Hyperglycemic Crises Flashcards
Normal Physiological Response to Increased Serum Glucose
Increased serumglucose
Detected by the pancreatic beta cells and insulinwill be released
insulin will
↓glucagonsecretionfrom pancreatic alpha cells
↓gluconeogenesis andglycogenolysis in theliver
↑glucoseuptake by muscle andadipose cells
Hyperglycemia
DKA & HHS
Results from problems relating to insulin (absolute deficiency or insulin resistance):
↓glucose utilization by peripheral tissues (muscle and adipose cells)
↑glycogenolysis and ↑gluconeogenesis by the liver
Leads to:
↑plasma osmolality (high solute – glucose) → draws water out of the cells → outside the cell the sodium concentration is now dilute
hyperglycemia
High serumglucose level (> 180 mg/dL) exceeds renal threshold causing
Glucosuria
Increase inosmotic pressure of the urine leading topolyuria
Loss of water → dehydration → worsens plasma osmolality (hyperosmolality) → potassium shifts out of cells → ↑ extracellularpotassium, ↓ intracellular potassium
Impaired renal function (AKI)
DKA
Epidemiology
More frequently seen in younger patients
Mostly seen inpatients with type 1diabetes
Accounts for ~14% of all hospital admissions for diabetics
Mortality rate of 5% in individuals < 40 years; ↑ mortality with advanced age
HHS
epidemiology
Usually associated with older individuals (≥ 65 years)
Patientswill usually have type 2 diabetes
Accounts for < 1% of all hospital admissions for diabetics
Mortality rate: 10%–20%
HHS & DKA
etiology
Infections(most common)
Inadequate or noncompliance withinsulintreatment
Acute illnesses (stroke,myocardial infarction,pancreatitis, surgery, trauma)
Medications - corticosteroids
Illicit drugs - cocaine
Alcohol
HHS
etiology
Dehydration
Medications – diuretics, beta-blockers
Endocrine disorders: Cushing syndrome
DKA
etiology
new onset diabetes - type 1
DKA
Clin Man
Rapid onset of symptoms (over 24 hours)
Polyuria
Polydipsia
Nausea andvomiting
Diffuse abdominalpain
Weakness
History ofweight loss → common with a new diagnosis oftype 1diabetes
DKA
PE Findings
Physical exam findings:
Vitals:
Tachycardia
Hypotension
Hypothermia
Rapid, deep respirations (Kussmaul respirations) → compensatoryhyperventilation (attempting to blow off carbon dioxide – acid)
Fruity breath → exhaledacetone
DKA and HHS
Evidence of severedehydration
Dry mucous membranes
Sunken eyes
Decreasedskin turgor
Decreasedurine output
HHS
Clin Man
Gradual development of symptoms (over days to weeks)
Polyuria
Polydipsia
Nausea andvomiting
Neurologic changes:
Lethargy
Delirium
Coma(in severe disease)
Seizures
Sensory deficits
Vision changes
HHS
PE Findings
Physical exam findings:
Vitals:
Tachycardia
Hypotension
Hypothermia
Altered mental status, lethargy, or coma
DKA
Dx
Serum glucose: >250 mg/dL
Serum bicarbonate: ↓↓ (< 18 mEq/L)
Anion gap: Yes(the higher the more severe the presentation)
Serum osmolality: Variable
Serum ketones (beta-hydroxybutyrate, acetone): Positive
Urine ketones: Positive
Arterial blood gas: pH < 7.3; ↓ pCO2 (increase resp to reduce CO2 and lessen acidosis)
HHS
Dx
Serum glucose: > 600 mg/dL
Serum bicarbonate: >18 mEq/L
Anion gap: Generally normal
Serum osmolality: >320 mOsm/L
Serum ketones (beta-hydroxybutyrate): Negative or small
Urine ketones: Negative or small
Arterial blood gas: pH > 7.3
Dx
both Na will be low, K will be high
DKA
IV fluid management
Admit patient to the intensive care unit (ICU)
Aggressive intravenous (IV) fluid replacement:
Begin withnormal saline (0.9% NaCl) (1 L/h for the first 1-2 hours, then run at a rate of ~250 ml/h)
If corrected Na is < 135 mEq/L, continuenormal saline
If corrected Na remains normal or elevated, consider changing to 0.45% saline
Onceglucosereaches 200 mg/dL, change todextrose5 % with ½normal saline at 150–250 mL/hr
Reduces risk ofhypoglycemia
Reduces risk ofcerebral edema (results from rapid decrease inglucose)
Monitorurine output andhemodynamics
fluid is to correct fluid osmolality, which should bring down glucose
DKA
IV insulin infusion
K+ must be > 3.3 mEq/L
Regular insulin 0.1 unit/kg as a bolus, then 0.1 unit/kg/h as an infusion or SQ
Hourly serum glucose monitoring
Repeat bolus if the plasma glucose does not ↓ by 10% in the first hour
Close monitoring of serumelectrolytes andanion gap (every 2–4 hours)
High potassium normal corrects with IV hydration and insulin
Providepotassium supplementation to maintain a K of 4–5 mEq/L
albuterol treatments will also bring K back into the cell.
DKA
Sodium bicarbonate(NaHCO3)
can be given over 2 hours if the pH is < 6.9
DKA
has resolved once..
DKA has resolved once the serumanion gap has normalized (< 12 mEq/L) andglucose is 150–200 mg/dL
HHS
IV fluid management
Admit patient to the intensive care unit (ICU)
Aggressive intravenous (IV) fluid administration:
HHSpatients typically have a significant fluid deficit of ~4-10 L
Begin with anormal saline bolus: 1 L over the 1st hour
If the corrected Na is < 135 mEq/L, continuenormal saline
If the corrected Na remains normal or elevated, consider changing to 0.45% saline
Onceglucosereaches 300 mg/dL, change todextrose5% with ½normal saline at 150–250 mL/hr
Maintainglucose between 250 and 300 mg/dL
Monitorurineoutput andhemodynamics
Management of HHS
IV Insulin infusion
(K+ must be > 3.3 mEq/L)
Regular insulin 0.1 unit/kg as a bolus, then 0.1 unit/kg/h as an infusion or SQ
Hourly serum glucose monitoring
Repeat bolus if the plasma glucose does not ↓ by 10% in the first hour
Close monitoring of serumelectrolytes (every 2–4 hours)
High potassium normal corrects with IV hydration and insulin
Providepotassium supplementation to maintain a K of 4–5 mEq/L
HHS
is considered resolved when..
HHS is resolved when the patient’s mental status has improved, serumosmolalityis < 315 mOsmol/kg, andglucoseis 250–300 mg/dL
