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DKA

DKA

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Published by: tiffarub on Feb 08, 2012
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09/11/2013

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Tiffany MattoxFebruary 7, 2012DKA1.
 
Describe the pathophysiologic changes in DKAa.
 
Why do blood glucose levels increase?Overexertion and exhaustion of the pancreas release of insulin. b.
 
What are commonly seen blood glucose levels?70-110c.
 
What fluid and electrolytes disturbances commonly occur?The hyperglycemia-induced osmotic diuresis depletes sodium, potassium, phosphates, andwater, as well as ketones and glucose.d.
 
What cause the fluid and electrolyte disturbances?The most common scenarios for diabetic ketoacidosis (DKA) are underlying or concomitantinfection, missed insulin treatments , and newly diagnosed, previously unknown diabetes . Other associated causes make up roughly 20% in the various scenarios.e.
 
What acid-base disturbances are commonly seen?Serum HCO3, Serum Pf.
 
Why do the acid base disturbances occur?Hepatic gluconeogenesis, glycogenolysis secondary to insulin deficiency, and counter-regulatory hormone excess result in severe hyperglycemia, while lipolysis increasesserum free fatty acids. Ketone bodies are produced from acetyl coenzyme A mainly in themitochondria within hepatocytes when carbohydrate utilization is impaired because of relative or absolute insulin deficiency, such that energy must be obtained from fatty acidmetabolism. High levels of acetyl coenzyme A present in the cell inhibit the pyruvatedehydrogenase complex, but pyruvate carboxylase is activated. Thus, the oxaloacetategenerated enters gluconeogenesis rather than the citric acid cycle, as the latter is alsoinhibited by the elevated level of nicotinamide adenine dinucleotide (NADH) resultingfrom excessive beta-oxidation of fatty acids, another consequence of insulinresistance/insulin deficiency. The excess acetyl coenzyme A is therefore rerouted toketogenesis. Ketones include acetone, beta-hydroxybutyrate, and acetoacetate.Progressive rise of blood concentration of these acidic organic substances initially leadsto a state of ketonemia, although extracellular and intracellular body buffers can limit
 
ketonemia in its early stages, as reflected by a normal arterial pH associated with a basedeficit and a mild anion gap.When the accumulated ketones exceed the body's capacity to extract them, they overflowinto urine (ie, ketonuria). If the situation is not treated promptly, a greater accumulation of organic acids leads to frank clinical metabolic acidosis (ie, ketoacidosis), with a drop in pHand bicarbonate
[2]
serum levels. Respiratory compensation for this acidotic condition resultsin rapid shallow breathing (Kussmaul respirations).2.
 
Describe the medical management of a patient in DKA?a.
 
How is fluid status monitored in the acute stage of DKA?
o
 
B
lood tests for glucose every 1-2 h until patient is stable, then every 6 h
o
 
Serum electrolyte determinations every 1-2 h until patient is stable, then every 4-6h
o
 
Initial blood urea nitrogen (
BU
 N)
o
 
Initial arterial blood gas (A
BG
) measurements, followed with bicarbonate asnecessary
o
 
Also by weighing the patient. b.
 
How is hypovolemia corrected? How rapidly is fluid volume replaced? And why?Patients with DKA and HHS are invariably volume depleted, with an estimated water deficit of 
100 ml/kg of body weight.28The initial fluid therapy is directed towardexpansion of intravascular volume and restoration of renal perfusion. Isotonic saline(0.9% NaCl) infused at a rate of 500±1,000 mL/h during the first 2 h is usuallyadequate, but in patients with hypovolemic shock, a third or fourth liter of isotonicsaline may be needed to restore normal blood pressure and tissue perfusion.After intravascular volume depletion has been corrected, the rate of normal salineinfusion should be reduced to 250 mL/h or changed to 0.45% saline (250±500 mL/h)depending on the serum sodium concentration and state of hydration. The goal is toreplace half of the estimated water deficit over a period of 12±24 h.Once the plasma glucose reaches 250 mg/dl in DKA and 300 mg/dl in HHS,replacement fluids should contain 5±10% dextrose to allow continued insulinadministration until ketonemia is controlled while avoiding hypoglycemia. Anadditional important aspect of fluid management in hypoglycemic states is to replacethe volume of urinary losses. Failure to adjust fluid replacement for urinary lossesmay delay correction of electrolytes and water deficit.
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B
lood tests for glucose every 1-2 h until patient is stable, then every 6 hSerum electrolyte determinations every 1-2 h until patient is stable, then every 4-6 h
 
Initial blood urea nitrogen (
BU
 N)Initial arterial blood gas (A
BG
) measurements, followed with bicarbonate asnecessaryd.
 
How are elevated blood glucose levels corrected?Insulin is needed to help switch from a catabolic state to an anabolic state, with uptake of glucosein tissues and the reduction of gluconeogenesis as well as free fatty acid and ketone production.Initial correction of fluid loss is either by isotonic sodium chloride solution or by lactated Ringer solution. The recommended schedule for restoring fluids is as follows:
y
 
Administer 1-3 L during the first hour.
y
 
Administer 1 L during the second hour.
y
 
Administer 1 L during the following 2 hours
y
 
Administer 1 L every 4 hours, depending on the degree of dehydration and central venous pressure readingsWhen the patient becomes euvolemic, the physician may switch to half the isotonic sodiumchloride solution, particularly if hypernatremia exists. Isotonic saline should be administered at arate appropriate to maintain adequate blood pressure and pulse, urinary output, and mental status.e.
 
How quickly is blood glucose corrected>3.
 
What electrolytes are monitored in the acute stage of DKA? Why?The hyperglycemia-induced osmotic diuresis depletes sodium, potassium, phosphates, andwater, as well as ketones and glucose. Repeat laboratory tests are critical, including potassium,glucose, electrolytes, and, if necessary, phosphorus. Initial workup should include aggressivevolume, glucose, and electrolyte management.It is important to be aware that high serum glucose levels may lead to dilutional hyponatremia;high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels.a.
 
How are electrolytes imbalances corrected? How rapidly is this accomplished? Why?If the potassium level is greater than 6 mEq/L, do not administer potassium supplement.If the potassium level is 4.5-6 mEq/L, administer 10 mEq/h of potassium chloride. If the potassium level is 3-4.5 mEq/L, administer 20 mEq/h of potassium chloride.

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