HHS nursing: why it can kill up to 10x more than DKA (and how to catch it early)

Hyperosmolar hyperglycemic state (HHS) – also called HHNS or the older term HHNK – is the most dangerous acute complication of type 2 diabetes. The 2024 ADA/EASD consensus report puts its mortality at 5 to 10 times that of diabetic ketoacidosis (DKA). Reported inpatient rates vary widely by setting: under 1% for type 2 diabetes HHS admissions in recent US national data, about 5% in a US hospital cohort, 13% in Japan, and 15–20% in the older series cited by the Joint British Diabetes Societies (JBDS). Patients lose an average of about 9 liters of fluid before they reach the emergency department, blood glucose is at least 600 mg/dL by definition and often far higher, and a change in mental status is common. Yet HHS develops over days to weeks, meaning there are multiple missed opportunities to intervene before a patient arrives obtunded.

Understanding HHS is essential for any nurse working in medical-surgical, emergency, or critical care settings. The condition is mechanistically distinct from DKA, requires a specific treatment sequence, and demands vigilant monitoring for a different set of complications. This reference covers the full clinical picture: pathophysiology, precipitating factors, assessment findings, diagnostics, the HHS vs DKA comparison you will see on NCLEX, the treatment protocol, nursing priorities, and the complications that can turn a recovering patient into an emergency.

Pathophysiology

HHS develops from a relative, rather than absolute, insulin deficiency. This distinction is what separates it from DKA and explains the two defining features of the condition: extreme hyperglycemia and the absence of ketoacidosis.

Relative insulin deficiency and hyperglycemia

In type 2 diabetes, endogenous insulin production persists – patients still make insulin, just not enough to fully control blood glucose under physiologic stress. Counterregulatory hormones (glucagon, cortisol, catecholamines, growth hormone) surge in response to a precipitating event such as infection or dehydration. These hormones drive hepatic gluconeogenesis and glycogenolysis, flooding the bloodstream with glucose. Peripheral tissues can’t take up glucose without adequate insulin signaling. Blood glucose climbs, often well beyond 600 mg/dL.

Osmotic diuresis begins when glucose exceeds the renal reabsorption threshold (~180 mg/dL). Glucose in the urine drags water and electrolytes with it. The kidney excretes sodium, potassium, chloride, phosphate, and magnesium alongside the fluid. A patient who is elderly, institutionalized, or has impaired thirst sensation cannot compensate by drinking – fluid losses accumulate over days to weeks, reaching 100–220 mL/kg (an average of about 9 liters in adults) by presentation.

Why ketones don’t accumulate

The residual insulin in HHS – even small amounts – is sufficient to suppress lipolysis and ketogenesis at the liver. Fat cells remain partially under insulin’s influence, preventing the massive free fatty acid release that drives ketone production in DKA. Without significant ketone accumulation, blood pH remains normal or near-normal, and there is no Kussmaul breathing or fruity breath.

This is the fundamental HHS/DKA distinction. Both involve severe hyperglycemia and osmotic diuresis, while pure HHS lacks significant ketoacidosis. The line is blurrier in practice: mild ketonemia is common in HHS, and more than a third of patients with a hyperglycemic crisis show features of both (mixed DKA/HHS), a group with higher mortality than either alone.

Hyperosmolality and neurological effects

As blood glucose rises and fluid depletes, serum osmolality climbs well above the normal range of 280–290 mOsm/kg. The formula for effective serum osmolality is:

Effective osmolality = 2 × Na⁺ (mEq/L) + glucose (mg/dL) ÷ 18

As effective osmolality climbs, brain cells lose water through osmosis. Depressed mental status in HHS tracks with the degree of hyperosmolality rather than with glucose alone, ranging from mild confusion through obtundation to stupor and coma at the extreme end. JBDS notes that cognitive changes become more common once osmolality rises above about 330 mOsm/kg, and the American Family Physician review places coma most often above 340. Mental status is therefore a rough bedside proxy for osmolality, and a patient whose sensorium is deteriorating needs an osmolality check rather than reassurance. HHS is also dangerous because it can cause, or be triggered by, vascular events such as myocardial infarction, stroke, and arterial thrombosis.

