Hyperglycemic Emergencies

Andrew Dionne, MDMaineGeneral Medical Center

Topics

Diabetic Ketoacidosis Epidemiology Pathophysiology Diagnosis Treatment

Hyperosmolar Hyperglycemic State AKA Nonketotic Hyperglycemia, Hyperosmolar

Nonketotic Coma

DKA Statistics

Type 1 Diabetes Occasionally in Type 2

Infection, Trauma, Cardiac Newly diagnosed Type 2 DM

More common in young people & women Cost

Annual hospital cost $1 billion ¼ of health care dollars spent on Type 1 diabetics

DKA Hospitalizations

DKA Mortality

DKA Mortality

Mortality primarily due to precipitating illness Prognosis worse with

Old Age Coma Hypotension

HHS Statistics

<1% of all diabetes-related admissions More common in elderly & Type 2 diabetics Mortality

Variable 10-50% Most often due to the precipitating illness

Diabetic Ketoacidosis

Pathophysiology of DKA

Role of 2 Hormones Insulin Glucagon

Lack of insulin stimulates hyperglycemia Lack of insulin stimulates fat & muscle

breakdown Increase in fatty acids to liver stimulates ketosis Fluid loss stimulates hyperosmolarity

Role of Insulin

Ketoacidosis Lipolysis→Increased FFA→Converted to

Ketones in Liver Three ketones

Acetoacetic Acid; Beta-Hydroxybutyric Acid; Acetone Accumulation leads to acidosis (↓pH) &

formation of anion gap Differential Diagnosis

Alcoholic Ketoacidosis Starvation Ketosis

DKA vs. HHS

HHS lacks ketosis/acidosis Residual insulin sensitivity & secretion minimizes

ketotic repsonse HHS may have higher blood sugars

>1000 mg/dl Older patients with worse GFR

HHS often presents later with hyperosmolar symptoms

Causes of DKA/HHS New diagnosis of Diabetes Infection: Pneumonia, Gastroenteritis, UTI Pancreatitis Acute MI/ACS Stroke Trauma Alcohol/Drugs/Medications Missed Insulin/Compliance

Symptoms of DKA

Develops rapidly Earliest symptoms are due hyperglycemia

Polyuria, Polydipsia, Weight loss Neurologic symptoms Abdominal pain, nausea, vomiting

Up to 50% of DKA Associated with degree of acidosis ?Delayed gastric emptying/ileus

Physical Exam in DKA

Signs of dehydration Tachycardia, hypotension

Neurologic exam “Acetone breath” Kussmaul Respirations Fever is rare, even with infection

Evaluation in DKA

Laboratory Glucose Electrolytes CBC Serum Ketones Plasma Osmolality ABG (?venous pH) Urinalysis ?Amylase/Lipase

Other Electrocardiogram Chest X-Ray Blood Culture Urine Culture Sputum Culture

Labs in DKA: Glucose

Usually between 500-800 mg/dl “Euglycemic DKA”

Nutritional deficiency Pregnancy

Labs in DKA: Anion Gap

AG= Na – (Cl + HCO3) Normal <12; DKA >20 Accumulation of BHB & AA Differential of AG metabolic acidosis

Lactic Acidosis Drugs: ASA, Methanol, Ethylene Glycol CKD

Labs in DKA: Ketones

Test in serum & urine Nitroprusside reaction converts AA to acetone

Theoretically possible to have ketoacidosis from mainly BHB & have a negative test

Can test by adding Hydrogen Peroxide to urine (converts BHB to AA & allows NP reaction)

Labs in DKA: Sodium

Variable sodium levels Direct effect of hyperglycemia leads to

hyponatremia (↓1meq/L for every 62 mg/dl rise in BS)

Secondary effect of osmotic diuresis which causes loss of free water→hypernatremia

Most are mildly hyponatremic Pseudohyponatremia d/t hyperlidemia

Labs in DKA: Potassium Overall potassium deficit

Renal loss with osmotic diuresis & ketone excretion GI loss

However, on initial evaluation, K level is usually normal or elevated Hyperosmolarity Insulin deficiency ?Acidemia

Take great care in monitoring/repleting K

Labs in DKA: Other

Phosphate Usually body depleted, but initial levels may be

normal or high Amylase/Lipase

May be elevated, even without pancreatitis Elevated WBC Hyperlipidemia

Elevated TC & Trigs

Treatment of DKA

Initial Evaluation: ABCs; Exam; Labs; Causes Close Monitoring Fluid Replacement Insulin Therapy Electrolyte Replacement Resolution & Conversion to home therapies

