Management of Diabetic Ketoacidosis - Case Study Example

Management of Diabetic Keto Acidosis Introduction Diabetic ketoacidosis (DKA) though is a preventable disease remains a persistent life-threatening complication of type 1 diabetes. It is usually attributed to the errors in its management that are not common but importantly associated with a significant morbidity as well as mortality. Several acute hospitals have guidelines for the management of diabetes ketoacidosis, but it is rarely followed, moreover, those guidelines are usually out of date. Lately, there has been a gradual change in the way patients suffering from DKA are being managed. This is because there has been the developments of rapid tests as well as guidelines have also been improved to be in align with the current technologies. Most of the guidelines used are evidenced based where all the possible accumulated professional knowledge has agreed anonymously. Such guidelines are intended to be utilized by the health care professionals while executing their duties, the most currently accepted is the NICE guidelines (Fogel & Zimmerman 2009). Globally, it is estimated that 382 adults aged between 20 and 79 years are suffering from diabetes, and the figures are expected to rise up to a staggering 592 million persons by year 2035 (Lam & LeRoith 2012). In the UK, statistics of 2013 have shown that 1 out of 17 people are diabetic whether diagnosed or undiagnosed. In essence, it can be stated that there are 3.2 million people who have been diagnosed of diabetes while 630, 000 people have not been diagnosed but have diabetes this leads to a UK prevalence of 6.0% (QOF 2012/3). Diabetes has got a lot of burden in UK. Currently, the indirect and direct cost spent in managing diabetes stands at £23.7 billion annually and it is predicted to rise to a colossal level of £39.8 billion annually by 2035/6 (Hex, et al., 2012). Discussion Diabetic ketoacidosis is a condition that is brought about by the absence or inadequacies for insulin in the body. When there is low insulin in the body, a derangement in metabolism of fat, protein and carbohydrates leads to diabetes and complicate to DKA. The condition is characterised by three major features, and this include hyperglycaemia, acidosis and dehydration as well as electrolyte loss. Pathophysiology When there is low insulin in the body, the percentage of glucose that gets into the cells is significantly reduced thus making the liver elevate its function by producing more glucose in the blood. All these two factors leads to elevation of the blood glucose level (hyperglycaemia). In an attempt to excrete the excess glucose in the body, the kidney works significantly by excreting the glucose and water as well as electrolytes like sodium and potassium. The osmotic diuresis is coupled with excessive secretion of urine, and a term commonly referred to as polyuria ultimately leads to dehydration and colossal loss of electrolytes. Studies have shown that patients with severe diabetic ketoacidosis loose water up to 6.5 litres as well as 400 mEq of potassium and sodium within a period of 24 hours (Savage et al. 2011). Insulin deficiency poses another effect, which is the impairment of the breakdown of body fats into the free fatty acids and their glycerol components. The free fatty acids are usually converted into ketones bodies in a person’s liver. In diabetic ketoacidosis, there is mass production of the ketones bodies due to the lack of insulin hormone that would otherwise avert such a process from occurring. Accumulation of the ketones bodies in the blood finally leads to metabolic acidosis, this is because of the acidic nature of ketones (Sivanandan et al. 2011). The primary causes of diabetic acidosis can be grouped into three broad reasons, and they include undiagnosed or untreated diabetes mellitus, missed or insufficient insulin in the body and illness or infection. Insulin deficiency may occur due to a deficiency in the insulin dosage that is prescribed or from a small dose of insulin that the patient administers himself. Another major way is through errors that patients make because some assume that if they are eating less food or if they vomit food then they should lower the dosage of insulin. Infections may occasionally lead to high glucose level in the body. Therefore, diabetic patients should not decrease their daily dosage of insulin to compensate for their ability to less food intake when ill. In fact, illness can sometimes warrant an increase in the dosage of insulin. Some infections have been associated with insulin resistance. During a stressful situation which can either be physical or emotional, majority of the stress hormones get released into the blood stream. These hormones include glucagon, cortisol and epinephrine among others. These hormones significantly lead to the production of glucose by the liver thus interferes with the normal utilization of glucose by the fat tissues and muscles, thus countering the action of insulin. In addition, if insulin levels are not scaled up during a time of chronic illnesses and severe infection then the hyperglycaemia can ultimately lead to diabetic ketoacidosis (M S Eledrisi et al. 2006). Clinical manifestation The elevated blood glucose levels in diabetic acidosis usually leads to excessive urination because of the osmotic capability possessed by glucose. Moreover, several patients occasionally experience blurred vision coupled with headache and general body weakness. In an individual who has lost much of intravascular fluid depletion, they may present with orthostatic hypotension. This is the reduction in systolic blood pressure of a proximately 20 mmHg or above