Precipitating factors

Every HHS presentation has a trigger. Identifying and treating that trigger is as important as correcting the metabolic derangement itself.

Infection is the most common precipitant, present in 30–60% of cases in the 2024 consensus (57% in the series cited by the American Family Physician review). UTI and pneumonia are the leading culprits. Sepsis drives a massive counterregulatory hormone response that overwhelms residual insulin production.

Inadequate fluid intake is particularly relevant in elderly patients, nursing home residents, and anyone with impaired thirst sensation or limited access to fluids. These patients may go days without adequate hydration before the syndrome becomes apparent.

Missed medications or insulin – whether deliberate, accidental, or due to access barriers – removes the partial glycemic control keeping glucose in check.

New-onset or undiagnosed type 2 diabetes – HHS is sometimes the presenting crisis that reveals previously unrecognized diabetes.

Medications that impair insulin secretion or raise glucose (named in the 2009 ADA statement and the 2024 consensus):

• Corticosteroids (increase hepatic glucose output and induce insulin resistance)
• Thiazide diuretics (reduce insulin secretion, partly through potassium depletion)
• Sympathomimetic agents
• Antipsychotics, especially second-generation agents such as olanzapine and clozapine
• Immunosuppressants such as tacrolimus and cyclosporine are also recognized causes of drug-induced hyperglycemia

Acute medical events – stroke, myocardial infarction, surgery, acute pancreatitis, pulmonary embolism, and trauma all trigger counterregulatory hormone surges. HHS may be the presenting crisis, or the acute event may be discovered as the workup proceeds.

Clinical presentation

HHS announces itself differently from DKA. The temporal course is different, the patient population is different, and several key clinical features are absent.

What you will find

Profound dehydration: Dry mucous membranes, poor skin turgor, tachycardia, hypotension, and sunken eyes reflect the massive fluid deficit. Orthostatic hypotension is frequently present. Urine output may have been high earlier in the course (polyuria from osmotic diuresis) but decreases as volume depletion reduces renal perfusion. JBDS warns that patients often look less dry than they are, because hypertonicity pulls water out of cells and partly preserves intravascular volume – so a normal blood pressure does not exclude a large deficit.

Altered mental status: A change in cognitive state is common in HHS and is the feature that most often sets it apart from DKA, though JBDS stresses that it is not always present. Patients present across a spectrum from mild confusion and disorientation to stupor and frank coma. The degree of mental status change broadly tracks the degree of osmolality elevation. This is why rapid correction of osmolality is dangerous: if the brain has adapted to a high osmolar environment, too-rapid normalization can cause cerebral edema or osmotic demyelination.

Neurological findings: Beyond diffuse altered mental status, HHS can produce focal neurological deficits such as hemiparesis, visual disturbances, and seizures. These can mimic stroke and require careful differential diagnosis. Seizures occur in up to a quarter of patients and are often focal, although generalized, myoclonic, and movement-induced seizures are also described.

The absence of key DKA findings: There are no Kussmaul respirations (the deep, labored breathing that compensates for metabolic acidosis in DKA). There is no fruity breath (acetone from ketone bodies). Nausea and vomiting are less prominent than in DKA. Abdominal pain is uncommon.

Onset over days to weeks: Patients and family members often describe a gradual decline – increasing confusion over several days, drinking more, urinating frequently, eating poorly. This contrasts with DKA, which typically develops over hours to a few days.

Diagnostic evaluation

Key laboratory findings

The diagnostic workup for suspected HHS includes blood glucose, serum electrolytes and renal function, a venous blood gas, complete blood count, serum osmolality (measured and calculated), blood beta-hydroxybutyrate or urine ketones, an ECG, and investigation for the precipitating cause.

