Management of Electrolyte Emergencies: Emergency Medicine Board Review Manual
Management of Electrolyte Emergencies: Emergency Medicine Board Review Manual
Management of Electrolyte Emergencies: Emergency Medicine Board Review Manual
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Category/ Urinary
Volume Status Mechanism Sodium Treatment
Hypovolemic hyponatremia Renal losses: excess diuretic use,* osmotic diuresis, > 20 mEq/L Isotonic saline,
(ECF volume depletion) renal tubular acidosis, salt-losing nephritis, volume expansion
adrenal insufficiency, metabolic alkalosis
Extrarenal losses: vomiting, diarrhea, fistulas, < 10 mEq/L Isotonic saline,
tubes, burns, effusions, pancreatitis, ascites, muscle volume expansion
trauma, intestinal obstruction, systemic infections
Euvolemic hyponatremia Excess ADH: SIADH, drugs > 20 mEq/L Water restriction
(modest ECF volume Glucocorticoid deficiency
excess) Water intoxication: IV therapy, psychogenic polydipsia,
inappropriately diluted formula, excessive water feeding
Hypothyroidism
Reset osmostat
Hypervolemic hyponatremia Edema-forming states: congestive heart failure,* liver < 10 mEq/L Sodium and water
(ECF volume excess) failure, nephrotic syndrome restriction
Acute or chronic renal failure > 20 mEq/L Sodium and water
restriction, dialysis
ADH = antidiuretic hormone; ECF = extracellular fluid; IV = intravenous; SIADH = syndrome of inappropriate ADH secretion. (Adapted with
permission from Perkin RM, Novotny W, Harris GD, et al. Common electrolyte problems in pediatric patients presenting to the ED. Pediatr
Emerg Med Rep 2001;6:115; and Berl T, Anderson RJ, McDonald KM, et al. Clinical disorders of water metabolism. Kidney Int 1976;10:117.)
*Most common cause of hyponatremia in adult emergency department patients.
Water flows out of the relatively hypo-osmotic cells into tremia should include measurement of basic elec-
the ECF, causing apparent hyponatremia. Initially, this trolytes, urinary electrolytes, and a renal panel. Urinary
redistribution of TBW occurs without an alteration in sodium concentration of less than 10 mEq/L is expect-
total body sodium. The presence of an extraneous os- ed if losses are extrarenal. If the urine sodium and chlo-
motically active substance in plasma can be recognized ride concentrations are high (sodium > 20 mEq/L), the
when the calculated osmolality differs from the measured kidney is wasting sodium and chloride.
osmolality by more than 10 mOsm/L. The most common category of hyponatremia in the
In situations of hyperglycemia, the sodium concentra- adult ED patient population is hypovolemic hyponatre-
tion falls by approximately 1.5 mEq/L for every 100 mg mia. Adult patients develop hypovolemic hyponatremia
rise in serum glucose. The apparent hyponatremia will secondary to overuse of thiazide diuretics and in con-
usually resolve once the underlying disorder is treated. gestive heart failure (CHF).
Care should be taken to prevent the patient from becom- Hyponatremia with euvolemia occurs with the syn-
ing dehydrated secondary to osmotic diuresis. drome of inappropriate ADH secretion (SIADH).
True hyponatremia. “True hyponatremia” (plasma os- SIADH has been recognized in association with a variety
molality < 280) occurs with hypovolemia and hypervol- of pathologic processes, including malignancies, central
emia, depending on the imbalance of TBW in conjunc- nervous system (CNS) disorders (eg, infections), bleed-
tion with total body sodium concentration (Table 1). ing, trauma, acute psychosis, and pulmonary disorders.
Hyponatremia with hypovolemia occurs when there is Although the normal kidney is able to excrete up to 25 L
depletion of both water and sodium but the loss of sodi- of excess water intake,4 in cases of extreme polydipsia or
um is greater. Hyponatremia with euvolemia is a mis- in infants, water intoxication can cause hyponatremia
nomer, since there is actually a modest increase in TBW. with clinical euvolemia. Other causes of euvolemic hypo-
However, the TBW increase is equally distributed across natremia include glucocorticoid deficiency, hypothyroid-
all fluid compartments. In situations of hypervolemic ism, and drug use (carbamazepine chlorpropamide,
hyponatremia, total body sodium is increased but TBW is clofibrate, cyclophosphamide, desmopressin, thiazides,
increased even more. tolbutamide, opiates, oxytocin, vincristine).5 These pa-
Initial laboratory tests in the assessment of hypona- tients should be treated with water restriction because
50 kg woman with serum Na level of 105 mEq sciousness, flaccid or spastic quadriparesis, and bulbar
(correct at rate of 2 mEq/hr or < 0.5 mEq/L/hr) dysfunction. To avoid CPM, serum sodium should not
Sodium to be infused (mEq/L) be corrected faster than 0.5 mEq/L/hr with a target
= (total body water) (desired [Na] – actual [Na]) sodium concentration of 120 mEq/L.1 Figure 1 shows
the method for calculating the volume of hypertonic
Volume of 3% saline to be infused in 1 hour saline to be infused.
