COPD Case Study Assignment


Mr TLT is a 58 year old taxi driver who was admitted to Hospital Batu Pahat due to newly diagnosed chronic obstructive pulmonary disease.

He has had hypertension for the past one year and is taking T Amlodipine 5mg od. He is also a chronic smoker for the past 40 years who smokes about 20 sticks of cigarettes a day.

Mr TLT presented with shortness of breath which progressively increased in severity for the past 4 days. The shortness of breath was associated with a wheeze. There was also cough with production of mucoid sputum. The dyspnoea occurred after an episode of upper respiratory tract infection.

Mr TLT has been having intermittent chronic cough associtaed with mucoid sputum for the past 3 years. He has also been having persistent breathlessness for the past 1 year especially on exertion. He has not sought treatment prior to this admission.

On physical examination, Mr TLT was tacypnoiec with a respiratory rate of 28 breaths per minute. There was no cyanosis. Repiratory system examination showed use of accesory muscles as well as increased anterior posterior diameter of the chest and reduced cricosternal distance. On auscultation, vesicular breathing was heard with generalised rhonchi and coarse early inspiratory crepitations at the lower zone of both lungs. The cardiovascular system examination was normal. There were no other abnormalities on physical examination.

Investigations done include chest plain radiograph which showed a hyperinflated chest, tubular heart and absence of vascular markings at the peripheries. The ECG showed sinus rhythm with low voltage. No P pulmonale indicative of right atiral hypertrophy seen.

A working diagnosis of acute exacerbation of chronic obstructive airway disease due to upper respiratory tract infection was made.

Mr TLT was given nebulization of ipratropium bromide, salbutamol and normal saline for 2 times. His symptoms improved after being given the nebulization. He was discharged after three days when the dyspnoea had resolved. He was given metered dose inhaler of Ipratropium Bromide 40microgrammes tds and MDI salbutamol 200microgrammes PRN. He was given an appointment to assess his symptoms at the outpatient department in one month time.


I/C NUMBER : 510912-01-6343 AGE : 58

SEX : Male DATE OF ADMISSION : 2 June 2009

R/N NUMBER : 1143451


Chief complaint:

Mr TLT is a 58 year old taxi driver who presented with shortness of breath for the past four days.

History of present illness:

Mr TLT is a chronic smoker for the past 40 years who has been smoking about twenty sticks of cigarettes a day. He had been diagnosed with hypertension for the past one year and is currently on T Amlodipine 5 mg od.

Mr TLT has been having intermittent chronic cough for the past 3 years. The cough is productive at times. The sputum produced is mucoid in nature and about one tablespoonful in amount. There is no blood in the sputum. It is also not foul-smelling. Mr TLT then proceeded to have shortness of breath for the past one year. The dyspnoea is persistently present and described as requiring increased effort to breathe. It is worse on exertion and Mr TLT experinces reduced effort tolerance. He is now able to climb one and a half flights of stairs before becoming breathless. He has not consulted any doctors for these symptoms prior to admission.

Mr TLT then developed symptoms of upper respiratory tract infection such as rhinorrhea and sore throat one week prior to admission. He had fever of 38 degress celcius at that time which resolved with paracetamol. He also had a productive cough with mucoid sputum at this time. Mr TLT then developed increasing shortness of breath 4 days prior to admission. The shortness of breath worsened over the 4 days and was associated with noisy breathing. He was breathless even at rest but was still able to speak in sentences. There was also an increase in cough as well as production of sputum. The sputum was mucoid and non purulent. He also did not notice any blueness around his lips or at his fingers.

Systemic review: There was no loss of appetite or loss of weight. He had mild ankle oedema but no other signs of heart failure such as orthopnoea or paroxysmal nocturnal dyspnoea.

Past medical history

Mr TLT has not had any hospital admissions prior to this. He was diagnosed with hypertension last year as an incidental finding during a visit to the kilinik kesihatan for an upper respiratory tract infection. He is currently taking tablet Amlodipine 5 mg once daily.

Family history

Mr TLT is the eldest of 5 siblings. There is a strong family history of hypertension in that his mother as well as two other siblings are also hypertensive. There is no family history of asthma, diabetes or ischaemic heart disease.

