Diabetic Emergencies

Question 1

Summarize the basic pathophysiology of diabetic emergencies.

Answer 1

diabetic emergency: hyperglycemic states caused by severe insulin deficiencies (both endogenous and exogenous)
diabetic ketoacidosis
hyperglycemic hyperosmolar state

Question 2

Pathophysiology

Answer 2

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

Question 3

Absolute insulin deficiency

Answer 3

type 1
increase lipolysis –> increase FFA to liver –> increase ketogenesis –> decrease alkali reserve –> increase ketoacidosis

Question 4

Relative insulin deficiency

Answer 4

type II
absolute or minimal ketogenesis
increase glycogenolysis –> hyperglycemia

Question 5

Diabetic ketoacidosis (DKA)

Answer 5

hyperglycemia
hyperketonemia
metabolic acidosis

Question 6

DKA background

Answer 6

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

Question 7

DKA pathophysiology

Answer 7

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

Question 8

DKA patient presentation

Answer 8

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

Question 9

Hyperglycemic hyperosmolar state (HHS)

Answer 9

severe hyperglycemia
hyperosmolality
severe fluid depletion

Question 10

Compare and contrast the minor differences in the treatment of diabetic emergencies.

Answer 10

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)

Question 11

DKA labs

Answer 11

pH < 7.3 with AG
low bicarb
(+) beta-HB/ketones
elevated K+
low Na+
elevated glucose

Question 12

DKA fluids

Answer 12

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

Question 13

DKA fluids balanced crystalloids

Answer 13

lactated ringers, plasma-lyte, normasol
NS has excess chloride content, worsening acidosis

Question 14

DKA insulin

Answer 14

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

Question 15

DKA IV insulin

Answer 15

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)

Question 16

When plasma glucose reaches 200 mg/dL, decrease infusion rate to 0.02-0.05 U/kg/hr and

Answer 16

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

Question 17

What is going on as fluids and insulin are started in our pts?

Answer 17

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

Question 18

Transitioning to SQ insulin from IV when:

Answer 18

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

Question 19

DKA SQ insulin

Answer 19

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

Question 20

DKA electrolytes and lab abnormalities

Answer 20

electrolytes of concern: potassium, sodium, phosphate, anion gap
pH, SCr, WBC

Question 21

DKA potassium

Answer 21

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

Question 22

DKA sodium:

Answer 22

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

Question 23

DKA phosphate

Answer 23

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

Question 24

DKA bicarbonate

Answer 24

pH >/= 6.9, no bicarb
pH < 6.9 give 50-100 mmol bicarb q1-2h until ph >/=7

Question 25

Euglycemic DKA

Answer 25

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

Question 26

Recall formula for corrected anion gap.

Answer 26

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))

Question 27

HHS background

Answer 27

generally occurs in older adults
many pts have underlying heart failure or kidney disease
precipitating factors include heart attack, stroke, infection, recent procedure

Question 28

HHS pathogenesis

Answer 28

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

Question 29

Why doesn’t the body convert to ketosis?

Answer 29

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

Question 30

HHS patient presentation

Answer 30

weakness, polyuria, polydipsia, dehydration with reduced fluid intake, lethargy
severe: confusion, coma, seizures

Question 31

HHS lab findings

Answer 31

glucose: ~800-2400 mg/dL
ketosis is absent or mild
pH ~7.35
BUN often severely elevated > 100 mg/dL
serum osmolality 320+

Question 32

HHS goals of treatment

Answer 32

restore circulatory volume (fluids)
restore urine output to 50 mL/hour or more (fluids)
return blood glucose to normal (fluids + insulin)

Question 33

HHS fluids

Answer 33

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

Question 34

HHS insulin

Answer 34

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

Question 35

HHS electrolytes

Answer 35

sodium: monitor during fluid resuscitation
phosphorous: only supplement if phosphorous is < 1 mg/dL
potassium: may supplement while on insulin drip or PRN

Question 36

DKA + HHS complications

Answer 36

cerebral edema
hypoglycemia

Question 37

Cerebral edema

Answer 37

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

Question 38

Hypoglycemia

Answer 38

caused by too much insulin
tx: reduce insulin rate, give glucose, consider glucagon

Question 39

DKA + HHS follow-up

Answer 39

ensure pt has proper follow-up (endocrinologist, PCP, pharmacist, dietician)
assess ability to pay for meds
educate on discharge DM regimen
prevent readmission