(total body water) (desired [Na] – actual [Na]) Patients receiving hypertonic saline should be admit-
=
513 mEq/L ted to the intensive care unit (ICU). Caution should be
(0.6 x 50 kg)(107–105 mEq/L) taken to prevent volume overload. Loop diuretics may
= be given in conjunction with hypertonic saline to en-
513 mEq/L
hance free water loss.
= 0.117 L or 117 mL
HYPERNATREMIA
Correct at this rate for a maximum of 24 hours.
Hypernatremia is defined as a sodium concentration
Figure 1. Calculation of volume of hypertonic saline for cor- of more than 145 mEq/L. The normal response to ele-
recting hyponatremia. vation of plasma osmolality is increased thirst and re-
lease of ADH. The thirst mechanism is exquisitely sen-
sitive to hyperosmolarity, so severe hypernatremia is
they actually have volume retention and more or less nor- rare in conscious, mobile patients. Hypernatremia oc-
mal total body sodium. curs primarily in infants, the elderly, and debilitated
Hyponatremia with hypervolemia occurs in patients patients secondary to inadequate access to and intake
with renal failure, advanced CHF, hepatic cirrhosis, and of water, often in conjunction with excessive water loss.
nephrotic syndrome. Total body sodium is increased, Thus, because it occurs in a vulnerable population, hy-
but TBW is increased even more. Patients are relatively pernatremia has the worst prognosis of any electrolyte
intravascularly depleted (cirrhosis, nephrosis) or have abnormality and dramatically increases the mortality
circulatory compromise (CHF). The kidneys interpret for any coexisting disease.
this apparent intravascular insufficiency as hypovolemia Hypernatremia causes cerebral cellular dehydration.
and act to retain water. Treatment is complex and in- In situations of acute hypernatremia, water flows out of
volves sodium and water restriction in addition to treat- the intracellular fluid into the ECF. The loss of brain
ment of the underlying disease. In situations of renal volume puts mechanical traction on the cerebral ves-
failure, dialysis may be necessary. sels, which may tear. In situations of chronic hyperna-
tremia, the brain creates small intracellular proteins to
Treatment combat cellular dehydration (idiogenic osmoles). Hy-
Treatment depends on the clinical severity of the dis- pernatremia may develop in the setting of low, normal,
order and the category of hyponatremia. In all patients, or high (rarely) total body sodium (Table 2).
airway, breathing, and circulation (ABCs) should be The initial assessment of hypernatremia and its causes
managed initially. Patients in hypovolemic shock should should include an electrolyte panel and urinary elec-
be volume resuscitated with normal saline. In patients trolytes. In hypovolemic states in the absence of renal dis-
where adrenal insufficiency is possible (eg, hyponatrem- ease, urinary sodium should be concentrated. In cases
ia, hyperkalemia, and dehydration), a steroid bolus where there is renal dysfunction in water regulation, uri-
should be given. Mild asymptomatic hyponatremia nary electrolytes are variable and not helpful in diagnosis.
does not usually require treatment.
More aggressive therapy should be considered in Etiology
severely symptomatic hyponatremia: new altered level Hypovolemic hypernatremia is the most common
of consciousness, coma, and seizures, in conjunction form of hypernatremia. The presence of hypernatremia
with serum sodium less than 120 mEq/L. Hypertonic in this setting indicates severe TBW depletion.1 Patients
saline (3%, 513 mEq/L) can correct hyponatremia display signs of severe volume contraction, including flat
rapidly, but its use is controversial because rapid cor- neck veins, orthostatic hypotension, tachycardia, poor
rection of hyponatremia can cause volume overload skin turgor, and dry mucous membranes.
