Hyperosmolar hyperglycemic state
Hyperosmolar hyperglycemic state is a life-threatening hyperglycemic crisis of older patients with type 2 diabetes, marked by extreme hyperglycemia and profound dehydration without significant ketoacidosis, because residual insulin secretion suppresses lipolysis even as it fails to control glucose. It is diagnosed by marked hyperglycemia (often >600 mg/dL) with plasma hyperosmolality above 320 mOsm/kg and minimal ketosis, and treated with aggressive isotonic fluid resuscitation, intravenous regular insulin, and careful potassium repletion.
- Topic reviewThe full article, organized the way the exam asks it.
- ABIM-format MCQsVignettes with an explanation for every wrong answer.
- Key factsThe numbers and thresholds worth memorizing, up front.
- AI tutorMedBrain answers the question you're stuck on.
What this article covers
- Overview
A life-threatening hyperglycemic crisis characterized by extreme hyperglycemia, severe hyperosmolar dehydration, and altered mental status, without the significant ketoacidosis seen in diabetic ketoacidosis (DKA).
- Epidemiology
Occurs predominantly in patients with type 2 diabetes older than 65 years, often with underlying chronic kidney disease or other comorbidities that impair thirst response or access to water.
- Risk factors
Advanced age with type 2 diabetes, particularly in patients with impaired thirst sensation or limited independent access to water (nursing home residents, those with dementia or debility).
- Pathophysiology
A partial, not absolute, insulin deficiency underlies HHS: residual insulin secretion is sufficient to suppress lipolysis and ketone body production but inadequate to correct the underlying hyperglycemia.
- Clinical features
HHS is recognized by profound hyperglycemia and severe dehydration with altered mental status developing gradually over days, in contrast to the more acute, 24-hour evolution typical of DKA.
- Differential diagnosis
Diabetic ketoacidosis: shares hyperglycemia and dehydration, but distinguished by significant ketonemia and an anion-gap metabolic acidosis, a more acute (about 24-hour) onset, and more common…
- Diagnosis
The diagnostic criteria are established first at presentation: marked hyperglycemia (plasma glucose often 600 mg/dL), plasma hyperosmolality (320 mOsm/kg), and the absence of significant ketosis or…
- Management
First, begin aggressive isotonic fluid resuscitation with 0.9% saline, since total fluid deficits in HHS are often larger than in DKA; continue isotonic saline if the patient remains severely…
- Complications
Death, with mortality up to 50%, higher than in DKA, reflecting the older, more comorbid population and degree of dehydration typically present.
- Prognosis
Mortality remains as high as 50%, substantially higher than DKA, driven largely by the older age and comorbidity burden of the typical patient and the severity of dehydration at presentation.
- Prevention
Ensure reliable access to water and glucose monitoring in older, debilitated, or institutionalized patients with type 2 diabetes, since impaired thirst and limited independent access to fluids are major contributors.
Read the whole article
Subscribing to Internal Medicine opens every article, the full question bank and MedBrain, on the web, iPhone and Android.
Related articles
- Diabetic ketoacidosis
Diabetic ketoacidosis is a life-threatening hyperglycemic crisis of near-absolute insulin deficiency, most common in type 1 diabetes, producing an anion-gap ketoacidosis from unrestrained lipolysis and osmotic diuresis from severe hyperglycemia. It is diagnosed by hyperglycemia, ketonemia, and an anion-gap metabolic acidosis, and treated with intravenous isotonic saline, an intravenous regular insulin bolus and infusion, and aggressive potassium repletion guided by frequent electrolyte monitoring.
- Type 2 diabetes mellitus
Type 2 diabetes is hyperglycemia from insulin resistance with progressive relative insulin deficiency, diagnosed by a hemoglobin A1c of 6.5% or higher, a fasting glucose of 126 mg/dL or higher, or a 2-hour oral glucose tolerance test value of 200 mg/dL or higher. First-line treatment is lifestyle modification plus metformin, with an SGLT2 inhibitor or GLP-1 receptor agonist added early for patients with atherosclerotic disease, kidney disease, or heart failure.
- Insulin therapy in diabetes mellitus
Insulin therapy replaces or supplements endogenous insulin to control hyperglycemia, and is lifelong and mandatory in type 1 diabetes because of absolute beta-cell failure, while in type 2 diabetes it is added when oral and noninjectable agents fail to reach glycemic goals. First-line therapy is a basal-bolus regimen started at 0.4-1.0 units/kg/day in type 1 diabetes, or basal insulin glargine 10 units/day (or 0.1-0.2 units/kg/day) in type 2 diabetes, titrated to a fasting glucose target.
- Noninsulin antihyperglycemic drugs in type 2 diabetes mellitus
Noninsulin antihyperglycemic drugs are the oral and injectable agents used to lower glucose in type 2 diabetes mellitus once lifestyle modification alone is insufficient, chosen in a patient-centered stepwise sequence built around metformin. Metformin, titrated to 850-1000 mg PO twice daily (max 2550 mg/day), is first-line for essentially every patient; an SGLT2 inhibitor or GLP-1 receptor agonist is added next for established or high-risk atherosclerotic cardiovascular disease, heart failure, or chronic kidney disease, with further agents layered by hypoglycemia risk, weight effect, and cost.