Social history

Mr TLT used to work as a taxi driver but has stopped working full time 2 years ago. He still occasionally drives his taxi but spends more time at home with his family. He is a chronic smoker for the past 40 years and smokes about 20 sticks of cigarrettes a day. He drinks alcohol with his friends on weekends. He drinks one to two bottles of beer each time.


On general examination, Mr TLT was well nourished and alert but was tachypnoiec. He was able to speak in sentences but there was use of his accessory muscles. There was no clubbing or cyanosis seen. There was also no peripheral oedema, pallor or jaundice.

Vital signs:

Pulse rate: 72 beats per minute, regular with good volume. No bounding pulse.

Respiratory rate: 28 breaths per minute

Blood pressure: 129/73

Temperature: 37 degrees Celsius

SpO2: 95% under nasal prong oxygen 3 litres per minute

Examination of the respiratory system:

On inspection of the hands, there was no peripheral cyanosis or flapping tremors seen. There was also no clubbing, muscle wasting or palmar erythema seen. There was presence of nicotine stains. The jugular venous pressure is mildly elevated at 3.5 cm above the sternal angle. On palpation of the trachea, the trachea is central but the cricosternal distance is 2 fingers which is reduced. The apex beat could not be palpated.

On inspection of the chest, there is an increased anterior posterior diameter giving rise to a barrel shaped chest. The chest moves equally with respiration and there is use of accessory mucles with intercostal, subcostal and suprasternal retraction. There are no chest wall deformities. On palpation, chest expansion is reduced on both sides. Tactile fremitus is equal on both sides. On percussion, there is hyperresonance over both lungs with loss of liver and cardiac dullness. On auscultation vesicular breathing is heard. There is generalised expiratory rhonchi. There is also fine early inspiratory crepitations heard at the lower zones of both lungs.

Examination of the cardiovascular system:

The apex beat could not be palpated. There were no parasternal heaves or thrills palpable. On auscultation, normal first and second heart sounds were heard. There was mild bilateral pitting oedema.

Examination of the abdomen:

On inspection, the abdomen is flat and moves with respiration. There was no guarding or tenderness. The liver and spleen were not palpable. There was no organomegaly.

Examination of the neurological system was normal.


Provisional diagnosis:

Acute exacerbation of newly diagnosed chronic obstructive airway disease due to upper respiratory tract infection.

Evidence for:

Patients with chronic obstructive airway disease (COPD) usually present with a persistent dyspnoea and reduced effort tolerance which was present in the history given by Mr TLT. He is also at increased risk of developing COPD due to exposure to associated risk factors such as tobacco smoke. He has been a chronic smoker for the past 40 years. There is also the presence of chronic cough occasionally associated with mucoid sputum which further suggests COPD. Physical findings of a hyperinflated chest and vesicular breathing with generalised expiratory rhonchi also point to an obstructive airway disease.

During this admission Mr TLT had increasing severity of shortness of breath even at rest. This was associated with a wheeze that was described as noisy breathing. Sudden worsening of symptoms suggest an episode of acute exacerbation. The history of upper respiratory tract infection symptoms suggest that it was the trigger for this episode of exacerbation.

Differential diagnosis:

1) Congestive cardiac failure.

Mr TLT may have developed congestive cardiac failure as a primary event or as a complication of chronic lung disease. There is history of reduced effort tolerance. Patients with congestive cardiac failure may also present with a wheeze and sudden increase in dyspnoea. Physical examination of fine crepitations at both bases of the lungs may also indicate congestive cardiac failure. There is also evidence of mildly raised JVP as well as mild pittint ankle oedema.

Evidence against:

There is no history of any cause of heart failure such as ischaemic heart disease or cardiac valve defect. Mr TLT’s previous records during follow-up show well controlled blood pressure.

Additional investigations need to be carried out in order to rule out this condition. A chest plain radiograph may be done in order to look for evidence of heart failure such as cardiomegaly. An ECG may be done to look for right atrial hypertrophy. An echocardiogram should also be performed in order to assess the function of the ventricles.

