Transcript Electrolyte_Disturbances

Electrolyte Disturbances
Introduction
• Main electrolytes in the blood
– sodium, potassium, calcium, magnesium, chloride,
phosphate, and carbonate
• Most commonly, problems occur when the level
of sodium, potassium, or calcium is abnormal
• Levels can become high or low
• Often, electrolyte levels change when water
levels in the body change
Hypokalemia
• Most common electrolyte abnormality
• Definition < 3.6 mmol/L
– Most between 3.0 and 2.5 mmol/L
• >20% hospitalized patients (No
comparable data available for outpatients)
• Hypokalemia has been found in 20-40% of
those patients treated with diuretics
Hypokalemia
• Often asymptomatic and well-tolerated in
otherwise healthy individuals
• Can be life-threatening when severe
• May  the risks of morbidity and mortality in
patients with cv disease, even when mild or
moderate
 As a result, when identified it is important to
determine any underlying etiologies and treat
appropriately
Regulation of Potassium Balance
• Total body stores (intracellular and extracellular
fluid) are closely regulated by key hormones
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Insulin
β-adrenergic catecholamines
Aldosterone
Thyroid hormone
• Normal: High ratio of intracellular to extracellular
potassium
• Both insulin and β- adrenergic catecholamine 
cellular potassium uptake by stimulating cell
membrane Na+/K+-ATPase
Regulation of Potassium Balance
• Insulin: feedback system
– ↑↑ K+ stimulates insulin
– ↓↓ K+ inhibits insulin
• β-adrenergic: no feedback system
– β blockade ↑↑ serum K+
– β agonist ↓↓ serum K+
• Thyroid Hormone: + synthesis of Na+/K+ ATPase
• Aldosterone:
– ?? affects on the transcellular distribution of potassium
– major regulator of body stores of potassium via its effects on
the excretion of potassium by the kidney
Regulation of Potassium Balance
Clinical Manifestations of
Hypokalemia
• Often asymptomatic, usually when mild (3-3.5
mmol/L)
• Nonspecific symptoms with more severe
hypokalemia
– generalized weakness; lassitude; constipation
• Serum K+ < 2.5 mmol/L muscle necrosis
• Serum K+ <2.0 mmol/L ascending paralysis
and impairment of respiratory function
• Symptoms usually correlate with rapidity of 
serum K+
Hypokalemia and Cardiac
Manifestations
• In patients without underlying heart disease,
abnormalities in cardiac conduction is very rare,
even when the serum potassium <3.0 mmol/L
•  risk of development of a cardiac arrhythmia
(even with mild to moderate hypokalemia)
– heart failure, cardiac ischemia, and/or LVH
• Hypokalemia  the arrhythmogenic potential of
digoxin
Etiology of Hypokalemia
• Two main mechanisms:
1. Abnormal losses
• Increased renal potassium loss
• Excess potassium loss in stools
2. Transcellular potassium shift
• Drugs are the most common cause
Drug Induced Hypokalemia
• Transcellular Potassium Shift
– Β2-Adrenergic Drugs
• Increase Renal Potassium Loss
– Diuretics
– Mineralocorticoid/Glucocorticoid Effects
– Antibiotics
• Excess Potassium Loss in Stool
Β2-Adrenergic Drugs
• Bronchodilators
– a standard dose of nebulized albuterol ↓serum
K by 0.2 to 0.4 mmol/L
– second dose within one hour ↓ K by 1 mmol/L
• Decongestants
• Tocolytic Agents
– ↓ serum K to as low as 2.5 mmol/L after 4-6 hours
of IV administration
Drug-Induced Hypokalemia
Transcellular Shifts
• Xanthines
– Theophylline
• Severe hypokalemia with acute theophylline toxicity
– Caffeine
• Verapamil intoxication
• Chloroquin intoxication
– Inhibits potassium from exiting cells
• Insulin
– Moves potassium into cells
– Transient hypokalemia
– Intentional overdose of insulin; treatment of DKA
Thiazide and Loop Diuretics
• Most common cause of hypokalemia
• Block Cl-associated Na+ reabsorption ↑
delivery of Na+ to collecting tubules↑
