Endocrine · Year 2 · from Endocrine

Case 2: Type 2 Diabetes - Hyperosmolar Hyperglycemic State (HHS)

Patient Demographics

• Age: 72 years
• Sex: Female
• Occupation: Retired, lives in assisted living facility

Chief Complaint

"She's been confused and not herself for two days."

History of Present Illness

A 72-year-old woman with type 2 diabetes, hypertension, and mild dementia is brought from her assisted living facility for altered mental status. Staff noted progressive lethargy over 2 days, decreased oral intake, and increased urination. She had a urinary tract infection treated with antibiotics 1 week ago but did not complete the course. Her diabetes has been controlled on metformin and glipizide. She has had polyuria and polydipsia for the past week, which staff attributed to drinking more fluids in warm weather. Her blood glucose this morning was "HI" (>600 mg/dL) on the facility glucometer.

Physical Examination

• Vital Signs: BP 88/52 mmHg, HR 112 bpm, RR 18 (NOT Kussmaul), Temp 38.1°C
• General: Elderly woman, severely dehydrated, responsive only to painful stimuli
• HEENT: Extremely dry mucous membranes, sunken eyes
• Cardiovascular: Tachycardic, thready pulses
• Abdomen: Soft, non-tender
• Skin: Poor turgor, warm, dry
• Neurologic: Obtunded, localizes to pain, no focal deficits, sluggish pupils

Workup

• Laboratory Studies:
• Blood glucose: 892 mg/dL (extremely elevated)
• Serum osmolality: 358 mOsm/kg (severely elevated, normal 275-295)
• Venous pH: 7.31 (near normal - key difference from DKA)
• Serum bicarbonate: 20 mEq/L (mildly low)
• Anion gap: 14 (mildly elevated)
• Serum ketones: Trace positive (minimal ketosis)
• Sodium: 148 mEq/L (elevated, reflects severe dehydration)
• Corrected sodium: 162 mEq/L (even higher when corrected for glucose)
• Potassium: 4.8 mEq/L (total body depleted)
• BUN/Creatinine: 68/2.8 (severe prerenal azotemia)
• HbA1c: 9.8%
• Urinalysis: Glucose 4+, trace ketones, leukocyte esterase positive, nitrites positive (UTI)
• Urine culture: Pending
• CT head: No acute intracranial pathology

Diagnosis

Hyperosmolar hyperglycemic state (HHS) precipitated by urinary tract infection

Comparison: HHS vs DKA

Treatment

HHS MANAGEMENT (Similar principles to DKA with important differences):

1. AGGRESSIVE FLUID RESUSCITATION (Most Critical):

• 0.9% NS 15-20 mL/kg in first hour (1-1.5 L)
• Continue aggressive fluids - typical deficit 8-12 liters
• Goal: Replace 50% of deficit in first 12 hours
• Switch to 0.45% NS when corrected Na normal or high (usually needed)
• Fluids alone will significantly lower glucose

2. INSULIN:

• Start AFTER initial fluid bolus
• Lower rate than DKA: 0.05-0.1 units/kg/hr
• Target glucose reduction: 50-75 mg/dL/hr (NOT faster - risk of cerebral edema)
• Fluids contribute significantly to glucose lowering

3. POTASSIUM:

• Same replacement protocol as DKA
• Replace aggressively as K+ will drop with insulin and correction of acidosis

4. MONITORING:

• Glucose hourly
• Serum osmolality every 2-4 hours
• Mental status (should improve as osmolality normalizes)
• Neurologic checks for cerebral edema (avoid too-rapid correction)

5. TREAT PRECIPITANT:

• Antibiotics for UTI (ceftriaxone pending culture)
• Common precipitants: Infection, stroke, MI, medications

6. RESOLUTION:

• Osmolality <315 mOsm/kg
• Mental status returns to baseline
• Transition to SQ insulin and oral diabetes agents

Pathophysiology of HHS

1. Relative insulin deficiency: Enough insulin to prevent ketosis but not hyperglycemia
2. Gradual onset: Develops over days to weeks (vs. hours to days in DKA)
3. Severe hyperglycemia: Causes massive osmotic diuresis
4. Profound dehydration: Often 8-12 L fluid deficit
5. Hyperosmolarity: Causes neurologic dysfunction; severity correlates with mental status
6. Minimal ketosis: Sufficient insulin prevents uncontrolled lipolysis
7. Higher mortality: Due to profound dehydration, older age, and comorbidities

Clinical Pearl

HHS is characterized by extreme hyperglycemia (>600 mg/dL), hyperosmolarity (>320 mOsm/kg), and minimal ketosis, typically occurring in elderly patients with type 2 diabetes who have enough residual insulin to prevent ketogenesis but not hyperglycemia. Mental status changes correlate with serum osmolality. The key difference from DKA is the absence of significant ketoacidosis. Fluid resuscitation is the cornerstone of treatment - patients may have an 8-12 liter fluid deficit. Insulin is started at lower doses than DKA, and correction should be gradual to avoid cerebral edema. Mortality is higher than DKA (10-20%) due to older patient population, greater dehydration, and underlying comorbidities. Always identify and treat the precipitating factor, most commonly infection.

Clinical Image

Diagram showing the metabolic consequences of insulin deficiency and the classic symptoms of diabetes including polyuria, polydipsia, and weight loss that precede acute decompensation.

Image Source: Wikimedia Commons - "Main symptoms of diabetes" License: CC BY-SA 4.0 URL: https://commons.wikimedia.org/wiki/File:Main_symptoms_of_diabetes.svg

All cases for this lecture as Markdown