while the patient is standing. The marked fluid volume loss may also lead to a frank hypotension characterised with a weak and rapid pulse (Donahey & Folse 2012). The high ketones levels in the blood causes gastrointestinal symptoms such as severe abdominal pain, loss of appetite, nausea and vomiting. The abdominal pain that is experienced by these patients is usually so severe that it may be confused with an abdominal surgical condition. The breaths of the patient often smell the acetone, which is due to the profound elevated ketones level in blood. Moreover, the patient’s presents with fast breathing that is very deep but not labouring. This kuss-maul respiration is a compensatory mechanism in which the body tries to reduce the acidosis as well as countering the effect of the accumulation of ketone. Assessment and diagnostic findings The blood glucose levels of patients may vary broadly and range from 16.6 to 44.4 mmol/L, however some of the patients may have low blood glucose while others have more due to the varying degree of dehydration status. In essence, it is good to note that the severity of diabetic ketoacidosis is not directly linked to blood glucose level. This is because some patients may present with severe acidosis and have moderately elevated blood glucose while others may show no evidence of having diabetes ketoacidosis with glucose levels of 22.7 to 27.7mmol/L. The evidence of ketoacidosis is often reflected in conditions with low serum bicarbonates that ranges between 0-15mEq/L and in low pH values of less than 7.3. Generally a low PCO2 level is a reflection of respiratory compensation in metabolic acidosis, which is commonly referred to as Kussmaul respirations (Mohsen S Eledrisi et al. 2006). The electrolytes are usually altered with potassium and sodium levels significantly affected. These two electrolytes can be high, normal or low because they depend on the dehydration or the quantity of water loss from the body. Despite the blood plasma concentration, there is usually a total depletion of these electrolytes and others in the body thus warrant their replacement. There is an elevation of creatinine, hematocrit and blood urea nitrogen because of dehydration. Management Medical management Despite the fact that the primary target is treatment of hyperglycaemia, management of diabetic ketoacidosis should focus on restoring electrolytes, and correcting dehydration as well as acidosis. Rehydrating the patient is vital because it restores tissue perfusion, moreover the fluids that are replaced assist in the excretion of the excess glucose by the kidneys. Therefore, the patient may need approximately 6 to 10 litres of intravenous fluid to compensate for the fluid loss due to fast breathing, excessive urination, vomiting and diarrhoea. Immediately when the patient is admitted, intravenous normal saline is administered at a rapid rate of 0.5 to 1 litre per hour for the first 2 hours. Half strength normal saline is used in patients who are having high blood pressure or hypernatremia as well as those patients who are at risk of developing heart failure. When the glucose levels reach 16.6mmol/L or less, dextrose 5% intravenous fluid in water may be started to prevent the precipitous reduction of the blood glucose level that is a hyperglycemic crisis in diabetic patients (Hardern 2003). Fluid volume should be regularly monitored by observing the vital signs. This can include monitoring any changes in the heart rate and blood pressures. The lungs should be auscultated to get the air entry since the patient may suffer from pulmonary congestion. Input and output chart should be filled accordingly to monitor the body fluid volume. If the patient is in severe hypotension that is not responding to the intravenous fluids, then plasma expanders may be administered. In diabetic ketoacidosis, there is usually a major loss of potassium from all the body stores thus causing an intracellular and extracellular shift of this electrolyte. In addition, the serum level of potassium usually falls during the management of DKA this is because potassium electrolytes re-enter the cell. Factors that that may lead elevation of the plasma levels, and reductions in potassium levels include rehydration and insulin administrations that facilitate potassium re-entry into the cell. During administration of potassium, the patient’s heart function should be carefully monitored by the use of electrocardiogram to avoid causing arrhythmias. The ketones bodies accumulate in the blood due to the breakdown of fat, and the acidosis state that occurs is reversed by the use of insulin, which acts by inhibiting the breakdown of fat. Insulin is administered intravenously at a slow but steady rate. The blood glucose level is measured after every hour and when blood glucose levels reaches between 13.8 and 16.6 mmol/L, intravenous fluids such as normal saline or dextrose 5% in normal saline. This will help to prevent rapid reduction of the blood glucose level (Fasanmade et al. 2008). Nursing care The nursing management of a patient who is with diabetic ketoacidosis majorly focus on monitoring the fluid, electrolytes and blood glucose levels. It, therefore, involves fluid administration, insulin administration and all the medications involved in the management as well as averting any eminent complication. Urine output is carefully monitored to ensure that the kidneys are properly functioning before administration of potassium to prevent hyperkalemia. The patients heart should be monitored using electrocardiogram, since it shall help in detecting any arrhythmia that is a sign of abnormal potassium levels. The vital signs should be monitored hourly as well