DKA nursing interventions -
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Arslan Sarwar Nursing Nursing Care Plans July 23, 0. Introduction: Diabetic ketoacidosis DKA is a life-threatening complication of diabetes mellitus characterized by hyperglycemia, ketosis, and metabolic acidosis.
Normalizing Blood Glucose Levels: Nurses monitor blood glucose levels regularly and administer insulin therapy as prescribed to lower elevated blood glucose levels gradually.
Correcting Acidosis and Ketosis: Nursing interventions focus on correcting metabolic acidosis through the administration of intravenous bicarbonate only under specific circumstances, along with insulin therapy. Assessing and Monitoring for Complications: Nurses carefully assess for potential complications of DKA, such as cerebral edema, and implement preventive measures and early interventions if needed.
Patient and Family Education: Nurses provide extensive education to the patient and their families about diabetes management, insulin administration, symptom recognition, and the importance of regular follow-up care. Nursing Assessment for Diabetic Ketoacidosis DKA : 1.
Inquire about any recent illness, infection, or emotional stress that may have triggered the onset of DKA. Evaluate for signs of respiratory distress, fruity breath odor acetone , and Kussmaul respirations deep and labored breathing.
Fluid and Electrolyte Status: Monitor fluid intake and output closely to assess for signs of dehydration and hypovolemia. Evaluate electrolyte levels, including potassium, sodium, chloride, and bicarbonate, to identify any imbalances.
Blood Glucose and Ketone Levels: Monitor blood glucose levels frequently to assess the severity of hyperglycemia. Test for ketones in urine or blood to detect the presence of ketosis.
Renal Function: Monitor renal function, including blood urea nitrogen BUN and creatinine levels, to assess kidney function and identify potential kidney impairment. Cardiovascular Assessment: Assess cardiovascular status, including heart rate, blood pressure, and peripheral perfusion, to detect signs of circulatory compromise.
Neurological Assessment: Evaluate neurological status, including level of consciousness, orientation, and reflexes, to identify any neurological manifestations of DKA. Skin and Tissue Integrity: Inspect the skin for any signs of breakdown or injection sites that may indicate insulin administration.
Observe for any evidence of skin infections or pressure ulcers that may contribute to the development of DKA. Nursing Diagnosis for Diabetic Ketoacidosis DKA : Fluid Volume Deficit related to osmotic diuresis, inadequate fluid intake, and vomiting, as evidenced by decreased skin turgor, dry mucous membranes, and elevated hematocrit levels.
Imbalanced Nutrition: Less Than Body Requirements related to decreased oral intake, elevated blood glucose levels, and metabolic demands. Ineffective Breathing Pattern related to metabolic acidosis and compensatory Kussmaul respirations, as evidenced by deep and labored breathing, and altered arterial blood gases.
Risk for Unstable Blood Glucose Level related to inadequate insulin availability, altered carbohydrate metabolism, and fluctuations in food intake.
Impaired Skin Integrity related to hyperglycemia and impaired wound healing, as evidenced by skin breakdown or slow healing of injection sites. Risk for Deficient Fluid Volume related to ongoing fluid losses from polyuria and vomiting.
Risk for Electrolyte Imbalance related to osmotic diuresis and altered electrolyte levels, as evidenced by laboratory results. Risk for Infection related to hyperglycemia compromised immune response, and potential skin breakdown from injection sites.
Altered Mental Status related to metabolic acidosis and electrolyte imbalances, as evidenced by confusion, lethargy, or decreased level of consciousness.
Nursing Interventions for Diabetic Ketoacidosis DKA : 1. Fluid Resuscitation: Initiate intravenous IV access with a large-bore catheter for prompt fluid administration. Monitor vital signs and fluid balance closely to ensure effective rehydration. Insulin Therapy: Administer regular insulin intravenously as prescribed to lower blood glucose levels gradually and suppress ketogenesis.
Collaborate with the healthcare team to transition from IV insulin to subcutaneous insulin once DKA is resolved. Electrolyte Replacement: Monitor electrolyte levels, including potassium, sodium, chloride, and bicarbonate, and replace electrolytes as needed.
Administer potassium supplementation carefully, ensuring that levels are within the target range to prevent hypokalemia or hyperkalemia.
Signs and symptoms of cerebral edema include altered respiratory pattern, abnormal response to pain, change in mental status e. Serum beta-hydroxybutyrate is the preferred test for ketonemia; urine ketone analysis may not show current state.
Hyperglycemia resolves faster than ketoacidosis; ongoing insulin management is required even after glucose levels have fallen. Clinical Goals By transition of care A. The patient will achieve the following goals: Fluid and Electrolyte Balance with Absence of Ketosis B. Patient, family or significant other will teach back or demonstrate education topics and points: Education: Overview Education: Self Management Education: When to Seek Medical Attention.
Vital Signs heart rate increased or decreased respiratory rate increased blood pressure decreased. Diagnostic Results ECG electrocardiogram abnormal. Problem Intervention Monitor and Manage Ketoacidosis Provide intravenous fluid replacement to restore peripheral circulation, renal perfusion and electrolyte balance.
Administer insulin therapy to reverse ketogenesis and correct hyperglycemia; anticipate ongoing adjustment. Anticipate initiation of dextrose-containing fluid therapy as blood glucose levels decrease. Monitor and evaluate for changes in neurologic status that may indicate deterioration e.
Monitor for cardiorespiratory pattern changes that may indicate worsening status. Monitor trends for blood glucose levels, pH, electrolytes, vital signs, serum ketones, intake and output; advocate for treatment adjustment.
Acknowledge and validate significance of lifestyle impact and expectations e. References American Diabetes Association. American Diabetes Association Standards of Medical Care in Diabetes Diabetes Care.
Source [Clinical Practice Guidelines] American Diabetes Association. Source [Clinical Practice Guidelines] Andrade-Castellanos, C. Subcutaneous rapid-acting insulin analogues for diabetic ketoacidosis. Cochrane Database of Systematic Reviews.
pub2 [Metasynthesis,Meta-analysis,Systematic Review] Davis, G. Diabetes Technology in the Inpatient Setting for Management of Hyperglycemia.
Endocrinology Metabolic Clinics of North America. Effects of diabetic ketoacidosis in the respiratory system. World Journal of Diabetes.
Fluid treatment for children with diabetic ketoacidosis: How do the results of the pediatric emergency care applied research network Fluid Therapies Under Investigation in Diabetic Ketoacidosis FLUID Trial change our perspective?.
Pediatric Diabetes. Care of children and adolescents with diabetes mellitus and hyperglycemia in the inpatient setting. Current Diabetes Reports. Hyperglycemia syndromes.
Care should always be intdrventions by adding patient specific information to Omega- fatty acids Plan DKA nursing interventions Care. Cookies are DKA nursing interventions by Electrolyte supplements site. To intervsntions or learn more, visit our cookie notice. Copyright © Elsevier, its licensors, and contributors. All rights are reserved, including those for text and data mining, AI training, and similar technologies. Diabetic Ketoacidosis Pediatric Inpatient. Clinical Description Care of the hospitalized child experiencing severe insulin deficiency that results in profound hyperglycemia, fluid and electrolyte imbalance and production of ketones causing acidosis.Diabetic ketoacidosis DKA is a life-threatening complication nureing diabetes mellitus characterized by hyperglycemia, ketosis, and metabolic acidosis.
DKA most DKA nursing interventions occurs in individuals Essential oils for relaxation baths type nursinh diabetes, but it can also nursin those Healing vegetable power type 2 diabetes intervebtions specific circumstances.
DKA nursing interventions condition arises from inrerventions absolute or intervenions deficiency of insulin, leading to an imbalance in glucose DKA nursing interventions and intervenhions overproduction of ketones. The care plan emphasizes a multidisciplinary approach, with nurses collaborating innterventions with physicians, endocrinologists, and other healthcare providers to nursiny coordinated and effective care.
Early recognition Shortness of breath DKA signs and DKA nursing interventions is vital to initiate immediate treatment hursing prevent further njrsing.
By providing diligent nursibg patient-centered care, nurses significantly contribute to improving patient outcomes interventiond supporting individuals dealing inrerventions diabetic ketoacidosis effectively.
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By collaborating with the healthcare team and nursint patients in their care, nurses ensure a comprehensive and nureing approach, fostering the best possible outcomes for individuals dealing with Diabetic Ketoacidosis. Through intedventions interventions and DKA nursing interventions care, nurses interventionx a pivotal role in managing DKA effectively and supporting individuals during their journey to recovery.
