Two of the most common metabolic emergencies

Transcription

1 CLINICAL DIFFERENTIATING BETWEEN AND Authors: Christy McDonald Lenahan, MSN, RN, FNP-BC, and Brenda Holloway, DNSc, MSN, RN, FNP-BC, Lafayette, LA, Mobile, AL Earn Up to 8.5 CE Hours. See page 270. Two of the most common metabolic emergencies associated with diabetes mellitus are diabetic ketoacidosis () and hyperglycemic hyperosmolar state (). 1 Although each disorder results in severe hyperglycemia, the underlying pathophysiology, clinical presentation, and treatment are vastly different. 2 It is imperative that clinicians be keenly aware of these differences, considering the variation in clinical pathways associated with each hyperglycemic emergency. 3 This article will compare and contrast the epidemiology, associated risk factors, differential diagnoses, clinical presentation, diagnosis, and medical management of and. Epidemiology Although gender appears to have no effect on the incidence of, being a member of an ethnic minority, including African and Hispanic, places one at an increased risk for the development of. 4 Data suggest that the incidence of has steadily risen, from 80,000 hospital discharges in 1988 to 140,000 hospital discharges in 2009 for cases in which was listed as the primary diagnosis. 5 However, the average length of hospital stay for persons with a primary diagnosis of trended favorably with a declining pattern, from an average of 5.7 days in 1988 to 3.4 days in Overall, -related mortality ranges from 1% in adults to 5% in elderly patients or patients with additional comorbidities. 6 In children, mortality rates range from 2% to 5%. 7 From an economic perspective, direct and indirect costs associated with average $2.4 billion annually. 6 Christy McDonald Lenahan is Instructor, College of Nursing and Allied Health Professions, University of Louisiana at Lafayette, Lafayette, LA. Brenda Holloway is Professor, College of Nursing, University of South Alabama, Mobile, AL. For correspondence, write: Christy McDonald Lenahan, MSN, RN, FNP- BC, 411 East Saint Mary Blvd, Lafayette, LA 70503; cmd3978@louisiana.edu. J Emerg Nurs 2015;41: Copyright 2015 Published by Elsevier Inc. on behalf of Emergency Nurses Association. Persons of African American ethnicity and older persons are at an increased risk for the development of. 8 Rates of hospital admissions associated with are significantly lower than those associated with and account for less than 1% of all diabetic-related admissions. 3 It should be noted, however, that between the years of 1997 and 2009 there was a 52.4% increase in the hospitalization rate among children and adolescents. 9 Moreover, it is predicted that as the occurrence of type 2 diabetes mellitus (T2DM) continues to rise, so will the occurrence of. 1 Mortality rates associated with are significantly higher than those associated with and range from 10% to 20%. 1 Risk Factors Multiple risk factors such as younger age, lower body mass index, and new-onset type 1 diabetes mellitus (T1DM) are associated with the development of. 10 Diabetic children younger than 3 years were reported to have a 54% risk for, whereas those aged 3 years or older exhibited a 33% risk of the development of. 11 This trend of decreasing risk for with increasing age appears to remain constant because risk for in adolescents older than 14 years is 16% or less. 12 Although is significantly more common in persons with T1DM, it can also be seen as a complication in persons with T2DM. 13 According to Raghaven, 14 other risk factors for include underlying infection, disruption of insulin treatment, and new onset of diabetes. Several risk factors are associated with the development of ; however, infection, and more specifically pneumonia and urinary tract infection, appear to be the leading risk factors for the development of. 15 Often is a result of decreased fluid intake precipitated by an underlying infection. 1 Poor compliance or noncompliance with diabetes treatment regimens is another common risk factor for the development of. 16 Unlike, which is usually associated with T1DM, is more common in persons with T2DM, but it can be seen in persons with T1DM and is May 2015 VOLUME 41 ISSUE

