Managing diabetic emergencies: hyperglycemia and diabetic ketoacidosis
Review article for paramedics, emergency medical services, nursing, and health informatics
Keywords:
Diabetic ketoacidosis, hyperglycemic hyperosmolar state, diabetes management, epidemiology, insulin therapyAbstract
Background: Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) are severe hyperglycemic crises that can occur in individuals with diabetes. While they are often treated as separate conditions, they exist on a continuum of hyperglycemic emergencies related to inadequate diabetes management. Aim: This review aims to provide an overview of DKA and HHS, exploring their epidemiology, pathogenesis, diagnosis, and management strategies. The review focus on the main role of paramedics, emergency medical services, nursing, and health informatics in the management of DKA. Methods: The article synthesizes data from various epidemiological studies, clinical case reviews, and historical accounts of diabetic emergencies to highlight the clinical characteristics and treatment approaches for DKA and HHS. Results: The incidence of DKA has risen significantly, leading to over 140,000 hospitalizations annually in the United States. While DKA is more common in younger individuals with type 1 diabetes, HHS primarily affects older patients with type 2 diabetes. Both conditions share common treatment principles, including fluid rehydration, insulin therapy, and electrolyte replacement, with timely intervention critical for improving outcomes. Conclusion: DKA and HHS represent serious medical conditions that necessitate swift diagnosis and management.
Downloads
References
Kitabchi AE, Umpierrez GE, Miles JM, et al. Hyperglycemic crises in adult pa tients with diabetes. Diabetes Care 2009;32(7):1335–43. DOI: https://doi.org/10.2337/dc09-9032
Centers for Disease Control and Prevention. Mortality due to Hyperglycemic cri ses. 2013. Available at: http://www.cdc.gov/diabetes/statistics/complications_ national.htm. Accessed September 2, 2016.
Ennis ED, Stahl EJVB, Kreisberg RA. The hyperosmolar hyperglycemic syn drome. Diabetes Rev 1994;2:115–26.
Umpierrez GE, Kelly JP, Navarrete JE, et al. Hyperglycemic crises in urban blacks. Arch Intern Med 1997;157(6):669–75. DOI: https://doi.org/10.1001/archinte.157.6.669
von Stosch A. Versuch einer Pathologie und Therapie des Diabetes Mellitus. Berlin: Duncker und Humblot; 1828 [in German].
Parsons J. Case of infantile diabetes. Prov Med Surg J 1849;13(13):342–3. DOI: https://doi.org/10.1136/bmj.s1-13.13.342
Hindle R. Case of acute diabetes. Prov Med Surg J 1845;9(29):452–3. DOI: https://doi.org/10.1136/bmj.s1-9.29.452
Favell CF. Cases of diabetes. Prov Med J Retrosp Med Sci 1843;6(153):467–9. DOI: https://doi.org/10.1136/bmj.s1-6.153.467
Kussmaul A. Zur lehre vom diabetes mellitus. Dtsch Arch Klin Med 1874;14: 1–46 [in German].
Adolf Kussmaul (1822-1902)–Country Doctor to Clinical Professor. JAMA 1964; 189:58–9. DOI: https://doi.org/10.1001/jama.1964.03070010064017
Stadelmann E. Ueber die Ursachen der pathologischen ammoniakausschei dung beim diabetes mellitus und des coma diabeticum. Arch Exp Pathol Phar makol 1883;17:419–44 [in German]. DOI: https://doi.org/10.1007/BF02055590
Ku¨lz E. Ueber eine neue linksdrehende saure (pseudo-oxybuttersaure). Zeitschr f Biologie 1884;20:165–78 [in German].
Dreschfeld J. The Bradshawe lecture on diabetic coma. Br Med J 1886;2(1338): 358–63. DOI: https://doi.org/10.1136/bmj.2.1338.358
Banting FG, Best CH, Collip JB, et al. Pancreatic extracts in the treatment of dia betes mellitus: preliminary report. Can Med Assoc J 1962;87(20):1062–7.
