From the casebook of Mrs DundeeChest:
Mr G, a 66 year old ex-smoker was referred to the psychiatry clinic with an 18 month history of “general slowing down” and fluctuating memory difficulties. MR G’s GP wanted to know if he might be suitable for medication for his memory problems; his MMSE in early 2009 was 23/30. PMH was significant for COPD.
Mr G continued to work 2 nights a week in a supermarket, but felt more tired than usual, sleeping up to 12 hours a night and taking naps during the day. He’d lost a bit of weight, but his appetite remained good. Mr G mentioned that he sometimes felt ‘tingling’ in his hands, particularly on the right. He also told me of a ‘rash’ that had appeared on his back and limbs over the previous few weeks, which his GP had been treating with steroid cream. He described a chronic cough, but denied SOB or haemoptysis.
On examination, Mr G walked slowly but without any gait abnormality. He had reduced grip strength in the right hand. In terms of the ‘rash’ there were large areas of symmetrical hyperpigmentation over Mr G’s back, forearms and thighs. His MMSE was 28/30. His chest was clear to auscultation.
Question one:
Is there a single unifying diagnosis to explain all of Mr G’s symptoms and signs?
Question two:
What is your next line of investigation?
Mr G’s results were as follows:
Hb 10.3; MCV 89.0; Na 126; K 5.7; Ur 7.3; Cr 85; corr Ca 2.6; LFTs normal
Question three:
Can you explain the abnormalities?
Normocytic anaemia is the anaemia of chronic disease; hyponatraemia in combination with hyperkalaemia may in this context indicate secondary hypoadrenalism; the commonest cause of hypercalcaemia is bony metastases.
Question four:
What would you do next?
Chest x-ray confirms a right apical tumour.
The right apical tumour is obvious.
This man was referred to the psychiatric clinic because of memory loss and what was described as “general slowing down”. The referring clinician had come to the conclusion that the most likely cause was that of a temporal lobe specific dementia, an uncommon syndrome, presenting in an unusually young man.
I teach the medical students that they must treat every patient from fresh, with no preconceptions, and be open to any diagnosis. Take a full history, examine all systems in detail, and don’t become limited to the obvious diagnosis, or what the last clinician thought. This man clearly had a multi-system problem, with central and peripheral nervous system involvement, systemic upset, weight loss, dermatological manefestations, and, when questioned in detail, cough. Dementia does not explain many of those symtoms.
I also teach the students to remember that common things happen commonly. In fact I’ve heard myself say, more than once:
It is more likely that something common is presenting in an uncommon manner, than something uncommon presenting at all
Ockham’s razor tells us that if a single unifying diagnosis can explain the constellation of symptoms, it’s the most likely explanation. In this case there is a simple, common disease that explains all of the symptoms, but without taking a detailed history, carrying out a full examination, and being open to the differential diagnoses, and thinking of common diseases presenting uncommonly, it would have been missed.
Take home message – Lung cancer is very common, and 90 % are picked up by a CXR. Always think of lung cancer in any smoker presenting with compatible signs and symptoms.
[…] Case of the Week #4 […]
This was a really interesting case, thanks.
Would it have been possible for this man to have later developed Horner’s considering the brachial plexus involvement?
Certainly Pancoast’s tumour can presents with, or progress to, Horner’s. Not massively common, but quite characteristic.
Hi there, this is a really great case I’m a little bit confused though about this patient and his many paraneoplastic symptoms, he seems to have ACTH and ADH ectopic secretions (so probably small cell carcinoma?) but he’s also got hypercalaemia which could be due to ectopic PTH secretion which is found more in squamous cell carcinoma. But i can see it mentions bone marrow infiltration so it could be small cell that’s invaded and caused that.
Sorry, just trying to get my head round it! I was just wondering is it usually small cell carcinoma that causes Pancoast’s tumours? Does ‘Pancoast’ just describe the position of the tumour or it’s pattern of invading the brachial plexus and it can be any cell type?
Also is it really rare for squamous cell carcinomas to produce PTH? I think I read its the most common lung carcinoma, but despite this is it more likely that hypercalcaemia is caused by a bone marrow infiltration than ectopic PTH? Can all types of lung cancer cause bone marrow infiltration?
– Sorry thats a bit longwinded, withhh quite a few questions! thanks in advance for any help!
Thanks Emma. Lots of questions!
You’re over analysing things a wee bit, but I’ll try to simplify it a smidge.
Hyponatraemia can be caused by an ADH secreting tumour, or due to SIADH (secretion). The latter is more common.
The skin pigmentation *may* be due to ectopic ACTH production, or it may be due to adrenal metastasis, but neither were present, so it was one of those things. We see many non-specific rashes in association with malignancy.
Adrenal metastases are usually non functioning.
The biochemical abnormalities are not really extreme enough to represent primary hypoadrenalism, but a cortisol should probably be checked just in case!
There is no way of telling whether this is NSCLC or SCLC without a biopsy.
Ectopic PTHr homone production causes very high calcium levels, but the commonest cause of a calcium rise of any magnitude is bone mets. Only Squamous tumours make PTHr homone, but all NSCLC and SCLC subtypes can infiltrate bone.
Pancoast tumours are just the description of the location, not the subtype. But most of them are NSCLC, because 95 % of lung tumours are NSCLC.
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