Module 5: DKA & HHS Flashcards
anabolic effects of insulin on liver
- promotes glycogen synthesis 2. promotes fatty acid synthesis
anabolic effects of insulin on adipose
- promote fatty acid uptake 2. promote triglyceride formation & storage
anabolic effects of insulin on muscle
- promote protein synthesis 2. promote glycogen synthesis
anticatabolic effects of insulin on liver
inhibits 1. glycogenolysis 2. gluconeogenesis 3. ketogenesis
anticatabolic effects of insulin on adipose
inhibits lipolysis
anticatabolic effects of insulin on muscle
inhibit proteolysis
criteria for DKA
glucose > 250; arterial pH < 7.35; positive serum ketones; increased anion gap (Anion gap = Na+ - (HCO3- + Cl-)
criteria for HHS (DM2)
glucose >600; arterial pH > 7.3; serum bicarb > 15; >320 mOsm/L
effective osmolarity?
Eosm = 2(Na + K) + Blood glucose/18 don’t use BUN b/c isn’t considered effective OSM b/c doesn’t create an osmotic gradient b/c can flow into /out of cell
mixed DKA & HHS?
pH 7.3 or serum bicarb < 15; positive serum ketones; Esom >320
different types of ketosis?
diabetic ketoacidosis; starvation ketosis; alcoholic ketoacidosis; ketogenic (high fat) diets
symptoms of hyperglycemia?
polyuria; polydipsia; nocturia; polyphasic; weight loss; vomiting; abdominal pain; fatigue; confusion –> coma; blurred vision; vulvovaginitis; poor wound healing; asymptomatic
causes of polyuria
hyperglycemia; hypokalemia; hypercalcemia; renal disorders; psychogenic polydipsia; neurogenic/nephrogenic diabetes insipidus; drugs (diuretics, lithium, demeclocycline)
precipitating factors for DKA
- new onset DM1 2. omission of insulin therapy 3. acute illness (UTI, PNA, medication, MI, CVA, trauma, hyperthyroidism, intra-abdominal catastrophe)
risk factors for DKA at onset
age < 12; no first degree relative with diabetes; lower SES; high dose glucocorticoids/atypical antipsychotics; poor access to medical care; uninsured
why insulin omission
weight control, fear of hypoglycemia, teenage rebellion
cocaine use and DKA
14% of all DKA admissions more frequent admissions for DKA, more likely to miss taking insulin prior to admission, higher admission glucose
risk factors for DKA leading to ER visit/hospitalization
A1C; african american; female; psychiatric disorder; under insured; limited self care skills; illness; substance abuse
physical exam for DKA
temperature; tachycardia; orthostatic BP/hypotension; dry mucosa; fruity odor of breath; abdominal pain; drowsiness–>coma; heme positive stool?
why heme positive stool?
gastric bleeding from retching, from vomiting, Hct is concentrated d/t increased urination, will start to dilute once return fluids so don’t necessarily thing with drop in Hct and heme positive stool that its a GI bleed
what mOsm do you have decreased LOC
if decreased level of consciousness with eosm < 320 look for other source of change in mental status
generally see decreased LOC with mOsm > 320
what does corrected sodium tell you?
helps evaluate severity of dehydration use measured Na for anion gap, not the calculated corrected Na.
anion gap acidosis
ketoacidosis, lactic acidosis, chronic renal failure, salicylate, methanol, ethylene glycol, paraldehyde
what is winter’s formula?
if the equation doesn’t equal the resulted PCO2 then you have to think of something besides just a standard acid base imbalance
causes for mixed acid base issues
respiratory alkalosis - PNA; metabolic alkalosis - vomiting, diuretics
treatment goals for DKA
rehydrate; correct hyperglycemia; reverse ketosis; replace electrolytes;
how fast should you change serum osmolality in DKA?
3 mOsm/kg H2O/hour goal replace ~50% deficit in 8 hours
fluid choice for DKA replacement?
NS then NS or 1/2 NS based on clinical assessment/volume status/urine output/labs
which takes longer to clear, ketones or hyperglycemia
ketones
when do you start giving D5W in DKA?
when plasma glucose reaches 200 mg/dL; administer D5W at 100-200 mL/hour; giving D5W allows us to keep the insulin drip at a higher rate and to get rid of ketones faster.
concerns for insulin and K+?
K+ should be > 3.3 before giving insulin. bolus is optional: 0.1 units/kg regular insulin 0.1 units/kg/hr regular insulin as continuous infusion or 0.14 units/kg/hr if NO bolus decrease rate of insulin infusion when glucose is 200. goal is to decrease glucose ~50-75 mg/dL/hr (if it goes to fast worry about osmotic shifts especially in the brain)
do you give bicarbonate for DKA?
not routinely recommended. no improvement in outcome pH>6.9 but no studies evaluating outcome with pH<69
what happens to phosphate with DKA
normal to increased at presentation. decreases with treatment
how do you treat low phosphate?
with potassium phosphate only if low
complications of treating for low phosphate
hypocalcemia, metastatic calcification, hypomagnesemia
do you replace low calcium in DKA?
only if symptomatic w/ calcium gluconate
what lab studies you order in DKA?