as arterial blood gases and other findings which are recorded on the flow sheet. Al the laboratory results, changes in medications, as well as changes in fluid administration, are adequately documented for reference purposes. As the patient improves, the nurse should reassess all the factors that led the patient to develop DKA after which she/he provides the patient and the significant others on prevention (Wallace & Matthews 2004). Case scenario Age: 34 years Gender: male Ethnicity: White The patient was admitted in the ward from outpatient department with complains of fever and cough that had lasted for 4 days, and he could not eat food or drink water. The patient is known diabetic. He was diagnosed with diabetes 5 years ago and was being managed with an intensive insulin regimen which is insulin glargine 24 I.U before each meal. On examination: he was having tachycardia, fever of 39 degrees centigrade, pulse rate of 103 beats per minute, respiratory rate 23 breaths per minute and blood pressure of 100/60mmHg. He had poor skin turgor and rhonchi on the left lungs. Biochemical results: glucose level 25 mmol/L, urea 10.2mmol/L, creatinine level 1.4 mg/dl, potassium levels 5.3mEq, bicarbonates level 5.6mEq, sodium levels 152mEq/L and the oxygen saturation was 98%. full blood count done revealed elevated white blood cells, heamatocrit count of 48%, and haemoglobin of 14.3 g/L. The ketones bodies in urine gave strong positive result of 3+ and glucose in urine showed 800mg/dl, specific gravity 1040. Diagnosis From the assessment made, the patient was hyperglycaemic with ketosis and having metabolic acidosis. Therefore, a diagnosis of DKA and a respiratory tract infection with impaired renal function. Immediate medical and nursing management Intravenous normal saline 4 litres was administered to restore body fluid volume and I.V insulin 24 I.U was initiated to lower the blood sugar level (Mooradian & chehade 2012). Because of the normal potassium levels, 10mEq of potassium was added to each litre of normal saline. The serum potassium level was added 4 hourly and dose adjusted appropriately according to the cardiac functioning. When the glucose levels were stabilised subcutaneous insulin was instituted. The patient was put on electrocardiogram to monitor the electrical activity of the heart. Blood sugar levels were tested 4 hourly and the patient was referred to nutritionist for diet prescription and advise. Intravenous antibiotics were administered as prescribed. Dip stick urinalysis was done daily to monitor ketonuria and albuminuria. DAFNE approach was applied since it is very significant because it leads to blood sugar control, treatment satisfaction, psychological well being and improved quality of life of the patient (K. et al. 2010). Prevention of Diabetic acidosis The patient should be taught the risk factors that leads to the development of diabetes since this will equip the patient with the required knowledge to avoid them. The most paramount issue is to make the patient understand that the insulin is the key factor that prevents DKA. The patient should learn that even if they eat and vomit they should not assume that their blood glucose is not raised thus avoid insulin injection. Rather they should endeavour to take their usual insulin dose. Diabetic patient should be encouraged to drink fluids hourly because it prevents dehydration. The blood glucose level and the urine ketones should be assessed after every four hours (Williams & Pickup 2004). The patient should report to the physician or nurse when the blood glucose level is greater than 16.6mmol/L since this predispose an individual to DKA. The patient should report episodes of vomiting and diarrhoea to the physician, and this is because they can be severe and causes dehydration (Skinner 2002). Conclusion Majority of people who are having diabetes mellitus rarely develop diabetic ketoacidosis, this is associated with the drug adherence and monitoring of blood glucose levels. In situations where DKA ensues it is always evident that those patients were not properly monitoring their blood glucose levels. It follows that their blood glucose levels rise exponentially to higher limits thus exposing them to the risk of developing DKA. Hyperglycaemia coupled with other precipitating factors like illness and dehydration ultimately make an individual to end in DKA. Therefore, the diabetic patients should always be advised to monitor their blood sugars as well as maintaining hydration and treating any illness (K. et al. 2010). During DKA management, the primary targets are insulin administration, electrolytes restoration and reversing acidosis. Insulin should be steadily and continuously administered using an insulin pump to reduce high blood sugar. Intravenous normal saline should be administered to correct dehydration status of the patient as well as restoring the lost sodium ion in the urine. Potassium infusion is necessary because it restores the lost ions which are important in heart function. Any significant complications that the patient faces like going to diabetic coma should be referred accordingly. Reference Donahey, E. & Folse, S., 2012. Management of diabetic ketoacidosis. 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Quality and outcomes framework (QOF) 2012/3 http://www.hscic.gov.uk/article/2021/Websitesearch?q=quality+and+outcomes+framewo rk&go=Go&area=both Wallace, T.M. & Matthews, D.R., 2004. Recent advances in the monitoring and management of diabetic ketoacidosis. QJM : monthly journal of the Association of Physicians, 97, pp.773–780. Williams G & Pickup J (2004) 3rd Edition. Handbook of Diabetes . Oxford. Blackwell Publishing Read More