and central pontine myelinolysis (CPM). CPM occurs Euvolemic hypernatremia occurs with water deficit
a few days after rapid correction of a severe hypona- in the absence of solute loss. It does not lead to overt
tremic episode. Symptoms include altered level of con- signs of hypovolemia since only 8% of negative water
DI = diabetes insipidus. (Adapted with permission from Berl T, Anderson RJ, McDonald KM, et al. Clinical disorders of water metabolism. Kidney
Int 1976;10:117. Copyright © 1976 Blackwell Publishing Ltd.)
balance is at the expense of the intravascular volume. should be continued on their usual therapy (usually
Renal water losses occur with diabetes insipidus (DI). desmopressin acetate). Nephrogenic DI is usually treat-
DI occurs when the kidney is unable to concentrate ed with a combination of thiazide diuretics and sodium
urine because of a lack of ADH secretion (central or restriction. Oral fluid replacement should be adequate
neurogenic DI) or the kidney fails to respond to ADH to treat euvolemic hypernatremia.
(nephrogenic DI). Central DI can occur after neuro-
surgical procedures, head trauma, stroke, and CNS
infections. In nephrogenic DI, renal response to ADH DISORDERS OF POTASSIUM IMBALANCE
or renal medullary interstitial hypertonicity is decreased,
so the release of ADH does not result in increased water
resorption. POTASSIUM HOMEOSTASIS
Hypervolemic hypernatremia is the least common Potassium is the major intracellular cation. Normal
form of hypernatremia. It is infrequently seen in pa- ICF potassium concentration is 140 to 155 mEq/L.
tients with normal renal function since the kidney is Only 2% of body potassium is extracellular, with the
generally able to excrete any amount of excess sodium extracellular concentration of potassium ranging from
ingested. It is usually iatrogenic secondary to the admin- 3.5 to 5.5 mEq/L. The large ratio of intracellular to
istration of hypertonic sodium-containing solutions. extracellular potassium is the primary determinant of
Treatment includes water replacement and furosemide cell membrane potential and is maintained by the
therapy. Those with renal failure may need dialysis. Na+,K+ –ATPase pump. Alteration of this ratio has pro-
found effects on excitable tissue, namely muscle and
Treatment nerve. Despite the vital function of potassium in the
As always, treatment priorities are the ABCs. Normal body, potassium imbalances can be asymptomatic or
saline should be used to stabilize the patient in hypo- nonspecific, with dysrhythmia being the first definitive
volemic shock. While it is known that rapid correction of manifestation.
hypernatremia increases acute mortality, there are little Regulation of extracellular potassium concentration
data on the optimal treatment methods and rate.1 Acute can be divided into the maintenance of external potas-
hypernatremia should be corrected carefully over a min- sium balance, defined as the overall amount of potassi-
imum of 48 hours, with a maximum increase in serum um in the body, and internal potassium balance, the dis-
sodium of 2 mEq/L/hr.1 In cases of hypernatremia of tribution of potassium between the ICF and the ECF. In
unknown or chronic duration, serum sodium should be an individual with normal renal function, approximate-
corrected no faster than 0.5 to 0.7 mEq/L/hr.6 More ly 90% of the daily potassium load is excreted by the kid-
rapid correction can result in deterioration, possibly be- neys. The remainder is excreted in the feces. Aldos-
cause infused saline will diffuse along an osmotic gradi- terone enhances sodium and water conservation and
ent into brain cells that contain idiogenic osmoles, caus- potassium excretion into the urine. Acid-base status
ing cerebral edema. Patients with known central DI also modulates renal potassium handling. Acidemia
inhibits renal tubular potassium secretion, whereas are usually nonspecific and include weakness, fatigue,
alkalosis stimulates it. muscle pain, and palpitations. Hypokalemia can affect the
Distribution of potassium between the intracellular smooth muscle of the intestines, causing an ileus. It
and extracellular compartments is a rapid and dynamic should not cause mental status changes. The most serious
process responsible for the moment-to-moment main- manifestations of hypokalemia are cardiac dysrhythmia
tenance of plasma potassium concentration. Insulin, and rhabdomyolysis. Atrial and ventricular premature
independent of its glucose regulatory role, promotes contractions and supraventricular tachycardia can devel-
Na+,K+-ATPase activity to pump potassium into the cell. op. Underlying heart disease and digoxin use predispose
Catecholamines also modulate internal potassium bal- patients with hypokalemia to more severe dysrhythmias;
ance. β2-adrenergic stimulation facilitates cellular potas- likewise, hypokalemia exacerbates digoxin toxicity.
