Hyperglycemic Hyperosmolar State (HHS) is a life-threatening diabetic emergency characterized by severe hyperglycemia, hyperosmolality, and profound dehydration. Learn the latest diagnostic criteria, treatment approach, complications, and prevention strategies based on current guidelines.

Hyperglycemic hyperosmolar state (HHS) is a life-threatening acute complication of diabetes characterized by severe hyperglycemia, hyperosmolality, and profound dehydration, usually without significant ketoacidosis. It is more commonly seen in older adults with type 2 diabetes, although it can occur in people with any type of diabetes.

HHS is a medical emergency requiring prompt recognition, careful fluid replacement, correction of electrolyte abnormalities, insulin therapy, and identification and treatment of the precipitating illness.

The current approach is based primarily on the ADA Standards of Care in Diabetes—2026 and the international consensus report on hyperglycemic crises in adults endorsed by the American Diabetes Association (ADA), European Association for the Study of Diabetes (EASD), Joint British Diabetes Societies (JBDS), American Association of Clinical Endocrinology (AACE), and Diabetes Technology Society (DTS).

What Is HHS?

HHS results from a relative deficiency of insulin combined with increased counter-regulatory hormones. There is usually enough endogenous insulin to suppress substantial ketone production, but not enough to prevent severe hyperglycemia.

Severe hyperglycemia causes osmotic diuresis, resulting in:

Massive urinary water loss
Sodium and electrolyte depletion
Progressive dehydration
Increased serum osmolality
Reduced renal glucose clearance
Worsening hyperglycemia
Neurological dysfunction

HHS generally develops more gradually than diabetic ketoacidosis (DKA), often over several days to a week or longer.

Importantly, HHS and DKA are not completely separate disorders. Mixed DKA/HHS presentations are common, and approximately one-third of hyperglycemic emergencies may have overlapping features.

Diagnostic Criteria for HHS

According to the 2026 ADA Standards of Care, HHS requires four major components.

1. Severe hyperglycemia

Plasma glucose ≥600 mg/dL (≥33.3 mmol/L)

2. Hyperosmolality

Either:

Effective serum osmolality >300 mOsm/kg

Total serum osmolality >320 mOsm/kg

Effective osmolality can be calculated as:

Effective osmolality = 2 × Na⁺ + glucose (mmol/L)

Total osmolality can be calculated as:

Total osmolality = 2 × Na⁺ + glucose (mmol/L) + urea (mmol/L)

3. Absence of significant ketonemia

β-hydroxybutyrate <3.0 mmol/L, or
Urine ketones <2+

4. Absence of significant metabolic acidosis

Venous or arterial pH ≥7.30
Serum bicarbonate ≥15 mmol/L

All four components should be considered when establishing the diagnosis.

HHS vs DKA

Feature	HHS	DKA
Typical diabetes	Usually type 2	Usually type 1, but also type 2
Onset	Days to weeks	Hours to days
Glucose	≥600 mg/dL	≥200 mg/dL or known diabetes
Hyperosmolality	Prominent	Variable
Ketones	Absent/mild	Markedly elevated
pH	≥7.30	<7.30
Bicarbonate	≥15 mmol/L	<18 mmol/L
Dehydration	Very severe	Moderate–severe
Mental status changes	Common	Variable
Abdominal pain/vomiting	Less common	Common
Kussmaul respiration	Usually absent	Common in severe DKA

The distinction is clinically important, but patients can have mixed DKA/HHS, which generally carries a worse prognosis.

Common Precipitating Factors

HHS is frequently triggered by an acute illness or interruption of diabetes treatment.

Important precipitating factors include:

Infection

Common examples include:

Pneumonia
Urinary tract infection
Sepsis
Skin and soft-tissue infection

Infection is one of the most important precipitants of hyperglycemic crises.

Cardiovascular and cerebrovascular disease

Consider:

Acute myocardial infarction
Stroke
Heart failure
Other major cardiovascular stress

Other acute illnesses

Pancreatitis
Trauma
Surgery
Gastrointestinal illness
Severe dehydration

Medication-related factors

Medications that may worsen hyperglycemia include:

Glucocorticoids
Some antipsychotic medications
Other drugs that impair glucose metabolism

SGLT2 inhibitors are particularly important in relation to DKA, especially euglycemic DKA, although any patient presenting with a hyperglycemic crisis should have their medication history reviewed.

