When a client is first admitted with hyperglycemic hyperosmolar nonketotic syndrome

Treatment

Approach Considerations

Diagnosis and management guidelines for hyperglycemic crises are available from the American Diabetes Association. [8, 12, 32]

The main goals in the treatment of hyperosmolar hyperglycemic state (HHS) are as follows:

  • To vigorously rehydrate the patient while maintaining electrolyte homeostasis

  • To correct hyperglycemia

  • To treat underlying diseases

  • To monitor and assist cardiovascular, pulmonary, renal, and central nervous system (CNS) function

In an emergency situation, whenever possible, contact the receiving facility while en route to ensure preparation for a comatose, dehydrated, or hyperglycemic patient. When appropriate, notify the facility of a possible cerebrovascular accident or myocardial infarction (MI). Initiation of insulin therapy in the emergency department (ED) through a subcutaneous insulin pump may be an alternative to intravenous (IV) insulin infusion. [33]

Airway management is the top priority. In comatose patients in whom airway protection is of concern, endotracheal intubation may be indicated.

Rapid and aggressive intravascular volume replacement is always indicated as the first line of therapy for patients with HHS. Isotonic sodium chloride solution is the fluid of choice for initial treatment because sodium and water must be replaced in these severely dehydrated patients.

Although many patients with HHS respond to fluids alone, IV insulin in dosages similar to those used in diabetic ketoacidosis (DKA) can facilitate correction of hyperglycemia. [34] Insulin used without concomitant vigorous fluid replacement increases the risk of shock. Adjust insulin or oral hypoglycemic therapy on the basis of the patient’s insulin requirement once serum glucose level has been relatively stabilized.

All patients diagnosed with HHS require hospitalization; virtually all need admission to a monitored unit managed by medicine, pediatrics, or the intensive care unit (ICU) for close monitoring. When available, an endocrinologist should direct the care of these patients.

Frequent reevaluation of the patient’s clinical and laboratory parameters is necessary. Recheck glucose concentrations every hour. Electrolytes and venous blood gases should be monitored every 2-4 hours or as clinically indicated.

When an underlying disease is responsible for HHS, it must be promptly identified and treated. Resolution of HHS often lags while the underlying process remains unresolved. Some authors advocate prophylactic heparin treatment and broad-spectrum antibiotic coverage, but these measures have not yet been studied thoroughly enough to allow recommendation of their use.

When a client is first admitted with hyperglycemic hyperosmolar nonketotic syndrome

Standard Care for Dehydration and Altered Mental Status

Standard care for dehydration and altered mental status is appropriate, including airway management, IV access, crystalloid fluid replacement, and administration of any medications routinely given to coma patients.

Airway management

Protection of the airway is mandatory in patients presenting with mental status changes, obtundation, or unconsciousness. Patients may present with respiratory failure and circulatory collapse and must be ventilated mechanically.

If patients are presenting with metabolic acidosis, take care to hyperventilate them when mechanical ventilation is instituted. Hyperventilation generates respiratory alkalosis, which compensates for the metabolic acidosis and also decreases the risk of cerebral edema.

Intravenous access

IV access, large bore if possible, or central venous access is useful, provided attempts to obtain it do not significantly delay transfer to the nearest emergency department (ED). A centrally placed catheter offers an avenue for vigorous rehydration, especially if means for intravenous (IV) access are difficult secondary to profound dehydration.

Fluid resuscitation

Aggressive fluid resuscitation is key in the treatment of HHS. This is to avoid cardiovascular collapse and to perfuse vital organs. Fluid deficits in adults are large in HHS, being about 9 L on average.

According to American Diabetes Association guidelines, fluid resuscitation with 0.9% saline at the rate of 15-20 mL/kg/h or greater is indicated to expand the extracellular volume quickly in the first hour. This amounts to about 1-1.5 L in an average-sized person. (In patients with contraindications to rapid fluid resuscitation [ie, cardiac or renal disease], slower rates are indicated.) A greater rate of fluid resuscitation is needed in patients with severe volume depletion but should not exceed 50 mL/kg in the first 4 hours. The choice of fluids after initial resuscitation depends on the patient's hydration status, serum electrolytes, and urinary output. If the patient's sodium level is normal or elevated, 0.45% normal saline may be used at a rate of 10 mL/kg/h. If the patient is hyponatremic, 0.9% normal saline may be used instead. In the first 18-24 hours, the first half of the patient's fluid deficit should be corrected. The plasma osmolality should not change over 3 mmol/kg/hr during fluid resuscitation. [5]

