rest, worsening early in the morning for
the last 2 days. Patient also could not complete sentences during the attack. It was
aggravated by cold weather and cold drink and was relieved by inhaler of Salbutamol and
by lying down on two pillows. It was also associated with coughing up sputum,
wheezing, fever, and sweating. Otherwise, there were no palpitation, no chest pain, no
paroxysmal nocturnal dypsnea (PND), no edema, no runny nose, no sore throat, and no
nausea and vomiting.
The cough was on and off, productive with green sputum during early in the
morning and worsens during night. Otherwise, no hemoptysis, and no medications were
taken.
He claimed that having 3 to 4 times asthmatic attacks per day and went to
multiple Health Clinics for nebulizer. He has had more than one nocturnal symptom per
week.
Urine and bowel output were normal. No abdominal pain and no syncope.

Past Medical History

He was a known case of bronchial asthma since childhood. He was admitted to

Temerloh Hospital in April 2009 for the same asthmatic attack. He also had an episode of
coma due to motor vehicle accident (MVA) in 2001.

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Past Surgical History

He had an intestinal surgery in 2006 but patient not sure what is it.
Drug History

Currently, he is on inhaler but not compliance to the medications given by the

hospital due to no symptoms showed by the patient. He also takes traditional medication
for his asthma.
He is allergic to the seafood.

Family History

He is having a strong background of atopic asthma on his dad’s side and 2 of his
brothers also have bronchial asthma since childhood. Otherwise, no history of
malignancy and sudden death run in the family. No history of eczema and chronic
rhinitis.

Social History

He smokes since he was 15 year old until now. He smokes 28 cigarettes per day
which is equivalent to 19.6 pack-years.
He also occasionally consumed alcohol when he was working in Kuala Lumpur
but now had stopped.
He claimed that he did not have sexual promiscuity.
He also had history of drug abuse such as ectasy, syabu, heroin etc. for 9 years
since his 15 till 23 years old. Otherwise, no history of intravenous drugs use.
He works as a guard officer.
He is married with a child but his wife died in 2006 due to accident and stay at
single story house in 424(F), Bukit Kepayang, Triang 3, Pahang. The house is full with a
lot of cats and carpets. He stays with his stepmother and his child. He used to sleep in air-
conditioning bedroom at night.

General Examination

Patient was laying at 45, looked pink, well, and alert with branula attach on the
dorsum of right hand. No accessory muscle was use. He looked hydrated, slightly
tachypnoiec, and not cyanosed. The vital signs were:
 Blood pressure: 106/56 mmHg
 Pulse rate: 101 beats per minute (slightly tachycardic), regular and good
volume.
 Respiratory rate: 21 breath per minute (slightly tachypnoiec)
 Temperature: 37 C
 SpO2 saturation: 95% on air

Hands was warm, no sweating, no clubbing, no nicotine stain, no tremor, no

stigmata of infective endocarditis, no peripheral cyanosis, capillary refill was normal, no

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muscle wasting and flapping tremor. There was no radio-radial and radio-femoral delay.
There was no collapsing pulse.
No pallor and no jaundice. No central cyanosis, hydration was fair and oral
hygiene was good. There was no high-arched palate.
Jugular venous pressure was not raised. Trachea is centrally located and
cricosternal notch was reduced.
Lymphadenopathy and pedal oedema was absent.

Systemic Examination

Respiratory System
Both sides of the chest moved equally with respiration. No usage of accessory
muscles was present. There were no scars, swelling, deformity, discolouration, and spine
abnormality.
No ribs tenderness. Chest expansion was reduced in both lungs. However, tactile
fremitus was equal on both sides of the lung.
Lung percussion was hyper-resonance on both sides. Liver dullness was present
on 6th intercostal space in which indicates hyperinflated lungs.
Air entry was reduced in both lungs. Vesicular breath sounds and generalized
rhonchi can be heard. No crepitation can be heard.

