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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