Hyperglycemia emergency protocol -
Diagnosis DKA or HHS should be suspected whenever patients have significant hyperglycemia, especially if they are ill or highly symptomatic. There are no definitive criteria for the diagnosis of DKA.
To make the diagnosis and determine the severity of DKA or HHS, the following should be assessed: Plasma levels of electrolytes and anion gap Glucose Creatinine Osmolality and beta-hydroxybutyric acid beta-OHB if available Blood gases arterial required for the severely ill Serum and urine ketones Fluid balance Level of consciousness Precipitating factors and complications.
DKA is more challenging to diagnose in the presence of the following conditions: Mixed acid-base disorders e.
associated vomiting, which will raise the bicarbonate level If there has been a shift in the redox potential favouring the presence of beta-OHB rendering serum ketone testing negative If the loss of keto-anions with sodium or potassium in osmotic diuresis has occurred, leading to a return of the plasma anion gap toward normal Ketones in both the serum and urine should be measured.
If there is an elevated anion gap and serum ketones are negative, beta-OHB levels should be measured. Measurement of serum lactate should be considered in hypoxic states.
Pregnant women in DKA typically present with lower glucose levels than non-pregnant women, and there are case reports of euglycemic DKA in pregnancy.
Management FIGURE 1 Patients with DKA and HHS are best managed in an intensive care unit or step-down setting with specialist care. In adult patients with DKA , 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 Search for precipitating cause [Grade D, Consensus].
In adult patients with HHS , a protocol should be followed that incorporates the following principles of treatment: Fluid resuscitation Avoidance of hypokalemia Avoidance of rapidly falling serum osmolality Search for precipitating cause, and Possibly insulin to further reduce hyperglycemia [Grade D, Consensus].
Volume status including fluid intake and output , vital signs, neurological status, plasma concentrations of electrolytes, anion gap, osmolality and glucose need to be monitored closely, initially as often as every 2 hours.
In individuals with DKA, IV 0. For persons with a HHS, IV fluid administration should be individualized based on the patient's needs [Grade D, Consensus]. Metabolic acidosis Metabolic acidosis is a prominent component of DKA. Patients with HHS have minimal or no acidosis. In individuals with DKA, an infusion of short-acting IV insulin of 0.
If you have trouble keeping your blood sugar within your target range, schedule an appointment to see your health care provider. Your provider can help you make changes to better manage your diabetes. Here's information to help you get ready for your appointment and know what to expect from your health care provider.
Illness or infections can cause your blood sugar to rise, so it's important to plan for these situations. Talk to your health care provider about creating a sick-day plan.
Questions to ask include:. On this page. Preparing for your appointment. Home blood sugar monitoring Routine blood sugar monitoring with a blood glucose meter is the best way to be sure that your treatment plan is keeping your blood sugar within your target range.
Hemoglobin A1C test During an appointment, your health care provider may conduct an A1C test. More Information. A1C test. Home treatment Talk to your health care provider about managing your blood sugar. Your health care provider may suggest the following: Get physical.
Regular exercise is often an effective way to control blood sugar. But don't exercise if you have ketones in your urine. This can drive your blood sugar even higher. Take your medication as directed. If you develop hyperglycemia often, your health care provider may adjust the dosage or timing of your medication.
Follow your diabetes eating plan. It helps to eat smaller portions and avoid sugary beverages and frequent snacking. If you're having trouble sticking to your meal plan, ask your health care provider or dietitian for help.
Check your blood sugar. Monitor your blood glucose as directed by your health care provider. Check more often if you're sick or if you're concerned about severe hyperglycemia or hypoglycemia. Adjust your insulin doses. Changes to your insulin program or a supplement of short-acting insulin can help control hyperglycemia.
A supplement is an extra dose of insulin used to help temporarily correct a high blood sugar level. Ask your health care provider how often you need an insulin supplement if you have high blood sugar.
Emergency treatment for severe hyperglycemia If you have signs and symptoms of diabetic ketoacidosis or hyperosmolar hyperglycemic state, you may be treated in the emergency room or admitted to the hospital.
Treatment usually includes: Fluid replacement. 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.
Thirty years of personal experience in hyperglycemic crises: diabetic ketoacidosis and hyperglycemic hyperosmolar state. Maust MS, Muramatsu RS, Egan K, Ahmed I. Perphenazine-associated hyperosmolar hyperglycemic state. J Clin Psychopharmacol.
Rock W, Elias M, Lev A, Saliba WR. Haloperidol-induced neuroleptic malignant syndrome complicated by hyperosmolar hyperglycemic state. Chen WY, Chen CC, Hung GC.
Hyperglycemic hyperosmolar state associated with low-dose quetiapine treatment in a patient with bipolar disorder. Curr Drug Saf. Ahuja N, Palanichamy N, Mackin P, Lloyd A. Olanzapine-induced hyper-glycaemic coma and neuroleptic malignant syndrome: case report and review of literature.
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Am J Med. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes.