When the blood glucose concentration, initially checked hourly, reaches 250 mg/dL, change the infusion to 5% dextrose in 0.45-0.7% normal saline. This helps to prevent a precipitous fall in glucose, which may be associated with cerebral edema. [6]  In pediatric patients with suspected HHS, correcting fluid deficits over a longer period (48 h) may help to reduce the risk of cerebral edema. [16]

The IV fluids should also include 20-40 mEq/L of potassium chloride to treat hypokalemia, which is seen in patients with HHS. 

Patients with persistent hypotension may require pressor support in the ICU while rehydration is being accomplished.

Medications for coma patients

Basic medications given to coma patients in the field may include dextrose (50 mL of 50% dextrose in water [D50]). This is of benefit to many comatose patients with few adverse effects.

When possible, fingerstick glucose measurement is obtained before dextrose administration. Whenever fingerstick glucose measurement is unavailable or is likely to be delayed, D50 must be administered to comatose patients on an empiric basis without delay. Undiagnosed and untreated hypoglycemia, which may present with signs and symptoms very similar to those of HHS, is readily reversible but can be rapidly lethal if not treated promptly.

Insulin Therapy for Correction of Hyperglycemia

All patients with HHS require IV insulin therapy; however, immediate treatment with insulin is contraindicated in the initial management of patients with HHS. The osmotic pressure that glucose exerts within the vascular space contributes to the maintenance of circulating volume in these severely dehydrated patients. Institution of insulin therapy drives glucose, potassium, and water into cells. This results in circulatory collapse if fluid has not been replaced first.

IV insulin administration is accomplished most effectively in the ICU, where cardiovascular and respiratory support is available if needed. Infuse insulin separately from other fluids, and do not interrupt or suspend the infusion of insulin once therapy has been started.

The following steps may be used as a guideline for insulin infusion, as per American Diabetes Association recommendations [5, 35] : 

  • If hypokalemia (K < 3.3mEq/L) has been excluded, an IV bolus of regular insulin of 0.10 U/kg/h should be administered.

  • Begin a continuous insulin infusion of 0.1 U/kg/h.

  • Monitor blood glucose by means of bedside testing every hour; if glucose levels are stable for 3 hours, decrease the frequency of testing to every 2 hours.

  • If plasma glucose levels do not achieve a reduction of 50 mg/dL in the first hour, check volume status. If volume status is normal, it is okay to double insulin infusion every hour until a drop in glucose of 50-75 mg/dL is obtained.

  • Set the target blood glucose level at 300 mg/dL; this target level may be adjusted downward after the patient is stabilized.

  • Once blood glucose concentration reaches 300 mg/dL, decrease the insulin infusion rate by 0.5-1.0 U/h. Add dextrose to the IV fluids.

  • Do not discontinue the insulin drip. Continue IV insulin at a goal glucose level of 250-300 mg/dL until the patient becomes more alert and hyperosmolarity has resolved.

Once the patient is alert and able to eat, an insulin regimen consisting of short-/rapid-acting insulin and long-acting insulin is needed to wean the patient off of IV insulin therapy and to control glucose levels. If the patient already had an insulin regimen before the onset of HHS, it is okay to continue the current regimen and adjust to better glycemic control. If the patient is new to insulin or a newly diagnosed diabetic, total subcutaneous insulin dosages should not exceed 0.5-1 U/kg/day. The IV insulin infusion should be continued for about 1-2 hours after subcutaneous insulin administration to avoid hyperglycemia. 

When the glucose level has been between 200 and 300 mg/dL for at least 1 day and the patient’s level of consciousness has improved, glycemic control may be tightened. The recommended level of glycemia for most patients with type 2 diabetes mellitus (DM) is 80-120 mg/dL. This correlates to the hemoglobin A1c value of 7% recommended by the American Diabetes Association.

All patients who have experienced HHS will probably require intensive management of their diabetes initially, and this includes insulin therapy. The severe hyperglycemia with which these patients present implies profound beta cell dysfunction. In most instances, sufficient recovery of endogenous insulin production is a reasonable expectation, with safe dismissal of the patient from the hospital on oral therapy. After maintaining adequate glycemic control with insulin for several weeks after HHS, consider switching patients to an oral regimen.