2 CLINICAL/Lenahan and Holloway seen more commonly in older persons. 1,17 Typically, the onset of is seen during or after the sixth decade of life. 1 Differential Diagnosis Ketoacidosis alone does not indicate an exclusive diagnosis of. Differential diagnoses that should be explored via clinical history and plasma glucose levels in patients presenting with ketoacidosis include starvation ketosis and alcoholic ketoacidosis. 18 Alternative causes of high anion gap metabolic acidosis also should be excluded prior to the diagnosis of. These causes include lactic acidosis caused by strenuous exercise, cancer, sepsis, or respiratory failure; excessive ingestion of salicylate or alcohol derivative; and acute or chronic renal failure. 18 Additionally, should be considered a differential diagnosis when assessing for because approximately 50% of patients presenting with may also present with ketoacidosis. 19 Differential and/or concomitant diagnoses to be considered when evaluating a patient for include diabetes insipidus,, myocardial infarction, and pulmonary embolism. 1 Patients presenting with diabetes insipidus and will exhibit signs and symptoms such as polydipsia and polyuria, similar to signs and symptoms of. Myocardial infarction and pulmonary embolism are precipitating factors for. 15,20 Laboratory values should be assessed as indicated per patient presentation and history of present illness for accurate diagnosis. 20 Additional differential diagnoses associated with include infection, pregnancy, lack of insulin, and ingestion of drugs such as cocaine. 21 Clinical Presentation Numerous similarities exist between clinical presentations of and and may include malaise, fatigue, anorexia, and existence of a preceding illness or infection. 22 The onset of is generally more rapid than that of, with developing over the course of a few days. 1 Differences that distinguish from are commonly the result of the compensatory mechanisms that are activated as a result of the metabolic acidosis associated with. 23 These differences include the existence of Kussmaul respirations, presenting as a rapid and labor intensive breathing pattern, and abdominal pain. 22 Kussmaul respirations occur as the body attempts to compensate for existing metabolic acidosis, and often a fruity odor resulting from exhaled acetone can be detected on the breath of patients with. 24 Abdominal pain may be present in persons with with no underlying disease; however, the pain can be the result of an underlying disorder such as acute pancreatitis and warrants an abdominal workup including but not limited to a physical examination, complete blood cell count, complete metabolic profile, serum lactic acid, glycosylated hemoglobin, serum amylase, serum lipase, anion gap, arterial blood gases, and necessary abdominal imaging as indicated by examination. 25 As with, the clinical presentation of may include malaise, fatigue, anorexia, and the existence of a preceding illness or infection. 22 Development of is more gradual than is and may take days to weeks to develop. 1 Neurologic disturbances are commonly seen in early as opposed to, in which neurologic disturbances are seen later in the disease process 22 and are a result of abnormal osmolality and electrolyte imbalances. 26 According to Hemphill, 1 neurologic disturbances seen in can include but are not limited to drowsiness and lethargy, delirium, coma, focal or generalized seizures, visual changes or disturbances, hemiparesis, and sensory deficits. Diagnosis Diagnostic criteria for both and are based on several laboratory values (Table 1) including plasma glucose, arterial ph, serum bicarbonate, urine and serum ketones, effective serum osmolality and anion gap (see Appendix), and mental status. 27 Plasma glucose levels in persons with are typically lower than in persons with, but they are generally greater than 250 mg/dl. 18 Arterial ph can range from 7.25 in persons with mild to less than 7.00 in persons with severe. 18 Urine and serum ketones are present in persons with and serum osmolality is variable but usually less than 320 mosm/kg. 18 Serum bicarbonate can range from 15 to 18 meq/l in persons with mild, 10 to 15 meq/l in persons with moderate, and less than 10 meq/l in persons with severe. 18 In persons with, the anion gap a difference of the serum cations sodium and potassium and the serum anions chloride and 202 JOURNAL OF EMERGENCY NURSING VOLUME 41 ISSUE 3 May 2015