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Mao S, Liu Z, Ding M. Central pontine myelinolysis in a patient with epilepsia partialis continua and hyperglycaemic hyperosmolar state. Ann Clin Biochem. Nyenwe EA, Kitabchi AE. Evidence-based management of hyperglycemic emergencies in diabetes mellitus. Wolfsdorf J, Glaser N, Sperling MA.
Diabetic ketoacidosis in infants, children, and adolescents: A consensus statement from the American Diabetes Association. Gogos CA, Giali S, Paliogianni F, Dimitracopoulos G, Bassaris HP, Vagenakis AG.
Interleukin-6 and C-reactive protein as early markers of sepsis in patients with diabetic ketoacidosis or hyperosmosis. Leung CB, Li PK, Lui SF, Lai KN. Acute renal failure ARF caused by rhabdomyolysis due to diabetic hyperosmolar nonketotic coma: a case report and literature review.
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search close. PREV Dec 1, NEXT. C 6 Phosphate replacement should be considered in patients with HHS only if hypophosphatemia is severe less than 1. C 6 Insulin therapy should be initiated in patients with HHS once fluid replacement has been started. C 6 Patients should be assessed and treated for underlying causes of HHS.
Causes and Risk Factors. Clinical Presentation. Diagnostic Testing. Calculating corrected serum sodium and effective serum osmolality.
Diagnostic criteria for DKA include blood glucose level of mg per dL INSULIN THERAPY. IDENTIFY AND TREAT THE CAUSE.
Your health care provider sets your Hyperglycrmia blood sugar range. Hyperglycemia emergency protocol Hgperglycemia people who have diabetes, Mayo Clinic e,ergency recommends the following Herbal medicine for hair loss blood sugar levels before meals:. For many Hyperglycemia emergency protocol who have diabetes, the American Diabetes Association generally recommends the following target blood sugar levels:. Your target blood sugar range may differ, especially if you're pregnant or you have other health problems that are caused by diabetes. Your target blood sugar range may change as you get older. Sometimes, reaching your target blood sugar range can be a challenge.The treatment Hyperglyce,ia Hyperglycemia emergency protocol and Hyperglyceia in adults Htperglycemia be reviewed here. The epidemiology, pathogenesis, clinical features, evaluation, and diagnosis of these disorders protpcol Hyperglycemia emergency protocol separately, Hyperglycemia emergency protocol.
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Find in Hyperglycemia emergency protocol Formulary Print Share. View Hyperglycemia emergency protocol. Language Chinese Emrgency. Hyperglycemia emergency protocol Energy balance and overall well-being B Hyperglyecmia, MD Michael Emmett, MD Protofol Editor: Hyperglyccemia M Nathan, MD Deputy Protoocl Katya Rubinow, MD Literature review current Low glycemic shopping list Jan Hypetglycemia This topic last updated: Oct 05, They are part of the spectrum of hyperglycemia, and each represents an extreme in the spectrum.
In addition, ketoacidosis with mild hyperglycemia or even normal blood glucose has become more common with the increased use of sodium-glucose cotransporter 2 [SGLT2] inhibitors. To continue reading this article, you must sign in with your personal, hospital, or group practice subscription.
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Treatment of diabetic ketoacidosis in adults. Treatment of hyperosmolar hyperglycemic state in adults. Diabetic ketoacidosis in adults: Rapid overview of emergency management.
Ketone response to treatment of diabetic ketoacidosis. Patient data flow sheet.
: Hyperglycemia emergency protocol| Key Messages for People with Diabetes | Learn how UpToDate can help you. Select the option that best describes you. View Topic. Font Size Small Normal Large. Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment. Formulary drug information for this topic. No drug references linked in this topic. Find in topic Formulary Print Share. View in. Language Chinese English. Authors: Irl B Hirsch, MD Michael Emmett, MD Section Editor: David M Nathan, MD Deputy Editor: Katya Rubinow, MD Literature review current through: Jan PLoS One. Zeitler P, Haqq A, Rosenbloom A, Glaser N Drugs and Therapeutics Committee of the Lawson Wilkins Pediatric Endocrine Society. Hyperglycemic hyperosmolar syndrome in children: pathophysiological considerations and suggested guidelines for treatment. J Pediatr. Fourtner SH, Weinzimer SA, Levitt Katz LE. Hyperglycemic hyperosmolar non-ketotic syndrome in children with type 2 diabetes. Chen HF, Wang CY, Lee HY, et al. Short-term case fatality rate and associated factors among inpatients with diabetic ketoacidosis and hyperglycemic hyperosmolar state: a hospital-based analysis over a 15—year period. Intern Med. Bhowmick SK, Levens KL, Rettig KR. Hyperosmolar hyperglycemic crisis: an acute life-threatening event in children and adolescents with type 2 diabetes mellitus. Endocr Pract. Rosenbloom AL. Hyperglycemic hyperosmolar state: an emerging pediatric problem. Fadini GP, de Kreutzenberg SV, Rigato M, et al. Characteristics and outcomes of the hyperglycemic hyperosmolar non-ketotic syndrome in a cohort of 51 consecutive cases at a single center. Diabetes Res Clin Pract. Morales AE, Rosenbloom AL. Death caused by hyperglycemic hyperosmolar state at the onset of type 2 diabetes. Piniés JA, Cairo G, Gaztambide S, Vazquez