sium uptake, while α-adrenergic stimulation releases Severe hypokalemia can cause a classic pattern of
potassium from cells. In acidemia, hydrogen ions move electrocardiograph (ECG) changes, including flattened
into cells in exchange for potassium ions in order to T waves, development of the U wave and a depressed
maintain plasma pH. ST segment, flat or inverted T wave, and prominent
U wave (Figure 2). Workup of hypokalemia should
HYPOKALEMIA include an electrolyte panel to assess for acidosis, anion
Etiology gap, and renal function. Measurement of urinary potas-
Hypokalemia is defined as a plasma potassium level sium is also helpful. Acidosis suggests lower GI losses,
less than 3.5 mEq/L. Although hypokalemia is common, RTA, or diabetic ketoacidosis (DKA). A urine potassium
life-threatening hypokalemia (potassium < 2.5 mEq/L) level less than 20 mEq suggests diarrheal losses, while
is unusual.5 In hypokalemia, the cell membrane is hyper- urine potassium more than 20 mEq suggests RTA, DKA,
polarized secondary to an increase in the ratio of intra- diuretic use, hyperaldosteronism, and vomiting. A low
cellular to extracellular potassium, causing decreased urinary chloride level suggests decreased renal perfu-
membrane excitability and delayed conduction of the sion and secondary hyperaldosteronism.5 Plasma mag-
action potential. nesium and calcium levels should also be evaluated
The 2 most common causes of hypokalemia in the since regulation of potassium is affected by plasma lev-
ED setting are diuretic use and malnutrition associated els of these electrolytes.
with alcohol abuse. Other causes include inadequate in-
take (rare if other homeostatic mechanisms are not Treatment
affected), renal potassium wasting, increased extrarenal Treatment should focus on first addressing the
potassium losses, and transcellular shifts of potassium. ABCs, correcting the potassium deficit, and addressing
Often, a combination of factors contributes to the hy- the underlying disorder. Hypokalemia with ventricular
pokalemic state. Etiologies of renal potassium wasting dysrhythmia is a medical emergency. Hypokalemia
include osmotic diuresis, renal tubular acidosis (RTA), should also be treated aggressively in patients taking
nephrotoxic drugs, and magnesium deficiency. Hyper- digoxin and in patients with angina or myocardial in-
aldosteronism and Cushing’s syndrome can result in farction. A rule of thumb is that each potassium deficit
potassium depletion due to increased action of aldos- of 0.3 mEq/L reflects a total body potassium deficit of
terone on the kidney. Common causes of increased 100 mEq.7 It is preferable to administer potassium oral-
extrarenal potassium losses are cutaneous (sweating and ly. Intravenous infusions can cause hyperkalemia and
burns) and gastrointestinal (GI) losses. Vomiting also dysrhythmias. If potassium is administered at a rate of
contributes to hypokalemia by causing elevated aldos- more than 20 mEq/hr, cardiac monitoring is needed to
terone and alkalosis, which favors potassium excretion check for dysrhythmias. The maximum IV potassium
in the urine in exchange for HCO2 and sodium. replacement rate should be 0.3 to 1 mEq/kg/hr to a
Alkalemia, insulin excess, catecholamine excess, and maximum of 40 mEq/hr. Potassium should be ad-
cellular proliferation can cause hypokalemia by shifting ministered through a large vein, as it burns and is scle-
potassium into the cells. The rare familial syndrome of rosing.
hypokalemic periodic paralysis causes a transient Treatment for patients with a potassium deficit to
change in the internal balance of potassium. 2.5 mEq/L is 20–40 mEq KCL orally. For those with a
potassium level less than 2.5 mEq/L or less than
Diagnosis 3 mEq/L and on digoxin, treatment is 20 mEq KCL/hr
Mild hypokalemia (plasma potassium, 3–3.5 mEq/L) IV. If a patient is acidotic and hypokalemic, it is
is rarely symptomatic. In severe hypokalemia, symptoms advisable to first replace potassium before treating the
HYPERKALEMIA
Hyperkalemia is defined as plasma potassium greater Increasing spread of
than 5.5 mEq/L. It is the most deadly electrolyte distur- QRS and T
bance. The first manifestation of hyperkalemia may be a
Increasing serum K
life-threatening cardiac arrhythmia. Hyperkalemia de-
creases the ICF/ECF potassium concentration ratio, de- Absent P Wave
polarizing excitable tissues, decreasing conduction velo-
city, and increasing the rate of repolarization.8
Table 3. Drugs That May Cause Hyperkalemia functions such as muscular contractility, neurotransmis-
sion, and hormonal secretion. The majority (99%) of
Drug Mechanism body calcium is complexed to hydroxyapatite in bone,
Potassium supple- May cause hyperkalemia in con- serving as a dynamic reservoir of available calcium. Die-
ments junction with renal insufficiency, tary calcium is absorbed actively and passively in the gas-
potassium-sparing diuresis, diabetes trointestinal tract. Approximately 90% of plasma calcium
Potassium-sparing Inhibits potassium secretion in the is filtered through the kidneys and passively resorbed.