3 Lenahan and Holloway/CLINICAL TABLE 1 Diagnostic criteria of diabetic ketoacidosis and hyperglycemic hyperosmolarstate Plasma glucose N 250 mg/dl N 600 mg/dl Arterial ph Mild to moderate N 7.30 Severe b 7.00 Serum bicarbonate Mild meq/l N 18 meq/l Moderate meq/l Severe b10 meq/l Urine ketones Present Absent to small Serum ketones Present Absent to small Effective serum osmolality Variable N 320 mosm/kg Anion gap Mild N10 b12 Moderate to severe N12 Mental status Mild alert Commonly seen in later stages Moderate alert to drowsy Severe stupor/coma, Diabetic ketoacidosis;, hyperglycemic hyperosmolar state. bicarbonate can range from greater than 10 meq/l in mild to greater than 12 meq/l in moderate to severe. 18 Mental status can range from alert in persons with mild to alert or drowsy in persons with moderate to stupor or coma in persons with severe. 18 Typically, the presence of a plasma glucose level greater than 250 mg/dl and an arterial ph less than 7.3 and the presence of urine and/or serum ketones are considered diagnostic criteria for. 27 Plasma glucose levels seen in persons with are usually significantly higher than those seen with and are normally greater than 600 mg/dl when is diagnosed. 18 Arterial ph is typically greater than 7.30 and serum bicarbonate is routinely greater than 18 meq/l in persons with. 18 Urine and serum ketones may be present, but often they are present only in small amounts. 18 Although effective serum osmolality may vary in, it is consistently greater than 320 mosm/kg in. 18 Anion gaps associated with are frequently reported as less than 12 meq/dl. 18 In persons with severe, stupor and coma are often present. 18 Diagnosis of is ordinarily based on plasma glucose levels greater than 600 mg/dl, an effective serum osmolality of greater than 330 mosm/kg, and the absence of severe ketoacidosis. 27 Medical Management in the Adult Patient Management of requires fluid and electrolyte replacement, administration of insulin, and treatment of any underlying cause if one is present or suspected (Table 2). 22 Fluid deficits in patients presenting with range from 3 to 5 L and should be replenished by a rapid normal saline solution bolus of 1 L with an additional infusion of normal saline solution at 250 to 500 ml/h for several hours thereafter in patients with low serum sodium levels or an additional infusion of half normal saline solution in patients with high to normal serum sodium levels. 18,22 Fluid replacement may vary depending on patient hemodynamics, electrolyte levels, and urinary output. 18 Of special concern is the pediatric population in which rapid fluid correction to correct hyperosmolality can result in cerebral edema and potential death, with mortality rates as high as 24%. 28 Electrolyte imbalances of serum potassium, phosphate, magnesium, and bicarbonate may be present in both and. 29 Rapid shifts in serum potassium are present as a result of extracellular shifts related to insulin deficiency and acidosis. 22 In persons with specifically, death in the initial phases of resuscitation is usually related to hyperkalemia, whereas the most common cause of death in later phases of resuscitation is related to hypokalemia; thus, May 2015 VOLUME 41 ISSUE

4 CLINICAL/Lenahan and Holloway TABLE 2 Management of diabetic ketoacidosis and hyperglycemic hyperosmolar state in the adult patient Fluid replacement Expected deficit: 3-5 L Expected deficit: N 10 L Initial bolus: 1 L Initial bolus: 500 ml Continuous: 500 ml/h for several hours Continuous: 1-2 L over first 2 h; replace ½ estimated fluid loss over first 12 h Add dextrose once blood glucose falls below 250 mg/dl Electrolyte replacement Potassium Treat after patient has voided Treat after patient has voided N 5.3 meq/l: no treatment b 5.2 meq/l: meq/l/h meq/l: 10 meq/l/h b4.0 meq/l: 20 meq/l/h b 3.5 meq/l: Hold insulin meq/l/h Phosphate b 1.5 mg/dl: dipotassium phosphate Same as at 0.5 mg/dl Magnesium b 1.8 mg/dl and symptomatic Same as b50 kg: 1-2 gm N50 kg: 2-3 gm b 1.2 mg/dl and symptomatic b50 kg: 2-3 gm N50 kg: 3-4 gm Bicarbonate Only replace if ph b 6.9 Not recommended Insulin therapy Loading dose: 0.1 units/kg of body Same as weight of regular insulin (not to exceed 10 units) Subsequent infusion: 0.1 units/kg Or of body weight of regular insulin per hour (not to exceed 10 units/h) If blood glucose does not decrease by 10% in the first hour a second loading dose may be given: 0.14 units/kg of body weight of regular insulin/h Fluid replacement and if blood glucose does not decrease by mg/dl/h give a bolus of 0.1 units/kg of body weight of regular insulin Resolution Blood glucose: b 200 mg/dl Serum osmolality: b 315 mosm/kg Serum bicarbonate: N 18 meq/l Normal mental state observed ph: N7.3 Patient is able to eat Anion gap: b12, Diabetic ketoacidosis;, hyperglycemic hyperosmolar state. serum potassium levels should be measured every 2 hours until the patient is deemed stable, and all patients should be monitored continuously with a cardiac monitor. 21 Potassium should be administered only after serum potassium levels are known and after the patient has voided. Urinary potassium loss is a common occurrence in persons with and is caused by extracellular potassium egression seen in acidosis. 30 Hypophosphatemia is another common 204 JOURNAL OF EMERGENCY NURSING VOLUME 41 ISSUE 3 May 2015

