1. suppressed immune system
2. impaired vascular responses
3. hyperreactive platelets and coagulation
4. inflammation
5. increased oxidative stress

1. Inhibits lipolysis
2. Inhibits inflammatory growth factors
3. Enhances vasodilation by stimulating endothelial nitric oxide
4. Inhibits proinflammatory cytokines

Preprandial: < 140 mg/dL

Random: < 180 mg/dL

Usually refers to use of regular insulin, dosed based on BG, without any scheduled insulin

Disadvantages:

1. Ineffective for hyperglycemia when used as monotherapy
2. Gives no incentive to adjust scheduled therapy
3. Usually not individualized dosing
4. Reactive approach rather than proactive
5. Often leads to fluctuation of BG levels

1. Most effective in achieving pre-specified BG levels
2. Allows rapid dosing adjustment
3. Has been shown to decrease mortality and morbidity in some studies

1. Very labor intensive (requires q 1-2 hr glucose monitoring)
2. Increased risk of hypoglycemia

1. Critical Illness
2. Hyperglycemic Crisis
3. Preoperative, intraoperative, and postoperative care
4. Post heart surgery
5. Post organ transplantation
6. Cardiogenic shock
7. High dose glucocorticoid therapy
8. Prolonged NPO in type 1 diabetes

Begin transition to SubQ when patients begin to eat regular meals or transferred to lower intensity care

• Daily SubQ requirements: Approx. 75-80% of total daily IV
• 40-50% of daily SubQ dose should be basal
• 50-60% of daily SubQ dose should be prandial, divided among the meals

IV insulin has short half-life (0.5-1 hr), therefore first dose of SubQ insulin should be administered before DCing IV insulin

Basal insulin can be initiated at any time of the day

Administer short or rapid acting insulin 1-2 hrs prior to discontinuing IV infusion

• Pay attention to changes in patient's nutritional status and/or medications
• Ensure a hypoglycemic protocol is in place
• Treat mild hypoglycemia promptly
• Less aggressive dosing in certain patients (increased insulin sensitivity, decreased insulin clearance, diminished glycogen stores)

• A1C should be used to differentiate between stress hyperglycemia and undiagnosed DM
• Patient with newly diagnosed DM should receive appropriate education and follow up
• Patients with stress hyperglycemia still need appropriate follow up with a physician

• Absolute deficiency of insulin OR
• Insufficient insulin coupled with increased counterregulatory stress hormones

• hyperglycemia -> glucosuria -> osmotic diuresis -> dehydration and loss of Na+ and K+
• increased lipolysis -> increased FFA -> increased ketone bodies -> increased ketonemia and metabolic acidosis
• Evolves over a short period of time (< 24 hrs)

• Insufficient insulin AND Insulin resistance

• Residual insulin is sufficient enough to inhibit lipolysis therefore minimizing ketosis, but not hyperglycemia
• Hyperglycemia -> glucosuria -> osmotic diuresis -> severe dehydration (hyperosmolality) -> loss of electrolytes and impaired renal function (eventually less excretion of glucose and accumulation)
• Reduction in urinary excretion of glucose leads to more severe hyperglycemia than in DKA
• Evolves over days and weeks

1. Hyperglycemia (HHS > DKA)
2. Dehydration (HHS > DKA)
3. Electrolyte imbalance
4. Consistent features (metabolic acidosis in HKA, hyperosmolality in HHS)

• Decreased Na and H2O reabsorption and increased urinary Na loss lead to a net loss of total body Na
• Need to correct Na based on glucose level before accessing total Na deficit

• Dehydration and acidosis (DKA) cause shifting K out of cells
• Insulinopenia leads to impaired K entry into cells
• Increased K in ECF leads to increase urinary loss

1. Infection (by far)
2. Inappropriate insulin therapy
3. New-onset of diabetes mellitus
4. CVD (heart attack, stroke)
5. Pregnancy
6. Trauma
7. Hyperthyroidism
8. Pancreatitis
9. Drugs (corticosteroids, sympathomimetics)

Symptoms:

1. history of polyuria, polydipsia, weight loss
2. N/V, abdominal pain
3. fruity odorous breath (DKA)
4. weakness and muscle cramps
5. altered mental status

Signs:

1. dehydration
2. hyperventilation
3. coma (more frequent in HHS)

1. Fingerstick
2. Chemistry panel
3. Urinanalysis
4. Arterial blood gas
5. Serum osmolality
6. Serum ketone and acetone levels
7. CBC and cultures if infection is suspected
8. EKG if hypokalemic
9. A1C to determine acute episode or poor control

Risk of mortality increases in the very young or very old

Negative prognostic factors:

1. hypotension
2. hypothermia
3. coma

• continuous IV insulin infusion
• if plasma glucose does not fall by 50-75 mg/dL in the first hr, increase infusion rate every hour until steady decline is reached

Maintenance insulin infusion when plasma glucose reaches 200 in DKA or 300 in HHS

1. decrease insulin drip and add dextrose to IV fluids
2. adjust infusion rate and dextrose amount to maintain 150-200 until DKA resolves or 250-300 until HHS resolves

• Rapid acting insulin may be used in mild DKA
• Administer bolus dose then q 1-2 hr injections to achieve glucose around 250 mg/dL
• Dose is then adjusted until DKA resolves
• No differences in efficacy compared to CIII
• Allows treatment on general medicine floor or ED which cuts cost

• Need repletion of both intravascular and extravascular volume
• Use crystalloids
• 0.9% NaCl should be used
• Subsequent fluid depends on serum Na+ concentration:

If normal or elevated: 0.45% NaCl

If low: 0.9% NaCl

• When plasma glucose reach 200 mg/dL in DKA or 300 mg/dL in HHS, switch to D5W 0.45% NaCl
• Infusion rate must be adjusted for cardiac and renal dysfunction
• Monitor BP and I/O to better assess fluid status

Sodium (replaced adequately with fluid replacement)

Potassium

• Goal ~ 4-5 mEq/L
• Usually depleted due to urinary loss but serum concentration may be low, normal, or high
• Replacement dose depends on serum K level
• Low (< 3.3): treatment immediately, hold insulin
• Normal (3-5.2): treat while patient is on insulin
• High (> 5.2): no replacement until level drops and recheck q 2hrs
• Must consider renal function

• Acidosis will correct with insulin therapy
• Sodium bicarb may be necessary only in severe acidosis (pH < 6.9) -> treat with bicarb and K until pH > 7.0