Hyperosmolar Hyperglycemic State (HHS)
Hyperosmolar Hyperglycemic State (HHS)
Hyperosmolar Hyperglycemic State (HHS)
HYPERGLYCEMIC STATE
(HHS)
• Relative insulin deficiency and inadequate fluid intake are the underlying causes of HHS.
• Insulin deficiency increases hepatic glucose production (through glycogenolysis and gluconeogenesis) and impairs glucose
utilization in skeletal muscle
• Hyperglycemia induces an osmotic diuresis that leads to intravascular volume depletion, which is exacerbated by inadequate
fluid replacement.
• The absence of ketosis in HHS is not completely understood.
• Presumably, the insulin deficiency is only relative and less severe than in DKA.
• Lower levels of counterregulatory hormones and free fatty acids have been found in HHS than in DKA in some studies.
• It is also possible that the liver is less capable of ketone body synthesis or that the insulin/glucagon ratio does not favor
ketogenesis
• Underlying mechanism of HHS is a relative or absolute reduction in effective circulating insulin with a concomitant elevation
of counterregulatory hormones.
• Decreased renal clearance and decreased peripheral utilization of glucose lead to hyperglycemia.
• Hyperglycemia and hyperosmolarity result in an osmotic diuresis and an osmotic shift of fluid to the intravascular space,
resulting in further intracellular dehydration.
• This diuresis also leads to loss of electrolytes, such as sodium and potassium.
• Unlike patients with DKA, patients with HHS do not develop significant ketoacidosis, but the reason for this is not known.
– May be availability of insulin in amounts sufficient to inhibit ketogenesis but insufficient to prevent hyperglycemia.
– Additionally, hyperosmolarity may decrease lipolysis, limiting the amount of free fatty acids available for ketogenesis.
– In addition, levels of counterregulatory hormones are found to be lower in patients with HHS than in those with DKA.
• All patients with HHS require IV insulin therapy; however, immediate treatment
with insulin is contraindicated in the initial management of patients with HHS.
The osmotic pressure that glucose exerts within the vascular space contributes to
the maintenance of circulating volume in these severely dehydrated patients.
Institution of insulin therapy drives glucose, potassium, and water into cells. This
results in circulatory collapse if fluid has not been replaced first.
• After the kidneys show evidence of being perfused, initiating insulin therapy is
safe. This is accomplished most effectively in the ICU, where cardiovascular and
respiratory support is available if needed. Infuse insulin separately from other
fluids, and do not interrupt or suspend the infusion of insulin once therapy is
started.
• The following steps may be used as a guideline for insulin infusion:
• Begin a continuous insulin infusion of 0.1 U/kg/h
• Monitor blood glucose by means of bedside testing every hour; if glucose levels
are stable for 3 hours, decrease the frequency of testing to every 2 hours
• Set the target blood glucose level at 14mmol/l; this target level may be adjusted
downward after the patient is stabilized
Kimaiga H.O, MBChB (University of Nairobi)