DKA and HHS may also be thought of as occurring on a spectrum of disease manifestation. On one end of the spectrum lie absolute insulin deficiency and profound ketosis and acidosis, which is DKA.

DKA tends to occur in patients with type 1 diabetes, who, because of destruction of β-cells, exhibit absolute insulin deficiency. On the other end of the spectrum is extreme hyperglycemia without ketosis and acidosis. As the analogy implies, patients may present with various manifestations of both disorders.

For example, a patient with DKA may have used enough insulin to partially suppress ketosis but still manifest profound hyperglycemia. Patients with HHS may also have varying degrees of ketosis and mild acidosis, depending on the degree to which they have been able to produce insulin and the extent of associated factors such as dehydration.

Insulin deficiency causes a lack of glucose utilization in insulin-dependent tissues such as muscle and adipose and therefore leads to hyperglycemia.

Lack of insulin also stimulates hyperglycemia by increasing hepatic gluconeogenesis. This is a common mechanism in both DKA and HHS. Deprived of glucose utilization, the body must look elsewhere for fuel to survive. In addition to hyperglycemia, lack of insulin increases degradation of triglycerides into free fatty acids in adipose tissue, which travel to the liver and are converted to the ketoacids β-hydroxybutyric acid, acetone, and acetoacetate.

Unopposed conterregulatory hormone effect causes further increases in glucose production from the liver and degradation of triglycerides.

The surge of ketoacid formation from unrestrained ketone body formation can be profound. DKA develops when the surge of ketoacid production is so powerful that a metabolic acidosis results.

In HHS, there remains sufficient insulin presence to suppress ketosis enough to prevent the development of metabolic acidosis. Dehydration is another common finding in DKA and HHS.

Because of osmotic pressure, unregulated diuresis follows. Patients frequently complain of preceding polyuria and polydipsia. Considerable electrolyte loss may result, especially potassium depletion.

Further dehydration and volume contraction can lead to worsening of hyperglycemia. Patients presenting in HHS and DKA typically exhibit a history of polyuria and polydipsia.

Frequently, one can identify a precipitating factor leading to DKA. Such factors can include inappropriate use of insulin non-compliance , cardiovascular disease, or infection, which may be the most common causes of DKA.

Patients with DKA may also manifest leukocytosis simply due to DKA. It is important to not overlook other possible causes of DKA and HHS, however. Myocardial infarction may precipitate hyperglycemia and DKA via an increase in counterregulatory hormones, such as epinephrine.

Drugs such as thiazides, sympathomimetics, second-generation antipsychotics, and corticosteroids may also precipitate HHS and DKA. Other disorders that may precipitate diabetes include pancreatitis and illicit drug use.

Additionally, and especially in patients with type 1 diabetes, decline in diabetes control and hyperglycemia may indicate the onset of an autoimmune thyroid disease, such as Grave's disease or Hashitoxicosis. Patients may develop progressive hyperglycemia over weeks or days, although patients with DKA may experience more rapid onset than those with HHS.

Symptoms of both HHS and DKA include polyuria and polydipsia due to hyperglycemia and signs of dehydration, including lack of skin turgor, hypotension, dry oral mucosae, tachycardia, weakness, and altered sensorium. Patients with DKA typically exhibit signs of acidosis, such as abdominal pain sometimes severe , nausea, vomiting, and Kussmaul respirations, and may also exhibit guaiac-positive vomitus.

Hypothermia, should it be present, is a poor prognostic indicator. Laboratory findings in patients with DKA include hyperglycemia, ketosis, and metabolic acidosis.

Patients who are suspected of DKA or HHS should undergo measurement of electrolytes with anion gap, glucose serological , creatinine and blood urea nitrogen, serum ketones, urinalysis with ketones, complete blood count, A1C, and arterial blood gas testing.

Additionally, electrocardiogram, chest X-ray, and urine, sputum, and blood cultures may be warranted. If children are otherwise healthy and there are no signs of infection, it may be acceptable to omit an infection workup.

Significant ketosis has been shown in up to one-third of patients with HHS, again indicative of the continuum of pathology between DKA and HHS. Buildup of ketoacids is responsible for anion gap metabolic acidosis in DKA.

It is important, however, to remember other causes of anion gap metabolic acidoses, including starvation, lactic acidosis especially in patients using metformin , salicylates, ethanol, methanol, ethylene glycol, paraldehyde, renal insufficiency, and isopropyl alcohol intoxication.

Serum potassium levels are typically elevated in response to the presence of acidosis and insulin deficiency, but total body potassium is depleted. Patients presenting with hypokalemia in the setting of DKA are particularly potassium-depleted and require aggressive monitoring and potassium repletion.

