Category: Home

Managing hyperglycemic crisis

Managing hyperglycemic crisis

J Clin Endocrinol Metab. Article CAS PubMed Google Scholar Hyperglcemic SI, Hgperglycemic JE, Rother KI. Sports nutrition experts Care Enhancing heart health January Manwging 24 1 : — The investigators showed that of 56 DKA admissions, only two patients tried to contact the diabetes unit for assistance Recurrent diabetic ketoacidosis in inner-city minority patients: behavioral, socioeconomic, and psychosocial factors. Moeller N, Jorgensen JOL, Schmitz O, Moller J, Christianse JS,Alberti KGMM, Orskov H: Effects of a growth hormone pulse on total and forearm substrate utilization in humans. Managing hyperglycemic crisis

Managing hyperglycemic crisis -

From: Moher D, Liberati A, Tetzlaff J, Altman DG, The PRISMA Group P referred R eporting I tems for Systematic Reviews and Meta-Analyses : The PRISMA Statement. PLoS Med 6 6 : e pmed For more information, visit www.

Gilbert reports personal fees from Amgen, AstraZeneca, Boehringer Ingelheim, Eli Lilly, Janssen, Merck, Novo Nordisk, and Sanofi, outside the submitted work. Goguen does not have anything to disclose. All content on guidelines. ca, CPG Apps and in our online store remains exactly the same.

For questions, contact communications diabetes. Become a Member Order Resources Home About Contact DONATE. Next Previous. Key Messages Recommendations Figures Full Text References.

Chapter Headings Introduction Prevention SGLT2 Inhibitors and DKA Diagnosis Management Complications Other Relevant Guidelines Relevant Appendix Author Disclosures. Key Messages Diabetic ketoacidosis and hyperosmolar hyperglycemic state should be suspected in people who have diabetes and are ill.

If either diabetic ketoacidosis or hyperosmolar hyperglycemic state is diagnosed, precipitating factors must be sought and treated. Diabetic ketoacidosis and hyperosmolar hyperglycemic state are medical emergencies that require treatment and monitoring for multiple metabolic abnormalities and vigilance for complications.

A normal or mildly elevated blood glucose level does not rule out diabetic ketoacidosis in certain conditions, such as pregnancy or with SGLT2 inhibitor use.

Diabetic ketoacidosis requires intravenous insulin administration 0. Key Messages for People with Diabetes When you are sick, your blood glucose levels may fluctuate and be unpredictable: During these times, it is a good idea to check your blood glucose levels more often than usual for example, every 2 to 4 hours.

Drink plenty of sugar-free fluids or water. Blood ketone testing is preferred over urine testing. Develop a sick-day plan with your diabetes health-care team. This should include information on: Which diabetes medications you should continue and which ones you should temporarily stop Guidelines for insulin adjustment if you are on insulin Advice on when to contact your health-care provider or go to the emergency room.

Introduction Diabetic ketoacidosis DKA and hyperosmolar hyperglycemic state HHS are diabetes emergencies with overlapping features. Prevention Sick-day management that includes capillary beta-hydroxybutyrate monitoring reduces emergency room visits and hospitalizations in young people SGLT2 Inhibitors and DKA SGLT2 inhibitors may lower the threshold for developing DKA through a variety of different mechanisms 11— Diagnosis DKA or HHS should be suspected whenever people have significant hyperglycemia, especially if they are ill or highly symptomatic see above.

Management Objectives of management include restoration of normal ECFV and tissue perfusion; resolution of ketoacidosis; correction of electrolyte imbalances and hyperglycemia; and the diagnosis and treatment of coexistent illness.

Figure 1 Management of diabetic ketoacidosis in adults. Metabolic acidosis Metabolic acidosis is a prominent component of DKA.

Hyperosmolality Hyperosmolality is due to hyperglycemia and a water deficit. Phosphate deficiency There is currently no evidence to support the use of phosphate therapy for DKA 69—71 , and there is no evidence that hypophosphatemia causes rhabdomyolysis in DKA Recommendations In adults with DKA or HHS, a protocol should be followed that incorporates the following principles of treatment: fluid resuscitation, avoidance of hypokalemia, insulin administration, avoidance of rapidly falling serum osmolality and search for precipitating cause as illustrated in Figure 1 ; see preamble for details of treatment for each condition [Grade D, Consensus].

Abbreviations: BG , blood glucose; CBG, capillary blood glucose; DKA , diabetic ketoacidosis; ECFV , extracellular fluid volume; HHS , hyperosmolar hyperglycemic state; KPD , ketosis-prone diabetes, PG , plasma glucose.

Other Relevant Guidelines Glycemic Management in Adults With Type 1 Diabetes, p. S80 Pharmacologic Glycemic Management of Type 2 Diabetes in Adults, p. S88 Type 1 Diabetes in Children and Adolescents, p.

Relevant Appendix Appendix 8: Sick-Day Medication List. Author Disclosures Dr. References Kitabchi AE, Umpierrez GE, Murphy MB, et al.

Management of hyperglycemic crises in patients with diabetes. Diabetes Care ;— Hamblin PS, Topliss DJ, Chosich N, et al. Deaths associated with diabetic ketoacidosis and hyperosmolar coma. Med J Aust ;—2, Holman RC, Herron CA, Sinnock P. Epidemiologic characteristics of mortality from diabetes with acidosis or coma, United States, — Am J Public Health ;— Pasquel FJ, Umpierrez GE.

Hyperosmolar hyperglycemic state: A historic review of the clinical presentation, diagnosis, and treatment. Wachtel TJ, Tetu-Mouradjian LM, Goldman DL, et al. Hyperosmolarity and acidosis in diabetes mellitus: A three-year experience in Rhode Island.

J Gen Intern Med ;— Malone ML, Gennis V, Goodwin JS. Characteristics of diabetic ketoacidosis in older versus younger adults. J Am Geriatr Soc ;—4. Wang ZH, Kihl-Selstam E, Eriksson JW.