JA. Course and prognosis of patients with diabetic non ketotic hyperosmolar state. Diabetes Metab. Huang CC, Kuo SC, Chien TW, et al. Predicting the hyperglycemic crisis death PHD score: a new decision rule for emergency and critical care. Am J Emerg Med. Chu CH, Lee JK, Lam HC, Lu CC. Prognostic factors of hyperglycemic hyperosmolar nonketotic state. Chang Gung Med J. Boonen E, Van den Berghe G. Endocrine responses to critical illness: novel insights and therapeutic implications. J Clin Endocrinol Metab. Matz R. Management of the hyperosmolar hyperglycemic syndrome. Am Fam Physician. Gupta S, Prabhu MR, Gupta MS, Niblett D. Severe non-ketotic hyperosmolar coma—intensive care management. Eur J Anaesthesiol. Rains JL, Jain SK. Oxidative stress, insulin signaling, and diabetes. Free Radic Biol Med. Maletkovic J, Drexler A. Diabetic ketoacidosis and hyperglycemic hyperosmolar state. Endocrinol Metab Clin North Am. Keenan CR, Murin S, White RH. High risk for venous thromboembolism in diabetics with hyperosmolar state: comparison with other acute medical illnesses. J Thromb Haemost. Lin PY, Wang CY, Wang JY. Hyperosmolar hyperglycemic state induced myocardial infarction: a complex conjunction of chronic and acute complications with diabetes mellitus. J Cardiovasc Med Hagerstown. Milano A, Tadevosyan A, Hart R, Luizza A, Eberhardt M. An uncommon complication of hyperosmolar hyperglycemic state: bilateral above knee amputations. Sakakura C, Hagiwara A, Kin S, et al. A case of hyperosmolar nonketotic coma occurring during chemotherapy using cisplatin for gallbladder cancer. Trence DL, Hirsch IB. Hyperglycemic crises in diabetes mellitus type 2. Roefaro J, Mukherjee SM. Olanzapine-induced hyperglycemic non-ketonic coma. Ann Pharmacother. Munshi MN, Martin RE, Fonseca VA. Hyperosmolar nonketotic diabetic syndrome following treatment of human immunodeficiency virus infection with didanosine. Yildiz M, Gül C, Ozbay G. Hyperosmolar hyperglycaemic nonketotic coma associated with acute myocardial infarction: report of three cases. Acta Cardiol. Gooch BR. Cushing's syndrome manifesting as pseudo-central hypothyroidism and hyperosmolar diabetic coma. Kitabchi AE, Umpierrez GE, Fisher JN, Murphy MB, Stentz FB. Thirty years of personal experience in hyperglycemic crises: diabetic ketoacidosis and hyperglycemic hyperosmolar state. Maust MS, Muramatsu RS, Egan K, Ahmed I. Perphenazine-associated hyperosmolar hyperglycemic state. J Clin Psychopharmacol. Rock W, Elias M, Lev A, Saliba WR. Haloperidol-induced neuroleptic malignant syndrome complicated by hyperosmolar hyperglycemic state. Chen WY, Chen CC, Hung GC. Hyperglycemic hyperosmolar state associated with low-dose quetiapine treatment in a patient with bipolar disorder. Curr Drug Saf. Ahuja N, Palanichamy N, Mackin P, Lloyd A. Olanzapine-induced hyper-glycaemic coma and neuroleptic malignant syndrome: case report and review of literature. J Psychopharmacol. Cerimele JM. Hyperosmolar hyperglycemic state in a patient taking risperidone. Prim Care Companion J Clin Psychiatry. This is a very dangerous and life-threatening emergency situation. Even in type 2 diabetes, severe hyperglycemia can lead to unconsciousness and can be life-threatening. Signs of such an emergency situation may include, for example, severe fatigue, nausea, dizziness, visual disturbances, increased thirst and frequent urination. This is also referred to as hyperosmolar hyperglycemic syndrome. Here is a video of YouTube. When the iframes is activated, a connection to YouTube is established and, if necessary, cookies from YouTube are also used. For further information click on here: YouTube privacy policy. Bundesärztekammer et al. Version 4. Teilpublikation der Langfassung. Version 1. et al. Cookie Settings Wir verwenden Cookies, um grundlegende Funktionen dieser Webseite zu ermöglichen und um unser Angebot ständig verbessern zu können. Required Third party content. 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| Learn first aid for someone who is having a diabetic emergency | 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. Misra S, Oliver NS. Utility of ketone measurement in the prevention, diagnosis and management of diabetic ketoacidosis. Chiasson JL, Aris-Jilwan N, Belanger R, et al. Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state. CMAJ ;— Lebovitz HE. Diabetic ketoacidosis. Lancet ;— Cao X, Zhang X, Xian Y, et al. The diagnosis of diabetic acute complications using the glucose-ketone meter in outpatients at endocrinology department. Int J Clin Exp Med ;—5. Munro JF, Campbell IW, McCuish AC, et al. Euglycaemic diabetic ketoacidosis. Br Med J ;— Kuru B, Sever M, Aksay E, et al. Comparing finger-stick beta-hydroxybutyrate with dipstick urine tests in the detection of ketone bodies. Turk J Emerg Med ;— Guo RX, Yang LZ, Li LX, et al. Diabetic ketoacidosis in pregnancy tends to occur at lower blood glucose levels: Case-control study and a case report of euglycemic diabetic ketoacidosis in pregnancy. J Obstet Gynaecol Res ;— Oliver R, Jagadeesan P, Howard RJ, et al. Euglycaemic diabetic ketoacidosis in pregnancy: An unusual presentation. J Obstet Gynaecol ; Chico A, Saigi I, Garcia-Patterson A, et al. Glycemic control and perinatal outcomes of pregnancies complicated by type 1 diabetes: Influence of continuous subcutaneous insulin infusion and lispro insulin. Diabetes Technol Ther ;— May