Both amylase and lipase may be elevated in the setting of DKA and are not necessarily indicative of pancreatitis. The cornerstones of treatment of DKA and HHS are fluids, insulin, correction of electrolyte abnormalities, and close monitoring.

In the absence of underlying renal and cardiac disease, initial fluid resuscitation should consist of isotonic fluids to restore renal perfusion.

Subsequently, fluids may be altered or titrated based on degree of dehydration and electrolyte abnormalities. Titration of fluids is based on hemodynamic improvement, urine output, laboratory improvement, and clinical response.

Patients with underlying cardiac and renal disease may require lower initial fluid resuscitation rates and more frequent monitoring of clinical status to avoid fluid overload. Insulin therapy for DKA and HHS is typically administered intravenously, although uncomplicated mild to moderate DKA may be managed with subcutaneous insulin therapy.

Typically, in the absence of hypokalemia, patients receive a bolus of intravenous regular insulin at 0. Doses may be titrated based on clinical response, which will vary based on the degree of insulin resistance. For example, patients with type 2 diabetes who present in DKA will typically require a higher dose of insulin than those with type 1 diabetes because of higher insulin resistance.

If subcutaneous insulin is to be used to treat uncomplicated DKA, patients typically receive an initial dose of 0. Such approaches may be associated with a lower cost of hospitalization by avoiding intensive care unit placement.

Electrolytes, glucose, blood urea nitrogen, osmolality, creatinine, and pH arterial or venous should be drawn every hours to monitor patients' responses to therapy and to allow titration of insulin and fluids. It is important to note that hyperglycemia typically resolves before ketosis; therefore, dextrose should be added to fluids as glucose declines as described above.

Ketosis should be measured via β-hydroxybutyric acid whenever possible because that is the prevalent ketone body produced in DKA. The nitroprusside reaction, which is still used in many laboratories to detect ketone formation, does not detect β-hyrdoxybutyric acid and therefore may yield false-negative results.

Most patients presenting in DKA exhibit hyperkalemia as a result of insulin deficiency and acidosis despite total body potassium depletion. Treatment with insulin, restoration of normal circulatory volume, and resolution of acidosis allow total body potassium depletion to manifest itself as hypokalemia during treatment of DKA.

Including mEq of potassium in each liter of fluid is usually sufficient to maintain a potassium concentration within normal limits. This will help to avoid cardiac arrhythmia and skeletal muscle dysfunction because insulin initiation can cause an acute decline in serum potassium concentration.

Use of bicarbonate to raise pH is controversial. Patients also frequently exhibit hypophosphatemia at presentation in DKA, but phosphate repletion has not demonstrated a beneficial effect on clinical outcomes in DKA. Patients receiving phosphate therapy should be monitored closely for hypocalcemia, which can result from phosphate administration.

Patients should resume rapid-acting insulin at meals and intermediate- or long-acting insulin when they are able to eat substantial carbohydrate.

It is important to continue intravenous insulin for several hours after resumption of subcutaneous insulin to avoid recurrent hyperglycemia and a possible return to ketosis.

The most common complications that occur when treating adults with ketoacidosis are hypokalemia and hypoglycemia. Potassium depletion is the most life-threatening electrolyte abnormality in the treatment of DKA. As previously described, total body potassium at presentation in DKA is low despite hyperkalemia because of metabolic acidosis.

Delayed potassium supplementation can lead to considerable hypokalemia as the serum potassium concentration drops precipitously in the presence of insulin and resolution of ketoacidosis.

In the setting of normal renal function, patients should receive potassium supplementation in their fluids when the potassium level approaches normal values. Hypoglycemia is also a potential complication of DKA.

The threat of hypokalemia and hypoglycemia both also illustrate the importance of frequent reassessment of patients treated for DKA. Care must also be taken in intravenous fluid administration. Patients with underlying medical conditions such as renal insufficiency or congestive heart failure are susceptible to fluid overload.

Patients should be assessed for such disorders before initiation of fluid resuscitation. Cerebral edema is yet another potential complication of DKA and HHS.

It occurs more frequently in pediatric patients than in adults. Signs of cerebral edema include mental status changes, vomiting, headache, lethargy, elevated diastolic blood pressure, decorticate or decerebrate posturing, cranial nerve palsies, or Cheyne-Stokes respiration.

Treatment options include use of mannitol or hypertonic saline to decrease cerebral edema, although there have been no large controlled trials clearly demonstrating benefit.

Dr Shah reported receiving research support through Mayo Clinic from the US Food and Drug Administration and the Centers of Medicare and Medicaid Innovation and receiving grants from the Agency for Healthcare Research and Quality, the National Heart, Lung and Blood Institute, the National Science Foundation, and the Patient Centered Outcomes Research Institute.