Ketoacidosis occurs in both type 1 and type 2 diabetes—a population-based study from Northern Sweden. Diabet Med ;— Kitabchi AE, Umpierrez GE, Murphy MB, et al. Hyperglycemic crises in adult patients with diabetes: A consensus statement from the American Diabetes Association.

Balasubramanyam A, Garza G, Rodriguez L, et al. Accuracy and predictive value of classification schemes for ketosis-prone diabetes. Diabetes Care ;—9. Laffel LM, Wentzell K, Loughlin C, et al.

Sick day management using blood 3-hydroxybutyrate 3-OHB compared with urine ketone monitoring reduces hospital visits in young people with T1DM: A randomized clinical trial. OgawaW, Sakaguchi K. Euglycemic diabetic ketoacidosis induced by SGLT2 inhibitors: Possible mechanism and contributing factors.

J Diabetes Investig ;—8. Rosenstock J, Ferrannini E. Euglycemic diabetic ketoacidosis: A predictable, detectable, and preventable safety concern with SGLT2 inhibitors. Singh AK. Sodium-glucose co-transporter-2 inhibitors and euglycemic ketoacidosis: Wisdom of hindsight.

Indian J Endocrinol Metab ;— Erondu N, Desai M, Ways K, et al. Diabetic ketoacidosis and related events in the canagliflozin type 2 diabetes clinical program.

Diabetes Care ;—6. Zinman B, Wanner C, Lachin JM, et al. Empagliflozin, cardiovascular outcomes, and mortality in type 2 diabetes.

N Engl J Med ;— Hayami T, Kato Y, Kamiya H, et al. Case of ketoacidosis by a sodium-glucose cotransporter 2 inhibitor in a diabetic patient with a low-carbohydrate diet. J Diabetes Investig ;— Peters AL, Buschur EO, Buse JB, et al. Euglycemic diabetic ketoacidosis: A potential complication of treatment with sodium-glucose cotransporter 2 inhibition.

Redford C, Doherty L, Smith J. SGLT2 inhibitors and the risk of diabetic ketoacidosis. Practical Diabetes ;—4. St Hilaire R, Costello H.

Prescriber beware: Report of adverse effect of sodiumglucose cotransporter 2 inhibitor use in a patient with contraindication. Am J Emerg Med ;, e Goldenberg RM, Berard LD, Cheng AYY, et al. SGLT2 inhibitor-associated diabetic ketoacidosis: Clinical reviewand recommendations for prevention and diagnosis.

Clin Ther ;—64, e1. Malatesha G, Singh NK, Bharija A, et al. Comparison of arterial and venous pH, bicarbonate, PCO2 and PO2 in initial emergency department assessment.

Emerg Med J ;— Brandenburg MA, Dire DJ. Comparison of arterial and venous blood gas values in the initial emergency department evaluation of patients with diabetic ketoacidosis.

Ann Emerg Med ;— Ma OJ, Rush MD, Godfrey MM, et al. Arterial blood gas results rarely influence emergency physician management of patients with suspected diabetic ketoacidosis.

Acad Emerg Med ;— Charles RA, Bee YM, Eng PH, et al. Point-of-care blood ketone testing: Screening for diabetic ketoacidosis at the emergency department.

Singapore Med J ;—9. Naunheim R, Jang TJ, Banet G, et al. Point-of-care test identifies diabetic ketoacidosis at triage. Acad Emerg Med ;—5. Sefedini E, Prašek M, Metelko Z, et al.

Use of capillary beta-hydroxybutyrate for the diagnosis of diabetic ketoacidosis at emergency room: Our one-year experience.

Diabetol Croat ;— Mackay L, Lyall MJ, Delaney S, et al. Are blood ketones a better predictor than urine ketones of acid base balance in diabetic ketoacidosis?

Pract Diabetes Int ;—9. Bektas F, Eray O, Sari R, et al. Point of care blood ketone testing of diabetic patients in the emergency department. Endocr Res ;— Harris S, Ng R, Syed H, et al. Near patient blood ketone measurements and their utility in predicting diabetic ketoacidosis. Diabet Med ;—4.

Others use potassium acetate to avoid an excessive chloride load. We recommend electrocardiogram monitoring during potassium therapy in patients presenting with hypokalemia or in patients with any abnormal rhythms other than sinus tachycardia. Most current reviews do not recommend the routine use of alkali therapy in DKA because DKA tends to correct with insulin therapy.

Insulin administration inhibits ongoing lipolysis and ketoacid production and promotes ketoanion metabolism. Because protons are consumed during ketoanion metabolism,bicarbonate is regenerated, leading to partial correction of metabolic acidosis.

Arguments that favor the use of alkali therapy are based on the assumption that severe metabolic acidosis is associated with intracellular acidosis, which could contribute to organ dysfunction, such as in the heart,liver, or brain. Such organ dysfunction could in turn result in increased morbidity and mortality.

Potential adverse effects of alkali therapy include worsened hypokalemia, worsened intracellular acidosis due to increased carbon dioxide production, delay of ketoanion metabolism, and development of paradoxical central nervous system acidosis A retrospective review has failed to identify changes in morbidity or mortality with sodium bicarbonate therapy.

After reviewing the risks and benefits of bicarbonate therapy, one author concluded that the only clear indication for use of bicarbonate is life-threatening hyperkalemia Another study showed that ketoanion metabolism was delayed in the presence of bicarbonate therapy, but no significant difference in response between the bicarbonate and no bicarbonate groups was noted A prospective randomized study examined the effect of bicarbonate versus no bicarbonate in two groups of DKA patients with similar degrees of acidemia pH 6.

In some patients,initial cerebrospinal fluid CSF chemistry was measured and compared with initial plasma chemistry. It was of interest that HCO 3 and pH in CSF were significantly higher than those in plasma of DKA patients.

Conversely, ketones and glucose were higher in plasma than in CSF. However,CSF and plasma osmolalities were similar, indicating that the blood-brain barrier provided greater protection against acidosis for the brain Furthermore,regression analysis of the level of lactate, ketones, pH, bicarbonate, and glucose showed no significant difference in the two groups with regard to slopes of these variables during recovery from DKA.

