Exam 2 Metab Emergencies Flashcards
What are causes of hypoglycemia
a) Delay in eating after taking insulin
b) poor caloric intake (dieting, vomiting)
c) increased or unusual physical exertion
d) increased physiologic stress (illness such as infection, trauma, emotional upset)
e) EXCESS EXOGENOUS INSULIN (addition of other DM meds esp sulonylureas in addition to insulin
f) impaired counter-regulatory hormone axis (glucagon, epinephrine, cortisol - don’t “kick in”)
g) variable absorption at injection site
What is the definition and initial mgmt of hypoglycemia
def: <70 mg/dL
15-20 g oral CHO preferred
- 3 to 5 glu tab/candy or 1/2 c juice/non-diet soda
If NPO
IV dextrose 1 amp D50
Glucagon 1 mg IM or SC
What can you expect in pt with hypoglycemia after initial tx of oral glucose, IV dextrose or IM glucagon (glucose has increased into normal range)
When blood glu increases into normal range, usually pt mental status normalizes (diaphoresis and tachycardia typically resolve)
- sometimes stroke like sx with focal neurological exam - these findings resolve with resolution of hypoglycemia
- keep observing pt
sx of hypoglycemia include
irritability, diaphoresis and tachycardia, blurry vision and feeling weak
What labs do you order if you are worried a pt might be hypoglycemic
Finger stick glucose
UA/microscopy
Urine hCG
After hypoglycemia has resolved, what should we keep in mind about our pt?
the condition can reoccur!
- observe pt for time checking serial blood sugars, investigating why this happened and “fixing the problem”
- if the hypogly is bc of a sulfonylurea, admit the pt bc sulfonylurea half life is long, condition most likely will reoccur
sx of DKA
Fruity breath odor
Tachycardia
Diffusely tender abd with involuntary guarding and hypoactive BS
vomiting and confusion
tachycardia, tachypnea, hypoTN, frequent urination
skin cool and dry
focal neurologic defects
What are common lab values associated with DKA
- hypoNA (pseudo due to hyperglycemia)
- decreased bicarb
- increased BUN/Cr
- hypergly
- urine ketones
- acidotic ABG, normal PO2, low PCO2 (resp compensation)
**increased Anion gap (normal MUDPILES
methanol toxicity, uremia, DKA, Paraldehyde, iron toxicity/INH, lactic acidosis, ethylene glycol, salicylate
What is MUDPILES associated with
causes of increased anion gap Methanol toxicity Uremia DKA Paraldehyde Iron toxicity/INH Lactic Acidosis Ethylene glycol Salicylate
Ddx if: hyperglycemia, hypoTN, hypoNa, hypoK, dehydration, alter LOC, diffuse abd pain, acidosis, elevated anion gap
DKA
*first give IV fluids with isotonic saline
What are the potential causes of hyperglycemic crisis in DM
DKA
Hyperosmolar hyperglycemic state (HHS) - aka hyperglycemic hyperosmolar non-ketotic state
*both precipitated by: illness, infection, trauma, surgery, MI, Insulin omission
Etiology of DKA? s/sx
usually T1DM (old term IDDM) due to insulin insufficiency in the setting of a precipitant
s/sx dev over hr/d
*N/V abd pain, hyperventilation with fast and deep Kussmaul respirations, hypoTN/shock, dehydration, metab acidosis with increased anion gap, hypergly, serum ketones, Polyuria, polydipsia, wt loss
How are DKA and DM dx related
DKA is the first sign of DM in 25% of T1DM, so lack of DM hx does not exclude dx
DKA dx studies?