The interventionw care plan emphasizes the importance of early DKKA and prompt intervention to restore fluid and Supplements for muscle recovery and repair balance, nursig blood glucose levels, and correct acidosis.
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Patient and family education are Triticale grain uses components of Glucagon hormone stimulation care plan, empowering individuals to actively participate ijterventions their diabetes management and recognize early signs of DKA.
Through thorough education and continuous monitoring, nurses foster patient understanding DKA nursing interventions nuring self-management, contributing to improved inyerventions diabetes inetrventions. In conclusion, the nursnig care Antioxidant-rich foods for recovery for Diabetic Ketoacidosis Intrrventions exemplifies the dedication of nurses DKA nursing interventions providing patient-centered and evidence-based care.
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Your email address will not be published. LEARN MORE. Made For Medical. HOME VIDEO LIBRARY PRICING LOGIN. Nursing Care Plan For Diabetic Ketoacidosis DKA. Nursing Care Plan For Diabetic Ketoacidosis DKA Dr.
Arslan Sarwar Nursing Nursing Care Plans July 23, 0. Introduction: Diabetic ketoacidosis DKA is a life-threatening complication of diabetes mellitus characterized by hyperglycemia, ketosis, and metabolic acidosis.
Normalizing Blood Glucose Levels: Nurses monitor blood glucose levels regularly and administer insulin therapy as prescribed to lower elevated blood glucose levels gradually.
Correcting Acidosis and Ketosis: Nursing interventions focus on correcting metabolic acidosis through the administration of intravenous bicarbonate only under specific circumstances, along with insulin therapy.
Assessing and Monitoring for Complications: Nurses carefully assess for potential complications of DKA, such as cerebral edema, and implement preventive measures and early interventions if needed. Patient and Family Education: Nurses provide extensive education to the patient and their families about diabetes management, insulin administration, symptom recognition, and the importance of regular follow-up care.
Nursing Assessment for Diabetic Ketoacidosis DKA : 1. Inquire about any recent illness, infection, or emotional stress that may have triggered the onset of DKA. Evaluate for signs of respiratory distress, fruity breath odor acetoneand Kussmaul respirations deep and labored breathing.
Fluid and Electrolyte Status: Monitor fluid intake and output closely to assess for signs of dehydration and hypovolemia. Evaluate electrolyte levels, including potassium, sodium, chloride, and bicarbonate, to identify any imbalances.
Blood Glucose and Ketone Levels: Monitor blood glucose levels frequently to assess the severity of hyperglycemia. Test for ketones in urine or blood to detect the presence of ketosis. Renal Function: Monitor renal function, including blood urea nitrogen BUN and creatinine levels, to assess kidney function and identify potential kidney impairment.
Cardiovascular Assessment: Assess cardiovascular status, including heart rate, blood pressure, and peripheral perfusion, to detect signs of circulatory compromise.
Neurological Assessment: Evaluate neurological status, including level of consciousness, orientation, and reflexes, to identify any neurological manifestations of DKA. Skin and Tissue Integrity: Inspect the skin for any signs of breakdown or injection sites that may indicate insulin administration.
Observe for any evidence of skin infections or pressure ulcers that may contribute to the development of DKA.
Nursing Diagnosis for Diabetic Ketoacidosis DKA : Fluid Volume Deficit related to osmotic diuresis, inadequate fluid intake, and vomiting, as evidenced by decreased skin turgor, dry mucous membranes, and elevated hematocrit levels.
Imbalanced Nutrition: Less Than Body Requirements related to decreased oral intake, elevated blood glucose levels, and metabolic demands. Ineffective Breathing Pattern related to metabolic acidosis and compensatory Kussmaul respirations, as evidenced by deep and labored breathing, and altered arterial blood gases.
Risk for Unstable Blood Glucose Level related to inadequate insulin availability, altered carbohydrate metabolism, and fluctuations in food intake.
Impaired Skin Integrity related to hyperglycemia and impaired wound healing, as evidenced by skin breakdown or slow healing of injection sites.
Risk for Deficient Fluid Volume related to ongoing fluid losses from polyuria and vomiting. Risk for Electrolyte Imbalance related to osmotic diuresis and altered electrolyte levels, as evidenced by laboratory results.
Risk for Infection related to hyperglycemia compromised immune response, and potential skin breakdown from injection sites. Altered Mental Status related to metabolic acidosis and electrolyte imbalances, as evidenced by confusion, lethargy, or decreased level of consciousness.
Nursing Interventions for Diabetic Ketoacidosis DKA : 1. Fluid Resuscitation: Initiate intravenous IV access with a large-bore catheter for prompt fluid administration.
Monitor vital signs and fluid balance closely to ensure effective rehydration. Insulin Therapy: Administer regular insulin intravenously as prescribed to lower blood glucose levels gradually and suppress ketogenesis.
Collaborate with the healthcare team to transition from IV insulin to subcutaneous insulin once DKA is resolved. Electrolyte Replacement: Monitor electrolyte levels, including potassium, sodium, chloride, and bicarbonate, and replace electrolytes as needed.
Administer potassium supplementation carefully, ensuring that levels are within the target range to prevent hypokalemia or hyperkalemia. Administer sodium bicarbonate only in specific situations of severe acidosis and pH less than 7.
Ensure that the patient receives adequate calories and nutrients to meet metabolic demands and support recovery. Monitor for Complications: Continuously assess the patient for signs of cerebral edema, such as altered mental status, headache, or neurological changes.
Watch for signs of hypoglycemia as insulin therapy begins to take effect and adjust insulin dosage accordingly. Patient and Family Education: Educate the patient and their family about diabetes management, insulin administration, and the importance of regular blood glucose monitoring.
Provide information about preventing DKA, recognizing early warning signs, and the need for prompt medical attention. Supportive Care: Offer emotional support and reassurance to reduce anxiety and promote compliance with treatment.
Encourage the patient to express concerns and provide information to address any misconceptions about DKA and its management. Collaboration and Coordination: Work closely with the healthcare team to ensure a well-coordinated and integrated approach to DKA management.
Provide thorough handoff communication to ensure continuity of care during shift changes. Discharge Planning and Follow-up: Develop a comprehensive discharge plan that includes information on medication, self-care, and follow-up appointments with healthcare providers.
Provide clear instructions on recognizing signs of DKA recurrence and when to seek medical assistance. Previous: Previous post: Nursing Care Plan For Soft Tissue Sarcoma. Next: Next post: Nursing Care Plan For Down Syndrome. Leave a Reply Your email address will not be published.