2) Bronchiectasis

Patients with bronchiectasis have a history of chronic cough as well as production of copious amounts of sputum. They may also have persistent shortness of breath, reduced effort tolerance and wheeze.

Evidence against:

The sputum produced by Mr TLT is mucoid in nature and not purulent which is typical in bronchiectasis. It is also not copious and foul smelling in nature. On physical examination, coarse crepitations would be heard in bronchiectasis as opposed to the fine crepitations heard in Mr TLT. There is also no evidence of clubbing.

Chest plain radiograph should be done in order to look for thickened bronchial walls or cystic shadows.


1. Shortness of breath and reduced effort tolerance

Mr TLT’s chief complaint is shortness of breath. This may be attributed to the increase in number of goblet cells and later on fibrosis of the bronchial walls causing airway obstruction seen in chronic obstructive airway disease. The shortness of breath may be partially relieved with the use of nebulization of ipratropium bromide, salbutamol and normal saline or with the use of metered dose inhalers. Chest physiotherapy may also be useful.

Mr TLT also has had reduced effort tolerance and persistent dyspnoea for the past a year. As such he may require the use of ipratropium bromide in a metered dose inhaler upon discharge in order to feel less breathless due to the bronchodilator effect of the ipratropium bromide.

2. Upper respiratory tract infection

Mr TLT may require antibiotics as he still has symptoms of upper respiratory tract infection such as sore throat. Furthermore patients who present with an acute exacerbation are at greater risk of having a bacterial infection. This is because of the depressed immune state that the patient is in as a result of the acute illness as well as due to any steroids that would be given as part of the management plan. The appropriateness of usage of antibiotics in chronic obstructive airway disease will be further discussed below.

3. Adequate inhaler technique

Mr TLT would need to be taught about the correct technique to be used when using metered dose inhalers. He would probably require daily use of ipratropium bromide metered dose inhalers to reduce his breathlessness. In the event that he is unable to learn proper technique, he may be encouraged to buy an aerochamber.

4. Smoking cessation

Mr TLT should be counseled on smoking cessation as it has been proven that smoking cessation would alter the course of progression in COPD and is associated with lower all-cause mortality. He should be counseled on the various options of smoking cessation which will be discussed further below.


1) Full Blood Count

Justification: In order to view the total white count as well as the differential count to see if there is an infection which has caused this episode of exacerbation. There may also be secondary polycythemia if the patient has chronic pulmonary hypertension.


White cell count : 7.91 X 109/L

Red blood cell : 4.48 X 1012/L

Haemoglobin : 133.00 g/dl

Haematocrit : 42.00 ratio

Mean cell volume : 93.80 fL

Mean cell haemoglobin : 29.70 pg

Mean cell haemoglobin conc. : 317.00 g/l

Platelets : 141.00 X 109/L

Differential count

Neutrophils : 60.10% 4.76 X 109/L

Lymphocytes : 25.30% 2.00 X 109/L

Monocytes : 13.80% 1.09 X 109/L

Eosinophils : 0.50% 0.04 X 109/L

Basophils : 0.30% 0.02 X 109/L

Interpretation: This is a normal full blood count result with normal total white count as well as normal haemoglobin levels.

2) Plain chest radiograph

Justification: Done in order to look for evidence of chronic obstructive airway disease such as hyperinflated chest or evidence of congestive cardiac failure such as cardiomegaly and prominent upper lobe vessels.

Results: Hyperinflation of the chest with the 7th anterior rib crossing the diaphragm. No other abnormalities seen.

Interpretation: Hyperinflation of the lung fields is consistent with the provisional diagnosis of chronic obstructive airway disease.

3) Sputum FEME, culture and sensitivity (not done)

Justification: In order to look for any bacteria which may have been the cause of the exacerbation . If there any organism cultured, proper antibiotics can be given based on the sensitivity test.

4) Arterial blood gas (not done)

Justification: May be necessary in severe cases of breathlessness to look for respiratory failure and associated changes in blood pH.

5) Blood urea serum electrolytes and creatinine

Justification: To look for renal impairment which may be present due to Mr TLT having hypertension. Renal impairment may also affect the dosage and type of antibiotics used.