Glu, ketones, K, Na, Cl, bicarb, BUN/Cr
1) Glu generally >250 (usually at least in 400-500)
2) KETONES: urine and serum+
3) K+: high, low or normal - tends to be slightly high on initial labs but gen the body has sig K+ deficit (K tends to fall with hypergly tx, so watch closely and be prepared with supplement)
4) pseudohypoNa (corrected Na for glu formula)
5) Cl: low in anion gap
6) bicarb: LOW
7) BUN/Cr elevated (dehydration)
8) anion gap elevated
9) serum osmolarity elevated
DKA dx studies continued
WBC, ABG, UA and CXR, EKG
elev WBC even in absence of infection (stress rxn, demargination)
ABG: acidosis overall
UA and CXR: may show infection (infection could precipitate DKA)
EKG: may show MI, electrolyte abn, arrhythmias (MI can precipitate DKA)
What is the general primary goal in DKA tx?
stop the body from breaking down fats and using fat for fuel (ie ketones)
Therapeutic goals DKA tx
a) restore circulatory volume
b) reduce blood glu
c) correct serum osm
d) clear serum ketones
e) correct electrolytes and anion gap
f) treat underlying causes
outline the mgmt of DKA
1) ABCS
2) Isotonic saline (0.9 NS IV)
3) correct electrolyte disorders: follow K/Na, replete phosphate
4) **reverse acidosis and ketogenesis
5) control blood glu: insulin bolus IV (not always); continuous IV insulin infusion
Fluid mgmt of DKA?
Give IV fluids aggressively
- 1-2 L NS in 1st hr (more if in shock, less if cardiomyopathy or HF)
- 250-500 mL/hr next 4 hr
- then reduce to 100-250 ml/hr
- monitor urine output (0.5-1 ml/kg/hr)**
- Change to 5% dextrose when blood glu <250 mg/dL – goal is to reverse ketogenesis not attain normoglycemia)
How do we treat DKA acidosis
Give bicarb? generally bicarb NOT used to treat pt in DKA bc would further drive K into the cell (hypoK!)
*gen rule: let them be acidotic and focus on correcting the ketogenesis, only give bicarb if hyperK and want to drive K into the cell
what are complications of using bicarb to treat acidosis
hyperNa, hypoK, paradoxical CSF acidosis and residual serum alkalosis
can lead to SEVERE CEREBRAL EDEMA and brain damage (first discovered in children)
When is it appropriate to use Bicarb to treat acidosis?
when significant hyperK is evident
*bicarb can be livesaving to lower serum K by pushing K into the cells
What is the mainstay of reversing Ketoacidosis
Fluid administration and insulin
- with insulin present, glu enters cells and body will d/c lypolysis
- blood glu will lower and ketones will clear
When glucose normalizes after DKA (no longer hypergly, how should you approach the insulin infusion
it may seem sensible to stop insulin infusion at this time, but if the anion gap is still elevated, Insulin admin MUST CONTINUE
*it is the presence of insulin that stops the lipolysis
Etiology of HHS
Mainly T2DM, typically in presence of precipitant (infection, MI, other stressors - often in older nursing home pt)
S/sx HHS
s/sx: insidious (d to wk) onset, weakness, polydipsia, polyuria, dehydration, alter LOC
*no abd pain or kussmaul respirations (bc no ketogenesis/acidosis) but may have an even higher glucose than DKA
Pathophysiology of HHS
- Hyperglycemia then glycosuria then dehydration
- Dehydration to hemoconcentration (results in worsening hyperglycemia; Glu 500+)
- Dehydration (plasma osm >320) often 5-10 L deficient
- relative insulin deficiency (insufficient to prevent hypergly and glycosuria but sufficient to prevent lipolysis and ketogenesis; absence of ketones/no acidosis)
Tx of HHS
Fluid & electrolyte replacement - NS for circulatory collapse,
- then .45% NS
- once blood glu <250, use 5%D in .5 NS or .9NS
Insulin IV
- if fluid replacement alone is inadequate to decrease glucose
- transition to SQ
- transition to home regimen or optimize tx
TREAT UNDERLYING PROBLEM
What is the most common irregularly irregular rhythm
A fib
*irregularly irregular rhythm associated with tachy = a fib with RVR (rapid ventricular response)
Etiology and dx studies for thyroid storm
Catecholamine binding sites increased (heart and nerve tissues; increased sensitivity to circulating catecholamines)
Dx: TSH low, FT4, FT3 high
H&P typical findings for thyroid storm
All the normal hyperTH sx plus”
- hypermetab (wt loss/diarrhea)
- excessive adrenergic response
- hyperpyrexia
- a fib with possible HF
- shock, coma, death
Tx of thyroid storm
ABC B blocker (treat tachy and/or a fib) PTU and/or methimazole ASA/tylenol Fluids Electrolytes Nutritional support cooling blanket
How do PTU and methimazole work to treat thyroid storm
PTU: decreases TH synthesis and blocks conversion of thyroxine (T4) to T3
Methimazole: decreases TH synthesis (no inhibition of peripheral conversion)
*in contrast to PTU, methimazole does NOT sig inhibit T4 to T3 conversion
What is myxedema Coma? cause? seasonality?
