Strategies For Treating Children With DKA: Best Essay On DKA And Cerebral Edema.

Causes of Diabetic Ketoacidosis

Question:

Discuss about the Diabetic Ketoacidosis (DKA) and Cerebral Oedema.

Diabetic ketoacidosis is caused as a result of reduced effective circulating insulin in blood. The condition usually arise among patients with type I diabetes mellitus, associated with a genetic defect in the insulin producing tissue, i.e. islets of langerhans in the pancreas tissue (Kumar & Manjusha 2017). The situation leads to the activation of hormones that alleviate glucose production, followed by increased lyiposysis and ketone body production, which causes the metabolic acidosis and hyperglycemia along with dehydration and loss of electrolytes (Usher-Smith et al., 2012). Thus, it is important to maintain the fluid balance among the patients experiencing DKA. In paediatric care, DKA is one of the significant areas of concern. One of the key dangerous complications related to DKA that leads to fatal consequences is the cerebral oedema, which has been estimated to be the cause of 70 to 80 % deaths of under 12 years old children, experiencing DKA (Usher-Smith et al., 2011). Children with type I diabetes are risk prone to develop dangerous consequences of DKA, significantly due to late diagnosis, late referral and late initiation of treatment. Thus, a high index of suspicion is required for diagnosing DKA during initial assessment (Kumar & Manjusha 2017).

It has also been estimated that the majority of the cerebral oedema cases leads fatal consequences, with a mortality rate of 25 % to 30 %, whereas 35% to 40 % patients survives with severe neurological defects. As the DKA is associated with significant amount of fluid and electrolyte loss, the treatment procedure is related to the maintenance of fluid balance through the IV fluid supplement. It has been estimated that within the overall cases of DKA, up to 1 % children develop cerebral oedema as a complication DKA (Savage et al., 2011).

The recent statistics showed that in UK and US, a prevalence of 0.5 to 1.5 % DKA cases include cerebral oedema, which constitutes 90 % mortality related to DKA (Yaneva, Konstantinova & Iliev, 2016). Whereas, dependence between the CO development and the initiation of DKA treatment, high fluid volume, delayed potassium substitution, hyperglycemia, low serum phosphate are the signs of cerebral oedema. In spite of providing a significant effort to reduce the risk of cerebral oedema related to DKA, the mortality rate has remained constant through past decades. Although several studies have been performed to identify methods to treat CO, no such strong methods have been found, rather a need for a lager trial has been found for finding appropriate therapeutic recommendations (Brown, 2004). For instance, Hsia et al., (2015) revealed that reducing the intended fluid rate during initial 24 hours to 2500 mL/m2/d and increasing the IBV fluid sodium content have no effect upon reducing the incident of adverse outcomes like CO among children, making fluid balance therapy questionable for CO.

Significance of DKA in Paediatric Care

It has been evident that this fluid rebuilt process has a significant contribution in developing cerebral oedema. Thus, while deciding the treatment for DKA patient, this factor should be kept in mind. While managing DKA in children, several unique aspects must be considered. Thus, paediatric care facilities need to develop goals and care plans for each child, based on the child’s condition and the evidences from the previous successful cases. In this assignment, the pathophysiology and clinical manifestation of DKA and cerebral oedema would be demonstrated, along with the demonstration of best strategies for treating children with DKA (Fritsch et al., 2011). The selection of the most appropriate treatment strategy would be identified through evidence based procedure.

The diabetic ketoacidosis or DKA is a complex metabolic disorder. The diabetic ketoacidosis is related to other severe and chronic disorder. The disorder is significantly a secondary complication of the chronic disease diabetes mellitus. It is typically diagnosed with the vital signs of low blood pH, high blood sugar level and presence of ketoacidis in either blood or urine (Seewi et al., 2010).

The complications related to the disease are due to shortage of insulin, as a result of which body starts burning fatty acids, thereby producing acidic ketone bodies. As a result of insulin deficiency, the level of glucagon is increased, causing the release of glucose by liver via the process of gluconiogenesis or glycogeenesis (Lamb, 2014). This high level of glucose spills over the urine along with water and minerals, causing osmotic dieresis. It causes the development of symptoms like polyuria, dehydration and polydipsia.