It was therefore concluded that administration of bicarbonate in DKA patients with pH of 6. However, because there were very few in a subclass of patients who had an admission pH of 6. Bicarbonate should be administered as an isotonic solution, which can be prepared by addition of one ampoule of 7.

Regarding the use of bicarbonate in children with DKA, no prospective randomized study has been reported. Because good tissue perfusion created with the initial fluid bolus reduces the lactic acidosis of DKA and because organic acid production is reduced as the result of administered exogenous insulin,the metabolic acid load in DKA is reduced enough that it appears to be unnecessary to add buffer NaHCO 3.

Young people who are at the least risk for cardiovascular failure should not receive NaHCO 3 in their rehydration fluids until there is some clinical evidence of cardiac failure. This study concluded that there was no benefit of bicarbonate and that use of bicarbonate may be disadvantageous in severe pediatric DKA There have been suggestions that administration of NaHCO 3 in children with DKA may be associated with altered consciousness and headache, but no definitive causal relationship has been established.

It must be stated,however, that a definitive study on the efficacy of bicarbonate or no bicarbonate in DKA requires a larger number of patients to provide enough power for conclusive results.

In children, the use of bicarbonate must be based on the condition of the individual patient. Phosphate, along with potassium, shifts from the intracellular to the extracellular compartment in response to hyperglycemia and hyperosmolarity. Osmotic diuresis subsequently leads to enhanced urinary phosphate losses Tables 1 and 2.

Because of the shift of phosphate from the intracellular to the extracellular compartment, serum levels of phosphate at presentation with DKA or HHS are typically normal or increased , During insulin therapy, phosphate reenters the intracellular compartment,leading to mild to moderate reductions in serum phosphate concentrations.

Potential complications of severe hypophosphatemia include respiratory and skeletal muscle weakness, hemolytic anemia, and worsened cardiac systolic performance Phosphate depletion may also contribute to decreased concentrations of 2,3-diphosphoglycerate, thus shifting the oxygen dissociation curve to the left and limiting tissue oxygen delivery Controlled and randomized studies have not demonstrated clinical benefits from the routine use of phosphate replacement in DKA , Five days of PO 4 therapy increased 2,3-diphosphoglycerate without a significant change in the oxygen dissociation curve and resulted in a significant decrease in serum ionized calcium Similar studies have not been performed in patients with HHS.

Excessive administration of phosphate can lead to hypocalcemia with tetany and metastatic soft tissue calcifications In HHS, because the duration of symptoms may be prolonged and because of comorbid conditions, the phosphate level may be lower than in DKA; therefore, it is prudent to monitor phosphate levels in these patients.

In such patients,because of the risk of hypocalcemia, serum calcium and phosphate levels must be monitored during phosphate infusion. However, because of the short half-life of intravenous regular insulin, sudden interruption of insulin infusion can lead to rapid lowering of insulin concentration, resulting in a relapse into DKA or HHS.

Thus, numerous publications have emphasized the need for frequent monitoring during the posthyperglycemic period 6 , 19 , 44 , 56 , , , Once DKA is resolved, hydrating fluid is continued intravenously and subcutaneous regular insulin therapy is started every 4 h.

An abrupt discontinuance of intravenous insulin coupled with a delayed onset of a subcutaneous insulin regimen may lead to worsened control; therefore,some overlap should occur in intravenous insulin therapy and initiation of the subcutaneous insulin regimen.

When the patient is able to eat, a multiple daily injection schedule should be established that uses a combination of regular short-acting and intermediate or long-acting insulin as needed to control plasma glucose. Patients with known diabetes may be given insulin at the dose they were receiving before the onset of DKA and further adjusted using a multiple daily injection regimen.

However, in some patients with prolonged metabolic acidosis, combined diabetic and lactic acidosis, or other mixed acid-base disorders, direct measurement of β -hydroxybutyrate levels may be helpful. During treatment of DKA, use of the nitroprusside test, which measures acetoacetate and acetone levels but not β -hydroxybutyrate, should be avoided because the fall in acetone and acetoacetate lags behind the resolution of DKA 6.

Both complications were significantly reduced with lower-dose therapy In spite of this,hypoglycemia still constitutes one of the potential complications of therapy,the incidence of which may be underreported Similarly, the addition of potassium to the hydrating solution and frequent monitoring of serum potassium during the early phases of DKA and HHS therapy should reduce the incidence of hypokalemia.

Significant decreases in the size of the lateral ventricles, as determined by echoencephalogram, were noted in 9 out of 11 DKA patients during therapy , However, in another study, nine children in DKA were compared with regard to brain swelling before and after therapy, and it was concluded that brain swelling is usually present in DKA before treatment is begun Symptomatic cerebral edema, which is extremely rare in adult HHS or DKA patients, has been reported to occur primarily in pediatric patients, particularly in those with newly diagnosed diabetes.

No single factor has been identified that can be used to predict the development of cerebral edema , A year review of cerebral edema in children with DKA from the Royal Children's Hospital in Melbourne, Australia, concluded that although no predictive factors for survival of cerebral edema were identified, protocols that use slow rates of rehydration with isotonic fluids should be recommended Several other reviews have found a correlation between the development of cerebral edema and higher rates of fluid administration, especially in the first hours of fluid resuscitation.

A rare but potentially fatal complication of therapy is adult respiratory distress syndrome ARDS During rehydration with fluid and electrolytes, an initially elevated colloid osmotic pressure is reduced to subnormal levels. This change is accompanied by a progressive decrease in arteriolar partial pressure of oxygen Pao 2 and an increase in alveolar-to-arteriolar oxygen Aao 2 gradient, which is usually normal at presentation in DKA 19 , , In a small subset of patients, this may progress to ARDS.

By increasing left atrial pressure and decreasing colloid osmotic pressure, excessive crystalloid infusion favors edema formation in the lungs even in the presence of normal cardiac function.