Rabinowitch IM. Diabetic coma and diabetic mortality rates. Can Med Assoc J 1929;21(5):583–6.
Clements RS Jr, Vourganti B. Fatal diabetic ketoacidosis: major causes and ap proaches to their prevention. Diabetes Care 1978;1(5):314–25. DOI: https://doi.org/10.2337/diacare.1.5.314
Felig P. Diabetic ketoacidosis. N Engl J Med 1974;290(24):1360–3. DOI: https://doi.org/10.1056/NEJM197406132902405
Graves EJ, Gillium BS. Detailed diagnosis and procedures: National Discharge Survey, 1995. National Center for Health Statistics. Vital Health Stat 13 1997; 13(130):1–146.
Wagner A, Risse A, Brill HL, et al. Therapy of severe diabetic ketoacidosis. Zero mortality under very-low-dose insulin application. Diabetes Care 1999;22(5): 674–7. DOI: https://doi.org/10.2337/diacare.22.5.674
Pasquel FJ, Umpierrez GE. Hyperosmolar hyperglycemic state: a historic review of the clinical presentation, diagnosis, and treatment. Diabetes Care 2014; 37(11):3124–31. Management of Hyperglycemic Crises 601 DOI: https://doi.org/10.2337/dc14-0984
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 2011;94(2):172–9. DOI: https://doi.org/10.1016/j.diabres.2011.06.018
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 2008;25(7):867–70. DOI: https://doi.org/10.1111/j.1464-5491.2008.02461.x
Karges B, Rosenbauer J, Holterhus PM, et al. Hospital admission for diabetic ketoacidosis or severe hypoglycemia in 31,330 young patients with type 1 dia betes. Eur J Endocrinol 2015;173(3):341–50. DOI: https://doi.org/10.1530/EJE-15-0129
Maahs DM, Hermann JM, Holman N, et al. Rates of diabetic ketoacidosis: inter national comparison with 49,859 pediatric patients with type 1 diabetes from En gland, Wales, the U.S., Austria, and Germany. Diabetes Care 2015;38(10): 1876–82. DOI: https://doi.org/10.2337/dc15-0780
Miller KM, Foster NC, Beck RW, et al. Current state of type 1 diabetes treatment in the U.S.: updated data from the T1D Exchange clinic registry. Diabetes Care 2015;38(6):971–8. DOI: https://doi.org/10.2337/dc15-0078
Rosenbloom AL. Hyperglycemic hyperosmolar state: an emerging pediatric problem. J Pediatr 2010;156(2):180–4. DOI: https://doi.org/10.1016/j.jpeds.2009.11.057
Savage MW, Dhatariya KK, Kilvert A, et al. Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis. Diabet Med 2011; 28(5):508–15. DOI: https://doi.org/10.1111/j.1464-5491.2011.03246.x
Otieno CF, Kayima JK, Omonge EO, et al. Diabetic ketoacidosis: risk factors, mechanisms and management strategies in sub-Saharan Africa: a review. East Afr Med J 2005;82(12 Suppl):S197–203. DOI: https://doi.org/10.4314/eamj.v82i12.9382
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 2005;11(1):23–9. DOI: https://doi.org/10.4158/EP.11.1.23
Wachtel TJ, Silliman RA, Lamberton P. Prognostic factors in the diabetic hyper osmolar state. J Am Geriatr Soc 1987;35(8):737–41. DOI: https://doi.org/10.1111/j.1532-5415.1987.tb06351.x
Basu A, Close CF, Jenkins D, et al. Persisting mortality in diabetic ketoacidosis. Diabet Med 1993;10(3):282–4. DOI: https://doi.org/10.1111/j.1464-5491.1993.tb00060.x
Malone ML, Gennis V, Goodwin JS. Characteristics of diabetic ketoacidosis in older versus younger adults. J Am Geriatr Soc 1992;40(11):1100–4. DOI: https://doi.org/10.1111/j.1532-5415.1992.tb01797.x