ME, Young C, King J. Resource utilization in treatment of diabetic ketoacidosis in adults. Am J Med Sci ;— Levetan CS, Passaro MD, Jablonski KA, et al. Effect of physician specialty on outcomes in diabetic ketoacidosis. Diabetes Care ;—5. Ullal J, McFarland R, Bachand M, et al. Use of a computer-based insulin infusion algorithm to treat diabetic ketoacidosis in the emergency department. Diabetes Technol Ther ;—3. Bull SV, Douglas IS, Foster M, et al. Mandatory protocol for treating adult patients with diabetic ketoacidosis decreases intensive care unit and hospital lengths of stay: Results of a nonrandomized trial. Crit Care Med ;—6. Waller SL, Delaney S, Strachan MW. Does an integrated care pathway enhance the management of diabetic ketoacidosis? Devalia B. Adherance to protocol during the acutemanagement of diabetic ketoacidosis: Would specialist involvement lead to better outcomes? Int J Clin Pract ;—2. Salahuddin M, Anwar MN. Study on effectiveness of guidelines and high dependency unit management on diabetic ketoacidosis patients. J Postgrad Med Inst ;—3. Corl DE, Yin TS, Mills ME, et al. Evaluation of point-of-care blood glucose measurements in patients with diabetic ketoacidosis or hyperglycemic hyperosmolar syndrome admitted to a critical care unit. J Diabetes Sci Technol ;— Kreisberg RA. Diabetic ketoacidosis: New concepts and trends in pathogenesis and treatment. Ann Intern Med ;— Mahoney CP, Vlcek BW, DelAguila M. Risk factors for developing brain herniation during diabetic ketoacidosis. Pediatr Neurol ;—7. Rosenbloom AL. Intracerebral crises during treatment of diabetic ketoacidosis. Adrogue HJ, Barrero J, Eknoyan G. Salutary effects of modest fluid replacement in the treatment of adults with diabetic ketoacidosis. Use in patients without extreme volume deficit. JAMA ;— Fein IA, Rachow EC, Sprung CL, et al. Relation of colloid osmotic pressure to arterial hypoxemia and cerebral edema during crystalloid volume loading of patients with diabetic ketoacidosis. Ann Intern Med ;—5. Owen OE, Licht JH, Sapir DG. Renal function and effects of partial rehydration during diabetic ketoacidosis. Diabetes ;— Kitabchi AE, Ayyagari V, Guerra SM. But don't exercise if you have ketones in your urine. This can drive your blood sugar even higher. Take your medication as directed. If you develop hyperglycemia often, your health care provider may adjust the dosage or timing of your medication. Follow your diabetes eating plan. It helps to eat smaller portions and avoid sugary beverages and frequent snacking. If you're having trouble sticking to your meal plan, ask your health care provider or dietitian for help. Check your blood sugar. Monitor your blood glucose as directed by your health care provider. Check more often if you're sick or if you're concerned about severe hyperglycemia or hypoglycemia. Adjust your insulin doses. Changes to your insulin program or a supplement of short-acting insulin can help control hyperglycemia. A supplement is an extra dose of insulin used to help temporarily correct a high blood sugar level. Ask your health care provider how often you need an insulin supplement if you have high blood sugar. Emergency treatment for severe hyperglycemia If you have signs and symptoms of diabetic ketoacidosis or hyperosmolar hyperglycemic state, you may be treated in the emergency room or admitted to the hospital. Treatment usually includes: Fluid replacement. 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. Inzucchi SE, et al. Glycemic control and vascular complications in type 2 diabetes mellitus. Comprehensive medical evaluation and assessment of comorbidities: Standards of Medical Care in Diabetes — Diabetes Care. The big picture: Checking your blood glucose. Castro MR expert opinion. Mayo Clinic, Rochester, Minn. July 7, Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment. Take care of your diabetes during sick days and special times. |
| For more information | There is a group of individuals with diabetes that present with DKA but do not have the typical features of type 1 diabetes. There are various terms given to characterize this condition, such as flatbush diabetes, type 1. There are several classification systems used to describe KPD that take into account pathophysiology and prognosis. Individuals with KPD have very little beta cell function, may or may not have beta cell antibodies, and some may require temporary or lifelong insulin therapy 9. Sick-day management that includes capillary beta-hydroxybutyrate monitoring reduces emergency room visits and hospitalizations in young people SGLT2 inhibitors may lower the threshold for developing DKA through a variety of different mechanisms 11— The presentation of the DKA is similar to those who develop DKA without SGLT2 inhibitor exposure, except that the blood glucose BG levels on presentation may not be as elevated as expected. In most cases, there is usually a known precipitant as a contributing factor, such as insulin dose reduction or omission, bariatric surgery or other surgery, alcohol, exercise, or low carbohydrate or reduced food intake 16— DKA or HHS should be suspected whenever people have significant hyperglycemia, especially if they are ill or highly symptomatic see above. As outlined in Figure 1 , to make the diagnosis and determine the severity of DKA or HHS, the following should be assessed: plasma levels of electrolytes