QJM Advance Access originally published online on April 25, 2008
QJM 2008 101(7):593-594; doi:10.1093/qjmed/hcn059
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The use of the sliding scale also needs to be reviewed
Sir,
Apart from the issue of administration of intravenous insulin to patients who are able to eat normally, and in whom subcutaneous insulin is not contraindicated1 the other consideration worth addressing is the continuing prevalence of the sliding scale insulin (SSI) regime in clinical practice, exemplified by its use, albeit via intravenous infusion, in 10 of the patients in the study.1 This should be a cause of concern, given the fact that the American Diabetic Association (ADA) guidelines discourage the use of the SSI, citing concerns about its potential to exacerbate both hyperglycaemia and hypoglycaemia.2 Indeed, in one study, the sole use of the SSI (without either basal insulin or a separate nutritional insulin order) was associated with a ‘daily average glucose reading that was ... higher than that for those ... not prescribed a sliding scale at all.’3 The alternative is to base treatment on an initial evaluation of the admission glycosylated haemoglobin (HbA1c) level, and to calculate the dose of basal insulin on the basis of body weight.4 The basal requirement should then be supplemented by short acting ‘prandial’ insulin (dose also based on body weight) administered with each meal so as to dampen down the postprandial surge in blood glucose. Even the subsequent fine tuning of prandial insulin (so-called correction dose insulin) can be made without recourse to SSI, the recommended strategy being a calculation based on a percentage of the initial total insulin dose.4 Indeed, the ADA guidelines are at pains to point out that correction dose insulin should not be confused with the sliding scale because, as opposed to SSI, correction dose insulin does not refer to a set amount of insulin administered for hyperglycaemia without regard to the timing of the food.2 Accordingly, it is appropriate to criticise, not only the use the intravenous insulin regime in patients who are able to eat,1 but also the use of a sliding scale which is based neither on a correction of prandial insulin requirements, nor on the intention to supplement basal insulin requirements. The SSI, however, permeates all aspects of clinical practice, including the management of diabetic ketoacidosis (DKA).5 In the ‘recovery’ phase of DKA, the recovery phase being defined as the one characterized by a fall in blood glucose to levels, below 14 mmol/l,6,7 the main rival to the SSI is a regime based either on a ‘match’ between the dose of insulin and the dextrose content of the rehydrating fluid,6 the ‘insulin/rehydrating fluid’ match or a ‘match’ between the doses of insulin, the dextrose content of the rehydrating fluid and the patient's body weight,7 the ‘insulin/rehydrating fluid/body weight’ match. In the ‘insulin/rehydrating fluid’ match a 2.5 units/h continuous infusion of insulin is matched with 1 l/4 h infusion of 5% dextrose, and a 10 units/h infusion of insulin is matched with a 1 l/4 h infusion of 10% dextrose).6 In this regime, the comparison between 2.5 units/h insulin (with matching 5% dextrose) and 10 units/h insulin (with matching 10% dextrose) showed no difference in the rate of resolution of acidosis. However, at the expense of higher final levels of blood glucose (higher by 
2.0 mmol/l), the 10 units/h regime achieved a significantly more rapid resolution of ketonaemia.6 In the ‘insulin/rehydrating fluid/body weight’ match insulin 0.05–0.1 units/kg body weight per hour is matched with either 5% dextrose or 10% dextrose.7 Comparative rates of resolution of acidosis and ketonaemia are not available for the ‘insulin/rehydrating fluid/body weight’ regime but, in view of the fact that it generates a dose of insulin in the range 2.5–6.0 units/h it is reasonable to extrapolate that it compares favourably with the ‘insulin/rehydrating fluid’ regime in its rate of resolution of acidosis. In contrast with the evidence base for the rate of resolution of acidosis and ketonaemia obtained from the ‘insulin/rehydrating fluid’ match,6 there is no documentation of the rate of resolution of these parameters following the use of the SSI during the recovery phase of DKA. Accordingly, this is one more reason for phasing out the SSI, a reason justified, in my view, by the misgiving that ‘the major deficit of sliding scale insulin is that it allows the house officer to write a arbitrary insulin regime and leave the patient's diabetes management in the hands of floor nursing staff.’8
Medical Division
Manchester Medical Society
C/o John Rylands University Library
Oxford Road
Manchester M13 9PP
email: oscarjolobe{at}yahoo.co.uk
References
1. Penfold S, Gouni R, Hamilton P, Richardson T, Kerr D. Immediate in-patient management of hyperglycaemia-confusion rather than consensus? Q J Med (2008) 101:87–90.[Web of Science]
2. Clement S, Braithwaite SS, Magee MF, et al. on behalf of Writing Committee Diabetes Care. Diabetes Care (2004) 27:553–90.
3. Schnipper JL, Barsky EE, Shaykevich S, Fitzmaurice G, Penedrgrass ML. Inpatient management of diabetes and hyperglycaemia among general medicine patients at a large teaching hospital. J Hosp Med (2006) 1:145–50.[CrossRef][Medline]
4. Donaldson S, Villanueva G, Rondinelli L, Maldwin D. Rush University Guidelines and Protocols for the management of hyperglycaemia in hospitalized patients. Diabetes Educ (2006) 32:954–62.
5. Wallace TM, Matthews DR. Recent advances in the monitoring and management of diabetic ketoacidosis. Q J Med (2004) 97:773–80.[Web of Science]
6. Krentz AJ, Hale PJ, Singh BM, Nattrass M. The effect of glucose and insulin infusion on the fall of ketone bodies during treatment of diabetic ketoacidosis. Diabet Med (1989) 6:31–6.[Web of Science][Medline]
7. Eledrisi MS, Alshanti MS, Shah MF, Brolosy B, Jaha N. Overview of the diagnosis and management of diabetic ketoacidosis. Am J Med Sci (2006) 331:243–51.[CrossRef][Web of Science][Medline]
8. Lorber DL. Sliding scale insulin (letter). Diabetes Care (2001) 24:2011–12.
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