-
what is the normal value of sodium?
135-145 mEq per L
-
what are 2 etiologies of hyponatremia?
- 1) due to decrease in sodium
- 2) due to expansion of fluid volume
-
what is the prevalence of hyponatremia?
what kind of patients have this?
- common in elderly
- after surgeries
- in paitents with CHF and cirrhosis (ascites)
-
what is considered mild hyponatremia?
lab value, symptoms?
- 125-134 meq/L
- usually asymptomatic
-
what is considered moderate hyponatremia?
lab value, symptoms?
- 115-125 meq/L
- anorexia, nausea, vomiting, muscle weakening, cramping (mostly nonspecific GI symtpoms)
- may be due to digoxin and etc so check therapeutic ranges for all meds
-
what is considered a severe hyponatremia?
lab value, symptoms?
- <115 meq/L or rapid onset (<48 h)
- gait disturbances, falls, impaired mental function, tremors, seizures
-
hyponatremia can be associated with what kind of risks?
- death or CV events
- falls and fractures
- impairment of gait and attention
- higher mortality
- poorer outcome in patients with pneumonia
- mechanical ventilation
-
what are two water-sodium balance mechanisms?
- free-water exchange between ICF and ECF
- arginine vasopressin (AVP or aka ADH (antidiuretic hormone)): maintain osmolality at 280-295 mOsm/kg and BP and volume
-
what are three different types of hyponatremia?
- isotonic
- hypertonic
- hypotonic
-
what is isotonic hyponatremia?
- this has normal osmolality
- aka pseudo-hyponatremia
- due to elevated lipids or proteins (hence in hyperlipidemic patients)
- not likely to occur often
-
what is hypertonic hyponatremia?
- osmolality: >295 mOsm/kg
- presence of effective osmoles (glucose, glycine, mannitol): due to additional solutes
-
what kind of "hyponatremia" would a diabetic patient present? how do you adjust this?
- hypertonic hyponatremia because of increased glucose and decreased sodium. however this is NOT a hyponatremia
- for every 100mg/dL increase of glucose, sodium should be decreased 1.7mEq/L
-
what is hypotonic hyponatremia?
- osmolality: <280 mOsm/kg
- excess water relative to solute in the ECF.
- decrease in solute = depletion (common in renal problem patients)
- increase in water = dilution (common in CHF and cirrhosis patients)
-
how do you differentiate different hyponatremias?
- important to measure serum osmolality
- (normal 280-295 mOsm/kg)
-
what is calculated osmolarity equation? (given during exam)
how about osmolal gap?
calculated osmolarity = 2 Na + glucose/18 + BUN/2.8
osmolal gap = measured - calculated
-
what is normal glucose level?
100 mg/dL
-
what are three kinds of hypotonic hyponatremia?
- hypovolemic
- hypervolemic
- euvolemic
-
what is hypovolemic hypotonic hyponatremia?
what are the symptoms?
- depletional! contraction of ECF fluid due to extra renal losses or diuretic use (THIAZIDE)
- diarrhea, vomit, excess sweating, burns, thiazide diuretic, adrenal insufficiency
- assess fluid status
-
what is hypervolemic hypotonic hyponatremia?
what are the associated conditions?
- dilutional or marked expansion increased in ECF fluid with edema
- CHF, cirrhosis, nephrosis/renal failure
-
what is euvolemic hypotonic hyponatremia?
what are the associated conditions?
- dilutional
- normal or slightly decreased Na content and increased total body water and ECF volume
- NO edema
- primarily polydipsia, low solute intake
- hypothyroidism, hypocortisolism, syndrome of inappropriate secretion of antidiuretic hormone (SIADH)
-
what does SIADH stand for? what kind of hyponatremia is it associated with?
- syndrome of inappropriate secretion of antidiuretic hormone
- euvolemic hypotonic hyponatremia
-
what is diuretic induced hyponatremia called?
when does this develop?
what ist eh mechanism?
what kind of diuretic is it associated with? why not the other diuretic?
