DKA

Brain

Normally, ketone bodies are produced in minuscule quantities, feeding only part of the energy needs of the heart and brain. In DKA, the body enters a starving state. Eventually, neurons (and so the brain) switch 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 osmolar load of the blood, are acidic. As a result, the pH of the blood begins to move downward towards an acidotic state. The normal pH of human blood is 7.35-7.45, in acidosis the pH dips below 7.35. Very severe acidosis may be as low as 6.9-7.1. The acidic shift in the blood is significant because the proteins (i.e. body tissues, enzymes, etc.) in the body will be permanently denatured by a pH that is either too high or too low, thereby leading to widespread tissue damage, organ failure, and eventually death.

Glucose begins to spill into the urine as the proteins responsible for reclaiming it from urine (the SGLT family) reach maximum capacity (the renal threshold for glucose). As glucose is excreted in the urine, it takes a great deal of body water with it, resulting in dehydration. Dehydration further concentrates the blood and worsens the increased osmolality of the blood. Severe dehydration forces water out of cells and into the bloodstream to keep vital organs perfused. This shift of intracellular water into the bloodstream occurs at a cost as the cells themselves need the water to complete chemical reactions that allow the cells to function.

Symptoms and Signs

• Sluggish, extreme tiredness.
• Fruity smell to breath/compare to nail polish remover, similar to peardrops.
• Extreme thirst, despite large fluid intake.
• Constant urination
• Extreme weight-loss.
• Oral Thrush may be present, or/ yeast infections that fail to go away, this is because the normal fungal/flora present in oral cavity/cervix in women, the balance is upset and bacterial began to feast on the high sugar from urine output/ dry mouth from extreme thirst.
• Muscle wasting.
• Agitation / Irritation / Aggression / Confusion

Late signs

At this point, DKA is life-threatening and medical attention should be sought immediately.

• Emesis (vomiting), although this is not always a sign of late-stage ketoacidosis, and can occur both in early-stage ketoacidosis and in non-ketoacidic hyperglycaemia.
• Confusion.
• Abdominal pain.
• Loss of appetite.
• Flu-like symptoms.
• Lethargy and apathy.
• Extreme weakness.
• Kussmaul breathing ("air hunger"). Patients breathe more deeply and/or rapidly.
• Unconsciousness (diabetic coma) after prolonged DKA. At this stage, speedy medical attention is imperative.

Complications

People with diabetic ketoacidosis need close and frequent monitoring for complications. Surprisingly, the most common complications of DKA are related to the treatment:

• Hypokalemia and often, potassium depletion
• Cerebral edema
• Hyperglycemia
• Ketoacidemia
• Fluid and electrolyte depletion
• Aspiration
• Unrecognized renal tubular necrosis
• Pulmonary edema
• Myocardial Infarction

Treatment

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 lowered blood potassium (hypokalemia) 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 exhausted 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). Kussmaul's respirations are the body's attempt to remove carbon dioxide from the blood that would otherwise form carbonic acid and further worsen the ketoacidosis. See also arterial blood gas.

On presentation to hospital, patients in DKA are typically suffering dehydration 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).

References

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