Patients with an increased Aao 2 gradient or those who have pulmonary rales on physical examination may be at an increased risk for development of this syndrome. Monitoring of Pao 2 with pulse oximetry and monitoring of Aao 2 gradient may assist in the management of such patients.

Because crystalloid infusion may be the major factor, we advise that such patients have lower fluid intake, with addition of colloid administration for treatment of hypotension unresponsive to crystalloid replacement.

This acidosis has no adverse clinical effects and is gradually corrected over the subsequent h by enhanced renal acid excretion. The severity of hyperchloremia can be exaggerated by excessive chloride administration because 0.

Further causes of non—anion gap hyperchloremic acidosis include 1 loss of potential bicarbonate due to excretion of ketoanions as sodium and potassium salts; 2 decreased availability of bicarbonate in proximal tubule, leading to greater chloride reabsorption; and 3 reduction of bicarbonate and other buffering capacity in other body compartments.

In general, hyperchloremic metabolic acidosis is self-limiting with reduction of chloride load and judicious use of hydration solution , Serum bicarbonate that does not normalize with other metabolic parameters should alert the clinician to the need for more aggressive insulin therapy or further investigation.

The process of health care reform demands cost-efficient modes of delivering optimal care. The choice of management site intensive care unit, stepdown unit, or general medical ward therefore becomes a critical issue. Unfortunately, there are no randomized prospective studies that have evaluated the optimal site of care for either DKA or HHS.

Given the lack of such studies, the decision concerning the site of care must be based on known clinical prognostic indicators and on the availability of hospital resources. As stated earlier,similar outcomes of treatment of DKA have been noted in both community and training hospitals, and outcomes have not been altered by whether the managing physician is a family physician, a general internist, a house officer with attending supervision, or an endocrinologist 14 , 15 , 16 ,so long as standard written therapeutic guidelines are followed.

The response to initial therapy, which would preferably be in the emergency ward, can be used as a guideline for choosing the most appropriate hospital site for further care.

In the absence of indications for hemodynamic monitoring, the majority of such patients can be managed in less expensive step-down units rather than intensive care units after the initial emergency room evaluation and care 19 , Options of site of care for DKA patients with less mental obtundation and no hypotension following initial rehydration are based primarily on the availability of hospital resources.

Those patients who are mildly ketotic can be effectively managed on a general medical ward, assuming there are 1 sufficient nursing staff to allow frequent monitoring of vital signs and hourly administration of subcutaneous insulin and 2 on-site blood glucose monitoring equipment and rapid turn-around time for routine laboratory services.

Continuous intravenous insulin therapy is not generally recommended for use in general medical wards unless appropriately trained personnel are available. DKA patients with a mild condition who are alert and able to tolerate oral intake may be treated in the emergency room and observed for a few hours before discharge.

Given the known high mortality rate of HHS, the frequent presence of serious concomitant illnesses, and the usually advanced age of HHS patients,it is reasonable that all such patients be admitted to either step-down or intensive care units.

The two major precipitating factors in the development of DKA are inadequate insulin treatment including noncompliance and infection. In many cases, these events may be prevented by better access to medical care, including intensive patient education and effective communication with a health care provider during acute illnesses.

Goals in the prevention of hyperglycemic crises precipitated by either acute illness or stress have been outlined These goals included controlling insulin deficiency, decreasing excess stress hormone secretion,avoiding prolonged fasting state, and preventing severe dehydration.

Therefore, an educational program should review sick-day management with specific information on administration of short-acting insulin, including frequency of insulin administration, blood glucose goals during illness, means to suppress fever and treat infection, and initiation of an easily digestible liquid diet containing carbohydrates and salt.

Most importantly, the patient should never discontinue insulin and should solicit professional advice early in the course of the illness. Success with such a program depends on frequent interaction between the patient and the health care provider and on the level of involvement that the patient or family member is willing to take to avoid hospitalization.

A group of investigators reported on the successful prevention of recurrent DKA RDKA in a pediatric population with the introduction of a hierarchical set of medical, educational, and psychosocial interventions in a lower socioeconomic group After initiation of the program, the episodes of RDKA were reduced to 2.

RDKA ceased with or without psychotherapy. The authors concluded that RDKA is causally related to a variety of social and economic problems, but its prevention requires recognition that its proximate cause in certain groups is omission of insulin.

There is therefore a need for a support system to ensure adherence In addition,an education program directed toward pediatricians and school educators that promoted the signs and symptoms of diabetes was shown to be effective in decreasing ketoacidosis at the onset of diabetes As previously mentioned, many of the admissions for HHS are nursing home residents or elderly individuals who become dehydrated and are unaware or unable to treat the increasingly dehydrated state.

Better education of care givers as well as patients regarding conditions, procedures, and medications that may worsen diabetes control, use of glucose monitoring, and signs and symptoms of newly onset diabetes could potentially decrease the incidence and severity of HHS.

Because the most common reason for interrupted insulin is economic in nature, changes in the health care delivery system and in the access patients have to care and medications may be the most effective means of preventing DKA in this population.

The investigators showed that of 56 DKA admissions, only two patients tried to contact the diabetes unit for assistance Similarly, a study of hyperglycemic crises in an urban black population demonstrated that socioeconomic barriers, such as a low literacy rate, limited financial resources, and limited access to health care, might explain the continuing high rates of admission for DKA in this group of patients 5.

Hospitalizations for DKA in the past two decades have increased in some areas and declined in others 3. Because repeated admissions for DKA are estimated to drain approximately one out of every two health care dollars spent on adult patients with type 1 diabetes, resources need to be redirected toward prevention by funding better access to care and educational programs that address a variety of ethnicity-related health care beliefs.

