You are on page 1of 10

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.
2.
3.

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
1.
2.
3.

Lower levels of counterregulatory hormones


High levels of endogenous insulin inhibiting lypolysis
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.

Signs of volume depletion.

Sxs correlate with degree of hyperglycemia and


hyperosmolality.

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
Most pts will require admission in the ICU

or monitoring for the first 24hrs of care.

You might also like