Tiffany Mattox February 7, 2012 DKA

1. Describe the pathophysiologic changes in DKA a. Why do blood glucose levels increase? Overexertion and exhaustion of the pancreas release of insulin. b. What are commonly seen blood glucose levels? 70-110 c. What fluid and electrolytes disturbances commonly occur? The hyperglycemia-induced osmotic diuresis depletes sodium, potassium, phosphates, and water, 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 concomitant infection, 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 P f. Why do the acid base disturbances occur? Hepatic gluconeogenesis, glycogenolysis secondary to insulin deficiency, and counterregulatory hormone excess result in severe hyperglycemia, while lipolysis increases serum free fatty acids. Ketone bodies are produced from acetyl coenzyme A mainly in the mitochondria within hepatocytes when carbohydrate utilization is impaired because of relative or absolute insulin deficiency, such that energy must be obtained from fatty acid metabolism. High levels of acetyl coenzyme A present in the cell inhibit the pyruvate dehydrogenase complex, but pyruvate carboxylase is activated. Thus, the oxaloacetate generated enters gluconeogenesis rather than the citric acid cycle, as the latter is also inhibited by the elevated level of nicotinamide adenine dinucleotide (NADH) resulting from excessive beta-oxidation of fatty acids, another consequence of insulin resistance/insulin deficiency. The excess acetyl coenzyme A is therefore rerouted to ketogenesis. Ketones include acetone, beta-hydroxybutyrate, and acetoacetate. Progressive rise of blood concentration of these acidic organic substances initially leads to 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 base deficit and a mild anion gap. When the accumulated ketones exceed the body's capacity to extract them, they overflow into 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 pH and bicarbonate[2] serum levels. Respiratory compensation for this acidotic condition results in 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 Blood 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 4-6 h o Initial blood urea nitrogen (BUN) o Initial arterial blood gas (ABG) measurements, followed with bicarbonate as necessary 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.28 The initial fluid therapy is directed toward expansion of intravascular volume and restoration of renal perfusion. Isotonic saline (0.9% NaCl) infused at a rate of 5001,000 mL/h during the first 2 h is usually adequate, but in patients with hypovolemic shock, a third or fourth liter of isotonic saline may be needed to restore normal blood pressure and tissue perfusion. After intravascular volume depletion has been corrected, the rate of normal saline infusion should be reduced to 250 mL/h or changed to 0.45% saline (250500 mL/h) depending on the serum sodium concentration and state of hydration. The goal is to replace half of the estimated water deficit over a period of 1224 h. Once the plasma glucose reaches 250 mg/dl in DKA and 300 mg/dl in HHS, replacement fluids should contain 510% dextrose to allow continued insulin administration until ketonemia is controlled while avoiding hypoglycemia. An additional important aspect of fluid management in hypoglycemic states is to replace the volume of urinary losses. Failure to adjust fluid replacement for urinary losses may delay correction of electrolytes and water deficit.
F +RZDUHEORRGJOXFRVHOHYHOVPRQLWRUHG"+RZRIWHQ"

Blood tests for glucose every 1-2 h until patient is stable, then every 6 h Serum electrolyte determinations every 1-2 h until patient is stable, then every 4-6 h

Initial blood urea nitrogen (BUN) Initial arterial blood gas (ABG) measurements, followed with bicarbonate as necessary d. How are elevated blood glucose levels corrected? Insulin is needed to help switch from a catabolic state to an anabolic state, with uptake of glucose in 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 y y y

Administer 1-3 L during the first hour. Administer 1 L during the second hour. Administer 1 L during the following 2 hours Administer 1 L every 4 hours, depending on the degree of dehydration and central venous pressure readings

When the patient becomes euvolemic, the physician may switch to half the isotonic sodium chloride solution, particularly if hypernatremia exists. Isotonic saline should be administered at a rate 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, and water, as well as ketones and glucose. Repeat laboratory tests are critical, including potassium, glucose, electrolytes, and, if necessary, phosphorus. Initial workup should include aggressive volume, 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.

Monitor serum potassium levels hourly, and the infusion must be stopped if the potassium level is greater than 5 mEq/L. The monitoring of serum potassium must continue even after potassium infusion is stopped in the case of (expected) recurrence of hypokalemia. In severe hypokalemia, not starting insulin therapy is advisable unless potassium replacement is under way; this is to avert potentially serious cardiac dysrhythmia that may result from hypokalemia. Potassium replacement should be started with initial fluid replacement if potassium levels are normal or low. Add 20-40 mEq/L of potassium chloride to each liter of fluid once the potassium level is less than 5.5 mEq/L. Potassium can be given as follows: two thirds as KCl, one third as KPO4.

b. How are acid base disturbances monitored? How often? Sodium bicarbonate only is infused if decompensated acidosis starts to threaten the patient's life, especially when associated with either sepsis or lactic acidosis. If sodium bicarbonate is indicated, 100-150 mL of 1.4% concentration is infused initially. This may be repeated every half hour if necessary. Rapid and early correction of acidosis with sodium bicarbonate may worsen hypokalemia and cause paradoxical cellular acidosis.

c. How are acid base disturbances corrected? How quickly is this accomplished and why? Sodium bicarbonate. If sodium bicarbonate is indicated, 100-150 mL of 1.4% concentration is infused initially. Rapid and early correction of acidosis with sodium bicarbonate may worsen hypokalemia and cause paradoxical cellular acidosis.

4. Describe the nursing management of a patient in DKA. a. How is fluid status assessed? How often? By monitoring input and output and weighing the patient. Every hour. b. What are the complications of fluid replacement and how are they prevented? Cerebral edema, Cardiac dysrhythmia, Pulmonary edema, Myocardial injury, Diabetic retinopathy, Hypoglycemia, Hypokalemia. By monitoring fluid replacement Performing cardiac monitoring on patients with DKA during correction of electrolytes always is advisable. Diuretics and oxygen therapy often suffice for the management of pulmonary edema. By monitoring glucose levels closely, and also monitoring fluid intake very closely.

c. How are blood glucose levels assessed and how often? Monitor the patient's blood glucose and electrolyte levels every 1 to 2 hours, and administer I.V. potassium supplements as ordered if his serum potassium level drops below 5.3 mEq/L. d. What are the complications of lowering blood glucose levels and how are they prevented? The complications of lowering blood glucose levels could send the patient into a hypovolemic state. In order to maintain blood glucose levels you have to continuously monitor the patients fluid and electrolyte balances as well as the blood glucose levels. d. How are electrolyte disturbances assessed? How often?
y