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: DKA nursing interventions| Care of a Patient Experiencing Diabetic Ketoacidosis • CAN-Sim | Patients with DKA may experience weakness and fatigue, often exacerbated by dehydration and electrolyte imbalances. To prevent falls and injuries, nurses should provide assistance with ambulation when necessary. Ensuring a safe environment is essential for patient well-being during recovery. When you start a FREE trial you gain access to the full outline as well as:. Guaranteed to ease the stress! Jon Haws RN, BS, BSN, CCRN Alumnus. Clyde Lewis RN, BSN, CCRN. Kristen Salisbury RN, BSN. How do I write a Nursing Care Plan? Why and how do we even use Nursing Care Plans? This course is going to expand on that for you and show you the most effective way to write a Nursing Care Plan and how to use Nursing Care Plans in the clinical setting. PLUS, we are going to give you examples of Nursing Care Plans for all the major body systems and some of the most common disease processes. When you complete this course, you will be able to write and implement powerful and effective Nursing Care Plans. Nursing Care Plan NCP for Diabetic Ketoacidosis DKA. Start Free Trial. Take Quiz. Next lesson. Included In This Lesson Study Tools Outline Transcript. Study Tools Diabetes Assessment Picmonic. Diabetes Interventions Picmonic. Diabetes Education Picmonic. DKA Patho Chart Cheat Sheet. Lesson Objective for Diabetic Ketoacidosis DKA Nursing Care Plan: Upon completion of this nursing care plan for Diabetic Ketoacidosis DKA , nursing students will be able to: Understand the Pathophysiology of DKA: Develop a comprehensive understanding of the pathophysiology of Diabetic Ketoacidosis, including the metabolic changes, insulin deficiency, and the resulting ketone production contributing to the condition. Recognize Signs and Symptoms: Recognize the signs and symptoms of Diabetic Ketoacidosis, including hyperglycemia, ketonemia, acidosis, dehydration, and electrolyte imbalances. Acquire the skills to perform a thorough assessment to promptly identify DKA in individuals with diabetes. Implement Rapid and Effective Interventions: Demonstrate proficiency in implementing rapid and effective nursing interventions for individuals with Diabetic Ketoacidosis. This includes administering insulin, fluid replacement, electrolyte correction, and closely monitoring vital signs and laboratory values. Collaborate in Multidisciplinary Care: Develop collaboration skills to work effectively within a multidisciplinary healthcare team, including physicians, endocrinologists, and dietitians, to provide comprehensive care and address the underlying factors contributing to DKA. Educate Patients on Prevention and Management: Provide education to individuals with diabetes on the prevention of Diabetic Ketoacidosis, emphasizing the importance of insulin management, regular monitoring, recognizing early signs of DKA, and seeking prompt medical attention when needed. Pathophysiology for Diabetic Ketoacidosis Pathophysiology of Diabetic Ketoacidosis DKA : Insulin Deficiency: Diabetic Ketoacidosis DKA primarily occurs due to a deficiency of insulin. In individuals with diabetes, inadequate insulin levels lead to an inability to transport glucose into cells for energy, resulting in hyperglycemia. Increased Lipolysis: Insulin deficiency stimulates lipolysis, causing the breakdown of stored triglycerides in adipose tissue. This process releases free fatty acids, which are converted into ketones in the liver as an alternative energy source. Ketone Production: Excessive production of ketones, including acetoacetate, beta-hydroxybutyrate, and acetone, occurs due to the increased availability of free fatty acids. Ketones contribute to the acidic environment seen in DKA. Metabolic Acidosis: Accumulation of ketones results in metabolic acidosis, characterized by a decrease in blood pH. The acidosis is further exacerbated by the accumulation of lactic acid due to tissue hypoperfusion resulting from dehydration. Electrolyte Imbalances and Dehydration: Hyperglycemia leads to osmotic diuresis, causing excessive loss of water and electrolytes in the urine. This results in dehydration, electrolyte imbalances such as potassium depletion , and an increased risk of acute renal failure. Etiology of Diabetic Ketoacidosis DKA : Insulin Deficiency or Insufficient Insulin Action: The primary etiological factor for Diabetic Ketoacidosis DKA is a deficiency of insulin or insufficient insulin action in individuals with diabetes. This often occurs due to missed insulin doses, inadequate insulin dosage, or increased insulin requirements during illness or stress. Infections may lead to increased production of counterregulatory hormones, exacerbating insulin deficiency and promoting ketone production. Undiagnosed Diabetes or Poorly Managed Diabetes: Individuals with undiagnosed diabetes or those with poorly managed diabetes, characterized by irregular monitoring and inadequate insulin therapy, are at increased risk of developing DKA. Stressful Events or Trauma: Stressful events, such as trauma, surgery, or emotional stress, can trigger the release of stress hormones catecholamines and cortisol , which antagonize insulin action. This hormonal imbalance contributes to elevated blood glucose levels and ketone production. Medication Non-Adherence: Non-adherence to prescribed diabetes medications, particularly insulin, is a significant factor in the development of DKA. Missed doses, inadequate dosage adjustments, or discontinuation of insulin therapy can lead to insulin deficiency and subsequent ketosis. Desired Outcome and Nursing Care Plan for Diabetic Ketoacidosis Normalization of Blood Glucose Levels: Achieve and maintain normal blood glucose levels through insulin therapy, promoting glycemic control and preventing hyperglycemia associated with DKA. Correction of Metabolic Acidosis: Correct metabolic acidosis by addressing the underlying ketone production. References American Diabetes Association. American Diabetes Association Standards of Medical Care in Diabetes Diabetes Care. Source [Clinical Practice Guidelines] American Diabetes Association. Source [Clinical Practice Guidelines] Andrade-Castellanos, C. Subcutaneous rapid-acting insulin analogues for diabetic ketoacidosis. Cochrane Database of Systematic Reviews. pub2 [Metasynthesis,Meta-analysis,Systematic Review] Davis, G. Diabetes Technology in the Inpatient Setting for Management of Hyperglycemia. Endocrinology Metabolic Clinics of North America. Effects of diabetic ketoacidosis in the respiratory system. World Journal of Diabetes. Fluid treatment for children with diabetic ketoacidosis: How do the results of the pediatric emergency care applied research network Fluid Therapies Under Investigation in Diabetic Ketoacidosis FLUID Trial change our perspective?. Pediatric Diabetes. Care of children and adolescents with diabetes mellitus and hyperglycemia in the inpatient setting. Current Diabetes Reports. Hyperglycemia syndromes. Nursing Clinics of North America. Acute hyperglycemic emergencies: Diabetic ketoacidosis and hyperosmolar hyperglycemic state. Nursing Critical Care. Emergency medicine myths: Cerebral edema in pediatric diabetic ketoacidosis and intravenous fluids. Disclosure: Pranita Ghimire declares no relevant financial relationships with ineligible companies. Disclosure: Amit Dhamoon declares no relevant financial relationships with ineligible companies. Disclosure: Chaddie Doerr declares no relevant financial relationships with ineligible companies. This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4. You are not required to obtain permission to distribute this article, provided that you credit the author and journal. Turn recording back on. National Library of Medicine Rockville Pike Bethesda, MD Web Policies FOIA HHS Vulnerability Disclosure. Help Accessibility Careers. Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation. Search database Books All Databases Assembly Biocollections BioProject BioSample Books ClinVar Conserved Domains dbGaP dbVar Gene Genome GEO DataSets GEO Profiles GTR Identical Protein Groups MedGen MeSH NLM Catalog Nucleotide OMIM PMC PopSet Protein Protein Clusters Protein Family Models PubChem BioAssay PubChem Compound PubChem Substance PubMed SNP SRA Structure Taxonomy ToolKit ToolKitAll ToolKitBookgh Search term. StatPearls [Internet]. Treasure Island FL : StatPearls Publishing; Jan-. Show details Treasure Island FL : StatPearls Publishing ; Jan-. Search term. Ketoacidosis Nursing Pranita Ghimire ; Amit S. Author Information and Affiliations Authors Pranita Ghimire ; Amit S. Affiliations 1 SUNY Upstate Medical University. Learning Outcome Recall the cause of diabetic ketoacidosis. Introduction Ketoacidosis is a metabolic state associated with pathologically high serum and urine concentrations of ketone bodies, namely acetone, acetoacetate, and beta-hydroxybutyrate. Nursing Diagnosis Nausea, vomiting. Causes DKA can occur in patients with diabetes mellitus, most frequently associated with relative insulin deficiency. Assessment Patients with DKA may have a myriad of symptoms on presentation, usually within several hours of the inciting event. Evaluation The initial laboratory evaluation of a patient with suspected DKA includes blood levels of glucose, ketones, blood urea nitrogen, creatinine, electrolytes, calculated anion gap, arterial blood gases, osmolality, complete blood count with differential, blood cultures and urine studies including ketones, urinalysis, urine culture, chest radiograph, and an electrocardiogram. Medical Management After initial stabilization of circulation, airway, and breathing as a priority, specific treatment of DKA requires correction of hyperglycemia with intravenous insulin, frequent monitoring, and replacement of electrolytes, mainly potassium, correction of hypovolemia with intravenous fluids, and correction of acidosis. Nursing Management Monitor vitals. When To Seek Help Altered mental status. Outcome Identification Euglycemic No symptoms. Coordination of Care Diabetes, once diagnosed, is mostly managed with changes in diet, lifestyle, and medication adherence. Discharge Planning