Na+ reabsorption  ↑ K+ secretion
• Direct relation with dose
•  response of hypokalemia with more dietary
Na+ intake
Diuretics
• Furosemide or Bumetanide with
Metolazone  Moderate-Severe
Hypokalemia
• Associated mild to moderate alkalosis
• Acetazolamide promote K+ reabsorption
– Interferes with H+ linked sodium
reabsorption metabolic acidosis
Drugs with Mineralocorticoid or
Glucocorticoid Effects
• Fludrocortisone
– Oral mineralocorticoid
– promotes renal K+ excretion
– If used inappropriately can lead to K+ wasting
• Prednisone and Hydrocortisone
– Glucocorticoids
– indirectly  K+ secretion via effect on filtration
rate and distal sodium delivery
– ↓ by 0.2 to 0.4 mmol/L
Other drugs causing renal wasting
of potassium
• High dose antibiotics
–  Na+ delivery to nephrons
– PCN, Naficillin, Ampicillin, Carbenicillin
• Drugs assoiciated with Mg depletion
– Aminoglycosides
– Cisplantin
– Foscarnet
– Amphotericin B
Non-Drug Causes of Hypokalemia
• Transcellular shifts
• Inadequate dietary intake
• Abnormal losses of potassium
– Looses in stool
– Loss through the kidney
Non-Drug Causes Due to
Transcellular Shifts
• Hyperthyroidism
– Severe <3.0 mmol/L 
sudden onset of severe
muscle weakness and
paralysis
– 2 to 8% of patients with
hyperthyroidism in Asian
countries
• Familial Hypokalemic
Periodic Paralysis
– autosomal dominant
– Mutations of gene
encoding the
dihydropyridine receptor
– Sudden attacks of muscle
paralysis, K+ < 2.5 mmol/L
– Provoked by high intake of
CHO, sodium, or by
exertion
– Subside < 24 hours
Non-Drug Causes Due to
Transcellular Shifts
• Delirium tremens
– Abrupt ↓ serum K+ by
1mmol/L
– Β2-adrenergic stimulation
• Barium compounds
– Block exit of K+ from cells
– Vomiting and diarrhea
– Muscle weakness,
paralysis, rhabdomyolysis
• Severe pernicious
anemia
– Treatment with vitamin
B12 rapid uptake of
K+ by new cells
formed
– Transfusion with
frozen washed red
cells
Non-Drug Causes Due to
Inadequate Dietary Intake
•  potassium intake by <1gram/day (25
mmol/day)
• Renal excretion of potassium fails to
decrease promptly
• With starvation or near-starvation
depletes body K+ stores compensated
by tissue breakdown that releases K+
Non-Drug Causes Due to Abnormal
Losses of Potassium
• Stool losses
• Renal losses
– Metabolic Alkalosis
• Chloride sensitive: vomiting, nasogastric drainage
• Chloride insensitive: hyperaldosteronism, Cushing’s syndrome
• Genetic abnormalities: Liddle’s syndrome, 11β-hydroxysteroid
dehyrogenase deficiency, Bartter’s syndrome, Gitelmans’s
syndrome
– Metabolic Acidosis
• Type I or classic distal renal tubular acidosis
• Type II or proximal renal tubular acidosis
Treatment of Hypokalemia
• Potassium replacement
• Note, that supplemental potassium
administration is the most common cause of
severe hyperkalemia in hospitalized patients
• Greatest risk with IV replacement
– If given, rate should be no more than 20 mmol/hour
and monitor cardiac rhythm
• PO administration safer because enters
circulation slower
Treatment of Hypokalemia
• On average, serum potassium  by 0.3
mmol/L for each 100 mmol reduction in
total body stores
• A portion of administered potassium is
always excreted, even in presence of
serious potassium depletion
Treatment of Hypokalemia
• Three salts available
– Potassium chloride
– Potassium phosphate
– Potassium bicarbonate
• KCl most often used because of its unique
effectiveness with the most common cause of
potassium depletion
• Liquid or tablet form of KCl available
• Initially, 1 mcg of KCL  serum K+ by 0.1 mmol/L
Treatment of Hypokalemia
• Typically, 40 to 100 mmol of supplemental K+
each day to maintain wnl serum K+ with daily
use of diuretics
• Hypokalemia persists in patients taking diuretics
despite aggressive potassium replacement in
10% of patients
