w5 critical care

What does diabetes do to blood?

Thickens it

What does thick blood increase the risk of?

Increased bp & hr = risk of stroke/MI

Cataracts & glaucoma = no circulation

Peripheral neuropathy = no circulation to feet

Diabetes diagnosising

Non fasting BG > 200

Fast BG >126

HbA1c > 7%

Diabetes type 1

Autoimmune destruction of beta cells

• no insulin produced, glucose not absorbed

Diabetes type 2

Produce some insulin but is insulin resistant

DKA- key findings

Lack of insulin → seen in DM1

• hyperglycemia BG > 250

• metabolic acidosis pH < 7.3 → bc ketones are acidic

• ketosis (from lipolysis)

HHS- key findings

relative lack of insulin produced → seen in DM2

• extreme hyperglycemia BG > 600

• serum osmo > 320 → bc profound dehydration

• pH > 7.3 → more alkaline

If patient comes in with BG at 500, what can we rule out?

HHS

If patient comes in with BG at 750, what could it be?

DKA or HHS

If patients BG is > 600 and we need to figure out if they have DKA or HHS, what do we need to do?

ABG

• alkaline→ HHS

• acidic→ DKA

TEST FOR KETONES IIN URINE

• ketones→ DKA

Assessment findings in DKA & HHS

BOTH

• altered mental status→ HHS will be worse tho from dehydration

• decreased cardiac output & low blood pressure

• electrolyte imbalances & decreased urine output→ from dehydration

HHS

• dehydration→ affects Na+ = seizure risk

  • if BG 750 and pt came in w/ seizure = HHS

• seizures

• myoclonic jerks

• facial paralysis

DKA

• kussmaul respiration→ rapid & deep bc pt trying to blow off acid

• GI effects (abd pain/vomiting)

• fruity breath

what do you suspect if the patient with DKA/HHS has elevated WBC?

patient likely has infection→ its the possible underlying cause

= tx the underlying cause to rid of the DKA/HHS

Will BUN/Cr be elevated of decreased in DKA/HHS?

elevated because of the dehydration

what will serum osmo be in HHS?

>320

electrolytes in DKA/HHS

sodium→ low from rising BG

potassium→ initially high

Mg, P, Cl→ below range

• patient will need electrolyte replacement

what is the concern w/ electrolyte replacement in DKA/HHS?

FVO

IV compatibility→ may need multiple IV sites

how frequently do we recheck electrolyte values in DKA/HHS?

q2-4hrs

what is used as the primary diagnoses to see if the patient is out of DKA/HHS?

anion gap

anion gap goal

<12 = DKA/HHS has resolved

how do we reach our goal of anion gap <12?

treat it → insulin, potassium, fluids, etc.

if patients blood glucose is at 170, does that mean they are not in DKA or HHS now?

not unless the anion gap is <12

• if the anion gap is still >12 that means we need to continue insulin drip→ BG will continue dropping

to prevent hypoglycemia if BG dropping and anion gap still not <12 what do we do?

once BG <200 in DKA or <250 in HHS we can add 5% dextrose to running fluid

if patient develops hypotension and requires aggressive fluid therapy what do you need to check?

if patient is tolerating the amount of fluid without developing signs of FVE

treatment of DKA/HHS initial

• establish IV access

• cardiac monitor

• 0.9% NS IV bolus→ rehydrate pt to increase BP to help medications circulate

  • 0.9% NS good for pts with low Na

  • 0.45% NS good for pts with high Na

treatment of DKA/HHS after initial

recheck K+ after bolus

→ if K+ > 5.2 = give insulin

→ if K+ between 3.3-5.2 = give insulin + replace K+ IV

→ if K+ < 3.3 = HOLD INSULIN & give K+ replacement until K+ gets back above 3.3-5.2

if patients BG drops

need to change IV flow

IV admin goals for DKA/HHS

DKA up to 6L 0.9% NS

HHS up to 9L 0.9% NS

• as we rehydrate pt monitor serum osmo we want to see if drop = rehydrated

• watch for FVE

insulin therapy DKA/HHS

IV regular insulin bolus→ 0.1 units/kg

• expect BG to drop 50-70pts an hour

• recheck BG q1hr

once BG < 200-250 in DKA or < 300 in HHS

• may decrease insulin drip

BUT continue checking BG until signal to check anion gap

• BG 150-200 DKA

• BG 250-300 HHS

when can we transition the patient to subQ insulin?

