Diabetic ketoacidosis (DKA) is a life-threatening emergency caused by a relative or absolute deficiency of insulin. This deficiency in available insulin results in disorders in the metabolism of carbohydrates, fat, and protein. The main clinical features of DKA are hyperglycemia, acidosis, dehydration, and electrolyte losses such as hypokalemia, hyponatremia, hypocalcemia, hypomagnesemia, and hypophosphatemia.
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. The overproduction of ketones ensues, causing them to accumulate in the blood and urine and turn the blood acidic. The most common early symptoms of DKA are the insidious increase in polydipsia and polyuria (Hamdy & Khardori, 2021).
The most common scenarios for DKA are underlying or concomitant infections such as pneumonia and urinary tract infections, missed or disrupted insulin treatments, and newly diagnosed, previously unknown diabetes. Drugs that affect carbohydrate metabolisms, such as corticosteroids, thiazides, sympathomimetic agents, and pentamidine may precipitate DKA (Lizzo et al., 2022). The overall mortality rate for DKA is 0.2 to 2%, with persons at the highest end of the range residing in developing countries (Hamdy & Khardori, 2021).
Fluid resuscitation and maintenance, insulin therapy, electrolyte replacement, and supportive care are the mainstays of management in DKA (Lizzo et al., 2022). Hypoglycemia is the most common complication of DKA, followed by hypokalemia, cerebral edema, acute respiratory failure, and even myocardial infarction and cerebrovascular accident.
Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS) or hyperosmolar hyperglycemic state (HHS) is a condition characterized by the presence of hyperglycemia, hyperosmolarity, and dehydration. HHS is one of two serious metabolic derangements that occur in clients with diabetes mellitus. There is enough production of insulin to reduce ketosis but not to control hyperglycemia. Persistent hyperglycemia causes osmotic diuresis, which results in fluid and electrolyte imbalances. Clients with HHS may present with symptoms of hypotension, tachycardia, marked dehydration, and neurological manifestation such as seizures, hemiparesis, and alterations in the sensorium. The clinical features of HHS and DKA overlap and are observed simultaneously in up to one-third of cases. However, unlike clients with DKA, most clients with HHS do not develop significant ketoacidosis (Avichal & Blocher, 2021).
Nursing Care Plans
The nursing care plan for clients with Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Nonketotic Syndrome includes the provision of information about the disease process/prognosis, self-care, and treatment needs, monitoring and assistance of cardiovascular, pulmonary, renal, and central nervous system (CNS) function, avoiding dehydration, and correcting hyperglycemia and hyperglycemia complications.
Here are four (4) nursing care plans (NCP) and nursing diagnoses for clients with Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Nonketotic Syndrome:
- Risk For Deficient Fluid Volume
- Risk For Infection
- Deficient Knowledge
- Imbalanced Nutrition: Less Than Body Requirements
Deficient Fluid Volume
Without insulin, the amount of glucose entering the cells is reduced, and the production and release of glucose by the liver are increased, leading to hyperglycemia. 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.
May be related to
- Decreased intake of fluids due to diminished thirst sensation or functional inability to drink fluids.
- Excessive gastric losses due to nausea and vomiting.
- Hyperglycemia-induced osmotic diuresis.
Possibly evidenced by
- Diluted urine
- Sudden weight loss
- Dry skin and mucous membranes, poor skin turgor
- Hypotension, tachycardia
- Delayed capillary refill
- The client will remain normovolemic as evidenced by urinary output greater than 30 ml/hr, normal skin turgor, good capillary refill, normal blood pressure, palpable peripheral pulses, and blood glucose levels between 70-200 mg/dL.
- The client will display normal electrolyte levels and stable vital signs.
Nursing Assessment and Rationales
1. 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. Poor compliance with insulin through the omission of insulin injections occurs due to a lack of client or guardian education, or as a result of psychological stress, particularly in adolescents (Hamdy & Khardori, 2021).
2. 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.