Electrolyte Replacement

Profound potassium depletion necessitates careful replacement. Patients may initially present with normal or elevated potassium levels. With rehydration, the potassium concentration is diluted. With the institution of insulin therapy, potassium is driven into cells, exacerbating hypokalemia. A precipitous drop in the potassium concentration may lead to cardiac arrhythmia.

Potassium may be added to the infusion fluid and should be started at a level of 3.5 mEq/L or less and with adequate urine output. Usually, replenishing potassium with 20-30 mEq of potassium chloride in each liter of IV fluid is sufficient. The goal is to keep a potassium level of between 4 and 5 mEq. It is important to replenish potassium before starting insulin infusion, especially when levels are below 3.5 mEq, to avoid cardiovascular compromise. Check the potassium level at least every 4 hours until the blood glucose concentration is stabilized.

Phosphate, magnesium, and calcium are not replaced routinely, even though patients may have whole body deficits in these electrolytes. A patient who is symptomatic with tetany requires replacement therapy for calcium.

Monitoring During Treatment

The mortality associated with HHS remains high. The profound electrolyte and metabolic abnormalities present during treatment warrant careful cardiorespiratory monitoring. When gas exchange has been compromised, endotracheal intubation and mechanical ventilation are indicated.

Neurologic monitoring is indicated in all patients with HHS who present with altered mental status. Hyperosmolarity may trigger many neurologic syndromes. If a patient has seizures, phenytoin is not the agent of choice, because it inhibits endogenous insulin secretion and because, in general, it is ineffective in persons with HHS. Volume resuscitation and appropriate decrease is osmolality will decrease the chance of seizures.

Telemetry monitoring may be required in patients with electrolyte imbalances while treatment occurs. This is especially important with potassium abnormalities and electrocardiographic changes. Patients with HHS may also require telemetry monitoring if cardiac workup suggests a cardiac etiology, such as MI, for HHS. 

Diet

Provide adequate nutritional support for all patients. Once the patient's mental status is back to normal and the patient is able to eat, starting an oral diet is indicated. Some HHS patients are unable to eat for several days as a consequence of the comorbidities with which they present.

Patients in the ICU who require prolonged mechanical ventilation, patients with impaired airway defenses, and all patients with prolonged mental status changes are candidates for enteral or parenteral nutrition. The use of parenteral nutrition often induces insulin resistance and leads to increased insulin requirements.

Once HHS is resolved, provide dietary counseling for all patients. This probably is most effectively delivered by a registered dietitian who has expertise in counseling patients with diabetes.

Consultations

Generally, no consultation is absolutely required to manage HHS in the ED; however, in occasional cases, consultations may be useful.

A consultation with an endocrinologist is suggested for patients with HHS. Consider a consultation with a neurologist for most patients with altered mental status. A neurologist should monitor the cases of any patients with underlying neurologic disease (eg, cerebrovascular accident or a history of seizures). A pulmonologist or critical care specialist should monitor the cases of patients requiring intubation and mechanical ventilation. Other consultations (eg, with infectious disease or psychiatry) may be obtained as appropriate.

Long-Term Monitoring

Primary care follow-up is necessary for additional diabetic teaching and any appropriate immunizations. Visiting home nurse referral may be necessary to enhance compliance.

After any episode of HHS, enroll patients in a program of routine diabetes care. Adhere to American Diabetes Association guidelines for the care of people with diabetes. For patients with diabetes that was unrecognized before HHS, perform a routine diabetic care exam. This includes a routine eye exam and foot exam, as well as lab work to check for nephropathy and evaluation for signs of macrovascular disease. Advise patients treated with insulin to wear a bracelet or chain identifying them as having diabetes.

  1. Pasquel FJ, Umpierrez GE. Hyperosmolar hyperglycemic state: a historic review of the clinical presentation, diagnosis, and treatment. Diabetes Care. 2014 Nov. 37 (11):3124-31. [QxMD MEDLINE Link]. [Full Text].

  2. Nugent BW. Hyperosmolar hyperglycemic state. Emerg Med Clin North Am. 2005 Aug. 23(3):629-48, vii. [QxMD MEDLINE Link].

