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Diabetic ketoacidosis

From Wikipedia, the free encyclopedia


Diabetic ketoacidosis (DKA) is one consequence of untreated diabetes mellitus (chronic high blood sugar, or hyperglycemia), and is linked to an impaired glucose cycle. In a diabetic patient, DKA begins with deficiency in insulin. This is most commonly due to undiagnosed diabetes mellitus, or in patients who have been diagnosed with diabetes, failure to take prescribed insulin. DKA has a 100% mortality rate if left untreated.



A key component of DKA is that there is no or very little circulating insulin and so it occurs mainly (but not exclusively) in type 1 diabetes, because type 1 diabetes is (essentially) caused by a lack of insulin production in the pancreas. It is much less common in type 2 diabetes because that is closely related to cell insensitivity to insulin, not shortage or absence of insulin. Some type 2 diabetics have lost their own insulin production and must take external insulin; they have some susceptibility to DKA. Although glucagon plays a role as an antagonistic hormone to insulin when there are low blood glucose levels, mainly by stimulating the process of glycogenolysis in hepatocytes (liver cells), insulin is the much more important hormone with more widespread effects throughout the body. Its presence or absence can by itself regulate most of DKA's pathological effects; notably, it has a short half-life in the blood of only a few minutes (typically about 6), so little time is needed between cessation of insulin release internally and the reduction of insulin levels in the blood.

Most cells in the body are sensitive to one or more of insulin's effects; the main exception being erythrocytes, neurons, liver cells, some intestinal tissue, and pancreatic beta-cells who do not require insulin to absorb glucose from the blood. The difference is due to different glucose transporter (GLUT) proteins. Most cells contain only GLUT-4 proteins which move to the cell surface membrane when stimulated by a second messenger cascade initiated by insulin, thus enabling uptake of glucose. Conversely, when insulin concentrations are low, these transporters dissociate from the cell membrane, and so prevent uptake of glucose.

Other effects of insulin include stimulation of the formation of glycogen from glucose and inhibition of glycogenolysis; stimulation of fatty acid (FA) production from stored lipids and inhibition of FA release into the blood; stimulation of FA uptake and storage; inhibition of protein catabolism and of gluconeogenesis, in which glucose is synthesised (mostly from some amino acid types, released by protein catabolism). A lack of insulin therefore has significant effects, all of which contribute to increasing blood glucose levels, to increased fat metabolism and protein degradation. Fat metabolism is one of the underlying causes of DKA.

Muscle wasting

Muscle wasting occurs primarily due to the lack of inhibition of protein catabolism; insulin inhibits the breakdown of proteins, and since muscle tissue is protein, a lack of insulin encourages muscle wasting, releasing amino acids both for to produce glucose (via gluconeogenesis) and for the synthesis of ATP via partial respiration of the remaining amino acids.

In those suffering from starvation, blood glucose concentrations are low due to both low consumption of carbohydrates and because most of the glucose available is being used as a source of energy by tissues unable to use most other sources of energy, such as neurons in the brain. Since insulin lowers blood glucose levels, the normal bodily mechanism here is to prevent insulin secretion, thus leading to similar fat and protein catabolic effects as in type 1 diabetes. Thus the muscle wastage visible in those suffering from starvation also occurs in type 1 diabetics, normally resulting in weight loss.

Ketone body production

Despite possibly high circulating levels of plasma glucose, the liver will act as though the body is starving if insulin levels are low. In starvation situations, the liver produces another form of fuel: ketone bodies. Ketogenesis, that is fat metabolic processing (beginning with lipolysis), makes ketone bodies as intermediate products in the metabolic sequence as fatty acids (formerly attached to a glycerol backbone in triglycerides) are processed. The ketone bodies beta-hydroxybutyrate and acetoacetate enter the bloodstream and are usable as fuel for some organs such as the brain, though the brain still requires a substantial proportion of glucose to function. If large quantities of ketone bodies are produced, the metabolic imbalance known as ketosis may develop, though this condition is not necessary harmful. The negative charge of ketone bodies causes decreased blood pH. An extreme excess of ketones can cause ketoacidosis.

In starvation conditions, the liver also uses the glycerol produced from triglyceride metabolism to make glucose for the brain, but there is not nearly enough glycerol to meet the body's glucose needs.


