Presentation

What is Hyperosmolar Hyperglycemic State (HHS)?

• A life-threatening acute complication of diabetes

• Primarily associated with type 2 diabetes

• Characterized by:

  • Severe hyperglycemia (BG often >600 mg/dL)

  • Profound dehydration

  • Hyperosmolality

  • Minimal or absent ketones

  • No significant metabolic acidosis

What distinguishes HHS from diabetic ketoacidosis (DKA)?

• HHS has sufficient insulin to prevent lipolysis and ketone production

• HHS lacks ketoacidosis (pH usually >7.3)

• HHS has higher glucose and osmolality than DKA

• HHS has more severe dehydration and neurologic symptoms

• Onset is slow and insidious, unlike DKA

Why does HHS not produce significant ketones?

• There is enough circulating insulin to suppress:

  • Lipolysis

  • Ketogenesis

• BUT insulin is insufficient for effective glucose uptake, leading to hyperglycemia

Why is HHS often diagnosed late?

• Symptoms develop over days to weeks

• Early signs are nonspecific (fatigue, polyuria, thirst)

• Often mistaken for aging or chronic illness

• Delayed recognition contributes to high mortality

What is the mortality rate of HHS?

• 10–20%, significantly higher than DKA

• Related to:

  • Delayed diagnosis

  • Severe dehydration

  • Hyperosmolality

  • Comorbidities (infection, MI)

Which population is most at risk for HHS?

• Older adults (>60–65 years) with type 2 diabetes

• Often have:

  • Impaired thirst mechanisms

  • Cognitive impairment

  • Limited healthcare access

  • Poorly controlled or undiagnosed diabetes

• Living alone or institutionalized increases risk

What is the most common precipitating factor for HHS?

• Infection (most common trigger), including:

  • Pneumonia

  • Urinary tract infections

  • Sepsis

• Infections increase insulin resistance and catabolic stress

How does dehydration contribute to HHS?

• Reduced fluid intake → glucose concentration rises

• Leads to osmotic diuresis

• Causes severe extracellular and intracellular dehydration

• Results in extreme hyperosmolality

What medications can precipitate HHS?

• Corticosteroids → increase glucose production and increase insulin resistance

• Thiazide diuretics → cause dehydration and raise blood glucose

• Atypical antipsychotics → impair glucose metabolism and increase insulin resistance

• Missed insulin or oral hypoglycemics → insufficient insulin to control blood glucose

• Non-adherence (forgetfulness, cost, access) → prolonged hyperglycemia → severe dehydration → HHS

List additional precipitating factors for HHS.

• Acute illness

• Dialysis treatments

• Excessive carbohydrate intake

• Increased insulin resistance

• Poor kidney function

• Inadequate fluid intake

What is the underlying pathophysiology of HHS?

• Relative insulin deficiency

• Extreme hyperglycemia (>600 mg/dL)

• Osmotic diuresis → massive fluid loss (8–12 L)

• Increased plasma osmolality (>320 mOsm/kg)

• Cellular dehydration → neurologic dysfunction

How do counter-regulatory hormones worsen HHS?

• Elevated:

  • Glucagon

  • Cortisol

  • Catecholamines

• Stimulate:

  • Gluconeogenesis

  • Glycogenolysis

• Increase glucose production and fluid loss

• Perpetuate hyperosmolar crisis

What are the hallmark laboratory findings of HHS?

• Plasma glucose >600 mg/dL

• Serum osmolality >320 mOsm/kg

• Arterial pH >7.3

• Minimal or absent ketones (serum & urine)

• Elevated BUN and creatinine from dehydration

What are the early clinical manifestations of HHS?

• Polyuria

• Polydipsia

• Unintentional weight loss

• Fatigue

• Often unnoticed initially

What neurologic manifestations are seen in HHS?

• Confusion

• Lethargy

• Agitation

• Seizures

• Coma

• Severity correlates with serum osmolality

What physical signs indicate severe dehydration in HHS?

• Dry mucous membranes

• Hypotension (often MAP <65)

• Tachycardia

• Poor skin turgor

• Decreased urine output

What conditions must be ruled out when diagnosing HHS?

