Abnormal Pharmacology and Nausea

Try out this pharmcology case and test your clinical knowledge. The answers are at the bottom.


A 32yearold woman presents to A&E with vomiting and nausea. She tells you that she was recently diagnosed with a UTI from her GP and started on gentamicin.



High BMI (41) 

Recurrent UTIs 





SpO2: 94%
Temperature: 37.5
BP: 154/89
HR: 112
RR: 34


Abdomen SNT

POC Bladder US: 500 ml pre-void, 298 mls post-void

Good anal tone

Enlarged prostate

Q1: Calculate her NEWS2 score. What is the significance of this result?

Some initial bloods are taken


Q2: Comment on the bloods. What is the diagnosis?

Shortly after presenting to A&E she collapses and becomes unresponsive. A pulse is palpable. An ECG is performed which shows:

Image 1: Case courtesy of Dr Ian Bickle, Radiopaedia.org. From the case rID: 50303


Q3: Comment on the ECG. What is the likely complication? 

Q4: How would you manage this complication?



Reveal the Answers

 Answer to Question 1

Resp: 3

SpO2: 1

Air/O2: 2

BP: 0

Pulse: 2

Consciousness: 0

(initially)Temperature: 0

Total: NEWS 8

A NEWS score of 8 indicates a ‘high’ level of risk and warrants anurgent/emergency assessment by senior clinicians. This patient is very unwell and ITU should also be informed.These patients are often automatically triaged by critical care outreach teams once their NEWS reaches 7.

Answer to Question 2

The most striking abnormality is in her renal function. This is most likely an AKI as even though we do not have previous renal function results to compare with, the normal calcium and phosphate point to an acute deterioration in renal function (in CKD hypocalaemia often leads to an increase in PTHsecondary hyperparathyroidism which subsequently sequesters phosphate in the blood). Similarly, the lack of a normocytic anaemia secondary to a chronic reduction in the ability of the kidneys to produce EPO points to an acute kidney pathology.

Her Urea: Creatinine ratio is < 100 and as such implies an intrinsic renal cause of her deterioration, as opposed to a prerenal cause e.g. dehydration/shock or renal artery stenosis. The most likely culprit here is an inappropriately high gentamicin dose by her GP, as the drug is dosed by a patient’s ideal body weight NOT their actual body weight due to gentamicin’s poor lipid solubility. Gentamicin is renally excreted and at toxic doses can lead to acute tubular necrosis and subsequent AKI.

The uraemia is driving her metabolic acidosis, with partial respiratory compensation (hyperventilation).

Her electrolyte disturbance is a common picture in AKIs, with sodium being haemodiluted due to the extra fluid retained and potassium being withheld within the bloodstream due to the acidosis.

Answer to Question 3

This is in essence ventricular tachycardia with features of:

Broad QRS > 120ms


However, the distinguishing feature of thetall, tented Twaves points to the underlying cause of this arrythmiasevere hyperkalaemia. This is likely secondary to her AKI combined with her ACE inhibitor, which further increases blood potassium levels.

Answer to Question 4

An AE approach should be adopted, and she will likely require intubation and ventilation. Hyperkalaemia is usually managed as follows:

Calcium chloride (10ml of 10%)This stabilizes the cardiac membrane and prevents further arrythmias

Insulin/dextrose infusion (50 units actrapid in 50 mls 20% dextrose)this drives the potassium into cells, reducing the serum K+ concentration

In more severe cases, calcium chelators e.g. calcium resonium and haemofiltration can also be used



Image 1: https://liftl.com/wp-content/uploads/2018/08/ECG-Hyperkalemia-serum-potassium-9.3.jpg



Dr Amol Joshi
University of Cambridge

About The Author

This case is written by Dr Amol Joshi who has an interest in writing medical puzzles.

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