Gibb FW, Teoh WL, Graham J, et al. Risk of death following admission to a UK hospital with diabetic ketoacidosis. Diabetologia 2016;59(10):2082–7. DOI: https://doi.org/10.1007/s00125-016-4034-0
Huang CC, Weng SF, Tsai KT, et al. Long-term mortality risk after hyperglycemic crisis episodes in geriatric patients with diabetes: a national population-based cohort study. Diabetes Care 2015;38(5):746–51. DOI: https://doi.org/10.2337/dc14-1840
Gregg EW, Williams DE, Geiss L. Changes in diabetes-related complications in the United States. N Engl J Med 2014;371(3):286–7. DOI: https://doi.org/10.1056/NEJMc1406009
Javor KA, Kotsanos JG, McDonald RC, et al. Diabetic ketoacidosis charges relative to medical charges of adult patients with type I diabetes. Diabetes Care 1997;20(3):349–54. DOI: https://doi.org/10.2337/diacare.20.3.349
Klingensmith GJ, Tamborlane WV, Wood J, et al. Diabetic ketoacidosis at dia betes onset: still an all too common threat in youth. J Pediatr 2013;162(2): 330–4.e1. DOI: https://doi.org/10.1016/j.jpeds.2012.06.058
Dabelea D, Rewers A, Stafford JM, et al. Trends in the prevalence of ketoacido sis at diabetes diagnosis: the SEARCH for diabetes in youth study. Pediatrics 2014;133(4):e938–45. 602 DOI: https://doi.org/10.1542/peds.2013-2795
Randall L, Begovic J, Hudson M, et al. Recurrent diabetic ketoacidosis in inner city minority patients: behavioral, socioeconomic, and psychosocial factors. Diabetes Care 2011;34(9):1891–6. DOI: https://doi.org/10.2337/dc11-0701
Maldonado MR, Chong ER, Oehl MA, et al. Economic impact of diabetic ketoa cidosis in a multiethnic indigent population: analysis of costs based on the precipitating cause. Diabetes Care 2003;26(4):1265–9. DOI: https://doi.org/10.2337/diacare.26.4.1265
Musey VC, Lee JK, Crawford R, et al. Diabetes in urban African-Americans. I. Cessation of insulin therapy is the major precipitating cause of diabetic ketoaci dosis. Diabetes Care 1995;18(4):483–9. DOI: https://doi.org/10.2337/diacare.18.4.483
Umpierrez G, Freire AX. Abdominal pain in patients with hyperglycemic crises. J Crit Care 2002;17(1):63–7. DOI: https://doi.org/10.1053/jcrc.2002.33030
Barnard KD, Skinner TC, Peveler R. The prevalence of co-morbid depression in adults with type 1 diabetes: systematic literature review. Diabet Med 2006;23(4): 445–8. DOI: https://doi.org/10.1111/j.1464-5491.2006.01814.x
Canadian Diabetes Association Clinical Practice Guidelines Expert Committee, Goguen J, Gilbert J. Hyperglycemic emergencies in adults. Can J Diabetes 2013;37(Suppl 1):S72–6. DOI: https://doi.org/10.1016/j.jcjd.2013.01.023
Garg SK, Walker AJ, Hoff HK, et al. Glycemic parameters with multiple daily in jections using insulin glargine versus insulin pump. Diabetes Technol Ther 2004; 6(1):9–15. DOI: https://doi.org/10.1089/152091504322783350
Implementation of treatment protocols in the Diabetes Control and Complica tions Trial. Diabetes Care 1995;18(3):361–76. DOI: https://doi.org/10.2337/diacare.18.3.361
Ly TT, Nicholas JA, Retterath A, et al. Effect of sensor-augmented insulin pump therapy and automated insulin suspension vs standard insulin pump therapy on hypoglycemia in patients with type 1 diabetes: a randomized clinical trial. JAMA 2013;310(12):1240–7. DOI: https://doi.org/10.1001/jama.2013.277818
