A 70 year old woman with type 2 diabetes, chronic kidney disease and hypertension was admitted as a result of generalised deterioration. Drugs on admission included ramipril 5mg od and gliclazide M/R 60mg od. A urine dipstick was positive for nitrites, leukocytes and protein. She was commenced on trimethoprim, intravenous fluids and enoxaparin for venous thrombo-embolism prophylaxis. 48 hours later she was making little improvement.
A microbiologist called at 14.00 and left a message with the healthcare assistant (as all doctors were busy) to say that the infection was resistant to trimethoprim but sensitive to amoxicillin. The message was disseminated to the F1 doctor on the ward who placed the details on his jobs list.
You attend the evening handover at 20.45. This patient is not discussed. You are called to see her at 03.00 as she is complaining of chest pain. An ECG revealed large T waves and reduced p waves consistent with hyperkalaemia. An urgent blood sample revealed a potassium level of 6.8 (3.5 to 5.5 mmol/L). Her potassium level on admission was 5.9 mmol/L (with her normal baseline of 5.0 mmol/L).
What factors contributed to her signs and symptoms?
Accurate handover and preparing for discharge
Two potential factors could be related to her hyperkalaemia. The first question to answer is whether or not she is dehydrated. Signs suggestive of this include reduced skin turgor, low jugular venous pressure.
How could such an event have been averted?
In the first instance, it is important to assess a patient when you acquire the knowledge that he/she is administered an ineffective antibiotic. The patient’s potassium was slightly raised on admission suggesting that it should have been monitored daily and her ACE inhibitor temporarily withdrawn at the outset. It is also advisable to check side effects of all drugs prescribed for the patient via the BNF. Biochemically, the urea will be disproportionately raised. However, she was commenced on intravenous fluids so one would hope that this was addressed.
The other is polypharmacy. Ramipril (an ACE inhibitor), trimethoprim and, to some extent, enoxaparin, can all increase potassium levels in the blood. Trimethoprim is often overlooked as a cause of such a metabolic disturbance. Moreover, the patient’s urine sample culture results suggest that her infection was resistant to this drug and should have been dealt with during the afternoon.
This would have been particularly relevant if the patient’s urinary tract infection was sensitive to trimethoprim and amoxicillin as the temptation to continue with the former would be significant.
When you look at the drug chart, you notice that a pharmacist has written the admitting potassium value next to the ramipril prescription with a note to monitor the potassium. Pharmacists write this information for a very good reason. The information written should acts as aide memoires to monitor levels or to change medications in light of the patient’s present physical state and not ignored.
If you are unable to complete all tasks, those left outstanding should be discussed at handover to allow prioritisation. This emphasizes the importance of effective communication during the handover period. The incident should also be reported to allow reflection of the event both in terms of handover and iatrogenic causes of hyperkalaemia
Accurate handover and preparing for discharge