  3. [Guideline] Wolfsdorf JI, Glaser N, Agus M, et al. ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic ketoacidosis and the hyperglycemic hyperosmolar state. Pediatr Diabetes. 2018 Oct. 19 Suppl 27:155-77. [QxMD MEDLINE Link]. [Full Text].

  4. Adeyinka A, Kondamudi NP. Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC, Hyperosmolar Hyperglycemic Nonketotic Syndrome). 2018 Jan. [QxMD MEDLINE Link]. [Full Text].

  5. Bhansali A, Sukumar SP. Hyperosmolar hyperglycemic state. World Clin Diabetol. 2016. 2(1):1-10. [Full Text].

  6. Kitabchi AE, Umpierrez GE, Murphy MB, et al. Management of hyperglycemic crises in patients with diabetes. Diabetes Care. 2001 Jan. 24(1):131-53. [QxMD MEDLINE Link]. [Full Text].

  7. Trence DL, Hirsch IB. Hyperglycemic crises in diabetes mellitus type 2. Endocrinol Metab Clin North Am. 2001 Dec. 30(4):817-31. [QxMD MEDLINE Link].

  8. Kitabchi AE, Umpierrez GE, Murphy MB, Kreisberg RA. Hyperglycemic crises in adult patients with diabetes: a consensus statement from the American Diabetes Association. Diabetes Care. 2006 Dec. 29(12):2739-48. [QxMD MEDLINE Link].

  9. Campanella LM, Lartey R, Shih R. Severe hyperglycemic hyperosmolar nonketotic coma in a nondiabetic patient receiving aripiprazole. Ann Emerg Med. 2009 Feb. 53(2):264-6. [QxMD MEDLINE Link].

  10. Ahuja N, Palanichamy N, Mackin P, Lloyd A. Olanzapine-induced hyperglycaemic coma and neuroleptic malignant syndrome: case report and review of literature. J Psychopharmacol. 2010 Jan. 24(1):125-30. [QxMD MEDLINE Link].

  11. MKSAP: Medical Knowledge Self-Assessment Program VIII. Philadelphia, Pa: American College of Physicians; 1988.

  12. [Guideline] Kitabchi AE, Umpierrez GE, Murphy MB, et al. Hyperglycemic crises in diabetes. Diabetes Care. 2004 Jan. 27 Suppl 1:S94-102. [QxMD MEDLINE Link]. [Full Text].

  13. Bradford AL, Crider CC, Xu X, Naqvi SH. Predictors of Recurrent Hospital Admission for Patients Presenting With Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State. J Clin Med Res. 2017 Jan. 9 (1):35-9. [QxMD MEDLINE Link]. [Full Text].

  14. Agrawal S, Baird GL, Quintos JB, et al. Pediatric Diabetic Ketoacidosis With Hyperosmolarity: Clinical Characteristics and Outcomes. Endocr Pract. 2018 Aug. 24 (8):726-32. [QxMD MEDLINE Link]. [Full Text].

  15. MacIsaac RJ, Lee LY, McNeil KJ, Tsalamandris C, Jerums G. Influence of age on the presentation and outcome of acidotic and hyperosmolar diabetic emergencies. Intern Med J. 2002 Aug. 32(8):379-85. [QxMD MEDLINE Link].

  16. Kershaw MJ, 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 May. 22(5):645-7. [QxMD MEDLINE Link].

  17. 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 Jan-Feb. 11(1):23-9. [QxMD MEDLINE Link].

  18. Singhi SC. Hyperglycemic hyperosmolar state and type 2 diabetes mellitus: yet another danger of childhood obesity. Pediatr Crit Care Med. 2005 Jan. 6(1):86-7. [QxMD MEDLINE Link].

  19. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care. 2009 Jul. 32 (7):1335-43. [QxMD MEDLINE Link]. [Full Text].

  20. Kao Y, Hsu CC, Weng SF, et al. Subsequent mortality after hyperglycemic crisis episode in the non-elderly: a national population-based cohort study. Endocrine. 2016 Jan. 51 (1):72-82. [QxMD MEDLINE Link].

  21. Issa M, Alqahtani F, Ziada KM, et al. Incidence and Outcomes of Non-ST Elevation Myocardial Infarction in Patients Hospitalized with Decompensated Diabetes. Am J Cardiol. 2018 Oct 15. 122 (8):1297-302. [QxMD MEDLINE Link].

