Transcript ELECTROLYTE ABNORMALITIES

ELECTROLYTE
ABNORMALITIES
BY: Anthony M. Letizio D.O.
Hyponatremia
Defn: plasma sodium concentration
less than 134mEq/L.
Clinical Manifestations: vary with the degree
of hyponatremia, and the rapidity of
onset. Moderate or gradual onset causes
confusion, muscle cramps, lethary,
anorexia, and nausea. Severe or rapid
onset can cause seizures and/or coma.
Etiology and Classifications
Hypotonic Hyponatremia
1) Euvolemic – SIADH, water intoxication,
renal failure, glucocorticoid deficiency,
hypothryoidism, thiazide diuretics,
NSAIDs, carbamazepine, amitriptyline,
thioridazine, vincristine,
cyclophosphamide, colchicine,
tolbutamide, chlorpropamide, Ace
inhibitors, clofibrate, oxytocin, SSRI’s, and
amiodarone.
Hypotonic Hyponatremia
2) Hypovolemic – Renal Losses
(diuretics, partial urinary tract
obstruction, salt-losing renal
disease), Extrarenal losses:
gastrointestinal (vomiting, diarrhea),
extensive burns, third spacing
(peritonitis, pancreatitis, ileus), and
adrenal insufficiency.
Hypotonic Hyponatremia
3) Hypervolemic – CHF, nephrotic
syndrome, cirrhosis, and pregnancy
Isotonic Hyponatremia (normal
serum osmolality)
1) Pseudohyponatremia (increased
serum lipids and serum proteins).
2) Isotonic infusion (glucose,
mannitol).
Hypertonic Hyponatremia
1) Hyperglycemia - each 100 mg/dL
increment in blood sugar level above
normal decreases plasma sodium
concentration by 1.6 mEq/L.
2) Hypertonic infusions – (glucose,
mannitol)
Diagnostic Approach
Useful lab tests: serum electrolytes,
glucose, BUN, creatinine, urine sodium,
serum and urine osmolality, uric acid, and
TSH.
Urine sodium determines the source. It
will be low in patients with GI losses or
third spacing. It will be high in patients
taking diuretics. Pseudohyponatremia
should be suspected when the measured
and the calculated osmolarities are
mismatched
Treatment
Euvolemic – SIADH fluid restriction unless
acutely symptomatic which you can give
hypertonic saline infusions.
The serum sodium concentration should
be corrected only halfway to normal in the
initial 24 hours, but not faster than 1
mEq/hr to prevent cerebral edema,
myelinolysis, and seizures.
Treatment
Hypovolemic – give normal saline
infusion
Hypervolemic – strict fliud and
sodium restiction.
Hypernatremia
Defn: Plasma sodium concentration
greater than 144 mEq/L.
Clinical Manifestations: Vary with
degree of hypernatremia and rapidity
of onset: they range from confusion
and lethargy to seizures and coma.
Isovolemic Hypernatremia
(decreased total body water, normal
total body sodium, and extracellular
fluid.
Causes include diabetes insipidus
both neurogenic and nephrogenic,
and skin loss (hyperhemia),
iatrogenic, reset osmostat
Hypervolemic Hypernatremia
(increased total body water,
markedly increased total body
sodium and extracellular fluid)
Causes include iatrogenic
(administration of hypernatremic
solutions), mineralocorticoid excess
(Conn’s syndrome, Cushing’s
syndrome) and salt ingestion
Hypovolemic Hypernatremia
Loss of water and sodium. (water
loss is greater than sodium loss)
Causes include renal losses (diuretics
and glycosuria), Gastrointestinal,
respiratory, skin losses, inadequate
access to water in the disabled or
elderly, and adrenal deficiencies.
Treatment
Isovolemic – Replace fliud with
dextrose in water D5W. Correct half
of the estimated water deficit in the
first 24 hours. The correction rate
should not exceed 1 mEq/L/hr in
acute cases, and 0.5mEq/L/hr in
chronic cases.
Treatment
Hypovolemic – Replace fluid with
isotonic saline initially until it is felt
that the person is becomes
euvolemic. This often occurs before
the sodium concentration is
completely corrected. Then switch to
½ normal saline or D5W. The rate of
correction should not exceed 2
mEq/kg/hr
Treatment
Hypervolemic – Replace fluid with
D5W after loop diuretics are used to
increase excretion of sodium.
Recommended to monitor
electrolytes q8-12 hours during this.
Hypokalemia
Defn: plasma potassium
concentration less than 3.3 mEq/L
Clinical Manifestations: Mild muscle
weakness to overt paralysis
(including respiratory paralysis), and
rhabdomyolysis. Atrial and
ventricular arrhythmias may develop
and ECG changes.
Hypokalemia
Mild causes flattening of T waves,
ST-segment depression, PVC’s,
prolonged QT intervals.
Severe causes prominent U waves,
atrioventricular conduction
disturbances, and V-Tach, Fib.