diuretics distal nephron Minute-to-minute plasma calcium levels are regulat-
Angiotensin- Causes relative hypoaldosteronism by ed by 3 hormonal mechanisms: vitamin D, parathyroid
converting enzyme inhibiting angiotensin II production hormone (PTH), and calcitonin. These hormones in-
inhibitors fluence intestinal absorption, renal resorption and ex-
Nonsteroidal anti- Diminishes renin release and may cretion, and internal mobilization of body calcium
inflammatory drugs inhibit aldosterone synthesis from bone. PTH is released in response to a fall in se-
Digitalis preparation Inhibits the Na+,K+-ATPase pump and rum calcium. It causes active renal resorption of calci-
overdose can inhibit potassium uptake by um and stimulates bone resorption by osteoclastic activ-
cells; therapeutic doses are not ity. PTH and sunlight also mediate hydroxylation of
associated with hyperkalemia dietary vitamin D into its active form, 1,25-dihydroxy-
Heparin Associated with hypoaldosteronism by cholecalciferol (1,25-DHCC), in the kidney and liver.
inhibiting aldosterone biosynthesis Activated vitamin D increases the intestinal absorption
Succinylcholine Prolongs muscle depolarization and of calcium. Calcitonin is released when serum calcium
enhances potassium efflux rises; it causes deposition of calcium into the skeleton
β Blockers Inhibits β2 stimulation of cellular and suppresses PTH release.
potassium uptake Normal serum calcium levels range from 8.5 to
10.5 mg/dL; however, only 40% to 50% of serum calci-
Adapted from Palevsky PM, Singer I. Disorders of potassium metabo- um is ionized, or physiologically active. (The normal
lism. In: Wolfson AB, editor. Endocrine and metabolic emergencies. range of ionized calcium is 2.1–2.6 mEq/L [1.0–
New York: Churchill Livingstone; 1990, with permission from Elsevier.
1.3 mmol/L]). The majority of plasma calcium is com-
Copyright © 1990.
plexed to serum anions (phosphate, bicarbonate, cit-
rate, lactate) and serum proteins (primarily albumin).
the potassium level is more than 6 mEq/L and ECG Although ionized calcium levels remain unchanged, the
manifestations of hyperkalemia are present. An asymp- ratio of bound serum calcium and ionized serum calci-
tomatic patient with a laboratory test result showing um is subject to change with decreased albumin states.
severe hyperkalemia should have a blood sample retest- Corrected serum calcium (in mg/dL) using serum albu-
ed and a simultaneous ECG. min levels can be calculated with the following formula:
Initial treatment of severe hyperkalemia is aimed at
Corrected serum calcium (mg/dL) =
preventing or reversing the deleterious effects of hyper-
(serum calcium [mg/dL] + 0.8) × (4 – serum albumin [g/dL])
kalemia on the myocardium. If ECG changes are pre-
sent, calcium is given intravenously as a temporizing Acid-base status influences the ratio of bound and
measure for membrane stabilization. Sodium bicarbon- ionized serum calcium. Acidosis decreases and alkalosis
ate, insulin (glucose is given simultaneously to prevent increases calcium binding to albumin.
hypoglycemia), and high-dose inhaled albuterol are
also used to shift potassium intracellularly. Kayexalate HYPOCALCEMIA
and diuretics actually correct the hyperkalemia by in- Etiology
creasing potassium excretion (Table 4). Acute hypocalcemia (ionized calcium level < 2.0 mEq/L
[< 1.0 mmol/L]) is rare in ambulatory patients.6 This dis-
order can result from decreased calcium intake, defi-
DISORDERS OF CALCIUM IMBALANCE ciency of the hormones that cause calcium release into
the blood, or chelation of calcium to substances that ren-
der the calcium inert. Primary hypoparathyroidism is
CALCIUM HOMEOSTASIS rare and is usually congenital. Typically, secondary hypo-
Plasma and intracellular calcium are strictly regulated parathyroidism is an iatrogenic complication of surgi-
because plasma and intracellular calcium mediate vital cal removal or vascular disruption during parathyroid,
IV = intravenous.
