Carlos Suarez, age 74, arrives at the emergency department by ambulance after collapsing at home. Emergency personnel report that he is confused and can’t tell them what caused his collapse. His vital signs are temperature 102.4° F, respirations 22 breaths/minute, pulse 110 beats/minute, and blood pressure 90/60 mm Hg. He has dry mucous membranes, poor skin turgor, and bilateral wheezing in both lungs. A fingerstick blood glucose level reads high on the meter, indicating a value above 600 mg/dl.
Mr. Suarez’s wife states that she called 911 after finding her husband lying in the bedroom unresponsive. She says he has a history of hypertension, for which he’s taking chlorothiazide (a thiazide diuretic), and hyperlipidemia, which he controls with atorvastatin. Two days ago, he finished a 5-day course of antibiotics prescribed for bronchitis. She also says her husband has been drinking fluids—and urinating—more frequently than usual.
STAT laboratory tests show a plasma glucose level of 1,050 mg/dl, plasma osmolarity above 320 mOsm/kg, serum sodium level below 120 mEq/L, serum potassium level of 4.0 mEq/l, arterial pH 7.45, and a white blood cell (WBC) count of 30,000/mm3. Plasma ketones are absent.
Although Mrs. Suarez says her husband has never been diagnosed with diabetes mellitus, his extremely high blood glucose level certainly suggests he has diabetes. Based on his other assessment findings, you’d be correct to assume he’s experiencing an acute complication of diabetes. But which one?
Is it DKA or HHS?
Serious acute complications of diabetes include diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar syndrome (HHS). Untreated, both can lead to death. However, their exact causes, clinical presentations, and treatment differ. Which condition do you think Mr. Suarez has? Read on for more clues.
DKA results from uncontrolled hyperglycemia associated with type 1 diabetes; it’s rare in patients with type 2 diabetes. In DKA, extreme hyperglycemia leads to lipolysis, which induces a ketotic and acidotic state.
HHS, on the other hand, stems from uncontrolled hyperglycemia associated with type 2 diabetes. In fact, some patients learn they’re diabetic only after an HHS episode. Ketosis is absent even with severe hyperglycemia. The Centers for Disease Control and Prevention estimates the prevalence of HHS at approximately 17.5 cases per 1,000 individuals per year. (DKA, in comparison, has a prevalence rate of 4.7 cases per 1,000 individuals.) With the diabetes incidence rising dramatically, you can expect the incidence of HHS to rise, too.
Although HHS is less familiar than DKA to many healthcare professionals, its mortality is 15% higher. Some clinicians may overlook or misdiagnose HHS because of its slow onset and insidious signs and symptoms. This may lead to treatment delays, contributing to the higher mortality.
To ensure accurate diagnosis and prompt treatment, healthcare professionals must be able to rapidly differentiate DKA and HHS.
Making the right call
If you guessed Mr. Suarez has HHS, kudos to you. He has classic findings—severe hyperglycemia without ketosis, high plasma osmolarity, normal pH, a recent history of infection, and current diuretic therapy.
In HHS, hyperglycemia causes polyuria-induced dehydration and induces cortisol and glucagon release. Dehydration, in turn, triggers movement of intracellular fluids out of cells. Combined with dehydration, cortisol and glucagon release exacerbates hyperglycemia. Intracellular fluid depletion further destabilizes metabolic homeostasis; as a result, sodium, potassium, and magnesium are lost to diuresis.
Polyuria occurs when the kidney reaches its glucose threshold—the level that triggers frequent urination as a means of glucose removal. Generally, plasma glucose activates the kidney’s excretory response at levels of 180 to 250 mg/dl. However, the protective effect of glucose removal from the body eventually disappears as fluid volume is depleted and the kidneys become less effective at excreting glucose. The degree of osmolarity determines alterations in consciousness and the morbidity risk.
Factors that predispose a patient to HHS include:
• type 2 diabetes with uncontrolled hyperglycemia
• decreased fluid intake
• underlying illness
• infection (present in 60% of cases)
• certain drugs, such as steroids, diuretics, and beta blockers
• history of myocardial infarction, thrombosis, compromised renal function, or dialysis
• age above 60 (especially in patients in hospitals and long-term care facilities).
Onset of HHS occurs over 12 days, on average. If misdiagnosed, the patient may suffer a serious medical emergency by the time it’s correctly diagnosed.
Suspect HHS in a patient with type 2 diabetes who has severe hyperglycemia, polyuria, polydipsia, profound dehydration, weakness, altered mental state or neurologic changes, or stroke-like symptoms. But keep in mind that some patients, like Mr. Suarez, have no known history of diabetes.
Laboratory findings typical of HHS include:
• plasma glucose level above 600 mg/dl
• blood urea nitrogen above 30 mEq/dl
• plasma osmolarity above 320 mOsm/kg
• abnormal electrolyte levels
• blood pH above 7.3
• minimal to absent ketones.
Blood and urine cultures should be obtained to determine if the patient has an underlying medical condition that might have triggered HHS.
Acute management of HHS involves prompt fluid and electrolyte replacement and insulin administration. The goal of fluid replacement is to increase circulatory volume and restore intracellular fluids. Typically, normal saline solution is given; once the patient is rehydrated, some clinicians administer half-normal saline solution with regular insulin added.
The American Diabetes Association recommends correcting the serum sodium level based on the degree of hyperglycemia: For each 100 mg/dl glucose above 100 mg/dl, add 1.6 mEq to the sodium value for a corrected serum sodium value. To reduce the plasma glucose level, regular insulin usually is given.
For Mr. Suarez, proper treatment means admission to the intensive care unit to correct hyperglycemia, severe dehydration, and electrolyte imbalances. His unresolved bronchial infection is the apparent reason for his elevated WBC count, which warrants another course of antibiotic therapy. He should receive an I.V. insulin infusion and normal saline solution to correct severe dehydration and hyperglycemia. Once his blood glucose measures less than 250 mg/dl, dextrose can be added to the I.V. infusion to prevent hypoglycemia.
To help prevent HHS and other diabetes complications, teach patients, family members, or other caregivers the importance of monitoring blood glucose levels regularly, following dietary recommendations, and staying well hydrated. If the patient has a specific risk factor for HHS, provide information to aid self-management of that condition. As needed, refer the patient to a diabetes educator so he can learn the self-care behaviors required to manage diabetes and avoid complications.
American Diabetes Association. Hyperglycemic crises in patients with diabetes mellitus (position statement). Diabetes Care. 2001;24(suppl 1):S83-S90.
American Diabetes Association. Newly released CDC study on diabetes reflects growing diabetes epidemic; illustrates need for heightened research and prevention and improved health care for diabetes. Available at: www.diabetes.org/uedocuments. Accessed August 13, 2006.
American Diabetes Association. What is hyperosmolar hyperglycemic nonketotic syndrome (HHNS)? Available at: www.diabetes.org/type-2-diabetes/treatment-conditions/hhns.jsp. Accessed June 20, 2006.
The Art and Science of Diabetes Self-Management. Desk Reference for Healthcare Professionals. Chicago, Ill: American Association of Diabetes Educators; 2006.
Kitabchi AE, Umpierrez GE, Murphy MB, et al. Hyperglycemic crises in diabetes. Diabetes Care. 2004;27(suppl 1):S94-S102. Available at: www.guideline.gov. Accessed August 14, 2006.
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Cynthia Tucker, RN, BSN, CDE, CPT is Diabetes Education Coordinator at Peninsula Regional Medical Center in Salisbury, Maryland.