April 18, 2016 - Diabetic Emergencies

Question 1

Alpha-Cells of the Pancreas

Answer 1

Secrete glucagon

Question 2

DKA

Answer 2

Diabetic Ketoacidosis

A life-threatening medical emergency that occurs when the body is hyperglycemic, in a state of ketosis, and is experiencing acidosis.

Occurs primarily in patients with DM1

During a shortage of insulin, the body switches to burning fatty acids and producing acidic ketone bodies that cause most of the symptoms and complications.

Question 3

HHS

Answer 3

Hyperosmolar Hyperglycemic State

A life-threatening medical emergency that occurs primarily in DM2 (but can be seen in DM1). This can be differentiated from DKA with the measurement of ketone bodies which are the underlying process in DKA and are usually not (or barely) detectable in HHS.

Question 4

Pathophysiology of DKA

Answer 4

DKA arises because of a lack of insulin in the body. The lack of insulin and corresponding elevation of glucagon leads to increased release of glocuse by the liver (normally suppressed by insulin) from glycogen via glycogenolysis and gluconeogenesis. High glucose levels spill over into the urine, taking water and solutes (like Na and K) with them in a process known as osmotic diuresis, which can lead to dehydration.

The absence of insulin also leads to the release of FFAs from adipose tissue through lipolysis which are then converted into ketone bodies in the liver. The ketone bodies have a low pKa and therefore turn the blood acidic through metabolic acidosis. The body can attempt to compensate by adjusting the breathing to become alkalotic in which case the patient hyperventilates to blow off CO2 and in the extreme case is Kussmaul repsiration.

Question 5

Pathophysiology of HHS

Answer 5

HHS is often precipitated by a stressor such as infection, MI, stroke, or acute illness such as sepsis.

A relative insulin deficiency leads to a serum glucose that is usually higher than 33 mmol/L, and a resulting serum osmolarity that is greater than 320 mOsm. This leads to osmotic diuresis which in turn leads to volume depletion which causes a further increase in blood glucose levels. Ketones are not present because the small amount of insulin present is enough to inhibit hormone-sensitive lipase mediated fat tissue breakdown and suppress ketone formation.

On the differential diagnosis should be DKA. This can be differentiated from DKA be the absence of ketones in the blood and the urine. In contrast to DKA, serum glucose levels in HHS are extremely high (usually greater than 40-50), however anion-gap metabolic acidosis is absent or mild.

Question 6

DKA vs HHS

Answer 6

DKA is usually more acidotic and less dehydrated, while HHS is more dehydrated but not acidotic

DKA is usually in younger patients (more DM1), while HHS is usually in older patients (more DM2)

DKA is usually DM1, while HHS is usually DM2

In DKA the duration of decline is usually hours to days, while in HHS it is usually days to weeks

In DKA underlying disease is unusual, while in HHS it is common

In DKA, mortality is 1-10%, while in HHS it is 12-46%

Question 7

Laboratory Investigations of DKA and HHS

Answer 7

In DKA there will be a lower pH, urine ketones, serum ketones, and a high anion gap

In HHS, glucose will be higher, bicarb will be higher (no acidosis), and the effective serum osmolarity will be higher

Question 8

Anion Gap

Answer 8

AG = Na - (Cl + HCO3)

Question 9

Principles of Treatment for Adult PKA

Answer 9

1. Fluid resuscitation
2. Avoidance of hypokalemia
3. Insulin administration
4. Avoidance of rapidly falling serum osmolality
5. Search for precipitating cause

Question 10

Principles of Treatment for Adult HHS

Answer 10

1. Fluid resuscitation
2. Avoidance of hypokalemia
3. Avoidance of rapidly falling serum osmolality
4. Search for preciptating cause
5. Possibly insulin to further reduce hyperglycemia

Question 11

How Dehydration Occurs in DKA and HHS

Answer 11

Osmotic diuresis from hyperglycemia

Vomiting from ketosis/hyperglycemia

Poor fluid intake from obtundation / lack of access (children / elderly)

Restoring ECFV improves tissue perfusion and decreases glucose by dilution and increasing urinary glucose losses

Question 12

Electrolyte Abnormalities in DKA

Answer 12

Sodium - hyperglycemia causes fluid shift from intracellular to extracellular which causes “apparent hyponatremia”

Potassium - moves extracellularly and is lost from osmotic diuresis (consider replacing and also ECG if abnormal)

Phosphate - moves extracellularly and is lost from osmotic diuresis (consider replacing if severely abnormal - but note this will cause a decrease in potassium so use potassium phosphate)

Bicarbonate - not recommended for treating acidosis and should only be cautiously considered if pH is less than 6.9, the patient is in severe shock, or the patient is facing life-threatening hyperkalemia.

Question 13

Complications of DKA and HHS

Answer 13

Treatment Related - cerebral edema, pulmonary edema, seizures from hypoglycemia, dysrhythmias from kypokalemia

Non-Treatment Related - thrombotic stroke, DVT, pulmonary embolism, pancreatitis, renal failure

* In a dehydrated state you are hypercoaguable *