- this is ONLY associated with hypovolemic hypotonic hyponatremia (all three "hypo")
- typically within 2 weeks of therapy initiation (can also occur alter with increase dose or other causes of hyponatremia develop)
- more Na loss than water: blocks Na reabsorption in distal tubules thus increased Na and water removal. decreased effective circulating volume and ADH is released. increased re-absorption of free water in the collecting duct and stimulate thirst.
- usually mild but could be severe
- THIAZIDE: not loop diuretic because when body senses water loss, sodium is reabsorbed back more in distal/proximal tube, not loop. less free water excretion in thiazide
-
what are some common causes of SIADH?
- LOSS OF FLUID conditions:
- thiazide diuretics
- volume depletion: vomiting, diarrhea, laxative abusemalignant tumor
- neuropsychiatric
- pulmonary dysfunction
- endocrine (hypothyroidism, glucocorticoid deficiency)
- postoperative
- alcohol withdrawal
- renal/adrenal dysfunction
- volume expansion (cirrhosis, HF, nephritic syndrome)
-
what is drug induced SIADH associated with?
what are usual findings?
what is important to manage?
- associated with euvolemic hypotonic hyponatremiano peripheral or pulmonary edema
- osmolarity >100 mOsm/kg, urine Na >20mEq/L
- rule out other causes first! (not just drug induced)
-
what are the drugs associated with drug induced SIADH?
- (euvolemic hypotonic hyponatremia)
- antipsychotics
- antidepressants (older SSRI, tricyclic, venlafaxime)
- anticonvulsants (carbamazepine)
- narcotic
- hallucinogenics
- CV drugs (ACEi (lisinopril, captopril), amiodarone)
- antineoplastic (esp lung cancer agents)
- sulfonylurea
-
what is the mechanism of drug induced SIADH?
- water intake exceeds the kidney's function to excrete due to AVP release or enhanced renal sensitivity to AVP
- increased central AVP production
- increased renal sensitivity to AVP
- AVP release due to serotonin
-
what are the risk factors for drug induced SIADH? (list three medications and risks)
- SSRI: >65yo, concomitant diuretic, elevated potassium, female, baseline serum Na <139 mEq/L, lower BMI
- carbamazepine: higher dose and duration, elevated serum concentrations
- vincristine, vinblastine: asian race
-
what are prevention management for drug-induced SIADH?
- screen risk factors
- use lowest dose possible
- routine monitoring of Na in high risk patients
-
what are managements for mild-mod drug induced SIADH?
- d/c offending agent
- identify underlying cause
- fluid restriction and maintain negative water balance (<1200 ml/day)
- monitor urine output and insensible losses
-
how do you manage acute symptomatic/severe drug induced SIADH? (if severe, could cause seizure)
- correct no more than 8-12 mEq/L in 24 hours.
- fluid restriction +/- furosemide
- sodium chloride +/- furosemide (not helpful in renal failure) (1g of NaCl has 17 mEq Na)
- NaCl infusion: 0.9% (isotonic), use hypertonic (3%, 5%) with extreme caution
- for chronic hyponatremia: demeclocycline 600-1200mg in div doses (onset 3-6d, monitor nephrotox) or lithium 900-1200mg qd (slow onset, use if underlying bipolar but otherewise limit)
- arginine vasopressin receptor (AVP) antagonists for euvolemic or hypervolemic hyponatremia
-
what are AVP antagonist regimens?
what are drug interactions?
when are they used?
- Conivaptan (Vaprisol) for IV: 20mg IV bolus then 20mg as CI for 24h for up to 4 days, max 40mg qd
- Tolvaptan (Samsca) for PO: 15mg po qd to max 60mg qd (ask cardiologist, $200/tab)
- CYP 3A4 interaction
- use for SIADH, euvolemic and hypervolemic hypOnatremia
- NOT for hypOvolemic b/c could cause dehydration
-
When is NaCl infusion regimen used?
when do you d/c? what is the rate of infusion?
