Diabetic Ketoacidosis

An episode of diabetic ketoacidosis often evolves over a 24 hour period [8]. The main symptoms are nausea, vomiting, extensive thirst, excessive production of urine as well as abdominal pain. Hyperglycemia is also present most of the time. Breathing is laboured and deep in severe cases of diabetic ketoacidosis. The abdomen may be tender and in a minority of patients, vomiting of blood may be noted. The vomiting of blood is as a result of oesophageal erosion. Confusion, lethargy, stupor and ultimately coma may be seen in patients with severe cases of diabetic ketoacidosis.

Following physical examination, there is often clinical evidence of dehydration such as decreased skin turgor and presence of a dry mouth. In small children with diabetic ketoacidosis, cerebral edema may be presented and when this is present, headache, coma and loss of pupillary light reflex are also seen.

The condition is diagnosed when the combination of hyperglycemia, acidosis and ketones in the blood is demonstrated [9]. To demonstrate acidosis, arterial blood gas measurement is often performed. Ketones can be measured in the blood and urine.

Also, blood samples may be taken to measure urea and creatinine (important measures of kidney function) as well as electrolytes. Other tests to rule out infection and acute pancreatitis may be carried out. Some of the tests include, complete blood count, C-reactive protein, etc.

People who are diagnosed with diabetic ketoacidosis are either treated in the emergency room or admitted to the hospital [10]. Treatment if often based on a three pronged approach covering the following:

• Fluid replacement
• Electrolyte replacement
• Insulin therapy

For diabetic ketoacidosis, the overall rate of mortality is 2% or less. However, prognosis is poor when there is presence of deep coma at the time of diagnosis is made [7].

In properly treated patients, prognosis is excellent, especially in younger patients who do not have any forms of intercurrent infections. The worst prognosis is seen in older patients with illnesses such as myocardial infarction, sepsis or pneumonia who are treated outside an intensive care unit.

In diabetic ketoacidosis, the most common scenarios are underlying or concomitant infection (seen in 40% of cases), missed insulin treatments (seen with 25% of cases) or newly diagnosed or unknown diabetes (seen in 15% of cases) [2]. There are other etiologic factors for this condition.

In type 1 diabetes mellitus, the following are etiologic factors [3]:

• Acute insulin deficiency
• Poor compliance with insulin mostly through injection omissions or lack of patient education
• Urinary tract infection (UTI) and other bacterial infections, recurrent sicknesses
• Stress (emotional, surgical or medical)
• Idiopathic causes
• Blockage of insulin infusion catheter pump
• Mechanical failure of the insulin infusion pump

In type 2 diabetes, the main etiologic factors are:

• Intercurrent illnesses such as myocardial infarction or pneumonia
• Medication use (Clozapine, pentamidine, corticosteroids)

4.6 to 8.0 per 100 people with type 1 diabetes develop this condition each year. In the United States, over 135,000 hospital admissions happen each year as a result of diabetic ketoacidosis [4]. The estimated cost has been put at $2.4 billion, around a quarter of what it costs to take care of people with type 1 diabetes. The number of cases in the United States has been on the increase. The risk is higher in people who have eating disorders and those who are unable to afford insulin.

In developed countries, the incidence of diabetic ketoacidosis remains unknown. However, it may be higher in industrialised nations [5].

A racial predisposition towards whites is notable with this condition and this as a result of the fact that type 1 diabetes is mostly seen in this racial group.

Diabetic ketoacidosis refers to a complex disordered metabolic state which is most of the time characterised by hyperglycemia, ketonuria and ketoacidosis [6]. DKA often occurs as a result of absolute or relative insulin deficiency which is followed most of the time by an increase in counter-regulatory hormones such as glucagon, cortisol, epinephrine and growth hormone. This kind of hormonal imbalance is referred to as glycogenolysis and lipolysis.

Severe hyperglycemia is caused by hepatic gluconeogenesis, glycogenolysis and excessive counter regulatory hormone. Lipolysis on the other hand causes an increase in serum free fatty acids. Hepatic metabolism of free fatty acids alternative source of energy or ketogenesis leads to accumulation of acidic intermediate and end metabolites such as ketones and ketoacids. The ketones formed include acetoacetate, acetone and beta-hydroxybutyrate.

