Hyperglycemic Hyperosmolar State (HHS)

Hyperglycemic Hyperosmolar State (HHS)

Lindsey Van Sambeek, MD PGY-2
The Ohio State University
Department of Emergency Medicine


1-Minute Review Video

Take Home Points

  1. HHS presents similarly to DKA with hyperglycemia, insulin resistance, and dehydration
  2. HHS typically has no ketoacidosis as the body’s residual endogenous insulin production inhibits lipolysis.
  3. Typical presentation is altered mental status and signs of dehydration
  4. Treatment includes fluid resuscitation, insulin administration, and electrolyte replacement

Typically Asked Questions

  1. What is the typical fluid deficit for HHS?
  2. Given a set of serum lab values, which one matches the typical presentation of HHS?
  3. What is the typical initial management for HHS?
  4. How do DKA and HHS differ?


HHS is typically found in elderly patients with Type 2 diabetes mellitus, other co-morbidities, and a precipitating infection. Precipitating factors can range from myocardial infarction to a simple urinary tract infection. The pathophysiology is somewhat complicated but ultimately causes dehydration/hyperosmolarity and hyperglycemia: insulin resistance or deficiency causes hyperglycemia, inflammatory cytokines and hormones increase hepatic gluconeogenesis and glycogenolysis, and concomitant osmotic diuresis, which eventually overwhelms renal excretion of glucose.  Patients may have a water deficit of up to 12 liters or more. In contrast to DKA, HHS typically has no ketoacidosis (small amounts of endogenous insulin prevent lipolysis and thus limited ketone production). Some medications increase the risk of HHS: diuretics, beta-blockers and calcium channel blockers, mannitol, glucocorticoids, antipsychotics (quetiapine, ziprasidone), phenytoin.


Patients typically present with altered mental status and signs of dehydration (tachycardia, hypotension, dry mucous membranes, etc.). only a small percentage of patients present in a coma. Focal neurological symptoms are not common but do occur. These symptoms can delay the diagnosis. Patients with prolonged vasodilation may also be hypothermic.


Diagnosis of HHS is typically done with blood work. Common lab findings include hyperglycemia (typically higher than 400mg/dL) and elevated serum osmolality (typically higher than 315mOsm/kg. Due to low levels of endogenous insulin being produced acidosis and elevated serum ketones are absent.  Imaging and further diagnostic testing is usually unnecessary except to look for a precipitating factor


Volume repletion is the most critical intervention. Fluids should be adjusted to account for the various comorbidities patients may have (heart failure, renal failure, etc.) as well as any electrolyte abnormalities that may be present (Hypernatremia, hyponatremia, hypokalemia hyperglycemia).

Total body potassium depletion is often greater in HHS than it is in DKA, thus potassium repletion is often needed. It should be replaced to maintain a level of 3.3-5.0 mEq/L. Potassium levels should be checked frequently. Magnesium and phosphate should be replaced as needed. After fluid resuscitation has started, then one can start slow correction of hyperglycemia with

Insulin is often started as an IV infusion. The starting dose is approximately 0.1-0.14 U/kg/hr, with a goal of reducing glucose by 50 mg/dL/hr. Volume resuscitation should precede insulin administration as insulin can cause a shift in the osmotic load and lead to further volume depletion. As in DKA, insulin should be held if potassium is critically low.

Patients diagnosed with HHS should be further managed in the ICU setting.

Beyond The Boards


Edited By Farhad Aziz, MD, Assistant Professor Department of Emergency Medicine, The Ohio State University


  • Graffeo CS. Chapter 222. Hyperosmolar Hyperglycemic State. In: Tintinalli JE, Stapczynski J, Ma O, Cline DM, Cydulka RK, Meckler GD, T. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e New York, NY: McGraw-Hill; 2011.
  • Rivers CS, Weber DE. Preparing for the Written Board Exam in Emergency Medicine. Vol 2. Milford, OH: Emergency Medicine Educational Enterprises; 2000.

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