- for acute symptomatic or severe hypotonic hyponatremia only
- d/c when Na increases by 10-12 mEq/L or to 120 mEq/L
- total correction should NOT exceed 8-12 mEq within the first 24 h
- initial rate is 1-2 mEq/L per hr for several hours then decrease
-
how much mEq sodium is in 0.9% NaCl?
154 mEq/L
-
how do you calculate total body water?
weight (kg) x body water
- 0.6 = children and men <70 yo
- 0.5 = elderly men >70yo, female <70 yo
- 0.45 = elderly women > 70 yo
-
how do you calculate infusion rate for NaCl?
- first:
- change in Na per L of infusion = (infusion Na content - baseline serum Na) / (total body water + 1L)
- second:
- infusion rate = target serum Na increase / change in Na/L of infusion
-
which is more common? hypo or hypernatremia?
hyponatremia
-
What happens if the change of Na is more than 12mEq/L over 24 hours?
CNS issues
-
what is hypernatremia? (definition, lab value)
what kind of patients will experience this?
- Na >145 mEq/L
- a deficit of water in relation to sodium content in the body
- most common in those with impaired thirst response or in those without access to water (altered mental status, intubated patients, infants, elderly)
-
what happens to the brain when the body has too much sodium?
- too much serum sodium causes water to diffuse out of the brain via BBB because water likes to go to concentrated area.
- thus the brain shrinks.
-
what are clinical features of hypernatremia?
- CNS dysfunction
- infants: hyperpnea, muscle weakness, restlessness, high pitched cry, insomnia, lethargy, coma
- adults: muscle weakness, confusion, coma
-
what are three etiologies of hypernatremia?
- isovolemic
- hypovolemic
- hypervolemic
-
what is hypovolemic hypernatremia?
what is this related to?
- water loss > Na loss
- related to renal, adrenal, GI, lung, skin systems
-
what is hypervolemic hypernatremia?
- Na gain > water gain
- sodium overload, mineralocorticoid excess
-
what is isovolemic hypernatremia?
when is this observed?
loss of water
- central diabetes insipidus (decreased AVP secretion causes this)
- nephrogenic diabetes insipidus (decreased renal response to AVP; can be drug induced)
- osmotic diuresis (urinary Osm <300)
- skin loss
- primary polydipsia
- iatrogenic
-
nephrogenic diabetes insipidus is associated with what kind of electrolyte imbalance?
isovolemic hypernatremia
-
what drugs induce nephrogenic diabetes insipidus hypernatremia?
- lithium toxicity (check level before d/c)
- cidofovir
- foscarnet
- demeclocycline
- sodium bicarbonate
- hypertonic NaCl
- hypercalcemia, hypokalemia
-
what is the mechanism of lithium induced nephrogenic diabetes insipidus hypernatremia?
what is urinary osmolality?
what are risk factors for this?
what is lithium therapeutic range?
- inhibits opening of aquaporins in nephrons and cause polyuria
- urinary osmolality <250 mOsm/kg
- chronic kidney disease (CrCl <60), miltiple daily doses, long term tx (>15yo), higher trough serum lithium level
- 0.8 - 1.2 (1.2 for mania bipolar)
-
what is the first step to manage hypernatremia?
- correct underlying cause (including hyperglycemia)
- withhold lactulose and diuretic
- treat other electrolyte disturbance
- moderate lithium
- correct feeding preparation
-
how do you manage hypovolemic hypernatremia?
- calculate water deficit = total body water x [initial serum Na /140) - 1]
- goal: 0.5 - 1 mEq/L per hr, not to exceed 10 mEq/L per day
- 0.9% NaCl 200-300 ml/hr until hemodynamically stable then 0.45% NaCl or D5W to correct water deficit
-
how do you manage central diabetes insipidus hypernatremia (isovolemic)?
- AVP analogs because AVP secretion is decreased: desmopressin (PO) and DDAVP (intranasal)
- this is not AVP antagonist (this is for hyponatremia)
-
how do you manage sodium overload hypernatremia?