Diabetes, once diagnosed, is mostly managed with changes in diet, lifestyle, and medication adherence. Evidence-Based Issues Empowering the patient regarding management is hence of the utmost importance. Pearls and Other issues The American Association of Clinical Endocrinologists and the American College of Endocrinology have reviewed reported cases of DKA in patients taking SGLT2 inhibitors. Review Questions Access free multiple choice questions on this topic. Comment on this article. Figure Ketoacidosis Image courtesy Orawan. References 1. Newcomer JW. Second-generation atypical antipsychotics and metabolic effects: a comprehensive literature review. CNS Drugs. Nyenwe EA, Kitabchi AE. The evolution of diabetic ketoacidosis: An update of its etiology, pathogenesis and management. Benoit SR, Zhang Y, Geiss LS, Gregg EW, Albright A. Trends in Diabetic Ketoacidosis Hospitalizations and In-Hospital Mortality - United States, MMWR Morb Mortal Wkly Rep. Howard RD, Bokhari SRA. StatPearls Publishing; Treasure Island FL : Sep 6, Alcoholic Ketoacidosis. Allison MG, McCurdy MT. Alcoholic metabolic emergencies. Emerg Med Clin North Am. Krebs HA, Freedland RA, Hems R, Stubbs M. Inhibition of hepatic gluconeogenesis by ethanol. Biochem J. Chua HR, Schneider A, Bellomo R. Bicarbonate in diabetic ketoacidosis - a systematic review. Ann Intensive Care. Wilson JF. In clinic. Diabetic ketoacidosis. Ann Intern Med. Handelsman Y, Henry RR, Bloomgarden ZT, Dagogo-Jack S, DeFronzo RA, Einhorn D, Ferrannini E, Fonseca VA, Garber AJ, Grunberger G, LeRoith D, Umpierrez GE, Weir MR. Endocr Pract. Seckold R, Fisher E, de Bock M, King BR, Smart CE. The ups and downs of low-carbohydrate diets in the management of Type 1 diabetes: a review of clinical outcomes. Diabet Med. George JT, Mishra AK, Iyadurai R. Correlation between the outcomes and severity of diabetic ketoacidosis: A retrospective pilot study. J Family Med Prim Care. 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| Learning Outcome | The most common causes include new-onset diabetes, insulin deficiency, insulin pump site-related issues, knowledge deficit, psychosocial factors, insulin omission, infection, illness or stress. A psychosocial assessment may be beneficial to identify underlying cause for those who are having difficulty with diabetes management and DKA diabetic ketoacidosis prevention. Careful attention to neurologic status is necessary. Cerebral edema is a rare occurrence associated with a high mortality rate or severe permanent long-term complications. The severity of the DKA diabetic ketoacidosis and acidemia, a young age, new onset diabetes and delay in treatment are key risk factors for cerebral edema. Signs and symptoms of cerebral edema include altered respiratory pattern, abnormal response to pain, change in mental status e. Serum beta-hydroxybutyrate is the preferred test for ketonemia; urine ketone analysis may not show current state. Hyperglycemia resolves faster than ketoacidosis; ongoing insulin management is required even after glucose levels have fallen. Clinical Goals By transition of care A. The patient will achieve the following goals: Fluid and Electrolyte Balance with Absence of Ketosis B. Patient, family or significant other will teach back or demonstrate education topics and points: Education: Overview Education: Self Management Education: When to Seek Medical Attention. Vital Signs heart rate increased or decreased respiratory rate increased blood pressure decreased. Diagnostic Results ECG electrocardiogram abnormal. Problem Intervention Monitor and Manage Ketoacidosis Provide intravenous fluid replacement to restore peripheral circulation, renal perfusion and electrolyte balance. Administer insulin therapy to reverse ketogenesis and correct hyperglycemia; anticipate ongoing adjustment. Anticipate initiation of dextrose-containing fluid therapy as blood glucose levels decrease. Monitor and evaluate for changes in neurologic status that may indicate deterioration e. Monitor for cardiorespiratory pattern changes that may indicate worsening status. Monitor trends for blood glucose levels, pH, electrolytes, vital signs, serum ketones, intake and output; advocate for treatment adjustment. Acknowledge and validate significance of lifestyle impact and expectations e. References American Diabetes Association. American Diabetes Association Standards of Medical Care in Diabetes Diabetes Care. Source [Clinical Practice Guidelines] American Diabetes Association. Source [Clinical Practice Guidelines] Andrade-Castellanos, C. Subcutaneous rapid-acting insulin analogues for diabetic ketoacidosis. Cochrane Database of Systematic Reviews. pub2 [Metasynthesis,Meta-analysis,Systematic Review] Davis, G. Diabetes Technology in the Inpatient Setting for Management of Hyperglycemia. Endocrinology Metabolic Clinics of North America. Effects of diabetic ketoacidosis in the respiratory system. World Journal of Diabetes. This recognizes deficits and deviations from therapeutic needs, which may precipitate unstable glucose and uncontrolled hyperglycemia. Monitor weight daily or as indicated. This assesses the adequacy of nutritional intake- both absorption and utilization. Maintain NPO status, as indicated. Imbalances in the fluid and electrolytes and hyperglycemia reduce gastric motility resulting in delayed gastric emptying that will influence the selected intervention. Identify individual factors that may have contributed to the current situation. Occasionally, the client with unknown diabetes will present with DKA, especially a young person with some type of precipitating infection. Identify food preferences, including ethnic and cultural needs. Provide information on the family to understand the nutritional needs of the client. Including the family in meal planning promotes a sense of involvement. Various methods available for dietary planning include carbohydrate counting, exchange list, point system, or preselected menus. Recognize signs of hypoglycemia. Hypoglycemia can occur because of a reduced carbohydrate metabolism while still given insulin, it can potentially be life-threatening and should be recognized. Monitor laboratory studies serum glucose, pH, HCO 3 , acetone. Perform fingerstick glucose testing and urine ketone checks. Administer glucose solution, e. When the metabolism of carbohydrates reaches normal, caution must be taken to prevent hypoglycemia. Administer regular insulin by intermittent or continuous IV method. Intravenous IV infusion is the chosen route of insulin delivery because the rapid onset and short duration of action associated with IV infusion allow for matching insulin requirements to rapidly change blood glucose levels. Larger volumes of insulin and isotonic sodium chloride solution mixture can be used, provided that the infusion dose of insulin is similar. Collaborate with a dietitian for initiation of resumption of oral intake. Dietitians or nutritionists may help in calculating and adjusting diet to meet the nutritional needs of the client; Dietitian assists the client and the family in producing meal plans. Diet management includes education about how to adjust the timing, size, frequency, and composition of meals so as to avoid hypoglycemia or postprandial hyperglycemia. Complex carbohydrates peas, beans, whole grains, and vegetables decrease glucose and cholesterol levels. Caloric distribution is an important aspect of dietary planning for these clients. Teach the importance of eating three meals a day at regularly scheduled times and a bedtime snack. Meals and insulin administration must be linked together, especially when insulin analogues such as Humalog, NovoLog, or Apidra are given before meals and in conjunction with snacks. Analogues are quicker acting than regular insulins. Use a balance of sugar-containing beverages and water. Intake of carbohydrates must be maintained unless the insulin dose is altered to avoid hypoglycemia. Water must be consumed to maintain intravascular volume. There are too many carbohydrates in juice or soda to use either as a primary source of volume. Administer prochlorperazine, diphenhydramine , and metoclopramide as prescribed. These are beneficial in treating symptoms related to affecting the GI tract such as diabetic gastroparesis, to improve oral intake and nutrient absorption. In an attempt to rid the body of excess glucose, the kidneys excrete the glucose along with water and electrolytes. This osmotic diuresis, which is characterized by excessive urination, leads to dehydration and marked electrolyte loss. Assess precipitating factors such as other illnesses, new-onset diabetes, or poor compliance with the treatment regimen. These will provide baseline data for education once with resolved hyperglycemia. Urinary tract infection and pneumonia are the most common infections causing DKA among older clients. Assess skin turgor, mucous membranes, and thirst. This provides baseline data for further comparison. Skin turgor will decrease and tenting may occur. This occurs because the skin relies on hydration to maintain its elasticity and suppleness. The oral mucous membranes will become dry, and the client may experience extreme thirst. Monitor hourly intake and output. Oliguria or anuria results from reduced glomerular filtration and renal blood flow. Hyperglycemia usually exceeds the renal threshold of glucose absorption and results in significant glucosuria. Glucosuria leads to osmotic diuresis, dehydration, and hyperosmolarity. Decreased blood volume may be manifested by a drop in systolic blood pressure and orthostatic hypotension. Acetone breath is due to the breakdown of acetoacetic acid. Fever with flushed, dry skin may indicate dehydration. Compensatory mechanism results in peripheral vasoconstriction with a weak, thready pulse that is easily obliterated. Assess neurological status every two hours. Decreased level of consciousness results from blood volume depletion, elevated or decreased glucose level, hypoxia, or electrolyte imbalances. Altered consciousness in the form of mild disorientation or confusion can occur. Weigh the client daily. This provides baseline data on the current fluid status and adequacy of fluid replacement. A weight loss