Lab Case 201 Interpretation

A 60 year old male presents to ED with a 1 week history nausea, decreased oral intake and occasional vomiting. He has a background of poorly controlled hypertension on  Perindopril.

Metabolic acidosis – pH 7.26 and HCO3 16mmol/l

Compensation- Expected CO2 = 1.5x HCO3 +8 = 32mmHg

AG = Na – (Cl+HCO3) = 19

Delta gap = AG-12/24-HCO3 = 0.87

The above VBG shows a metabolic acidosis with a raised AG and a delta gap that confirms a isolated HAGMA. There is a moderately raised potassium, more than expected for the degree of acidosis and a moderately increased creatinine. There is a mildly elevated lactate and a normal BSL. The common causes of a HAGMA are toxins, lactic acidosis, renal failure and ketones. In this clinical context the most likely cause is the renal failure, as the patients BSL is normal, lactate only mildly raised and there is no history of toxin ingestion. The renal failure is most likely secondary to the underlying uncontrolled hypertension and exacerbated by the use of an ACE inhibitor.  The raised potassium is due to the renal failure and the use of ACE inihibitors.

Agents used in management of hyperkalaemia

Agent MOA Dose Onset of Action Duration of Action

Ca Gluconate

Stabilisation of myocardium 10ml 10% IV <5min 30-60min
Sodium HCO3 Redistribution 1mEq/kg IV 15min 1-2 hours
Salbutamol Redistribution 10-20mg neb 15min 1 hour
Glucose and insulin Redistribution 50g 25-50ml and 10 units actrapid 20-30min 2-4 hours
Calcium Resonium Elimination 30g oral or rectal 2 hours 4-6 hours
Frusemide (fluid overloaded patients) Elimination 40mg IVI/Oral 1 hour 6 hours
Dialysis Elimination