Normally, ketone bodies are produced in minuscule quantities, feeding only part of the energy needs of the heart and brain. However, in DKA, the body enters a starving state. Eventually, neurons (and so the brain) switches from using glucose as a primary fuel source to using ketone bodies.

As a result, the bloodstream is filled with an increasing amount of glucose that it cannot use (as the liver continues gluconeogenesis and exporting the glucose so made). This significantly increases its osmolality. At the same time, massive amounts of ketone bodies are produced, which, in addition to increasing the osmolal load of the blood, are acidic. As a result, the pH of the blood begins to change. Glucose begins to spill into the urine as the proteins responsible for reclaiming it from urine reach maximum capacity. As it does so, it takes a great deal of body water with it, resulting in dehydration.

Dehydration worsens the increased osmolality of the blood, and forces water out of cells and into the bloodstream in order to keep vital organs perfused. A vicious cycle is now set up, positively feeding back upon itself, and if untreated will lead to coma and death.


Treatment consists of hydration to lower the osmolality of the blood, replacement of lost electrolytes, insulin to force glucose and potassium into the cells, and eventually glucose simultaneously with insulin in order to correct other metabolic abnormalities, such as elevated blood potassium (hyperkalemia) and elevated ketone levels. Many patients require admission to a step-down unit or an intensive care unit (ICU) so that vital signs, urine output, and blood tests can be monitored frequently. Brain edema is not rare, and so this may suggest intensive monitoring as well. In patients with severe alteration of mental status, intubation and mechanical ventilation may be required. Survival is dependent on how badly-deranged the metabolism is at presentation to a hospital, but the process is only occasionally fatal.

DKA occurs more commonly in type 1 diabetes because insulin deficiency is most severe, though it can occur in type 2 diabetes. In about a quarter of young people who develop type 1 diabetes, insulin deficiency and hyperglycemia lead to ketoacidosis before the disease is recognized and treated. This can occur at the onset of type 2 diabetes as well, especially in young people. In a person known to have diabetes and being adequately treated, DKA usually results from omission of insulin, mismanagement of acute gastroenteritis, the flu, or the development of a serious new health problem (e.g., bacterial infection, myocardial infarction).

Insulin deficiency switches many aspects of metabolic balance in a catabolic direction. The liver becomes a net producer of glucose by way of gluconeogenesis (from protein) and glycogenolysis (from glycogen, though this source is usually exhaused within hours). Fat in adipose tissue is reduced to triglycerides and fatty acids by lipolysis. Muscle is degraded to release amino acids for gluconeogenesis. The rise of fatty acid levels is accompanied by increasing levels of ketone bodies (acetone, acetoacetate and beta-hydroxybutyrate; only one, acetone, is chemically a ketone -- the name is an historical accident). As ketosis worsens, it produces a metabolic acidosis, with anorexia, abdominal distress, and eventually vomiting. The rising level of glucose increases the volume of urine produced by the kidneys (an osmolar diuresis). The high volume of urination (polyuria) also produces increased losses of electrolytes, especially sodium, potassium, chloride, phosphate, and magnesium. Reduced fluid intake from vomiting combined with amplified urination produce dehydration. As the metabolic acidosis worsens, it induces obvious hyperventilation (termed Kussmaul respiration).

On presentation to hospital, patients in DKA are typically dehydrated and breathing both fast and deeply. Abdominal pain is common and may be severe. Consciousness level is typically normal until late in the process, when obtundation (dulled or reduced level of alertness or consciousness) may progress to coma. Dehydration can become severe enough to cause shock. Laboratory tests typically show hyperglycemia, metabolic acidosis, normal or elevated potassium, and severe ketosis. Many other tests can be affected.

At this point the patient is urgently in need of intravenous fluids. The basic principles of DKA treatment are:

  • Rapid restoration of adequate circulation and perfusion with isotonic intravenous fluids
  • Gradual rehydration and restoration of depleted electrolytes (especially sodium and potassium), even if serum levels appear adequate
  • Insulin to reverse ketosis and lower glucose levels
  • Careful monitoring to detect and treat complications

Treatment usually results in full recovery, though death can result from inadequate treatment or a variety of complications, such as cerebral edema (occurs mainly in children).

See also

  • Diabetic coma

External links

  • American Diabetes Association
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