Inadequate diabetes treatment

HHS may occur because of:

Missed medications
Insufficient insulin therapy
Newly diagnosed diabetes
Poor access to medications
Inadequate monitoring
Cognitive impairment
Difficulty obtaining food, fluids, insulin, or glucose-monitoring supplies

Clinical Presentation

HHS often develops more slowly than DKA.

Typical symptoms include:

Polyuria
Polydipsia
Severe thirst
Weakness
Fatigue
Weight loss
Blurred vision
Dehydration
Dizziness
Confusion
Reduced consciousness
Seizures in severe cases
Coma

Physical findings may include:

Tachycardia
Hypotension
Dry mucous membranes
Poor skin turgor
Weak peripheral pulses
Altered mental status
Reduced urine output in severe dehydration

Neurological abnormalities are particularly important. Changes in cognition are common in HHS and correlate with the degree of hyperosmolality.

Initial Evaluation

HHS should be treated as a medical emergency.

Initial assessment should include:

Bedside assessment

Airway, breathing, circulation
Mental status
Vital signs
Hydration status
Fluid balance
Urine output
Weight when feasible

Laboratory investigations

Obtain:

Plasma glucose
Serum sodium
Potassium
Chloride
Bicarbonate
Urea
Creatinine
Serum osmolality
β-hydroxybutyrate
Venous blood gas
CBC
Magnesium
Phosphate when clinically indicated
HbA1c

Additional investigations should be directed toward identifying the precipitating cause.

Other investigations

Depending on clinical presentation:

ECG
Troponin
Chest X-ray
Blood cultures
Urine analysis and culture
Infection screening
Brain imaging when indicated
Additional cardiac or neurological investigations

The ECG is particularly useful because potassium abnormalities may cause potentially dangerous cardiac changes.

Monitoring During Treatment

During treatment:

Blood glucose

Check approximately every 1–2 hours.

Electrolytes and renal function

Repeat approximately every 4 hours, or more frequently when clinically indicated.

Serum osmolality

In HHS, serum osmolality should generally be monitored approximately every 4 hours during the acute phase.

Continuous assessment should include:

Blood pressure
Heart rate
Respiratory status
Neurological status
Fluid input/output
Urine output
Signs of fluid overload

Management of HHS

The major treatment goals are:

Restore circulating volume
Correct dehydration
Reduce hyperosmolality gradually
Correct electrolyte abnormalities
Control hyperglycemia
Identify and treat the precipitating illness
Prevent complications

The main therapeutic components are intravenous fluids, insulin, potassium/electrolyte replacement, and treatment of the underlying cause.

1. Fluid Replacement

Fluid therapy is the cornerstone of HHS management.

In adults without significant cardiac or renal compromise, current consensus guidance recommends starting:

0.9% sodium chloride or a balanced crystalloid at approximately 500–1,000 mL/hour during the first 2–4 hours.

The subsequent rate should be individualized according to:

Blood pressure
Heart rate
Hydration status
Sodium concentration
Urine output
Fluid balance
Renal function
Cardiac status

The estimated fluid deficit should generally be corrected over approximately 24–48 hours, rather than too rapidly.

Balanced crystalloids such as Ringer’s lactate may be useful and may reduce hyperchloremic metabolic acidosis compared with large-volume 0.9% saline.

Special caution

Older adults and patients with:

Heart failure
Advanced kidney disease
Dialysis dependence
Significant comorbidities

require more cautious fluid administration.

Smaller boluses, such as approximately 250 mL, with frequent reassessment may be appropriate in patients at high risk of fluid overload.

2. Avoid Rapid Correction of Hyperosmolality

One of the most important principles in HHS treatment is:

Do not correct glucose and osmolality too rapidly.

The recommended limits include:

Glucose decline: ≤90–120 mg/dL/hour
Sodium decline: ≤10 mmol/L per 24 hours
Osmolality decline: approximately 3–8 mOsm/kg/hour

These limits are intended to reduce the risk of neurological complications.

