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How to recognize and intervene for hyperosmolar hyperglycemic syndrome

How to recognize and intervene for hyperosmolar hyperglycemic syndrome


Charles, age 62 and overweight, recently had a brief bout of pneumonia and has since suffered other health problems. He complains that he can’t seem to drink enough water, no matter how much he ingests. He states he needs to urinate more than ever, and complains of headache and blurry vision. A blood test during a physician visit reveals his serum glucose level exceeds 600 mg/dL. Charles has never been diagnosed with diabetes mellitus, but now the physician tells him he has hyperosmolar hyperglycemic syndrome (HHS).

HHS is a potentially life-threatening condition that’s most often associated with type 2 diabetes but occasionally occurs with type 1 diabetes. In about 20% of cases, it’s the first manifestation of type 2 diabetes. Less common than other diabetes-related hyperglycemic syndromes, it has a significantly higher mortality (10% to 20%) than diabetic ketoacidosis (about 1%). Although HHS has commonly been seen as a problem in the elderly, an increasing number of younger patients are being diagnosed with it.

Other names for HHS include:

  • nonketotic hyperosmolar coma (NKHC)
  • hyperosmolar hyperglycemic nonketosis or nonketotic syndrome (HHNK or HHNS)
  • hyperosmolar hyperglycemic nonketotic coma (HHNC)
  • hyperglycemic hyperosmolar state.

Some HHS patients experience coma, and others have only mild ketosis. (Generally, HHS isn’t associated with significant ketoacidosis.) For this reason, many clinicians prefer the term hyperosmolar hyperglycemic syndrome because it reflects the two primary manifestations of the disease process.

The symptom triad commonly linked to HHS includes:

  • extremely high blood glucose level (hyperglycemia)
  • extremely low fluid level (dehydration and hyperosmolality)
  • altered level of consciousness, neurologic disturbances, or both.

The most common risk factor linked to HHS is a current or recent infection. Other risk factors
include other diseases, drugs that lower glucose tolerance or increase fluid loss, older age, and poor man­agement of diabetes. (See Causes and risk factors by clicking the PDF icon above.)


Insufficient insulin effect is the primary pathophysiologic process in HHS. In many patients with type 2 diabetes, the pancreas still produces insulin but insulin response is decreased. Other factors besides poor insulin response lead to increased levels of counterregulatory hormone levels, including glu­cagon, cortisol, catecholamines, and growth hormone. These hormonal increases and poor insulin response combine to cause hyperglycemia.

In type 2 diabetes, the body still produces some insulin—usually enough to avoid ketoacidosis but not enough to control serum glucose. As the serum glucose level rises, osmotic diuresis begins to deplete body fluid. Typically, when the serum glucose level reaches approximately 180 mg/dL, the kidneys initiate glucose wasting in the urine (glycosuria). The higher the glucose level, the greater the diuresis. This further decreases fluid levels and increases solute concentration in the blood, which leads to hyperosmolality. Additional dehydration triggers further hyperglycemia. Some electrolyte loss (most notably potassium) also accompanies diuresis.

Signs and symptoms

HHS generally develops over several days to weeks. Common signs and symptoms include profound thirst (polydipsia) and diuresis (polyuria), along with mental status or other neurologic changes. Frequent nausea, vomiting, weakness, and weight loss also may occur with HHS onset. Other findings may include poor skin turgor, tachycardia, and hypotension. Some patients maintain a normal mental status, whereas others have lethargy, coma, or visual disturbances. (See Assessment findings by clicking the PDF icon above.)

Diagnostic tests

Patients with known or suspected HHS typically undergo various tests, including:

  • serum levels of glucose, blood urea nitrogen (BUN), creatinine, electrolytes (with a calculated anion gap), and osmolality
  • serum and urine ketones
  • urinalysis
  • arterial blood gas (ABG) analysis
  • complete blood count (CBC) with differential.

