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Diabetic ketoacidosis
ICD9 = 250.1| ICDO = | Image = | Caption = | OMIM = | OMIM_mult = | MedlinePlus = 000320 | eMedicineSubj = emerg | eMedicineTopic = 135 | DiseasesDB = 3709 | }} Diabetic ketoacidosis (DKA) is one consequence of severe, out-of-control diabetes mellitus(chronichigh blood sugar, or hyperglycemia). In a diabetes sufferer, DKA begins with relative deficiency in insulin. In the most common cases, this is due to failure to take prescribed insulin. Insulin requirements may rise due to physiologic stressthat causes release of catecholamines, glucagon, and cortisol. This stress may be emotionalor physical, although the most common cause by far is infection(e.g., pneumoniaor urinary tract infection). Simply having uncontrolled hyperglycemiamay be sufficient to trigger an attack if significant dehydrationoccurs.
MechanismThis process is vastly more common in type 1 diabetes than in type 2. A key component of DKA is that there is essentially no circulating insulin. Normally, the balance between storing energy and releasing energy in the body is controlled by the insulin-to-glucagon ratio. In type 1 diabetics, who do not produce any insulin on their own, the absence of insulin leads to DKA. Without insulin, cells cannot transport glucoseout of the bloodstreamand into themselves. This occurs because glucagon tells cells not to use glucose from outside but instead to secrete non-carbohydrate sources that can be used to make glucose, on which red blood cellsare absolutely dependent and the brainmostly dependent for energy. Some amino acidscan be converted to glucose (by gluconeogenesis), so those sources are typically locally available protein. This is the only source in muscletissue; the livercan also use the "glycerol backbone" made available in its fatprocessing. Since neither protein nor amino acids are stored as raw material, amino acids used in glucose production must come from protein currently in use for other purposes. This explains the thin, wasted appearance of those that have been starved: even in the face of adequate fat stores, muscle will be broken down to make glucose. In starvationsituations, then, the liver must produce another form of fuel. The brain, in particular, is protected by the blood-brain barrierwhich makes it unable to use fats for fuel. If it is to avoid using glucose, it must have a new energy source. The liver provides this by making ketone bodiesfrom fats, then secreting them into the bloodstream. Normally, ketone bodies are produced in minuscule quantities, feeding only part of the energy needs of the heartand brain. In DKA, they rapidly become a major component of the brain's fuel. 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 osmolalload of the blood, are acidic. As a result, the pHof the blood begins to change. Glucose begins to spill into the urineas 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 organsperfused. The vicious cycleis now set, and if untreated will lead to comaand death. TreatmentTreatment consists of hydrationto lower the osmolalityof the blood, replacement of lost electrolytes, insulin to force glucose and potassiuminto the cells, and eventually glucose simultaneously with insulin in order to correct other metabolicabnormalities, such as elevated blood potassium (hyperkalemia) and elevated ketone levels. Most patients require admission to step-down unit or intensive care unit(ICU) so that vital signs, urine output, and blood tests can be monitored on an hourly basis. In patients with severe alteration of mental status, intubationand mechanical ventilationis 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 the insulin deficiency is more severe, though it can occur rarely in type 2 diabetes. In about a quarter of young people that develop type 1 diabetes, the 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. When a person is known to have diabetes and is being adequately treated, DKA usually results from omission of insulin, mismanagement of acute gastroenteritis(the "flu"), or an overwhelming new health problem (e.g., bacterial infection, myocardial infarction). Insulin deficiency switches many aspects of metabolic balance in a catabolicdirection. The liver becomes a net producer of glucose by way of gluconeogenesisand glycogenolysis. Fat in adipose tissueis reduced to triglyceridesand fatty acids by lipolysis. Muscle is degraded to release amino acids for gluconeogenesis. The rise of fatty acid levels is accompanied by a rise of ketones (acetone, acetoacetateand beta-hydroxybutyrate). As the 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 vomitingcombined with amplified urination produce dehydration. As the metabolic acidosisworsens, it induces obvious hyperventilation(termed Kussmaul respiration). On presentation to hospital, the patient in DKA is typically dehydrated and breathing both fast and deeply. Abdominal painis common and may be severe. The level of consciousness is normal until late in the process, when obtundation(dulled or reduced level of alertness or consciousness) may progress to coma. The 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:
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