Endocrine Emergencies & Management Diabetic Ketoacidosis (DKA) & Hyperglycemic Hyperosmolar Syndrome (HHS) Endocrine Emergencies & Management

Learning Goals Understand the physiology of DKA and HHS. Apply the revised Insulin infusion nomogram to patients experiencing DKA and HHS.

DKA Triad: Medical Emergency Diabetic Ketoacidosis (DKA) can occur in both type 1 & 2 diabetes mellitus. It presents with three common characteristics: Hyperglycemia Hyperketonemia Metabolic Acidosis

Hyperglycemia Without insulin… Glucose does not move into the cell Glucose accumulates in the bloodstream (leading to serum hyperosmolality) Cells begin to starve; lipolysis occurs to compensate PLEASE SEE COMMENT

Electrolyte imbalances Hyperosmolality As glucose concentration increases in the bloodstream, the kidneys attempt to excrete the glucose (along with water, potassium, phosphate, and magnesium) Leads to: Polyuria Polydipsia Dehydration Electrolyte imbalances

Lipolysis Cells go into survival mode and breakdown fat for glucose Adipose tissue (fat stores) are broken down Produces byproduct of ketones which accumulates in bloodstream (hyperketonemia)

Hyperketonemia Cells use insulin to break down ketones Without sufficient insulin, ketones accumulate in bloodstream along with the glucose (exacerbating serum hyperosmolality) Excessive ketones changes the pH of blood to become more acidic (metabolic acidosis)

Metabolic Acidosis Blood pH < 7.3 Anion gap of 10-12 mEq/L Body tries to compensate: Hyperventilating (Kussmaul respirations) to decrease CO2 levels in blood and correct pH Excrete ketones through renal system Mental status changes, lethargy, and hypotension (LATE SIGNS! TREAT AGRESSIVELY!)

Classifying the Severity Mild Moderate Severe Plasma Glucose >250 Arterial pH 7.25 – 7.30 7.00 - <7.24 <7.0 Serum Bicarb 15 – 18 10 - <15 <10 Urine Ketone Positive Serum Ketone Anion Gap >10 >12 Mental Status Alert Alert/Drowsy Stuperous

Hyperglycemic Hyperosmolar Syndrome (HHS) Complication of type 2 diabetes When glucose cannot move into the cell, it accumulates in the bloodstream (leading to hyperglycemia and hyperosmolality) Since insulin is still produced in type 2 diabetes, it is sufficient to prevent lipolysis (which causes ketone byproducts) HHS does not cause ketoacidosis PLEASE SEE COMMENT

Differences in DKA & HHS Correct acidosis Lower blood glucose Rehydrate Correct electrolytes Resolve cause Criteria for resolved DKA: pH > 7.3 Bicarbonate ≥ 15 mEq/L Blood glucose < 200 mg/dL Anion gap < 12 Patient is able to eat HHS: Lower blood glucose Rehydrate Correct electrolytes Resolve cause Criteria for resolved HHS: BG 200 – 300 mg/dL Patient is able to eat

Critical Note… Goal of DKA is to reverse the metabolic acidosis and normalize serum glucose Remember: Hyperglycemia is not causing the acidosis—the ketones are! It takes twice as long for insulin to treat ketones than it does for glucose. Requires meticulous care and frequent monitoring for 12-24 hours until acidosis is reversed.

Treatment Rehydrate Correct electrolyte deficits & acidosis Restore glucose metabolism Provide glucose when necessary Prevent complications

Focus on restoring the volume Rehydration Focus on restoring the volume 1 liter of 0.9% NaCl bolus followed with maintenance fluids Na+ levels during fluid resuscitation Serum Na+ ≥ 135 mEq/L then 0.45% NaCl is used Serum sodium ≤135 mEq/L then 0.9% NaCl is used Give IV fluids until anion gap is closed or volume deficit is corrected.

Correcting Electrolyte Deficits & Acidosis Correcting labs are crucial to your patient’s outcome Chem 10, Magnesium & Phosphate are routinely ordered every 2 hours ABG/VBG will show you if your acidosis is correcting

Do NOT start an insulin drip if potassium is < 3.3 mEq/L Electrolytes Magnesium Phosphate Potassium ≥ 1.8 mg/dL ≥ 1.5 mg/dL ≥ 5.1 mEq/L The new order set has specific directions to replace each of these electrolytes. However the physician may chose to write their own orders. Do NOT start an insulin drip if potassium is < 3.3 mEq/L

Respiratory Alkalosis ABG / VBG Test Normal Ranges pH 7.35 – 7.45 pCO2 35 – 45 mmHg pO2 80 – 100 mmHg O2 Sat 95 – 100% HCO3- 22 – 26 mmHg pH CO2 HCO3- Respiratory Acidosis < 7.35 > 45 mmHg Normal Metabolic Acidosis < 22 mEq/L Respiratory Alkalosis > 7.45 < 35 mmHg Metabolic Alkalosis > 26 mEq/L

Anion Gap Goal is to decrease anion gap to <12 in DKA patients Calculated measurement of ions in the blood: Sodium – (Chloride + Bicarbonate) Anion gap is high when you have DKA, because of the ketoacids (anions). Goal is to decrease anion gap to <12 in DKA patients

The lungs can blow off the CO2 (acids). Using Bicarbonate HCO3 + H  H2CO3  H2O + CO2 The lungs can blow off the CO2 (acids). New Order Set: For pH less than 6.9, dilute 100 mEq Sodium Bicarbonate in 400 mL of D5W. Infuse over 2 hours. For pH 6.9 - 7.0, dilute 50 mEq Sodium Bicarbonate in 200 mL of D5W. Infuse over 1 hour.

Glucose Target is: 150 – 200 mg/dL while in DKA 200 – 300 mg/dL while in HHS Reduce glucose levels by 50-75 mg/dL every hour until goal is reached Glucometer reading “HI” (>500): Get a serum glucose STAT Blood glucose levels hourly while on insulin drip

Insulin Drip Regular Insulin IV drip Loading dose (if critically ill) = 0.1 units/kg Start infusion rate = 0.1 unit/kg/hour Nomogram titration is based upon finger stick blood glucose/sugar (FSBS). Pump is programmed in units/kg/hour PLEASE SEE COMMENT

DKA Nomogram

HHS Nomogram

Insulin Management Do NOT stop insulin infusion unless you have hypoglycemia (< 70 mg/dL) or DKA is resolved Criteria for resolved DKA: Venous pH > 7.3 Bicarbonate ≥ 15 mEq/L Blood glucose < 200 mg/dL Anion gap < 12 Patient is able to eat

Converting Insulin IV to SubQ Call physician to initiate subcutaneous insulin AND Wait to discontinue your insulin IV drip until 2 hours after subcutaneous insulin is initiated

Glucose Administration Use dextrose-based IV fluids once target glucose has been reached When blood glucose reaches 200 mg/dL, change IV fluids to D51/2 NS per MD order Remember…Glucose levels correct faster than ketonemia. Need to correct the ketones that are causing the acidosis!

Preventing Complications Hypoglycemia Hourly monitoring of blood glucose level during insulin infusion Hypokalemia Caused by inadequate potassium replacement or inappropriate bicarbonate administration Cerebral Edema (Rare, but severe complication) Avoid excessive hydration and rapid decrease in plasma osmolarity Maintain a slow, gradual decrease in serum glucose