Hyperglycemic Crises and Inpatient Control of Diabetes Flashcards
What is DKA
Diabetic Ketoacidosis
Complication in T1 pts
Hyperglycemia + Ketosis + Acidosis
Pathophysiology of DKA
Decreased insulin concentration
Increased counterregulatory hormones
Counterregulatory hormones
Catecholamines
Cortisol
Glucagon
Growth Hormones
DKA Hyperglycemia from
Increased glyconeogenesis
Accelerated glycogenolysis
Impaired glucose utilizaiton
DKA Lipolysis from
Insulin deficiency
Counterregulatory hormones
DKA Transient insulin resistance from:
Hormone imbalance
Elevated FFA
Increased FFA oxidation in liver leads to
Increased ketone bodies (beta-hydroxybutyrate and acetoacetate) which leads to acidosis
DKA symptoms
N/V Ab pain Polyuria Polydispsia Confusion Fatigue Fruity odor on breath (ketones)
DKA presentation
Elevated glucose Low arterial pH Low serum bicarbonate Elevated anion gap Decreasing mental status Decreased sodium Increased phosphate
Treatment Goals
Correct dehydration, hyperglycemia, electrolyte imbalances
ID and correct precipitating factors
Frequent pt monitoring
Treatment Initial Fluid Therapy
Initial: Normal Saline 15-20 mL/kg/hr or 1-1.5 L in the first hr
Treatment Maintenance Fluid Therapy
1/2 NS at 250-500 mL/kg OR NS at 250-500 mL/hr if low serum Na
Once glucose is ~200 mg/dL –> add 5% dextrose to fluids
Correct fluid deficits within 24 hrs
Treatment Insulin Therapy
Initial IV bolus of regular insulin 0.1u/kg
Continuous infusion regular insulin 0.1u/kg/hr
When serum glucose reaches 200, decrease insulin to 0.02-0.05 u/kg/hr
Maintain glucose between 150-200
Treatment Potassium Replacement
Replace K+ when levels fall below UNL
20-30 mEq/L fluid maintenance
Goal: 4-5 mEq/L
Delay insulin until K+ is >3.3 bc it pushes it intracellularly
Treatment of Bicarb and Phosphate Replacement
Bicarb: pH < 6.90
Phosphate is pushed intracellularly by insulin
Transitioning to SQ insulin
Glucose < 200 + 2 of the following:
Bicarb >15
pH >7.3
Anion gap <12
Overlap for 1-2 hrs
If insulin naive:
Start multi-dose insulin regimen at 0.5-0.8 u/kg/day
Cerebral Edema Signs and Symptoms
Headache Level of consciousness deterioration Seizures Incontinence Pupilary changes Bradycardia Decreased BP
Prevention of Cerebral Edema
Avoid excessive hydration
Avoid rapid reduction in plasma osmolarity
Gradual decrease in serum glucose
Maintain glucose at 250-300 until mental status normalized
Treatment of Cerebral Edema
Mannitol infusion
Mechanical ventilation
What is HHS
Hyperglycemic Hyperosmolar Syndrome Usually from restricted water intake Days to weeks Dehydration- osmotic diuresis Relative insulin deficiency (prevents lipolysis -- no acidosis)
Presentation of HHS
Hemiparesis and seizures A lot higher glucose than DKA Normal pH Normal bicarb High osmolarity --> diuresis Worse mental status
Treatment for HHS
Fluid therapy: NS or 1/2 NS
Once glucose is ~300 add dextrose
Insulin therapy: Decrease rate when glucose is ~300
Challenges to inpatient glycemic control
Acute illness
Inconsistent caloric intake
Changes in medications
Limitations in glucose monitoring and insulin administration
Goals in Critically Ill Patients
Initiate IV insulin when BG >180 mg/dL
BG target = 140-180
Avoid hypoglycemia
Goals in Non-critically ill patients
Fasting BG <70
Management
Oral meds may need to be discontinued upon admission
Sliding scale insulin alone is not appropriate for hospitalized patients
Management of Critically ill patients
Continuous IV insulin is preferred method in this population
Management of Non-Critically Ill Patients
SQ insulin preferred (basal/bolus)