  22. Schaapveld-Davis CM, Negrete AL, Hudson JQ, et al. End-Stage Renal Disease Increases Rates of Adverse Glucose Events When Treating Diabetic Ketoacidosis or Hyperosmolar Hyperglycemic State. Clin Diabetes. 2017 Oct. 35 (4):202-8. [QxMD MEDLINE Link]. [Full Text].

  23. Pasquel FJ, Tsegka K, Wang H, et al. Clinical Outcomes in Patients With Isolated or Combined Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State: A Retrospective, Hospital-Based Cohort Study. Diabetes Care. 2020 Feb. 43 (2):349-57. [QxMD MEDLINE Link]. [Full Text].

  24. Chan KH, Thimmareddygari D, Ramahi A, Atallah L, Baranetsky NG, Slim J. Clinical characteristics and outcome in patients with combined diabetic ketoacidosis and hyperosmolar hyperglycemic state associated with COVID-19: A retrospective, hospital-based observational case series. Diabetes Res Clin Pract. 2020 Aug. 166:108279. [QxMD MEDLINE Link]. [Full Text].

  25. Chiasson JL, Aris-Jilwan N, Belanger R, et al. Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state. CMAJ. 2003 Apr 1. 168 (7):859-66. [QxMD MEDLINE Link]. [Full Text].

  26. Katz MA. Hyperglycemia-induced hyponatremia--calculation of expected serum sodium depression. N Engl J Med. 1973 Oct 18. 289 (16):843-4. [QxMD MEDLINE Link].

  27. Khardori R, Soler NG. Hyperosmolar hyperglycemic nonketotic syndrome. Report of 22 cases and brief review. Am J Med. 1984 Nov. 77 (5):899-904. [QxMD MEDLINE Link].

  28. Middleton P, Kelly AM, Brown J, Robertson M. Agreement between arterial and central venous values for pH, bicarbonate, base excess, and lactate. Emerg Med J. 2006 Aug. 23(8):622-4. [QxMD MEDLINE Link]. [Full Text].

  29. Rosa EC, Lopes AC, Liberatori Filho AW, Schor N. Rhabdomyolysis due to hyperosmolarity leading to acute renal failure. Ren Fail. 1997 Mar. 19(2):295-301. [QxMD MEDLINE Link].

  30. Slovis CM, Mork VG, Slovis RJ, Bain RP. Diabetic ketoacidosis and infection: leukocyte count and differential as early predictors of serious infection. Am J Emerg Med. 1987 Jan. 5 (1):1-5. [QxMD MEDLINE Link].

  31. Hu WS, Lin CL. Role of CHA2DS2-VASc score in predicting new-onset atrial fibrillation in patients with type 2 diabetes mellitus with and without hyperosmolar hyperglycaemic state: real-world data from a nationwide cohort. BMJ Open. 2018 Mar 22. 8 (3):e020065. [QxMD MEDLINE Link]. [Full Text].

  32. Kitabchi AE, Nyenwe EA. Hyperglycemic crises in diabetes mellitus: diabetic ketoacidosis and hyperglycemic hyperosmolar state. Endocrinol Metab Clin North Am. 2006 Dec. 35(4):725-51, viii. [QxMD MEDLINE Link].

  33. Munoz C, Villanueva G, Fogg L, et al. Impact of a subcutaneous insulin protocol in the emergency department: Rush Emergency Department Hyperglycemia Intervention (REDHI). J Emerg Med. 2011 May. 40(5):493-8. [QxMD MEDLINE Link].

  34. Kitabchi AE, Murphy MB, Spencer J, Matteri R, Karas J. Is a priming dose of insulin necessary in a low-dose insulin protocol for the treatment of diabetic ketoacidosis?. Diabetes Care. 2008 Nov. 31(11):2081-5. [QxMD MEDLINE Link]. [Full Text].

  35. Fowler M. Hyperglycemic Crisis in Adults: Pathophysiology, Presentation, Pitfalls, and Prevention. Clin Diabetes. 2009 Dec. 27 (1):19-23. [Full Text].