- loop diuretic (furosemide 20-40mg q6h)
- IV D5W
-
how do you manage nephrogenic diabetes insipidus hypernatremia (isovolemic)?
- correct hypercalcemia, hypokalemia (Ca and Na go together and K is opposite)
- thiazide diuretic + dietary sodium restriction (<2g NaCl daily)
- indomethacin 50mg TID (adjunct)
- if lithium induced, amiloride 5-10mg daily
-
normal range of potassium?
3.5-5.0 mEq/L
-
cause/etiology of hypokalemia?
- due to total body K deficit
- or when serum K is shifted into the ICF
-
clinical feature of mild hypokalemia (3-3.5 meq/l)
asymptomatic
-
clinical feature of moderate hypokalemia (2.5-3 meq/L)
cramping, weakness, malaise, myalgia
-
clinical feature of severe hypokalemia (<2.5meq/L)
- ECG ST segmentation depression or flattening, T wave inversion or U wave elevation
- life threatening cardiac arrhythmia, heart block
-
what other electrolyte disturbance could happen if hypokalemia? what should you do to fix?
- hypomagnesemia (<1.7 mg/dL (not meq/l))
- fix Mg first
-
what are the etiologies of hypokalemia?
- inadequate intake
- magnesium depletion
- increased excretion - diarrhea, laxative abuse
- renal losses - diuresis, loop or thiazide diuretics, non-reabsorbable anions (penicillin), high dose glucocorticoids
-
what are 2 mechanisms of drug induced hypokalemia? give drug examples with each.
transcellular shift: b2 agonist (albuterol), theophylline, caffeine, insulin overdose
enhanced fecal elimination: laxative, SPS, sorbitol
enhanced renal elimination: diuretic, high dose pcn, mineralocorticoids
-
when do you use IV K supplementation?
how do you administer?
- K<2.5 meq/L (severe)
- presence of cardiac arrhythmias, muscle spasm
- unable to tolerate PO
- 10-20 meq K diluted in 100ml NS over 1 h
- monitor EKG if admin >10meq/h
- do not exceed 40 meq/l
- after each 30-40 meq check K 30 min after infusion
-
K+ should never be given via which way?
IV push (this is lethal)
-
when do you give po K+ replacement therapy?
in milder cases
-
when K <3.5, every ___ meq/L decrease requires ____ meq supplement.
1meq/L decrease requires 100-400 meq supplem
-
hypokalemia due to chroni loop or thiazide diuretic use requires ____ meq orally (in div doses) then prevention.
40-100 meq
-
what other electrolyte should you always monitor when hypokalemia?
magnesium
-
what is the definition of hyperkalemia?
K >5.5 meq/L
-
clinical feature of mild hyperkalemia? (5.5 - 6 meq/L)
usually asymptomatic
-
clinical feature of moderate hyperkalemia? (6.1 - 6.9 meq/L)
heart palpitation
-
clinical feature of severe hyperkalemia (> 7 meq/L)
- potentially life threatening
- cardiac arrhythmia
- EKG changes (peaked t-wave, widened QRS complex)
-
what are the 4 etiologies of hyperkalemia?
- increased K intake
- impaired K excretion (K sparing diuretic, ACEi, ARB, NSAID, cyclosporine, tacrolimus, Bactrim)
- tubular un-responsiveness to aldosterone
- redistribution of K into the extracell space
-
beta blocker causes __ kalemia.
beta agonist causes __ kalemia.
-
for acute management of hyperkalemia, which agents may exhibit immediate effect?
- calcium gluconate or chloride 1g IV
- hemodialysis
-
for acute management of hyperkalemia, which agents may exhibit effect after 30 min ?