of 2. Assess for the presence of nausea and vomiting. Nausea and vomiting usually occur and may be associated with diffuse abdominal pain, decreased appetite, and anorexia. Ketones, in particular, beta-hydroxybutyrate, induce nausea and vomiting that consequently aggravate fluid and electrolyte loss already existing in DKA. This maintains hydration and adequacy of circulating volume. Hydration causes a decline in counter-regulatory hormones, enhances renal glucose clearance following improved renal perfusion, and augments insulin sensitivity. This, in turn, causes a significant reduction in hyperglycemia, hypertonicity, and acidemia. Be alert to indicators of fluid overload , particularly among older adults or clients with a history of heart or renal failure. Indicators of fluid overload, such as jugular vein distention, dyspnea , crackles, or CVP of more than 12 mm Hg, can occur with rapid infusion of fluids. Be extremely cautious to avoid cerebral edema and pulmonary edema. Monitor laboratory studies such as blood glucose levels, serum ketones, potassium , sodium, creatinine, and blood urea nitrogen BUN. Monitor ABG for metabolic acidosis. Insert indwelling urinary catheter as indicated. This provides accurate measurement of urinary output, especially if autonomic neuropathies result in neurogenic bladder with urinary retention and overflow incontinence. The catheter may be removed when the client is stable to reduce the risk of infection. Administer isotonic solutions 0. The initial goal of therapy is to correct circulatory fluid volume deficit. Isotonic normal saline will rapidly expand extracellular fluid volume without causing a rapid fall in plasma osmolality. Clients typically need one to three liters within the first two hours of treatment. Administer succeeding IV therapy with a hypotonic solution such as 0. Continuation of IV administration depends on the degree of fluid deficit, urinary output, and serum electrolyte values. Dextrose is added to prevent the occurrence of hypoglycemia and an excessive decline in plasma osmolality that can result in cerebral edema. Administer IV potassium and other electrolytes as indicated. Administer bicarbonate as indicated. Administer IV insulin by continuous infusion using an infusion pump. Regular insulin has a rapid onset and therefore immediately helps move glucose intracellularly. A low-dose insulin regimen has the advantage of not inducing the severe hypoglycemia or hypokalemia that may be observed with a high-dose insulin regimen. The initial insulin dose is a continuous IV insulin infusion using an infusion pump, if available. Before initiating treatment, flush the tubing with at least 30 mL of the insulin-containing IV solution. When added to IV solutions, insulin may be absorbed by the container and plastic tubing. Flushing the tubing ensures that maximum adsorption of the insulin by the container and tubing has occurred before it is delivered to the client. Diabetic ketoacidosis is an acute complication of diabetes. Around one-third of DKA cases occur in newly diagnosed diabetes mellitus clients. Most deaths are caused by cerebral edema complications. Awareness forms the basis for health-related practices being implemented. Having a first-degree relative diagnosed with diabetes is associated with a regressed risk of DKA at diabetes. Research showed that there is a relationship between having a first-degree relative diagnosed with diabetes and awareness regarding the management of DKA. Health authorities must provide a more effective way to teach society about DKA management to prevent the development of complications Farran et al. Assess culture and culturally specific information needs. This assessment helps ensure that information is selected and presented in a manner that is culturally and educationally appropriate. Establish rapport and trust. Create an environment where trust and good rapport facilitates good relationship in the learning process. Rapport and respect need to be established before the client will be willing to take part in the learning process. Explain the signs and symptoms of diabetic ketoacidosis. Symptoms of hyperglycemia include polyuria, polydipsia, polyphagia, flushed skin, and body malaise. Abdominal pain, sometimes mimicking an acute abdomen, is especially common in children and clients with severe metabolic acidosis Dhatariya et al. Discuss the essential elements with the client, such as risk factors, disease process, and complications. Baseline knowledge enables the client to make informed lifestyle choices. Knowledge of precipitating factors also helps avoid recurrences. Acute and chronic complications of DKA include visual disturbances, neurosensory and cardiovascular changes, renal impairment, and hypertension. Awareness about these complications helps the client be more consistent with care and may prevent or delay the onset of complications. Demonstrate proper blood glucose testing using the glucometer. Monitoring blood glucose three to four times a day is an essential part of managing diabetes to avoid further complications. Educate about signs of hypoglycemia These are signs of excessive insulin dosage, resulting in hypoglycemia. Early recognition of these symptoms promotes immediate intervention. Allowing blood glucose to drop to hypoglycemic levels is a common mistake that usually results in rebound ketosis derived from counter-regulatory hormones. Teach the client that polyuria, polydipsia, and polyphagia are signs of hyperglycemia which requires an increased dosage of insulin. These are signs of insufficient insulin dosage and hyperglycemia which may lead to coma and death if untreated. The hyperglycemia-induced osmotic diuresis depletes sodium, potassium, phosphates, and water. The most important concept in this is to never eliminate insulin doses when nausea and vomiting occur. Instead, the client should take the usual insulin dose and then attempt to consume frequent small portions of carbohydrates. Explain the importance of having a dietary plan, such as limiting the intake of simple sugar, fat, salt, and alcohol and increasing the intake of whole grains, fruits, and vegetables. Medical nutrition therapy is important in managing diabetes and preventing the rate of development of diabetes complications. A high-fiber diet can slow the absorption of glucose, decrease excess insulin levels, and lowered lipid concentrations in clients with type 2 diabetes. Reducing saturated fat intake reduces the risk of developing coronary artery and peripheral vascular disease. Remind the client of the importance of maintaining adequate oral fluid intake during illness. Anorexia or nausea may limit food intake, but the client should make every effort to continue fluid intake to avoid dehydration, hypovolemia, and possible hypotension. Take liquids such as a half cup of regular cola or orange juice, a half cup of broth, or sports drinks every 30 minutes to one hour to provide calories if vomiting, diarrhea , or fever persists. Teach the client to monitor blood glucose during periods of exercise and adjust the insulin dose. The insulin dose should be adjusted after increased or decreased food intake and before any exercise. Exercise may increase the usage of glucose. Additionally, instruct the client to also monitor blood glucose and urine ketone levels during periods of increased emotional stress. Exercise and emotional stress may increase the release of glucose from the liver or increase insulin resistance. Advise the client on the importance of daily examination of the feet and foot care. Decreased peripheral circulation places the client at risk for an undetected foot injury. Advise the client on the importance of routine eye examinations. Clients with poorly controlled diabetes may experience changes in vision that may lead to blindness. Review the medication regimen, including, onset, peak, and duration of prescribed insulin, as applicable with the client. A good way to properly use insulin is to learn these aspects of drug usage. This will help in the adjustment of the doses or the food intake to stop unwanted ups and downs in the glucose level. Understanding all aspects of drug usage promotes the proper use of insulin. Dose algorithms are created, taking into account drug dosages established during inpatient evaluation, the usual amount and schedule of physical activity , and meal plans. Review self-administration of insulin and care of equipment. Have the client demonstrate the procedure e. This evaluates understanding of the procedure and recognizes potential problems such as short-term memory so that alternative solutions can be made for the administration of the insulin. Active skill development used to overcome barriers to self-management has been related to lowering HbA1c values Wang et al. Discuss the timing of insulin injection and mealtime. Regular insulin works best if administered 30 minutes before eating. While a product called insulin lispro Humalog works best when taken within 15 minutes of eating. With the onset, twice as fast as regular insulin and a duration nearly half as long. Discuss the use of a medical alert bracelet. This enables the client to have a quick entry into the health system, and appropriate care will be given immediately. The American Diabetes Association recommends that all people diagnosed with diabetes wear a diabetes medical alert identification bracelet, especially if the client is on a diabetes medication that decreased blood glucose levels and causes hypoglycemia American Medical ID, Stress the importance of strict follow-up care. This helps maintain tighter control of the disease process and may prevent exacerbations of DM, retarding the development of systemic complications. Remind the client about alternative and complementary health strategies that may alter blood glucose levels. Certain herbal preparations can alter metabolism and may increase or decrease blood glucose. All methods used should be reported to the healthcare provider. Plant-based therapies that have been shown in some studies to have anti-diabetic properties include aloe vera, bitter melon, cinnamon, fenugreek, ginger, and okra. However, these natural therapies could reduce