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
HHNS occurs less often than DKA, but has a
much higher mortality.
 Pathophysiology
HHNS is attributed to three factors
1. Decreased insulin utilization
2. Increased gluconeogenesis & glycogenolysis
3. 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
1. Lower levels of counterregulatory hormones
2. High levels of endogenous insulin inhibiting lypolysis
3. Hyperosmolar state inhibiting lypolysis
 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.
 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.
 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.
 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 NS can be used once serum glucose reaches
250-300mg/dL.
 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.
 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.
 Disposition
Mostpts will require admission in the ICU
or monitoring for the first 24hrs of care.