Urea : 3.7mmol/L

Sodium : 135 mmol/L

Potassium : 3.7 mmol/L

Creatinine : 65 umol/L

Interpretation: Normal result. There is no renal impairment

6) Electrocardiogram

Justification: To look for evidence of right ventricular hypertrophy or right atrial hypertrophy which may be seen in chronic lung disease.

Results: ECG with sinus rhythm. There is no P pulmonale seen. There is low voltage seen. No ischaemic changes seen. No left ventricular hypertrophy.

Interpretation: Normal ECG with low voltage is seen in a hyperinflated chest such as in patients with COPD


Working diagnosis:

Acute exacerbation of chronic obstructive airway disease due to upper respiratory tract infection

My proposed plan of management is as follows:

Acute management

1. Provide supplemental oxygen via nasal prong 3L/min and maintain SpO2 above 90%. Arterial blood gas should be done in order to ensure adequate oxygenation without carbon dioxide retention of acidosis.

2. Close monitoring of vital signs and SpO2 hourly until the patient’s breathlessness improves. Nursing staff to inform if patient deteriorates such as increased respiratory rate or drop in oxygen saturation below 92%.

3. Give nebulization of Ipratropium Bromide:Salbutamol:Normal Saline in ratio of 2:2:1 every four hours until breathlessness decreases.

4. Oral prednisolone 40mg once daily for 10 days

5. Postural drainage and chest physiotherapy may be performed.

6. Oral antibiotics such as T. Cefuroxime may be given. This was not given in this patient with further discussion below.

Long term management

1. MDI ipratropium bromide 40 microgrammes tds

2. MDI salbutamol 200 microgrammes PRN

3. Counseling on proper inhaler technique.

4. Couseling on smoking cessation.


Mr TLT was warded for a total of 3 days. His breathlessness improved after nebulization with ipratropium bromide, salbutamol and normal saline for one day. He no longer required nebulization after one day. Mr TLT was also able to ambulate without feeling breathless. He was able to eat and to sleep well without being bothered by the dyspnoea. His vital signs were also normal and his respiratory rate improved to about 20 breaths per minute. There was still some ronchi heard on auscultation but it was much reduced. He was afebrile during his stay.

Mr TLT was discharged after 3 days of admission and educated on chronic obstructive airway disease. He was also counseled on the importance of smoking cessation. He was given an appointment with the medical outpatient department in one month time in order to review his symptoms after being given MDI ipratropium bromide. He was told to return to the hospital if he had similar episodes.


Discharge Plan

1. Medications:

i. MDI Salbutamol 200µg PRN

ii. MDI Ipratropium Bromide 40µg TDS

iii. T. Amlodipine 5mg once daily

iv. T. Prednisolone 20mg od for 7 days.

2. Counseling on COPD and use of metered dose inhaler

Mr TLT should be taught about the correct technique in using a metered dose inhaler. The technique should then be assessed before discharge. In the event that Mr TLT is unable to coordinate well, he may be advised to purchase an aerochamber.

3. Counseling on smoking cessation

The approach to counseling a patient on smoking cessation as well as various options will be further discussed below.

4. Education on the symptoms of an acute exacerbation and advise to return to the hospital if there is development of those symptoms.

5. For follow-up at the medical outpatient department for review of symptoms while on MDI ipratropium bromide. He should also be taught about pulmonary rehabilitation. A spirometry appointment may also be made.


Dr Tan Hai Liang

Medical Department,

Hospital Batu Pahat

Family physician,

Klinik Kesihatan Batu Pahat,

83000 Batu Pahat, 10 June 2009

Dear esteemed colleague,

Patient’s name: Teo Lai Thing

Patient’s I/c number: 510912-01-6343

Problem: Chronic Obstructive Airway disease

Thank you for seeing this 58 year old gentleman who is hypertensive for the past 1 year currently on T. Amlodipine 5mg once daily.

He presented to Hospital Batu Pahat with shortness of breath for 4 days that was increasing in severity. A diagnosis of chronic obstructive airway disease was made. He was discharged uneventfully on the third day of admission with the following medication: MDI Salbutamol 200µg PRN, MDI Ipratropium Bromide 40µg TDS and T. Amlodipine 5mg once daily.

