A complicated hyperglycaemic emergency
Editor – I read with interest the article by Vidyarthi and Chowdhury describing a hyperosmolar non-ketotic diabetic emergency complicated by diabetes insipidus (Clin Med June 2010 pp 264–5).
I agree that these complex cases are best managed in a critical care environment where point of care testing is available to guide therapy. I feel a number of other features merit clarification, however. Firstly, the authors fail to emphasise that hyperglycaemia causes water shift from intracellular fluid (ICF) to extracellular fluid (ECF). Correction of hyperglycaemia thus causes in a influx of water back into the ICF causing a rise in serum sodium despite reduced free water losses. As this rise is accompanied by an influx of water into the brain, osmotic demyelination syndrome (central pontine myeliniolysis) should not arise, as long as serum osmolarity is falling. Conversely cerebral oedema can be a risk if serum osmolarity falls very rapidly with volume expansion. However, this danger may have been over-emphasised in this case where serum osmolarity paradoxically rose with therapy, attributed by the authors to diabetes inspidus of uncertain aetiology. I feel administration of large volumes of 0.9% saline may have contributed to this outcome. The patient described was in early shock with a mean arterial blood pressure of 75 mmHg. Six litres of 0.9% saline were given for volume correction, certainly an over estimate of any ECF deficit – and potentially risking ECF volume overload and hyperchloraemic metabolic acidosis. Interestingly, the patient subsequently passed very dilute urine and became hypernatraemic beyond the rise expected by fall in serum glucose – so that they then were at risk of osmotic demyelination, a state that corrected with use of DDAVP. A similar scenario is well described in the correction of hyponatraemia associated with a volume deficit1 where appropriate suppression of a hypovolaemic ADH signal results in a water diuresis (with low urinary osmolarity) and over-shoot hypernatraemia. I feel the case described is exactly analogous, with removal of hypovolaemia leading to water diuresis and significant over-elevation of serum sodium. This response is transient and physiological, although short duration treatment with DDAVP is appropriate.2
Footnotes
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- Royal College of Physicians
References
- Mohmand HK
- Perianayagam A
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