Nonketotic hyperglycemia, often called Hyperosmolar Hyperglycemic State (HHS), is a severe metabolic complication requiring immediate medical attention. It is most frequently observed in individuals with Type 2 Diabetes, where blood glucose concentration rises extremely high, typically exceeding 600 milligrams per deciliter (mg/dL). The defining feature is severe hyperosmolarity, meaning the blood becomes highly concentrated, while the production of ketone bodies remains minimal or absent. This metabolic derangement creates a profoundly dehydrated state that affects every organ system and carries a significantly higher mortality rate than other acute diabetic complications.
Understanding the Triggers
Nonketotic hyperglycemia begins when the body experiences intense physiological stress against chronic high blood sugar. Acute illnesses, such as infection like pneumonia or a urinary tract infection, are the most frequent triggers. Other acute events, including stroke, myocardial infarction, or recent surgery, can also initiate the syndrome. These events flood the body with counter-regulatory hormones like cortisol, which oppose the action of insulin and accelerate the liver’s production of glucose.
A second major cause involves issues with medication adherence or management, particularly in older adults who may have limited access to fluids. The underlying mechanism involves an insufficient, but not absent, amount of circulating insulin. This small amount of insulin is enough to suppress lipolysis, preventing the production of acidic ketones. However, this insulin level is inadequate to facilitate glucose uptake, leading to a relentless accumulation of sugar in the bloodstream.
Certain prescription medications can also contribute to the onset by impairing glucose tolerance or increasing fluid loss. Glucocorticoids (steroids) raise blood glucose levels by promoting insulin resistance. Diuretics, used to manage fluid retention, accelerate the loss of water and electrolytes, intensifying dehydration. As blood sugar climbs, it pulls water from cells into the bloodstream, where the kidneys filter it out excessively in a process called osmotic diuresis.
Recognizing the Acute Warning Signs
The signs of nonketotic hyperglycemia usually develop gradually over several days to weeks, allowing the body to accumulate a large fluid deficit, often averaging 8 to 12 liters in an adult. This slow onset leads to profound signs of severe dehydration, including excessive thirst, frequent urination in the early stages, and a lack of sweating. Healthcare providers often note poor skin turgor, dry mucous membranes, and a rapid heart rate coupled with low blood pressure, reflecting depleted circulatory volume.
The most distinguishing features are the severe neurological symptoms, which result from hyperosmolarity drawing water out of brain cells. As the brain shrinks due to dehydration, patients often present with an altered mental status ranging from confusion and lethargy to deep stupor or coma. Focal neurological deficits, such as temporary partial paralysis (hemiparesis), visual disturbances, or generalized seizures, can occur due to cellular stress.
The neurological presentation often misleads initial diagnosis, sometimes mimicking a stroke or other acute brain injury. Unlike Diabetic Ketoacidosis (DKA), patients with nonketotic hyperglycemia do not exhibit signs related to high ketone levels. This means the patient will not have the rapid, deep breathing pattern known as Kussmaul respirations, nor will their breath carry the characteristic fruity scent associated with acetone. The absence of these telltale signs of acidosis is a key distinction.
Essential Steps for Medical Treatment
Treatment for nonketotic hyperglycemia must be initiated immediately within a hospital setting to reverse life-threatening physiological derangements. The initial therapeutic goal is the replacement of lost body fluid to correct severe dehydration and reduce hyperosmolarity. Intravenous fluid resuscitation begins with isotonic saline solution (0.9% sodium chloride), administered rapidly to restore circulating blood volume and improve tissue perfusion.
This aggressive fluid therapy must occur before the administration of insulin to avoid a sudden shift of water into cells, which could worsen hypotension and lead to circulatory collapse. As rehydration progresses, clinicians monitor serum sodium levels to determine if the intravenous fluid should be switched to a hypotonic solution, like 0.45% saline, to correct the water deficit more effectively. Continuous monitoring of serum electrolytes is necessary throughout this process, particularly potassium.
Total body potassium stores are often depleted from excessive urination, though initial serum potassium levels may appear normal or elevated due to blood concentration. Once insulin therapy begins, potassium rapidly shifts back into the cells, necessitating replacement to prevent heart rhythm disturbances. Insulin therapy is introduced after fluid resuscitation is underway, often involving a low-dose, continuous intravenous infusion of regular insulin. This helps gradually lower the blood glucose level, minimizing the risk of a too-rapid decrease in plasma osmolality that could lead to cerebral edema.
The final component of management involves identifying and treating the underlying precipitating illness that triggered the event, such as an infection. If an infection is suspected, broad-spectrum antibiotics are started without delay. Other underlying conditions, like a recent heart attack or stroke, must be addressed simultaneously. This multi-pronged approach ensures the immediate metabolic crisis is resolved while treating the root cause to prevent recurrence.