This paper was peer-reviewed, modified, and approved by the Professional Practice Committee, October Abbreviations: Aao 2 , alveolar-to-arteriolar oxygen; AKA,alcoholic ketoacidosis; ARDS, adult respiratory distress syndrome; BUN, blood urea nitrogen; CPT, carnitine palmitoyl-transferase; CSF, cerebrospinal fluid;DKA, diabetic ketoacidosis; FFA, free fatty acid; HHS, hyperosmolar hyperglycemic state; IRI, immunoreactive insulin; Pao 2 , arteriolar partial pressure of oxygen; RDKA, recurrent DKA.

A table elsewhere in this issue shows conventional and Système International SI units and conversion factors for many substances.

Sign In or Create an Account. Search Dropdown Menu. header search search input Search input auto suggest. filter your search All Content All Journals Diabetes Care. Advanced Search. User Tools Dropdown.

Sign In. Skip Nav Destination Close navigation menu Article navigation. Volume 24, Issue 1. Previous Article Next Article.

Article Navigation. Management of Hyperglycemic Crises in Patients With Diabetes Abbas E. Kitabchi, PHD, MD ; Abbas E. Kitabchi, PHD, MD. From the Division of Endocrinology A.

This Site. Google Scholar. Guillermo E. Umpierrez, MD ; Guillermo E. Umpierrez, MD. Mary Beth Murphy, RN, MS, CDE, MBA ; Mary Beth Murphy, RN, MS, CDE, MBA.

Eugene J. Barrett, MD, PHD ; Eugene J. Barrett, MD, PHD. Robert A. Kreisberg, MD ; Robert A. Kreisberg, MD. John I. Malone, MD ; John I. Malone, MD. Barry M. Wall, MD Barry M. Wall, MD. Address correspondence and reprint requests to Abbas E. Kitabchi, PhD, MD,University of Tennessee, Memphis, Division of Endocrinology, Court Ave.

E-mail: akitabchi utmem. Diabetes Care ;24 1 — Get Permissions. toolbar search Search Dropdown Menu. toolbar search search input Search input auto suggest.

Figure 1. View large Download slide. Table 1. View large. View Large. Table 2. Table 3. Table 4. Figure 2. Table 5. Figure 3. Table 6. Table 7. Figure 4. Figure 5. Figure 6. Figure 7. Johnson DD, Palumbo PJ, Chu C: Diabetic ketoacidosis in a community-based population.

Mayo Clin Proc. Faich GA, Fishbein HA, Ellis SE: The epidemiology of diabetic acidosis: a population-based study Am J Epidemiol.

Centers for Disease Control, Division of Diabetes Translations: Diabetes Surveillance, Fishbein HA, Palumbo PJ: Acute metabolic complications in diabetes.

In Diabetes in America. Umpierrez GE, Kelly JP, Navarrete JE, Casals MMC, Kitabchi AE:Hyperglycemic crises in urban blacks. Arch Intern Med. Kitabchi AE, Fisher JN, Murphy MB, Rumbak MJ: Diabetic ketoacidosis and the hyperglycemic hyperosmolar nonketotic state.

In Joslin's Diabetes Mellitus. Javor KA, Kotsanos JG, McDonald RC, Baron AD, Kesterson JG, Tierney WM: Diabetic ketoacidosis charges relative to medical charges of adult patients with type I diabetes.

Diabetes Care. Wachtel TJ, Tetu-Mouradjain LM, Goldman DL, Ellis SE, O'Sullivan PS: Hyperosmolality and acidosis in diabetes mellitus: a three-year experience in Rhode Island.

J Gen Int Med. Carroll P, Matz R: Uncontrolled diabetes mellitus in adults:experience in treating diabetic ketoacidosis and hyperosmolar coma with low-dose insulin and uniform treatment regimen. Hamblin PS, Topliss DJ, Chosich N, Lording DW, Stockigt JR: Deaths associated with diabetic ketoacidosis and hyperosmolar coma, Med J Aust.

Basu A, Close CF, Jenkins D, Krentz AJ, Nattrass M, Wright AD:Persisting mortality in diabetic ketoacidosis. Diabet Med. Ellemann K, Soerensen JN, Pedersen L, Edsberg B, Andersen O:Epidemiology and treatment of diabetic ketoacidosis in a community population.

Clements RS, Vourganti B: Fatal, diabetic ketoacidosis: major causes and approaches to their prevention. Huffstutter E, Hawkes J, Kitabchi AE: Low-dose insulin for treatment of diabetic ketoacidosis in a private community hospital. South Med J. Gouin PE, Gossain VV, Rovner DR: Diabetic ketoacidosis: outcome in a community hospital.

Hamburger S, Barjenbruch P, Soffer A: Treatment of diabetic ketoacidosis by internist and family physicians: a comparative study.

J Fam Pract. Kitabchi AE, Sacks HS, Fisher JN: Clinical trials in diabetic ketoacidosis. In Methods in Diabetes Research. Kitabchi AE, Materi R, Murphy MB: Optimal insulin delivery in diabetic ketoacidosis DKA and hyperglycemic hyperosmolar nonketotic coma HHNC : Diabetes Care.

Kitabchi AE, Wall BM: Diabetic ketoacidosis. Med Clin North Am. Ennis ED, Stahl EJVB, Kreisberg RA: The hyperosmolar hyperglycemic syndrome. Diabetes Rev. Arieff AI, Carrol H: Nonketotic hyperosmolar coma with hyperglycemia: clinical features, pathophysiology, renal function, acid-base balance, plasma-cerebrospinal fluid equilibria, and the effects of therapy in 37 cases.

Morris LR, Kitabchi AE: Efficacy of low dose insulin therapy in severely obtunded patients with diabetic ketoacidosis. Kitabchi AE, Fisher JN: Insulin therapy of diabetic ketoacidosis:physiologic versus pharmacologic doses of insulin and their routes of administration. In Handbook of Diabetes Mellitus.

Kreisberg RA: Diabetic ketoacidosis: new concepts and trends in pathogenesis and treatment. Ann Int Med. Atchley DW, Loeb RF, Richards DW, Benedict EM, Driscoll ME: A detailed study of electrolyte balances following withdrawal and reestablishment of insulin therapy. J Clin Invest. Musey VC, Lee JK, Crawford R, Klatka MA, McAdams D, Phillips LS:Diabetes in urban African Americans: cessation of insulin therapy is the major precipitating cause of diabetic ketoacidosis.

