Acid–Base, Electrolyte and Renal Emergencies 141Acute Renal Failure
4 Insert a large-bore i.v. cannula and send blood for FBC, U&Es, LFTs, CK,
magnesium, lipase and thyroid function.
5 Perform an ECG and look for:
(i) Prolongation of PR and QT intervals.
(ii) ST segment depression.
(iii) Widened QRS and torsades de pointes.
MANAGEMENT1 Commence rehydration wit h 0.9% norma l sa line i.v. at 250 mL/h.
2 Look for and treat the underlying cause.
3 Administer oral magnesium supplements to asymptomatic patients.
4 Start parenteral magnesium in more severe cases:
(i) Give patients with seizures, torsades de pointes, or cardiac arrest
50% magnesium sulphate 8 mmol or 2 g i.v. over 5–10 min.
(ii) Give other symptomatic patients 50% magnesium sulphate
8 mmol (2 g) i.v. at a slower rate over 30–60 min.
5 Refer the patient to the medical team and discuss further elemental mag-
nesium treatment.
ACUTE RENAL FAILURE
Acute kidney injury
Acute renal failure is now encompassed in the term ‘acute kidney injury’ (AKI)
t hat denotes t he spect r u m of rapid loss of k id ney f unct ion f rom minor cha nges to
the requirement for renal replacement therapy.
The RIFLE classification is used for diagnostic staging of acute kidney injury and
allows differentiation between mild and severe, as well as early and late cases. The
RIFLE criteria refer to:
Risk: serum creatinine · 1.5; or urine production <0.5 mL/kg per hour for 6 h
Injury: serum creat · 2; or urine production <0.5 mL/kg per hour for 12 h
Failure: serum creat · 3 or >355 μmol/L (with acute rise >44); or urine output
<0.3 mL/kg per hour for 24 h ‘oliguria’, or anuria for 12 h
Loss: persistent AKI wit h complete loss of k idney f unction for >4 weeks
End-stage k idney disease: complete loss of k idney f unction for >3 mont hs.
DIAGNOSIS1 Acute renal failure leads to an abrupt, sustained increase in serum urea and
creatinine secondary to decreased glomerular filtration rate (GFR), usually
associated wit h oliguria or anuria.