Mr Teo has been a chronic smoker for the past 40 years and smokes up to 20 sticks of cigarettes a day. We have counselled him about the benefits of smoking cessation while in the ward. He is currently considering it and would like to learn more about the various options of smoking cessation.

Kindly assess the patients keenness for smoking cessation as well as provide him with additional information on the options available to quit smoking.

Thank you.



1) Communication skills

What are the benefits of smoking cessation in COPD patients and how should counseling be done?

Counseling for smoking cessation should play a significant role in the holistic management of a patient with chronic obstructive airway disease. This is because studies have shown that smoking cessation changes the clinical course of COPD by preserving lung function. One study of patients reviewed at 14.5 years after stopping smoking showed that smoking cessation intervention showed 18% reduction in all-cause mortality compared with usual care without smoking cessation intervention. Patients who had stopped smoking had lower rates of death due of coronary heart disease , cerebrovascular disease, lung cancer, and other respiratory disease as compared with those assigned to usual care who continue to smoke. [1]

Fig. 4. Effect of smoking cessation on mortality cause at 14.5 years in the Lung Health Study.

(A) Comparison of smoking cessation intervention with usual care. (B) Comparison according to smoking status.

I therefore looked up for counseling methods for smoking cessation. The American College of Chest Physicians recommend that physicians should be the first line in introducing smoking cessation. [2] There are 5 As that a doctor should perform for a patient who is a smoker:

• Ask about tobacco use at every visit

• Advise tobacco users to quit

• Assess the willingness to attempt quitting

• Assist the patient with methods for quitting

• Arrange for follow-up contact via phone or face to face

If the patient is not yet willing to quit, there are 5 Rs which should be identified together by the patient and the doctor:

• Relevance of quitting for the patient

• Risks of illness related to continued tobacco use

• Rewerds/benefits of smoking cessation

• Roadblocks for quitting, internal and external

• Repetition of the motivation intervention at each encounter

There are two means of intervention in smoking cessation namely pharmacological and behavioural. The pharmacological means include nicotine replacement therapy or buproprion. Behavioural interventions include counseling programs that teach problem-solving skills and support groups. [3]

In conclusion, I learned that doctors have an important role in actively encouraging patients who smoke to stop as there are many proven benefits of smoking cessation. The steps discussed above on techniques in the counseling of patients would be helpful to me in the future.

2) Professionalism, ethics and personal development

Should antibiotics be given for episodes of exacerbation of chronic obstructive airway disease?

Mr TLT was not given antibiotics during this episode of exacerbation. Certain quarters support the use of prophylactic antibiotics in all exacerbations due to the knowledge that most exacerbations are caused by the common organisms of Streptococcus pneumoniae (S. pneumoniae), Haemophilus influenzae (H. influenzae), Pseudomonas aeruginosa (P. aeruginosa) and Moraxella catarrhalis (M. catarrhalis).

Sputum culture may not be useful as even in the clinical stable state, some patients have sputum positive for bacteria. As such a broad spectrum antibiotic is usually used to cover different bacteria. However, is this use of antibiotics justified in that do patients benefit from it or is the overjudicious use of antibiotics merely promoting antibiotic resistant bacteria?

Current Global initiative for chronic Lung Disease guidelines [4] recommend that antibiotics should be given in:

i) patients with exacerbations of COPD and the three cardinal symptoms of increased

dyspnoea, increased sputum volume and increased sputum purulence.

ii) patients with exacerbation of COPD with two of the cardinal symptoms if increased

purulence of sputum is one of the two symptoms

iii) patients with severe exacerbations of COPD that requires mechanical ventilation

A meta-analysis by Ram et al [5] of 11 placebo controlled RCTs with 917 patients attempted to analyse the value of antibiotics in the management of acute COPD exacerbations. The results show that there is a decrease in short-term mortality, treatment failure and sputum purulence with antibiotic therapy compared to placebo. The authors concluded that antibiotics therapy is appropriate in exacerbations of COPD associated with increased cough and sputum purulence. They further found that antibiotics have the greatest effect for patients with severe exacerbations who are admitted to the hospital. They were unable to comment on exacerbations with non-purulent sputum, what antibiotics were the best to be used and also the duration of therapy due to the lack of RCTs done on these aspects.