Hypokalemia
Causes of Hypokalemia
Alkalosis (each 0.1 increase in pH
decreases serum potassium by 0.4 to
0.6 mEq/L
Insulin administration
Vitamin B12 therapy for
megaloblastic anemias, acute
leukemias
Hypokalemic periodic paralysis which
is a rare familial disorder
Causes of Hypokalemia
Beta-Adrenergic agonist (terbutaline),
decongestants, bronchodilators,
theophylline, and caffeine.
Barium poisoning, toluene, verapamil, and
chloroquine intoxication.
Correction of digoxin intoxication with
digoxin antibody fragments (digibind)
Increased renal excretion due to drugs
including the diuretic carbonic anhydrase
inhibitors such as acetazolamide
Causes of Hypokalemia
Amphotericin B
High-dose sodium penicillin, nafcillin,
ampicillin, or carbenicillin
Cisplatin
Aminoglycosides
Corticosteroids, mineralcorticoids
Foscarnet sodium
Causes of Hypokalemia
Renal tubular acidosis distal type 1 or
proximal type 2
Diabetic ketoacidosis
Magnesium deficiency
Postobstruction diuresis, diuretic phase of
acute tubular necrosis
Osmotic diuresis such as mannitol
Bartter’s syndrome which is hyperplasis of
the juxtaglomerular cells
Causes of Hypokalemia
Increased mineralocorticoid activity both
primary and secondary aldosteronism,
Cushings syndrome, or physiological
increases in mineralocorticoid activity
during dehydration.
Chronic metabolic alkalosis from loss of
gastric fluid
GI losses including vomiting, nasogartic
suctioning, diarrhea, laxative abuse villous
adenomas and fistulas
Inadequate dietary intake seen in people
with anorexia nervosa
Causes of Hypokalemia
Cutaneous losses such as sweating
High dietary sodium intake,
excessive use of licorice
Hypomagnesemia
Treatment
Replace potassium either IV or oral
or both. Oral increases the
potassium more quickly than IV
because you have to give IV slowly.
Each 10 meq should raise the
potassium level 0.1 mmol/L
May have to adjust patients diuretics
or other drugs such as amphotericin
which decrease the potassium
Treatment
Check a magnesium level which has
to be normal for maintainence of
serum potassium levels.
Advice patients to eat foods that are
high in potassium such as fruits.
Hyperkalemia
Defn: plasma potassium
concentration greater than 4.9
mEq/L
Clinical Manifestations include
generalized weakness, irritability,
paresthesias, decreased deep tendon
reflexes, flaccid paralysis, cardiac
arrhythmias, and ileus
Hyperkalemia
Mild causes peaking of T waves, and
PVC’s
Severe causes peaking of T waves,
widening of QRS complex, depressed
ST segments, prolongation of PR
interval, sinus arrest, deep S waves,
PVC’s, V-Tach, Fib, and cardiac arrest
Hyperkalemia
Causes of Hyperkalemia
Pseudohyperkalemia – Hemolyzed specimen,
severe thrombocytosis (platelet count of less
than 10 x 6/ml), severe leukocytosis (wbc less
than 10 x 5/ml, fist clenching during phlebotomy,
and drawing blood from a limb into which
potassium is being infused.
Excessive potassium intake
Decreased renal excretion from potassium
sparing diuretics, insufficiency, tubular
unresponsiveness, type 4 RTA, ACE inhibitors,
heparin administration, NSAIDs, TMP-SMX, BBlockers, and pentamidine.
Causes of Hyperkalemia
Acidemia (each 0.1 decrease in pH
increases the serum potassium by
0.4 to 0.6 mEq/L.
Insulin deficiency
Drugs such as succinycholine,
markedly increased digitalis levels,
arginine, and B-adrenergic blockers
Hypertonicity, hemolysis, tissue
necrosis, rhabdomyolysis, burns
Treatment
IV calcium gluconate helps stabilize the
myocardial cell membranes, it does not
lower the potassium.
Give glucose and insulin which will lower
plasma potassium transiently for 4 to 6
hours.
Sodium bicarbonate can be used.
Kayexalate orally or per rectum.
Remove the cause and patients may need
dialysis.
Hypomagnesemia
Defn: plasma magnesium
concentration less than 1.8mg/dL
Clinical Manifestations:
Neuromuscular weakness,
hyperreflexia, fasciculations,
tremors, convulsions, delirium, and
coma
Causes of Hypomagnesemia
Defective absorption (malabsorption)
Inadequate dietary intake (alcoholics)
Parenteral therapy without magnesium
Chronic diarrhea, villous adenoma, prolonged
nasogastric suction, and fistulas
Diuretic usage
Renal tubular acidosis
Endocrine disturbances such as diabetic
ketoacidosis, hyperaldosteronism,
hyperthyroidism, hyperparathryroidism, SIADH,
bartter’s syndrome, hypercalciuria, and
hypokalemia
Causes of Hypomagnesemia
Cisplatin, alcohol, cyclosporine, digoxin,
pentamidine, mannitol, amphotericin B,
foscarnet, and methotrexate
Gentamicin, ticarcillin, carbenicillin
Hypoalbuminemia, cirrhosis, insulin and
glucose, theophylline, epinephrine, acute
pancreatitis, CABG, sweating, burns,
prolonged exercise, lactation, hungrybones disease.