*Use as a bolus only if QRS is widened.
thyroid, or carotid surgery. Infiltration of the parathyroid Trousseau’s sign (carpal spasm after inflation of a blood
gland by metastasis or by infiltrative disorders destroys pressure cuff to 20 mm Hg above systolic blood
parathyroid tissue. Hypomagnesemia and hypermagne- pressure for 3 minutes) are signs of hypocalcemia. CNS
semia impair PTH release. manifestations of hypocalcemia include depression, con-
Vitamin D deficiency can cause hypocalcemia be- fusion, and seizures. Psychiatric symptoms include de-
cause of decreased absorption of dietary calcium but is pression, psychosis, and dementia. Bradycardia, hypoten-
rare in the United States because of milk fortification. sion, CHF, and cardiac arrest can result from decreased
However, lack of sunlight exposure, small bowel or bil- myocardial contractility.
iary disease, or pancreatic failure can decrease vita- Initial assessment should include measurement of
min D absorption. Many drugs can cause hypocalcemia, serum electrolytes, serum calcium, ionized calcium,
including cimetidine, phosphates, dilantin, loop diuret- and phosphate and an ECG. The ECG may demon-
ics, and glucocorticoids. Renal disease can result in lack strate a prolonged QT interval, although changes are
of activation of vitamin D. nonspecific.
Since calcium forms complexes with different sub-
stances, increased concentration of anions, proteins, Treatment
and fatty acids in the plasma can result in ionized hypo- Asymptomatic patients can be treated with oral calci-
calcemia. In hyperphosphatemia, the phosphate com- um supplementation. Severe presentations (seizure, dys-
plexes with serum calcium to cause hypocalcemia. rhythmias, hypotension) with high clinical suspicion for
Citrate (found in blood products as a preservative and hypocalcemia should be treated immediately. Sympto-
in contrast material), exogenous bicarbonate, and alka- matic patients should be treated with elemental calcium
losis enhance plasma binding of calcium. Hypocal- 100 to 300 mg IV in a monitored setting.9 (10% calcium
cemia can occur in pancreatitis as a result of calcium gluconate = 9.3 mg elemental calcium/mL and 10% cal-
complexing with free fatty acids. Fluoride forms com- cium chloride = 27.2 mg elemental calcium/mL). Cal-
plexes with calcium in cases of fluoride poisoning. cium is best administered through a central vein since it
Calcium can also move into cells as a result of cellular is sclerosing.
injury, as occurs in sepsis, shock, and burns. When treating hypocalcemia, serum magnesium
should be checked and corrected if low, since hypo-
Diagnosis magnesemia can cause refractory hypocalcemia. When
The clinical manifestations of hypocalcemia are pro- metabolic acidosis accompanies hypocalcemia, calcium
tean. In the ED, patients will usually have neuromuscular must be replaced before acidosis is corrected because
and cardiovascular signs and symptoms. Decreased se- calcium and hydrogen compete for protein-binding
rum calcium causes neuromuscular hyperexcitability. sites and an increase in pH could result in a rapid de-
Paresthesias, weakness, cramps, fasciculations, and tetany crease in ionized calcium and cardiac arrest. Patients on
are some peripheral neuromuscular signs. Latent tetany digoxin should be monitored carefully because calcium
elicited by Chvostek’s sign (spasm of the muscles of facial can exacerbate digoxin toxicity. In hyperphosphatemia,
movement when tapping over the facial nerve) and soft tissue calcifications can result when the product of
Clinical manifestations of hypomagnesemia are non- associated with respiratory depression, coma, and heart
specific, inconsistent, and variable in severity and do block. Treatment includes discontinuing magnesium
not correlate with plasma magnesium levels. Patients and forced diuresis. In severe cases, IV calcium is the
are usually symptomatic at magnesium levels less than first-line treatment to promote membrane stability.
