Pathophysiological Mechanisms of Diabetic Ketoacidosis - Essay Example

? Pathophysiological Mechanisms of Diabetic Ketoacidosis and the Risk Factors Associated with it Diabetes is one of the main healthcare concerns in medicine. The paper is aimed to explore the condition specifically the pathophysiological mechanisms of diabetic ketoacidosis. In addition, other pertinent issues such as the risk factors associated with the subject will be presented. Pathophysiological Mechanisms of Diabetic Ketoacidosis and the Risk Factors Associated with it Patients who are diagnosed with Type 1 diabetes mellitus (T1DM) are highly susceptible to develop a condition known as the Diabetic Ketoacidosis (DKA). This condition causes hospitalization to more than 100,000 individuals annually in the US, translating to a cumulative hospitalization costs reaching $ 1 billion (Buse, Menke and Sisca, 2005). Statistics show that in England 11% of patients with Type I diabetes had occurrence of DKA within the period of 2004 to 2009, compared with US that has “. . . 4.6 to 8 episodes per 1000 patients” (Savage et al., 2011). Mortality rates from both countries ranges from 2% to 5%, with UK having the lower incidents, at 2% of the patients diagnosed with DKA. Advances in the management of diabetes among patients resulted to several benefits such as reducing the incidence of DKA (Buse, Menke and Sisca, 2005). This paper will tackle the risk factors as well as the signs and symptoms of DKA among different age groups including infants, children, and adults. According to Daniel Levin (2008), Cerebral Edema in Diabetic Ketoacidosis (CEDKA) has close association with the cause of mortality in children and adolescents. This will also be examined throughout the discussion. Diabetic Ketoacidosis (DKA) is a reversible condition that most T1DM patients are at risk of having. It can also occur to patients diagnosed with type 2 diabetes that are experiencing high physiological stress, but this occurrence is more of a rare case (MedBroadcast Clinic Team, n.d.). DKA is a dangerous condition that occurs when insulin levels in the body is not enough to allow the cells to convert glucose to energy. As a result of insulin deficiency, the body breaks down fats and converts them to fatty acids that eventually become another acid called ketones (CardioSmart, 2011). The excessive production of ketones, a toxic substance, in the body significantly adjusts the pH of the blood making it highly acidic. This condition can be readily managed, but failure to detect it early will lead a patient to coma and eventually death (MedBroadcast Clinic Team, n.d.). Initial evaluation and diagnosis of patients diagnosed with DKA is crucial in order to reduce the inherent mortality rates associated with the condition. Furthermore, signs and symptoms of the condition should be observed and necessary treatments should be employed. Discussion According to David Trachtenbarg (2005), the initial evaluation of DKA includes the diagnosis and treatment of precipitating factors, such as infection and “. . . noncompliance with insulin therapy”. The method of using insulin pump therapy was associated, in the past, as a risk factor for DKA. However, recently, the implication was debunked by studies that proved that the frequency of DKA occurrence was the same with using the pump therapy and the more conventional injection therapy (Trachtenbarg, 2005). Savage et. al. (2011) enumerates three diagnostic criteria. First is the presence of ketonemia at 3 mmol/l and significant levels of ketonuria. Next is the presence of over 11 mmol/l of blood glucose or known diabetes mellitus, and last is the reduced levels of venous bicarbonate and venous, with values of 15 mmol/l and 7.3 respectively. The pathophysiology of DKA is important in order to accurately determine its occurrence. Trachtenbarg (2005) also pointed out three key features of diabetic acidosis, namely hyperglycemia, ketosis, and acidosis. Hyperglycemia can be diagnosed in reference to the hyperosmolar hyperglycaemic state and also by observation of the classic osmotic symptoms, which is characterized by weight loss, polydipsia and polynuria (Shipman and Dhatariya, 2011). “It occurs secondary