NUR440 Case Study 6 DKA
NUR440 Case Study 6 DKA
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Date Created: 11/14/15
Case 6 DKA Mrs S is a 28yearold patient with a 12year history of type I diabetes mellitus Her husband states that she has had a bad cold for several days Yesterday she stayed in bed and slept all day She was too ill to check her blood sugar and since she was not really eating she did not take her insulin This morning she was not able to stand up and vomited twice A Gram stain of Mrs S s blood contains grampositive cocci in clusters Her admission vital signs are BP 9060 HR 118 bpm sinus tachycardia RR 32min T 1023quot F 02 sat via pulse oximetry 96 Her serum glucose is 398 mgdl and she is positive for serum ketones She is admitted with a diagnosis of DKA Her baseline ABGs on 2 L of oxygen are pH 725 PCOZ 28 HC03 14 Pa0292 02 sat 96 Her respirations are deep rapid and labored She has bronchial breath sounds in the right axillary area There is bilateral chest expansion and no evidence of cyanosis A regular insulin bolus is given and a regular insulin drip is initiated Mrs S s IV uids are infusing at 800 mlhr Her vital signs after 2 hours in the unit are BP 12070 HR 78 bpm normal sinus rhythm RR 22min 02 sat 100 Her serum glucose is 250 mgdl and serum potassium is 40 mEqL She is more alert and is feeling hungry 1 What is insulin s function in the body What is the most significant basic defect in the development of DKA Insulin has four major functions first of all it is the only hormone produced in the body that lowers blood glucose levels in the bloodstream Insulin is responsible for the storage of carbohydrate fats and proteins Insulin also assists with the transportation of potassium into the cell The most basic defect in the development of DKA is a lack of insulin Infection is often the major cause of the development of DKA With insulin being the key to the transfer of glucose from the bloodstream into the cell in DKA a lack of insulin contributes to increasing levels of glucose in the bloodstream and the cells starve When the cells are deprived of their energy source due to the lack of insulin the liver is then stimulated to release glucagon Glucagon increases the amount of glucose in the bloodstream by breaking down fats and proteins glycogenolysis and converts them to glucose Blood glucose levels then rise to 300800 mgdl of blood Also during times of deficient insulin fat is converted to glucose a process known as gluconeogenesis The free fatty acids are metabolized into ketones resulting in ketoacidosis which will be seen in the urine as ketonuria and in the bloodstream as ketonemia What is the cause of Ms S experiencing DKA Describe the pathophysiologic rationale for your answer Ms S s DKA most likely developed from her infection grampositive cocci Stress and illness causes an increase in the release of hormones such as catecholamines cortisol glucagon and growth hormones these hormones counteract or oppose the action of insulin If doses of insulin are not increased in times of infection or stress insulin deficient states develop When insulin levels are low fats breakdown very quickly and ketones accumulate in the bloodstream resulting in acidosis At the same time the kidneys cannot resorb glucose so glucose is then excreted in the urine causing dehydration As mentioned above cortisol levels increase in times of illness and stress Cortisol stimulates gluconeogenesis increasing the production of glucose by the liver up to ten times As you can see this would increase the blood glucose level even further List the classic signs and symptoms of DKA Which signs and symptoms did Ms S experience What are the pathophysiologic causes of these signs and symptoms The classic signs and symptoms of DKA headache malaise elevated blood glucose greater than 250 mgdL polyuria polydipsia polyphagia glycosuria and ketonuria Nausea vomiting dehydration and fatigue will follow if the insulin stores are not corrected The fact that Ms S is a well known diabetic would be the first clue she also presented with hypotension tachycardia tachypnea malaise not wanting to get out of bed or check her blood sugar vomiting ketones in urine serum glucose of 398 mgdL and she had a bad cold Her ABG s later on admission showed a decreased HCO3 and decreased pH indicating acidosis What is an anion gap Why is the anion gap important to follow in the treatment of DKA The anion gap is the difference between measured cations and anions in the blood A loss of HCO3 causes an increase in the anion gap If we are unable to view the patient s ABG s the anion gap is a good indicator of acidosis An elevated anion gap indicates acidosis the normal anion gap is 8 16 mEqL If we follow the anion gap in DKA we will watch for a gradual decline in the anion gap this will indicate the HCO3 is returning to normal and the metabolic acidosis is resolving What acid base disturbance is Ms S experiencing What compensatory mechanisms are in effect at this time Ms S is experiencing metabolic acidosis and the lungs are trying to compensate by blowing off the C02 as evidenced by the increased RR What is the primary nursing diagnosis for Ms S What are the goals for treatment both independent and collaborative What interventions are imperative to initiate immediately What interventions are important within the next 1224 hours Decreased cardiac output related to dehydration and DKA as evidenced by tachycardia and hypotension Ms S s treatment goals will be to resolve dehydration restore insulin stores decrease serum glucose replenish electrolytes if needed and reverse the ketoacidosis It is imperative Ms S continue to receive IV uids to reverse the dehydration depending on the potassium level and the physician s order 20 mEq potassium L may be appropriate insulin replacement monitoring of ABG s strict intake and output The patient may also need more invasive hemodynamic monitoring if the DKA does not resolve Continuous monitoring of Ms S s response to the treatment will include blood glucose every hour frequent potassium checks serum osmolality serum sodium and BUNCreatinine to evaluate renal function Ms S should also be monitored over the next 1224 hours for uid volume overload hyperkalemia hypokalemia hyponatremia and hypoglycemia It is imperative Ms S s neurological status be continuously monitored neurological changes may occur slowly Headaches and confusion are signs of cerebral edema What are potential lab abnormalities for a patient in DKA Potential lab abnormalities may include hyponatremia hypokalemia hyperkalemia hypoglycemia hyperglycemia hypophosphatemia and abnormal arterial blood gas results What nursing considerations are important in planning Ms S s discharge Extremely important considerations for Ms S would be to educate her on the disease process of diabetes as well as the DKA Explain to her the exact etiology of the DKA so she can understand what lead up to her hyperglycemia Discussion and learning objectives may be directed towards acceptable levels of blood glucose definition of hyperglycemia and its causes harmful effects signs and symptoms and how to manage her insulin and diet when she is unable to eat Her family members should also be involved in the teaching process so they will learn to recognize the signs and symptoms
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