A rise in serum sodium during the initial treatment of HHS does not automatically mean that hypotonic fluid should be started. As glucose falls, water shifts back into cells and serum sodium can rise.

If osmolality is not declining despite adequate fluid replacement and appropriate insulin therapy, 0.45% sodium chloride may be considered.

3. Intravenous Insulin

Insulin should be used carefully because fluids alone can produce a substantial reduction in glucose.

For HHS with:

No significant ketosis, or
Mild/moderate ketonemia
No significant acidosis

the consensus recommendation is:

Regular/short-acting IV insulin infusion: 0.05 units/kg/hour.

If the patient has significant ketonemia or metabolic acidosis suggesting mixed DKA/HHS, use:

IV insulin infusion: 0.1 units/kg/hour.

Rapid-acting subcutaneous insulin regimens used for uncomplicated mild DKA are not recommended for HHS.

4. Potassium Management

Total-body potassium is usually depleted in HHS despite a normal or high initial serum potassium.

Insulin and correction of dehydration can cause serum potassium to fall rapidly.

Therefore:

Monitor potassium closely.
Replace potassium when indicated.
Aim for serum potassium approximately 4–5 mmol/L.
Potassium replacement is generally started when serum potassium falls below approximately 5.0 mmol/L, assuming adequate renal function and urine output.

If potassium is <3.5 mmol/L, potassium replacement should take priority and insulin should generally be delayed until potassium has been corrected to >3.5 mmol/L, because insulin can precipitate severe hypokalemia and potentially fatal arrhythmias.

5. Dextrose During Treatment

As plasma glucose falls, dextrose-containing fluids may eventually be necessary to prevent hypoglycemia while allowing insulin to continue when clinically required.

The exact glucose threshold and dextrose strategy should follow the institutional HHS protocol and the patient’s osmolality, neurological status, and insulin requirement.

The key principle is:

Do not stop treatment simply because glucose has normalized if significant hyperosmolality or other metabolic abnormalities remain.

6. Treatment of the Precipitating Cause

Correcting glucose alone is not sufficient.

Search actively for the underlying trigger.

If infection is suspected

Obtain appropriate cultures.
Start appropriate antimicrobial therapy when clinically indicated.
Look for pneumonia, UTI, sepsis, skin infection, and other sources.

If myocardial infarction is suspected

Perform:

ECG
Cardiac biomarkers
Appropriate cardiovascular assessment

If stroke is suspected

Perform urgent neurological assessment and appropriate brain imaging.

Other precipitating conditions should be treated according to standard emergency protocols.

7. Thrombosis Prevention

HHS is associated with significant dehydration and a prothrombotic state.

Unless contraindicated or thrombosis is already being treated, prophylactic-dose low-molecular-weight heparin is recommended for hospitalized patients to reduce thrombotic risk.

Patients with clinical evidence of venous or arterial thrombosis require full diagnostic evaluation and therapeutic anticoagulation when appropriate.

8. Level of Care

Because HHS is a serious hyperglycemic emergency, many patients require high-dependency or intensive monitoring.

ICU-level care should be strongly considered for:

Altered mental status
Hemodynamic instability
Severe dehydration
Significant electrolyte abnormalities
Severe hyperosmolality
Sepsis
Myocardial infarction
Stroke
Significant renal dysfunction
Respiratory compromise
Other critical illness

The 2026 ADA Standards specifically identify HHS and severe hyperglycemic crises as conditions requiring appropriate high-level inpatient management.

When Is HHS Resolved?

There is not complete international agreement on a single definition of HHS resolution.

The international consensus report considers HHS resolved when:

Serum osmolality is <300 mOsm/kg
Hyperglycemia has been corrected
Blood glucose is <250 mg/dL (13.9 mmol/L)
Urine output is >0.5 mL/kg/hour
Cognitive status has improved

Clinical recovery and normalization of the precipitating illness are also essential.

Major Complications

HHS itself and its treatment can cause serious complications.

Important complications include:

Neurological complications

Cerebral edema
Seizures
Coma
Neurological deterioration
Osmotic demyelination syndrome

Rapid changes in serum osmolality should therefore be avoided.

