Diabetic ketoacidosis in adults
BMJ 2015; 351 doi: https://doi.org/10.1136/bmj.h5660 (Published 28 October 2015) Cite this as: BMJ 2015;351:h5660All rapid responses
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Patient education is a critical component of the prevention of ketoacidosis and a clear understanding of insulin action is an essential component of this. However, it is uncommon to encounter fear of insulin therapy acutely in people admitted with DKA (the scope of this review) as they are unwell with a life-threatening metabolic derangement and generally understand insulin is required for recovery.
Concerns around insulin therapy are most frequently encountered in type 2 diabetes, where an elective decision to progress to insulin is discussed.
We are not aware of robust experimental data confirming that the intracellular glucose concentration is low in insulin deficient states. In DKA, the switch from intracellular glucose metabolism to fatty acid oxidation and ketogenesis is primarily driven by insulin deficiency and it is important to note that not all intracellular glucose transporters are insulin sensitive.
Box 3 is correct - hyperkalaemia is often seen at presentation with DKA as a consequence of insulin deficiency. Hypoglycaemia occurs later with insulin therapy.
Competing interests: No competing interests
A key point to emphasise in patient education is that in DKA, while there is hyperglycaemia, there is intracellular hypoglycaemia, and it is the administration of insulin which remedies this by allowing cells to access circulating glucose to use for their energy requirements. This realisation should help abate some of the fears that patients have about insulin administration.
(In Box 3., I think that the authors intended hypokalaemia to be a potential cause of arrhythmias and cardia arrest, rather than the hyperkalaemia listed).
Competing interests: No competing interests
Here is what I thought I knew before reading this article ;
A. DKA presents with hyperkalaemia
B. This hyperkalaemia is improved by insulin and fluids therapy
C. Insulin therapy can precipitate hypokaleamia if titration and care are not well minded.
After reading, I became somehow confused.
Some clarification may help.
Competing interests: No competing interests
Misra et al give a broad overview of the management of diabetic ketoacidosis (DKA). When discussing intravenous fluids, the authors mention the risk of hyperchloraemic acidosis. However, when discussing potassium replacement, they do not mention what kind of potassium should be used. As suggested by the ISPAD Clinical Practice Consensus Guidelines 2014 and ISPED Reccomendations for the management of diabetic ketoacidosis in pediatric patients, potassium replacement should be started at 40 mmol/L. They also suggest that potassium phosphate may be used with potassium chloride or acetate as administration of potassium entirely as potassium chloride contributes to the risk of hyperchloremic metabolic acidosis, whereas administration entirely as potassium phosphate can result in hypocalcemia.
Furthermore, it is important to recognize that the characteristic features of hyperglycemic hyperosmolar state (HHS) and DKA may in some cases overlap. Some patients with HHS, especially when severely dehydrated, may present with mild or moderate acidosis (due to hypoperfusion/lactic acidosis) and some children with type 1 diabetes may have severe hyperglycemia (high carbohydrate containing beverages are frequently used to quench thirst before diagnosis). Therefore, therapy must be carefully adapted to address the inpatient-specific pathophysiology and biochemical alterations.
Competing interests: No competing interests
Pathophysiology of Diabetic Ketoacidosis (Re: Diabetic ketoacidosis in adults)
To the Editor of British Medical Journal
In the Clinical Review “Diabetic ketoacidosis in adults”(1) there are discrepancies with the literature (including the authors' references).
1. In the paragraph “What is DKA?” the authors write “DKA is an extreme metabolic state caused by insulin deficiency”. Since the Nobel Prize was awarded 1977 to Rosalyn S Yalow for the development of new methods of biochemical analysis that make it possible to measure insulin concentration in human plasma, these methods have been used worldwide. In 1981, the monograph “Diabetic coma: ketoacidotic and hyperosmolar” (the authors' reference 1) was published and on page 67, Figure 6.3 has the names of 12 authors who have reported sufficient amounts of plasmatic insulin in patients with DKA. In contrast, absolute deficiency of plasmatic insulin has been reported in diabetic patients with hyperglycemic hyperosmolar syndrome(2) as well as in diabetic patients on routine control without subjective complaints(3). Where are the published concrete reports on the deficiency of plasmatic insulin in patients with DKA? What is the “safe level” of plasmatic insulin concentration that makes development of DKA impossible?
2. In the paragraph “How does DKA present” the authors write “Typically, patients develop … an altered mental state, including coma” and in the paragraph “Bicarbonate” they write “Bicarbonate is not routinely recommended”. Without bicarbonate therapy, lethality of coma in DKA is up to 100% (e g, the authors reference 27 – Basu et al); if in the therapy is included also sodium bicarbonate, the lethality of coma is zero (e g (4)). Where are the published reports on zero lethality of coma in DKA without alkalising therapy?
Dr. Viktor Rosival, PhD
SYNLAB Department of Laboratory Medicine, Dérer's Hospital,
Limbová 5, SK-833 04 Bratislava, Slovakia.
e-mail: rosivalv@hotmail.com
References
1. Misra O, Oliver NS. Diabetic ketoacidosis in adults. BMJ 2015; 351: Oct 28:h5660.
2. Vinik A, Seftel H, Joffe BJ. Metabolic findings in hyperosmolar, non-ketotic diabetic stupor. Lancet 1970:2:797-9.
3. Matsuyama T, Hoffman WH, Dunbar JC, et al. Glucose, insulin, pancreatic glucagen and glucagon-like immunoreactive materials in the plasma of normal and diabetic children. Horm Metab Res 1975;7:452-6.
4. Umpierrez GE, Kelly JP, Navarrete JE, et al. Hyperglycemic crises in urban blacks. Arch Intern Med; 1997;157:669-75.
Competing interests: No competing interests