1.2 mg/dL. Neuromuscular (muscle weakness, tremor, Dialysis is the definitive treatment in patients who have
hyperreflexia, and tetany) and cardiovascular (supra- kidney failure, dysrhythmias, and persistent hemody-
ventricular and ventricular dysrhythmias, including namic instability.
ventricular tachycardia, ventricular fibrillation, and tor-
sades de pointes) symptoms are the manifestations of
hypomagnesemia seen in the ED. Patients with CHF on DISORDERS OF PHOSPHOROUS IMBALANCE
diuretics are especially prone to hypomagnesemia and
vulnerable to its effects. Digoxin-induced dysrhythmias Phosphorous is found in the body in the form of
are more likely with hypomagnesemia. Hypomagnes- phosphate. It forms an essential component of nucleic
emia also complicates digoxin toxicity since magnesium acids, ATP, and hydroxyapatite in bone. In the serum,
is an essential cofactor for the Na+,K+-ATPase pump, phosphate serves a vital function as an acid-base buffer.
which is inhibited by digoxin. Phosphate abnormalities are rarely diagnosed in the
Serum electrolytes and calcium level should be as- ED, although they are not uncommon in very sick hos-
sessed. Hypomagnesemia can cause hypocalcemia since pitalized patients.
magnesium is required for normal synthesis and release Phosphate is absorbed by the intestines and kidney,
of PTH. It can also result in refractory hypokalemia stored in bone, and renally excreted. It is regulated by
since it is a cofactor in the Na+,K+-ATPase pump. Electro- PTH and vitamin D hormones. Vitamin D coregulates
cardiography should be done, although findings are phosphate, causing increased intestinal absorption of
nonspecific. phosphate and calcium. Approximately 90% of serum
Because the serum magnesium level is an inaccurate phosphate is passively reabsorbed in the proximal tu-
representation of intracellular magnesium, it should not bule of the kidney. PTH inhibits further absorption of
be used to guide therapy. If hypomagnesemia is suspect- phosphate in the distal tubules while increasing calcium
ed and the patient is symptomatic, treatment should be absorption. PTH also regulates calcium and phosphate
determined by severity of symptoms. Oral magnesium activation from bone.
can be given when symptoms are not severe. In patients
who are symptomatic, ABCs must first be addressed. A HYPOPHOSPHATEMIA
patient with dysrhythmia or seizures should be given IV This disorder is classified as mild (2.5–2.8 mg/dL),
magnesium. In patients with normal renal function, moderate (1.0–2.5 mg/dL), and severe (< 1 mg/dL).
25 to 50 mg/kg can be given initially.9 This should be Malnutrition is an uncommon cause of hypophosphat-
diluted and given over 30 to 60 minutes. Bolus adminis- emia because phosphate is ubiquitous in the diet. How-
tration can cause bradycardia, hypotension, and heart ever, up to 50% of alcohol abusers are hypophosphat-
block; therefore, magnesium should be administered emic. Important risk factors include DKA, malnutrition,
with caution in patients with heart block or renal insuf- diuretic or antacid therapy, sepsis, and alcoholism.
ficiency. Because most magnesium is excreted in the Causes can be categorized as disorders that increase
urine, restoring total body magnesium to normal levels renal excretion, decrease GI absorption, or shift phos-
can take days. phate from the serum into the cells (Table 6).
Manifestations of hypophosphatemia are usually
HYPERMAGNESEMIA hematologic and neuromuscular, resulting from im-
Significant hypermagnesemia is rare and is seen al- paired energy metabolism and production of ATP. Mild
most exclusively in the setting of renal insufficiency and hypophosphatemia is usually asymptomatic. With se-
accidental overdose (antacids and cathartics). Treat- vere hypophosphatemia, myocardial depression, hypo-
ment of toxemia or preterm labor with magnesium are tension, impaired responsiveness to vasopressors, and
iatrogenic causes of hypermagnesemia. Clinical mani- respiratory insufficiency are common. Other manifesta-
festations of hypermagnesemia correlate well with tions of hypophosphatemia include hemolysis, leuko-
serum levels. Early signs are nausea, vomiting, weak- cyte dysfunction, and decreased oxygen delivery to the
ness, cutaneous flushing, and hyporeflexia. At serum tissues.
levels of 5 to 6 mg/dL, hypotension and ECG changes Patients with mild to moderate hypophosphatemia
develop. Magnesium levels of more than 9 mg/dL are can be treated with oral phosphate supplements. Those
Copyright 2005 by Turner White Communications Inc., Wayne, PA. All rights reserved.