to insulin deficiency, gluconeogenesis, and underutilization of glucose . . .” that results to the production of glucagon which stimulates gluconeogenesis and ketogenesis. Stress can also add up to the release of glucagon and also affects glucose utilization due to the increased concentrations of epinephrine, cortisol and growth hormones ((MedBroadcast Clinic Team, n.d.). Ketosis happens due to enhanced lipolysis that produces ketone bodies such as acetone, acetoacetate, and 3-beta-hydroxybutyrate in high concentrations thus resulting to metabolic acidosis. Hyperglycemia causes osmotic diuresis while ketone causes nausea and vomiting, both of which contributes to severe fluid depletion and electrolyte imbalance that threatens the life of a patient (Savage et al., 2011). On the presence of the said pathological mechanisms, DKA can occur in less than 24 hours and the sign and symptoms of the condition will start to be observable. Patients would usually show signs of polyuria, plydipsia, polyphadia, weakness, and Kussmaul’s respirations. Symptoms of nausea and vomiting, abdominal pains, and a fruity breath odor can be observed. Also, coffee-ground emesis due to hemorrhagic gastritis is present with 25 percent of vomiting patients (Trachtenbarg, 2005). In addition, symptoms complications of DKA includes confusion, decreased perspiration, dry cool skin, excessive thirst and urination, fatigue, and presence of ketones in the urine. Dehydration also happens due to the excessive concentrations of ketones in the urine which draws out more water, and excreted excessively with frequent urination (MedBroadcast Clinic Team, n.d.). According to the study of Wolfsdorf, Glaser and Sperling (2006), the approach to DKA varies between infants, children and adolescents. However, the pathophysiology of DKA among different age groups is the same. Cases of DKA in younger children are difficult to determine and can sometime lead to misjudgement of the case to other illness or disease. The treatment would also be more complex with children due to the higher risks of children to develop the severe complication of cerebral edema. On the other hand, DKA has different risk factors for pregnant women as compared to children and adults. According to Michael Pischke (2001), the reason behind why pregnant women has a higher or special risk factor of having DKA is due to the increased insulin resistance and accelerated ketosis during pregnancy. In addition to that, infections can also contribute to the increased risk. The most common cause of mortality among patients diagnosed with DKA is the occurrence of serious complications such as hypokalaemia and hyperkalaemia, hypoglycaemia, and cerebral edema. Hypokalaemia and hyperkalaemia is associated with severe dehydration and can lead to pre-renal failure. Hypoglycaemia is a condition that occurs during treatment wherein the blood glucose is allowed to drop that can cause cardiac arrhythmias, acute brain injury and death. Cerebral edema has been observed to usually occur a few hours after the start of treatment, but the exact phenomenon is unknown (Savage et al., 2011). Cerebral edema is a kind of DKA complication that can cause neurological deterioration to affected patients. According to the case study conducted by Glaser et. al. (2001), the “. . . initial pressure of arterial carbon dioxide was found to be an important predictor of the risks of cerebral edema.” This study had determined that high initial urea nitrogen concentrations and low partial pressure of arterial carbon dioxide creates a biochemical feature that increases the risk of having cerebral edema. Also, the increase in sodium concentration during therapy and the use of bicarbonate during treatment would increase the risk factor (Glaser, et al., 2001). A clinical and biochemical monitoring for DKA patients have been outlined in the published study of Wolsdorf et al. (2007). The key to a successful management of DKA is meticulous monitoring, which will allow timely adjustments in treatment. This is done by using a documentation flow chart of hourly clinical observations. The study conducted by Glaser et al. (2004) about the mechanism of cerebral edema proposed an effective treatment and