Serum osmolality: Both measured and calculated values are useful, and the two carry different cutoffs – a distinction that is easy to get wrong. The 2024 ADA/EASD consensus report defines the hyperosmolarity criterion for HHS as a calculated effective osmolality above 300 mOsm/kg (2 × Na⁺ + glucose ÷ 18), or a total serum osmolality above 320 mOsm/kg. Effective osmolality excludes urea, which crosses cell membranes freely and so does not drive the water shifts that alter mental status; that is why its threshold sits lower. Applying the 320 figure to the effective-osmolality formula understates severity and can make a patient who meets the HHS definition appear to fall below the diagnostic threshold. Coma is most often seen once osmolality exceeds about 340 mOsm/kg. JBDS uses a total osmolality above 350 mOsm/kg as one of its triggers for high-dependency care.

Glucose: At least 600 mg/dL by definition and often considerably higher. Values above 1,000 mg/dL are not uncommon in elderly patients with prolonged, unrecognized illness.

Sodium: Measured serum sodium is often low at presentation, because glucose draws water out of cells and dilutes the extracellular sodium (JBDS calls this relative pseudohyponatremia; it is a true dilutional fall, not a laboratory artifact). The corrected sodium formula accounts for this:

Corrected Na⁺ = measured Na⁺ + 1.6 × [(glucose − 100) ÷ 100]

The 2024 consensus uses the 1.6 factor; JBDS uses a 2.4 mmol/L rise in sodium for each 100 mg/dL (5.5 mmol/L) fall in glucose. As glucose falls with treatment, measured sodium is expected to rise, and that rise alone is not a reason to switch to hypotonic fluid. JBDS advises that a rise much larger than 2.4 mmol/L per 100 mg/dL glucose fall suggests fluid replacement is inadequate, and that a rising sodium matters mainly when osmolality is not falling at the same time.

Potassium: Serum potassium may appear normal or even elevated at presentation despite total-body depletion. Once insulin is given and volume is restored, potassium shifts intracellularly and serum levels fall. JBDS notes that these shifts are usually less pronounced than in DKA, because patients are less acidotic and receive a lower insulin rate, but hyperkalemia can accompany acute kidney injury and patients taking diuretics may be profoundly hypokalemic. In the studies summarized by the 2024 consensus, about half of HHS patients became hypokalemic during treatment and 9% fell below 2.5 mEq/L. Check electrolyte management principles for a full review of the potassium-insulin relationship.

BUN and creatinine: Often elevated from prerenal acute kidney injury secondary to severe volume depletion; by RIFLE criteria about half of adults admitted with DKA or HHS have AKI. A BUN:creatinine ratio above 20:1 fits a prerenal pattern. Track these values over the first 24 hours to monitor renal recovery with fluid resuscitation.

pH and bicarbonate: pH ≥7.30 and bicarbonate ≥15 mEq/L by definition; most patients have a bicarbonate of 18 or more. If pH falls below 7.30 or bicarbonate drops below 15, consider a concurrent metabolic acidosis – either mixed DKA/HHS, lactic acidosis from hypoperfusion, or sepsis-related acidosis.

Ketones: Blood beta-hydroxybutyrate is below 3.0 mmol/L and urine ketones are less than 2+ on dipstick. Mild ketonemia (beta-hydroxybutyrate about 1.0–3.0 mmol/L) can occur in HHS. Significant ketonemia (3.0 mmol/L or more, or ketonuria of 2+ or more) with acidosis points to mixed DKA/HHS.

CBC with differential: Leukocytosis is common from physiologic stress. The 2009 ADA statement notes that a WBC above 25,000/mm³ may designate infection and needs further evaluation. Obtain blood cultures before antibiotics if sepsis is suspected.

Refer to the nursing lab values cheat sheet for normal reference ranges across all these parameters.

HHS vs DKA: the comparison you need to know

The HHS versus DKA comparison is one of the highest-yield differentials in nursing education. It appears on NCLEX, in clinical vignette questions, and at the bedside in every emergency department. Know every row of this table.

The clinical memory anchor: HHS = little or no ketones, no significant acidosis, profound osmolality, profound AMS, elderly patient, gradual onset. DKA = ketones, acidosis, Kussmaul breathing, fruity breath, younger patient, rapid onset.

Treatment

HHS treatment follows a defined sequence: fluids first, then low-dose insulin once potassium is confirmed safe, while the underlying cause is found and treated. Doing these steps out of order creates preventable harm. Patients with HHS should be managed in an intensive care or high-dependency setting under the 2024 consensus.