and anion gap , plasma glucose PG , creatinine, osmolality and beta-hydroxybutyric acid beta-OHB if available , blood gases, serum and urine ketones, fluid balance, level of consciousness, precipitating factors and complications 1. Arterial blood gases may be required for more ill individuals, when knowing the adequacy of respiratory compensation and the A-a gradient is necessary. Otherwise, venous blood gases are usually adequate—the pH is typically 0. Point-of-care capillary blood beta-OHB measurement in emergency is sensitive and specific for DKA and, as a screening tool, may allow more rapid identification of hyperglycemic persons at risk for DKA 24— There are no definitive criteria for the diagnosis of DKA. DKA is more challenging to diagnose in the presence of the following conditions: 1 mixed acid-base disorders e. associated vomiting, which will raise the bicarbonate level ; 2 if there has been a shift in the redox potential, favouring the presence of beta-OHB rendering serum ketone testing negative ; or 3 if the loss of keto anions with sodium or potassium in osmotic diuresis has occurred, leading to a return of the plasma anion gap toward normal. It is, therefore, important to measure ketones in both the serum and urine. If there is an elevated anion gap and serum ketones are negative, beta-OHB levels should be measured. Negative urine ketones should not be used to rule out DKA Measurement of serum lactate should be considered in hypoxic states. Pregnant women in DKA typically present with lower PG levels than nonpregnant women 36 , and there are case reports of euglycemic DKA in pregnancy 37, 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. The issues that must be addressed in the individual presenting with DKA or HHS are outlined in Table 2. A summary of fluid therapy is outlined in Table 3 , and a management algorithm and formulas for calculating key measurements are provided in Figure 1. People with DKA and HHS are best managed in an intensive care unit or step-down setting 1,31,32 with specialist care 39, Protocols and insulin management software systems 41 may be beneficial 42,43 , but there can be challenges with achieving adherence 44, Volume status including fluid intake and output , vital signs, neurological status, plasma concentrations of electrolytes, anion gap, osmolality and glucose need to be monitored closely, initially as often as every 2 hours 1,31, Capillary blood glucose CBG measurements are unreliable in the setting of severe acidosis Precipitating factors must be diagnosed and treated 1,31, Restoring ECFV improves tissue perfusion and reduces plasma glucose levels both by dilution and by increasing urinary glucose losses. ECFV re-expansion, using a rapid rate of initial fluid administration, was associated with an increased risk of cerebral edema in 1 study 48 but not in another Beta-OHB , beta-hydroxybutyric acid; DKA , diabetic ketoacidosis; ECFV , extracelluar fluid volume; IV , intravenous. There have been no randomized trials that have studied strategies for potassium replacement. It is reasonable to treat the potassium deficit of HHS in the same way. Metabolic acidosis is a prominent component of DKA. People with HHS have minimal or no acidosis. Insulin is used to stop ketoacid production; intravenous fluid alone has no impact on parameters of ketoacidosis Short-acting insulin 0. There is no conclusive evidence supporting the use of an initial insulin bolus in adults and it is not recommended in children. Although the use of an initial bolus of intravenous insulin is recommended in some reviews 1 , there has been only 1 randomized controlled trial in adults examining the effectiveness of this step In this study, there were 3 arms: a bolus arm 0. Unfortunately, this study did not examine the standard dose of insulin in DKA 0. In children, using an initial bolus of intravenous insulin does not result in faster resolution of ketoacidosis 57,58 and increases the risk of cerebral edema see Type 1 Diabetes in Children and Adolescents chapter, p. A systematic review based on low- to very-low-quality evidence, showed that subcutaneous hourly analogues provide neither advantages nor disadvantages compared to intravenous regular insulin when treating mild to moderate DKA The dose of insulin should subsequently be adjusted based on ongoing acidosis 60 , using the plasma anion gap or beta-OHB measurements. Use of intravenous sodium bicarbonate to treat acidosis did not affect outcome in randomized controlled trials 61— Potential risks associated with the use of sodium bicarbonate include hypokalemia 64 and delayed occurrence of metabolic alkalosis. Hyperosmolality is due to hyperglycemia and a water deficit. However, serum sodium concentration may be reduced due to shift of water out of cells. The concentration of sodium needs to be corrected for the level of glycemia to determine if there is also a water deficit Figure 1. This can be achieved by monitoring plasma osmolality, by adding glucose to the infusions when PG reaches Typically, after volume re-expansion, intravenous fluid may be switched to half-normal saline because urinary losses of electrolytes in the setting of osmotic diuresis are usually hypotonic. The potassium in the infusion will also add to the osmolality. If osmolality falls too rapidly despite the administration of glucose, consideration should be given to