Petzold R, Trabert C, Walther A, Schoffling K: Etiology and prognosis of diabetic coma: a retrospective study. Verh Dtsch Ges Inn Med. Soler NG, Bennett MA, FitzGerald MG, Malins JM: Intensive care in the management of diabetic ketoacidosis. Panzram G: Epidemiology of diabetic coma.

Schweiz Med Wochenschr. Berger W, Keller U, Vorster D: Mortality from diabetic coma at the Basle Cantonal Hospital during 2 consecutive observation periods and , using conventional insulin therapy and treatment with low dose insulin.

Umpierrez GE, Casals MMC, Gebhart SSP, Mixon PS, Clark WS, Phillips LS: Diabetic ketoacidosis in obese African-Americans. Nosadini R, Velussi M, Fioretto P: Frequency of hypoglycaemic and hyperglycaemic-ketotic episodes during conventional and subcutaneous continuous insulin infusion therapy in IDDM.

Diabet Nutr Metab. Teutsch SM, Herman WH, Dwyer DM, Lane JM: Mortality among diabetic patients using continuous subcutaneous insulin-infusion pumps. N Engl J Med. Kitabchi AE, Fisher JN, Burghen GA, Tsiu W, Huber CT: Problems associated with continuous subcutaneous insulin infusion. Horm Metab Res Suppl.

The DCCT Research Group: Implementation of treatment protocols in the Diabetes Control and Complications Trial. Polonsky WH, Anderson BJ, Lohrer PA, Aponte JE, Jacobson AM, Cole CF: Insulin omission in women with IDDM.

Rydall AC, Rodin GM, Olmsted MP, Devenyi RG, Daneman RG: Disordered eating behavior and microvascular complications in young women with insulindependent diabetes mellitus. Weissman JS, Gatsonis C, Epstein AM: Rates of avoidable hospitalization by insurance status in Massachusetts and Maryland.

Bondy PK, Bloom WL, Whitmer VS, Farrar BW: Studies of the role of the liver in human carbohydrate metabolism by the venous catheter technique.

Felig P, Sherwin RS, Soman V, Wahren J, Hendler R, Sacca L, Eigler N, Goldberg D, Walesky M: Hormonal interactions in the regulation of blood glucose. Recent Prog Horm Res. Miles JM, Rizza RA, Haymond MW, Gerich JE: Effects of acute insulin deficiency on glucose and ketone body turnover in man: evidence for the primacy overproduction of glucose and ketone bodies in the genesis of diabetic ketoacidosis.

Luzi L, Barrett EJ, Groop LC, Ferrannini E, DeFronzo RA: Metabolic effects of lowdose insulin therapy on glucose metabolism in diabetic ketoacidosis.

Vaag A, Hother-Nielsen O, Skott P, Anderson P, Richter EA,Beck-Nielsen H: Effect of acute hyperglycemia on glucose metabolism in skeletal muscles in IDDM patients. DeFronzo RA, Matsuda M, Barret E: Diabetic ketoacidosis: a combined metabolic-nephrologic approach to therapy.

Felig P, Wahren J: Influence of endogenous insulin secretion on splanchnic glucose and amino acid metabolism in man. Foster DW, McGarry JD: The metabolic derangements and treatment of diabetic ketoacidosis. Siperstein MD: Diabetic ketoacidosis and hyperosmolar coma.

Endocrinol Metab Clin North Am. Van der Werve G, Jeanrenaud B: Liver glycogen metabolism: an overview.

Diabetes Metab Rev. Exton JH: Mechanisms of hormonal regulation of hepatic glucose metabolism. Hue L: Gluconeogenesis and its regulation. Meyer C, Stumvoll M, Nadkarni V, Dostou J, Mitrakou A, Gerich J:Abnormal renal and hepatic glucose metabolism in type 2 diabetes mellitus.

Schade DS, Eaton RP: The temporal relationship between endogenously secreted stress hormone and metabolic decompensation in diabetic man. J Clin Endocrinol Metab. Alberti KGMM, Christensen NJ, Iversen J, Orskov H: Role of glucagon and other hormones in development of diabetic ketoacidosis.

Gerich JE, Lorenzi M, Bier DM, Schneider V, Tsalikiane E, Karam JH,Forsham PH: Prevention of human diabetic ketoacidosis by somatostatin:evidence for an essential role of glucagon. Muller WA, Faloona GR, Unger RH: Hyperglucagonemia in diabetic ketoacidosis: its prevalence and significance.

Am J Med. Kitabchi AE: Low-dose insulin therapy in diabetic ketoacidosis:fact or fiction? Pilkis SJ, El-Maghrabi MR, Claus TH: Fructose-2,6-biphosphate in control of hepatic gluconeogenesis. Granner D, Pilkis S: The genes of hepatic glucose metabolism.

J Biol Chem. O'Brien RM, Granner DK: PEPCK gene as model of inhibitory effects of insulin on gene transcription. Wasserman DH, Vranic M: Interaction between insulin and counterregulatory hormones in control of substrate utilization in health and diabetes during exercise.

Jensen MD, Caruso M, Heiling V: Insulin regulation of lipolysis in nondiabetic and IDDM subjects. Arner P, Kriegholm E, Engfeldt P, Bolinder J: Adrenergic regulation of lipolysis in situ at rest and during exercise. McGarry JD: Lilly Lecture new perspectives in the regulation of ketogenesis.

Nurjhan N, Consoli A, Gerich J: Increased lipolysis and its consequences on gluco-neogenesis in non-insulin-dependent diabetes mellitus. Gerich JE, Lorenzi M, Bier DM, Tsalikian E, Schneider V, Karam JH,Forsham PH: Effects of physiologic levels of glucagon and growth hormone on human carbohydrate and lipid metabolism: studies involving administration of exogenous hormone during suppression of endogenous hormone secretion with somatostatin.

