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)
- pH >7.30
- HCO3− >15 mEq/L
- No ketoacidosis or severe ketosis
Initial presentation of DM in 20% of patients.
Precipitating factors are:
- Acute infection 30–40% (pneumonia, UTI, sepsis)
- Acute pancreatitis
- Renal failure
- Severe burns
- 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
- 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):
Management of Hyperosmolar Hyperglycemic State (HHS)
|Fluid replacement||Correction of hyperglycemia||Electrolyte 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 may be as high as ...
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