Besides a serum glucose level above 600 mg/dL, Charles also has an elevated BUN, creatinine, electrolytes, and osmolality; his serum and urine ketone levels are minimal. ABG results are within the normal range. Urinalysis and CBC findings reflect his recent pneumonia.

Electrocardiography, chest X-ray, and various cultures should be done to help rule out causative factors and monitor current status. Because HHS patients have fluid deficits at diagnosis, regular tests are needed during treatment to check levels of critical electrolytes, blood glucose, and ABGs and help prevent further complications. (See Typical diagnostic findings by clicking the PDF icon abive.)

Diagnostic criteria

According to the American Diabetes Association, diagnostic criteria for HHS include:

  • serum glucose level above 600 mg/dL
  • arterial pH above 7.30
  • serum bicarbonate level above 18 mEq/L
  • serum or urine ketones absent or present only in small amounts
  • serum osmolality above 320 mOsm/kg
  • variable anion gap
  • stupor or coma.


Successful HHS treatment entails correcting dehydration (or hyperosmolality), hyperglycemia, and electrolyte imbalances; identifying comorbid precipitating factors; and monitoring the patient continuously. Because of the need for aggressive and labor-intensive treatment, patients should be admitted to an intensive or intermediate care unit, with continuous cardiac monitoring and possibly invasive hemodynamic monitoring. Depending on patient status, intubation and mechanical ventilation may be necessary.

Fluid therapy to correct dehydration or hyperosmolality

HHS patients may have fluid deficits of 8 to 10 L. The main goals of fluid therapy are to bolster intravascular, interstitial, and intercellular fluid (all depleted due to the aggressive diuresis of HHS) and to improve renal perfusion. As ordered, give isotonic fluid (typically 0.9% saline solution) first and infuse up to 1 to 1.5 L during the first hour, unless the patient has cardiac problems or multiple comorbidities.

After this, depending on electrolyte levels, expect to infuse normal or hypotonic 0.45% saline
solution at a rate of 250 to 500 mL/hour for several hours. Eventually, reduce rates to 100 or 125 mL/hour, as ordered. Monitor electrolyte and osmolality values and urine output regularly to help identify how much fluid to deliver and when to give it. Calculate fluid replacement to correct the estimated deficit within the first 24 hours.

As the patient’s blood glucose level decreases and nears 300 mg/dL, 5% dextrose may be added to I.V. fluid to ensure blood glucose doesn’t drop too rapidly or too far. In patients with cardiac or renal compromise, strictly monitor serum osmolality and system status during fluid resuscitation to avoid iatrogenic fluid overload.

Insulin therapy to correct hyperglycemia

I.V. infusion of low-dose regular insulin is a mainstay in HHS and other hyperglycemic emergencies. However, treatment with subcutaneous rapid-acting insulin analogs, such as insulin lispro and insulin aspart, have proven effective alternatives. In HHS patients, initial fluid boluses can profoundly affect hyperglycemia, so be sure to monitor insulin therapy carefully whether giving insulin I.V. or subcutaneously. Check the blood glucose level at least hourly, making changes to insulin delivery rates as needed and appropriate. As a general rule, strive to reduce the blood glucose level by about 50 to 75 mg/dL/hour, and no more than 100 mg/dL/hour. Too-rapid reduction can cause such complications as cerebral edema. When the blood glucose level approaches 300 mg/dL, dextrose may be added to the I.V. fluid infusion to avoid too-rapid reduction of glucose or hypoglycemia.

Reduce insulin and I.V. fluids gradually, based on regular blood glucose checks, until both are discontinued and the patient maintains a blood glucose level within a normal range. By this time, both hyperglycemia and hyperosmolality should be corrected.

Because Charles is newly diagnosed with diabetes and hasn’t received insulin before, administer his insulin therapy cautiously, as ordered, to gauge his response. Know that small intermittent boluses of I.V. insulin may be used instead of a continuous I.V. infusion.