EKG Manifestations
Prolonged QT interval, T-wave
flattening, prolonged PR interval, AFib, torsades de pointes
Lab Manifestations of
Hypomagnesemia
Hypokalemia refractory to potassium
replacement
Hypocalcemia refractory to calcium
replacement
Treatment Hypomagnesemia
Correct the magnesium deficiency
Mild – Oral magnesium
Moderate – IV magnesium sulfate
over 6 hour periods
Severe – serum mag of less than 1
mg/dL give 2grams magnesium in
over 1 hour period
Monitor ECG, blood pressure, pulse,
respiration, DTR’s, and urine output
Hypermagnesemia
Defn: plasma magnesium
concentration greater than 2.3
mg/dL
Clinical Manifestations: Paresthesias,
hypotension, confusion, decreased
DTR’s paralysis, coma, apnea
Acute hypermagnesemia suppresses
parathyroid hormone secretion
causing hypocalcemia
Causes of Hypermagnesemia
Renal failure due to a decreased GFR
Decreased renal excretion due to salt
depletion
Abuse of antacids and laxatives which
contain magnesium
Endocrinopathies including
mineralocorticoid and thyroid
horomone
Rhabdomyolysis
Causes of Hypermagnesemia
Acute diabetic ketoacidosis
Pheochromocytoma
Lithium, volume depletion, familial
hypocalciuric hypercalcemia
EKG Manifestations
Shortened PR interval, heart block,
peaked T-waves, and increased QRS
duration
Treatment for Hypermagnesemia
Identify and correct the underlying
disorder
Dialysis is needed for severe
hypermagnesium
Hypophosphatemia
Defn: plasma phosphate concentration
less than 2.5 mg/dL
Clinical Manifestations: Proximal muscle
weakness, waddling gait, bone pain,
myalgias, osteopenia, apprehension,
paresthesia, seizures, coma, ataxia,
encephalopathy, hemolytic anemia,
leukocyte and platelet dysfunction,
rhabdomyolysis, ventilator dependence,
respiratory failure, dysrhythmias,
hypotension, cardiomyopathy, decreased
contractility, CHF, and metabolic acidosis
Causes of Hypophosphatemia
Decreased intake
Malabsorption, vomiting, diarrhea
Phosphate-binding antacids
Renal loss including RTA, Met acidosis,
Fanconi’s syndrome, vitamine D- resistant
rickets, ATN, hyperparathyroidism, familial
hypophosphatemia, acute volume
expansion, glycosuria, acetazolmide, and
kidney transplantation
Causes of Hypophosphatemia
Transcellular – caused by withdrawal
of alcohol, DKA, glucose, insulin
and/or catecholamine infusion,
anabolic steriods, and other
hormones such as insulin, glucagon,
epinephrine and dopamine. Total
parenteral nutrition, theophylline
overdose, severe hyperthermia,
acute leukemias and Burkitt’s
lymphoma.
Treatment
Mild to moderate can be oral
replaced daily.
Severe cases require IV phosphate
salts until serum phosphate is
greater than 1.5 mg/dL
Hyperphosphatemia
Defn: plasma phosphate
concentration greater than 5mg/dL
Clinical Manifestations: Soft tissue
calcifications in the kidney, cornea,
lung, blood vessels, and skin.
Treatment
Renagel (Sevelamer) is the agent of
choice. It is an oral agent given TID
with meals. It binds phosphate in
the gut and prevents its absorption.
May also use insulin and glucose
infusion to prompt cell phosphate
uptake when rapid phosphate
decreases are needed.
May also need dialysis.
Hypercalcemia
Symptoms – constipation, anorexia,
nausea, vomiting, pancreatitis, ulcers,
confusion, obtundation, pyschosis,
lassitude, depression, coma,
nephrolithiasis, renal insufficiency,
polyuria, decreased urine-concentrating
ability, nocturia, nephrocalcinosis,
myopathy, weakness, osteoporosis,
pseudogout, bone pain, HTN, metastatic
calcifications, pruritis
EKG changes
Shortening of the
QT interval
Treatments
Vigorous IV hydration,
bisphosphonates, loop diuretics,
phosphate repletion, calcitonin,
mithramycin, glucocorticoids, and
indomethacin
Hypocalcemia
Symptoms – neuromuscular
irritability with the Chvostek’s and
Trousseau’s sign, tetany,
paresthesias, myopathy, seizures,
muscle spasm or weakness, soft
tissue calcifications, ocular cataracts,
arrhythmias, CHF
ECG changes
Increases QT
interval
Treatment
IV calcium gluconate, improve
nutritional status, replace calcium
orally, treat underlying diseases.