There are important steps to be taken if diabetic ketoacidosis is to be dealt with. This includes the following:

• Commitment to the management of diabetes 
• Continuous monitoring of blood sugar level 
• Adjustment of insulin dosage as needed
• Consistent check of ketone levels

Diabetic ketoacidosis (DKA) is a complication of diabetes that is often life-threatening [1]. The condition is an acute one and it is mainly seen in people with the type 1 diabetes. It is however not rare in patients with type 2 diabetes.

This condition refers to relative or absolute insulin deficiency. It is often aggravated by dehydration, hyperglycemia, and derangements in intermediary metabolism as a result of acidosis. Some of the main causes of this condition are disruption in insulin treatment, new onset of diabetes and underlying infections.

Clinically, it can be defined as an acute state of severe and uncontrolled diabetes associated with ketoacidosis often requiring emergency treatment with intravenous fluids and insulin.

Diabetic ketoacidosis refers to an often serious complication common with patients of diabetes. The complication makes the blood have high level of acids. The acid is referred to as ketones.

Diabetic ketoacidosis arises when the body is not able to produce enough insulin. Insulin usually plays a very important role in helping sugar to get into the cells. The sugar is the main source of energy for the muscles and other tissues to enter the cells. When the insulin is not enough, the body starts to break down fat as if struggles to replace sugar as fuel. As this process goes on, there will be a build-up of the toxic acids (ketones). As this goes on, diabetic ketoacidosis or DKA will develop.

People who have diabetes need to understand the symptoms of DKA so as to seek emergency care as soon as these signs are seen.

1. Glaser NS, Marcin JP, Wootton-Gorges SL, et al. Correlation of clinical and biochemical findings with diabetic ketoacidosis-related cerebral edema in children using magnetic resonance diffusion-weighted imaging. J Pediatr. Jun 25 2008.
2. Umpierrez GE, Jones S, Smiley D, et al. Insulin analogs versus human insulin in the treatment of patients with diabetic ketoacidosis: a randomized controlled trial. Diabetes Care. Jul 2009;32(7):1164-9. 
3. Herrington WG, Nye HJ, Hammersley MS, Watkinson PJ. Are arterial and venous samples clinically equivalent for the estimation of pH, serum bicarbonate and potassium concentration in critically ill patients?. Diabet Med. Jan 2012;29(1):32-5.
4. Mrozik LT, Yung M. Hyperchloraemic metabolic acidosis slows recovery in children with diabetic ketoacidosis: a retrospective audit. Aust Crit Care. Jun 26 2009
5. Bowden SA, Duck MM, Hoffman RP. Young children (< 5 yr) and adolescents (>12 yr) with type 1 diabetes mellitus have low rate of partial remission: diabetic ketoacidosis is an important risk factor. Pediatr Diabetes. Jun 2008;9(3 Pt 1):197-201. 
6. Eledrisi MS, Alshanti MS, Shah MF, Brolosy B, Jaha N. Overview of the diagnosis and management of diabetic ketoacidosis. American Journal of Medical Science 2006 331 (5): 243–51.
7. Powers AC (2005). "Diabetes mellitus". In Kasper DL, Braunwald E, Fauci AS, et al.. Harrison's Principles of Internal Medicine (16th ed.). New York, NY: McGraw-Hill. pp. 2152–2180. ISBN 0-07-139140-1.
8. Glaser N. New perspectives on the pathogenesis of cerebral edema complicating diabetic ketoacidosis in children. Pediatric Endocrinology Reviews 2006 3 (4): 379–86. 
9. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care 2009; 32:1335.
10. Arieff AI, Carroll HJ. Nonketotic hyperosmolar coma with hyperglycemia: clinical features, pathophysiology, renal function, acid-base balance, plasma-cerebrospinal fluid equilibria and the effects of therapy in 37 cases. Medicine (Baltimore) 1972; 51:73.

• DKA
  Guest, 2018-10-04 23:22
• Ketoacidosis
  Guest, 2017-11-24 04:23