Endocrine Emergencies- Hyperglycemia

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Endocrine Emergencies- Hyperglycemia

Hyperglycemia

Condition in which blood glucose is elevated above normal level

Types of hyperglycemia

Diabetic Ketoacidosis (DKA)

Hyperglycemic Hyperosmolar Nonketotic Coma (HHNC)

DKA or HHNC can be first sign of diabetes mellitus in a patient with no known history

Epidemiology

DKA most often occurs in Type 1 DM

DKA Onset often associated with a stressor on body (trauma, Infection, MI, Stroke)

DKA -25% occurs in patient with no known history

HHNS commonly elderly patients with Type 2 DM, but can occur in young patients also

Incidence of HHNS higher than that of DKA.

20-30% patients with no history of DM present with acute onset of HHNS

Diabetic Ketoacidosis

Relative or absolute insulin defciency

Due to lack of insulin, tissues are unable to uptake glucose

Blood has extremely elevated glucose (problem is tissue can't uptake without insulin to aid in creating channel into cell)

Blood-Brain barrier does not require insulin for glucose to diffuse across- Brain is receiving more than adequate glucose

Tissues starving for glucose (except brain).

Three syndromes in DKA

Metabolic Acidosis

Cells not receiving glucose to produce energy due to lack of insulin to aid in moving glucose into cell (no channel created)

Cells starving for energy/glucose

Triggers release of glucagon which further increase blood glucose levels (glucose is not problem...need insulin to push into cell)

Free fatty acids now circulate in abundance in bloodstream and metabolized into ketones. Acetone begins to accumulate in blood

Acetone released in respirations in small part. This is the cause of the fruity (acetone) smell on breath

Ketones are not used with shift from aerobic metabolism; Increased acidosis (Metabolic Acidosis) is present. Large amount of ketones eliminated by kidneys in urine.

Osmotic Diuresis

Osmosis is movement of water across semipermeable membrane from low concentration to high particle concentration

Diuresis equals urination- Excessive normally the case

As BGL approaches 225 mg/dl, glucose spills over into urine for elimination

Glucose molecules then pull water across semipermeable membrane (osmotic effect)

Results in significant urine production

Volume depletion and dehydration result from the large water loss

Electrolyte Disturbance

Large amount of ketones in the urine (remember during metabolic acidosis free fatty acids were metabolized into ketones)

Ketones are strong organic acids and must be buffered to be excreted

Sodium is typically the buffer, but where sodium goes water follows.

As sodium buffers the ketones it draws large amounts of water into renal tubules and produces excessive urine

Further increase in dehydration and volume depletion

Loss of large amounts of fluid results in excretion of other electrolytes such as potassium, calcium, magnesium, and phosphorus

So what is Diabetic Ketoacidosis?

Obviously the diabetic portion is related to fact that lack of insulin prevented glucose from entering cells. This started the entire cascade.

Ketoacidosis is simply the metabolic acidosis from the ketone production from fat metabolism (cells had to get energy somewhere since glucose couldn't enter cell)

The ketones were a byproduct of that process.

Excess ketones had to be eliminated in urine. Osmotic diuresis pulled huge fluid (water) into renal tubule and formed urine. This brought vital electrolytes with it also. The sodium buffer to eliminate ketones further shifted water from the body into urine for elimination of the ketones.

Hyperglycemic Hyperosmolar Nonketotic Syndrome ( HHNS)

Excessively elevated blood glucose and hyperosmolar extracellular fluid without production and accumulation of mass ketones

HHNS often has blood glucose levels over 600 mg/dl

Absolute or relative insulin deficiency OR decreased tissue response to insulin that is present and circulating

Results in decreased uptake of glucose by the tissues (cellular level)

Elevated blood glucose levels creates hyperosmolar extracellular space that pulls fluid from the cell and dehydrates the intracellular space

Initially, pulling fluid out of cell into bloodstream helps maintain perfusion and blood pressure

As BGL reaches 250, glucose spills into urine and osmotic diuresis (just like in DKA) pulls more fluid from body.

Profoundly depletes intravascular volume (perfusion) which decreases perfusion to kidneys and impairs their ability to remove the excess glucose

Commonly results in death from circulatory collapse

Key electrolytes have been pulled from tissues into extracellular space. So, blood levels for electrolytes may appear normal, but the tissue levels dangerously low

Why no Ketones in HHNS?

Not well understood. Some schools of thought are that the decreased tissue/cellular response to insulin is problem more than absolute insulin defieciency. If so, some circulating insulin does exist...perhaps just enough that it prevents the mass release of counterregulatory hormones and prevents ketoacidosis from occuring.

No mass ketones/acetone in blood is why the HHNS patient will not have acetone breath (sweet fruity).

Endocrine Emergencies- DKA/HHNS/Hypoglycemia

Hyperglycemia