• May add a 2nd diuretic that inhibits K+ excretion
– Amiloride, triamterene, or spironolactone
Hyperkalemia
• Diagnosed in up 8% of hospitalized patients
• Primary cause of morbidity and death is
potassium's effect on cardiac function
• Mortality rate can be as high as 67% if severe
hyperkalemia is not treated rapidly
• Hyperkalemia is defined as a potassium level
>5.5 mEq/L
5.5 - 6.0 mEq/L
6.1 - 7.0 mEq/L
7.0 mEq/L and greater
Mild
Moderate
Severe
Causes of Hyperkalemia
•  or impaired K+ excretion
– acute or chronic renal failure (most common)
– K+ sparing diuretics, urinary obstruction, sickle cell
disease, Addison disease, and SLE
• Additions of potassium into extracellular space
– K supplements, rhabdomyolysis, hemolysis
• Transmembrane shifts
– acidosis and medication effects (eg, acute digitalis
toxicity, BB, succinylcholine)
• Factitious or pseudohyperkalemia
– improper blood collection, lab error, leukocytosis, and
thrombocytosis
Clinical Manifestation
• Hyperkalemia frequently discovered as an incidental
laboratory finding
• However may experience:
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Generalized fatigue
Weakness
Paresthesias
Paralysis
Palpitations
• EKG findings
– Early: peaked T waves, shortened QT interval, and ST segment
depression
– Later: bundle branch block, resulting in widened QRS, increases in
the PR interval, and decreased amplitude of the P wave
Hyperkalemia
Approach to Hyperkalemia
• Is this a true measurement?
– Look at prior measurements
– Repeat stat
• Is patient symptomatic or have underlying
reason to explain for the ↑↑ K+?
– Renal insufficiency
– Medications (BBlockers, K+sparing diuretics, K+
supplements, digitalis)
• EKG findings?
Approach to Hyperkalemia
• ABC’s
• IV access and cardiac monitor
• EKG
• Discontinue any potassium-sparing drugs or
dietary potassium
• If the hyperkalemia is severe (>7.0 mEq/L) or
the patient is symptomatic begin treatment, do
not wait for tests
– Individualize treatment based upon the patient's
presentation, potassium level, and EKG
Treatment of Hyperkalemia
• Calcium gluconate
– Stabilizes cell membrane
– 2 amps IV; onset few minutes
• Insulin
– Drives K into cells
– 10 units regular + 1-2 amps D5W; onset 15-30min
• Bicarbonate
– Drives K into cells in exchange for H
– 1-3 amps IV; onset 15-30 minutes
• Kayexlate
– Exchanges Na for K in GI tract
– 30-90 grams po/pr; onset 1-2 hours
• Diuretics
– Furosemide ≥ 40 mg IV; onset 30 minutes
• Hemodialysis
Sodium and Water Homeostasis
• Disorders of sodium are generally due to
changes in total body water, not body sodium
• Two key hormones:
– Antidiuretic hormone (ADH)
• Primary hormone regulator of sodium concentration
– Aldosterone
• Primary hormone regulator of total body sodium (and
therefore volume)
Antidiuretic Hormone (ADH)
• Stimuli for secretion: hyperosmolality, ↓↓ effective
arterial volume (EAV)
• Action: open water channels in collecting ducts 
passive water reabsorption into medulla
• Urine osmolality- indirect assay of ADH activity
– Uosm range 60 mOsm/L (no ADH activity) to 1200
mOsm/L (max ADH activity)
• ↑↑ ADH = Syndrome of inappropriate ADH (SIADH)
• ↓↓ ADH = Central diabetes insipidus
Aldosterone
• Stimuli for secretion:
– hypovolemia (via renin and angiotensin II)
– hyperkalemia
• Action: isoosmotic reabsorption of sodium in
exchange for potassium or H+
• ↑↑ aldosterone = Conn’s Syndrome ( HTN,
hypokalemia, metabolic alkalosis)
• ↓↓ aldosterone = hypovolemia, hyperkalemia,
metabolic acidosis
Hyponatremia
• A common clinical problem and frequently
develops in hospitalized patients
• Although morbidity varies widely in severity,
serious complications can arise form the
disorder itself as well as from errors in
management
• Defined as the excess of water relative to
sodium