Johnson SR, Cooper MN, Jones TW, et al. Long-term outcome of insulin pump therapy in children with type 1 diabetes assessed in a large population-based case-control study. Diabetologia 2013;56(11):2392–400. DOI: https://doi.org/10.1007/s00125-013-3007-9
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 1991;6(6):495–502. DOI: https://doi.org/10.1007/BF02598216
Gerich JE, Martin MM, Recant L. Clinical and metabolic characteristics of hyper osmolar nonketotic coma. Diabetes. 1971;20(4):228–38. DOI: https://doi.org/10.2337/diab.20.4.228
Ben Salem C, Fathallah N, Hmouda H, et al. Drug-induced hypoglycaemia: an update. Drug Saf 2011;34(1):21–45. DOI: https://doi.org/10.2165/11538290-000000000-00000
Caro JJ, Ward A, Levinton C, et al. The risk of diabetes during olanzapine use compared with risperidone use: a retrospective database analysis. J Clin Psy chiatry 2002;63(12):1135–9. DOI: https://doi.org/10.4088/JCP.v63n1208
Buse JB, Cavazzoni P, Hornbuckle K, et al. A retrospective cohort study of dia betes mellitus and antipsychotic treatment in the United States. J Clin Epidemiol 2003;56(2):164–70. DOI: https://doi.org/10.1016/S0895-4356(02)00588-7
Gianfrancesco F, Grogg A, Mahmoud R, et al. Differential effects of antipsy chotic agents on the risk of development of type 2 diabetes mellitus in patients with mood disorders. Clin Ther 2003;25(4):1150–71. DOI: https://doi.org/10.1016/S0149-2918(03)80073-5
Ananth J, Parameswaran S, Gunatilake S. Side effects of atypical antipsychotic drugs. Curr Pharm Des 2004;10(18):2219–29. DOI: https://doi.org/10.2174/1381612043384088
Lipscombe LL, Austin PC, Alessi-Severini S, et al. Atypical antipsychotics and hyperglycemic emergencies: multicentre, retrospective cohort study of adminis trative data. Schizophr Res 2014;154(1–3):54–60. Management of Hyperglycemic Crises 603 DOI: https://doi.org/10.1016/j.schres.2014.01.043
Peters AL, Buschur EO, Buse JB, et al. Euglycemic diabetic ketoacidosis: a po tential complication of treatment with sodium-glucose cotransporter 2 inhibition. Diabetes Care 2015;38(9):1687–93. DOI: https://doi.org/10.2337/dc15-0843
Perspective Taylor SI, Blau JE, Rother KI. SGLT2 inhibitors may predispose to ketoacidosis. J Clin Endocrinol Metab 2015;100(8):2849–52. DOI: https://doi.org/10.1210/jc.2015-1884
Erondu N, Desai M, Ways K, et al. Diabetic ketoacidosis and related events in the canagliflozin type 2 diabetes clinical program. Diabetes Care 2015;38(9): 1680–6. DOI: https://doi.org/10.2337/dc15-1251
Tang H, Li D, Wang T, et al. Effect of sodium-glucose cotransporter 2 inhibitors on diabetic ketoacidosis among patients with type 2 diabetes: a meta-analysis of randomized controlled trials. Diabetes care 2016;39(8):e123–4. DOI: https://doi.org/10.2337/dc16-0885
Kibbey RG. SGLT-2 inhibition and glucagon: cause for alarm? Trends Endocrinol Metab 2015;26(7):337–8. DOI: https://doi.org/10.1016/j.tem.2015.05.011
Waldhausl W, Kleinberger G, Korn A, et al. Severe hyperglycemia: effects of rehydration on endocrine derangements and blood glucose concentration. Dia betes. 1979;28(6):577–84. DOI: https://doi.org/10.2337/diab.28.6.577
