Specific Management

In DKA there are a number of specific biochemical and haematological considerations that need to be monitored and managed.


Phosphate levels are affected in DKA in a similar way as potassium. However phosphate supplementation does not change the correction of glucose, bicarbonate or pH. Phosphate should not be routinely given [3,4,7].


There is also a magnesium deficiency in DKA. The symptoms are difficult to recognise and overlap with calcium, potassium and sodium deficiencies.

They are paresthesia, tremor, carpopedal spasm, agitation, seizures and cardiac arrhythmias. Correction of magnesium should be considered in symptomatic patients or those with hypokalaemia.

In magnesium deficiency treatment of hypokalaemia with potassium is often refractory to treatment. The mechanism still remains unexplained.


Adequate fluid and insulin therapy will resolve the acidosis in DKA and the use of bicarbonate is not indicated (R). The acidosis may be an adaptive response as it improves oxygen delivery to the tissues by causing a right shift of the oxygen dissociation curve. Excessive bicarbonate may cause a rise in the CO2 partial pressure in the cerebrospinal fluid (CSF) and may lead to a paradoxical increase in CSF acidosis [42]. In addition, the use of bicarbonate in DKA may delay the fall in blood lactate: pyruvate ratio and ketones when compared to intravenous 0.9% sodium chloride infusion [43]. Intensive care teams may occasionally use intravenous bicarbonate if the pH remains low and inotropes are required.

Level 2 care


Anti-thrombo-embolic therapy

The risk of DVT and PE is high in DKA. Patients should receive low weight molecular heparin as per the hospital protocol.