Other Systemic Examination

Cardiovascular System
The chest wall shape was normal. There were no visible apex beat, no extra
pulsation observed, and no surgical scars.
The apex beat was present at 5th intercostal space and slightly lateral to mid-
clavicular line. There were no parasternal heaves, thrills and palpable P 2. No other
pulsation found.
Carotid pulse was adequate in volume.
The first and second heart sounds were present and normal. There were no
murmur and added heart sound heard.

Gastrointestinal System
Abdomen was soft, non-tender and not distended. No liver, spleen, kidneys or
other masses palpable. Shifting dullness was negative. Bowel sounds were present and
normal.

CNS & PNS

Patient was well oriented with time, place and person. The speech, cranial nerves,
sensation, motor function and reflexes, cerebellar function and gait were normal.

Summary

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 Mr Salleh, a 29 year-old Malay gentleman who is a chronic smoker with a known
case of asthma since childhood, presented to Emergency department with short of
breath and cough 2 days prior to admission. It was associated coughing up sputum,
wheezing, fever, and sweating.

Provisional Diagnosis

Acute Exacerbation of Bronchial Asthma (AEBA) 2o to Respiratory Tract Infection

As evidence by strong family history of bronchial asthma since childhood, history

of recurrent episodic of shortness of breath, associated with wheezing, productive cough
and fever, he is most likely having AEBA 2o to respiratory tract infection. He is also a
chronic smoker and stays in the house that is full with cats and carpets. Physical
examination revealed areas of hyper resonance area with generalized rhonchi. A pre and
post nebulizer of peak expiratory flow (PEF) measurement needs to be done to ascertain
the diagnosis.

Differential diagnosis

1. Chronic Obstructive Pulmonary Disease (COPD)

COPD can be differentiated from asthma from several views. COPD has a strong
association with smoking while asthma has slight association. COPD will have chronic
cough without underlying family history of atopic diseases. The gold standard in
differentiating COPD and asthma is based on spirometry and PEF monitoring.

2. Pneumothorax
Severe onset of shortness of breath with sharp pain on the side of pneumothorax is
very suggestive of pneumothorax. However, patient did not experience any of the
symptoms.

3. Acute pulmonary edema

Left ventricular failure can cause accumulation of fluid in both lungs that lead to
development of cardiac asthma. The clinical symptoms would include wheezing,
orthopnea, and cough. However, in this patient there were no PND and no oliguria.
There was no fine bibasal crepitation upon auscultation and chest X- ray does not
revealed features suggesting heart failure.

DISCUSSION
Investigations

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 1. Chest X-ray
o Objective: to look for evidence of infection and pneumothorax
o Impression: Not done.
2. Full blood count (FBC) (done on 12th September 2009)
o Objective: to look for evidence of infection
 Red Blood Cell 5.56 (4-6)
 Haemoglobin 12.2 g/dL (12-18)
 Haematocrit 40.8 % (37-51)
 Platelet 200 K/uL (140-440)
 White Blood Cells 9.6 K/uL (4-11)
o Impression: WBC is increased and indicates sign of infection.
3. Renal profile (RP) (done on 12th September 2009)
o Objective: To look for renal impairment for treatment purposes
 Urea 3.4 mmol/L (1-8)
 Sodium 139 mmol/L Abnormal (135-145)
 Potassium 4.0 mmol/L (3-5)
 Chloride 103 mmol/L Abnormal (98-106)
 Creatinine 62 umol/L (62-106)
o Impression: Urea and creatinine within normal range. Kidneys are
functioning normally.
4. Arterial blood gases (done on 12th September 2009)
o Objective: To look for any sign of acidosis
 pH 7.48 (N: 7.35-7.45)
 pCO2 35 mmHg (N: 35-45mmHg)
 pO2 44 mmHg (N: 75-100mmHg)
 SpO2 96%
 HCO3- 26 mmol/L (N: 24.1 meq/L)
o Impression: Patient in slightly alkalosis state due to hyperventilation.
5. AFB sputum microscopy (done on 14th September 2009)
o Objective: To look for Tuberculosis (TB) infection
 No TB bacteria found
o Impression: Negative TB infection
6. Electrocardiogram (ECG) (not done)
o Objective: To look for signs of heart diseases
7. Spirometry
o Objective: To rule out COPD
8. Peak Expiratory Flow (PEF) (done on 12th September 2009)
o Objective: Measures functional lung volumes.
 Pre nebulizer = 100
 Post nebulizer = 120
o Impression: Improved after nebulizer treatment.