increasing the sodium concentration of the infusing solution 1, Water imbalances can also be monitored using the corrected plasma sodium. Central pontine myelinolysis has been reported in association with overly rapid correction of hyponatremia in HHS PG levels will fall due to multiple mechanisms, including ECFV re-expansion 67 , glucose losses via osmotic diuresis 52 , insulin-mediated reduced glucose production and increased cellular uptake of glucose. Once PG reaches Similar doses of intravenous insulin can be used to treat HHS, although these individuals are not acidemic, and the fall in PG concentration is predominantly due to re-expansion of ECFV and osmotic diuresis Insulin has been withheld successfully in HHS 68 , but generally its use is recommended to reduce PG levels 1, 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 However, because hypophosphatemia has been associated with rhabdomyolysis in other states, administration of potassium phosphate in cases of severe hypophosphatemia may be considered for the purpose of trying to prevent rhabdomyolysis. Reported mortality in DKA ranges from 0. Mortality is usually due to the precipitating cause, electrolyte imbalances especially hypo- and hyperkalemia and cerebral edema. 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]. Negative urine ketones should not be used to rule out DKA [Grade D, Level 4 35 ]. In adults with DKA, intravenous 0. For adults with HHS, intravenous fluid administration should be individualized [Grade D, Consensus]. In adults with DKA, an infusion of short-acting intravenous insulin of 0. The insulin infusion rate should be maintained until the resolution of ketosis [Grade B, Level 2 60 ] as measured by the normalization of the plasma anion gap [Grade D, Consensus]. Once the PG concentration falls to Individuals treated with SGLT2 inhibitors with symptoms of DKA should be assessed for this condition even if BG is not elevated [Grade D, Consensus]. 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. Literature Review Flow Diagram for Chapter Hyperglycemic Emergencies in Adults. 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, — Search Menu. Article Navigation. Close mobile search navigation Article Navigation. Volume Journal Article. Development and implementation of a hyperglycemic emergency protocol Get access. Miyares, Pharm. Clinical Hospital Pharmacist, Internal Medicine, and Director, Postgraduate Year 1 Residency Program. Pharmacy Department Jackson Memorial Hospital N. mmiyares jhsmiami. Oxford Academic. Google Scholar. Ariel Zlicha, Pharm. Jeanette N. Rodriguez, Pharm. Cite Cite Marta A. Select Format Select format. ris Mendeley, Papers, Zotero. enw EndNote. bibtex BibTex. txt Medlars, RefWorks Download citation. Permissions Icon Permissions. Close Navbar Search Filter American Journal of Health-System Pharmacy This issue Pharmacology Books Journals Oxford Academic Enter search term Search. Extract Diabetic ketoacidosis DKA and hyperosmolar hyperglycemic state HHS are serious complications of diabetes mellitus. Issue Section:. You do not currently have access to this article. Download all slides. Comments 0. Add comment Close comment form modal. I agree to the terms and conditions. You must accept the terms and conditions. Add comment Cancel. Submit a comment. Comment title. You have entered an invalid code. Submit Cancel. Thank you for submitting a comment on this article. Your comment will be reviewed and published at the journal's discretion. Please check for further notifications by email. Recently, one case report has shown that a patient with diagnosed acromegaly may present with DKA as the primary manifestation of the disease In addition, an earlier report of pituitary gigantism was presented with two episodes of DKA with complete resolution of diabetes after pituitary apoplexy Successful treatment of DKA and HHS requires correction of dehydration, hyperglycemia, and electrolyte imbalances; identification of comorbid precipitating events; and above all, frequent patient monitoring. Protocols for the management of patients with DKA and HHS are summarized in Fig. Protocol for management of adult patients with DKA or HHS. Bwt, body weight; IV, intravenous; SC, subcutaneous. Initial fluid therapy is directed toward expansion of the intravascular, interstitial, and intracellular volume, all of which are reduced in hyperglycemic crises 53 and restoration of renal perfusion. In the absence of cardiac compromise, isotonic saline 0. Subsequent choice for fluid replacement depends on hemodynamics, the state of hydration, serum electrolyte levels, and urinary output. In general, 0. Fluid replacement should correct estimated deficits within the first 24 h. In patients with renal or cardiac compromise, monitoring of serum osmolality and frequent assessment of cardiac, renal, and mental status must be performed during fluid resuscitation to avoid iatrogenic fluid overload 4 , 10 , 15 , Aggressive rehydration with subsequent correction of the hyperosmolar state has been shown to result in a more robust response to low-dose insulin therapy During treatment of DKA, hyperglycemia is corrected faster than ketoacidosis. The mainstay in the treatment of DKA involves the administration of regular insulin via continuous intravenous infusion or by frequent subcutaneous or intramuscular injections 4 , 56 , Randomized controlled