Rare complication of hypothyroidism
- severe deficiency in TH leads to encephalopathy
- winter mth after cold exposure
- other precipitating events: CVA, surgery, trauma, meds, infection
What are cardinal features of myxedema coma? onset and population at risk?
Hypothermia, hyporeflexia, CNS depression/coma, bradycardia, slow verbal responses
onset: may be rapid or insidious (elderly at highest risk)
What is myxedema vs pretibial myxedema?
Myxedema: puffiness of hands and face; thickened nose, swollen lips, and enlarged tongue secondary to nonpitting edema with abn deposits of mucin in the skin and other tissues (mucin prevent pitting)
“pretibial myxedema” is an uncommon skin disorder that occurs not in cases of hypoTH, but in HYPERTH, usually Graves
(pretibial is misnomer bc can occur other places)
What are causes of hyperglycemia
Illness, infection
Trauma, surgery
Myocardial Infarction
Insulin Omission
What is the mainstay of Treating acidosis (ketoacidosis)
FLUID AND INSULIN
- with insulin, glu will enter cells and body will immediately dc lipolysis as a source for fuel
- blood glu will lower and ketones will clear
what is the prognosis and dx of myxedema coma? when should we suspect it?
Mortality 60-70% (tx drops to 15-20%)
- high bx not easy to dx.. need high level of suspicioun
- supsect when clinical manifestations of hx of hypoTH accompanied by disturbances of consciousness, hypothermia, hypoventilation, hypoTN
what dx studies suggest myxedema coma
CMP: hypogly,hypoNa
TSH: high
FT4/3: low or undetectable
CT head: norm unless trauma precipitated
CXR: normal unless pericardial effusion or pneumonia precipitating event
EKG: BRADYCARDIA, FLATTENING or inversion of T waves, possible conduction abn
AG: HYPOXEMIA with HYPERCARBIA (if hypoventilation)
Mgmt of Myx coma
ABC TH: T4 (T3 alone not rec) Glucocorticoid (given until AI r/o) IV fluids isotonic Correct electrolytes Rewarming blankets Find precipitating cause *slow recovery (metab abn take time)
Thin male, responsive to pain, no evidence of head trauma, Lungs CTA bilat, heart mild tachy no MRG, weak peripheral pulses
Hemoccult neg, no masses, no LE edema
HUGE ddx
this is AI though
*not enough cortisol produced by adrenal glands
ADDISONS
Primary vs secondary vs tertiary AI
Primary: problem at adrenal gland (addisons)
Secondary: at pituitary (ACTH release inhibited) - often panhypopituitariasm bc isolated ACTH def rare
Tertiary: supppression of HPA axis (usually due to w/drawal of steroids)
What causes acute adrenal crisis
may result from acute exacerbation of chronic insufficiency usually sepsis or surgical stress
can be caused by adrenal hemorrhage (ex septicemia induced waterhouse friderichsen syndrome
fulminant meniningococcemia), anticoag complicaitons or congenital abnormalities ,
Mgmt of adrenal crisis
ABCs, IV fluids, correct electrolytes
HYDROCORTISONE, mineralocorticoic (Florinef) if needed, identify/treat underlying cause
Acute adrenal crisis: suspect bacterial etiology (sepsis)
culture and then empiric broad spectrum abx
*note: if any reason to suspect adrenal crisis, treat immediately with hydrocortisone
When should we think of adrenal crisis
shock oterhwise unexplained and inadequate response to vasopressors and volume replacement
