How does dka cause dehydration

Due to the lack of insulin, cells are not receiving an adequate fuel source to produce energy. Even though the blood is loaded with glucose, the cells go into a starvation mode. This triggers the release of glucagon and other counter-regulatory hormones that promote the breakdown of triglycerides into free fatty acids and initiate gluconeogenesis to produce more glucose for the starving cells. This further elevates the blood glucose level as the body begins to metabolize protein and fat to produce a source of energy.

Due to the insulin deficiency and release of large amounts of glucagon, free fatty acids circulate in abundance in the blood and are metabolized into acetoacetic acid and B-hydroxybutric acid - both of which are strong organic acids and are referred to as ketones.

As acetoacetic acid is metabolized it produces acetone, which begins to accumulate in the blood. In normal metabolism, ketones would be used as fuel in the peripheral tissue; however, due to the starvation state of the cells, the ketones are not used.

An increase in ketone production and a decrease in peripheral cell use lead to metabolic acidosis — also called ketoacidosis. This is reflected in a decreasing pH value typically less than 7. The patient will also begin to eliminate large amounts of ketones through excretion in the urine. A glucose molecule produces an osmotic effect by drawing water across a semipermeable membrane.

As an excessive amount of glucose enters the renal tubules, it draws a large amount of water that ends up producing a significant amount of urine. This is known as osmotic diuresis and leads to volume depletion and dehydration in the patient. Large amounts of ketones also collect in the urine. Because ketones are strong organic acids, they must be buffered in order to be excreted. Sodium is typically used as the buffer. As we have been instructed, where sodium goes, water follows.

Thus, the sodium used to buffer the ketones also draws a large amount of water into the renal tubules, which produces excessive urine and leads to further volume depletion and dehydration. The loss of large amounts of fluid also leads to the excretion of other electrolytes, such as potassium, calcium, magnesium and phosphorous.

This produces electrolyte imbalance and disturbances. The term diabetic ketoacidosis literally explains what the patient is experiencing. The term diabetes is often thought of as dealing with a glucose derangement or imbalance. However, this is not true. Diabetes simply means an increase in urine output. Thus, diabetic in DKA implies an increase in urine output that occurs from osmotic diuresis. The term ketoacidosis is fairly self explanatory.

It refers to the metabolic acidosis resulting from ketone production from fat metabolism. The DKA patient is therefore prone to metabolic acidosis from:. The slow and gradual onset of signs and symptoms is related to the accumulating effect of the dehydration from osmotic diuresis and buildup of acid from ketone production. As the cells slowly become dehydrated and acidotic, the signs and symptoms begin to appear. And as the brain cells slowly dehydrate and are affected by the increasing acidic state over hours and days, the mental status slowly begins to alter.

Osmotic diuresis typically produces the classic signs and symptoms of hyperglycemia:. Osmotic diuresis leads to dehydration and a potential hypovolemic state from fluid loss, producing the following signs:. The deep and rapid respiratory rate blows off carbon dioxide, which is necessary for the production of carbonic acid.

In patients suspected of having diabetic ketoacidosis, serum electrolytes, blood urea nitrogen BUN and creatinine, glucose, ketones, and osmolarity should be measured. Urine should be tested for ketones. Patients who appear significantly ill and those with positive ketones should have arterial blood gas measurement. DKA is diagnosed by an arterial pH 7. Acidemia is serum pH A presumptive diagnosis can be made when urine glucose and ketones are strongly positive.

Urine test strips and some assays for serum ketones may underestimate the degree of ketosis because they detect acetoacetic acid and not beta-hydroxybutyric acid, which is usually the predominant ketoacid.

Symptoms and signs of a triggering illness should be pursued with appropriate studies eg, cultures, imaging studies. Adults should have an ECG to screen for acute myocardial infarction and to help determine the significance of abnormalities in serum potassium. Other laboratory abnormalities include hyponatremia, elevated serum creatinine, and elevated plasma osmolality. Hyperglycemia may cause dilutional hyponatremia, so measured serum sodium is corrected by adding 1.

As acidosis is corrected, serum potassium drops. An initial potassium level 4. Rarely IV sodium bicarbonate if pH 7 after 1 hour of treatment. The most urgent goals for treating diabetic ketoacidosis are rapid intravascular volume repletion, correction of hyperglycemia and acidosis, and prevention of hypokalemia 1 Treatment reference Diabetic ketoacidosis DKA is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis.

Hyperglycemia causes an osmotic diuresis with Identification of precipitating factors is also important. Treatment should occur in intensive care settings because clinical and laboratory assessments are initially needed every hour or every other hour with appropriate adjustments in treatment. Intravascular volume should be restored rapidly to raise blood pressure and ensure glomerular perfusion; once intravascular volume is restored, remaining total body water deficits are corrected more slowly, typically over about 24 hours.

Initial volume repletion in adults is typically achieved with rapid IV infusion of 1 to 3 L of 0. Adults with diabetic ketoacidosis typically need a minimum of 3 L of saline over the first 5 hours. When blood pressure is stable and urine flow adequate, normal saline is replaced by 0. Pediatric maintenance fluids Maintenance requirements Dehydration is significant depletion of body water and, to varying degrees, electrolytes.

Symptoms and signs include thirst, lethargy, dry mucosa, decreased urine output, and, as the degree Initial fluid therapy should be 0. Hyperglycemia is corrected by giving regular insulin 0. Insulin adsorption onto IV tubing can lead to inconsistent effects, which can be minimized by preflushing the IV tubing with insulin solution. Children should be given a continuous IV insulin infusion of 0.

Ketones should begin to clear within hours if insulin is given in sufficient doses. Serum pH and bicarbonate levels should also quickly improve, but restoration of a normal serum bicarbonate level may take 24 hours. Rapid correction of pH by bicarbonate administration may be considered if pH remains 7 after about an hour of initial fluid resuscitation, but bicarbonate can lead to development of acute cerebral edema primarily in children and should not be used routinely.

If used, only modest pH elevation should be attempted target pH of about 7. When plasma glucose becomes Insulin dosage can then be reduced to 0. Insulin replacement may then be switched to regular insulin 5 to 10 units subcutaneously every 4 to 6 hours. When the patient is stable and able to eat, a typical split-mixed or basal-bolus insulin regimen is begun.

IV insulin should be continued for 1 to 4 hours after the initial dose of subcutaneous insulin is given. Children should continue to receive 0.

If serum potassium is 3. To understand this illness, you need to understand the way your body powers itself with sugar and other fuels.

Foods we eat are broken down by the body, and much of what we eat becomes glucose a type of sugar , which enters the bloodstream. Insulin helps glucose to pass from the bloodstream into body cells, where it is used for energy. Insulin normally is made by the pancreas, but people with type 1 diabetes insulin-dependent diabetes don't produce enough insulin and must inject it daily.

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