Ketoacidosis is referred to an extension of normal physiological mechanisms, compensating for starvation. For instance, in the fasting state, the changes in body metabolism changes from carbohydrate oxidation to fat oxidation. The ketoacids are formed from the free fatty acids which are produced in adipocytes and transported to the liver via albumins. In liver, these fatty acids are broken down and produce ketoacids. These newly produced ketoacids are then exported to the peripheral tissues from liver, i.e. brain and muscles. At these tissues, these ketoacids are oxidised by the process of beta oxidation (Gosmanov, Gosmanova & Dillard-Cannon, 2014). It is because; the beta-hydroxybutarate can serve as energy resource, when the insulin mediated glucose delivery system is not available. This procedure is recognized as a protective method during the starvation phase. At the time of ketosis, a small amount of acetone is produced, which causes the breath of the DKA patients a fruity smell (Wolfsdorf et al., 2014). As a result of the formation of ketone bodies, which have a low pKa, the blood becomes acidic as its pH lowers. However, initially, the buffering occurs through the bicarbonate buffering system. However, the system is not able to maintain the balance for longer time and it overwhelms, as no other system is supporting it (Cameron et al., 2014).

Complications Related to Cerebral Edema

In patients with diabetes mellitus, insulin resistance cannot meet the insulin demand rise’ blood sugar level rises along with dehydration and resistance to insulin increases further through vicious circle. As a result, an adult patient with DKA has a water shortage of 6 litres along with the deceased amount of key minerals like sodium, potassium, calcium, chloride, magnesium and phosphate (Mahler et al., 2011). In the patients with type I diabetes mellitus, DKA is a secondary complication of complete lack of insulin production by the pancreas tissues, islets of langerhans. On the other hand, in type 2 diabetes, insulin resistance occurs as a result of insufficient production of insulin. However, in type 2 diabetes, DKA is not common, as the amount of insulin that is produced in this disorder is usually sufficient for patients to suppress ketogenesis (Edge, 2015). However, ketosis-prone type 2 diabetes is referred to the cases when DKA occurs in patients with type 2 diabetes. Thus, upon treatment, if the normal insulin secretion resumes, the patient may have better results. Moreover, DKA is associated with the secretion of several counter-regulatory hormones in glucagon and adrenaline as well as cytokines, which ultimately causes inflammation (Glaser et al., 2013).

Cerebral oedema is another serious complications associated with DKA, which is the most dangerous consequences of DKA. It is associated with several critical factors. It is most likely to be developed among people, who are suffering from severe DKA. It is often argued that the condition is associated with over vigorous rehydration (Glaser et al., 2013). The factors contributing in the development of cerebral oedema are acidosis, low carbon dioxide, dehydration, increased inflammation and coagulation; these factors collaboratively reduces the blood flow to some particular parts of the brain, causing the swelling of brain tissue upon starting the fluid replacement treatment (Foster, Morrison & Fraser, 2011). The tissue swelling in brain causes the raised intracranial pressure, which ultimately leads to fatal consequences. Therefore, the treatment procedure has a significant contribution upon the development of this serious complication among patients.

As DKA is a secondary complication to the diabetic patients, the early signs and clinical manifestations are often not properly diagnosed. However, development of DKA is a slow process, although symptoms can be alleviated by several means. The initial clinical features of DKA are often mistaken with the normal symptoms of diabetes mellitus. The clinical representation of the condition can vary with the severity and comorbid conditions (Edge, 2015). Sometimes, the disease symptoms are progressed over 1 day or less than that, which include the signs and symptoms of polyuria and polydipsia, which are the most common symptoms of the disease. Besides these signs, vomiting, fatigue, flushing of skin, dry skin, thirst, dyspnea, losing weight, polyphagia, abdominal pain, preceding febrile illness, tachycardia, hypotension, frequent urination, high blood sugar level and presence of ketones in urine are common. Kussmaul respiration is a compensatory symptom of metabolic acidosis. In severe case, shock, oliguria and anuria are developed (Seewi et al., 2010). Patients in severe cases may experience drowsiness, confusion, progressive obtundation to loss of consciousness and coma. These signs are mainly arise as a result of the effect of the disorder upon brain, i.e. cerebral oedema. Finally, the inflammation in brain can lead to fatal consequences.

Prevalence of Cerebral Edema in DKA

There are several ways through which children with DKA are treated. It is important to follow particular protocol for paediatric patients, based on the hospital’s care protocol. In this context, maintaining fluid balance is the key concern because, in DKA patient’s excessive fluid loss causes severe complications, whereas patients with severe cases, i.e. cerebral oedema, it is important to eliminate the risk of excessive fluid build up in the patient’s body. The key therapy requirements are IV fluid therapy, insulin administration for keeping the adequate level of glucose in the body, as glucose level decreases with IV supplementation (Seewi et al., 2010). Continuous monitoring is required for eliminating the risk of developing cerebral oedema. It is crucial for children to monitor the neurological status continuously, for keeping the vital signs, i.e. blood glucose level, blood pressure, respiratory rate, breathing issue and  fluid content under control, which would help to reduce the progress of the disease towards the severe complications like cerebral oedema (Fritsch et al., 2011).