studies in patients with DKA have shown that insulin therapy is effective regardless of the route of administration The administration of continuous intravenous infusion of regular insulin is the preferred route because of its short half-life and easy titration and the delayed onset of action and prolonged half-life of subcutaneous regular insulin 36 , 47 , Numerous prospective randomized studies have demonstrated that use of low-dose regular insulin by intravenous infusion is sufficient for successful recovery of patients with DKA. Until recently, treatment algorithms recommended the administration of an initial intravenous dose of regular insulin 0. A recent prospective randomized study reported that a bolus dose of insulin is not necessary if patients receive an hourly insulin infusion of 0. If plasma glucose does not decrease by 50—75 mg from the initial value in the first hour, the insulin infusion should be increased every hour until a steady glucose decline is achieved Fig. Treatment with subcutaneous rapid-acting insulin analogs lispro and aspart has been shown to be an effective alternative to the use of intravenous regular insulin in the treatment of DKA. Treatment of patients with mild and moderate DKA with subcutaneous rapid-acting insulin analogs every 1 or 2 h in non—intensive care unit ICU settings has been shown to be as safe and effective as the treatment with intravenous regular insulin in the ICU 60 , The rate of decline of blood glucose concentration and the mean duration of treatment until correction of ketoacidosis were similar among patients treated with subcutaneous insulin analogs every 1 or 2 h or with intravenous regular insulin. However, until these studies are confirmed outside the research arena, patients with severe DKA, hypotension, anasarca, or associated severe critical illness should be managed with intravenous regular insulin in the ICU. Despite total-body potassium depletion, mild-to-moderate hyperkalemia is common in patients with hyperglycemic crises. Insulin therapy, correction of acidosis, and volume expansion decrease serum potassium concentration. To prevent hypokalemia, potassium replacement is initiated after serum levels fall below the upper level of normal for the particular laboratory 5. Generally, 20—30 mEq potassium in each liter of infusion fluid is sufficient to maintain a serum potassium concentration within the normal range. Rarely, DKA patients may present with significant hypokalemia. The use of bicarbonate in DKA is controversial 62 because most experts believe that during the treatment, as ketone bodies decrease there will be adequate bicarbonate except in severely acidotic patients. Severe metabolic acidosis can lead to impaired myocardial contractility, cerebral vasodilatation and coma, and several gastrointestinal complications A prospective randomized study in 21 patients failed to show either beneficial or deleterious changes in morbidity or mortality with bicarbonate therapy in DKA patients with an admission arterial pH between 6. Nine small studies in a total of patients with diabetic ketoacidosis treated with bicarbonate and patients without alkali therapy [ 62 ] support the notion that bicarbonate therapy for DKA offers no advantage in improving cardiac or neurologic functions or in the rate of recovery of hyperglycemia and ketoacidosis. Moreover, several deleterious effects of bicarbonate therapy have been reported, such as increased risk of hypokalemia, decreased tissue oxygen uptake 65 , cerebral edema 65 , and development of paradoxical central nervous system acidosis. Despite whole-body phosphate deficits in DKA that average 1. Phosphate concentration decreases with insulin therapy. Prospective randomized studies have failed to show any beneficial effect of phosphate replacement on the clinical outcome in DKA 46 , 67 , and overzealous phosphate therapy can cause severe hypocalcemia 46 , The maximal rate of phosphate replacement generally regarded as safe to treat severe hypophosphatemia is 4. No studies are available on the use of phosphate in the treatment of HHS. Patients with DKA and HHS should be treated with continuous intravenous insulin until the hyperglycemic crisis is resolved. Resolution of HHS is associated with normal osmolality and regain of normal mental status. When this occurs, subcutaneous insulin therapy can be started. To prevent recurrence of hyperglycemia or ketoacidosis during the transition period to subcutaneous insulin, it is important to allow an overlap of 1—2 h between discontinuation of intravenous insulin and the administration of subcutaneous insulin. Patients with known diabetes may be given insulin at the dosage they were receiving before the onset of DKA so long as it was controlling glucose properly. In insulin-naïve patients, a multidose insulin regimen should be started at a dose of 0. Human insulin NPH and regular are usually given in two or three doses per day. More recently, basal-bolus regimens with basal glargine and detemir and rapid-acting insulin analogs lispro, aspart, or glulisine have been proposed as a more physiologic insulin regimen in patients with type 1 diabetes. A prospective randomized trial compared treatment with a basal-bolus regimen, including glargine once daily and glulisine before meals, with a split-mixed regimen of NPH plus regular insulin twice daily following the resolution