Step 1: IV fluid resuscitation

Fluid is the most important initial treatment in HHS. Patients arrive with large volume deficits (100–220 mL/kg), and IV fluid alone lowers blood glucose through dilution and improved renal glucose excretion, even before insulin is given. The 2024 consensus cites a fall of about 50–70 mg/dL per hour with fluids alone and notes the drop may be steeper in HHS.

Initial fluid: 0.9% normal saline (NS) at 500–1,000 mL/hour for the first 2–4 hours in adults without cardiac or renal compromise, or about 1 L/hour with severe hypovolemia (2024 consensus). The consensus also allows a balanced crystalloid, although the evidence for that comes mainly from DKA; JBDS names 0.9% saline as the principal fluid in HHS, because it is relatively hypotonic compared with the patient’s serum. In older adults, pregnant patients, and those with heart failure or kidney disease, use smaller boluses (for example 250 mL) and reassess hemodynamics frequently to avoid volume overload.

Overall pace: Replace about 50% of the estimated deficit in the first 8–12 hours (JBDS: the first 12 hours, typically a positive balance of 3–6 L) and the rest over the following 12 hours. Full normalization of electrolytes and osmolality can take up to 72 hours.

Transition fluid: After the initial resuscitation phase, subsequent fluid choice depends on fluid balance, hemodynamics, and sodium concentration. The 2024 ADA/EASD consensus narrowed the role of hypotonic fluid: 0.45% NS is indicated specifically when osmolality is not declining despite adequate fluid and insulin therapy, rather than as a routine step-down once the patient stabilizes. Older protocols (and many order sets still in circulation) switch to 0.45% NS at 200–250 mL/hour by default, so check which your institution follows.

Rate of osmolality correction: This is a critical safety parameter. Osmolality should fall by no more than 3–8 mOsm/kg/hour, serum sodium should not decline by more than 10 mEq/L in 24 hours, and glucose should not fall faster than 90–120 mg/dL/hour (2024 consensus; JBDS aims for no more than about 90 mg/dL, or 5 mmol/L, per hour). Exceeding these rates risks cerebral edema and osmotic demyelination – the brain has adapted to a high-osmolality environment, and rapid fluid shifts can cause dangerous cerebral swelling. If osmolality is falling faster than 8 mOsm/kg/hour, JBDS advises reducing the fluid rate and/or the insulin rate.

Dextrose addition: Under the 2024 consensus, add dextrose (5% or 10%) once blood glucose falls below 250 mg/dL, and target glucose of 200–250 mg/dL until HHS resolves. This is a change from the 2009 protocol, which added dextrose at 300 mg/dL and targeted 200–300 mg/dL; you will still encounter the older thresholds in practice. JBDS uses a similar initial target of 10–15 mmol/L (about 180–270 mg/dL) until the patient is eating and drinking. Either way, the principle is unchanged: dropping glucose too rapidly before osmolality is corrected can cause cerebral edema.

Step 2: potassium replacement

Before starting insulin, check serum potassium and confirm it is above 3.5 mEq/L (the 2009 ADA protocol used 3.3 mEq/L). Confirm adequate urine output (about 0.5 mL/kg/hour) before adding potassium to fluids.

Insulin drives potassium from the extracellular space into cells. In HHS, total-body potassium is depleted despite serum levels that may look normal. If insulin is given when potassium is low or borderline, serum potassium can fall quickly enough to trigger arrhythmias and respiratory muscle weakness. This same principle applies in DKA management. The 2024 consensus pathway, with the JBDS HHS table alongside:

• If K⁺ >5.0 mEq/L: Give no potassium; start insulin when indicated and recheck potassium every 2 hours (JBDS withholds potassium above 5.5)
• If K⁺ 3.5–5.0 mEq/L: Add potassium to each liter of IV fluid to keep serum K⁺ at 4–5 mEq/L (consensus pathway 10–20 mEq/L; JBDS uses 40 mmol/L for K⁺ 3.5–5.5)
• If K⁺ <3.5 mEq/L: Hold insulin; replace potassium at 10–20 mEq/hour until K⁺ is above 3.5. Faster replacement needs central venous access, and JBDS calls for senior review and high-dependency care

Step 3: insulin therapy

Insulin plays a secondary role in early HHS management – fluids do most of the initial work, and most patients with HHS are insulin sensitive. Giving insulin before adequate fluid replacement can cause rapid glucose drops, unsafe osmolality shifts, and, per JBDS, cardiovascular collapse as water follows glucose out of the circulation.

