Hyperglycemic Emergencies

Andrew Dionne, MD MaineGeneral 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 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

LipolysisIncreased FFAConverted 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

Other

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

Electrocardiogram Chest X-Ray Blood Culture Urine Culture Sputum Culture

Labs in DKA: Glucose

Usually between 500-800 mg/dl Euglycemic DKA

Nutritional Pregnancy

deficiency

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 waterhypernatremia 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 be elevated, even without pancreatitis

Amylase/Lipase
May

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

Dont 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 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 Some studies have looked at frequent, rapid-acting insulin, but not enough data to support use except in mild DKA cases

Insulin IV bolus and continuous drip is standard of care

Insulin Therapy

Check Potassium first!

If

K <3.3, delay insulin until begin K repletion May drive insulin into the cells and lead to lifethreatening 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 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 NS as this will create isotonic solution

NS = 154 cation equiv NS = 77; 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 perfusionexcretion

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