Diabetic ketoacidosis (DKA) refers to a decompensation of diabetes mellitus, along with the hyperosmolar state and hypoglycaemias, which are the three major acute complications of diabetes mellitus. Unlike the chronic complications, this complication develops within hours and endangers the life of the patient and is considered a medical emergency.
The essential background of the CAD is the partial or total deficiency of insulin in the body. Partial deficiency occurs in patients with type 2 diabetes mellitus who still have a reserve pancreas. It also happens in patients with type 1 diabetes mellitus, using insufficient doses of insulin. In these patients the limited available insulin does not prevent glucose levels being above normal, but are sufficient to prevent ketosis. To develop CAD the combination of insulin deficiency and excess glucagons is especially needed.
To this is added a trigger, usually a sharp rise in energy requirements of the organism. Common examples are infectious diseases, particularly urinary and respiratory, surgeries, periods of fasting, increased physical activity or suspension or reduction of doses of hypoglycaemic agents. Another trigger may be the sudden increase in blood glucose concentrations, as a result of extra calorie intake due to a particularly heavy meal or alcohol intake.
It should be noted that in a small but significant number of patients with Type 1 diabetes mellitus, DKA is the initial manifestation of the disease. At this point it triggers a gradual increase in blood levels of glucose, which when they exceed 180 mg / dL, they exert an osmotic effect on water in the renal tubules, and hence increased diuresis (urine production).
The osmotic effect is proportional to the blood glucose level, so that the more the glucose level rises, the more fluid is lost by diuresis. Water loss is so intense that it endangers the patient, causing severe hypovolemia, leading to shock (severe hypotension and tissue hypoperfusion) and cardiovascular failure (arrhythmias and asystole).
Add to that the loss of electrolytes such as sodium, potassium, chloride and bicarbonate, leading to an electrolyte imbalance (hyponatremia, metabolic acidosis, hypochloremia), compounding the adverse effects of dehydration, particularly those affecting the heart (arrhythmias).
Besides affecting the central nervous system, it causes alterations in consciousness (lethargy, stupor, coma), confusion and seizures. Along with the changes described above, there is an increase of substances called counter-regulatory hormones, primarily glucagon, adrenaline and growth hormones.
These are released in response to the inability of glucose to enter cells, due to lack of insulin. Its effect is to increase blood glucose, trying to compensate for their “deficit” intracellular.
This increased concentration is due to glucose production in the liver and kidneys from substrates such as fatty acids, glycogen and amino acids (gluconeogenesis and glycogenolysis). The result of these processes is to exacerbate the hyperglycemia caused by the absence of insulin, as well as the accumulation of ketone bodies, byproducts of fatty acid oxidation-producing metabolic acidosis and thereby worsening the patient’s condition.
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