The most important strategy for DKA and cerebral oedema is fluid balance therapy. However, based on the hospital policy and national guidelines, the treatment should follow a common guideline. For instance, immediate assessment of the patient, resuscitation for shock, diagnosis of DKA, IV therapy to combat with dehydration, insulin therapy, monitoring, management of other symptoms and management of  cerebral oedema. However, based on the patient’s condition, mild non IV DKA therapy is also administered (Savage et al., 2011). However, it should be kept in mind that large amount of fluid can be harmful for paediatric DKA.

Initial/emergency assessment- The clinical history of polyuria, polydispia, weight loss, abdominal pain, vomiting, tiredness, confusion, dehydration, fruity smell breathing, kussmaul breathing, ketone bodies in urine, elevated blood glucose, low electrolyte level are assessed and reported. Based on this assessment, when DKA is confirmed, three lines of therapy are recommended (Usher-Smith et al., 2011). During initial assessment, the baseline acidosis and abnormalities in sodium potassium and urea concentrations were critical risk indicators related to cerebral oedema. In addition, early administration of insulin along with high volumes of fluid is also key risk factors for cerebral oedema among children with DKA. Thus, these observations would be taken into consideration during the treatment protocol designing (Edge et al., 2006).

Resuscitation- If the patient undergone shock, reduced peripheral pulses, reduced conscious level or undergoing coma, resuscitation is done for reviving the patient. At that time, the nasogastric tube is inserted and in severe shock, the patient should be administered with 100 % oxygen through face mask. When emergency fluids are necessary, isotonic fluid, like 0.9 % sodium chloride 10ml/kg over 20 to 30 minutes should be administered (Foster, Morrison & Fraser, 2011). If the patient is still hypotensive, further fluid administration would be needed.

Challenges in Treating Cerebral Edema

Mild DKA- In mild cases, when the dehydration is less than 5 % and no sign of vomiting is observed, IV fluid or repeat electrolytes are not provided; rather treated with subcutaneous insulin from the beginning.

Moderate DKA- If the patient is vomiting, but not in shock, the fluid requirement is calculated over 48 hours, 0.9 % saline is administered, whereas ECG for elevated T-waves are assessed; if there is no changes, KCl in 40 mmol/L is started. The low dose continuous insulin infusion at the rate of 0.1 unit/kg/hour is continued (Seewi et al., 2010). Here, the patient should be monitored critically, which should include hourly assessment of blood glucose level, fluid intake and output, neurological status, electrolyte therapy per 2 hours after IV therapy along with monitoring ECG for changes in T-wave elevation. If the blood glucose level falls to 15 mmol/l or >5mmol/hour, IV fluid therapy is started. It should be done upon the accurate assessment of volume deficit (Seewi et al., 2010). For first 12 hours 0.9 % sodium chloride is continued and during the reduced blood glucose level, 50g glucose is added to per 1000 mL saline. However, if the blood glucose level falls further, with 0.9 % sodium chloride, 7.5 % or 10 % glucose is added and maintained. If the patient is hypokalemic, the potassium replacement therapy should be started, whereas if the patient is hyperkalemic or anuric, potassium replacement should be ceased. Contentious monitoring is required for measuring the level of potassium retention. If the patient is clinically well and tolerating oral fluids, the patient therapy should be transmitted to SC insulin, i.e. SC insulin is started as per protocol, while ceasing IV insulin after 30 minutes (Glaser et al., 2013).

Insulin therapy- After initial diagnosis with DKA, if the patient is clinically is successfully tolerating fluid through oral routes, SC insulin therapy is started. For instance, the SC insulin therapy is started, along with oral hydration. However, if no improvement is documented and neurological deterioration is observed through the representation of warning signs like slow heart rate, headache, decreased conscious level, incontinence and hypoglycaemia; assessment for cerebral oedema is done (Wolfsdorf et al., 2014).

Management of cerebral oedema- cerebral oedema is a critical consequence of DKA, in which the fluid overload leads to inflammation in brain, hampering its function. At that time, patient should be managed with high precautions. If the patient is in fluid therapy, it should be reduced or ceased slowly, to maintain the fluid balance. The patient should be moved to ICU, followed by cranial imaging, once the patient is stable. Immediately after transferring the patient in ICU, patient’s head should be raised to 30 degree with the bed; oxygen should be administered immediately via mask (Cameron et al., 2014). Initially, the patient is administered with 0.5-1 g/kg mannitol through intravenous route over 20 minutes; if the patient’s condition is not improved, mannitol is repeated after 30 minutes. Consulting with a paediatric endocrinologist, 3 % NaCl may be administered. If needed, patient should be intubated; but aggressive ventilation should not be performed, as it is associated with poor outcomes in previous studies (Cameron et al., 2014).