- regular insulin 5-10U iv/sc with dextrose 10~50% 25-100g to avoid hypoglycemia
- albuterol 10-20mg by inhaler over 10 min (higher dose than 2.5mg for asthma)
-
if there is metabolic acidosis, what agent can you consider to acutely manage hyperkalemia?
sodium bicarbonate 50-100 meq
-
if you were to use loop diuretic 20-40 iv for acute management of hyperkalemia, what should you assess prior?
fluid status
-
what is one of the most effective agents to acutely manage hyperkalemia? how fast is the onset
- kayexalate 15-60g with sorbitol
- onset in 1 hr
-
goal of hyperkalemia long term management?
restrict dietary K intake to ____g/d
avoid ____
d/c drugs that interfere with K homeostasis
agument K+ excretion (use ____, ____)
if hypoaldosteronism is present, use ____.
chronic kayexalate (each g of resin removes ___ meq of K)
- maintain K <6 meq
- 2-3g
- K supplement
- loop, thiazide diuretic
- fludrocortisone
- 1 meq of K
-
if severe hyperkalemia and EKG changes, what would be a reasonable choice of therapy?
- calcium gluconate (antagonize K damage to heart)
- kayexalate (removes K)
-
what is normal Mg? (Careful with the units)
- 1.7-2.3 mg/dL
- 1.4 - 1.8 meq/L
-
definition of hypomagenesmia?
<1.4 meq/L
-
clinical features of hypomagnesemia
- may be present with hypokalemia and hypocalcemia
- tetny, twitch, tremor, generalized convulsion
- heart palpitation, cardiac arrhythmia, ECG change
-
what are two etiology of hypomagnesemia?
decreased intestinal absorption: small bowel disease, laxative abuse, alcoholism
increased renal excretion: thiazide, loop diuretic, AG, amphoB, cyclosporin, tacrolimus, cisplatin, pentamidine, foscarnet
-
how do you manage?
Mg 1.0-1.4 meq/L without symptoms
- milk of magnesia 5ml QID
- Mg antacid 15ml TID
- Mg Ox tab 400-800 QD
- these all increase K+ as well
-
how do you manage?
Mg <1.0 meq/L without severe symptoms
- day 1: 1 meq/kg iv inf or div im
- day 2-5: 0.5 meq/kg/d (iv)
- Mg sulfate
-
how do you manage?
Mg < 1.0meq/L with life threatening symptoms (arrhythmia, seizure)
- day 1: 2 g Mg sulfate mix with 6ml NS IV push over 1min then 1 meq/kg IV inf over 24 h
- day 2-5: 0.5 meq/kg/d (iv inf) (same as w/o severe sympt)
-
Kg in hypomagnesemia IV is based on what kind of weight?
lean body weight
-
definition of hypermagnesimia?
>2meq/L
-
clinical features of hypermagenesemia?
- above 6 is considered serious
- >6meq/L: loss of deep tendon reflex, EKG change
- 7-9 meq/L: drowsy, lethargy, somnolence
- 12 meq/L: resp depression, muscle paralysis, coma
- 15 meq/L: complete heart block, death
-
what are the etiologies of hypermagenesmia?
- decreased renal exc
- excessive intake
- drug induced: Mg containing antacid and vitamin, lithium
- others
-
how do you manage hypermagnesemia?
- reduce Mg intake
- IV calcium: 100-200mg hrly
- IV furosemide 40mg (do not use if dehydration, hotn or CrCl<30)
- supportive care
- dialysis patients (make sure dialysate is Mg-free)
-
normal range of calcium?
8.5-10.5 meq/L
-
definition of hypocalcemia?
- serum Ca <8.5 meq/L
- or
- ionized Ca <4.4 mg/dL
-
when should you use the formula to adjust Ca level?
what is the formula?
- when albmin <4
- adjusted Ca = 0.8 (4 - albumin) + total measured Ca
-
clinical features of hypocalcemia?
- altered mental status, seiure, paresthesia, tetany, hyperreflexia, muscle weak
- prolonged QT interval, cardiac arrhythmia
-
6 etiologies of hypocalcemia
- result of alterations in the effect of PTH and itamn D on the bone, gut and kidney
- loss of Ca from circulation: intravascular binding with citrate, lactate, foscarnet, EDTA
- postoperative hypoparathyroidism
- magnesium deficiency
- vitamin D deficiency
- others - thyroid surgery, sepsis, chemotherapy
-
what drugs induce hypocalcemia?