Initial insulin: The 2024 ADA/EASD consensus specifies a fixed-rate IV insulin infusion at 0.05 units/kg/hour for HHS without significant ketonemia – half the 0.1 units/kg/hour used for moderate-to-severe DKA. No bolus is given, and subcutaneous rapid-acting insulin is not recommended for HHS. If the patient already takes basal insulin, continue it at the usual dose.

Timing: JBDS goes further: unless significant ketonemia is present, it starts IV fluids alone and begins the 0.05 units/kg/hour infusion only once glucose has stopped falling with fluids. The consensus notes this approach as an option. Expect your unit protocol to follow one or the other.

Mixed DKA/HHS: If beta-hydroxybutyrate is 3.0 mmol/L or more, ketonuria is 2+ or more, pH is below 7.30, or bicarbonate is below 18 (consensus) or 15 (JBDS), treat as DKA with insulin at 0.1 units/kg/hour.

Target glucose reduction: JBDS treats a fall of up to about 90 mg/dL (5 mmol/L) per hour as ideal, and the consensus ceiling is 90–120 mg/dL per hour. Faster reduction increases the risk of neurological complications. If glucose is falling by less than 90 mg/dL per hour, JBDS advises checking fluid balance first, then starting or increasing insulin.

Transition to subcutaneous insulin: IV insulin can usually be stopped once HHS has resolved and the patient is eating and drinking. Give subcutaneous basal insulin 1–2 hours before stopping the IV infusion to prevent rebound hyperglycemia. Some patients previously managed on oral agents can later return to them after a period of stability.

Step 4: identify and treat the precipitating cause

Every case of HHS has a trigger. The metabolic crisis will recur if the underlying cause is not addressed.

• Obtain blood cultures and urine culture early – before antibiotics if possible
• Start antibiotics when there are clinical, laboratory, or radiological signs of infection; JBDS notes that sepsis in these patients may not cause a fever
• Obtain ECG and troponin to evaluate for myocardial infarction
• Review the medication list for offending agents (steroids, thiazides, antipsychotics)
• Consider CT head if focal neurological deficits suggest stroke

Step 5: DVT prophylaxis

Dehydration, hypernatremia, and hyperosmolality promote a prothrombotic state, and HHS is linked with both arterial events (MI, stroke, peripheral arterial thrombosis) and venous thromboembolism. The size of the VTE excess is debated: JBDS describes it as greater than in DKA, while a Taiwanese nationwide study cited in the 2024 consensus found rates similar to other hospitalized patients. Both guidelines recommend prophylactic-dose low-molecular-weight heparin (for example enoxaparin) unless contraindicated, and JBDS continues it for the whole admission. Full therapeutic anticoagulation is reserved for suspected thrombosis or acute coronary syndrome. Use mechanical prophylaxis per unit policy when anticoagulation is contraindicated.

Nursing priorities

Neurological monitoring

Assess and document mental status every 1–2 hours using a standardized tool (GCS or AVPU); JBDS asks for this frequency specifically to catch fluid overload, cerebral edema, and osmotic demyelination early. Neurological decline during treatment is an emergency. In an adult, check for hypoglycemia, an osmolality falling too fast, sepsis, or a new neurological event (stroke, seizure); cerebral edema is rare in adults but carries high mortality. Children and adolescents with HHS are managed under separate pediatric guidance.

Maintain the head of bed at 30–45 degrees for patients with reduced consciousness. Implement seizure precautions. If GCS drops below 8, prepare for airway protection – the patient may no longer be able to protect their own airway.