Pathophysiology of DKA

Patient education- Another important strategy is patient education. It has been revealed poor adherence with the therapies, follow ups, poor dietary guidelines and poor lifestyle management skills of the family. In this context, health promotional sessions are important for mild and moderate DKA patients and their parents. For instance, the pros and cons of the therapy, appropriate dietary guidelines for the child, the complications or risk factors of poor adherence with the treatment procedure are crucial factors for the parents and patients to understand (Foster, Morrison & Fraser, 2011). Several literatures found that ongoing patient education has improved the management and adherence of the patients with the therapeutic procedures and follow up procedures.

The most important strategy for DKA and cerebral oedema is fluid balance therapy. However, according to the Hospital policy, there is no best strategy to reduce the effect of the DKA and cerebral oedema. On the basis of the condition of the patient, the strategy can be applied to the patient. However, fluid balance therapy can be applied to the patients in a particular dose. As the retention of fluid decrease in the body, it is necessary to maintain the fluid balance in the body so that the patient can lead a healthy lifestyle. For instance, immediate assessment of the patient, resuscitation for shock, diagnosis of DKA, IV therapy to combat with dehydration, insulin therapy, monitoring, management of other symptoms and management of  cerebral oedema (Edge, 2015). However, most of the patient continues to practice the therapy even after the recovery. Hence, this type of practice needs to be reduced. If the fluid amount increases in the brain, the patient may face vital issues that are related to the brain. As a result, the patient may die due to the cerebral oedema. Hence, before applying the fluid balance therapy, the nurses need to remember the consequences of the therapy. To reduce the dehydration, fluid balance therapy is beneficial. The patients who are in shock, fluid balance therapy is not appropriate for them. Hence, in such cases, the fluid balance therapy should not be used. Instead of the fluid balance therapy, insulin therapy can be used (Glaser et al., 2013). The patients need to take the medication on time so that the side effects of the therapy can be reduced.

The nurses need to follow the hospital protocols so that the ethical issues regarding the therapies can be avoided. It should be kept in mind that large amount of fluid can be harmful for paediatric DKA. The nurses need to monitor the patients on the regular basis so that they can keep the record of the patient. It is the duty of the nurses that they should monitor the patient for example, the development or deterioration condition of the patient. If any noticeable changes are seen, they need to report to the responsible person so that the necessary actions can be taken (Gosmanov, Gosmanova & Dillard-Cannon, 2014). However, it is crucial for children to monitor the neurological status continuously, for keeping the vital signs, i.e. blood glucose level, blood pressure, respiratory rate, breathing issue and fluid content under control, which would help to reduce the progress of the disease towards the severe complications like cerebral oedema. For instance, immediate assessment of the patient, resuscitation for shock, diagnosis of DKA, IV therapy to combat with dehydration, insulin therapy, monitoring, management of other symptoms and management of cerebral oedema (Glaser et al., 2013). Patients in severe cases may experience drowsiness, confusion, progressive obtundation to loss of consciousness and coma. Based on this assessment, when DKA is confirmed, three lines of therapy are recommended. Hence, the patient should be monitored critically.

Clinical Manifestation of DKA

Conclusion

DKA is a significant cause of paediatric mortality and morbidity. However, appropriate management and continuous monitoring can lead to improved health outcomes of the patients. The management and therapeutic procedures of DKA is different from the therapeutic processes of adults. Thus, the nursing staffs and the paediatric care facilities need to be more careful and skilled, while dealing with children with DKA. One of the serious complications related to poorly managed DKA in children is cerebral oedema, which can lead to fatal consequences in several cases. In paediatric care services the DKA have significant negative impact as a result of high rate of mortality and morbidity. Although the condition can be managed with proper guidelines and follow up care, fluid therapy and insulin administration should be carefully monitored throughout the process. On the other hand, fluid therapy, if not monitored and balanced properly, can lead to severe complications, i.e. cerebral oedema. For this enough control of fluid intake and output are required. This assignment provided in depth demonstration of pathophysiology and clinical manifestation of DKA and cerebral oedema, followed by the analysis of the treatment strategies for DKA and cerebral oedema.