preventive methods for patients that have high risk of developing cerebral edema. The treatment included infusion of a certain amount of 0.9% saline solution to the patients until perfusion and hemodynamic stability were established. Insulin was also administered to the patients in small volumes through IV infusion. Bicarbonate was not used in the treatment, instead potassium replacements was used. Also, the Glasgow Coma Scale (GCS) was used to monitor neurological status of patients. Initial treatment of DKA includes fluid replacement, to resuscitate the fluids lost due to osmotic dieresis, and IV insulin administration. The insulin therapy via IV infusion is effective in managing plasma glucose and ketones. Other crucial treatments include Potassium replacement, Bicarbonate therapy and Phosphate replacement. However, strict clinical guidelines should be followed in order to reduce the risks of developing serious complications (Jevin, 2011). The University Hospital of Columbia and Cornell (2008) published a DKA guideline for treatment and management of the condition. The goals of the treatment include the replacement of volume deficit, correcting ketosis and acidosis, replacement of electrolyte deficits and water deficits, prevention of hypoglycaemia, and correction of hyperglycemia. Conclusion Diabetic Ketoacidosis is a life-threatening condition that occurs to T1DM patients on the basis of several risk factors. Accuracy on the initial evaluation and diagnosis is crucial in order to address the condition at the earliest possible time. The sign and symptoms associated with DKA should also be closely monitored in order to effectively administer proper treatment methods. References Buse, J. B., Menke, M., & Sisca T. S. (2005). A Comprehensive Review of Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State in Adults. Hopewell, NJ: Scherer Clinical Communications. CardioSmart. (2011). Diabetes: Diabetic Ketoacidogenesis. Retrieved from http://www.cardiosmart.org Glaser, N., Barnett, P., McCaslin, I., Nelson, D., Trainor, J., Louie, J., Kaufman, F., Quayle, K., Roback, M., Malley, R., & Kuppermann, N. (2001). Risk Factors for Cerebral Edema in Children with diabetic ketoacidosis. The New England Journal of Medicine, 344(4), 264-269. Glaser, N. S., Wootton-Gorges, S. L., Marcin, J. P., Buonocore, M. H., DiCarlo, J., Neely, E. K., Barnes, P., Bottomly, J., & Kuppermann, N. (2004). Mechanism of Cerebral Edema in Chidren with Diabetic Ketoacidosis. Elsevier. DOI: 10.1016/j.jpeds.2004.03.045 Jivan, D. (2011). Management of diabetic ketoacidosis. Journal of Endocrinology, Metabolism and Diabetes of South Africa, 16(1), 10-14. Retrieved from http://www.jemdsa.co.za/index.php/JEMDSA/article/viewFile/216/257 Levin, D. L. (2008). Cerebral edema in diabetic ketoacidosis. Pediatric Critical Care Medicine, 9(3), 320-329. MedBroadcast Clinical Team. (n.d.). Diabetic Ketoacidosis. CHealth. Retrieved from http://chealth.canoe.ca/channel_condition_info_details.asp?channel_id=143&relation_id=1711 &disease_id=154&page_no=1 Pischke, M. A. (2001). Diabetic Ketoacidosis. Physician Assistant Journal, 25(11), 42-48. Savage, M. W., Dhatariya, K. K., Kilvert, A., Rayman, G., Rees, J. A. E., Courtney, C. H., Hilton, L., Dyer, P. H., & Hamersley, M. S. (2011). Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis. Diabetic Medicine, 28, 508-515. DOI:10.1111/j.1464-5491.2011.03246.x Shipman, K., & Dhatariya, K. (2011). Diabetic ketoacidosis and new onset diabetes. Midlife and Beyond, 69-72. Retrieved from http://www.drketandhatariya.com/publications/case_reports/Geriatric%20Medicine%202011.pdf Trachtenbarg, D. E. (2005). Diabetic Ketoacidosis. American Family Physicians, 71(9), 1705-714. Retrieved from http://aafp.org/afp University Hospital of Coumbia and Cornell. (2008). Diabetic Ketoacidosis Guidelines. New York: Presbyterian. Wolfsdorf, J., Glaser, N., & Sperling M. A. (2006). Diabetes Ketoacidosis in Infants, Children, and Adolescents. Diabetes Care, 29(5), 1150-1159. Wolfsdorf, J., Craig, M. E., Daneman, D., Dunger, D., Edge, J., Lee, W., Rosenbloom, A., Sperling, M. A., & Hanas R. (2007). ISPAD Cllinical Practice Consensus Guidelines 2006-2007. Pedriatic Diabetes, 8, 28-43. Read More