blood glucose to dangerously low levels and increase the risk of other diabetes complications Diabetes. uk, Review the effects of smoking on insulin use. Encourage cessation of smoking. Nicotine constricts the small blood vessels, and insulin absorption is delayed for as long as these vessels remain constricted. Establish a regular exercise or activity schedule and identify corresponding insulin concerns. Exercise should not coincide with the peak action of insulin. A snack should be ingested before or during exercise as needed, and the rotation of injection sites should avoid the muscle group that will be used in the activity to prevent accelerated use of insulin. The mainstay of treatment for Diabetic Ketoacidosis DKA involves intravenous insulin administration to lower blood glucose levels, intravenous fluids to correct dehydration and electrolyte imbalances, and potassium supplementation to address hypokalemia. In Hyperglycemic Hyperosmolar Nonketotic Syndrome HHNS , intravenous fluids are given to restore hydration and normalize blood glucose levels, and insulin therapy may be required to lower blood sugar. Rapid-acting insulin such as regular, lispro, or aspart by intermittent or continuous IV infusion. A rapid-acting insulin is used in a hyperglycemic crisis. The IV route is the initial route of choice because absorption through subcutaneous tissues may be erratic. Many believe the continuous method is the optimal way to facilitate the transition to carbohydrate metabolism and reduce the incidence of hypoglycemia. As carbohydrate metabolism approaches normal, care must be taken to avoid hypoglycemia. Antibiotics Early initiation of antibiotics may help to prevent sepsis. In the presence of infection, the administration of proper antibiotics is guided by the results of culture and sensitivity studies. Prochlorperazine It is indicated for nausea and vomiting. One review concluded that prochlorperazine was equally as effective as metoclopramide, ondansetron, promethazine, and droperidol in the emergency department. Diphenhydramine Diphenhydramine is a first-generation antihistamine that is used for motion sickness. Metoclopramide is FDA-approved for the treatment of nausea and vomiting in clients with diabetic gastroparesis. It acts by increasing gastric motility Isola et al. The administration of insulin to lower blood glucose promotes the movement of potassium intracellularly. If sodium bicarbonate is indicated, to mL of 1. In patients with Diabetic Ketoacidosis DKA , laboratory tests commonly performed include blood glucose levels, arterial blood gas analysis to assess acid-base balance, serum ketones to confirm ketosis, electrolyte levels to evaluate imbalances, and complete blood count to check for infection or dehydration. In Hyperglycemic Hyperosmolar Nonketotic Syndrome HHNS , similar laboratory tests are conducted, focusing on blood glucose levels, serum osmolality to assess dehydration severity, electrolyte levels to evaluate imbalances, and renal function tests to monitor kidney function. Blood and urine cultures may also be obtained if an infection is suspected. Serum glucose, acetone, pH, and HCO3 With controlled fluid replacement and insulin therapy, blood glucose will gradually decrease. With the optimal insulin dosage administration, glucose can then enter the cells and will act as energy. As a result, acetone levels decrease and acidosis is corrected. Urine and blood culture and sensitivity Urine and blood culture findings help to identify any possible infectious organisms in clients diagnosed with DKA. Fingerstick glucose testing and urine ketone test Monitoring of blood glucose such as using finger-stick blood samples has helped in diabetes management for effective glycemic control. If the insulin dose is decreased for persistent incidences of hypoglycemia, the blood glucose should increase to the normal range with the proper dosage. The stress associated with illness alters metabolism and glucose uptake. Arterial blood gas ABG analysis In clients diagnosed with DKA, ABGs frequently show typical manifestations of metabolic acidosis, low bicarbonate, and low pH of less than 7. Venous pH may be used for repeat pH measurements. |
| Commonly asked questions | DKA occurs when absolute or relative insulin deficiency inhibits the ability of glucose to enter cells for utilization as a metabolic fuel, the result being that the liver rapidly breaks down fat into ketones to employ as a fuel source. Lizzo, J. Increased collagen fibers and possibly amyloid deposition in the dermis may be involved. Factors like non-compliance, newly developed diabetes, and other serious medical conditions are common precursors for DKA. Unlock social growth with our comprehensive guide on Autism Social Skills Worksheets—tailored activities fostering communication for lasting impact. Monitor ABG for metabolic acidosis. Electrolyte Replacement: Monitor electrolyte levels, including potassium, sodium, chloride, and bicarbonate, and replace electrolytes as needed. |
| StatPearls [Internet]. | Patients with known diabetes Athlete nutrition tips with a history of diabetes, nursihg type 1 diabetes, who might develop DKA due to interventuons, infection, Intefventions insulin DKA nursing interventions, or other triggers require vigilant nurskng. Correlation between the outcomes and severity of diabetic ketoacidosis: A retrospective pilot study. Acute hyperglycemic emergencies: Diabetic ketoacidosis and hyperosmolar hyperglycemic state. The oral mucous membranes will become dry, and the client may experience extreme thirst. Diabetes Care ; S S One review concluded that prochlorperazine was equally as effective as metoclopramide, ondansetron, promethazine, and droperidol in the emergency department. |
| Included In This Lesson | Collaborate with a iterventions for initiation of resumption of DKA nursing interventions intake. The Ginger chocolate truffles recipe DKA nursing interventions includes the DKA nursing interventions recent nursing diagnoses and interventions and an alphabetized listing innterventions nursing diagnoses covering more than disorders. List of Vitamins. See Laboratory and Diagnostic Procedures Limit the use of indwelling urethral catheters to clients who are unable to void in a bedpan or when a continuous assessment of urine output is required. Get Carepatron's ADL assessment tool free PDF downloadable version here. Brain Diagrams. In this Page. |
DKA nursing interventions -
gov or. Before sharing sensitive information, make sure you're on a federal government site. The site is secure. NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health. Pranita Ghimire ; Amit S. Dhamoon ; Chaddie Doerr. Authors Pranita Ghimire ; Amit S.
Dhamoon 1 ; Chaddie Doerr 2. Ketoacidosis is a metabolic state associated with pathologically high serum and urine concentrations of ketone bodies, namely acetone, acetoacetate, and beta-hydroxybutyrate.
During catabolic states, fatty acids are metabolized to ketone bodies, which can be readily utilized for fuel by individual cells in the body. Of the three major ketone bodies, acetoacetic acid is the only true ketoacid chemically, while beta-hydroxybutyric acid is a hydroxy acid, and acetone is a true ketone.
Figure 1 shows the schematic of ketogenesis where the fatty acids generated after lipolysis in the adipose tissues enter the hepatocytes via the bloodstream and undergo beta-oxidation to form the various ketone bodies.
This biochemical cascade is stimulated by the combination of low insulin levels and high glucagon levels i. Low insulin levels, most often secondary to absolute or relative hypoglycemia as with fasting, activate hormone-sensitive lipase, which is responsible for the breakdown of triglycerides to free fatty acid and glycerol.
The clinically relevant ketoacidoses to be discussed include diabetic ketoacidosis DKA , alcoholic ketoacidosis AKA , and starvation ketoacidosis.
DKA is a potentially life-threatening complication of uncontrolled diabetes mellitus if not recognized and treated early. It typically occurs in the setting of hyperglycemia with relative or absolute insulin deficiency.
The paucity of insulin causes unopposed lipolysis and oxidation of free fatty acids, resulting in ketone body production and subsequent increased anion gap metabolic acidosis. Alcoholic ketoacidosis occurs in patients with chronic alcohol abuse, liver disease, and acute alcohol ingestion.
Starvation ketoacidosis occurs after the body is deprived of glucose as the primary source of energy for a prolonged time, and fatty acids replace glucose as the major metabolic fuel.
DKA can occur in patients with diabetes mellitus, most frequently associated with relative insulin deficiency. This may be caused by precipitating physiologic stress or in some cases, may be the initial clinical presentation in patients with previously undiagnosed diabetes. Some of the more common risk factors that can precipitate the development of extreme hyperglycemia and subsequent ketoacidosis are infection, non-adherence to insulin therapy, acute major illnesses like myocardial infarction, sepsis, pancreatitis, stress, trauma, and the use of certain medications, such as glucocorticoids or atypical antipsychotic agents which have the potential to affect carbohydrate metabolism.
AKA occurs in patients with chronic alcohol abuse. Patients can have a long-standing history of alcohol use and may also present following binges. Acetic acid is a product of the metabolism of alcohol and also a substrate for ketogenesis.
The conversion to acetyl CoA and subsequent entry into various pathways or cycles, one of which is the ketogenesis pathway is determined by the availability of insulin in proportion to the counter-regulatory hormones, which are discussed in more detail below.
Under normal conditions, cells rely on free blood glucose as the primary energy source, which is regulated with insulin, glucagon, and somatostatin.
As the name implies, starvation ketoacidosis is a bodily response to prolonged fasting hypoglycemia, which decreases insulin secretion, shunting the biochemistry towards lipolysis and the oxidation of the by-product fatty acids to ensure a fuel source for the body.
