The Joint British Diabetes Societies guidelines for the management of diabetic ketoacidosis (these do not cover Hyperosmolar Hyperglycaemic Syndrome) are available in full at: (i) http://www.diabetes.org.uk/About_us/Our_Views/Care_recommendations/The-Management-of-Diabetic-Ketoacidosis-in-Adults; (ii) http://www.diabetes.nhs.uk/publications_and_resources/reports_and_guidance; (iii) http://www.diabetologists-abcd.org.uk/JBDS_DKA_Management.pdf. This article summarizes the main changes from previous guidelines and discusses the rationale for the new recommendations. The key points are: Monitoring of the response to treatment (i) The method of choice for monitoring the response to treatment is bedside measurement of capillary blood ketones using a ketone meter. (ii) If blood ketone measurement is not available, venous pH and bicarbonate should be used in conjunction with bedside blood glucose monitoring to assess treatment response. (iii) Venous blood should be used rather than arterial (unless respiratory problems dictate otherwise) in blood gas analysers. (iv) Intermittent laboratory confirmation of pH, bicarbonate and electrolytes only. Insulin administration

Diabetes UK Position Statements and Care Recommendations Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis

Diabet. Med. 28, 508–515 (2011)

Abstract
The Joint British Diabetes Societies guidelines for the management of diabetic ketoacidosis (these do not cover Hyperosmolar Hyperglycaemic Syndrome) are available in full at:

(i) http://www.diabetes.org.uk/About_us/Our_Views/Care_recommendations/The-Management-of-Diabetic-Ketoacidosis-in-Adults;
(ii) http://www.diabetes.nhs.uk/publications_and_resources/reports_and_guidance;
(iii) http://www.diabetologists-abcd.org.uk/JBDS_DKA_Management.pdf.


This article summarizes the main changes from previous guidelines and discusses the rationale for the new recommendations.

The key points are:

Monitoring of the response to treatment

(i) The method of choice for monitoring the response to treatment is bedside measurement of capillary blood ketones using a ketone meter.
(ii) If blood ketone measurement is not available, venous pH and bicarbonate should be used in conjunction with bedside blood glucose monitoring to assess treatment response.
(iii) Venous blood should be used rather than arterial (unless respiratory problems dictate otherwise) in blood gas analysers.
(iv) Intermittent laboratory confirmation of pH, bicarbonate and electrolytes only.


Insulin administration

(i) Insulin should be infused intravenously at a weight-based fixed rate until the ketosis has resolved.
(ii) When the blood glucose falls below 14 mmol/l, 10% glucose should be added to allow the fixed-rate insulin to be continued.
(iii) If already taking, long-acting insulin analogues such as insulin glargine (Lantus®, Sanofi Aventis, Guildford, Surry, UK) or insulin detemir (Levemir®, Novo Nordisk, Crawley, West Sussex, UK.) should be continued in usual doses.


Delivery of care

(i) The diabetes specialist team should be involved as soon as possible.
(ii) Patients should be nursed in areas where staff are experienced in the management of ketoacidosis.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1464-5491.2011.03246.x

Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis

Reactive oxidative species (ROS) toxicity remains an undisputed cause and link between Alzheimer’s disease (AD) and Type-2 Diabetes Mellitus (T2DM). Patients with both AD and T2DM have damaged, oxidized DNA, RNA, protein and lipid products that can be used as possible disease progression markers. Although the oxidative stress has been anticipated as a main cause in promoting both AD and T2DM, multiple pathways could be involved in ROS production. The focus of this review is to summarize the mechanisms involved in ROS production and their possible association with AD and T2DM pathogenesis and progression. We have also highlighted the role of current treatments that can be linked with reduced oxidative stress and damage in AD and T2DM.

/pdf/oxidative-toxicity-in-diabetes-and-alzheimer-s-disease-7evvayjmlz.pdf

Oxidative toxicity in diabetes and Alzheimer’s disease: mechanisms behind ROS/ RNS generation

This paper describes the design and fabrication of a "pop-up" electrochemical paper-based analytical device (pop-up-EPAD) to measure beta-hydroxybutyrate (BHB)-a biomarker for diabetic ketoacidosis-using a commercial combination BHB/glucometer. Pop-up-EPADs are inspired by pop-up greeting cards and children's books. They are made from a single sheet of paper folded into a three-dimensional (3D) device that changes shape, and fluidic and electrical connectivity, by simply folding and unfolding the structure. The reconfigurable 3D structure makes it possible to change the fluidic path and to control timing; it also provides mechanical support for the folded and unfolded structures that enables good registration and repeatability on folding. A pop-up-EPAD designed to detect BHB shows performance comparable to commercially available plastic test strips over the clinically relevant range of BHB in blood when used with a commercial glucometer that integrates the ability to measure glucose and BHB (combination BHB/glucometer). With simple modifications of the electrode and the design of the fluidic path, the pop-up-EPAD also detects BHB in buffer using a simple glucometer-a device that is more available than the combination BHB/glucometer. Strategies that use a "3D pop-up"-that is, large-scale changes in 3D structure and fluidic paths-by folding/unfolding add functionality to EPADs (e.g., controlled timing, fluidic handling and path programming, control over complex sequences of steps, and alterations in electrical connectivity) and should enable the development of new classes of paper-based diagnostic devices.

A Paper-Based "Pop-up" Electrochemical Device for Analysis of Beta-Hydroxybutyrate.

Diabetic ketoacidosis (DKA) is a rare yet potentially fatal hyperglycemic crisis that can occur in patients with both type 1 and 2 diabetes mellitus. Due to its increasing incidence and economic impact related to the treatment and associated morbidity, effective management and prevention is key. Elements of management include making the appropriate diagnosis using current laboratory tools and clinical criteria and coordinating fluid resuscitation, insulin therapy, and electrolyte replacement through feedback obtained from timely patient monitoring and knowledge of resolution criteria. In addition, awareness of special populations such as patients with renal disease presenting with DKA is important. During the DKA therapy, complications may arise and appropriate strategies to prevent these complications are required. DKA prevention strategies including patient and provider education are important. This review aims to provide a brief overview of DKA from its pathophysiology to clinical presentation with in depth focus on up-to-date therapeutic management.

/pdf/management-of-adult-diabetic-ketoacidosis-1m9ru63x0q.pdf

Management of adult diabetic ketoacidosis.

Diabetic ketoacidosis (DKA) is still a major contributor to morbidity and mortality in diabetes. The triad of hyperglycaemia, ketosis and acidosis can be diagnosed within a few minutes of the patient presenting, by measuring blood glucose and ketones using a meter, and venous blood pH on a blood gas analyser. Quantifying ketosis allows accurate distinction between simple hyperglycaemia and metabolic decompensation. We review the management of DKA, and the emerging role of near-patient testing in diagnosing ketosis and monitoring its resolution.

https://www.glucomen.co.uk/wp-content/themes/glucomen/assets/pdfs/qjm-2004-wallace-matthews.pdf

T.M. Wallace

Papers

Recent advances in the monitoring and management of diabetic ketoacidosis.