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Acute medical emergency seen in type 2 DM characterized by:

  • Impaired mental status
  • Hyperglycemia (plasma glucose >600 mg/dL)
  • Hyperosmolality (serum osmolality >320 mOsm/kg)
  • Dehydration
  • pH >7.30
  • HCO3 >15 mEq/L
  • No ketoacidosis or severe ketosis

Initial presentation of DM in 20% of patients.

Mortality 30–50%.

Precipitating factors are:

  • Acute infection 30–40% (pneumonia, UTI, sepsis)
  • CVA
  • MI
  • Acute pancreatitis
  • Renal failure
  • Thrombosis
  • Severe burns
  • Hypothermia
  • Trauma
  • Subdural hematoma
  • Endocrine (acromegaly, thyrotoxicosis, Cushing syndrome)
  • Drugs (β-blockers, calcium channel blockers, diuretics, steroids, and TPN)

Ketone production is minimal as pancreas still retains ability to secrete insulin to prevent fatty acid lipolysis.

Figure 211-1. Pathophysiology of HHS

  • Elderly individual with type 2 DM
  • Nausea/vomiting
  • Muscle weakness and cramps
  • Polyuria, and then oliguria
  • Slight hyperthermia common; if >38°C, suspect infection
  • Confusion, lethargy, seizures, hemiparesis, and coma

  • Extreme hyperglycemia (>1,000 mg/dL) is sufficient for diagnosis
  • Serum osmolality >320 mOsm/kg with higher osmolality leading to worse impairment of mental status. (Osmotic concentration is referred to as osmolality when expressed in milliosmoles/kilogram of solvent and as osmolarity when expressed in milliosmoles/liter of solvent.)
  • Effective serum osmolality calculated as:
    • 2(Na+ + K+) + (mg/dL of glucose/18) + (BUN/2.8) can give a quick assessment
  • Urine ketones are absent, which distinguishes from DKA
  • Serum Na+ concentration is usually normal or elevated because of severe dehydration
  • Serum K+ concentration is initially frequently high and goes down with treatment
  • Wide anion gap due to mild metabolic acidosis (multifactorial but HCO3- >15 mEq/L)
  • Prerenal renal insufficiency

  • Overall mortality ranges from 10% to 20%
  • Mortality rate increases with age and higher levels of osmolality
  • Mortality directly associated with age: 10% in patients <75 years and 35% in patients >75 years
  • Degree of dehydration should be assessed with decrease in body weight, tachycardia, oliguria, and hypotension
  • A complete neurological assessment with subsequent frequent assessments should be done

  • Goals of treatment include aggressive intravascular fluid replacement, correction of hyperglycemia, electrolyte replacement, and supportive care
  • Fluid replacement should always precede insulin replacement
  • Care should be taken to avoid pitfalls. Insulin infusion should not be begun before adequate correction of fluid status or with K+ <3.5 mEq/dL or hypophosphatemia
  • Also care should be maintained not to lower glucose by >100 mg/dL/h for risk of osmotic encephalopathy
  • Adequate subcutaneous insulin should be given before stopping insulin infusion

Management of hyperosmolar hyperglycemic state (HHS):

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Management of Hyperosmolar Hyperglycemic State (HHS)
Fluid replacementCorrection of hyperglycemiaElectrolyte management
Initial management
  • NS 15–20 mL/kg/h initially, until BP and organ perfusion normalize
  • Then, subsequent fluid management should focus on free water replacement
  • Total body water deficit ...

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