Fatigued and Vomiting with Malaise
Try out this endocrine case and test your clinical knowledge. The answers are at the bottom.
A 47-year-old woman presents to A&E with vomiting and malaise. She appears confused and collapses in the A&E resus department. Her husband who accompanies her says she had been sleeping in for hours for the last few days and was much more fatigued than he was used to.
Salbutamol 2 puffs INH
Prednisolone 60mg OD – last prescription issued 2 months ago
- SpO2: 81% 15L non-rebreathe mask
- Temperature: 37.1
- BP: 71/38
- HR: 139
- RR: 36
A: Patent – nurse maintaining jaw thrust
B: Non-rebreathe 15/min FiO2 100%. Chest clear, trachea central.
C: CRT 7s, HS very faint. ECG: no changes
D: GCS 7 (E2V1M4). PEARL. BM 2.1
E: Abdomen: SNT. No focal neurological signs detected.
Q1: What is the single most important step to perform as an F1 for this patient?
Q2: Calculate her NEWS2 score.
Initial bloods are taken:
Q3: Comment on the blood results. What is the likely diagnosis and why might this have occurred?
Q4: How should this patient be managed?
Reveal the Answers
This patient is critically unwell, as evidenced by her grossly deranged observations and low GCS. The single most important step as a junior doctor would be to immediately summon senior help – in most scenarios, the best way to do this would be to pull the emergency bedside buzzer and also put out a peri-arrest crash call via 2222/switchboard.
Total NEWS2: 16
There are multiple abnormalities in the blood tests:
- Paired hyponatraemia with hyperkalaemia – this often indicates an endocrine disturbance in the hypothalamic pituitary adrenal axis, as both cortisol and aldosterone have antagnositic effects on sodium and potassium control
- Low random cortisol
- Metabolic acidosis with no respiratory compensation. NB: The elevated lactate does not appear severe enough to fully account for the metabolic acidosis, indeed the anion gap is normal (Na + K) – (HCO3 + Cl) = 12.8 (normal range 8-14) – this indicates that there is minimal influence from external sources of protons e.g. lactate, ketones and that there is a secondary cause driving the metabolic acidosis.
Based on these findings, the likely diagnosis here is an Addisonian crisis secondary to poor medication (prednisolone) compliance. Corticosteroids at high doses can have mineralocorticoid activity, hence the derangement in sodium and potassium can be explained by the lack of mineralocorticoid action (aldosterone causes potassium excretion and sodium retention). Furthermore cortisol/corticosteroids promote vasoconstriction to increase blood pressure and increase serum glucose concentrations, both of which are grossly suppressed in this patient in the absence of her usual prednisolone dosing.
The patient should be intubated as soon as possible due to her low GCS and extremely high oxygen requirements.
The single most important medical treatment for her crisis however is to begin at hydrocortisone infusion – note that a mineralocorticoid is not required for acute management as the dose of hydrocortisone used has strong mineralocorticoid effects.
Her potassium should be very closely monitored as Addisonian patients have a predisposition to become very hyperkalemic – calcium gluconate may be a suitable option to stabilize the cardiac membrane if ECG changes occur.
The blood sugar can be corrected with 50-100 mls 20% IV dextrose, however the hydrocortisone will help improve this as well.
Dr Amol Joshi
University of Cambridge