3. 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. Severe dehydration, if not properly compensated, may lead to impaired renal function (Hamdy & Khardori, 2021).
4. Monitor vital signs, especially for orthostatic hypotension and Kussmaul’s respirations.
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. Kussmaul’s respiration (rapid and shallow breathing) represents a compensatory mechanism by the respiratory buffering system to raise arterial pH by exhaling more carbon dioxide. Fever with flushed, dry skin may indicate dehydration. Compensatory mechanism results in peripheral vasoconstriction with a weak, thready pulse that is easily obliterated.
5. 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. Although frank coma is uncommon, it may occur when the condition is neglected or if dehydration or acidosis is severe (Hamdy & Khardori, 2021).
6. Weigh the client daily.
This provides baseline data on the current fluid status and adequacy of fluid replacement. A weight loss of 2.2 lbs (1 kg) over 24 hours indicates a liter of fluid loss. Typical free water loss in DKA is approximately six liters or nearly 100 mL/kg of body weight. The initial half of this amount is derived from intracellular fluid and precedes signs of dehydration, while the other half is from the extracellular fluid and is responsible for signs of dehydration (Hamdy & Khardori, 2021).
7. 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.
Nursing Interventions and Rationales
1. Maintain a fluid intake of at least 2500 liters/day within cardiac tolerance when oral intake is resumed.
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. Hydration alone (intravenous and oral) has been shown to reduce glucose concentration by 17 to 80% over a duration of 12 to 15 hours (Javashree et al., 2019).
2. 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. Although initial aggressive fluid replacement is necessary in all clients, particular care must be taken in those with comorbidities such as renal failure or congestive heart failure (Hamdy & Khardori, 2021).
3. Monitor laboratory studies such as blood glucose levels, serum ketones, potassium, sodium, creatinine, and blood urea nitrogen (BUN).
DKA occurs when the blood glucose level is greater than 250 mg/dL. Elevated ketones are associated with DKA. Initially, hyperkalemia occurs in response to metabolic acidosis. As the fluid volume deficit progresses, the potassium level decreases. Both DKA result in hypokalemia. Increased blood sugar causes water to shift from intracellular into extracellular, resulting in serum sodium depletion. Elevated BUN and creatinine indicate cellular breakdown from dehydration or a sign of acute renal failure.
4. Monitor ABG for metabolic acidosis.
In clients diagnosed with DKA, ABGs frequently show typical manifestations of metabolic acidosis, low bicarbonate, and low pH of less than 7.3. Venous pH may be used for repeat pH measurements. When monitoring the response to treatment, guidelines recommend the use of venous blood rather than arterial blood in blood gas analyzers, except where respiratory problems preclude using arterial blood (Hamdy & Khardori, 2021).
5. 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.
6. Administer isotonic solutions (0.9% NaCl) initially.
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. A liter is administered every four hours following the first two hours, depending on the degree of dehydration and central venous pressure readings (Hamdy & Khardori, 2021).
7. Administer succeeding IV therapy with a hypotonic solution such as 0.45% normal saline.
Continuation of IV administration depends on the degree of fluid deficit, urinary output, and serum electrolyte values. After initial stabilization with isotonic saline, switch to half-normal saline at 200 to 1000 mL/hour. Half-normal saline matches losses due to osmotic diuresis (Hamdy & Khardori, 2021).
8. Add dextrose to IV fluid when serum blood glucose level is less than 180 mg/dL in DKA.
When blood sugar decreases to less than 180 mg/dL, isotonic sodium chloride solution is replaced with 5 to 10% dextrose with half isotonic sodium chloride solution (Hamdy & Khardori, 2021). Dextrose is added to prevent the occurrence of hypoglycemia and an excessive decline in plasma osmolality that can result in cerebral edema.
9. Administer IV potassium and other electrolytes as indicated.
If the potassium level is greater than 6 mEq/L, do not administer a potassium supplement. Instead, monitor until potassium levels are 4,5 to 6 mEq/L, then administer 10 mEq/hour of potassium chloride. The administration of insulin to lower blood glucose promotes the movement of potassium intracellularly. The infusion must be stopped if the potassium level is greater than 5 mEq/L (Hamdy & Khardori, 2021).
