**3. Pathophysiology of DKA**

Diabetic ketoacidosis (DKA) results from absolute or relative deficiency of circulating insu‐ lin and the combined effects of increased levels of the counterregulatory hormones: cate‐ cholamines, glucagon, cortisol and growth hormone [5].

At presentation, the magnitude of specific deficits of fluid and electrolytes in an individual patient varies depending upon the extent to which the patient was able to maintain intake of fluid and electrolytes, and the content of food and fluids consumed before coming to medi‐

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There is wide geographic variation in the frequency of DKA at onset of diabetes; rates inver‐ sely correlate with the regional incidence of type 1 diabetes. Frequencies range from 15 to

Type 2 diabetes mellitus (T2DM), associated with increased rates and severity of obesity, may account for as much as one half of newly diagnosed diabetes in those aged 10 to 21 years, depending on the socioeconomic and ethnic composition of the population [2]. Acute decompensation with DKA has been recognized to occur at the time of diagnosis in as many

cal attention and the duration and severity of illness [8].

DKA at diagnosis of type 1 diabetes occurs more commonly in [15,16]:

**•** children with absent first-degree relative with T1DM and

as 25% of children with type 2Diabetes Mellitus (T2DM0 [17].

The risk of DKA in established T1DM is 1–10% per patient per year

*In children with established diabetes (recurrent DKA)[4]*

Risk is increased in the following conditions [18 ]:

**•** peripubertal and adolescent girls

**•** limited access to medical services

**•** omission of insulin

**•** insulin pump therapy

**•** difficult or unstable family circumstances

**•** poor metabolic control or previous episodes of DKA

**•** psychiatric disorders, including those with eating disorders

**4. Epidemiology of DKA**

**4.1. Frequency of DKA**

At disease onset

70% in different regions of the world [9 -14].

**•** children younger than four years of age

**•** families of a lower socioeconomic class

*Absolute insulin deficiency* occurs in the following conditions:


*Relative insulin deficiency*, on the other hand, occurs when the concentrations of counterregu‐ latory hormones increase in response to stress in conditions such as:


The combination of low serum insulin and high counterregulatory hormone concentrations results in an accelerated catabolic state with increased glucose production by the liver and kidney (via glycogenolysis and gluconeogenesis), impaired peripheral glucose utilization re‐ sulting in hyperglycemia and hyperosmolality, and increased lipolysis and ketogenesis, causing ketonemia and metabolic acidosis [4].

Hyperglycemia and hyperketonemia cause osmotic diuresis, dehydration, and electrolyte loss. This stimulates stress hormone production, which induces insulin resistance and leads to a vicious circle, worsening the hyperglycemia and hyperketonemia. Fatal dehydration and metabolic acidosis will ensue if management is not initiated. Poor tissue perfusion or sepsis may lead to lactic acidosis which can aggravate the ketoacidosis [5].

At presentation, the magnitude of specific deficits of fluid and electrolytes in an individual patient varies depending upon the extent to which the patient was able to maintain intake of fluid and electrolytes, and the content of food and fluids consumed before coming to medi‐ cal attention and the duration and severity of illness [8].