No other disclosures were reported. Disclaimer: Dr McCoy affirms that the article is an honest, accurate, and transparent account of the study being reported; that no important aspects of the study have been omitted; and that any discrepancies from the study as planned have been explained.

Study contents are the sole responsibility of the authors and do not necessarily represent the official views of the National Institutes of Health. Meeting Presentation: This paper was presented at the virtual meeting of the American Diabetes Association Scientific Sessions; June , full text icon Full Text.

Download PDF Comment. Top of Article Key Points Abstract Introduction Methods Results Discussion Conclusions Article Information References. Figure 1. View Large Download. Figure 2. Table 1. Baseline Sociodemographic, Clinical, and Diabetes Treatment Characteristics of Patients With Type 1 Diabetes.

Table 2. Baseline Sociodemographic, Clinical, and Diabetes Treatment Characteristics of Patients With Type 2 Diabetes. Table 3. Factors Associated With Hyperglycemic Crises Among Adults With Type 1 or Type 2 Diabetes, eTable 1.

Code Sets for Included Health Conditions eTable 2. Classification Scheme for Glucose-Lowering Medications eTable 3. Patients With Type 2 Diabetes eTable 4. Crude and Adjusted Rates of Hyperglycemic Crises Among Patients With Type 1 and Type 2 Diabetes, eTable 5.

Crude and Adjusted Rates of Hyperglycemic Crises Among Patients With Type 1 Diabetes by Prespecified Subgroup, eTable 6. Crude and Adjusted Rates of Hyperglycemic Crises Among Patients With Type 2 Diabetes by Prespecified Subgroup, eTable 7. Centers for Disease Control and Prevention.

National Diabetes Statistics Report, US Department of Health and Human Services, Centers for Disease Control and Prevention; Umpierrez G, Korytkowski M. Diabetic emergencies—ketoacidosis, hyperglycaemic hyperosmolar state and hypoglycaemia. doi: Karslioglu French E, Donihi AC, Korytkowski MT.

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About one in five patients with T1D admitted for DKA will be readmitted for DKA within 30 days Several studies suggested that the omission of insulin is one of the most common precipitating factors of DKA, sometimes because patients are socio-economically underprivileged, and may not have access to or afford medical care In addition, they may have a propensity to use illicit drugs such as cocaine, which has been associated with recurrent DKA 58 , or live in areas with higher food deprivation risk Therefore, it is important to continuously re-assess socio-economic status of patients who had at least one episode of DKA.

The most recent data demonstrating a significant increase in DKA hospitalization rates in diabetic persons aged 45 years and younger 10 suggests that this group of patients may require particular attention to understand why they are more vulnerable than others to develop hyperglycemic crisis.

Education of the patient about sick day management is very vital to prevent DKA, and should include information on when to contact the health care provider, blood glucose goals, use of insulin, and initiation of appropriate nutrition during illness and should be reviewed with patients periodically.

Patients must be advised to continue insulin and to seek professional advice early in the course of the illness. Close follow up is very important, as it has been shown that three-monthly visits to the endocrine clinic will reduce the number of ER admission for DKA Close observation, early detection of symptoms and appropriate medical care would be helpful in preventing HHS in the elderly.

A study in adolescents with T1D suggests that some of the risk factors for DKA include higher HbA1c, uninsured children, and psychological problems In other studies, education of primary care providers and school personnel in identifying the signs and symptoms of DKA has been shown to be effective in decreasing the incidence of DKA at the onset of diabetes In another study outcome data of patients with diabetes under continuing care over a 7-year period were examined.

There is early evidence that use of continuous glucose monitoring CGM can decrease DKA incidence , Contrary to the initial observations connecting DKA episodes with insulin pump malfunction, the newer pumps are associated with reduced DKA risk without or with concomitant CGM application in T1D youth Considering DKA and HHS as potentially fatal and economically burdensome complications of diabetes, every effort for diminishing the possible risk factors is worthwhile.

SGLT-2 inhibitor-induced DKA in patients with T2D is a potentially avoidable condition in light of accumulating knowledge of potential triggers prompting the development of this hyperglycemic emergency A recent international consensus statement on the DKA risk management in patients with T1D treated with SGLT-2 inhibitors 76 can be effectively applied to the care of patients with T2D as well.

The DEEARAILS pneumonic can help recalling these clinical situations. Precipitating factors for DKA in patients taking SGLT2 inhibitors. This electronic version has been made freely available under a Creative Commons CC-BY-NC-ND license.