Cardiovascular and hemodynamic monitoring

Continuous cardiac monitoring is required throughout active treatment. Electrolyte shifts – particularly potassium – cause ECG changes that precede arrhythmias. Hypokalemia produces flattened T waves, U waves, and ST depression. Hyperkalemia causes peaked T waves, widened QRS, and sine wave pattern.

Monitor vital signs every 1–2 hours. Watch for orthostatic hypotension during position changes – these patients are prone to falls from both volume depletion and altered mental status.

Fluid balance

Strict intake and output documentation is non-negotiable. Insert a urinary catheter if the patient is obtunded or unable to reliably report urine output. Target urine output ≥0.5 mL/kg/hour as a sign of adequate renal perfusion.

Track cumulative fluid balance every 4–6 hours. Document all IV fluid administered, oral intake (if any), urine output, and insensible losses. This running total guides decisions about when to reduce fluid administration rates.

Weigh the patient daily. In critically ill patients receiving aggressive fluid resuscitation, daily weight reflects overall fluid status more reliably than any single vital sign.

Laboratory monitoring schedule

During active HHS management, expect the following monitoring intervals:

• Blood glucose: every 1–2 hours with a hospital-calibrated meter (2024 consensus); many units check hourly while insulin is running
• Electrolytes, renal function, venous pH: every 2–4 hours until stable (consensus treatment pathway), with potassium 2 hours after insulin starts
• Serum osmolality: every 4 hours per the 2024 consensus text; JBDS measures or calculates it every hour for the first 6 hours, then every 2 hours for the next 6, so that the rate of fall can be plotted. Continue until below 300 mOsm/kg with mental status improving – the resolution threshold
• Phosphate and magnesium: check with the other electrolytes. Both are often low in HHS, but neither guideline supports routine replacement. The consensus gives phosphate only if it is below 1.0 mmol/L with muscle weakness, respiratory compromise, or cardiac compromise, and JBDS reserves IV magnesium for severe, symptomatic depletion

Skin integrity and fall prevention

Severe dehydration compromises skin integrity – patients with HHS are at high risk for pressure injuries, especially over bony prominences. JBDS treats everyone with HHS as high risk for foot ulceration, particularly if obtunded or uncooperative: assess the feet on admission and daily, and provide heel protection and a pressure-relieving mattress. Reposition every 2 hours and document skin assessment at least daily.

Fall risk is elevated on two fronts: altered mental status and orthostatic hypotension. Use non-skid footwear, bed alarms, and bed in lowest position. Ensure call light is within reach and oriented patients understand the fall risk.

Complications

Cerebral edema

The most feared neurological complication of treatment. Rapid correction of serum osmolality causes water to shift into brain cells that have adapted to a hyperosmolar environment. In adults it is rare – the 2024 consensus estimates fewer than 0.1% of DKA and HHS events – but its reported mortality is about 30%, and it may be subclinical and visible only on imaging. Children are at higher risk.

Warning signs: new or worsening headache during treatment, sudden neurological deterioration, vomiting, declining GCS, pupillary changes, Cushing’s triad (bradycardia, hypertension, irregular respirations). Keep a low threshold for brain imaging. Immediate interventions include slowing the fluid and insulin rates, elevating the head of bed, and notifying the provider; the consensus suggests mannitol and mechanical ventilation for treatment.

Osmotic demyelination syndrome

Formerly called central pontine myelinolysis. It is linked to rapid correction of a low sodium, and patients with HHS can be relatively hyponatremic at presentation. Prevention is the same discipline as for cerebral edema: correct with 0.9% saline, keep the fall in osmolality to 3–8 mOsm/kg/hour, and keep the sodium change within 10 mEq/L in 24 hours. A deteriorating level of consciousness, new difficulty swallowing or speaking, or weakness after initial improvement should be reported at once.

Hypokalemia

A common and dangerous electrolyte complication. In the studies summarized by the 2024 consensus, 51% of HHS patients became hypokalemic during treatment and 9% fell below 2.5 mEq/L, a level associated with higher inpatient mortality. Insulin drives potassium intracellularly and volume resuscitation dilutes extracellular potassium. Monitor at least every 4 hours during treatment and replace promptly. Hypokalemia on ECG (U waves, flattened T waves) requires immediate attention.