Electrolyte abnormalities

Hypokalemia
Hyperkalemia
Hyponatremia
Hypernatremia
Hypophosphatemia
Hypomagnesemia

Cardiovascular complications

Arrhythmias
Myocardial ischemia
Heart failure
Pulmonary edema from excessive fluid administration

Renal complications

Acute kidney injury is common and often improves with restoration of renal perfusion and hydration.

Thromboembolic complications

Deep vein thrombosis
Pulmonary embolism
Arterial thrombosis

Treatment-related complications

Hypoglycemia
Hypokalemia
Fluid overload
Hyperchloremic metabolic abnormalities

Prevention of HHS

Prevention is an important component of diabetes management.

Patients and caregivers should be educated about:

Maintaining adequate hydration during illness
Monitoring glucose more frequently during acute illness
Recognizing symptoms of severe hyperglycemia
Taking diabetes medications according to an individualized sick-day plan
Recognizing infection early
Seeking medical attention for persistent severe hyperglycemia
Avoiding interruption of essential insulin therapy without medical advice
Having access to glucose-monitoring equipment and medications

The ADA 2026 Standards recommend structured education about recognition, prevention, and management of hyperglycemic crises for patients at increased risk.

Social and economic barriers should also be assessed, including difficulty obtaining insulin, medications, glucose-monitoring equipment, or healthcare.

Key Clinical Pearls

1. HHS is an emergency

Severe hyperglycemia with dehydration and altered mental status should immediately raise suspicion for HHS.

2. Fluids are the foundation of treatment

Restoration of circulating volume improves renal perfusion and helps lower glucose and osmolality.

3. Do not lower osmolality too quickly

The goal is controlled correction rather than rapid normalization.

4. Check potassium before giving insulin

Insulin can rapidly lower serum potassium.

5. Always look for the precipitating cause

Infection, myocardial infarction, stroke, medications, and inadequate diabetes treatment are important triggers.

6. Think about mixed DKA/HHS

Significant ketonemia or metabolic acidosis means the patient may have a mixed hyperglycemic crisis and requires the corresponding DKA insulin strategy.

7. Older patients require special attention

Older adults frequently have cardiovascular and renal comorbidities, making aggressive fluid replacement potentially dangerous.

8. HHS does not end when glucose normalizes

Osmolality, neurological status, hydration, renal function, and the underlying precipitating condition must also improve.

Practical HHS Treatment Algorithm

Suspected HHS

↓

Confirm diagnosis

Glucose ≥600 mg/dL

Hyperosmolality
No significant ketosis
No significant acidosis

↓

Assess ABC + neurological status + hemodynamics

↓

Start IV isotonic crystalloid

Usually 500–1,000 mL/hour initially in patients without cardiac/renal compromise

↓

Check potassium

K⁺ <3.5 mmol/L: replace potassium; delay insulin
K⁺ 3.5–5.0 mmol/L: replace potassium as needed
K⁺ >5.0 mmol/L: monitor closely; start insulin when appropriate

↓

IV insulin

HHS without significant ketosis/acidosis:

0.05 units/kg/hour

Mixed DKA/HHS:

0.1 units/kg/hour

↓

Monitor every 1–4 hours

Glucose
Electrolytes
Renal function
Serum osmolality
Urine output
Neurological status

↓

Control rate of correction

Glucose fall ≤90–120 mg/dL/hour
Osmolality fall 3–8 mOsm/kg/hour
Sodium fall ≤10 mmol/L/24 hours

↓

Treat precipitating illness

Infection / MI / stroke / medication / dehydration / other acute illness

↓

Continue until HHS resolves

Osmolality <300 mOsm/kg
Glucose <250 mg/dL
Urine output >0.5 mL/kg/hour
Cognition improved

↓

Transition to long-term diabetes management

Education + medication optimization + follow-up + prevention plan

Frequently Asked Questions

1. What glucose level defines HHS?

The current ADA diagnostic threshold is plasma glucose ≥600 mg/dL (≥33.3 mmol/L) together with hyperosmolality and absence of significant ketosis and acidosis.

2. Can HHS occur in type 1 diabetes?

Yes. HHS is more common in type 2 diabetes, particularly older adults, but it can occur in people with type 1 diabetes and other forms of diabetes.