- bisphosphonate
- cinacalcet
- calcitonin
- furosemide
- ketoconazole
-
how do you manage hypocalcemia?
- first look at albumin level and correct
- treat hypomagnesemia
- treat hypoparathyroidism, vitamin D deficiency (1,25 dihydroxyvitamin D3 (0.5-3mcg daily), ergocalciferol 50,000 IU daily)
-
how do you manage asymptomatic hypocalcemia?
oral elemental calcium 1-3g/d
-
how do you manage symptomatic hypocalcemia?
- Ca++ gluconate 1 ampule IV over 10-30min
- if persistent, rebolus IV and increase maintenance infusion rate
- check Ca, PO4, Mg q 4-6h
- monitor EKG
-
define hypercalcemia
>10.5
-
clinical features of hypercalcemia
- alterned mental status with confusion, lethargy, psychosis, coma
- hyporeflexia and muscle weakness
- constipation, shortening of QT interval, pancreatitis
-
clinical features associated with chronic hypercalcemia
bone changes, band keratopathy (corneal calcium deposition)
-
other clinical presentation with hypercalcemia
- hyperparathyroidism
- malignancy
- sarcoidosis
- vitamin A tox
-
4 etiologies of hypercalcemia
- increased intestinal Ca absorption
- hypervitaminosis D
- increased bone resorption
-
important drug that induces hypercalcemia
- thiazide
- (also causes hypokalemia, hypomagnesemia, hypercalcemia)
-
how do you manage hypercalcemia?
- d/c offending drug
- treat even if asymptomatic if >12 mg/dL
- increase urinary Ca excretion (isotonic saline NS 200-300ml/hr +/- loop diuretic 40-80 mg q1-4h)
-
how can you diminish bone resorption in hypercalcemia?
- calcitonin sq/im
- bisphosphonate: etidronate (Didronel), pamidronate (Acredia), zoledronic acid, ibandronate
-
how can you manage decreased intestinal Ca absorption in hypercalcemia?
corticosteroids
-
what is the normal level of phosphate?
2.5 - 3.5 mg/dL
-
define hypophosphatemia
<1 - 2 mg/dL (severe if <1)
-
what are clinical features of hypophsophatemia?
- CNS manifestation
- myalgia, bone pain, weakness
- severe rhabdomyolysis
- increase alkaline phosphate
- normal to low PO and Ca
-
what are drug induced causes of hypophosphatemia?
- decreased GI absorption (pohsphate binding subtance, glucocorticoid)
- increased urinary excretion
- internal redistribution (alcoholism, dextrose solution, re-feeding syndrome)
-
how do you manage mild to moderate hypophosphatemia without symptoms?
- oral phosphorus supplementation
- NeutraPhos
- Neutra Phos K
- Fleet Phospho soda
-
difference between NeutraPhos and NeutraPhosK?
- Neutra Phos: 7 meq/L each of Na and K, 8mmol PO
- Neutra Phos K: 12 meq/L of K, 8 mmol PO
-
how do you manage severe hypophosphatemia?
- PO <1mg/dL
- depends on potassium
- if K >3.5: sodium phosphate over 3h
- if K <3.5: potassium phosphate over 3h
-
define hyperphosphatemia
>4.5 mg/dL
-
clinical features of hyperphosphatemia
GI disturbance, lethargy, obstruction urinary tract, seiure, calciphylaxis
-
drug induced causes of hyperphosphatemia
- vitamin D
- bisphosphonate
- phosphorus containing enema
- excessive IV or PO of phosphorus
-
how do you manage hyperphosphatemia?
- correct and manage hypocalcemia first!
- goal Ca x PO <55 (precipitation if higher number)
- goal PO 2.7-4.6 in stage 3/4 CKD
- goal PO 3.5 - 5.5 in stage 5 CKD
- phosphate binder (avoid long term therapy)
- antacids containing calcium
- lantanum 1.5 - 3g daily in div doses
- sevelamer 800-1600mg with meals TID
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