Chupin M, Charbonnel B, Chupin F. C-peptide blood levels in keto-acidosis and in hyperosmolar non-ketotic diabetic coma. Acta Diabetol Lat 1981;18(2):123–8. DOI: https://doi.org/10.1007/BF02098997
Kitabchi AE, Umpierrez GE, Murphy MB, et al. Management of hyperglycemic crises in patients with diabetes. Diabetes Care 2001;24(1):131–53. DOI: https://doi.org/10.2337/diacare.24.1.131
Maldonado M, Hampe CS, Gaur LK, et al. Ketosis-prone diabetes: dissection of a heterogeneous syndrome using an immunogenetic and beta-cell functional classification, prospective analysis, and clinical outcomes. J Clin Endocrinol Metab 2003;88(11):5090–8. DOI: https://doi.org/10.1210/jc.2003-030180
Miles JM, Rizza RA, Haymond MW, et al. Effects of acute insulin deficiency on glucose and ketone body turnover in man: evidence for the primacy of overpro duction of glucose and ketone bodies in the genesis of diabetic ketoacidosis. Diabetes 1980;29(11):926–30. DOI: https://doi.org/10.2337/diab.29.11.926
Foster DW, McGarry JD. The metabolic derangements and treatment of diabetic ketoacidosis. N Engl J Med 1983;309(3):159–69. DOI: https://doi.org/10.1056/NEJM198307213090307
Laffel L. Ketone bodies: a review of physiology, pathophysiology and applica tion of monitoring to diabetes. Diabetes Metab Res Rev 1999;15(6):412–26. DOI: https://doi.org/10.1002/(SICI)1520-7560(199911/12)15:6<412::AID-DMRR72>3.0.CO;2-8
Miles JM, Haymond MW, Nissen SL, et al. Effects of free fatty acid availability, glucagon excess, and insulin deficiency on ketone body production in postab sorptive man. J Clin Invest 1983;71(6):1554–61. DOI: https://doi.org/10.1172/JCI110911
McGarry JD, Foster DW. Effects of exogenous fatty acid concentration on glucagon-induced changes in hepatic fatty acid metabolism. Diabetes. 1980; 29(3):236–40. DOI: https://doi.org/10.2337/diabetes.29.3.236
McGarry JD, Foster DW. Regulation of hepatic fatty acid oxidation and ketone body production. Annu Rev Biochem 1980;49:395–420. DOI: https://doi.org/10.1146/annurev.bi.49.070180.002143
Rains JL, Jain SK. Oxidative stress, insulin signaling, and diabetes. Free Radic Biol Med 2011;50(5):567–75. DOI: https://doi.org/10.1016/j.freeradbiomed.2010.12.006
Li J, Huang M, Shen X. The association of oxidative stress and pro-inflammatory cytokines in diabetic patients with hyperglycemic crisis. J Diabetes Complica tions 2014;28(5):662–6. DOI: https://doi.org/10.1016/j.jdiacomp.2014.06.008
Vaarala O, Yki-Jarvinen H. Diabetes: should we treat infection or inflammation to prevent T2DM? Nat Rev Endocrinol 2012;8(6):323–5. DOI: https://doi.org/10.1038/nrendo.2012.31
Pickup JC. Inflammation and activated innate immunity in the pathogenesis of type 2 diabetes. Diabetes Care 2004;27(3):813–23. 604 DOI: https://doi.org/10.2337/diacare.27.3.813
Kim F, Tysseling KA, Rice J, et al. Free fatty acid impairment of nitric oxide pro duction in endothelial cells is mediated by IKKbeta. Arterioscler Thromb Vasc Biol 2005;25(5):989–94. DOI: https://doi.org/10.1161/01.ATV.0000160549.60980.a8
Chaudhuri A, Umpierrez GE. Oxidative stress and inflammation in hyperglyce mic crises and resolution with insulin: implications for the acute and chronic complications of hyperglycemia. J Diabetes Complications 2012;26(4):257–8. DOI: https://doi.org/10.1016/j.jdiacomp.2012.04.016
