Course Work Example: Application of Evidence-based Care Delivery in Diabetes Ketoacidosis

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Course work
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Diabetes ketoacidosis is a severe occurrence, which presents itself in patients who have an insulin dependency. Its occurrence can be evident in patients with either type 1 or 2 diabetes. Effective management and prevention are necessary to resolve the complication. Some of the aspects of effective management include appropriate diagnosis using current laboratory tools, use of qualified clinicians, competent clinical criteria, insulin therapy, and electrolyte replacement.

Recognizing the pathophysiology behind diabetes ketoacidosis is significant. Byrne (2015) articulates that the destruction of beta cells cause insulin insufficiency. Additionally, the author affirms that the complication can occur when triggered by other factors such as poor control of insulin or infection. In his article, the author states that the complication is common in patients with type 1 diabetes. The author articulates that some other causes of the disease include pancreatitis and drugs, cerebral accidents and protracted vomiting, myocardial infarction, and pulmonary embolism. He affirms that diabetes ketoacidosis occurs when events such as ketosis, hyperglycemia, and acidosis take place within the body. He adds that the deficiency of insulin in the body prevents the exploitation of glucose within the tissues and increases gluconeogenesis in the liver, which causes hyperglycemia. Moreover, the author affirms that the deficiency in association with the increased production of hormone results in lyposis. As he explains, when lyposis occurs, the fatty acids break down into ketones. The ketones cause ketosis, which eventually results to acidosis. The author puts forward that a preliminary evaluation of the patient is necessary to identify immediate life-threatening concerns. As he adds, the initial assessment determines the cause of acute episodes and identifies some of the symptoms, which need prioritization during the treatment of a patient. As the author suggests, clinicians need to determine the best therapeutic interventions. Additionally, he adds that the interventions should take place within the first hour following the admission of a patient. Furthermore, Gosmanov, Gosmanova, & Cannon (2014) indicate that physicians ought to initiate the management of the hyperglycemic crisis. The authors provide the following primary points for the efficient management of diabetes ketoacidosis,

Before insulin therapy, the clinician should begin intravenous fluids on the patient.

Before the introduction of an insulin therapy, the clinician should ensure that the potassium level is >3.3 mEq/1.

The clinician should administer a priming insulin bolus at 0.1 U/kg/h, and commence on a continuous insulin infusion at 0.1 U/kg/h. More so, the authors assert that before the clinician regulates the insulin infusion rate, he or she should gauge the bedside glucose hourly.

The clinician should prevent hyperglycemia when administering insulin by initiating fluids, which contain dextrose. Either way, as the authors explain, they can reduce the rate of insulin rate to avoid hyperglycemia.

When diabetes ketoacidosis is resolved, the authors state that the clinician can transition to subcutaneous insulin only.

Additionally, the authors provide the following three key interventions for the treatment of diabetes ketoacidosis,

Fluid Therapy

Gosmanov, Gosmanova, & Cannon (2014) assert that the average fluid loss in a patient with diabetes ketoacidosis is 6-9 L. As they explain, during fluid therapy, clinicians work to replace the amount of fluid lost within 24-36 hours. They add that clinicians increase up to 50% of fluid during the first 8-12 hours of treatment. Moreover, the authors state that the solution of choice during treatment is a crystalloid fluid. As they add, the current suggestions are to initiate the reinstatement of lost fluid with an isotonic saline of 0.9% NaCI to the patient intravenously depending on the patients hemodynamic status. The authors state that safe practice of fluid revival in patients with diabetes ketoacidosis includes the provision of an initial bolus of isotonic saline at 15-20mL/kg/h followed by a hypotonic saline solution of 0.45% at a rate of 4-14 mL/kg/h. They suggest that as long as the patient is hemodynamically stable and the sodium is normal to high, clinicians can begin the fluid resuscitation. More so, they state that the instigation of 0.9% saline at a rate of 150250 mL/h is recommended until eunatremia is achieved in case the patient becomes hyponatremic based on corrected serum sodium. They affirm that both the volume resuscitation of intravascular and extravascular will eventually reduce hyperglycemia through the stimulation of osmotic diuresis only if the renal function is not affected and peripheral action of insulin is enhanced. The authors state that intravenous fluids should be switched to dextrose-containing 0.45% NaCl solution to prevent hypoglycemia, and the insulin infusion rate should be decreased if glucose levels are below 200-250 mg/dL. Furthermore, the authors recommend that clinicians should exercise caution in patients with congestive heart failure and chronic kidney disease because they tend to retain fluids.

Intravenous Insulin

Gosmanov, Gosmanova, & Cannon (2014) affirm that the treatment promotes the utilization of glucose by peripheral tissues, moderates glycogenolysis and gluconeogenesis as well as repress ketogenesis. They affirm that clinicians ought to perform initial volume resuscitation before they infuse the intravenous fluid to avoid worsening dehydration. The authors recommend an initial bolus of regular insulin of 0.1 U/kg to be followed with a continuous insulin infusion. Furthermore, they state that if the plasma fails to fall by at least 10% within the first hour of treatment, clinicians should add 0.1 U/kg bolus of insulin in the process of combination. Additionally, they state that if the plasma levels rise to 200-250 mg/dL, clinicians should reduce the insulin rate by 50% or 0.02-0.05 U/kg/h. From their perspective, many of patients who have diabetes ketoacidosis can become insulin sensitive rapidly through the administration of intravenous fluids and improvements in hyperglycemia. The authors affirm that if clinicians need to avoid hypoglycemia and rapid shifts of glucose between the extracellular and intracellular compartments, they should reserve insulin infusion for obese and insulin-resistant patients.