10. Administer bicarbonate as indicated.
Sodium bicarbonate is only infused if decompensated acidosis starts to threaten the client’s life, especially when associated with either sepsis or lactic acidosis. If sodium bicarbonate is indicated, 100 to 150 mL of 1.4% concentration is infused initially. Rapid and early correction of acidosis with sodium bicarbonate may worsen hypokalemia and cause paradoxical cellular acidosis (Hamdy & Khardori, 2021).
11. 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. The incidence of DKA was reduced with the introduction of pumps equipped with sensitive electronic alarm systems that alert users when the infusion catheter is blocked (Hamdy & Khardori, 2021).
12. 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.
Recommended nursing diagnosis and nursing care plan books and resources.
Ackley and Ladwig’s Nursing Diagnosis Handbook: An Evidence-Based Guide to Planning Care
We love this book because of its evidence-based approach to nursing interventions. This care plan handbook uses an easy, three-step system to guide you through client assessment, nursing diagnosis, and care planning. Includes step-by-step instructions showing how to implement care and evaluate outcomes, and help you build skills in diagnostic reasoning and critical thinking.
Nursing Care Plans – Nursing Diagnosis & Intervention (10th Edition)
Includes over two hundred care plans that reflect the most recent evidence-based guidelines. New to this edition are ICNP diagnoses, care plans on LGBTQ health issues, and on electrolytes and acid-base balance.
Nurse’s Pocket Guide: Diagnoses, Prioritized Interventions, and Rationales
Quick-reference tool includes all you need to identify the correct diagnoses for efficient patient care planning. The sixteenth edition includes the most recent nursing diagnoses and interventions and an alphabetized listing of nursing diagnoses covering more than 400 disorders.
Nursing Diagnosis Manual: Planning, Individualizing, and Documenting Client Care
Identify interventions to plan, individualize, and document care for more than 800 diseases and disorders. Only in the Nursing Diagnosis Manual will you find for each diagnosis subjectively and objectively – sample clinical applications, prioritized action/interventions with rationales – a documentation section, and much more!
All-in-One Nursing Care Planning Resource – E-Book: Medical-Surgical, Pediatric, Maternity, and Psychiatric-Mental Health
Includes over 100 care plans for medical-surgical, maternity/OB, pediatrics, and psychiatric and mental health. Interprofessional “patient problems” focus familiarizes you with how to speak to patients.
References and Sources
- Ahola, A. J., Harjutsalo, V., Thomas, M. C., Forsblom, C., & Groop, P.-H. (2021, January). Dietary intake and hospitalization due to diabetic ketoacidosis and hypoglycemia in individuals with type 1 diabetes. Scientific Reports, 11.
- American Medical ID. (2023). Diabetic Bracelets by American Medical ID. American Medical ID. Retrieved February 11, 2023.
- Aprilia, D., Decroli, E., Kam, A., Rahmadi, A., Manaf, A., & Syahbuddin, S. (2019). Sepsis in Type 1 Diabetes Mellitus with Diabetic Ketoacidosis. Proceedings of the 2nd International Conference on Tropical Medicine and Infectious Disease.
- Avichal, D., & Blocher, N. C. (2021, January 5). Hyperosmolar Hyperglycemic State: Practice Essentials, Pathophysiology, Etiology. Medscape Reference. Retrieved February 13, 2023, from
- Caballero, E. (2018, August 28). The “A to Z” of Managing Type 2 Diabetes in Culturally Diverse Populations. NCBI. Retrieved February 13, 2023.
- Dhatariya, K. K., Glaser, N. S., Codner, E., & Umpierrez, G. E. (2020). Diabetic ketoacidosis. Nature Reviews.
- Diabetes.co.uk. (2023). Herbal and Natural Remedies for Diabetes. Diabetes UK.
