What is the clinical spectrum of DKA and HONKC?
! Diabetic ketoacidosis and hyperosmolar coma represent the extremes of a clinical spectrum of
uncontrolled DM with hyperglycemia with variable levels of ketoacid accumulation (DKA) and
hyperosmolality (NKH). This is due to lack of insulin (deficiency or resistance) and excess glucagon.
! Hyperglycemia is a result of impaired peripheral glucose utilization due to insulin deficiency and
increased hepatic gluconeogenesis due to excess glucagon and to a lesser extent insulin deficiency.
! Ketoacid production is a result of increased free fatty acid production due to enhanced lipolysis
from insulin deficiency and altered hepatic metabolism of FFA due to excess glucagon facilitating
FFA entry into the mitochondria where converted to ketoacids. These ketoacids are B-
hydroxybutyrate (main ketone, especially in early DKA, NOT picked up with nitroprusside test)
and acetoacetate (rising pH favors the formation of this acid, should be strongly positive in late
DKA, picked up by nitropusside test.)
! Clinical variability is common, patients with type 2 DM can get DKA, while those with type 1 DM can
be hyperosmolar. It is known that much lower levels of insulin are needed to suppress lipolysis than to
promote glucose utilization. It is postulated that fat and muscle cells may have different sensitivities
insulin effects. A combination of the above leads to the clinical spectrum.
! Clinical pearls:
! ALWAYS look for precipitating factor-infection, ischemia, insufficient insulin, stress, meds
! Kussmaul breathing (think pH <7.2), abdominal pain 30 %, vomiting 80%, if febrile look for ID
! Prognosis determined by osmolality
What about the serum osmolality and its complications?
! Plasma osmolality is determined by solutes that are restricted to ECF= 2Na +Glu/18 +Bun/2.8, the
normal difference between the calculated and measured should be 10-15.
! If the osmolar gap is elevated, evaluate for the presence of other osmolyt