5 Lenahan and Holloway/CLINICAL manifestation of, and any serum phosphate less than 1.5 mg/dl should be treated with intravenous dipotassium phosphate at a rate of 0.5 ml/h. 21 A serum phosphate deficit of 0.5 to 1 mmol/l is normally present in patients presenting with. 31 Symptoms of hypomagnesaemia such as paresthesias, tremor, carpopedal spasm, seizures, and cardiac disturbances usually occur at levels below 1.2 mg/dl; thus, treatment should begin if levels fall below 1.8 mg/dl and symptoms of hypomagnesaemia are present. 31 Although bicarbonate imbalances can be present in persons with or, many studies indicate minimal efficacy of bicarbonate replacement when used in patients with a ph of greater than In patients with severe, current recommendations for insulin therapy include an intravenous loading dose of regular insulin at 0.1 units/kg of body weight, not to exceed a total loading dose of 10 units. 18,21 If a patient s initial blood glucose does not decrease by 10% within the first hour, an additional intravenous loading dose of 0.14 units/kg of body weight should be administered. 18,21 Subsequent to the initial loading dose, an intravenous infusion of regular insulin should begin at a rate of 0.1 units/kg of body weight per hour, not to exceed 10 units per hour. 18 In patients with who have an arterial ph between 7.00 and 7.25, an intravenous infusion of regular insulin at a rate of 0.1 units/kg of body weight per hour may be started without a loading dose. 21 Careful monitoring of blood glucose level should be conducted hourly in patients with or. 21 In persons with, once the blood glucose level falls below 250 mg/dl, 5% dextrose should be added to intravenous fluids. 21 Resolution of is acknowledged when blood glucose levels are less than 200 mg/dl, serum bicarbonate is greater than or equal to 18 meq/l, ph is greaterthan7.3,andtheaniongapislessthanorequalto 12 meq/l. 32 Management of requires fluid and electrolyte replacement and treatment of any underlying cause if one is present or suspected. 22 Variable guidelines for the use of insulin therapy in the management of are discussed later. Severe dehydration is often associated with, and deficits of 10 L or more can exist in patients presenting with this condition. 21 Considering the vast amount of fluid deficit associated with, clinicians should consider replacement of one half of the estimated fluid loss during the first 12 hours of treatment, with the remainder of the deficit being replaced in the following 12 hours. 1 An initial bolus of 500 ml of normal saline solution is considered appropriate, and 1 to 2 L of normal saline solution should be delivered within the first 2 hours of therapy. 1 Advanced age and comorbidities associated with should cause the clinician to be conscientious of potential complications associated with rapid fluid replacement and may require slower initial rates. 1 As with, cerebral edema is a concern in the pediatric population when rapid fluid resuscitation is performed in patients with. 32 Early signs of cerebral edema are headache and lethargy culminating to neurologic deterioration (seizures and coma) and respiratory arrest in later stages. 33 Symptoms typically occur 4 to 12 hours into treatment. 34 Hyperkalemia is often more severe in than in and results from an extracellular shift and osmotic diuresis. 29 -related hyperkalemia often will correct itself with the administration of fluids and insulin treatment, which encourage a shift of potassium back into the cell. 22 To prevent hypokalemia, it is suggested that potassium replacement be initiated via the addition of 20 to 30 meq of potassium in each liter of infused fluid once serum potassium levels fall below 5.2 meq/l. 18 No studies were found to support waiting until the patient voids prior to administering intravenous potassium in persons with. As with, the potential for cardiac disturbances remain secondary to hyperkalemia and hypokalemia affiliated with ; potassium levels should be checked every 2 hours, and patients should be monitored continuously with a cardiac monitor. 