Summary 6

Mr H, a 65 years old Malay gentlemen with underlying chronic obstructive airway disease and hypertension diagnosed two years ago presented with progressive breathlessness at home. He had worsening of breathlessness on the on the day of admission with persistent breathlessness for past one year. He had associated productive cough with non-purulent sputum for a week with no fever, running nose or sore throat. No wheezing or stridor was noted.

Question: Breathlessness without wheezing - what does it suggest? Breathlessness without stridor - what does it suggest?

The breathlessness does not get relieved with inhaler Salbutamol 200mcg six puffs at home which had improved his symptom twice this year. His breathlessness would aggravate on prolonged walking and this was his third hospital admission due to breathlessness with no intensive care unit admission of intubation before. He has no lower leg swelling, paroxysmal nocturnal dyspnoea or orthopnoea. He had lost five kilograms this year.

Question: Suggest a reason for the loss of weight.

He was on MDI Salbutamol 200mcg, MDI Berodual thrice daily, MDI Budesonide 400mcg twice daily and T. Amlodipine 10mg once daily. He was a chronic smoker for twenty years with ten cigarettes per day and stopped ten years ago. Worked as a policemen and was a passive smoker for twenty years.

On examination, he was alert, no cyanosis or altered mental consciousness. His blood pressure was 160/87 mmHg, heart rate was 78 beats per minute, SpO2 was 98% on nasal prong 5 litres oxygen and was tacypnoeic, 24 breaths per minute with use of accessory muscles. Jugular venous pressure was not raised, no flapping tremors, clubbing or pedal oedema was noted. Upon respiratory examination, no barrel chest or tracheal tug was noted and palpation revealed bilateral reduced chest expansion with hyperesonance on tactile vocal fremitus and percussion. Auscultation revealed prolonged expiratory phase over both lungs with vesicular breath sounds. No rhonchi or crepitation noted and vocal hyperesonance was present.

Question: Suggest a reason why in a patient diagnosed as AECOPD, there is no rhonchi on examination.

Chest examination revealed no apex beat deviation or parasternal heaves and heart sounds heard with no loud P2 or added sounds.
Laboratory investigations showed he had microcytic hypochromic anaemia (Haemoglobin 9.4 g/dL) with normal white blood cell count (8.61 X10^9/L) and arterial blood gas analysis noted presence of compensated chronic respiratory acidosis (pH 7.39, pCO2 46mmHg, PaO2 90mmHg, HCO3 28 mHg, SO2 98%).

Question: What does "compensated chronic respiratory acidosis" suggest in a patient with COPD?

Chest radiograph showed hyperinflation of the lungs, flattening of diaphragm, hyperlucent upper lung fields and cardiomegaly of ratio 0.7 with no bullae noted. Electrocardiogram showed sinus rhythm with no right ventricular hypertrophy.
He was treated as acute exacerbation of chronic obstructive disease secondary to lower respiratory tract infections and was given oxygen supplementation with face mask and nebulised bronchodilators with Salbutamol 200mcg 0.5ml), Atrovent (1ml) diluted in normal saline (0.5ml) was given four hourly. Intravenous hydrocortisone 200mg once and T.Augmentin 625mg tds was given. He was discharged on the third day with medications T. Amlodipine 10mg od, T. Prednisolone 30mg od for three days, MDI Salbutamol 200mcg, MDI Berodual, MDI Budesonide 400mcg and education on inhaler technique. He was given appointment for specialist clinic two weeks later.

Question: For this patient, what medication should be also considered?

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