when the DKA/HHS has resolved, anion gap < 12, improved LOC

what do you need to make sure to do when switching over to subQ insulin?

after giving the first dose of subQ insulin

NEED TO CONTINUE IV INSULIN FOR 2 hrs → let the subQ insulin to kick in

if patients Na+ level was low and we get it to increase to 150 but their baseline used to be 135 what do we need to do?

change to hypotonic solution like 0.45% NS→ help rehydrate while decreasing Na+

how do you know DKA/HHS is resolved

DKA

• BG < 200

• pH > 7.3 → out of metabolic acidosis

• anion gap < 12

HHS

• anion gap < 12

• serum osmo < 320

• mental alertness improved

diabetes education

• drink 2-3L water daily

• monitor BG q2-4hrs

  • even if not eating or sick bc inc cortisol can inc BG

• if BG > 240 check urine for ketones

• if patient is following orders and BG still remains above 250 need to increase insulin

• notify provider if

  • illness > 24hrs

  • BG > 240

• watch for low Mg levels → risk for torsades NEED TO REPLACE Mg

• can give Bicarb if severe acidosis

diabetes inspidus/arginine vasopressin disorder

body does not have enough ADH or is resistant to ADH

• we lose all H2O in body bc w/o ADH we cant retain

  • ADH only involved in retaining H2O not Na+ so w/o ADH we will lose water but Na+ will stay

diabetes inspidus/arginine vasopressin disorder: types

central DI

• AVP deficiency

• lack of ADH hormone, dont produce any of it

nephrogenic DI

• AVP resistant

• kidneys dont respond to ADH

diabetes inspidus/arginine vasopressin disorder: lab effects

• inc serum osmo (>300)→ pt dehydrated e.g. 330

• inc urine output→ e.g. 1000ml/hr

• inc serum Na+ (>145)→ needs fluids still bc dehydrated from peeing

so give 0.45% NS + dextrose (helps rehydrate pt + dec Na+ slower)

• dec urine osmo (<300)

• dec urine specific gravity (<1.005)→ pee looks like water

• BUN/Cr inc

diabetes inspidus/arginine vasopressin disorder: memory trick

every test that involves SERUM/BLOOD will be INCREASED

every test that involves URINE will be DECREASED

RF for the 2 types of DI

central DI: brain related lack of ADH

• e.g. pts with stroke, tumor, head trauma

• any brain related injury pts @ risk

nephrogenic DI: kidney issue

• e.g. pts with AKI, CKD, hypercalcemia, lithium

s/s of diabetes inspidus/arginine vasopressin disorder

• dehydration

• polyuria

• polydipsia

• nocturia

• hypernatremia

IF EXAM MENTIONS BG DO NOT PICK IT

diabetes inspidus/arginine vasopressin disorder: diagnosising

check brain MRI

• rule out issues related to possible central DI

water deprivation test: tells us if central or nephro DI

• administer subQ vasopression (ADH at its core)

  • if urine output drops from 1200 to 600ml/hr = responding to vasopressin = problem is central DI→ just lacking ADH

  • if urine output stays at 1200ml/hr after vasopressin = not responding to med= problem is nephrogenic DI→ kidneys not responding to ADH

diabetes inspidus/arginine vasopressin disorder: managing pt

• pt has diuresis = dehydrated = need fluid = low BP→ give fluid 0.45% NS + dextrose

• monitor Na+ lvl; one of most important indicators of fluid hydration→ if it drops too fast = too much fluid given

