Diabetic Emergencies Flashcards
Summarize the basic pathophysiology of diabetic emergencies.
diabetic emergency: hyperglycemic states caused by severe insulin deficiencies (both endogenous and exogenous)
diabetic ketoacidosis
hyperglycemic hyperosmolar state
Pathophysiology
the basic underlying mechanism for both disorders is a reduction in the net effective action of circulating insulin coupled with a concomitant elevation of counterregulatory hormones, such as glucagon, catecholamines, cortisol, and growth hormone
Absolute insulin deficiency
type 1
increase lipolysis –> increase FFA to liver –> increase ketogenesis –> decrease alkali reserve –> increase ketoacidosis
Relative insulin deficiency
type II
absolute or minimal ketogenesis
increase glycogenolysis –> hyperglycemia
Diabetic ketoacidosis (DKA)
hyperglycemia
hyperketonemia
metabolic acidosis
DKA background
usually occurs in T1DM or new-onset T2DM
leading precipitating factors: poor adherence to treatment regimen; infection (UTIs most common)
drugs: thiazides, steroids, sympathomimetics, atypical antipsychotics, SGLT-2 inhibitors
DKA pathophysiology
precipitating factor (non-adherence, infection, new diagnosis) –> increase catecholamines/cortisol/GH (oppose circulating insulin) –> increase hepatic glucose production/decrease peripheral insulin sensitivity –> lack of peripheral glucose uptake –> increase lipase in adipose tissue –> trigylcerides to glycerol + FFAs –> FFAs to ketones
DKA patient presentation
polyuria, polydipsia, weight loss, dehydration
NAUSEA/VOMITING + ABDOMINAL PAIN
changes in mental status
fruity breath
kussmaul respirations (deep, laborious breathing)
coma
Diagnosis: hyperglycemia, hyperketonemia, metabolic acidosis
Hyperglycemic hyperosmolar state (HHS)
severe hyperglycemia
hyperosmolality
severe fluid depletion
Compare and contrast the minor differences in the treatment of diabetic emergencies.
DKA goals of treatment: restore circulatory volume (fluids), inhibit ketogenesis and return of normal glucose metabolism (insulin), correct electrolyte imbalances (supplement electrolytes)
HHS goals of treatment: restore circulatory volume (fluids), restore urine output to 50 mL/hour or more (fluids), return blood glucose to normal (fluids + insulin)
DKA labs
pH < 7.3 with AG
low bicarb
(+) beta-HB/ketones
elevated K+
low Na+
elevated glucose
DKA fluids
administer 0.9% NS at 500-1000 mL/hr for first 1-4 hours –> evaluate corrected Na+ at 2-4 hours –> corrected Na normal/high: change to 1/2 NS and decrease rate by 50%, corrected Na low: continue NS and decrease the rate by 50% –> when blood glucose approaches 200 mg/dL, change to D5W w/ 0.45% NS @150-250 mL/hr until resolution ketoacidosis
DKA fluids balanced crystalloids
lactated ringers, plasma-lyte, normasol
NS has excess chloride content, worsening acidosis
DKA insulin
second step in management of DKA after fluids are initiated –> can be administered IV, SQ, IM, IV continuous infusion preferred and most commonly used –> hourly labs/BG checks
DKA IV insulin
insulin initiation - regular insulin: start 0.1 U/kg/hour +/- a bolus of 0.1 U/kg, check glucose every hour
if glucose doesn’t fall by >/= 10% (50-70 mg/dL) in 1st hour, repeat or increase bolus dose (0.1-0.4 U/kg)
When plasma glucose reaches 200 mg/dL, decrease infusion rate to 0.02-0.05 U/kg/hr and
change fluids from NS to 1/2 NS and D5W and decrease to 150-250 mL/hr; adjust rate of insulin or rate of dextrose administration to maintain plasma glucose level of 150-200 mg/dL
What is going on as fluids and insulin are started in our pts?