Subcutaneous Insulin

Gosmanov, Gosmanova, & Cannon (2014) assert that insulin doses through subcutaneous delivery are efficient. They affirm that insulin analogs such as aspart, glulisine, and lispro offered new paradigms when managing diabetes mellitus and therapy of diabetes ketoacidosis. The authors state that subcutaneous insulin is effective in patients with moderate diabetes ketoacidosis and those in the intensive care unit.

Potassium, Bicarbonate, and Phosphate Therapy

Gosmanov, Gosmanova, & Cannon (2014) indicate that clinicians ought to scrutinize serum potassium during the treatment of diabetes ketoacidosis. As they explain, events such as insulin administration and correction of hyperosmolality drive potassium intracellularly. As they add, the drive results in hypokalemia, which causes arrhythmias and cardiac arrest. They point out that the clinician should stop insulin treatment immediately and administer potassium intravenously if the serum potassium drops to <3.3 mEq/L during diabetes ketoacidosis treatment. Additionally, they add that when the serum potassium is between 3.3 and 5.3 mmol/L, the clinician should add small amounts of potassium of 20-30mEq/L to the intravenous fluid.

The authors state that in mild and moderate forms of diabetes ketoacidosis, bicarbonate therapy is not indicated because the metabolic acidosis will correct the insulin therapy. The lack of prospective randomized studies makes the use of bicarbonate in the treatment of diabetes ketoacidosis controversial (Gosmanov, Gosmanova, & Cannon, 2014). As they explain, according to reports, the administration of bicarbonate may result in marginal hypoxemia, cerebral edema in children and young adults, elevated hypokalemia, paradoxical central nervous system acidosis as well as an increase intracellular acidosis. Due to the extreme acidosis associated with the clinical results, bicarbonate therapy might be indicated if the pH is 6.9 or less. More so, the authors point out that in future randomized controlled trials, an infusion of 100 mmol of bicarbonate in 400mLof sterile water, added with 20mEq potassium chloride over 2 hours, and repeating the mixture until the pH is greater than 7.0 is recommended.

Regarding the phosphate therapy, the authors affirm that phosphate deficit in diabetes ketoacidosis averages to 1 mmol/kg. They assert that during the treatment of diabetes ketoacidosis insulin therapy will condense the serum phosphate concentration. However, the authors state that randomized trials have failed to disclose any positive effects of phosphate replacement on the outcomes of diabetes ketoacidosis. As the authors explain, phosphate replacement may result in extended hypoclacemia. Therefore, they assert that the replacement can be given to patients who have a serum phosphate concentration of less than 1.0mg/dL or in those who have levels between 1.0 and 2.0 mg/dL and cardiac dysfunction, respiratory depression as well as anemia. They add that during the initial phosphate replacement strategy, clinicians should infuse the patient with a potassium phosphate of 0.1 - 0.2 mmoL over a period of 6 hours. Additionally, the authors state that the infusion should depend on the extent of phosphate deficit. They recommend that clinicians should examine the phosphorous and calcium levels. As well, they indicate that clinicians should administer less phosphate replacement to patients who have renal complications and hypocalcemia.

Literature Review of Diabetes Ketoacidosis

As Dhatariya (2015) explains in his article, the evolution of diabetes ketoacidosis began in 1922-1923. According to him, early adopters of the medication wondered how to balance the glucose lowering effects to ensure that they prevent ketosis. The author affirms that during 1923-1944, several patients died because they received small doses of insulin. Therefore, he states that medical practitioners began to provide high-doses of insulin to manage diabetes ketoacidosis. More so, the author affirms that in 1972, reports showed that low-dose insulin could treat the complication. He asserts that Sonksen et al. published an article in 1972, which revealed that small doses infusions given to patients intravenously could reduce the glucose and ketone levels. However, he explains that an insistent fluid schedule together with a low dose of insulin was the standard of care for four decades. More to the point, the author affirms that over the last 30 years in the UK, consultants in diabetes and general medicine overtook the individuals who were appointed in the 1970s and 1980s. As he adds, it became known that patients who received care from specialists of diabetes had better outcomes compared to those who got it from general physicians.

Dhatariya (2015) articulates that as the late 1990s and early 2000s approached, diabetes specialists agreed that the best way to treat the complication is through aggressive fluid management and a small dose of intravenous insulin infusion. More so, he affirms that the specialists established that appropriate assessment of blood gases helped in the proper administration of the complication. Additionally, as the author claims, the professionals noted that since electrolyte deficiencies were common in patients with diabetes ketoacidosis, potassium replacement became a re...

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