Treatment of HHS

Initial Evaluation: ABCs; Exam; Labs; Causes Close Monitoring Fluid Replacement Insulin Therapy Electrolyte Replacement Resolution & Conversion to home therapies

Monitoring

Don’t expect much sleep ICU Status Blood sugar monitoring q1 hr BMP, venous pH q2-4 hrs Ketones? Close evaluation of vitals & neuro status Consider use of flowsheet

Fluid Replacement Mainstay of initial therapy Expand the intravascular volume & improve renal blood

flow Avg fluid loss for DKA: 3-6 Liters (8-10 in HHS) Isotonic saline

Rapidly infuse volume without acute lowering of plasma osmolarity

Switch to ½ NS in subacute phase if Na normal or high 15-20 ml/kg initially then decrease to 5-10ml/kg/hr Fluids alone my initially decrease BG by 35-70

Insulin Therapy

Role of Insulin Lower serum glucose (mainly by decreasing liver production) Reduce ketogenesis in liver by reducing lipolysis and glucagon

secretion Increase ketone utilization

Insulin IV bolus and continuous drip is standard of care Some studies have looked at frequent, rapid-acting insulin, but

not enough data to support use except in mild DKA cases

Insulin Therapy

Check Potassium first! If K <3.3, delay insulin until begin K repletion May drive insulin into the cells and lead to life-

threatening hypokalemia IV bolus of regular insulin: 0.1 U/Kg Continuous infusion, start at 0.1 U/Kg/hr Goal is to decrease glucose by 50-70 mg/dl per

hour; will require further titration of drip

Insulin Therapy

Addition of dextrose to IVF Avoid hypoglycemia Continue insulin drip while awaiting resolution of

ketoacidosis Continue nutrition while patient NPO

Once BS < 200 (<300 in HHS) start dextrose (usually D5 ½ NS)

Potassium Replacement

If initial K high, should not need more therapy than insulin, which will drive K into the cells

To prevent hypokalemia, add KCl to IVF if K<5.3 If K normal, 20-30 meq/liter of IVF is adequate If K low, may need more aggressive rx If using 40 meq KCl in saline, may use ½ NS as this

will create isotonic solution NS = 154 cation equiv ½ NS = 77; ½ NS + 40 meq KCl = 117 (~3/4 NS)

Bicarbonate Therapy Controversial subject Small RCT did not shown improved M/M with addition of NaHCO3

to standard rx in pts with pH of 6.9-7.1 Concerns with use:

Rapid rise in pCO2 may lead to fall in cerebral pH contributing to edema May increase hepatic ketogenesis Post-treatment metabolic alkalosis

Consider use with: pH <7.0, especially if decreased cardiac function or vasodil. Life-threatening hyperkalemia

Dose: 50-100 meq NaHCO3 (1-2 amps) over 2 hours Does not apply to HHS

Phosphate Therapy Most patients phosphate depleted Usually level will fall with initial therapy

Driven into the cells with resolving acidosis Improved renal perfusion→excretion

Most patients do not have symptoms related to hypophosphatemia

Routine use not necessary If evidence of cardiac dysfunction, hemolytic anemia, or

respiratory depression in pts with phos <1.0 mg/dl 20-30 meq/L of Potassium Phosphate, added to IVF

Resolution of DKA

Goals Resolve ketoacidosis

Normal AG Ketones may remain (+) because of slower resolution of

acetone Neurologically alert/intact

Plasma Osm <315 Taking PO nutrition

Resolution of DKA

Resume regular diet Add long-acting insulin, based on prior dosing or

24 hr insulin requirements on drip Stop insulin infusion 1-2 hrs after SQ insulin

dose

Complications Related to underlying illness Cerebral edema

Worsening mental status 12-24 hrs after starting rx 0.5-1% of cases, mostly in children Mortality 20-25% Reduce risk by gradual replacement of Na & H2O

deficits in hyperosmolar patients & adding dextrose to IV solution once appropriate

Non-cardiogenic pulmonary edema

Prevention

Improved access to medical care Education

When to contact doctor if illness occurs Increased use of short-acting insulin during illness Continued use of insulin & BS monitoring when illness

prevents eating Continued nutrition during times of illness