CBC, CMP, ABG, serum/urine ketones (for initial diagnosis, likely will go up when getting better), Q1H glucose, Q1-2H K+, Q2-4 hr electrolytes, calcium, phosphate, magnesium culture of blood, urine, sputum as indicated (to figure out infection as the precipitating factor to DKA)
what do you trend to know when to stop iv insulin?
bicarbonate, stop when bicarb is > 18 & patient tolerating PO
complications of treatment?
hypoglycemia, hyponatremia/hypernatremia, hypokalemia, hyperchloremia, hypotension (you want to correct this first before giving IV insulin), cerebral edema
what happens during recovery of DKA?
hyperchloremic metabolic acidosis. loss of ketones in urine & loss of buffering capacity Cl- is reabsorbed leading to hyperchloremic acidosis will likely resolve on its own over a couple of days
most feared complication of DKA
cerebral edema. most common < 5 year old; rare in patients > 20; occurs only 1% of the time & more common in newly diagnosed diabetics
why do you do hourly neuro checks?
cerebral edema - can have headache; impaired LOC; bradycardia; elevated blood pressure; urinary incontinence; vomiting; unequal/fixed dilated pupils
risk factors for cerebral edema with DKA
- treatment with HCO3 2. bad initial pCO2 3. bad initial BUN (r/t dehydration) not r/t rate of sodium or glucose correction
when should you start long active sub Q insulin?
start subQ2-3 hours prior to stopping IV insulin IV insulin only lasts 20 minutes in blood stream
what does basal insulin do?
controls glucose and ketone production between meals and overnight; withholding basal insulin in insulin deficient patients results in rapid rise in glucose and DKA should be about 50% of daily insulin requirements
what does prandial insulin do?
insulin required to cover meals; limits post prandial hyperglycemia; 10-20% of total daily insulin requirement at each meal
what does correction/supplemental insulin do?
used to correct hyperglycemia; used in combination w/ long acting insulin; should be adjusted based on recent glucose levels, previous insulin requirements & changes in patient’s medical condition
how do you calculate starting dose of basal insulin?
weight based, 50/50 basal/nutritional. ranges from 0.3 with malnourished, no h/o DM, cognitive impairment to 0.6 units/kg/day to DM2, obese & on glucocorticoids
what is the goal blood glucose?
140-180
how do you figure out basal insulin based on IV insulin infusion?
project 24 hour requirement based on most recent 4 hour period, do 80% of TDD; if not eating when receiving the IV insulin multiply that by 2
equation for correction/supplemental rapid acting insulin?
=1800/TDD
do studies show benefit w/ SSI?
nope! increase risk of hypoglycemia and hyperglycemia when used alone; it’s not proactive - it’s responding to hyperglycemia; generally not adjusted based on glucose levels & clinical status
flow diagram for hyperglycemic hyperosmolar state
when does hyperglycemic hyperosmolar state tend to happen
new/unrecognized diabetes; neglected diabetes; medications; concurrent illness; volume depetion; limited access to fluids; impaired thirst perception
what are some drugs causing hyperglycemia
glucocorticoids; cyclosporine/tacrolimus; sirolimus; everolimus; protease inhibitors, clozapine, TKI, bevacizumab, diuretics
predisposing factors for HHS
female; acute infection, NH resident; dementia
HHS clinical manifestations
polyuria, polydipsia, dehydration, neurological abnormalities; heme positive stool; normal temperature; lethargy & disorders of sensorium
HHS treatment
fluids, insulin (not as critical since not producing ketones like DKA)
reasons for early mortality in HHS
sepsis, shock, underlying illness,
causes of late mortality in HHS
thrombosis d/t dehydration, hypercoagulable state
HHS management
depends on reason for HHS
safest to start on sub Q when stopping IV insulin
depending on other medical conditions and if total insulin dose is <30 might be able to switch to oral diabetic medicaion
considerations for non-insulin therapies
sulfonylureas can prolong hypoglycemia
metformin contraindicated w/ decreased renal function, use of iodinated contrast dye, and any state of poor tissue perfusion
thiazolidinediones are associated w/ edema and CHF
GLP1 can cause N/V & act by lowering post prandial glucose so less effective is patient is NPO
SGLT2 may cause hyperkalemia and hypovolemia b/c it increases glucose in the urine
sick day management for diabetics
take diabetes medication even if eating less
check glucose at least 4 times a day, more often for severe illness
check ketones if glucose >250
push fluids (sugar free if able to eat, w/ sugar if can’t eat)
call health care provider: presistent vomiting/diarrhea; BS > 250 x 2 checks of BS does not decrease w/ extra insulin; moderate/large ketones
what is stress hyperglycemia?
no prior history of diabetes; inpatient hyperglycemia (check A1C to see where they’ve been); follow up testing for DM w/in 1 month of hospital discharge
adrenergic symptoms of hypoglycemia
palitations; diaphoresis; anxiety; agitation; hunger; tremor; pallor
neuroglycopenic symptoms of hypoglycemia
fatigue/listlessness; inappropriate behavior; cognitive impairment; focal neurologic deficits; seizure; loss of consciousness; death