Management

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 1. Nebulizer Atrovan:Ventoline:Normal Saline (1:2:1) 2 hourly
2. Metered dose inhaler (MDI) Budesonide 2 puff twice a day (BD)
3. IV Hydrocortisone 100 mg
4. PEFR charting
5. Advice to stop smoking
6. NPO2 3L/day
7. Tablet Tamiflu 75 mg BD for 5 days (prophylaxis for H1N1)
8. Tablet Erythromycin (EES) 800 mg BD
9. IV Augmentin 12 g

Discussion

Asthma is an inflammatory lung problem that is characterized by recurrent episodes

of dyspnoea, cough, and wheeze caused by reversible airways obstruction. There are
three factors that contribute to airway narrowing:
i. Bronchial muscle contraction – triggered by various stimuli
ii. Mucosal swelling/inflammation – caused by mast cell and basophil
degranulation resulting in the release of inflammatory mediators
iii. Increased mucus production
This patient develop recurrent episode of acute exacerbation of bronchial asthma after
exposed to many risk factors such as smoking, cats’ fur, carpets, cold weather, and cold
drink. These cause inflammation to bronchial that later cause obstruction.
Diagnosing an asthmatic attack can be challenging and measurements of lung
functions and demonstration of its reversibility greatly enhanced diagnostic confidence;
as asthma can be found in association with other co-morbidities, like COPD. The
demonstrations include:
1) Spirometry is the preferred way in measuring airflow limitation and reversibility.
- An increase in FEV1  15% increase after bronchodilator.
2) PEF important in aiding diagnosis and treatment.
- PEF is ideally compared to patient’s previous best measurement.
- An increase in  20% diurnal variation in PEF on  3 days in a week for 2
weeks.

Many attempts have been made to classified asthma;

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 1) Based on etiology. This is limited by existence of patients whom cannot be
ascertained which environmental factors causing the asthma.
2) By severity; which based on level of symptoms, airflow limitation and lung
function variability into: intermittent, mild persistent, moderate persistent and
severe persistent. This classification is useful when decisions are being made at
the initial management plan. As, for this patient, the severity was very severe as
patient could talk when he was presented to the Emergency department.
3) Asthma control; which may indicate disease prevention or even control. The
complete control of asthma is usually achieved by treatment. In this patient, he
can be classified as uncontrolled asthma since he is not compliance to the
medication given by the hospital.
Complication of asthma includes recurrent exacerbation, COPD and cor pulmonale.
Patient was discharged with certain medication to control his asthmatic attack from
becoming COPD in which is irreversible inflammatory lung problem:
1) Tablet prednisolone 30 mg OD for four days
2) Tablet Erythromycin 800 mg BD for five days
3) MDI Combivent 2 puff three times daily (TDS) for two months
4) Tablet Tamiflu 75 mg BD for three days
5) Tablet Augmentin 625 mg BD for four days
Patient will come again to the hospital after a month at medical outpatient department
(MOPD) with PEFR, FBC, and RP/BUSE for asthmatic assessment.

References
1. Oxford Handbook of Clinical Medicine, 7th Ed. 2007, Longmore, Wilkinson,
Turmuzei & Chee KC, Oxford University Press.
2. Global Initiative for Asthma (GINA)
3. In A Page Medicine, 2nd Ed. 2009, Kahan & Ashar, LWW.
4. http://en.wikipedia.org