Causes of Diabetic Ketoacidosis
Question:
Identify the clinical priorities in the management of this patient. The clinical priorities are the most important or pressing patient problems or issues based on the presented assessment data.
Many individuals die from diabetic ketoacidosis across the world. Scholars advocate that poor or pitiable patient education is possibly the critical determinant of the prevalence of the upheaval which constitutes diabetic ketoacidosis. It is important to note that in most cases, only about a quarter of the patients are initial presenters with the presently acquired or developed diabetes mellitus type whereas the remainder of the patient’s populace is recognized people with diabetes who possess severe illness which precipitate diabetic ketoacidosis or non-complaint with insulin therapy. According to Kumar, Galanter, and Ize-Ludlow (2014), Diabetic ketoacidosis is best recognized as a disorder which trails on the imbalance between the level of counter regulatory hormones and the level of insulin. In other words, DKA manifest itself because of the marked insulin deficiency in the face of higher levels of the hormone which oppose the impacts of insulin specifically glucagon. It is essential to note that even a small amount of insulin can lead to the formation of ketoacid. Some of the hormones which antagonize the effects of insulin include catecholamine, estrogen, cortisol, and glucagon. The graduate RNs should understand this case to help in saving lives within a minimum time. Knowing the symptoms and effects of diabetic ketoacidosis would help the RNs graduate to act professionally in treating the disease.
The triggers of diabetic ketoacidosis are quite essential to know. Patients presented with diabetic ketoacidosis are usually severely ill since diabetic ketoacidosis itself is a metabolic catastrophe, and other disorders may be too present. The common precipitants of diabetic ketoacidosis include severe underlying infection, poor compliance with the insulin therapy, and other inter-current diseases such as gangrenous bowel, stroke, and acute myocardial infarction (Klocker, Phelan, Twigg & Craig, 2013). In the same token, antipsychotic agents such as olanzapine and clozapine can as well precipitate DKA.
Patients suffering from diabetic ketoacidosis have marked electrolyte and fluid deficits. It is approximate that these patients more often have a fluid deficit of 101ml/kg and therefore require numerous hundred mill moles of sodium (3-10mmol/kg) and potassium ion (2-5+mmol/kg) and being deficient in magnesium and phosphate. Wolfsdorf, Allgrove, Craig, Edge, Glaser, Jain, and Hanas, (2014), argue that the replacement of the above deficits can be more difficult because of the existence of an array of factors comprising the derangement of pH which is related with diabetic ketoacidosis. There are a lot of mechanisms which be used to deplete fluid in diabetic ketoacidosis. The tools include an inability to take in the fluid because of reduced consciousness levels, vomiting which commonly associated with DKA, and osmotic diuresis as a result of hyperglycemia (Carmody & Philipson, 2015). It is worth noting that the depletion of the electrolyte is linked to the osmotic diuresis.
Additionally, the loss of potassium occurs as a result of the acidotic state as well as the fact that in spite of the total depletion of the body potassium, the levels of serum potassium often remain high, prejudicing to the renal loss. DKA is an extension of some of the standard physiological mechanisms which compensate for starvation (Erondu, Desai, Ways, and Meininger, 2015). Remarkably, during the fasting state, the body normally changes to fat oxidation from metabolism base carbohydrates. The patient might have developed the high condition levels of sugar in the body or illness. Missed insulin treatment left the patient with less insulin in his system thus triggering the condition. Other diseases caused the body of the patient to produce high levels of particular hormones, for example, cortisol and adrenaline and the hormones countered insulin effects.
Electrolyte and Fluid Deficits
The two highest priority clinical problems I would focus on include ensuring low blood sugar (hypoglycemia) and ensuring low potassium (hypokalemia). I would first monitor the patient’s blood sugar and record it. Besides, I will adjust his insulin dosage as required to meet his insulin target range. Together with other practitioners, the patient’s ketone level would be checked using the over-the-counter urine ketone test kit (Rosenstock & Ferrannini, 2015). I would monitor electrolyte and glucose levels, and administer intravenous insulin as well as fluid on the patient. Correcting the fluid loss would involve ringer solution or isotonic sodium solution (Tran et al. 2017). The two highest priority clinical problems ought to be addressed as soon as possible to help in saving the patient’s life. Insulin level must be reduced to normal to avoid the occurrence high pressure and heart attack.
Managing Diabetic ketoacidosis within a minimal period is vital for the life of a patient. In regards to the patient, the nurses would hurriedly bring him to the intensive care unit. The nurses would administer the patient’s glucose level and the level of potassium to ascertain what the patient is suffering from. The physicians together with the nurses will check on the patient’s electrolyte and the deficits of fluids. After establishing the patient’s condition, different doctors would be involved in correcting of the fluid loss with the intravenous fluids. Moreover, a physician would correct the electrolyte disturbance, specifically, potassium loss (Jefferies et al. 2015). Additionally, the doctors would correct hyperglycemia with insulin as well as correct acid-base balance. The doctors would after which intervene if treatment of concurrent infection is appropriate.