Electrolyte correction

Electrolyte shifts are common during correction of hyperosmolar and hyperglycemic states. Monitor electrolyte levels at least every 4 hours, or every 2 hours if needed. Monitor serum sodium and potassium levels closely. If needed, use isotonic and hypotonic saline solutions to adjust the patient’s sodium level. Despite major potassium loss during diuresis in early HHS stages, many patients initially present in a hyperkalemic state due to dehydration. When fluid and insulin therapy begin, the serum potassium level may drop dramatically. Once it falls below the high-normal range (around 5.0 mEq/L), begin replacement therapy to avoid hypo­kale­mia, as further drops are expected. The goal is to maintain potassium between 4 and 5 mEq/L during the treatment phase. The most common way to accomplish replacement therapy is to add 20 to 40 mEq of potassium to each L of I.V. fluid. Also give additional potassium infusions (10 to 20 mEq/hour) as needed to maintain appropriate levels. Monitor the serum magnesium level; if needed and ordered, replace magnesium in I.V. fluid.

Treatment complications

Hypoglycemia and hypokalemia are the main complications of treatment for hyperglycemic states. Hypoglycemia usually stems from overly aggressive insulin therapy and aggressive fluid resuscitation. Check the patient’s blood glucose level at least every hour to avoid hyperglycemia overtreatment and hypoglycemia development.

Hypokalemia occasionally occurs with the initial fluid bolus and serum potassium dilution. If this is expected, start replacement therapy with the initial bolus if ordered; otherwise, start it after the bolus is given. To help prevent hypokale­mia, check electrolyte levels at least every 4 hours, or as often as every 2 hours if needed.

Preventing HHS

Educating diabetic patients and their families is the most important way to prevent HHS. For patients with a family history of diabetes or significant diabetes risk factors, regular communication with a healthcare provider is the key to preventing HHS episodes. Cover the following topics with these patients and their families, as well as with nondiabetics who have diabetes risk factors:

  • importance of early communication with a healthcare provider when HHS signs and symptoms appear
  • importance of maintaining insulin or oral diabetic treatment during an illness
  • appropriate serum glucose goals
  • proper use of supplemental insulin or oral diabetics
  • importance of keeping medication on hand to suppress a fever and getting early treatment for infection
  • starting an easily digested liquid diet containing carbohydrates and sodium when nauseated
  • appropriate sick-day management, including monitoring blood glucose levels, urine output, oral intake, daily weight, and insulin or other drug administration.

Your ability to recognize HHS early and intervene effectively can help patients avoid complications and death. Early identification helps avoid excessive hospital admissions for hyperglycemic emergencies. Prompt access to health care after symptom onset is crucial to successful resolution. Especially if you care for elderly patients in long-term care facilities, stay alert for early signs and symptoms of dehydration and HHS.

To help prevent HHS, ensure appropriate and regular education of diabetic patients. Teach nondiabetic patients with diabetes risk factors, such as Charles, about the risk of complications related to diabetes onset.

Selected references

Brenner ZR. Management of hyperglycemic emergencies. AACN Clin Issues. 2006 Jan-Mar;17(1):56-65.

Eckman AS. Diabetic hyperglycemic hyperosmolar syndrome. MedlinePlus. Updated May 10, 2010. Accessed May 29, 2012.

Fowler M. Hyperglycemic crisis in adults: pathophysiology, presentation, pitfalls, and prevention. Clinical Diabetes. 2009 Dec 21;27(1):19-23.

Hemphill RR. Hyperosmolar hyperglycemic state. Medscape Reference. Updated May 16, 2012. Accessed May 29, 2012.

Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care. 2009 Jul;32(7):1335-43.

McNaughton CD, Self WH, Slovis C. Diabetes in the emergency department: acute care of diabetes patients. Clinical Diabetes. 2011; 29(2):51-9.

Ira Gene Reynolds is an adjunct nursing faculty member at Roseman University of Healthcare Sciences in South Jordan, Utah.

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