Recently missed an Addisonian crisis. Here’s a brief summary of the case.
61 y o female attended the ED after seeing her GP with vaginal bleeding. GP sent the patient to the ED for an inappropriate official reason (vaginal bleeding in a post menopausal lady unless torrential should be managed as a two week wait), but the lady looked unwell, and I think that was why the GP fabricated a reason.
This lady had a PMH of psychotic illness, rectal prolapse, and that was pretty much it. She was seen with a family member who looked after her. The history was vague. She wouldn’t talk much, she said she had felt unwell for a few days, tired, and lethargic. She had noticed the bleeding intermittently for the last few months. She had a grey waxy sheen to her skin, and her hair was matted and unkempt. Was this because of her mental health problem?
Systemic examination was unremarkable apart from a large rectal prolapse which I reduced, it was probably also the source of the blood. Her results were phoned through:
Na 129, K6.9 Urea 17.2 Creat 152. She had an elevated neutrophilia. ECG showed sinus tachy with what were on reflection tented t-waves. Her VBG showed a normal pH, slightly reduced HCO3- 15, and a BE of -5.
She was dry. She had a high K+. I started her on insulin/dex. Started a septic screen and began rehydrating her with normal saline. I did not giver her steroids but the medical SpR did about 1 hour after I saw her.
So why didn’t I think of Addisons? (apart from me being a bit thick).
The patient arrived in the ED by ambulance. The history was confused. The reason for attendance was really ‘unwell ?cause’ that the GP had recognised but then put more emphasis on the symptom of vaginal bleeding. I think this led me down a strange path. Possibly slowing my decision making with an anchoring bias. I’d found a pathology with the rectal prolapse, and solved it (premature closure). Did I think that this could explain the GI symptoms, AKI and dehydration? Possibly, given the mental health problems and poor communication, this lady was likely to present late enough to cause these things if she’d avoided nutrition and fluid because toileting was painful.
Did I also fall prey to confirmation bias? I think so. I had a theory, I’d found something to confirm this. I think I stopped looking for or considering differentials, despite the fact that I was thinking renal failure in someone with a normal venous pH, and only slightly disturbed bicarb. . I think there was also an element of fundamental attribution error (stereotyping), I probably placed too much emphasis on this woman’s serious mental health problem, as I tried to fit my theory together.
I may have rejected a new diagnosis of Addisons as a form of availability bias – I’ve never diagnosed primary Addisons, which means it’s not an explanation I often examine or reach for. This is also called Zebra Retreat. My normal cue for thinking about Hypoadrenalism is if people are on long term steroids and this lady wasn’t.
So how do we mitigate against cognitive errors?
One way I normally work is I try to write down my differential, weighing the relative merits of each one as best I can. However the time when I do this is when I’m less busy, and I know that when I am juggling a few Resus patients simultaneously I neglect my documentation, but those are probably exactly the times it needs to be done! Especially as writing my working out is so important to my ‘cognitive process’.
When I miss something I also like to read up on the thing I missed, as well as trying to understand why I missed it. Sometimes I write a reflection, sometimes (more often) I chat to my wife about it (she’s an ICU doc). I just wish more time was allowed for this kind of thing at work.
Some notes on Addisons.
Incidence 0.8 per 100 000 of population. More common in women than men.
The commonest cause of glucocorticoid deficiency is Iatrogenic, this technically isn’t Addisons. Consider replacement if patients have been on 7.5mg pred/day (30mg Hydrocortisone/day) for longer than one month. The mechanism here as I’m sure you know is suppression of the adrenal axis by negative feedback, causing adrenal atrophy.
Classically the causes are usually infection (TB, HIV), trauma, anything causing adrenal haemorrhage, and malignancy (mets like the adrenal glands as they are highly vascular).
Vague, frustrating and insidious. Tiredness is the commonest symptom. Skin hyperpigmentation (secondary to excess ACTH) looks quite subtle to me. It’s more pronounced in areas of increased friction like palms, knuckles and scars. GI symptoms can be severe enough to mimic an acute abdomen.
ED presentations are mostly crises, so you get hypotension, alongside the hyperkalaemia and hyponatraemia. You can also get hypoglycemia. On reflection I wonder how many potential mild cases we send back to GPs.
Mistakes and errors are common, especially with rare conditions and vague presentations. The ED environment sometimes feels like it’s designed to cause and not mitigate cognitive error, with multiple distractions and heavy time pressure. We all need to develop our own strategies for limiting our own cognitive errors as we develop as clinicians.
Don’t miss an Addisonian crisis. [Low Na, High K –> Give steroids]