Hypoglycemia

Occurs when insulin is not reduced or dextrose is not added as glucose falls. In DKA treatment studies, 16–28% of patients dropped below 70 mg/dL and about 2% below 40 mg/dL, and severe hypoglycemia was linked with higher mortality. Bedside glucose checks every 1–2 hours allow timely dose reduction, and adding dextrose at the 250 mg/dL threshold creates a buffer against further drops.

Acute kidney injury

AKI, mostly prerenal, affects about half of adults admitted with DKA or HHS and is more common in older patients and those with higher osmolality and glucose. It usually resolves with rehydration. Monitor creatinine and urine output closely and renal function at least daily. Failure of creatinine to improve with fluids suggests intrinsic renal injury or ongoing hypoperfusion.

Thromboembolism

Dehydration, hyperosmolality, and immobility combine to create a prothrombotic state, and HHS is associated with myocardial infarction, stroke, and peripheral arterial thrombosis as well as venous thromboembolism. Give prophylactic low-molecular-weight heparin as above. Assess lower extremities daily for signs of DVT (unilateral leg swelling, erythema, pain), and watch for chest pain, new neurological signs, or a cold, pulseless limb.

Rhabdomyolysis

Can occur in HHS and may worsen kidney injury. It is diagnosed by a creatine kinase (CK) more than 10 times the upper limit of normal. Consider checking CK in patients with markedly elevated osmolality, prolonged immobility, or myalgias.

Patient and family education

Before discharge, patients who are cognitively intact – and their families – need to understand what happened, why, and what to do differently.

Understanding the trigger: Explain what caused this episode in simple terms. If it was a UTI, discuss the importance of recognizing UTI symptoms early. If it was a medication issue, review the medication regimen and address any barriers to adherence.

Sick-day rules: During illness (fever, vomiting, diarrhea), blood glucose rises and fluid losses increase. Patients should:

• Check blood glucose every 4 hours when ill
• Never stop insulin; agree a written sick-day plan in advance, because some tablets (for example SGLT2 inhibitors and metformin) are often paused during a dehydrating illness
• Increase fluid intake aggressively
• Call the provider if glucose exceeds 300 mg/dL, they cannot keep fluids down, or they feel confused

Hydration habits: Older adults with decreased thirst perception should drink water on a schedule, not just when thirsty. A target of 6–8 glasses of water per day is appropriate for most patients without fluid restrictions.

When to go to the emergency department: Confusion or difficulty thinking clearly, glucose consistently above 500 mg/dL, inability to keep fluids down, extreme fatigue, or any sign of serious illness (high fever, chest pain, difficulty breathing).

Medication adherence and access: Review whether cost, complexity, or logistics contributed to missed medications. Connect patients with social work, patient assistance programs, or pharmacy resources as appropriate.

NCLEX tips

NCLEX tip 1: HHS presents in a type 2 diabetic patient, not type 1. When a question describes an older adult with gradual onset confusion and blood glucose above 600 mg/dL, think HHS.

NCLEX tip 2: The classic clinical finding in HHS is altered mental status from hyperosmolality, along with severe dehydration. Kussmaul breathing and fruity breath are DKA findings. Little or no ketones = no significant ketoacidosis = no respiratory compensation needed.

NCLEX tip 3: Osmolality calculation will appear on the NCLEX. Memorize: Effective osmolality = 2 × Na⁺ + glucose ÷ 18. Under the 2024 ADA/EASD consensus criteria, an effective osmolality above 300 mOsm/kg meets the hyperosmolarity criterion for HHS; the higher 320 mOsm/kg figure applies to total serum osmolality. Watch which one a question is asking for.

NCLEX tip 4: Always check potassium BEFORE starting insulin – both in DKA and HHS. Insulin drives potassium into cells. If serum K⁺ is already low or borderline and you give insulin, the patient can go into a fatal arrhythmia. Hold insulin if K⁺ <3.5 mEq/L.

