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These are the case findings in their original reveal order, moving from the broader presentation to the most discriminating evidence.
Clue 1
A 68-year-old man is driven to the emergency department by his son. Over the last four days his breathing has been getting steadily worse, and this morning he could not get from his bed to the bathroom without stopping twice on the way. He looks exhausted. Asked what happened, he manages three or four words at a time before he has to stop and take another breath.
Clue 2
He has smoked about a pack a day for forty years and has coughed most mornings for as long as he can remember — long enough that he stopped mentioning it to anyone. Each of the last two winters he has had an episode like this, both treated with steroid tablets and antibiotics, and he takes a long-acting inhaler every day. His grandson stayed with him the week before last with a streaming cold.
Clue 3
The cough itself has changed in two specific ways over the same four days. He is bringing up considerably more than he normally does — filling tissues rather than clearing his throat — and what comes up is no longer the clear stuff he is used to. It has turned green. There is no blood in it.
Clue 4
He will not lie back. He sits forward propped on his hands, recruiting his neck muscles with every breath and blowing out slowly through pursed lips, and his chest is noticeably barrel-shaped. Listening to him, the striking thing is how little there is to hear: breath sounds are quiet everywhere, expiration drags on far longer than inspiration, and there is a diffuse wheeze on the way out with no focal crackles anywhere. Respiratory rate 28, saturations 88 per cent on air, pulse 104, temperature 37.1 °C. His jugular venous pressure is not raised and his ankles are not swollen.
Diagnosis
COPD Exacerbation
Why the diagnosis fits
This is a case about recognising an acute deterioration on a chronic background, and the definition is unusually mechanical. An exacerbation is defined by the worsening of three cardinal symptoms — increased dyspnoea, increased sputum volume and increased sputum purulence — and he has all three, which is what classes it as Type 1. The background is established separately and matters just as much: forty pack-years, a chronic productive morning cough of many years, two previous winter episodes needing steroids and antibiotics, and daily long-acting bronchodilator therapy. The trigger fits too, since respiratory viral infections account for 70 to 80 per cent of exacerbations, and a grandson with a streaming cold was in the house the week before. The examination is a coherent picture of air trapping rather than of fluid or consolidation. He sits forward on his hands and breathes out through pursed lips, which is a person generating their own positive end-expiratory pressure to hold collapsing airways open. His chest is barrel-shaped, breath sounds are quiet everywhere, and expiration drags out with a diffuse wheeze — quiet lungs that take a long time to empty. Crucially there are no focal crackles, no raised jugular venous pressure and no ankle swelling, which is where pneumonia and heart failure would have declared themselves. The chest radiograph confirms that reading in both directions: hyperinflation with flattened diaphragms, increased retrosternal air space and attenuated peripheral vessels, and no consolidation, no effusion and a normal cardiac silhouette. What clinches the underlying diagnosis is the spirometry already on file — a post-bronchodilator FEV1/FVC of 0.54, below the 0.70 threshold that defines the disease, with an FEV1 of 44 per cent predicted placing him at GOLD grade 3. That the bronchodilator did not reverse it is the single most useful fact in separating this from asthma. Note that the number is retrieved rather than measured today: spirometry during an acute exacerbation is unreliable, and there is no reason to put a breathless patient through it.
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