Hyperosmolar Hyperglycemic Nonketotic syndrome

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Hyperosmolar Hyperglycemic Nonketotic syndrome

• Presented by Dr Moosally
• Prepared by Mick Svoboda

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HHNS

• Definition
• Severe hyperglycemia w/
• Serum glucose gt600mg/dL
• Plasma osmolarity gt 315mOsm/kg
• Bicarb gt 15
• Arterial pH gt 7.3
• Serum ketones - negative or mildly elevated
• Epidemiology
• HHNS occurs less often than DKA, but has a much
  higher mortality.

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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

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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.

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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.

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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.

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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.

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Treatment

• Electrolytes
• K
• Initial levels may be normal or high in the
  presence of acidemia
• Levels lt 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.

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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.

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Disposition

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