Jenkins D, Close CF, Krentz AJ, et al. Euglycaemic diabetic ketoacidosis: does it exist? Acta Diabetol 1993;30(4):251–3. DOI: https://doi.org/10.1007/BF00569937
Bas VN, Uytun S, Torun YA. Diabetic euglycemic ketoacidosis in newly diag nosed type 1 diabetes mellitus during Ramadan fasting. J Pediatr Endocrinol Metab 2015;28(3–4):333–5. DOI: https://doi.org/10.1515/jpem-2013-0497
GuoRX,YangLZ,Li LX,et al. Diabetic ketoacidosis in pregnancy tends to occur at lower blood glucose levels: case-control study and a case report of euglyce mic diabetic ketoacidosis in pregnancy. J Obstet Gynaecol Res 2008;34(3): 324–30. DOI: https://doi.org/10.1111/j.1447-0756.2008.00720.x
Stephens JM, Sulway MJ, Watkins PJ. Relationship of blood acetoacetate and 3 hydroxybutyrate in diabetes. Diabetes. 1971;20(7):485–9. DOI: https://doi.org/10.2337/diab.20.7.485
Sheikh-Ali M, Karon BS, Basu A, et al. Can serum beta-hydroxybutyrate be used to diagnose diabetic ketoacidosis? Diabetes Care 2008;31(4):643–7. DOI: https://doi.org/10.2337/dc07-1683
ArieffAI,CarrollHJ.Nonketotichyperosmolarcomawithhyperglycemia:clinicalfea tures, pathophysiology, renal function, acid-base balance, plasma-cerebrospinal fluid equilibria and the effects of therapy in 37 cases. Medicine (Baltimore) 1972; 51(2):73–94. DOI: https://doi.org/10.1097/00005792-197203000-00001
Slovis CM, Mork VG, Slovis RJ, et al. Diabetic ketoacidosis and infection: leuko cyte count and differential as early predictors of serious infection. Am J Emerg Med 1987;5(1):1–5. DOI: https://doi.org/10.1016/0735-6757(87)90280-4
Beigelman PM. Potassium in severe diabetic ketoacidosis. Am J Med 1973; 54(4):419–20. DOI: https://doi.org/10.1016/0002-9343(73)90037-5
Adrogue HJ, Lederer ED, Suki WN, et al. Determinants of plasma potassium levels in diabetic ketoacidosis. Medicine (Baltimore). 1986;65(3):163–72. DOI: https://doi.org/10.1097/00005792-198605000-00004
Umpierrez GE, DiGirolamo M, Tuvlin JA, et al. Differences in metabolic and hor monal milieu in diabetic- and alcohol-induced ketoacidosis. J Crit Care 2000; 15(2):52–9. DOI: https://doi.org/10.1053/jcrc.2000.7900
Cahill GF Jr. Starvation in man. N Engl J Med 1970;282(12):668–75. DOI: https://doi.org/10.1056/NEJM197003192821209
Umpierrez GE, Cuervo R, Karabell A, et al. Treatment of diabetic ketoacidosis with subcutaneous insulin aspart. Diabetes Care 2004;27(8):1873–8. DOI: https://doi.org/10.2337/diacare.27.8.1873
Hara JS, Rahbar AJ, Jeffres MN, et al. Impact of a hyperglycemic crises proto col. Endocr Pract 2013;19(6):953–62. DOI: https://doi.org/10.4158/EP13077.OR
Kitabchi AE, Umpierrez GE, Murphy MB, et al. Hyperglycemic crises in dia betes. Diabetes Care 2004;27(Suppl 1):S94–102. DOI: https://doi.org/10.2337/diacare.27.2007.S94
May ME, Young C, King J. Resource utilization in treatment of diabetic ketoaci dosis in adults. Am J Med Sci 1993;306(5):287–94. DOI: https://doi.org/10.1097/00000441-199311000-00003
Moss JM. Diabetic ketoacidosis: effective low-cost treatment in a community hospital. South Med J 1987;80(7):875–81. DOI: https://doi.org/10.1097/00007611-198707000-00017
Umpierrez GE, Latif KA, Cuervo R, et al. Subcutaneous aspart insulin: a safe and cost effective treatment of diabetic ketoacidosis. Diabetes. 2003; 52(Suppl 1):584A.