• A  serum sodium concentration <136 mmol/L
Approach to Hyponatremia
•
FIRST, determine tonicity
– Isotonic
•
Rare laboratory artifact due to hyperlipidemia or
hyperproteinemia check lipid panel and/or lft’s
– Hypertonic
•
Excessive presence of other effective osmole
– Glucose, mannitol, or glycine
– For each 100 mg/dL rise in glucose above 100 mg/dL
the Na ↓ 1.6 mEq/L
– Hypotonic
•
True excess of water relative to sodium
Approach to Hyponatremia
•
NEXT, if true excess of water relative to
sodium, in other words, hypotonic
hyponatremia, determine volume status
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•
Hypovolemic
Euvolemic
Hypervolemic
Vital signs, orthostatics, JVP, skin tugor,
mucous membranes, peripheral edema, BUN,
Cr, uric acid
Hypotonic Hyponatremia
• Three categories:
– Hypovolemic Hypotonic Hyponatremia
– Euvolemic Hypotonic Hyponatremia
– Hypervolemic Hypotonic Hyponatremia
Hypovolemic Hypotonic
Hyponatremia
• Primary Na loss secondary H20 gain
• Determine renal vs. extrarenal losses
– UNa > 20 mEq/L = renal losses
• Diuretics
• Hypoaldosteronism
• Salt-wasting nephropathy
– UNa < 10 mEq/L = extrarenal losses
• GI losses
• Third-spacing
• Insensible losses
Hypervolemic Hypotonic
Hyponatremia
• Determine if there is a ↓ EAV or advanced
renal failure
• UNa < 10 mEq/L = ↓ EAV
– CHF (↓ CO)
– Cirrhosis (ascites)
– Nephrotic Syndrome (hypoalbuminemia
edema)
• UNa > 20 mEq/L = advanced renal failure
Euvolemic Hypotonic
Hyponatremia
• Primary H2O gain
• Determine whether SIADH or ADH
suppression
– Uosm>100 = SIADH
– Uosm <100 = psychogenic polydipsia
• >12- 20 L/day
– Uosm variable = ADH physiology reset to
regulate lower serum Na concentration
Etiology of SIADH
• Endocrine
– Hypothyroidism, Adrenal Insufficiency
• Pulmonary
– Pneumonia, Asthma, COPD, pneumothorax
• CNS
– Trauma, infection, hemorrhage, hydrocephalus, CVA,
demyelinating diseases, acute psychosis
• Malignancy
– Small cell lung cancer, intracranial tumors
• Drugs
– Thiazides, antidepressants, antipsychotics
• Others: Post-operative state, pain, nausea
Approach to Hypotonic
Hyponatremia
Clinical Manifestation of
Hyponatremia
• Severity of symptoms related to how rapid and
to what degree the hyponatremia develops
• Often with Na+ >125 asymptomatic or may
have nonspecific symptoms
– Headache, nausea, vomiting, muscle cramps,
lethargy, restlessness, disorientation, depressed
reflexes
• More severe or rapidly developed hyponatremia
– Seizures, coma, permanent brain damage, respiratory
arrest, brain-stem herniation, and possibly death
Management of Hyponatremia
• The optimal treatment of hypotonic
hyponatremia requires balancing the risks of
hypotonicity against those of therapy
• The presence of symptoms and their severity
largely determine the pace of correction
• Too rapid correction  ↑ serum osmolality in
setting of low brain osmolality  rapid water egress
 acute brain dehydration  central pontine
myelinosis
Management of Hyponatremia
• No consensus about the optimal treatment of
symptomatic hyponatremia
• Most reported cases of osmotic dymyelination
occurred after corrections of only 9 to 10 mmol/L
in 24 hours or 19 mmol/L in 48 hours
• Targeted rate of correction that does not exceed
8 mmol/L on any day of treatment
• The initial rate of correction can still be 1 to 2
mmol/L/hour x several hours in patients with
severe symptoms
Management of Hyponatremia
• Hypovolemic Hyponatremia
– Volume replacement, often with 0.9%NaCl
• Hypervolemic Hyponatremia
– Sodium (1-3 g/day) and water (1.0-1.5 L/day) restriction
• SIADH
– Free water restriction
– If chronic demeclocycline
– If neurologic emergency loop diuretic + hypertonic
saline
Calculating fluid replacement
In cases of hypovolemic or severe SIADH with
neurological manifestations . . .