How the medical team would evaluate the patient’s responses to the interventions
The patient’s response towards the medications is significant since it helps the medical practitioners to know the progress of the patient. According to Peters, Buschur, Buse, Cohan, Diner, and Hirsch, (2015), the medical team would expect the patient to remain normovolemic which will be evidenced by the urinary outputs becoming greater or higher than 31 ml/hr. In the same vein, the medical evaluate the patient’s pressure by it becoming normal. The blood glucose levels will be expected to range between 69 – 200 mg/dL (Misra & Oliver, 2015). Notably, for the medical team to be satisfied with the patient’s condition, they would need to see when the blood glucose levels not to be more than 250 mg/dL.
Conclusion
In conclusion, Diabetic ketoacidosis (DKA) is a possibly life-threatening complication of diabetes mellitus, and this makes it a medical emergency once presented in a healthcare facility. Nurses and medical practitioners ought to know how to recognize or identify as well as maintain Diabetic ketoacidosis. The medical professionals ought also to understand how to maintain insulin level as well as electrolyte balance to help patients survive this severe condition. Patients suffering from Diabetic ketoacidosis (DKA) need close and regular blood glucose monitoring. Patients are required to visit their doctors’ regular check-ups to obtain normal blood glucose. The condition continues to have higher rates of mortality and morbidity in spite of the advances developed in the treatments of diabetes mellitus. Notably, persons with ketosis-prone diabetes ought to have proper glucose management and impaired insulin secretion to avoid the disease becomes chronic. Diabetic ketoacidosis (DKA) manifest itself as result of the marked insulin deficiency in the face of higher levels of the hormone which oppose the impacts of insulin specifically glucagon. It is essential to note that even a small amount of insulin can lead to the formation of ketoacid. Some of the hormones which antagonize the effects of insulin include catecholamine, estrogen, cortisol, and glucagon
References
Carmody, D., Naylor, R. N., & Philipson, L. H. (2015). Insulin dosing in pediatric diabetic ketoacidosis: where to start?. Jama, 313(22), 2274-2275.
Cherubini, V., Skrami, E., Ferrito, L., Zucchini, S., Scaramuzza, A., Bonfanti, R., … & Chiari, G. (2016). High frequency of diabetic ketoacidosis at diagnosis of type 1 diabetes in Italian children: a nationwide longitudinal study, 2004–2013. Scientific reports, 6.
Erondu, N., Desai, M., Ways, K. and Meininger, G., 2015. Diabetic ketoacidosis and related events in the canagliflozin type 2 diabetes clinical program. Diabetes Care, p.dc151251.
Jefferies, C. A., Nakhla, M., Derraik, J. G., Gunn, A. J., Daneman, D., & Cutfield, W. S. (2015). Preventing diabetic ketoacidosis. Pediatric Clinics, 62(4), 857-871.
Klocker, A. A., Phelan, H., Twigg, S. M., & Craig, M. E. (2013). Blood β?hydroxybutyrate vs. urine acetoacetate testing for the prevention and management of ketoacidosis in Type 1 diabetes: a systematic review. Diabetic Medicine, 30(7), 818-824.
Kumar, A., Galanter, W. L., & Ize-Ludlow, D. (2014). Is Diabetic Ketoacidosis Prevention at Reach for Single Health System Intervention?. In Diabetes, Hypoglycemia & Obesity: Pediatric Endocrinology (pp. SUN-0142). Endocrine Society.
Misra, S., & Oliver, N. S. (2015). Utility of ketone measurement in the prevention, diagnosis and management of diabetic ketoacidosis. Diabetic Medicine, 32(1), 14-23.
Peters, A. L., Buschur, E. O., Buse, J. B., Cohan, P., Diner, J. C., & Hirsch, I. B. (2015). Euglycemic diabetic ketoacidosis: a potential complication of treatment with sodium–glucose cotransporter 2 inhibition. Diabetes care, 38(9), 1687-1693.
Rewers, A., Dong, F., Slover, R. H., Klingensmith, G. J., & Rewers, M. (2015). Incidence of diabetic ketoacidosis at diagnosis of type 1 diabetes in Colorado youth, 1998-2012. Jama, 313(15), 1570-1572.
Rosenstock, J., & Ferrannini, E. (2015). Euglycemic diabetic ketoacidosis: a predictable, detectable, and preventable safety concern with SGLT2 inhibitors. Diabetes Care, 38(9), 1638-1642.
Tran, T. T., Pease, A., Wood, A. J., Zajac, J. D., Mårtensson, J., Bellomo, R., & Ekinci, E. I. (2017). Review of evidence for adult diabetic ketoacidosis management protocols. Frontiers in endocrinology, 8, 106.
Wolfsdorf, J. I., Allgrove, J., Craig, M. E., Edge, J., Glaser, N., Jain, V., … & Hanas, R. (2014). Diabetic ketoacidosis and hyperglycemic hyperosmolar state. Pediatric diabetes, 15(S20), 154-179.
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