Diabetic Ketoacidosis

Diabetic Ketoacidosis

Introduction

Diabetic ketoacidosis (DKA) is considered a cardinal feature of Type 1 diabetes and insulin dependence. However, several reports have described young obese African-American subjects presenting with DKA, but lacking autoimmune markers and having physical characteristics that are more typical of Type 2 diabetes. Although the degree of acidosis on presentation can be severe , in many it is possible to withdraw insulin after initial therapy. In the UK, this clinical scenario has been reported in adult subjects of African or Caribbean descent , and recently, in an adolescent obese white subject .

In other words it can be sai that Diabetic ketoacidosis (DKA) is a state of inadequate insulin levels resulting in high blood sugar and accumulation of organic acids and ketones in the blood. It is also common in DKA to have severe dehydration and significant alterations of the body's blood chemistry(Pinero 2001).

DKA is usually seen in people who have type 1 (insulin-dependent) diabetes. Most often, these are diabetics younger than 25 years, but the condition may occur in diabetics of any age. Males and females are equally affected.

The condition known as diabetic ketoacidosis occurs when the body has no insulin. This leaves the muscle, fat, and liver cells unable to use glucose (sugar) in the blood as fuel. Other hormones such as glucagon, growth hormone, and adrenaline cause fat to break down within the cells of these tissues into glucose and fatty acids. These fatty acids are converted to ketones by a process called oxidation. The body is literally consuming muscle, fat, and liver cells for fuel(Shimabukuro 1998).

In diabetic ketoacidosis the body shifts from its normal metabolism using carbohydrates for fuel to a fasting state using fat for fuel. The resulting increase in blood sugar because it cannot be transported into cells for future use causes increased urination and dehydration. Commonly, 10% of total body fluids may be lost. Significant loss of potassium from urination is also common.

Discussion

We report two UK adolescent black subjects with similar presentations.

A 17-year-old black Non-Obese boy (subject 1) presented with nausea, vomiting, polyuria and polydipsia. his maternal grandmother had Type 2 diabetes. His weight was 65 kg and body mass index (BMI) 26.1 kg/m2. He had acanthosis nigricans. he had glycosuria and ketonuria. his blood glucose was 22.0 mmol/l, pH 7.284, bicarbonate 9.8 mmol/l and HbA1c 15.2%. She was treated successfully with intravenous fluids and insulin. He was later converted to a subcutaneous insulin regimen, to which twice daily metformin was added. Within 2 months of discharge he stopped complying with his insulin therapy, but continued metformin(Aizawa 1997).

A 16-year-old black Obese boy (subject 2) presented with abdominal pain, vomiting, polyuria and polydipsia. There were two small lesions discharging pus over his left lateral malleolus. Three months previously he had fractured his left tibia and fibula playing football. This had required operative intervention. His maternal grandmother and uncle had Type 2 diabetes. His weight was 135 kg and BMI 39.9 kg/m2. He had acanthosis nigricans. He had glycosuria and ketonuria. His blood glucose was ...