Glaser NS, Ghetti S, Casper TC, et al, Pediatric Emergency Care Applied Research Network DKAFSG. Pediatric diabetic ketoacidosis, fluid therapy, and cerebral injury: the design of a factorial randomized controlled trial. Pediatr Diabetes 2013;14(6):435–46. Management of Hyperglycemic Crises 605 DOI: https://doi.org/10.1111/pedi.12027
Van Zyl DG, Rheeder P, Delport E. Fluid management in diabetic-acidosis Ringer’s lactate versus normal saline: a randomized controlled trial. QJM 2012;105(4):337–43. DOI: https://doi.org/10.1093/qjmed/hcr226
Umpierrez G, Korytkowski M. Diabetic emergencies- ketoacidosis, hypergly caemic hyperosmolar state and hypoglycaemia. Nat Rev Endocrinol 2016; 12(4):222–32. DOI: https://doi.org/10.1038/nrendo.2016.15
Abramson E, Arky R. Diabetic acidosis with initial hypokalemia. Therapeutic im plications. JAMA 1966;196(5):401–3. DOI: https://doi.org/10.1001/jama.196.5.401
Lever E, Jaspan JB. Sodium bicarbonate therapy in severe diabetic ketoacido sis. Am J Med 1983;75(2):263–8. DOI: https://doi.org/10.1016/0002-9343(83)91203-2
Green SM, Rothrock SG, Ho JD, et al. Failure of adjunctive bicarbonate to improve outcome in severe pediatric diabetic ketoacidosis. Ann Emerg Med 1998;31(1):41–8. DOI: https://doi.org/10.1016/S0196-0644(98)70279-3
Latif KA, Freire AX, Kitabchi AE, et al. The use of alkali therapy in severe diabetic ketoacidosis. Diabetes Care 2002;25(11):2113–4. DOI: https://doi.org/10.2337/diacare.25.11.2113
Gamba G, Oseguera J, Castrejon M, et al. Bicarbonate therapy in severe dia betic ketoacidosis. A double blind, randomized, placebo controlled trial. Rev Invest Clin 1991;43(3):234–8.
Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. N Engl J Med 2001;344(4):264–9. DOI: https://doi.org/10.1056/NEJM200101253440404
Fraley DS, Adler S. Correction of hyperkalemia by bicarbonate despite constant blood pH. Kidney Int 1977;12(5):354–60. DOI: https://doi.org/10.1038/ki.1977.122
Published
How to Cite
Issue
Section
Copyright (c) 2017 International journal of health sciences
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
Articles published in the International Journal of Health Sciences (IJHS) are available under Creative Commons Attribution Non-Commercial No Derivatives Licence (CC BY-NC-ND 4.0). Authors retain copyright in their work and grant IJHS right of first publication under CC BY-NC-ND 4.0. Users have the right to read, download, copy, distribute, print, search, or link to the full texts of articles in this journal, and to use them for any other lawful purpose.
Articles published in IJHS can be copied, communicated and shared in their published form for non-commercial purposes provided full attribution is given to the author and the journal. Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgment of its initial publication in this journal.
This copyright notice applies to articles published in IJHS volumes 4 onwards. Please read about the copyright notices for previous volumes under Journal History.