- Din, L., & Preuss, C. V. (2022, September 21). Prochlorperazine – StatPearls. NCBI. Retrieved February 11, 2023.
- Doenges, M. E., Moorhouse, M. F., & Murr, A. C. (2010). Nursing Care Plans: Guidelines for Individualizing Client Care Across the Life Span. F.A. Davis Company.
- Farran, B. A., Bin Elaiwah, R. I., Aldarsouny, A. T., Alshamrani, A. M., Almaslamani, A. M., Alsubie, B. F., Zainab, M. M., Alkulaib, M. O., & Khalifah, A. (2020, June). Level of awareness of diabetic ketoacidosis among diabetes mellitus patients in Riyadh. Journal of Family Medicine and Primary Care, 9(6).
- Hamdy, O., & Khardori, R. (2021, January 19). Diabetic Ketoacidosis (DKA): Practice Essentials, Background, Pathophysiology. Medscape Reference. Retrieved February 8, 2023.
- Hinkle, J. L., & Cheever, K. H. (2018). Brunner & Suddarth’s Textbook of Medical-surgical Nursing. Wolters Kluwer.
- Isola, S., Hussain, A., Dua, A., Singh, K., & Adams, N. (2022, November 9). Metoclopramide – StatPearls. NCBI. Retrieved February 11, 2023.
- Javashree, M., Williams, V., & Iver, R. (2019, November 12). Fluid Therapy For Pediatric Patients With Diabetic Ketoacidosis: Current Perspectives. NCBI. Retrieved February 9, 2023.
- Khan, T., & Khardori, R. (2020, October 15). Diabetic Foot Ulcers: Practice Essentials, Pathophysiology, Etiology. Medscape Reference. Retrieved February 9, 2023.
- Khardori, R., & Griffing, G. T. (2022, December 19). Type 1 Diabetes Mellitus: Practice Essentials, Background, Pathophysiology. Medscape Reference. Retrieved February 11, 2023.
- Linton, A. D. (2015). Introduction to Medical-Surgical Nursing. Elsevier.
- Lizzo, J. M., Goyal, A., & Gupta, V. (2022, July 12). Adult Diabetic Ketoacidosis – StatPearls. NCBI. Retrieved February 8, 2023.
- Murao, M., Murao, K., Nagata, T., & Shimizu, M. (2022, January). Repeated insulin injection without site rotation affects skin thickness – ultrasonographic and histological evaluation. Journal of Diabetes Investigation, 13(6), 997-1003.
- Murphy-Lavoie, H. M., Ramsey, A., Nguyen, M., & Singh, S. (2022, July 4). Diabetic Foot Infections – StatPearls. NCBI. Retrieved February 9, 2023.
- Swearingen, P. L. (Ed.). (2015). All-in-one Nursing Care Planning Resource: Medical-surgical, Pediatric, Maternity, and Psychiatric-mental Health. Elsevier.
- Thakare, P. S., & Ankar, R. (2021, May). To Assess the Knowledge Regarding Signs and Symptoms of Diabetic Ketoacidosis and Its Prevention among Diabetes Patients in Wardha District, Maharashtra, India. Journal of Evolution of Medical and Dental Science, 10(19).
- Umpierrez, G., & Korytkowski, M. (2016, April). Diabetic emergencies — ketoacidosis, hyperglycaemic hyperosmolar state and hypoglycaemia. Nature Reviews, 17.
- Wang, C. M.B., Inouye, J., Davis, J., & Wang, C.-Y. (2013, July). Diabetes Knowledge and Self-Management Effects on Physiological Outcomes in Type 2 Diabetes. Nursing Forum, 48(4).
- Yin, C., Lu, S., Wei, D., Xiong, J., Zhu, L., Yan, S., & Meng, R. (2021). Effects of nutritional support combined with insulin therapy on serum proteins, inflammatory factors, pentraxin-3, and serum amylase levels in patients with diabetic ketoacidosis complicated with acute pancreatitis. Medicine, 100(51).
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