Diabetic Emergencies Michael J Fowler MD Division of

Diabetic Emergencies Michael J. Fowler MD Division of Diabetes and Endocrinology Vanderbilt University

The patients never stop making water and the flow is incessant. . . Life is short, unpleasant and painful, thirst unquenchable, drinking excessive. . . If for a while they abstain from drinking, their mouths become parched and their bodies dry; the viscera seem scorched up; the patients are affected by nausea, restlessness and a burning thirst, and within a short time, they expire. Aretaeus of Cappadocia 2 nd Century A. D.

Case #1 • 21 year old male with history of poorly controlled type one diabetes presents to the ED with symptoms of nausea, vomiting and abdominal pain. He states the symptoms began developing last night. Because he hadn’t been eating anything, he skipped using insulin at supper.

Case #1 (cont’d) • • • Physical exam: Oral mucosa is slightly dry Tachycardic with regular heart rate in the 130’s Deep, regular respirations Acetone odor Mild diffuse abdominal tenderness, no R/G/R hyperactive bowel sounds • No foot or hand lesions • Insulin injection sites and blood glucose test sites are without evidence of infection

Labs • • Na- 130 (low) K – 5. 4 (High) Cl – 102 (low) CO 2 – 10 (low) Anion Gap – 18 (high) Glucose – 597 Ketones - positive > 1: 8

• Diagnosis, Doctor?

Anion Gap Metabolic Acidoses • • Methanol Uremia DKA Paraldehyde Isopropyl alcohol Lactic acidosis Ethylene glycol Salicylates

Diabetic Ketoacidosis/Hyperosmolar Crisis

Laboratory Findings • • • Anion gap metabolic acidosis Hyperkalemia Hyperglycemia Positive Ketones > 1: 2 dilution p. H less than 7. 35 Hyperchloremic nonketotic metabolic acidosis

Why? ? ?

Other Causes • • • Drugs Pregnancy Infarction Secondary Gain Incorrect insulin dosing or administration Unrefrigerated insulin

Diabetic Ketoacidosis

Potassium Flux

The Basic Problem Ketosis Insulin Glucagon Hyperglycemia Dehydration

Fat Cells

The Liver: Epicenter

Treatment • • • Fluids Insulin Potassium

Common Mistakes • Panic over dehydration leads to an IV flood • Inadequate or delayed Potassium • Ignore Co-diagnoses • Failure to reassess • Not starting long-acting insulin immediately • Use of bicarbonate

Ketoacidosis Hyperosmolar Crisis

Unusual DKA • • • Euglycemic DKA Alkalemic DKA “Nonketotic” DKA

Whom to Watch Most Closely

Case Study #2 32 yo Male with type 1 DM is admitted with acute bacterial meningitis and seizure episode. The patient was visiting relatives from out of state. He is currently obtunded and intubated and no family are present for questioning. His glucose upon arrival to the MICU is 262. His serum bicarb is 23 and serum ketones are absent. On exam you notice he is wearing an insulin pump

What do you do? A. Recommend cranking the insulin pump up to 10 units an hour and head back to the call room for a nap B. Remove the device and order a regular insulin sliding scale C. Recommend removal of the device, begin an IV insulin drip with frequent glucose monitoring, start IVF with 5% Dextrose, and obtain an endocrine consult

Case Study #3 Your team is called to the bedside of a morbidly obese 51 year old female with DM with altered mental status. She responds sluggishly to painful stimuli and the nurse reports her FSBG to be 22, respirations 16, HR 90, and blood pressure 144/61. Her IV infiltrated several hours ago and she currently has no IV access.

You Manage the Patient’s Hypoglycemia by: A. Drawing a stat blood sample and waiting to confirm the fingerstick with a serum glucose value before giving treatment B. Inserting a central line and administering an amp of D 50 C. Give Glucagon D. Leaving her alone to “sleep it off”

Causes of Hypoglycemia • • • Reduced intake malnutrition malabsorption adrenal insufficiency Renal/hepatic failure meal/insulin mismatch • Drug interactions with oral hypoglycemics • alcohol If a patient has an episode of significant hypoglycemia- FIND OUT WHY

Ketones

Clinical Signs • • • Dehydration Ketotic odor Kussmaul breathing Antecedent polyuria and polydipsia Abdominal pain and Nausea

Critical Calculations

Fluids • • • 500 -2000 isotonic fluid bolus 250 cc/hr thereafter For practical purposes LR is preferable to NS • Potassium should be added to the fluids as potassium gluconate

Insulin • IV insulin is used most commonly • Starting dose of 0. 1 u/kg/hour is a reasonable starting dose • Insulin resistance (due to illness or type 2 DM or both) may require higher doses of insulin • Dose is titrated based on clinical response • Basal insulin is started in the Emergency Room • Decline in glucose is rapid to a glucose of 200 mg/d. L

Potassium • Anion Gap is a useful marker of recovery • Start potassium supplementation as soon as normal renal function is verified

Nonketotic Hyperosmolar Crisis Hyperglycemia Dehydration

Caveats • • • Chronic Renal Insufficiency Overt Renal failure Pancreoprivic Diabetes Mellitus

Lactic Acidosis

Type 2 Diabetes

Clinical Diabetes

Cori Cycle

Lactate

Definition • • AG Metabolic acidosis with p. H < 7. 35 Lactic acid level is greater than 5 mmol/L Type A – Inadequate Oxygen availability Type B – Nonhypoxic etiology

Causes • Typically does not occur in the setting of good health

Metformin • Incidence of Lactic Acidosis is. 03/1000 patient years; typically 50% fatal • Enhances glucose uptake in peripheral tissues • Increases lactic acid production • Inhibits pyruvate conversion to acetyl Co. A

Metformin (continued) • Lactic acidosis is most likely to occur in drug overdose, renal insufficiency or dehydration/renal hypoperfusion • Hold drug for hypoxemia, dehydration, sepsis or use of IV contrast media

Treatment of Lactic Acidosis • • Prompt recognition Stop metformin Bicarb is controversial Ensure adequate hydration without inducing fluid overload (renal or cardiac failure) • Dialysis