1. Description of the problem
What every clinician needs to know
Diabetic patients are at greater risk for organ dysfunction, and in patients with acute coronary syndromes diabetes is also associated with increased mortality. In ICU patients, hyperglycemia and high blood glucose variability are associated with increased morbidity and mortality.
Admission hyperglycemia is associated with mortality in patients without a history of diabetes, but not in diabetic patients.
Clinical features of the condition
Hyperglycemic crisis can present as diabetic keto-acidosis (DKA) or hyperosmolar hyperglycemic coma (HHC).
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Normoglycemia is defined as a blood glucose concentration between 80 and 110 mg/dL. In ICU patients consensus recommendations are to maintain blood glucose at less than 150 mg/dL.
Patients with hyperglycemic crisis have polyuria, polydipsia, weight loss, weakness, signs of dehydration and altered mental state. In addition patients have increased blood glucose and white blood cell count, hyponatremia, elevated or normal potassium concentrations and increased osmolarity. Diabetic keto-acidosis is characterized by metabolic acidosis caused by ketoacids (measured in blood or urine). Patients with hyperosmolar hyperglycemic coma do not develop keto-acidosis because there is still enough insulin to suppress lipolysis.
Key management points
Blood glucose should be maintained between 80 and 150 mg/dL by means of a continuous (short acting) intravenous insulin infusion. Blood glucose should be controlled regularly and insulin dose should be adjusted in order to prevent hyperglycemia and hypoglycemia.
2. Emergency Management
Emergency management steps
Hyperglycemic crisis:
1. Fluid therapy: goal is to restore fluid deficits within 24h.
Start: isotonic saline 15-50 mL/kg body weight per hour. Adjust upon urine output and hemodynamic status, typically 250-500 mL/h.
When blood glucose is less than 200 mg/dL: proceed with glucose 5% infusions.
2. Insulin:
Start: iv bolus of 0.1 U/kg body weight, followed by continuous infusion at 0.2 U/kg body weight per h.
Titrate insulin at a decline of blood glucose of 50-75 mg/dL per hour. Decrease insulin rate when blood glucose is less than 200 mg/dL in DKA and less than 300 mg/dL in HHC to 0.02-0.05 U/kg per hour.
Subcutaneous insulin: when DKA /HHC is resolved and patient starts eating by mouth.
3. Potassium: total body potassium is depleted, therefore start potassium infusion (20-30 mmol/h) when serum K+ is below normal limit.
4. Bicarbonate: start bicarbonate infusion only when pH is less than 6.9.
Drugs and dosage
NaCl 0.9%
NaCl 0.45% in case of hypernatremia
Glucose 5% when blood glucose is less than 200 mg/dL
Insulin: short acting – Actrapid
3. Diagnosis
Establishing a specific diagnosis
Hyperglycemia is diagnosed by measurement of blood glucose on a whole blood sample (blood gas machine) or on plasma.
Point of care devices lack sensitivity and specificity.
Describe the diagnostic approach to the patient with this problem
Hyperglycemia: measurement of blood glucose.
Hyperglycemic crisis: measurement of blood glucose and pH. Measurement of keto-acids on a urine stick or on plasma.
Normal lab values
Blood glucose: 80-110 mg/dL
Pathophysiology
Hyperglycemia results from defects in insulin secretion, insulin action or both. In hyperglycemic crisis there is also activation of counter regulatory hormones such as catecholamines, cortisol, glucagon and growth hormone. DKA is characterized by lipolysis with formation of keto-acids, while in HHC there is enough insulin to suppress lipolysis.
Epidemiology
Hyperglycemia is associated with worse outcomes in ICU patients. Diabetes patients may present with hyperglycemic crisis.
Hyperglycemia:
1. At time of ICU admission: associated with worse outcomes.
a) In general ICU patients: only in patients without diabetes.
b) in cardiovascular ICU patients: also in patients with diabetes.
2. Blood glucose control:
The initial hallmark study by the Leuven group demonstrated survival benefit for strict blood glucose control in ICU patients. Follow up studies and meta-analyses demonstrated varying results. Differences in study design, standard of care, measurement of blood glucose, nutrition protocols and patient cohorts may explain these differences.
3. Blood glucose variability is associated with worse outcomes.
What’s the evidence?
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