3. Is HHS more dangerous than DKA?

HHS carries a substantial risk of morbidity and mortality. Historically, mortality has been considerably higher than for uncomplicated DKA, partly because patients with HHS are often older and have serious precipitating illnesses.

4. Can HHS and DKA occur together?

Yes. Mixed DKA/HHS is common. Significant ketonemia or metabolic acidosis in a patient with HHS should prompt treatment as a mixed hyperglycemic crisis.

5. Should insulin be given immediately in HHS?

Insulin is important, but fluid replacement should begin promptly and the rate of glucose/osmolality decline must be controlled. For uncomplicated HHS without significant ketosis or acidosis, IV insulin is generally started at 0.05 units/kg/hour after initial assessment and fluid therapy.

6. Why can sodium rise during HHS treatment?

As glucose falls, water shifts from the extracellular to intracellular compartment. Consequently, measured serum sodium may rise even while the patient’s overall hydration and osmolality are improving. A sodium rise alone is not an automatic indication for hypotonic fluid.

7. When should 0.45% saline be used?

The consensus report recommends considering 0.45% sodium chloride when serum osmolality is not declining despite adequate positive fluid balance and appropriate insulin therapy, rather than simply because serum sodium initially rises.

8. Why is potassium so important?

Total-body potassium is usually depleted because of osmotic diuresis. Insulin drives potassium into cells, potentially causing severe hypokalemia and arrhythmias. Potassium must therefore be monitored and replaced appropriately.

9. Can HHS be treated at home?

No. Suspected HHS requires urgent hospital evaluation and treatment because patients may have profound dehydration, electrolyte abnormalities, hyperosmolality, neurological impairment, and a serious precipitating illness. The ADA specifically recommends inpatient evaluation and treatment for suspected HHS.

10. How can HHS be prevented?

Prevention includes good long-term glycemic control, medication adherence, adequate hydration during illness, appropriate sick-day planning, early recognition and treatment of infection, glucose monitoring, and timely medical assessment when severe hyperglycemia or altered mental status develops.

Conclusion

Hyperglycemic hyperosmolar state is a life-threatening diabetic emergency characterized by severe hyperglycemia, hyperosmolality, and profound dehydration with little or no significant ketoacidosis.

Early recognition is essential. Management should prioritize careful intravenous fluid replacement, controlled correction of hyperosmolality, appropriate IV insulin, potassium and electrolyte management, thrombosis prevention, and aggressive identification and treatment of the precipitating illness.

The most important principle is to avoid overly rapid correction. In HHS, the goal is not simply to normalize glucose quickly—it is to restore perfusion and gradually correct hyperosmolality while preventing neurological and electrolyte complications.

Patients who survive HHS should receive a comprehensive discharge plan addressing diabetes treatment, medication access, sick-day management, glucose monitoring, education, and follow-up to reduce the risk of recurrence.

References

American Diabetes Association Professional Practice Committee. 6. Glycemic Goals, Hypoglycemia, and Hyperglycemic Crises: Standards of Care in Diabetes—2026. Diabetes Care. 2026;49(Suppl 1):S132-S149. doi:10.2337/dc26-S006.
American Diabetes Association Professional Practice Committee. 16. Diabetes Care in the Hospital: Standards of Care in Diabetes—2026. Diabetes Care. 2026;49(Suppl 1):S339-S367.
Umpierrez GE, Davis GM, ElSayed NA, et al. Hyperglycemic Crises in Adults With Diabetes: A Consensus Report. Diabetes Care. 2024;47(8):1257-1275. doi:10.2337/dci24-0032.
Umpierrez GE, Korytkowski M. Diabetic emergencies—ketoacidosis, hyperglycaemic hyperosmolar state and hypoglycaemia. Nat Rev Endocrinol. 2016;12:222-232.
Dhatariya KK, Joint British Diabetes Societies for Inpatient Care. The Management of Hyperosmolar Hyperglycaemic State (HHS) in Adults with Diabetes. JBDS guideline.

Clinical disclaimer: This article is intended for medical education and should not replace individual clinical assessment, institutional protocols, or specialist consultation. HHS is a medical emergency requiring hospital-based management.