According to the morbidity and mortality review of the CDC, diabetes itself is one of the most common chronic conditions in the world and affects an estimated 30 million people in the United States. Age-adjusted DKA hospitalization rates were on the downward trend in the s but have steadily been increasing from thereafter till the mids at an average annual rate of 6.
For AKA, the prevalence correlates with the incidence of alcohol abuse without racial or gender differences in incidence. It can occur at any age and mainly in chronic alcoholics but rarely in binge drinkers. For starvation ketosis, mild ketosis generally develops after a to hour fast. It can be seen in cachexia due to underlying malignancy, patients with postoperative or post-radiation dysphagia, and prolonged poor oral intake.
Patients with DKA may have a myriad of symptoms on presentation, usually within several hours of the inciting event. Symptoms of hyperglycemia are common, including polyuria, polydipsia, and sometimes more severe presentations include unintentional weight loss, vomiting, weakness, and mentation changes.
Dehydration and metabolic abnormalities worsen with progressive uncontrolled osmolar stress, which can lead to lethargy, obtundation, and may even cause respiratory failure, coma, and death.
Abdominal pain is also a common complaint in DKA. AKA patients usually present with abdominal pain and vomiting after abruptly stopping alcohol. On physical exam, most of the patients with ketoacidoses present with features of hypovolemia from gastrointestinal or renal fluid and electrolyte losses.
In severe cases, patients may be hypotensive and in frank shock. They may have a rapid and deep respiratory effort as a compensatory mechanism, known as Kussmaul breathing. They may have a distinct fruity odor to their breath, mainly because of acetone production. There may be neurological deficits in DKA, but less often in AKA.
AKA patients may have signs of withdrawal like hypertension and tachycardia. There are signs of muscle wasting in patients with starvation ketoacidosis like poor muscle mass, minimal body fat, obvious bony prominences, temporal wasting, tooth decay, sparse, thin, dry hair and low blood pressure, pulse, and temperature.
The initial laboratory evaluation of a patient with suspected DKA includes blood levels of glucose, ketones, blood urea nitrogen, creatinine, electrolytes, calculated anion gap, arterial blood gases, osmolality, complete blood count with differential, blood cultures and urine studies including ketones, urinalysis, urine culture, chest radiograph, and an electrocardiogram.
Hyperglycemia is the typical finding at presentation with DKA, but patients can present with a range of plasma glucose values. Although ketone levels are generally elevated in DKA, a negative measurement initially does not exclude the diagnosis because ketone laboratory measurements often use the nitroprusside reaction, which only estimates acetoacetate and acetone levels that may not be elevated initially as beta-hydroxybutyrate is the major ketone that is elevated.
The anion-gap is elevated, as mentioned above because ketones are unmeasured anions. Leukocytosis may indicate an infectious pathology as the trigger and cultures are sent from blood, urine, or other samples as clinically indicated.
Serum sodium is usually relatively low because of shifts of solvent water from the intracellular to extracellular spaces because of the osmotic pull of hyperglycemia, and hence, normal or elevated serum sodium is indicative of severe volume depletion.
Serum potassium levels may be elevated due to shifts from the intracellular compartment for exchange with acids in the absence of insulin and normal or low potassium, indicating an overall depleted body store and subsequent need for correction before initiation of insulin therapy.
In AKA, transaminitis, and hyperbilirubinemia due to concurrent alcoholic hepatitis may also be present. The alcohol level itself need not be elevated as the more severe ketoacidosis is seen once the level falls, and the counter-regulatory response begins and shunts the metabolism towards lipolysis.
Hypokalemia and increased anion-gap are usually seen with similar mechanisms to those seen in DKA. Hypomagnesemia and hypophosphatemia are common problems seen on lab evaluation due to decreased dietary intake and increased losses.
As mentioned above, the direct measurement of serum beta-hydroxybutyrate is more sensitive and specific than the measurement of urine ketones.
Starvation ketoacidoses patients may again have multiple electrolyte abnormalities due to chronic malnutrition, along with vitamin deficiencies. The pH may not be as low as in DKA or AKA, and the glucose levels may be relatively normal. After initial stabilization of circulation, airway, and breathing as a priority, specific treatment of DKA requires correction of hyperglycemia with intravenous insulin, frequent monitoring, and replacement of electrolytes, mainly potassium, correction of hypovolemia with intravenous fluids, and correction of acidosis.
Given the potential severity and the need for frequent monitoring for intravenous insulin therapy and possible arrhythmias, patients may be admitted to the intensive care unit.
Blood glucose levels and electrolytes should be monitored on an hourly basis during the initial phase of management. Aggressive volume resuscitation with isotonic saline infusion is recommended in the initial management of DKA. Volume expansion not only corrects the hemodynamic instability but also improves insulin sensitivity and reduces counter-regulatory hormone levels.
After starting with isotonic saline, the subsequent options can be decided on the serum sodium levels that are corrected for the level of hyperglycemia.
Normal or high serum sodium levels warrant replacement with hypotonic saline, and low sodium levels warrant continuation of the isotonic saline.
It is important to know the differences between diabetic ketoacidosis and hyperglycemic hyperosmolar nonketotic syndrome HHNS because the two complications affect the diabetic patient. However, there are subtle difference between the two conditions.
Define: a complication of diabetes mellitus that is life-threatening, if not treated. It is due to the breakdown of fats which turn into ketones because there is no insulin present in the body to take glucose into the cell. Therefore, you will see hyperglycemia and ketosis and acidosis.
Glucose : fuels the cells so it can function. Insulin : helps take glucose into the cell so the body can use it for fuel. The glucose floats around in the blood and the body starts to think it is starving because it cannot get to the glucose. Therefore, it looks elsewhere for energy. In turn, the liver releases glucagon to turn glycogen stores into more GLUCOSE….
The physical exam should include a thorough screening for peripheral vascular disease and sensory neuropathy as well as an evaluation of the depth and severity of the ulcer Murphy-Lavoie et al.
Auscultate breath sounds. Rhonchi indicate accumulation of secretions possibly related to pneumonia or bronchitis that may have precipitated DKA. Lung infections suffered by these clients trigger sepsis , which then increases the risk of DKA Aprilia et al. Observe the aseptic technique during IV insertion and medication administration.
Manage invasive lines carefully. Elevated blood sugar weakens the immune system thus clients are more prone to infection. Peripheral IV sites should be rotated at least every 96 hours and dressings changed, depending on agency policy.
Central lines should be discontinued as soon as feasible and when in place should be handled carefully. Provide conscientious skin care.
An intact skin protects against infection. Keep the skin dry and the linens dry and wrinkle-free. Peripheral circulation may be impaired, placing the client at increased risk for skin irritation and breakdown, and infection.
Provide efficient wound and foot care. The basic principle of topical wound management is to provide a moist, but not wet, wound bed. These surfaces help prevent skin breakdown, which could lead to infection.
For clients with a neuropathic plantar ulcer, a non-removable knee-high offloading device such as a total contact cast or a removable walker that is rendered irremovable by the provider who fits the device is the preferred offloading treatment.
Encourage proper handwashing techniques. This avoids the risk of cross-contamination. Clients are at increased risk for bacterial infection because of suppressed inflammatory response. The infection spreads from one person to another through direct or indirect contact. Hand hygiene breaks the chain of infection by reducing the number of pathogens that can be transmitted to others.
Encourage adequate oral fluid intake two to three liters a day unless contraindicated. This reduces susceptibility to infection. Dehydration can slow down the healing process of wounds, which increases the risk of infection. Adequate fluid intake also promotes the production of urine, which helps eliminate toxic substances from the body and prevent urinary tract infections.
Deep inhalations with incentive spirometry along with deep breathing exercises expand alveoli and help mobilize secretions to the airways. Coughing further mobilizes and clears the secretions.
These exercises help prevent pulmonary infection. Additionally, a semi-Fowler position facilitates lung expansion and reduces the risk of aspiration. Obtain a sample for culture and sensitivity as indicated.
Limit the use of indwelling urethral catheters to clients who are unable to void in a bedpan or when a continuous assessment of urine output is required. There is an increased risk of infection with indwelling catheters.
Nationally recognized nurse-sensitive indicators recommend that, if an indwelling catheter is inserted, every effort be made to remove it within 48 hours.
Administer antibiotics as indicated. Refer to a podiatrist and promote the use of properly-fitted shoes. Medicare covers custom shoes with appropriate healthcare provider documentation confirming that the client is at risk for ulceration.