fluids are restoring renal perfusion, normal osmolality, and volume status: excreting glucose and ketoacids, restoring electrolyte balance
insulin is restoring normal glycemic process: inhibiting glucagon, stopping lipolysis, reducing hyperosmolarity
Transitioning to SQ insulin from IV when:
BGL < 200 mg/dL and >/= 2 of the following: anion gap closes </= 12 mEg/L, bicarbonate level >/= 15 mEq/L, venous pH > 7.3
pt should not be NPO
OVERLAP IV and SQ insulin by 2-4 hours to prevent rebound ketoacidosis or hyperglycemia
DKA SQ insulin
transitioning to SQ from IV: can restart home regimen if it was working; consider SQ rapid acting insulin q 2 hr at 0.1 U/kg; if insulin naive pt, start multidose regimen of 0.5-0.8 U/kg/d divided 50/50 bolus; adding up total amount of IV insulin required by pt and convert to estimated daily requirement using basal/bolus or q 6 hr NPH insulin
DKA electrolytes and lab abnormalities
electrolytes of concern: potassium, sodium, phosphate, anion gap
pH, SCr, WBC
DKA potassium
DO NOT start insulin if K < 3.3 mmol/L
K > 5 mmol/L: no supplementation
K 4-5 mmol/L: add 20 mEq KCl per liter to replacement fluids
K 3-4 mmol/L: add 40 mEq KCl per liter to replacment fluids
K < 3 mmol/L: add 10-20 mEq/hour until K > 3 mmol/L then supplement 40 mEq
DKA sodium:
administer 0.9% NS at 500-1000 mL/hr for first 1-4 hours –> evaluate corrected Na at 2-4 hours –> corrected Na normal/high: change to 1/2 NS and decrease rate by 50%, corrected Na low: continue NS and decrease rate by 50% –> when BG is 200 mg/dL, change to D5W with 0.45% NS @ 150-250 mL/hr until resolution of ketoacidosis
DKA phosphate
phosphate concentration decreases with insulin therapy, no studies show benefits in replacing phosphate acutely
may be supplemented as potassium phosphate in fluids in pts presenting with phosphate < 1 mg/dL
DKA bicarbonate
pH >/= 6.9, no bicarb
pH < 6.9 give 50-100 mmol bicarb q1-2h until ph >/=7
Euglycemic DKA
pt presents with normal or slightly elevated BG (~200 mg/dL)
urine still (+) for ketones - may be caused by poor oral intake, pregnancy, or SGLT2 inhibitors
Recall formula for corrected anion gap.
anion gap evaluates metabolic acidosis
a gap >/= 12 mEq/L suggests metabolic acidosis
when gap closes or becomes < 12, can begin to think about transition from IV to SQ insulin
The anion gap ((Na + K) - (Cl + bicarbonate))
HHS background
generally occurs in older adults
many pts have underlying heart failure or kidney disease
precipitating factors include heart attack, stroke, infection, recent procedure
HHS pathogenesis
insulin deficiency or resistance which leads to –> reduced utilization of glucose in liver, muscle, and fat which leads to –> increased hepatic glucose output via hyperglucagonemia which leads to –> massive glucosuria which leads to –> poorly perfused kidneys which leads to –> decreased ability to clear excess BG which leads to –> hyperosmolality which may lead to –> mental confusion, coma, seizures
Why doesn’t the body convert to ketosis?
reduced levels of GH may play a role, small amounts of endogenous insulin may be enough to restrain ketogenesis, or a plethora or other reasons…we don’t know
HHS patient presentation
weakness, polyuria, polydipsia, dehydration with reduced fluid intake, lethargy
severe: confusion, coma, seizures
HHS lab findings
glucose: ~800-2400 mg/dL
ketosis is absent or mild
pH ~7.35
BUN often severely elevated > 100 mg/dL
serum osmolality 320+
HHS goals of treatment
restore circulatory volume (fluids)
restore urine output to 50 mL/hour or more (fluids)
return blood glucose to normal (fluids + insulin)
HHS fluids
administer 0.45% or 0.9% sodium chloride NS at 500-1000 mL/hr for first 1-4 hours –> evaluate corrected Na at 2-4 hours –> corrected Na normal/high: reduce the rate, corrected Na low: consider NS –> when BS is 300 mg/dL, change to D5W with 0.45% NS at 150-250 mL/hour until resolution of HHS
HHS insulin
insulin initiation IV - regular insulin
start 0.1 U/kg/hour +/- a bolus of 0.1 U/kg; check glucose every hour and adjust dose of insulin to obtain initial glucose of 300 mg/dL; then decrease infusion to 0.02-0.05 U/kg/hour and maintain glucose of 200-300 mg/dL until pt is mentally alert; transition to SQ via methods like DKA
HHS electrolytes
sodium: monitor during fluid resuscitation
phosphorous: only supplement if phosphorous is < 1 mg/dL
potassium: may supplement while on insulin drip or PRN
DKA + HHS complications
cerebral edema
hypoglycemia
Cerebral edema
may be caused when plasma osmolality is reduced too fast
sx: HA, lethargy, decreased level of consciousness
can lead to seizures, bradycardia, respiratory arrest
tx: mannitol + mechanical ventilation
DO NOT hydrate too FAST
Hypoglycemia
caused by too much insulin
tx: reduce insulin rate, give glucose, consider glucagon
DKA + HHS follow-up
ensure pt has proper follow-up (endocrinologist, PCP, pharmacist, dietician)
assess ability to pay for meds
educate on discharge DM regimen
prevent readmission
