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Journal Scan

August 2016

Diabetic ketoacidosis

Summarized from Nyenwe E, Kitabchi A. The evolution of diabetic ketoacidosis: An update of its etiology, pathogenesis and management. Metabolism 2016; 65: 507-21

Diabetic ketoacidosis (DKA), which is an acute, potentially life-threatening complication of poorly controlled diabetes, is the subject of a recent comprehensive review article.  

The authors discuss epidemiological issues, revealing increasing incidence of DKA and decreasing mortality. 

Once inevitably fatal, DKA now has a reported mortality rate of <1 % in adults and 5 % in the elderly who also have one or more chronic illnesses, in addition to diabetes.

They reveal that although DKA more commonly affects those with type 1 diabetes, around a third of cases occur in those with type 2 diabetes.

This introductory section also reminds that DKA is characterized by the presence of three cardinal biochemical features: raised blood glucose (hyperglycemia); presence of ketones in blood and urine (ketonemia, ketonuria); and metabolic acidosis.

Insulin deficiency is central to the development of these three biochemical abnormalities.

The very rare occurrence of euglycemic DKA (DKA with normal blood glucose) is highlighted by reference to recent reports of this condition in patients treated with a relatively new class of antidiabetic drug (the SGLT 2 inhibitors) that reduces blood glucose by inhibiting renal reabsorption of glucose. 

There follows discussion of factors that precipitate DKA (omission or inadequate dosing of insulin, and infection are the most common triggers), and the possible mechanisms responsible for ketosis-prone type 2 diabetes.

This latter condition, which was recognized as an entity only relatively recently, is distinguished by the development of severe but transient failure of pancreatic β-cells to manufacture insulin, with resulting DKA. No triggers have yet been identified for development of DKA in ketosis-prone type 2 diabetes.

Full recovery of β-cell function and consequent return of normal insulin production following DKA, is usual for patients with ketosis-prone type 2 diabetes.  

Just how deficiency of insulin leads to the acute and severe biochemical abnormalities of DKA is explained under three headings: carbohydrate metabolism; lipid and ketone metabolism; and water and electrolyte disturbances.

This detailed description of the pathogenesis of DKA includes discussion of recent research that provides evidence of a temporary inflammatory, procoagulant state among patients with DKA. 

A section on diagnosis of DKA includes comprehensive detail of the signs and symptoms of the condition, along with detail of expected laboratory test results, and the differential diagnosis of patients who present with unexplained ketoacidosis. 

Finally, the treatment of DKA is fully discussed; the authors provide a recommended treatment protocol that reflects the three main goals: improvement of circulatory volume and tissue perfusion; correction of hyperglycemia and thereby hyperosmolarity; and correction of electrolyte imbalance, along with resolution of ketosis.

Treatment requires administration of iv fluids, insulin, potassium and, in some circumstances, bicarbonate and phosphate. Each of these treatment elements is discussed fully in turn, and many controversies surrounding treatment of DKA over the years are addressed.

The authors emphasize the necessity of intensive biochemical and physical monitoring during treatment of DKA, and highlight complications that can arise.   

This review, which draws on 146 references, including many recent studies provides an up-to-date, authoritative account of all aspects of DKA. A valuable resource for clinical and laboratory trainees involved in the care of diabetic patients.


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Chris Higgins

has a master's degree in medical biochemistry and he has twenty years experience of work in clinical laboratories.

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