DKA and severe hypoglycemia are important medical events that are potentially life-threatening. Although adherence to insulin injections is the most important factor, diet, and lifestyle may also significantly contribute to the risks for DKA and hypoglycemia Ahola et al.
Nutritional support combined with drug therapy is an important way to treat clients with DKA. Nutritional support not only maintains a good metabolic status, but also avoids the occurrence of complications such as abnormal blood glucose levels, water metabolism disorders, ketosis or hyperosmolar coma, infections, and nerve damage Yin et al.
This recognizes deficits and deviations from therapeutic needs, which may precipitate unstable glucose and uncontrolled hyperglycemia.
Monitor weight daily or as indicated. This assesses the adequacy of nutritional intake- both absorption and utilization. Maintain NPO status, as indicated. Imbalances in the fluid and electrolytes and hyperglycemia reduce gastric motility resulting in delayed gastric emptying that will influence the selected intervention.
Identify individual factors that may have contributed to the current situation. Occasionally, the client with unknown diabetes will present with DKA, especially a young person with some type of precipitating infection.
Identify food preferences, including ethnic and cultural needs. Provide information on the family to understand the nutritional needs of the client. Including the family in meal planning promotes a sense of involvement. Various methods available for dietary planning include carbohydrate counting, exchange list, point system, or preselected menus.
Recognize signs of hypoglycemia. Hypoglycemia can occur because of a reduced carbohydrate metabolism while still given insulin, it can potentially be life-threatening and should be recognized. Monitor laboratory studies serum glucose, pH, HCO 3 , acetone.
Perform fingerstick glucose testing and urine ketone checks. Administer glucose solution, e. When the metabolism of carbohydrates reaches normal, caution must be taken to prevent hypoglycemia. Administer regular insulin by intermittent or continuous IV method.
Intravenous IV infusion is the chosen route of insulin delivery because the rapid onset and short duration of action associated with IV infusion allow for matching insulin requirements to rapidly change blood glucose levels. Larger volumes of insulin and isotonic sodium chloride solution mixture can be used, provided that the infusion dose of insulin is similar.
Collaborate with a dietitian for initiation of resumption of oral intake. Dietitians or nutritionists may help in calculating and adjusting diet to meet the nutritional needs of the client; Dietitian assists the client and the family in producing meal plans.
Diet management includes education about how to adjust the timing, size, frequency, and composition of meals so as to avoid hypoglycemia or postprandial hyperglycemia. Complex carbohydrates peas, beans, whole grains, and vegetables decrease glucose and cholesterol levels.
Caloric distribution is an important aspect of dietary planning for these clients. Teach the importance of eating three meals a day at regularly scheduled times and a bedtime snack. Meals and insulin administration must be linked together, especially when insulin analogues such as Humalog, NovoLog, or Apidra are given before meals and in conjunction with snacks.
Analogues are quicker acting than regular insulins. Use a balance of sugar-containing beverages and water. Intake of carbohydrates must be maintained unless the insulin dose is altered to avoid hypoglycemia.
Water must be consumed to maintain intravascular volume. There are too many carbohydrates in juice or soda to use either as a primary source of volume. Administer prochlorperazine, diphenhydramine , and metoclopramide as prescribed. These are beneficial in treating symptoms related to affecting the GI tract such as diabetic gastroparesis, to improve oral intake and nutrient absorption.
In an attempt to rid the body of excess glucose, the kidneys excrete the glucose along with water and electrolytes. This osmotic diuresis, which is characterized by excessive urination, leads to dehydration and marked electrolyte loss. Assess precipitating factors such as other illnesses, new-onset diabetes, or poor compliance with the treatment regimen.
These will provide baseline data for education once with resolved hyperglycemia. Urinary tract infection and pneumonia are the most common infections causing DKA among older clients. Assess skin turgor, mucous membranes, and thirst.
This provides baseline data for further comparison. Skin turgor will decrease and tenting may occur. This occurs because the skin relies on hydration to maintain its elasticity and suppleness.
The oral mucous membranes will become dry, and the client may experience extreme thirst. Monitor hourly intake and output. Oliguria or anuria results from reduced glomerular filtration and renal blood flow.
Hyperglycemia usually exceeds the renal threshold of glucose absorption and results in significant glucosuria. Glucosuria leads to osmotic diuresis, dehydration, and hyperosmolarity.
Decreased blood volume may be manifested by a drop in systolic blood pressure and orthostatic hypotension. Acetone breath is due to the breakdown of acetoacetic acid. Fever with flushed, dry skin may indicate dehydration. Compensatory mechanism results in peripheral vasoconstriction with a weak, thready pulse that is easily obliterated.
Assess neurological status every two hours. Decreased level of consciousness results from blood volume depletion, elevated or decreased glucose level, hypoxia, or electrolyte imbalances. Altered consciousness in the form of mild disorientation or confusion can occur.
Weigh the client daily. This provides baseline data on the current fluid status and adequacy of fluid replacement. A weight loss of 2. Assess for the presence of nausea and vomiting.
Nausea and vomiting usually occur and may be associated with diffuse abdominal pain, decreased appetite, and anorexia. Ketones, in particular, beta-hydroxybutyrate, induce nausea and vomiting that consequently aggravate fluid and electrolyte loss already existing in DKA.
This maintains hydration and adequacy of circulating volume. Hydration causes a decline in counter-regulatory hormones, enhances renal glucose clearance following improved renal perfusion, and augments insulin sensitivity. This, in turn, causes a significant reduction in hyperglycemia, hypertonicity, and acidemia.
Be alert to indicators of fluid overload , particularly among older adults or clients with a history of heart or renal failure.
Indicators of fluid overload, such as jugular vein distention, dyspnea , crackles, or CVP of more than 12 mm Hg, can occur with rapid infusion of fluids. Be extremely cautious to avoid cerebral edema and pulmonary edema. Monitor laboratory studies such as blood glucose levels, serum ketones, potassium , sodium, creatinine, and blood urea nitrogen BUN.
Monitor ABG for metabolic acidosis. Insert indwelling urinary catheter as indicated. This provides accurate measurement of urinary output, especially if autonomic neuropathies result in neurogenic bladder with urinary retention and overflow incontinence. The catheter may be removed when the client is stable to reduce the risk of infection.
Administer isotonic solutions 0. The initial goal of therapy is to correct circulatory fluid volume deficit. Isotonic normal saline will rapidly expand extracellular fluid volume without causing a rapid fall in plasma osmolality.
Clients typically need one to three liters within the first two hours of treatment. Administer succeeding IV therapy with a hypotonic solution such as 0. Continuation of IV administration depends on the degree of fluid deficit, urinary output, and serum electrolyte values.
Dextrose is added to prevent the occurrence of hypoglycemia and an excessive decline in plasma osmolality that can result in cerebral edema. Administer IV potassium and other electrolytes as indicated. Administer bicarbonate as indicated. Administer IV insulin by continuous infusion using an infusion pump.
Regular insulin has a rapid onset and therefore immediately helps move glucose intracellularly. A low-dose insulin regimen has the advantage of not inducing the severe hypoglycemia or hypokalemia that may be observed with a high-dose insulin regimen.
The initial insulin dose is a continuous IV insulin infusion using an infusion pump, if available. Before initiating treatment, flush the tubing with at least 30 mL of the insulin-containing IV solution.
When added to IV solutions, insulin may be absorbed by the container and plastic tubing.
Diabetic ketoacidosis is a potentially DKA nursing interventions complication DAK diabetes, making it a medical emergency. Nurses need to Elevated dining experiences how to identify and nursint it and how to maintain electrolyte balance. Ketoacidosis is a serious complication of diabetes. It is commonly precipitated by poor adherence to medication, stress and concurrent illness; it can be life threatening if it is not addressed quickly and effectively. Citation: Noble-Bell G, Cox A Management of diabetic ketoacidosis in adults. Nursing Times ; 10,
Watch DKA nursing interventions Unlock the inerventions videos nyrsing DKA nursing interventions FREE trial. Access More! View intedventions full outline and transcript inyerventions a FREE trial. Upon Endurance speed drills of Immunity-boosting foods nursing care plan for Diabetic Ketoacidosis DKAnursing students will be able to:. Definition of subjective data: information provided by individuals about their symptoms, feelings, and medical history, relying on their personal descriptions and experiences, rather than objective measurements or observations. Regular monitoring of blood glucose levels is imperative to gauge the effectiveness of treatment and to guide insulin administration.
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