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Show details Feingold KR, Anawalt B, Blackman MR, et al. Contents www. Search term. Hyperglycemic Crises: Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State Aidar R Gosmanov , M.

Author Information and Affiliations Aidar R Gosmanov , M. Professor of Medicine, Division of Endocrinology, Department of Medicine, Albany Medical College, Albany, NY and Endocrinology Section, Stratton VAMC, Albany, NY.

Email: moc. liamg vonamsoga. Elvira O. Abbas E. Professor of Medicine and Molecular Sciences Emeritus, Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Tennessee Health Science Center, Memphis, TN. ABSTRACT Diabetic ketoacidosis DKA and hyperglycemic hyperosmolar state HHS are acute metabolic complications of diabetes mellitus that can occur in patients with both type 1 and 2 diabetes mellitus.

Diabetic Ketoacidosis In DKA, there is a severe alteration of carbohydrate, protein, and lipid metabolism 8. CLINICAL FEATURES Symptoms and Signs DKA usually evolves rapidly within a few hours of the precipitating event s. Pitfalls of Laboratory Tests and Diagnostic Considerations for Interpreting Acid Based Status in DKA False positive values for lipase may be seen if plasma glycerol levels are very high due to rapid breakdown of adipose tissue triglycerides glycerol is the product measured in most assays for plasma lipase.

TREATMENT OF DKA The goals of therapy in patients with hyperglycemic crises include: 1 improvement of circulatory volume and tissue perfusion, 2 gradual reduction of serum glucose and osmolality, 3 correction of electrolyte imbalance, and 4 identification and prompt treatment of co-morbid precipitating causes 8.

Fluid Therapy DKA and HHS are volume-depleted states with total body water deficit of approximately 6 L in DKA and 9 L in HHS 16 , , Insulin Therapy The cornerstone of DKA and HHS therapy is insulin in physiologic doses.

Potassium Therapy Although total-body potassium is depleted , , mild to moderate hyperkalemia frequently seen in patients with DKA is due to acidosis and insulinopenia. Bicarbonate Therapy The use of bicarbonate in treatment of DKA remains controversial. Phosphate Therapy There is no evidence that phosphate therapy is necessary in treatment for better outcome of DKA Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN.

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Umpierrez GE, Casals MM, Gebhart SP, Mixon PS, Clark WS, Phillips LS. You'll receive fluids — usually through a vein intravenously — until your body has the fluids it needs. This replaces fluids you've lost through urination.

It also helps dilute the extra sugar in your blood. Electrolyte replacement. Electrolytes are minerals in your blood that are necessary for your tissues to work properly. A lack of insulin can lower the level of electrolytes in your blood.

You'll receive electrolytes through your veins to help keep your heart, muscles and nerve cells working the way they should. Insulin therapy.

Insulin reverses the processes that cause ketones to build up in your blood. Along with fluids and electrolytes, you'll receive insulin therapy — usually through a vein.

Request an appointment. What you can do Be aware of any pre-appointment restrictions. If your health care provider is going to test your blood sugar, you may need to stop eating or drinking anything but water for up to eight hours before your appointment.

When you're making an appointment, ask if there are any restrictions on eating or drinking. Write down key personal information, including any major stresses or recent life changes.

Make a list of all medications, vitamins and supplements you take. Create a record of metered glucose values. Give your health care provider a written or printed record of your blood glucose values, times and medication. Using the record, your health care provider can recognize trends and offer advice on how to prevent hyperglycemia or adjust your medication to treat hyperglycemia.

Write down questions to ask your health care provider. If you need more information about your diabetes management, be sure to ask. Check if you need prescription refills. Your health care provider can renew your prescriptions while you're at the appointment.

For hyperglycemia, questions you may want to ask include: How often do I need to monitor my blood sugar? What is my target range? How do diet and exercise affect my blood sugar? When do I test for ketones?

How can I prevent high blood sugar? Do I need to worry about low blood sugar? What are the symptoms I need to watch for? Will I need follow-up care? Sick-day planning Illness or infections can cause your blood sugar to rise, so it's important to plan for these situations. Questions to ask include: How often should I monitor my blood sugar when I'm sick?

Does my insulin injection or oral diabetes pill dose change when I'm sick? When should I test for ketones? What if I can't eat or drink?

When should I seek medical help? By Mayo Clinic Staff. Aug 20, Show References. Hyperglycemia high blood glucose. American Diabetes Association. Accessed July 6, What is diabetes?

National Institute of Diabetes and Digestive and Kidney Diseases. Wexler DJ. Management of persistent hyperglycemia in type 2 diabetes mellitus. Hirsch IB, et al. Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis.

Managing diabetes.