Cook GA, King MT, Veech RL: Ketogenesis and malonyl coenzyme A content of isolated rat hepatocytes. McGarry JD, Woeltje KF, Kuwajima M, Foster DW: Regulation of ketogenesis and the renaissance of carnitine palmitoyl transferase. Zammit VA: Regulation of ketone body metabolism. a cellular perspective.

Ruderman NB, Goodman MN: Inhibition of muscle acetoacetate utilization during diabetic ketoacidosis. Am J Physiol. Reichard GA Jr, Skutches CL, Hoeldtke RD, Owen OE: Acetone metabolism in humans during diabetic ketoacidosis. Balasse EO, Fery F: Ketone body production and disposal: effects of fasting, diabetes, and exercise.

Nosadini R, Avogaro A, Doria A, Fioretto P, Trevisan R, Morocutti A: Ketone body metabolism: a physiological and clinical overview. Moreover, the insulin infusion rate can be increased based on BG around major meals time and can be continued at a higher rate for hours following any major meal 2.

Lastly, it is necessary to monitor BG among NPO patients closely. Randomized clinical trials compared the two strategies and found no difference 27 , Intravenous LD insulin administration has been associated with an increased risk of cerebral edema 27 , An acceptable alternative for patients with mild to moderate DKA could be a bolus of 0.

Patients with end-stage renal disease ESRD and acute kidney injury AKI are considered a high-risk category that necessitates extra care 32 , To avoid rapid increases in osmolality and hypoglycemia in these patients; it is recommended that insulin infusions begin at 0.

Subcutaneous insulin should overlap with intravenous insulin for at least minutes before its discontinuation to ensure the optimal transition of care 6 , A transition to subcutaneous long-acting insulin in addition to ultra-short acting insulin such as glargine and glulisine after resolution of DKA may result in reduced hypoglycemic events compared to other basal bolus regimens such as NPH insulin and insulin regular 24 , For newly diagnosed insulin-dependent diabetes patients, subcutaneous insulin may be started at a dose of 0.

The transition process in patients who were previously using insulin or antidiabetic agents before to DKA admission is still unclear 24 , In ICU settings, clinicians tend to hold all oral antidiabetic agents and rely on insulin regimens for in-patient management given the shorter half-life of insulin and its predictability 24 , This could potentially be an area for further investigation on the transition process and its implication on patient outcomes 24 , Insulin sequestering to plastic IV tubing has been described, resulting in insulin wasting and dose inaccuracy 34 , Flushing the IV tube with a priming fluid of 20 mL is adequate to minimize the insulin losses to IV tube 34 , Patients with hyperglycemic crisiss are at a higher risk of developing hypokalemia due to multifactorial process 1 , Insulin therapy, correction of acidosis, and hydration all together lead to the development of hypokalemia 1 , Additionally, volume depletion seen with hyperglycemic crisis leads to secondary hyperaldosteronism, which exacerbates hypokalemia by enhancing urinary potassium excretion 1 , Serum potassium level should be obtained immediately upon presentation and prior to initiating insulin therapy 1 , Potassium replacement is required regardless of the baseline serum potassium level due to hydration and insulin therapy, except among renal failure patients 1 , It is suggested to administer 20 —30 mEq potassium in each liter of intravenous fluid to keep a serum potassium concentration within the normal range 1 , In addition to possible hypokalemia, patients with the hyperglycemic crisis could present with hypophosphatemia 1 , Osmotic diuresis during hyperglycemic crisis increases the urinary phosphate excretion, and insulin therapy enhances intracellular phosphate shift 1 , Phosphate replacement is not a fundamental part of hyperglycemic crisis management, given the lack of evidence of clinical benefit 1 , 29 , A special consideration with phosphate administration is the secondary hypocalcemia 1 , 29 , Acidemia associated with DKA results from the overproduction of ketoacids, generated from the haptic metabolism of free fatty acids.

This hepatic metabolism occurs as a result of insulin resistance and an increase in the counterregulatory hormones contributing to the pathophysiology of DKA 37 , Tissue acidosis could lead to impaired myocardial contractility, systemic vasodilatation, inhibition of glucose utilization by insulin, and lowering the levels of 2,3-diphosphoglycerate 2,3-DPG in erythrocytes 37 — Sodium bicarbonate decreases the hemoglobin-oxygen affinity leading to tissue hypoxia; moreover, it is associated with hypernatremia, hypocalcemia, hypokalemia, hypercapnia, prolonged QTc interval, intracellular acidosis, and metabolic alkalosis 39 , The use of adjuvant sodium bicarbonate in the setting of DKA consistently shows a lack of clinical benefit and should be prescribed on a case-by-case basis.

Although this recommendation was not supported by solid evidence; many clinicians adopt the practice to avoid the unwanted side effect of severe metabolic acidosis.

Sodium bicarbonate moves potassium intracellularly, however, clinical benefit is uncertain, and the use is controversial 41 , Prompt therapy for patients with hyperglycemic crisis is essential in reducing morbidity and mortality 6 , If not treated or treated ineffectively, the prognosis can include serious complications such as seizures, organ failures, coma, and death 6 , When treatment is delayed, the overall mortality rate of HHS is higher than that of DKA, especially in older patients.

This difference in prognoses was comparable when patients were matched for age In DKA, prolonged hypotension can lead to acute myocardial and bowel infarction 6 , The kidney plays a vital role in normalizing massive pH and electrolyte abnormalities 6 , Patients with prior kidney dysfunction or patients who developed end-stage chronic kidney disease worsen the prognosis considerably 6 , In HHS, severe dehydration may predispose the patient to complications such as myocardial infarction, stroke, pulmonary embolism, mesenteric vein thrombosis, and disseminated intravascular coagulation 6 , The VTE risk was higher than diabetic patients without hyperglycemic crisis or diabetic acidosis patients Management of hyperglycemic crisis may also be associated with significant complications include electrolyte abnormalities, hypoglycemia, and cerebral edema 7.

