What is the pathophysiology and management of Hyperosmolar Hyperglycemic State (HHS), a condition characterized by severe hyperglycemia and impaired renal function?

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Last updated: April 4, 2025 • View editorial policy

From the Guidelines

Hyperosmolar Hyperglycemic State (HHS) is a serious metabolic emergency that requires immediate attention, and the most effective treatment approach involves individualization based on a careful clinical and laboratory assessment, as stated in the most recent guidelines 1.

Pathophysiology of the Disease Process

The pathophysiology of HHS involves insulin deficiency leading to hyperglycemia, which causes osmotic diuresis, resulting in profound dehydration and electrolyte imbalances. As blood glucose levels exceed 600 mg/dL, cellular dehydration occurs, affecting brain function and potentially leading to coma.

Relevant Assessment Data

Subjective

  • Increased thirst
  • Polyuria
  • Weakness
  • Confusion
  • Visual disturbances

Objective

  • Blood glucose >600 mg/dL
  • Serum osmolality >320 mOsm/kg
  • Minimal ketosis
  • pH >7.3
  • Altered mental status
  • Signs of dehydration (dry mucous membranes, poor skin turgor)
  • Tachycardia
  • Hypotension
  • Warm, dry skin

Nursing Diagnoses: Outcome (Patient’s Goals)

Short-term

  • Restore fluid balance within 24-48 hours
  • Normalize blood glucose levels to 140-180 mg/dL
  • Improve mental status

Long-term

  • Prevent recurrence through diabetes management education
  • Maintain stable blood glucose levels

Nursing Interventions

  • Administering IV fluids (typically 0.9% saline at 15-20 mL/kg/hr initially)
  • Insulin therapy (regular insulin IV at 0.1 units/kg/hr)
  • Electrolyte replacement (particularly potassium)
  • Frequent monitoring of vital signs, neurological status, intake and output, and blood glucose levels hourly
  • The use of continuous intravenous insulin is the standard of care for critically ill and mentally obtunded patients with DKA or hyperosmolar hyperglycemia, as recommended by the latest guidelines 1.

Evidence-base Rationale

The rationale for these interventions includes correcting dehydration to improve circulation and organ perfusion, gradually reducing blood glucose to prevent cerebral edema, and restoring electrolyte balance to prevent arrhythmias. According to the most recent study 1, there is no significant difference in outcomes for intravenous human regular insulin versus subcutaneous rapid-acting analogs when combined with aggressive fluid management for treating mild or moderate DKA.

Evaluation of Goal and Patient Response to Interventions

Evaluation involves monitoring for:

  • Improved mental status
  • Stabilized vital signs
  • Normalized laboratory values
  • Adequate urine output
  • The patient's understanding of diabetes management to prevent recurrence of HHS Clear communication with outpatient providers either directly or via hospital discharge summaries facilitates safe transition of care, as emphasized in the guidelines 1.

From the Research

Pathophysiology of the Disease Process

  • Hyperosmolar Hyperglycaemic State (HHS) is a medical emergency associated with high mortality, characterized by marked hypovolaemia, osmolality ≥320 mOsm/kg, marked hyperglycaemia ≥30 mmol/L, without significant ketonaemia (≤3.0 mmol/L), without significant acidosis (pH >7.3) and bicarbonate ≥15 mmol/L 2
  • It occurs less frequently than diabetic ketoacidosis (DKA) and affects those with pre-existing or new type 2 diabetes mellitus, increasingly affecting children and younger adults
  • Mixed DKA/HHS may occur

Relevant Assessment Data

Subjective

  • Clinical features of HHS include marked hypovolaemia, hyperglycaemia, and altered cognitive status
  • Patients may present with symptoms such as thirst, polyuria, and weakness #### Objective
  • Laboratory results: osmolality ≥320 mOsm/kg, glucose ≥30 mmol/L, ketonaemia ≤3.0 mmol/L, pH >7.3, and bicarbonate ≥15 mmol/L
  • Vital signs: hypotension, tachycardia, and decreased urine output

Nursing Diagnoses: Outcome (Patient’s Goals)

Short-term

  • Improve clinical status and replace fluid losses within 24 hours
  • Gradual decline in osmolality (3.0-8.0 mOsm/kg/h) to minimize the risk of neurological complications
  • Blood glucose 10-15 mmol/L in the first 24 hours #### Long-term
  • Prevent hypoglycaemia and hypokalaemia
  • Prevent harm (VTE, osmotic demyelination, fluid overload, foot ulceration)
  • Identify and treat underlying precipitants

Nursing Interventions

  • Intravenous (IV) 0.9% sodium chloride to restore circulating volume (fluid losses 100-220 ml/kg, caution in elderly) 2
  • Fixed rate intravenous insulin infusion (FRIII) should be commenced once osmolality stops falling with fluid replacement unless there is ketonaemia
  • Glucose infusion (5% or 10%) should be started once glucose <14 mmol/L
  • Potassium replacement according to potassium levels

Evidence-base Rationale

  • The Joint British Diabetes Societies (JBDS) HHS care pathway consists of 3 themes (clinical assessment and monitoring, interventions, assessments and prevention of harm) and 5 phases of therapy (0-60 min, 1-6, 6-12, 12-24 and 24-72 h) 2
  • HHS resolution criteria are: osmolality <300 mOsm/kg, hypovolaemia corrected (urine output ≥0.5 ml/kg/h), cognitive status returned to pre-morbid state and blood glucose <15 mmol/L

Evaluation of Goal and Patient Response to Interventions

  • Monitor patient's clinical status, laboratory results, and vital signs to evaluate the effectiveness of interventions
  • Adjust interventions as needed to achieve patient's goals and prevent complications 2

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.