A Edge, J. (2015). BSPED Recommended Guideline for the Management of Children and Young People under the age of 18 years with Diabetic Ketoacidosis 2015. bsped.org.uk. Retrieved 5 August 2017, from https://www.bsped.org.uk/clinical/docs/DKAguideline.pdf

Brown, T. B. (2004). Cerebral oedema in childhood diabetic ketoacidosis: is treatment a factor?. Emergency medicine journal, 21(2), 141-144.

Cameron, F. J., Scratch, S. E., Nadebaum, C., Northam, E. A., Koves, I., Jennings, J., ... & Inder, T. E. (2014). Neurological consequences of diabetic ketoacidosis at initial presentation of type 1 diabetes in a prospective cohort study of children. Diabetes care, 37(6), 1554-1562.

Edge, J. A., Jakes, R. W., Roy, Y., Hawkins, M., Winter, D., Ford-Adams, M. E., ... & Dunger, D. B. (2006). The UK case–control study of cerebral oedema complicating diabetic ketoacidosis in children. Diabetologia, 49(9), 2002-2009.

Foster, J. R., Morrison, G., & Fraser, D. D. (2011). Diabetic ketoacidosis-associated stroke in children and youth. Stroke research and treatment, 2011.

Fritsch, M., Rosenbauer, J., Schober, E., Neu, A., Placzek, K., & Holl, R. W. (2011). Predictors of diabetic ketoacidosis in children and adolescents with type 1 diabetes. Experience from a large multicentre database. Pediatric diabetes, 12(4pt1), 307-312.

Glaser, N. S., Ghetti, S., Casper, T. C., Dean, J. M., & Kuppermann, N. (2013). Pediatric diabetic ketoacidosis, fluid therapy, and cerebral injury: the design of a factorial randomized controlled trial. Pediatric diabetes, 14(6), 435-446.

Glaser, N. S., Wootton-Gorges, S. L., Buonocore, M. H., Tancredi, D. J., Marcin, J. P., Caltagirone, R., ... & Kuppermann, N. (2013). Subclinical cerebral edema in children with diabetic ketoacidosis randomized to 2 different rehydration protocols. Pediatrics, 131(1), e73-e80.

Gosmanov, A. R., Gosmanova, E. O., & Dillard-Cannon, E. (2014). Management of adult diabetic ketoacidosis. Diabetes, metabolic syndrome and obesity: targets and therapy, 7, 255.

H Lamb, W. (2014). Pediatric Diabetic Ketoacidosis Treatment & Management: Approach Considerations, Fluid Replacement, Insulin Replacement. Emedicine.medscape.com. Retrieved 5 August 2017, from https://emedicine.medscape.com/article/907111-treatment

Hsia, D. S., Tarai, S. G., Alimi, A., Coss?Bu, J. A., & Haymond, M. W. (2015). Fluid management in pediatric patients with DKA and rates of suspected clinical cerebral edema. Pediatric diabetes, 16(5), 338-344.

Kumar MV, & Manjusha K. (2017). Precipitating factors, clinical profile and metabolic abnormalities of diabetic ketoacidosis in children with type 1 diabetes and their role in predicting the outcome. J. Evid. Based Med. Healthc, 4(8), 393-400. DOI: 10.18410/jebmh/2017/76

Mahler, S. A., Conrad, S. A., Wang, H., & Arnold, T. C. (2011). Resuscitation with balanced electrolyte solution prevents hyperchloremic metabolic acidosis in patients with diabetic ketoacidosis. The American journal of emergency medicine, 29(6), 670-674.

Savage, M. W., Dhatariya, K. K., Kilvert, A., Rayman, G., Rees, J. A. E., Courtney, C. H., ... & Hamersley, M. S. (2011). Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis. Diabetic Medicine, 28(5), 508-515.

Seewi, O., Vierzig, A., Roth, B., & Schönau, E. (2010). Symptomatic cerebral oedema during treatment of diabetic ketoacidosis: effect of adjuvant octreotide infusion. Diabetology & metabolic syndrome, 2(1), 56.

Usher-Smith, J. A., Thompson, M. J., Sharp, S. J., & Walter, F. M. (2011). Factors associated with the presence of diabetic ketoacidosis at diagnosis of diabetes in children and young adults: a systematic review. Bmj, 343, d4092.

Usher-Smith, J. A., Thompson, M., Ercole, A., & Walter, F. M. (2012). Variation between countries in the frequency of diabetic ketoacidosis at first presentation of type 1 diabetes in children: a systematic review. Diabetologia, 55(11), 2878-2894.

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.

Yaneva, N. Y., Konstantinova, M. M., & Iliev, D. I. (2016). Risk factors for cerebral oedema in children and adolescents with diabetic ketoacidosis. Biotechnology & Biotechnological Equipment, 30(6), 1142-1147.