DM 5 hyperglycemia

  1. diabetic ketoaciosis
    • aka a diabetic coma
    • lack of or profound deficiency of insulin
    • breakdown of fats cause there is no insulin bringing glucose to the cell. when fat is broken down it makes ketones
    • seen in type 1 rarely in type 2
    • reasons:
    • - illness
    • - inadequate insulin dosage
    • - undiag type 1
    • - poor self management
    • - read brunner sick day rule- prevention
    • 1. incre BS
    • 2. + ketones
    • 3. develop metabolic acidiosis bc of + ketones
  2. sick day rule
    • never eliminate insulin secondary to n/v
    • take nl does insulin- freq small CHO
    • fluids- prevent dehydration
    • check CBG more often than usual
    • if vomiting, NPO call the MD
    • call MD is ketones or CBG is > 250
    • infection and inflammation can cause BS to increa
    • dehydration can cause EOD
  3. DKA
    classic features
    • hyperglycemia
    • FVD and lytes loss (NA and K) glucose molecules cant move so the water will move to create balance. fluid will pull into the blood stream. well perfuse kidneys
    • acidosis- no insulin to make
  4. DKA
    • less glucose enter cells without insulin
    • gluconeogensis increased
    • osmostic diuresis- can loss liters
    • excessive urination
    • dehydration
    • lytes imbalance
    • lipolysis results in ketone bodies which leads to acidosis
  5. DKA
    • polyuria
    • polydipsia
    • polyphagia- alter ketones, incr ketones
    • hot and dry sugar high
    • acetone breath- fruity bc u are breath off sugar
    • kussmaul's respiration- hyperventilation trying to get rid of CO2 bc of the acid
  6. DKA
    more manifestations
    • blurred vision
    • headache, weakness
    • orthostatic hypotension
    • tachycardia
    • poor skin turgor
    • GI- anorexia, n/v, abd pain (lipolysis ketones)
    • +/- mental status changes- plays with nerve function CNS changes
    • kidneys can have a normal amt of glucose 180 mg/dl
  7. DKA
    diagnostic finding
    • glucose 300 +
    • serum bicarbonate < 15 mEq/L (norm 18-22)
    • ph under 7.35
    • + urine ketones
    • incre serum ketones
    • Na- hypo
    • K- hypo
    • incre BUN (over working kidneys and dehydration), HCT (dehydration)
  8. DKA
    • ********* reverse dehydration********
    • treat hyperglycemia
    • balance electrolytes
    • resolve acidosis- when BS is resolve this usually resolves itself
  9. DKA management more
    • fluid and electrolyte replacement******:
    • NS as fast as 1L/hr (6-10L) reesta volume
    • 1/2 NS (hypotonic) after u/o and BP has improved- u want to go slow. push the fluid into cells but not too fast bc cause cells to have too much fluid ie cerebral edema(this means u have more glucose in the vascular and u want to move fluid into the cells)
    • when glu reaches 250 give IV D5W to maintain it- this pt they are getting insulin so glucose can maintain
    • K + replacement early in treatment even with normal lab result
    • - assess hypokalemia
    • - assess EKG, K level, urine out *** if you not putting out u can get hyperkalemia which will lead to arrythimas
    • insulin can pushes K into cells as well which is further causing hypo
    • this pt will get IV K supplements
  10. DKA management
    monitor fluid volume status
    • VS
    • I&O- makes kidney is still so we are not causing FVO
    • lung sounds
    • skin turgor
    • monitor lytes
    • monitor renal function
  11. DKA management
    treatment acidosis
    • Insulin IV (only regular)
    • - bolus: start off with this lower BS, ketones
    • - continuous infusion: then this after
    • we don't stop the IV insulin until they started SC insulin. think about how long R insulin last. u want to make sure pt is cover. so once they recieve sc insulin then dc IV insulin
    • Insulin SC: stop after IV insulin stops then put on dextrose with this. u want to slowly drop the BS
    • monitor glu q 1hr while on insulin infusion
    • adm solutions with glu once CBG > 250 (switch to dexrose
    • why don't give Na bicarb- bc it can cause hyperkalemia and acidotic
    • once bicarbnate is normal they will stop IV insulin and dextrose slowly
  12. Hyperglycemic hyperosmolar Nonketonic syndrome
    • HHNS
    • type 2 dm
    • lack of insulin production or resistant (u still have some insulin to work with)
    • blood glu > 600
    • serum osmolarity is > 350 mOsm/L
    • dehydration
    • mental status changes- slight decre onset usually slowly
  13. HHNS
    classic features
    • hyperglycemia
    • hyperosmolarity- lots of BS in blood more flood in blood
    • mental status changes
    • ketosis: minimal or absent
  14. HHNS
    • incre resistant to insulin and/or excessive CHO intake contribute to hyperglycemia
    • incre serum osmolarity pulls water out of body cells to create balance- polyuria, dehydration, mental status changes
    • enough insulin available to prevent breakdown of fats and ketosis, acidosis
  15. HHNS
    who is at risk
    • over age 50, undiag type 2
    • precip event: acute illness, infection, stroke
    • medication: thiazides
    • often has s/s for weeks before dx
    • - polyuria and polydipsia
  16. HHNS manifestations
    • few symptoms early, so glu very high when diagnosed
    • dehydration symptoms
    • excessive thirst
    • change in mental status
    • infection/imflammation
    • seizures
    • hallucinations
    • may be mistaken for a stroke
    • - hemiperesis, visual field loss
  17. HHNS dx
    • blood glucose > 600
    • serum osmolarity > 350
    • elevated BUN and crt
    • absent: serum/urine ketones
    • change in lytes levels
  18. HHNS management
    • similiar to DKA
    • higher amt of IVF
    • careful fluid replacement to avoid cerebral edema
    • IV insulin: tx hyperglycemia
    • careful monitoring of neuro s/s
    • education prevention
Card Set
DM 5 hyperglycemia
high BS