Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemia syndrome (HHS) are life-threatening emergencies that occur in patients with type 1 and type 2 diabetes.

Diabetic ketoacidosis (DKA) is defined by the following triad: Hyperglycaemia (or diagnosis of diabetes), Metabolic acidosis, and ketonemia.

Hyperosmolar hyperglycemia syndrome (HHS) is defined as a hyperglycaemic syndrome with high serum osmolality and dehydration.

These diabetic emergencies usually occur in an overlapping manner. Early diagnosis and management following preventive recommendations are essential to improve the evolution of patients. This is particularly important for those who have “euglycemic” DKA, a term used to describe DKA accompanied by lower than expected blood glucose.

What is your pathophysiology?

Both DKA and SHH result from absolute or relative insulin deficiency along with increased levels of circulating counterregulatory hormones.

Pathophysiology of DKA

In the usual clinical situation, an increase in the regulation of hormones contributes to the increase of gluconeogenesis and the deterioration of the use of glucose by peripheral tissues, causing DKA.

The main counterregulatory hormone is glucagon, responsible for the development of DKA, since the increase of other counterregulatory hormones (catecholamines, cortisol and growth hormone) are not necessarily observed. However, even glucagon is not absolutely essential, since DKA has also been described in patients after pancreatectomy.

In the liver, the gluconeogenic enzymes fructose, bisphosphatase, phosphoenolpyruvate carboxykinase (PEPCK), glucose-6-phosphatase and pyruvate carboxylase are stimulated by the increase of glucagon in proportion to insulin and by the increase in circulating cortisol concentrations.

Hepatic gluconeogenesis, but renal gluconeogenesis also intervenes. In adipose tissue, the combination of severe insulin deficiency and high concentrations of counterregulatory hormone activates hormone-sensitive lipase causing an increase in circulating free fatty acids.

Pathophysiology of SHH

The pathogenesis of SHH differs from that of DKA in that the degree of dehydration is more severe, secondary to osmotic diuresis and, the absence of ketosis / significant ketonemia. A higher concentration of insulin in patients with circulating hepatic SHH could partly explain the absence of significant ketosis.

Patients with HHS have lower concentrations of free fatty acids, cortisol, growth hormone and glucagon than those with DKA. Patients with HHS may have mild metabolic acidosis due to kidney failure and dehydration.

What are the precipitating causes?

The most frequent precipitating factors of DKA and SHH are:

• Inadequate insulin therapy.

• Infection followed by new-onset diabetes.

• Metabolic Stressors.

• Certain medications, including glucocorticoids, excessive diuretics, atypical antipsychotics, and others, may predispose to severe hyperglycemia, DKA, and SHH.

Ketoacidosis may include an elevation of urinary acetoacetate or serum β-hydroxybutyrate. The measurement of the ketone bodies at the point of care and the test strips for the measurement of β-hydroxybutyrate are expensive and not always available in many institutions, but it is likely that in the future they will become the standards of care, since they also provide accurate information to guide the treatment.

Patients with DKA may present with some or all of the following symptoms:

• Polyuria, polydipsia, nausea and vomiting.

• abdominal pain, visual disturbances and lethargy.

• sensory alteration and tachycardia, Kussmaul breathing, with a fruity smell on the breath.

• In general, patients have a marked hypovolemia, with orthostatic hypotension.

Patients with HHS usually have an altered level of consciousness, which can mask the usual symptoms of hyperglycemia. In patients with blood glucose> 600 mg / dl and negligible ketone concentrations, there is a direct relationship between hyperosmolality and sensory depression.

How should acute cases be managed?

The management of DKA and SHH includes liquids (usually administered intravenously), electrolytes and insulin.

It is very important to identify the cause of the acute decompensation of diabetes, which should not delay the treatment.

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