21 Phosphate and magnesium imbalances are less common in persons with, but levels should be monitored and replacement begun when levels fall below normal limits. 35 Bicarbonate is not recommended in the treatment of. 21 Clinical guidelines for insulin therapy in the treatment of are variable and are related to the potential for euglycemia obtained with fluid therapy alone. 1 Some authors suggest using thesameinsulinguidelinesforand, 1 whereas more conservative authors suggest not giving any insulin as part of the initial therapy in persons with ;instead,theysuggest that glucose levels be monitored hourly and that insulin therapy be initiated as a bolus of 0.1 units/kg of body weight only if serum glucose levels do not decrease by 50 to 70 mg/dl per hour with appropriate fluid management. 21 As with, blood glucose levels should be monitored hourly in the patient with. 21 The addition of dextrose in intravenous fluids is not suggested for persons with unless blood glucose levels fall below 300 mg/dl and unless signs of oliguric renal failure and/or cardiovascular collapse are present. 21 Resolution of is acknowledged when serum osmolality levels fall below 315 mosm/kg, the patient returns to a normal mental state, and the patient is able to eat. 36 May 2015 VOLUME 41 ISSUE

6 CLINICAL/Lenahan and Holloway Prevention Clinicians should be mindful of preventive measures when treating patients with diabetes. Diabetic ketoacidosis alone is responsible for 500,000 US hospital days per year and a total economic cost of $2.4 billion annually. 18 Moreover, mortality rates can exceed 15% in patients with compared with mortality rates of less than 5% in patients with. 37 Multiple preventive measures such as increased access to medical care, education, and communication can decrease the occurrence of and. 18 Considering the high incidence of and precipitated by illness or infection, education of patients with T1DM and T2DM regarding sick day management is of particular importance. 3 Appropriate educational interventions for sick day management include (1) initiation of contact with the health care provider early in the illness, (2) maintaining an insulin regimen during the illness, (3) treatment of the underlying illness, (4) maintaining ingestion of carbohydrates and sodium despite nausea, and (5) recruitment of family members or caregivers to assist with sick day management, especially in elderly persons. 18 Conclusion Clinicians must be vigilant in differentiating between hyperglycemic emergencies such as and. A thorough history, physical examination, and evaluation of available laboratory data can assist the clinician in differentiating from and quickly lead to the appropriate clinical pathway. Although and have many similarities, significant differences exist in pathology, diagnostic criteria, management, and resolution of each disorder, and thus accurate diagnosis is critical. Appendix. Calculations a Effective Serum Osmolality 2(Na + +K + ) + glucose Anion Gap a Na + (Cl + HCO 3 ) or (Na + +K + ) (Cl + HCO 3 ) It is a common practice to omit potassium from the formula when calculating anion gap and is considered clinically acceptable. REFERENCES 1. Hemphill RR. Hyperosmolar hyperglycemic state. medscape.com/article/ overview. Updated April 30, Accessed 2. Kitabchi AE. Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: treatment. treatment-of-diabetic-ketoacidosis-and-hyperosmolar-hyperglycemicstate-in-adults. Published June 26, Updated July 3, Accessed 3. ChaitnogiN,SubausteJS,KochCA,GeraciSA.Diagnosisandmanagement of hyperglycemic emergencies. Hormones. 2011;10(4): hormones.gr/738/article/article.html. Accessed 4. Usher-Smith J, Thompson MJ, Sharp S, Walter FM. Factors associated with the presence of diabetic ketoacidosis at diagnosis of diabetes in children and young adults: a systematic review. BMJ. 2011;343:d Centers for Disease Control and Prevention. Diabetes public health resource. Updated May 17, Reviewed November 19, Accessed 6. Clinical Key Staff. Diabetic ketoacidosis. topics/endocrinology/diabetic-ketoacidosis.html. Published Accessed 7. Lamb WH. Pediatric diabetic ketoacidosis. com/article/ overview. Updated April 25, Accessed 8. Epocrates Staff. Hyperosmolar hyperglycemic state. epocrates.com/u/ /hyperosmolar+hyperglycemic+state/basics/ Epidemiology. Published Accessed 9. Bagdure D, Rewers A, Campagna E, Sills MR. Epidemiology of hyperglycemic hyperosmolar syndrome in children hospitalized in USA. Pediatr Diabetes. 