Endocrine and Metabolic Emergencies Flashcards
Fundamentals of tx of DKA?
- volume repletion
- insulin
- correction of lytes and acid-base imbalance
- tx precipitating cause
- avoid complications
Most impt initial step in tx of DKA?
- Rapid fluid admin
- NS recommended initially
- then alt w/ 0.45% NS
- BG and ketone conc will fall after fluid admin andb/f implementation of any other therapeutic modality (rise in GFR allows for glucose and ketone body clearance)
- increased insulin perfusion facilitates action of insulin
- *insulin and fluid key to tx
Insulin therapy in DKA?
***- admin at 0.1 units/kg/hr after fluid bolus
- continus IV infusion of small doses through pump:
less complications
- loading dose not necessary
- monitor freq.
- DONT do IM or SubQ (erratic absorption)
What causes K+ def in DKA?
- combo of acidosis, osmotic diuresis, and vomiting
- initial serum conc usually normal or high due to:
intracellular exchange of K+ for H+
total body fluid deficit
diminished renal fxn
K+ therapy in DKA?
- necessary for replacement in 1st 24-36 hrs - don’t have to replace as much as previously thought
- will normalize w/ fluid tx
- if tx rapidly - K+ conc will fall rapidly -
can lead to cardiac arrhythmias, resp paralysis, parlytic ileus and rhabdo - development of severe hypokalemia is potentially most life threatening lyte derangement during tx of DKA
- want to maintain extracellular K conc during acute phase and replace intracellular deficit over days
Complications of DKA?
- hypoglycemia
- cerebral edema
- hypokalemia
- hypophosphatemia
- adult resp distress syndrome
Causes of DKA?
- new onset diabetic
- compliance issues
- d/c of insulin
- insults to body: infection (Pneumonia, UTI) or MI, PE
What is hyperosmolar hyperglycemic state? Who does it occur in?
- AKA nonketotic hyperosmolar state
- occurs in pts w/ poorly controlled or undx type II DM
syndromes:
-severe hyperglycemia
-hyperosmolality
-relative lack of ketonemia
How is hyperosmolar hyperglycemic state defined?
- serum glucose usually over 600 mg/dL
- elevated plasma osmolality of over 315 mOsm/kg
- bicarb over 15
- arterial pH over 7.3
- serum ketones that are negative to mildly positive
Shared sxs b/t DKA and hyperosmolar hyperglycemic state?
- hyperglycemia, hyperosmolality, severe vol depletion, lyte disturbances, and sometimes acidosis (usually due to hypoperfusion - lactic acidosis)
Diff b/t DKA and hyperosmolar hyperglycemic state?
- DKA:
glucose: over 250
pH: lower than 7.3
bicarb: less than 15
urine ketone: +
serum osmolarity: variable
anion gap: greater 10
AMS: alert/drowsy to stupor/coma
-HHNS:
glucose: over 600
pH: greater than 7.3
bicarb: greater than 15
urine ketone: small
serum osmolarity: over 320
anion gap: less than 12
AMS: stupor/coma
Epidemiology of HHNS?
- poorly controlled or undx DM II
- less freq than DKA
- mortality rates higher than DKA:
15-30% compared to 5% in DKA
Increases w/ advanced age
Who is at greatest risk for HHNS?
- iability to access water
- nonambulatory nursing home pt
Presentation of HHNS?
- elderly, often brought in by caretaker due to abnorm VS and AMS
- often precip by acute illness: pneumonia, UTI (50% cases)
- most have some levels of baseline cog impairment
- sxs: weakness, anorexia, fatigue, cough, SOB, abd pain
Tx of HHNS?
- volume repletion
- correct lytes
- ID and tx precip cause
- gradual correction of hyperglycemia
- manage concurrent illnesses
S/S of hypoglycemia?
Neurogenic (increased ANS activity):
- sweating
- pallor
- tachy
- palpitations
- tremor/shaking
- nervousness/anxiety
- tingling, paresthesias (mouth and fingers)
Neuroglycopenic (not enough sugar to feed brain):
- HA
- drowsiness
- lightheadedness/syncope
- mental dullness/confusion
- amnesia
- seizures
- coma
Hypoglycemia thresholds - assoc manifestations?
Vary depending on individual
- drop 65-68 mg/dl: secretion of insulin counter-reg hormones glucagon and epi
- 54 mg/dL: neurogenic sxs
- 47 mg/dL: sxs of cog dysfxn (neuroglycopenic)
- Danger zone: under 50 mg/dL
- poorly controlled diabetes w/ persistent hyperglycemia results in higher glucose thresholds
- lower thresholds w/ repeated hypoglycemia episodes
What is hypoglycemia unawareness? Pts at greatest risk?
- development of low serum sugar values w/o physiologic ability to react:
places pts at greater risk for coma and other neuro sequelae - pts at greatest risk:
extremes of age
comorbidities
meds
Hypoglycemia tx for outpt?
- 15-20 g of glucose (effects should be noticeable in 15 min)
- may only be transient so retest plasma glucose in 15 min w/ add txs as necessary
- glucagon should be Rx for all pts at sig risk
- alt of insulin regimen or dosage adjustment of ral med may help
Hypoglycemia tx in ED?
- take blood sugar on anyone who comes in w/ AMS!
- initial: admin 1g/kg dextrose, D50W in adults and infusion of D10W to follow for maintenance of glucose above 100 mg/dL
- repeat glucose q 30 min for 2 hrs
- oral replacement (300 g carb given PO)
- glucagon 1 mg IM or IV, (slower response than dextrose)
- octreotide can be given after glucose therapy has been initiated in pt w/ sulfonylurea ingestion
Other etiologies of hypoglycemia if pt not a diabetic?
- ETOH
- sepsis
Fxn of adrenal medulla?
- controlled by nervous system
- when stim secretes epi and NE into adrenal veins
adrenal cortex - components and hormones secreted?
- glomerulosa: mineralocorticoids: aldosterone
- fasciculata: glucocorticoids- cortisol
- reticularis: sex hormones
Fxn of ACTH?
- stim synthesis and secretion of adrenocortical hormones (cortisol, androgens, aldosterone)
- primarily stim cortisol