• Stroke

• Sepsis

• Intoxication

• Intracranial infection

• Hepatic encephalopathy

• Uremic encephalopathy

What is the FIRST and most critical intervention in HHS?

• Aggressive fluid resuscitation

• Isotonic fluids (0.9% normal saline)

• Typically 15–20 mL/kg/hr initially

Why must fluids be given before insulin in HHS?

• Restores intravascular volume

• Improves tissue perfusion

• Gradually reduces serum osmolality

• Prevents hemodynamic collapse and cerebral edema

When should insulin therapy be initiated in HHS?

• Only after:

  • Initial fluid replacement has started

  • Potassium is >3.3 mEq/L

What is the standard insulin regimen for HHS?

• IV regular insulin

• 0.1 units/kg/hour continuous infusion

Why is potassium monitoring critical in HHS?

• Total body potassium is severely depleted

• Serum levels may appear normal initially

• Insulin drives potassium into cells → hypokalemia risk

• Hypokalemia can cause life-threatening arrhythmias

How is potassium managed during HHS treatment?

• K⁺ ≥ 3.3 mEq/L
  → Start insulin
  → Also give potassium replacement if K⁺ < 5.3

• K⁺ < 3.3 mEq/L
  → HOLD insulin
  → Give potassium first until K⁺ ≥ 3.3

Why:

• Insulin drives potassium into cells, lowering blood K⁺.

• If K⁺ is already too low (<3.3), insulin can cause severe hypokalemia and arrhythmias.

Bottom line (one line to remember):

• Only hold insulin if K⁺ < 3.3.

• If K⁺ is 3.3–5.2, give insulin + potassium together.

What is the desired rate of glucose reduction in HHS?

• 50–70 mg/dL per hour

• Rapid drops increase risk of cerebral edema

When should dextrose be added to IV fluids in HHS?

• When glucose falls below 250–300 mg/dL

• Typically add 5% dextrose

• Prevents hypoglycemia while continuing insulin

What monitoring is required after stabilization of HHS?

• ICU-level monitoring

• Frequent vital signs (BP, HR, RR, temp)

• Labs every 2–4 hours:

  • Glucose

  • Electrolytes

  • BUN/creatinine

  • Serum osmolality

What supportive care measures are included in HHS management?

• Treat underlying cause (often infection)

• Blood cultures and imaging if indicated

• Broad-spectrum antibiotics

• DVT prophylaxis (LMWH)

• Aspiration precautions

• Nutritional support

What are major complications of HHS?

• Neurologic injury (confusion, seizures, coma)

• Cerebral dehydration

• Acute kidney injury

• Cardiac arrhythmias

• Thromboembolism

• Possible permanent cognitive dysfunction

What prognostic indicators suggest worse outcomes in HHS?

• Age >65 years

• Severe infection

• Serum osmolality >350 mOsm/kg

• Delayed diagnosis

• Delayed fluid resuscitation

What is the key teaching point from the HHS case study?

• Early aggressive fluid therapy is lifesaving

• Correct sequencing (fluids → electrolytes→ insulin) prevents complications

• Identifying and treating the trigger (UTI) is essential

• Post-discharge education prevents recurrence

1. IV fluids FIRST

   • Corrects dehydration

   • Improves perfusion and lowers glucose on its own

2. Check electrolytes (especially K⁺)

   • Replace potassium if < 5.3

   • Hold insulin if K⁺ < 3.3

3. Start insulin

   • Only after fluids are running and potassium is safe (≥ 3.3)

Key exception to remember:

• Insulin is NOT started if potassium is < 3.3 mEq/L.

NCLEX-style takeaway:
Fluids stabilize first, electrolytes make it safe, insulin fixes the problem.

How is recurrence of HHS prevented?

• Optimized glycemic control

• Medication adherence

• Regular glucose monitoring

• Sick-day management education

• Adequate hydration

• Reliable follow-up care

Why is post-discharge follow-up essential after HHS?

• Reduces rehospitalization

• Reduces mortality

• Ensures medication access

• Addresses social determinants (cost, cognition, access to water)

• Coordinates long-term diabetes care

What is the key clinical pearl for HHS management?

• Fluids first, always

• Early recognition + aggressive hydration saves lives

• Prevention and education are just as critical as acute treatment