• weigh daily→ 2lb lost in 24hr ok BUT 3lb gained = too much fluid

• careful for overcorrection

• seizure precautions→ inc serum Na+

diabetes inspidus/arginine vasopressin disorder: meds

desmopressin (DDVAP): FIRST LINE for CENTRAL DI

• can give subQ, intranasal (preferred), oral

• slows down the amount of water leaving the system & promote fluid retention

• will make urine output dec, serum osmo dec, urine osmo inc, USG inc, BP inc,

HR dec, RR dec

carbamazepine (tegretol): NOT FIRST LINE for CENTRAL DI

• used as trigger to release ADH (usually not needed)

chlorpropamide: for NEPHROGENIC DI

• enhances effect of ADH on the kidneys, makes kidneys more susceptible

*chlorpropamide + hydrochlorothiazide used together for nephrogenic DI

hydrochlorothiazide (microzide): for NEPHROGENIC DI

• helps dec H2O in renal system + kidneys more susceptible to ADH

• is a diuretic but in DI its MOA promote H2O retention & dec urine output

NSAIDs (indomethacin)

• inc urine concentration in kidneys

how do you know if your giving too much desmopressin?

s/s of FVE (O2 dec, BP inc, crackles, serum osmo <275 etc.)

diabetes inspidus/arginine vasopressin disorder: complications

massive dehydration → cardiac arrest

overcorrection → circulatory overload

SIADH

too much ADH pt cant pee, excess H2O in system

SIADH: memory trick

everything in SERUM is DECREASED

everything in urine is INCREASED

SIADH: lab effects

• dec serum osmo

• dec serum Na+ → mild <125-135 = give 0.9% NS; advanced <120 = give 3% NS

• dec urine output

• inc USG

• inc urine osmo

• BUN/Cr WNL

SIADH: causes + RF

causes

• cancer

• chemo

• too much vasopressin (giving too much ADH)

rf

• malignancies

• hormone deficiencies

• CNS issues

SIADH: effects

neurological (from dec Na+)

• HA, lethargy, confusion, somnolence, seizure→ SEIZURE PRECAUTIONS

gi

• N/V, no appetite, diarrhea→ FVE→ inc bp→ inc stomach perfusion = inc motility

gu

• dark urine, high USG, dec output

SIADH: treatment priority

• fluid restrictions 800-100ml/day

• foley cath + monitor urine output

• daily weight

SIADH: IV protocol

Na+ > 120 use 0.9% NS in small amounts help inc Na+

Na+ < 120 use 3% NS can give 200-300ml/day→ thru CENTRAL venous cath

SIADH: meds

furosemide (lasix): GIVEN LAST

• pt not peeing w/SIADH = diuretic wont do anything till kidneys work

conivaptan (vaprisol)

• IV vasopressin antagonist (the narcan to ADH hormone)

• makes the pt start peeing , inc urine output→ if pt develops FVD/dec BP = titrate down

*ONCE conivaptan or tolvaptan START MAKING PT PEE= GIVE LASIX TO SPEED UP

tolvaptan (samsca)

• oral vasopressin antagonist (the oral narcan to ADH hormone)

• does the same thing as conivptan, but used for less severe , pt who isn’t confused, put who can swallow

demeclocycline (antibiotic)

• off label use, produces urine output

• only for MILD cases

SIADH: tx order

1. fluid restrictions

2. vasopressin antagonist (conivaptan/tolvaptan)

3. demeclocycline (if mild)

4. furosemide

hypothyroidism

thyroid not working, everything slow

hypothyroidism: causes

• too much antithyroid meds→ overcorrection

• disruption of pituitary gland or hypothalamus

• genetics

hypothyroidism: complications

• hair loss

• fatigue

• mood/memory changes

• dec HR, RR, BP, temp

• RISK RESP DEPRESSION → pt not breathing enough → resp acidosis (need synthroid or intubation if severe)

• ABG imbalance

• inc cholesterol from slowed metabolic rate → pt at risk of MI

• constipation → no GI motility

if pt with hypothyroidism suddenly shows signs of hyperthyroidism what do we need to do?

titrate thyroid medication down

hypothyroidism: labs

elevated TSH; decreased T3/T4

*synthroid should decrease TSH and inc T3/T4

hypothyroidism: meds

levothyroxine (synthroid)

• speeds up thyroid

• takes 6-8hrs to take affect IV

• take w/ full glass h2o, empty stomach, 1hr b4 meals or 3 hrs after meals

• increases effect of warfarin = pt more prone to bleeding = titrate warfarin down

• can increase need for insulin & digoxin bc it increases metabolic rate = metabolize meds faster

• how do we know were giving enough?