  36. Islam N, Zito PM. Insulin, Lispro. 2018 Jan. [QxMD MEDLINE Link]. [Full Text].

  37. Lu CL, Chang HH, Chen HF, et al. Inverse relationship between ambient temperature and admissions for diabetic ketoacidosis and hyperglycemic hyperosmolar state: A 14-year time-series analysis. Environ Int. 2016 Jul 6. [QxMD MEDLINE Link].

  38. Hamdy O. Diabetic ketoacidosis. Medscape Drugs and Diseases. 2017 Mar 23. [Full Text].

  • Glucose metabolism chart

When a client is first admitted with hyperglycemic hyperosmolar nonketotic syndrome

When a client is first admitted with hyperglycemic hyperosmolar nonketotic syndrome

Author

Coauthor(s)

Chief Editor

George T Griffing, MD Professor Emeritus of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for Physician Leadership, American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical and Translational Research, Endocrine Society, International Society for Clinical Densitometry, Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Additional Contributors

Acknowledgements

Howard A Bessen, MD Professor of Medicine, Department of Emergency Medicine, University of California, Los Angeles, David Geffen School of Medicine; Program Director, Harbor-UCLA Medical Center

Howard A Bessen, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Joseph Michael Gonzalez-Campoy, MD, PhD, FACE Medical Director and CEO, Minnesota Center for Obesity, Metabolism, and Endocrinology

Joseph Michael Gonzalez-Campoy, MD, PhD, FACE is a member of the following medical societies: American Association of Clinical Endocrinologists, Association of Clinical Researchers and Educators (ACRE), and Minnesota Medical Association

Disclosure: Nothing to disclose.

George T Griffing, MD Professor of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, InternationalSocietyfor Clinical Densitometry, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Lewis S Nelson, MD, FACEP, FAACT, FACMT Associate Professor, Department of Emergency Medicine, New York University School of Medicine; Attending Physician, Department of Emergency Medicine, Bellevue Hospital Center, New York University Medical Center and New York Harbor Healthcare System

Lewis S Nelson, MD, FACEP, FAACT, FACMT is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David S Schade, MD Chief, Division of Endocrinology and Metabolism, Professor, Department of Internal Medicine, University of New Mexico School of Medicine and Health Sciences Center

David S Schade, MD is a member of the following medical societies: American College of Physicians, American Diabetes Association, American Federation for Medical Research, Endocrine Society, New Mexico Medical Society, New York Academy of Sciences, and Society for Experimental Biology and Medicine

Disclosure: Nothing to disclose.

Don S Schalch, MD Professor Emeritus, Department of Internal Medicine, Division of Endocrinology, University of Wisconsin Hospitals and Clinics

Don S Schalch, MD is a member of the following medical societies: American Diabetes Association, American Federation for Medical Research, Central Society for Clinical Research, and Endocrine Society

Disclosure: Nothing to disclose.

Paulina B Sergot, MD Staff Physician, Department of Emergency Medicine, New York University/Bellevue Hospital Center

Paulina B Sergot, MD is a member of the following medical societies: American Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

What happens in hyperglycemic hyperosmolar nonketotic syndrome?

HHNS is an emergency caused by very high blood sugar, often over 600 mg/dL. Your kidneys try to get rid of the extra blood sugar by putting more sugar into the urine. This makes you urinate more and you lose too much body fluid, causing dehydration.

What is the treatment for hyperglycemic hyperosmolar syndrome?

Treatment. Treatment of HHS requires a four-pronged approach: (1) vigorous intravenous rehydration, (2) electrolyte management, (3) intravenous insulin, and (4) diagnosis and management of precipitating and coexisting problems.

What signs would be present in a patient who had hyperglycemic hyperosmolar nonketotic syndrome?

What are the symptoms of hyperosmolar hyperglycemic syndrome (HHS)?.
High blood sugar level (over 600 mg/dL)..
Confusion, hallucinations, drowsiness or passing out..
Dry mouth and extreme thirst that may eventually get better..
Frequent urination..
Fever over 100.4 degrees Fahrenheit..
Blurred vision or loss of vision..

What is the initial treatment for a patient experiencing hyperosmolar hyperglycemic nonketotic coma HHNC )?

Hyperosmolar hyperglycemic state is diagnosed by severe hyperglycemia and plasma hyperosmolality and absence of significant ketosis. Treatment is IV saline solution and insulin. Complications include coma, seizures, and death.