of DKA. Hypoglycemia and hypokalemia are two common complications with overzealous treatment of DKA with insulin and bicarbonate, respectively, but these complications have occurred less often with the low-dose insulin therapy 4 , 56 , Frequent blood glucose monitoring every 1—2 h is mandatory to recognize hypoglycemia because many patients with DKA who develop hypoglycemia during treatment do not experience adrenergic manifestations of sweating, nervousness, fatigue, hunger, and tachycardia. Hyperchloremic non—anion gap acidosis, which is seen during the recovery phase of DKA, is self-limited with few clinical consequences This may be caused by loss of ketoanions, which are metabolized to bicarbonate during the evolution of DKA and excess fluid infusion of chloride containing fluids during treatment 4. Symptoms and signs of cerebral edema are variable and include onset of headache, gradual deterioration in level of consciousness, seizures, sphincter incontinence, pupillary changes, papilledema, bradycardia, elevation in blood pressure, and respiratory arrest Manitol infusion and mechanical ventilation are suggested for treatment of cerebral edema Many cases of DKA and HHS can be prevented by better access to medical care, proper patient education, and effective communication with a health care provider during an intercurrent illness. Paramount in this effort is improved education regarding sick day management, which includes the following:. Emphasizing the importance of insulin during an illness and the reasons never to discontinue without contacting the health care team. Similarly, adequate supervision and staff education in long-term facilities may prevent many of the admissions for HHS due to dehydration among elderly individuals who are unable to recognize or treat this evolving condition. The use of home glucose-ketone meters may allow early recognition of impending ketoacidosis, which may help to guide insulin therapy at home and, possibly, may prevent hospitalization for DKA. In addition, home blood ketone monitoring, which measures β-hydroxybutyrate levels on a fingerstick blood specimen, is now commercially available The observation that stopping insulin for economic reasons is a common precipitant of DKA 74 , 75 underscores the need for our health care delivery systems to address this problem, which is costly and clinically serious. The rate of insulin discontinuation and a history of poor compliance accounts for more than half of DKA admissions in inner-city and minority populations 9 , 74 , Several cultural and socioeconomic barriers, such as low literacy rate, limited financial resources, and limited access to health care, in medically indigent patients may explain the lack of compliance and why DKA continues to occur in such high rates in inner-city patients. These findings suggest that the current mode of providing patient education and health care has significant limitations. Addressing health problems in the African American and other minority communities requires explicit recognition of the fact that these populations are probably quite diverse in their behavioral responses to diabetes Significant resources are spent on the cost of hospitalization. Based on an annual average of , hospitalizations for DKA in the U. A recent study 2 reported that the cost burden resulting from avoidable hospitalizations due to short-term uncontrolled diabetes including DKA is substantial 2. However, the long-term impact of uncontrolled diabetes and its economic burden could be more significant because it can contribute to various complications. Because most cases occur in patients with known diabetes and with previous DKA, resources need to be redirected toward prevention by funding better access to care and educational programs tailored to individual needs, including ethnic and personal health care beliefs. In addition, resources should be directed toward the education of primary care providers and school personnel so that they can identify signs and symptoms of uncontrolled diabetes and so that new-onset diabetes can be diagnosed at an earlier time. Recent studies suggest that any type of education for nutrition has resulted in reduced hospitalization In fact, the guidelines for diabetes self-management education were developed by a recent task force to identify ten detailed standards for diabetes self-management education An American Diabetes Association consensus statement represents the authors' collective analysis, evaluation, and opinion at the time of publication and does not represent official association opinion. 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 32, Issue 7. Previous Article Next Article. Article Navigation. Consensus Statements July 01 Hyperglycemic Crises in Adult Patients With Diabetes Abbas E. Kitabchi, PHD, MD ; Abbas E. Kitabchi, PHD, MD. Corresponding author: Abbas E. Kitabchi, akitabchi utmem. This Site. |
| Chapter 15: Hyperglycemic Emergencies in Adults | When this Hyperglyecmia, subcutaneous insulin therapy can Health-conscious energy source started. Pediatr Hyperglycemia emergency protocol Care ;—9. Causes and Risk Factors. If the person is unconscious, call the emergency service or immediately. High risk for venous thromboembolism in diabetics with hyperosmolar state: comparison with other acute medical illnesses. |
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