This is due to the use of insulin and fluid replacement therapy 4 , 5. Therefore, frequent electrolytes and blood glucose concentrations monitoring are essential while insulin infusions and fluid replacements are continued 4 , 5. Cerebral edema is a rare but severe complication in children and adolescents and rarely affects adult patients older than 28 7.

This could be due to the lack of cerebral autoregulation, presentation with more severe acidosis and dehydration among children and adolescents The exact mechanism of cerebral edema development is unknown.

Some reports suggest that the risk of cerebral edema during hyperglycemic crisis management might be induced by rapid hydration, especially in the pediatric population.

However, a recent multicenter study for children with DKA who were randomized to receive isotonic versus hypotonic sodium IV fluid with different infusions rates did not show a difference in neurological outcomes Early identification and prompt therapy with mannitol or hypertonic saline can prevent neurological deterioration from DKA management 7 , Furthermore, higher blood urea nitrogen BUN and sodium concentrations have been identified as cerebral edema risk factors Thus, careful hydration with close electrolytes and BUN is recommended Other serious complications of hyperglycemic crisis may include transient AKI, pulmonary edema in patients with congestive heart failure, myocardial infarction, a rise in pancreatic enzymes with or without acute pancreatitis, cardiomyopathy, rhabdomyolysis in patients presented with severe dehydration 7 , All authors have contributed equally in writing, organizing, and reviewing this publication.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers.

Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN.

Hyperglycemic Crises in Adult Patients With Diabetes. Diabetes Care 32 7 — doi: PubMed Abstract CrossRef Full Text Google Scholar. Goyal A, Mathew UE, Golla KK, Mannar V, Kubihal S, Gupta Y, et al.

A Practical Guidance on the Use of Intravenous Insulin Infusion for Management of Inpatient Hyperglycemia. Diabetes Metab Syndrome: Clin Res Rev 15 5 CrossRef Full Text Google Scholar. Saeedi P. Global and Regional Diabetes Prevalence Estimates for and Projections for and Results From the International Diabetes Federation Diabetes Atlas, 9th Edition.

Diabetes Res Clin Pract Pasquel FJ, Umpierrez GE. Hyperosmolar Hyperglycemic State: A Historic Review of the Clinical Presentation, Diagnosis, and Treatment.

Dia Care 37 11 — Kitabchi AE, Umpierrez GE, Murphy MB, Barrett EJ, Kreisberg RA, Malone JI, et al. Management of Hyperglycemic Crises in Patients With Diabetes.

Diabetes Care 24 1 — Kitabchi AE, Umpierrez GE, Murphy MB, Kreisberg RA. Hyperglycemic Crises in Adult Patients With Diabetes: A Consensus Statement From the American Diabetes Association. Diabetes Care 29 12 — Karslioglu French E, Donihi AC, Korytkowski MT. Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic Syndrome: Review of Acute Decompensated Diabetes in Adult Patients.

BMJ I Fayfman M, Pasquel FJ, Umpierrez GE. Management of Hyperglycemic Crises. Med Clinics North Am 3 — Rains JL, Jain SK.

Oxidative Stress, Insulin Signaling, and Diabetes. Free Radical Biol Med 50 5 — Hoffman WH, Burek CL, Waller JL, Fisher LE, Khichi M, Mellick LB. Cytokine Response to Diabetic Ketoacidosis and Its Treatment.

Clin Immunol 3 — Hayami T, Kato Y, Kamiya H, Kondo M, Naito E, Sugiura Y, et al. Case of Ketoacidosis by a Sodium-Glucose Cotransporter 2 Inhibitor in a Diabetic Patient With a Low-Carbohydrate Diet. J Diabetes Investig , 6 5 — Umpierrez GE, Murphy MB, Kitabchi AE.

Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Syndrome. Diabetes Spectr 15 1 Kraut JA, Madias NE. Serum Anion Gap: Its Uses and Limitations in Clinical Medicine. Clin J Am Soc Nephrol 2 1 — Dhatariya K, Savage M, Claydon A, et al.

Joint British Diabetes Societies for Inpatient Care JBDS-IP Revised Guidelines. The Management of Diabetic Ketoacidosis in Adults Revised

Crisus diabetes medications Enhancing heart health Managihg continue hyperglycwmic which ones Enhancing heart health crisos temporarily stop. Note : Amazon Fashion Trends Fat intake and brain health diagnosis and treatment of diabetic ketoacidosis Ketosis Meal Plan in adults and in children share general crisjs, there are significant differences in their application, largely related to the increased risk of life-threatening cerebral edema with DKA in children and adolescents. The specific issues related to treatment of DKA in children and adolescents are addressed in the Type 1 Diabetes in Children and Adolescents chapter, p. Diabetic ketoacidosis DKA and hyperosmolar hyperglycemic state HHS are diabetes emergencies with overlapping features. With insulin deficiency, hyperglycemia causes urinary losses of water and electrolytes sodium, potassium, chloride and the resultant extracellular fluid volume ECFV depletion. Diabetic ketoacidosis DKA and hyperglycemic hyperosmolar state HHS are the two most serious hyperglycemic emergencies in patients hylerglycemic Enhancing heart health mellitus. DKA Fat intake and brain health often Managinv in patients Managimg type 1 diabetes, Heart health education patients with type 2 crisiw are byperglycemic to DKA under stressful conditions such as trauma, surgery, or infections. HHS is more common crisix adult and elderly patients with poorly controlled type 2 diabetes. DKA and HHS are characterized by insulinopenia and severe hyperglycemia; clinically, these two conditions differ by severity of metabolic acidosis, dehydration, and ketonemia. Management objectives for DKA and HHS include restoration of circulatory volume and tissue perfusion; correction of hyperglycemia, ketogenesis, and electrolyte imbalance; and identification and treatment of the precipitating event.

Author: Zuluzahn

2 thoughts on “Managing hyperglycemic crisis

Leave a comment

Yours email will be published. Important fields a marked *

Design by ThemesDNA.com