NCLEX tip 5: The initial IV fluid is 0.9% normal saline (isotonic) – not 0.45% NS. Isotonic saline expands volume without dropping osmolality too rapidly. Under the 2024 consensus and JBDS, 0.45% NS is used only if osmolality stops falling despite an adequate positive fluid balance. Older textbooks and question banks may still key a routine switch to 0.45% once the patient is hemodynamically stable and the corrected sodium is normal or high.

NCLEX tip 6: Dextrose is added to IV fluids while blood glucose is still well above normal – below 250 mg/dL under the 2024 consensus, and at 300 mg/dL under the older protocol many question banks still use. Either way the reasoning is the point: dextrose maintains a safe glucose level while osmolality continues to correct, which prevents cerebral edema.

NCLEX tip 7: The primary difference between HHS and DKA is the presence or absence of ketoacidosis. HHS: little or no ketones (beta-hydroxybutyrate <3.0 mmol/L), pH ≥7.30, bicarbonate ≥15. DKA: beta-hydroxybutyrate ≥3.0 mmol/L, pH <7.30 and/or bicarbonate <18 under the 2024 criteria (older sources use <15). Blood glucose is higher in HHS, but the ketone/pH status is the defining distinction.

NCLEX tip 8: HHS has a much higher mortality than DKA – 5 to 10 times higher per the 2024 consensus, while DKA mortality is under 1% in high-income settings. Older textbooks quote 15–20% for HHS. If a question asks which hyperglycemic crisis is more dangerous, the answer is HHS.

NCLEX tip 9: Seizures can occur in HHS from severe hyperosmolality, in up to a quarter of patients. They are often focal, although generalized seizures also occur. Implement seizure precautions for any patient with markedly elevated osmolality (effective osmolality well above the 300 mOsm/kg criterion) or significant altered mental status.

NCLEX tip 10: Thromboprophylaxis with low-molecular-weight heparin is a priority in HHS because dehydration and hyperosmolality create a prothrombotic state. Expect to see this as a nursing priority in NCLEX vignettes.

NCLEX tip 11: The most common precipitating cause of HHS is infection – particularly UTI and pneumonia. A question that gives you an older adult with HHS and a recent upper respiratory illness or urinary symptoms is pointing you toward the trigger.

NCLEX tip 12: In HHS, fluid resuscitation is the primary initial treatment – not insulin. Fluids alone lower blood glucose (about 50–70 mg/dL per hour in the 2024 consensus, sometimes faster in HHS). Insulin is a secondary intervention at a low fixed rate, started after volume is partially restored and potassium is confirmed safe.

NCLEX tip 13: Corrected sodium must be calculated in HHS. Hyperglycemia pulls water out of cells and dilutes the serum sodium, so the measured sodium appears low and rises as glucose falls. Use the formula: corrected Na⁺ = measured Na⁺ + 1.6 × [(glucose − 100) ÷ 100].

NCLEX tip 14: Mental status in HHS correlates with serum osmolality. A patient who remains confused despite falling glucose should prompt a check of osmolality – osmolality may still be critically elevated even as glucose is trending down.

Summary

HHS is a true medical emergency with mortality rates that demand rapid, systematic nursing response. The clinical picture – older patient with type 2 diabetes, gradual onset, extreme hyperglycemia, little or no ketones, profoundly elevated osmolality, and significant altered mental status – distinguishes it clearly from DKA. The treatment sequence follows a defined order: aggressive fluid resuscitation first, potassium confirmation before insulin, controlled glucose and osmolality reduction, and investigation of the underlying trigger.

The nursing role in HHS is intensive: glucose checks every 1–2 hours, close tracking of the rate of fall in osmolality, frequent electrolyte assessment, vigilant neurological checks, strict fluid tracking, and continuous cardiac monitoring through electrolyte shifts. Understanding the underlying diabetes mellitus and the electrolyte physiology of potassium movement makes the treatment rationale clear and guides safe, confident bedside decision-making.

Written by Lindsay Smith, AGPCNP. Reviewed for clinical accuracy against the 2024 ADA/EASD hyperglycemic crises consensus report, the Joint British Diabetes Societies HHS guideline (2022), the ADA Standards of Care in Diabetes (2026), NCBI StatPearls, and published peer-reviewed literature on hyperglycemic crises. Last verified October 2026.

References

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