Phosphate
Phosphate levels are affected in DKA inmuch the same way as
potassium (that is, extracellular shift but depleted total body
levels). A small study found that the addition of phosphate to
standard treatment did not reduce the time taken to reach
recovery indices of bicarbonate, pH, or glucose.16 Differences in
magnesium and 2,3DPG levels and in P50 (the PaO2 at which
haemoglobin is 50% saturated) were not statistically significant.
In another study phosphate supplementation (15 or 45
mmol) did not affect the rate of correction of [glucose],
[bicarbonate] or pH.17
PROGNOSIS
An overall mortality rate of 3.9% was reported from Birmingham
(United Kingdom) for the period 1971 to 1991.2 Many of
these deaths occurred in patients with significant comorbidity;
it may not be possible to reduce the mortality rate further.
The mortality rate increases with age: 1.9% in those aged 12 to
69 and 19.6% in those aged 70 or more (95% CI for the difference
in mortality between the two age groups 9.9% to 25.4%).
If cerebral oedema complicates DKA the mortality rate is
over 90%. Although most cases occur in patients younger than
20 years it can occur in older patients. Avoiding falls in osmolality
greater than 5 mosm/h has been suggested as a way of
reducing the likelihood of developing cerebraloedema.9
FUTURE DEVELOPMENTS
There are insulin analogues (Aspart and LisPro) that are
ultra-fast acting insulins with shorter half lives than soluble
insulins currently in use. There is no evidence that the use of
such insulins increases the risk of DKA and the management
of patients with diabetes treated with these agents is no
different from that outlined above.
Continuous subcutaneous insulin infusions are commonly
used in continental Europe to treat type I diabetes mellitus
and their use is increasing in the UK. They were initially associated
with an increased risk of DKA because of equipment
failure.18 19 As the technology has improved this risk has fallen.