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Hyperosmolar Hyperglycemic Nonketotic syndrome

Hyperosmolar Hyperglycemic Nonketotic syndrome. Presented by Dr Moosally Prepared by Mick Svoboda. HHNS. Definition Severe hyperglycemia w/ Serum glucose >600mg/dL Plasma osmolarity > 315mOsm/kg Bicarb > 15 Arterial pH > 7.3 Serum ketones - negative or mildly elevated Epidemiology

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Hyperosmolar Hyperglycemic Nonketotic syndrome

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  1. Hyperosmolar Hyperglycemic Nonketotic syndrome Presented by Dr Moosally Prepared by Mick Svoboda

  2. HHNS • Definition • Severe hyperglycemia w/ • Serum glucose >600mg/dL • Plasma osmolarity > 315mOsm/kg • Bicarb > 15 • Arterial pH > 7.3 • Serum ketones - negative or mildly elevated • Epidemiology • HHNS occurs less often than DKA, but has a much higher mortality.

  3. Pathophysiology • HHNS is attributed to three factors • Decreased insulin utilization • Increased gluconeogenesis & glycogenolysis • Impaired renal excretion of glucose • End result - hyperglycemia and volume depletion through osmotic diuresis. • Total body water losses can reach 8-12 liters • Lack of ketoacidosis in HHNS attributed to • Lower levels of counterregulatory hormones • High levels of endogenous insulin inhibiting lypolysis • Hyperosmolar state inhibiting lypolysis

  4. Clinical Features • Usually elderly • HHNS pts often present with abnormal vital signs and changes in mentation. • Common complaints are nonspecific • Weakness, anorexia, fatigue, cough, dyspnea, or abdominal pain. • Pts are often poorly controlled or newly diagnosed type 2 DM. • 30-50% of cases are assoc. w/ pneumonia or UTIs.

  5. Physical findings • Sxs range from subtle changes in VS and confusion to profound shock and coma. • Sxs correlate with degree of hyperglycemia and hyperosmolality. • Signs of volume depletion. • Poor skin turgor, dry mucous membranes, hypotension. • CNS sxs • Tremor, clonus, hyper/hyporeflexia, hemiplegia or hemisensory defects.

  6. Laboratory studies • Serum glucose • Electrolytes • Serum osmolality/osmolarity • BUN, creatinine • Ketones • CBC • EKG • Ancillary studies if indicated • UA, blood cultures, CXR, cardiac enz, pancreatic enz, ABGs, head CT and LP.

  7. Treatment • Key is to improve tissue perfusion • Fluid resuscitation • NS preferred • Initial rates of 500-1500 mL/h during first two hrs. • More conservative therapy for pts w/ cardiac ds. • Once hypotension, tachycardia, and urinary output improve fluid can be changed to 1/2NS. • D5 ½NS can be used once serum glucose reaches 250-300mg/dL.

  8. Treatment • Electrolytes • K+ • Initial levels may be normal or high in the presence of acidemia • Levels < 3.3mEq/L represents severe deficit and are at risk for dysrhythmias. • Replacement can begin once urinary output is assured. • Replace at a rate of 10-20mEq/h. • Na+ • Replaced rapidly w/ the amount of NS required for fluid resuscitation. • Mag and Phos • No current guidelines for random replacement in the ED.

  9. Treatment • Insulin • As in DKA IV administration preferred over IM or SubQ due to poor adsorption. • IV infusion at rate of 0.1 units/kg/h R insulin • Loading dose is optional • Once serum glucose reaches 250-300mg/dL fluid can be to D5 1/2NS and insulin can be decreased to 0.05units/kg/h.

  10. Disposition • Most pts will require admission in the ICU or monitoring for the first 24hrs of care.

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