AKI Flashcards
You are the on call SHO for medicine. A nurse asks you to see a 65-year-old male patient who has come in feeling drowsy and with decreased urine output. She hands you the ECG saying another doctor mentioned “tented T waves”.
How would you assess the patient?
I would use an A to E approach.
A
- Ensure airway patency, if alert and speaking, can be assumed
B
- Monitor SpO2, give high flow oxygen if SpO2 < 90%
- Check RR
- Look, listen and feel the chest
C
- Monitor HR, BP
- Check CRT peripherally and centrally
- Look for signs of dehydration
- Serial 12-lead ECGs
- 2 x Large bore IV access - take bloods, quick VBG (potassium)
- Insert catheter and monitor UO
- If hypotensive, give small bolus of crystalloids
D
- AVPU/GCS, if GCS ≤ 8, call anaesthetist - intubation)
- Blood sugar, temperature
E
- Examine: Any focal neurological deficit? Abdominal exam? Rashes?
What bloods would you do?
VBG/ABG
FBC, CRP, U&E & Mg, LFTs (drowsy)
Blood cultures, urine MC&S
The potassium is 7.0 on the VBG. How would you manage this patient?
This is a severe hyperkalaemia (>6.5 mmol/L) and is a medical emergency.
Hopefully at this point I would have sent off U&E and have an ECG.
Cardiac monitoring
Protect the heart:
* 10 mL of 10% Calcium Gluconate IV 5-10 min
* Repeat if ECG changes persist
Shift K+
* 10U soluble insulin in 25g glucose (e.g. 125mL of 25% glucose)
* Salbutamol 10-20mg via nebulizer
Remove K+
* Sodium zirconium cyclosilicate
Monitor K+ and glucose
* Hypoglycaemia occurs in 11-75%, most commonly 2-3.5h after insulin, 6h in CKD
* Consider 10% IV glucose at 50ml/h if pre-treatment glucose < 7.0 mmol/h
Prevent recurrence
- Withhold drugs which increase K+: ACEi, ARB, MRA
Look for cause
- Pre-renal, renal, post-renal
Insulin stimulates intracellular uptake of K+ by 0.65-1.0 mmol/L
Salbutamol Neb SE: tremor, palpitation, headachae)
Sodium zirconium cyclosilicate - a non-absorbed binder that exchanges H+ and Na+ for K+ and ammonium in the gut. 10g TDS approved for use in the acute setting. Onset within 1h, lowering serum K+ by 1.1 mmol/L within 48h
The serum potassium comes back as 6.8. The U&Es show an AKI stage 3; the patient had normal renal function on previous blood tests 6 months ago. What are the possible causes of this AKI?
Pre-renal
* Volume depletion (most common)
* Heart and liver failure
* Low BP (hypoperfusion)
Renal
- Renal Tubular Acidosis (RTA)
- Contrast induced nephropathy
- Glumerulonephritis
Post-renal
- Stones
- Blader outlet obstruction (BOO)
- Benigh prostate hypertrophy (BPH)
- Malignancy
- Catheter problems
You commence treatment and repeat the potassium after 2 hours. The VBG result is 7.1 and there is now a metabolic acidosis. How would you proceed?
- Reassess ABCDE
- Has treatment been given? Is the cannula working? Any exogenous potassium being given?
- Send repeat serum sample to confirm
- Involve medical registrar and ITU registrar (dialysis may be needed)
- Move patient to HDU/resus setting
This is a question not only about treating a **refractory hyperkalaemia*
What are the indications for dialysis?
- Refractory hyperkalaemia
- Metabolic acidosis
- CKD stage 5
- Fluid overload unresponsive to treatment
- Symptoms of uraemia
You now have one minute to handover the patient in this scenario to your registrar/consultant as if you were at the Acute Medical Handover.
Situation: This is a 65 year old gentleman with refractory hyperkalaemia and metabolic acidosis.
Background: He was admitted in AKI and has no other known past medical history.
Assessment: The potassium is 7.1 and there are changes on the ECG consistent with hyperkalaemia. The patient is drowsy.
Recommendations: I would like an urgent review of this patient by the ITU registrar as he may need emergency dialysis given the lack of response to treatment so far. I will commence cardiac monitoring and continue treatment for the hyperkalaemia pending your review.