  • labs TSH/T4

  • energy level imporved; can complete ADL

hypothyroidism: education

tx begins slowly & LIFELONG

• dosage increases q2-3 weeks

• start at lowest dose

• monitor pt till we get at a nice middle

hyperthyroidism

thyroid doing too much, everything goes up

hyperthroidism: causes

• autoimmune disorders

• antibodies

• toxic goiter

• graves

• thyroiditis

hyperthyroidism: complications

• inc BP, HR, RR, temp

• restlessness

• yawning

• diarrhea→ pooping everywhere

• muscle wasting

• RISK FOR DEHYDRATION

• ABG imbalance→ metabolic alkalosis

if pt with hyperthyroidism is unstable and gets intubated how do we know the pt is responding well to tx?

• vitals

• labs

• metabolism of meds will DECREASE = pt will become more SEDATED even tho the sedation meds haven’t changed RAAS score will increase

hyperthyroidism: labs

decreased TSH; increased T3/T4

antithyroid med with increase TSH; decrease T3/T4

hyperthyroidism: diagnostic

EKG→ needed bc of increased cardiac workload and MI risk

hyperthyroidism: meds + order

*hyperthyroidism meds take ~5days to work = in meanwhile focus on s/s management (pt has inc BP, RR, HR, temp)

1. give beta blocker (propanolol, atenolol, etc.) → stabalize cardiac sys.

2. acetaminophen (antipyretic) + cooling measures → decrease temp

3. methimazole or propylthiouracil (antithyroid meds)

• slows thyroid

• impacts immune sys → dec function & dec WBC count/migration

  • neutropenic precautions (no sick ppl, ppe, etc.)

radioactive iodine

ablation therapy to tx hyperthyroidism rapidly

• kills thyroid gland to slow it down (dangerous)

• radioactive precautions (cant be near pregnant ppl or kids, no close contact, flush toilet frequently, separate bathrooms/clothes washing)

thyroidectomy

for hyperthyroidism surgery option if meds dont work

• preprocedure give IODINE SOLUTION (lugols) → suppress blood flow to thyroid = help to decrease HR, BP, temp, RR → helps pt be stable enough for surgery

• pt will need SYNTHROID for life

• BIGGEST CONCERN→ airway obstruction from site inflammation & swelling = if airway constricted → intubate pt (if cant advance bc hemorrhaging = tracheostomy)

• risk parathyroid gland damage = hypocalcemia risk → pt needs cardiac monitor + calcium gluconate

• if pts voice becomes more hoarse = airway narrowing = intubate pt + find cause

thyroid storm

very severe hyperthyroidism

• severe thyroidtoxicosis, too much synthroid

• pt will have high fever >104 = high fluid volume defecit risk

• pt will have tachycardia > 140 = MI risk

• pt will need to be INTUBATED + FLUID BOLUS + other hyperthyroid med regimen

• can give glucocorticoids → help w/ adrenal insufficiency from damage to adrenal gland

thyroid storm med priority order

1. intubate

2. fluid bolus

3. beta blocker

4. acetaminophen

5. antithyroid med (methimazole/propylthiouracil)

if pts thyroid storm cant be controlled with medication + intubation, pt will need….?

thyroidectomy

myxedema coma

pt in coma from severe hypothyroidism

1. INTUBATION (changes in sedation becoming less sedated = good metabolism of meds increasing)

2. CORTICOSTEROID

3. LEVOTHYROXINE IV BOLUS