2013;14(1): Butalia S, Johonson JA, Ghali WA, Rabi DM. Clinical and sociodemographic factors associated with diabetic ketoacidosis hospitalization in adults with type 1 diabetes. Diabet Med. 2013;30(5): Klingensmith GJ, Tamborlane WV, Wood J, et al. Diabetic ketoacidosis at diabetes onset: still an all too common threat in youth. J Pediatr. 2013;162(2): Wolfsdorf J, Glaser N, Sperling MA. Diabetic ketoacidosis in infants, children, and adolescents: a consensus statement from the American Diabetes Association. Diabetes Care. 2006;29(5): Lin MV, Bishop G, Benito-Herrero M. Diabetic ketoacidosis in type 2 diabetics: a novel presentation of pancreatic adenocarcinoma. J Geriatr Intern Med. 2010;25(4): Raghaven VA. Diabetic ketoacidosis. article/ overview. Updated April 10, Accessed September 15, Stoner GD. Hyperosmolar hyperglycemic state. Am Fam Physician. 2005;71(9): Published May 1, Accessed 16. Pietrangelo A. Diabetic hyperglycemic hyperosmolar syndrome. Published September 16, Accessed 206 JOURNAL OF EMERGENCY NURSING VOLUME 41 ISSUE 3 May 2015

7 Lenahan and Holloway/CLINICAL 17. American Diabetes Association. Hyperosmolar hyperglycemic nonketotic syndrome (HHNS). complications/hyperosmolar-hyperglycemic.html. Updated December 6, Accessed 18. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care. 2009;32(7): Lang A, Satterfield K. When there are acute changes in mental status in patients with diabetes. Podiatry Today. 2010;23(3): com/when-there-are-acute-changes-in-mental-status-in-patientswith-diabetes?page=2. Published March Accessed 20. Stunkard ME, Pikul VT, Foley K. Hyperosmolar hyperglycemic syndrome with rhabdomyolysis. Clin Lab Sci. 2011;24(1): McNaughton CD, Self WH, Slovis C. Diabetes in the emergency department: acute care of diabetes patients. Clin Diabetes. 2011;29(2): Maletkovic J, Drexler A. Diabetic ketoacidosis and hyperglycemic hyperosmolar state. Endocrinol Metab Clin. 2013;42(4): Thomas C. Metabolic acidosis clinical presentation. medscape.com/article/ clinical. Updated March 27, Accessed 24. KishoreP.Diabeticketoacidosis. endocrine_and_metabolic_disorders/diabetes_mellitus_and_disorders_ of_carbohydrate_metabolism/diabetic_ketoacidosis_dka.html. Revised June Accessed 25. Kadaria D, Murillo LC, Yataco JC, et al. Abdominal pathology in patients with diabetic ketoacidosis. Am J Med Sci. 2012;344(5): Chalela JA, Kasner SE. Acute toxic-metabolic encephalopathy in adults. Updated August 9, Accessed 27. Epocrates Staff. Diabetic ketoacidosis: diagnostic criteria. epocrates.com/u/ /diabetic+ketoacidosis/diagnosis/criteria. Published Accessed 28. Orlowski JP, Cramer CL, Fiallos MR. Diabetic ketoacidosis in the pediatric ICU. Pediatr Clin North Am. 2008;55(3): DeBeer K, Michael S, Thacker M, et al. Diabetic ketoacidosis and hyperglycaemic hyperosmolar syndrome clinical guidelines. Nurs Crit Care. 2008;13(1): Barbara Davis Center for Diabetes. treatment protocol. ucdenver.edu/academics/colleges/medicalschool/centers/barbaradavis/ Clinical/Resources/Documents/BDCTreatmentProtocol2012.pdf. Published Accessed 31. Trachtenbarg DE. Diabetic ketoacidosis. Am Fam Physician. 2005;71(9): html#afp p1705-b42. Published May 1, Accessed 32. Maciel AT, Park M. A physiochemical acid-base approach for managing diabetic ketoacidosis. Clinics. 2009;64(7): Kershaw MJR, Newton T, Barrett TG, Berry K, Kirk J. Childhood diabetes presenting with hyperosmolar dehydration but without ketoacidosis: a report of three cases. Diabet Med. 2005;22(5): Banh K, Tsukamaki J. Hyperglycemia. CDEM Self Study Modules. hyperglycemia.php. Published Accessed 35. Venkatraman R, Signhi SC. Hyperglycemic hyperosmolar nonketotic syndrome. Indian J Pediatr. 2006;73(1): Makrilakis K, Katsilambros N. Diabetic emergencies, diagnosis and clinical management: hyperosmolar non-ketotic hyperglycemia, part 4. Published May 27, Accessed 37. Kitabchi AE, Razavi L. Hyperglycemic crises: diabetic ketoacidosis (), and hyperglycemic hyperosmolar state (). pbworks.com/w/page/ /hyperglycemic%20crises% 3A%20Diabetic%20Ketoacidosis%20%28%29%2C%20And% 20Hyperglycemic%20Hyperosmolar%20State%20%28%29. Revised Accessed May 2015 VOLUME 41 ISSUE