In conclusion, it was appropriate that Mr TLT was not given antibiotics as he did not have the cardinal signs as mentioned by the GOLD guidelines and further supported by the systemic review.

3) Self directed life long learning

What are extrapulmonary manifestations of COPD and what are it’s therapeutic implications?

Chronic obstructive lung disease has long been known as a localized pulmonary disorder. However new evidence have shown that COPD may be a systemic disease that involves pathology in several extra-pulmonary systems.

An article by Remels et al [6] summarized the extrapulmonary manifestations as well as it’s implications on the holistic management of chronic obstructive airway disease. The article showed that there is skeletal muscle dysfunction as well as systemic inflammation in chronic obstructive airway disease.

There is loss of muscle mass associated with impaired protein metabolism. The loss of muscle mass which is called sarcopenia may progress to cachexia. Studies have also shown that there is increased apoptosis of muscle cells at the cellular level. Independent of the loss of muscle mass is the reduced muscle endurance. This finding has been attributed to abnormalities in mitochondria or to hypoxia. These findings have significant implications on management of a COPD patient which will be discussed below.

Systemic inflammation is also seen in patients with COPD. This is evidenced by elevated levels of the proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-a), interleukin-6, interleukin-8, and TNF-a receptors. The origin of the systemic inflammation is thought to be independent of the pulmonary manifestation of COPD. One postulation is the increase systemic inflammatory mediators such as neutrophils and lymphocytes in the circulation of patients with COPD. Another proposed mechanism is increased cytokine production due to chronic hypoxia.

The therapeutic implications of these findings is that muscle atrophy should be prevented by resistance exercise as well as combined strength and endurance exercise. Current Malaysian guidelines on the management of COPD [7] recommend pulmonary resistance including lower and upper limb exercises as well as inspiratory muscle training. This concurs with a Cochrane metaanalysis by Lacasse et al [8] which strongly support respiratory at least four weeks of exercise training as part of the of management for patients with COPD. The authors found that there was clinically and statistically significant improvements in quality of life as measured by dyspnea, fatigue and emotional function.

4. Critical thinking and research

What is the efficacy of systemic corticosteroids for acute exacerbations of chronic obstructive airway disese?

The use of systemic oral or intravenous corticosteroids is recommended by GOLD guidelines in the management of acute exacerbations of chronic obstructive airway disease. However the patient, Mr TLT was not given any systemic corticosteroids. This could be because he merely had a mild exacerbation.

I therefore looked up a Cochrane metaanalysis on the use of systemic corticosteroids for acute exacerbations of chronic obstructive airway disease [9]. The authors reviewed randomized controlled trials comparing parenteral or oral corticosteroids with placebo for the treatment of exacerbation of COPD. The primary outcomes measured were treatment failure (hospital readmission, return to emergency department), relapse and mortality.

The authors reviewed 11 studies involving 1081 participants. The results show a statistically significant difference between placebo and use of corticosteoids. There was less treatment failure in patients given corticosteroids. Relapse within 30 days were also reduced. However there was no statistically significant reduction in mortality.

As such the authors concluded that administration of oral or parenteral corticosteroids in the treatment of acute exacerbations of COPD reduces the likelihood of treatment failure. This is associated with early and continuing improvement during treatment with corticosteroids in lung function, breathlessness and blood gases and with a shorter hospital stay. This in turn has a positve impact on the economic cost of treating exacerbations, with fewer follow-up visits and hospital admissions. The authors also found that although there is an increased incidence of corticosteroid side effects such as fluid retention, hypertension and adrenal suppression, the effects are unlikely to persist after treatment ceases.



Patient (P): Patients who present with stable COPD

Intervention (I): Oral corticosteroids

Comparison (C): Placebo

Outcome (O): Effects on health status


How was the article identified: The Cochrane Library

Search keywords : corticosteroids, stable COPD

Citation: Walters JAE,Walters EH,Wood-Baker R.Oral corticosteroids for stable chronic obstructive pulmonary disease. Cochrane Database of Systematic Reviews 2005, Issue 3