1. Calculate Na+ deficit:
NA deficit= 0.6 x ideal body weight x (140 –
measured Na) (x 0.85 for women)
2. Choose appropriate infusate
3. Calculate # liters of chosen saline required
4. Calculate rate of infusion, keeping in mind the
danger of correcting too fast and at the same
time the consequences of the untreated
hypotonicity
CASE 1
• A 58 year-old man with small cell lung cancer
presents with confusion and lethargy. Clinically
euvolemic. IBW 80 kg.
• LAB: Na 112, K 3.9, Cr 0.5, Serum Osm 220,
Uosm 600, TSH 2.3, random serum cortisol 24
• How do you classify this patient’s hyponatremia?
Euvolemic Hypotonic Hyponatremia
Tumor-Induced SIADH
• How do you manage this patient?
CASE 1
1. Calculate Na deficit
0.6 x 80 x (120-112)= 384 mEq of Na
2. Choose infusate
3% NaCl (513 mmol/L of Na)
3. Calculate # liters of 3% NaCl required
384 mEq Na / 513 mmol/ L Na= 750 ml
4. Determine rate of infusion
750cc/24 hour= 31ml/hr
Hypernatremia
• Whereas, hyponatremia can be associated
with low, normal, or high tonicity
hypernatremia always denotes
hypertonicity
• Deficit of water relative to sodium
• Almost always due to loss of hypotonic
fluid and impaired access to free water
• Hypernatremia is a powerful thirst stimulus
Approach to Hypernatremia
• Determine volume status
– Hypovolemic
– Euvolemic
– Hypervolemic
Approach to Hypernatremia
• Determine volume status
– Hypovolemic, euvolemic water loss 
check Uosm
• Uosm <300
• Uosm 300-600
• Uosm >600
complete DI
renal H20 losses, partial DI,
reset osmostat
extrarenal H2O losses
– Hypervolemic  Na retention
• Exogenous NaCl infusion
• Mineralocorticoid excess
H20 loss and Hypernatremia
• Diabetes insipidus
– Central
• CNS trauma, surgery, hemorrhage, infection, granulomas,
tumor, idiopathic
– Nephrogenic
• Drugs: lithium, amphotericin, demeclocycline
• Metabolic: hypercalcemia, severe hypokalemia
• Others: polycystic kidney disease, sickle cell, Sjogren’s
syndrome, sarcoid, amyloid
• Renal losses: diuretics, osmotic diuresis
(glucose, urea, mannitol)
• Extra-renal losses: GI or insensible losses
Treatment of Hypernatremia
• Avoid rapid correction
– ↓ serum osmolality in setting of high brain osmolality water
ingress cerebral edema
• Hypovolemic Hypernatremia
– Replace volume & free water deficit
– Free water deficit= 0.6 x ideal body weight x [(measured
Na/140)-1] (x 0.85 for female)
• Hypervolemic Hypernatremia
– Loop diuretic + D5W
• DI
– Central DI: desmopressin (dDAVP)
– Nephrogenic DI: treat underlying cause; salt restriction +
thiazide diuretics
Calcium Homeostasis
• 40% of the calcium is bound to protein
• 50% is ionized and is in physiologic active
form
• Remaining 10% complexed to anions
• Corrected total calcium (mg/dL) =
(measured total calcium mg/dL) + 0.8 (4.4 measured albumin g/dL)
Calcium Homeostasis
• Three major hormones involved in calcium homeostasis
– parathyroid hormone (PTH)
– 1,25-dihydroxyvitamin D (calcitriol)
– Calcitonin
• PTH directly targets the bone and the kidneys to serum
calcium levels. Indirectly, through vitamin D, it causes
intestinal calcium absorption
• Vitamin D directly targets GI absorption of calcium to
increase calcium levels
• Calcitonin lowers calcium by targeting bone, renal, and
GI losses
Hypercalcemia
• Primary hyperparathyroidism
– most common cause
– occurs in 25 per 100,000 persons in the general
population and in 75 per 100,000 hospitalized
patients
• Hypercalcemia has been reported to occur in up
to 20 to 30% of patients with cancer
• The detection of hypercalcemia in a patient with
cancer signifies a very poor prognosis;
approximately 50% of such patients die within 30
days
Causes Of Hypercalcemia
• Hyperparathyroidism
– Primary: adenoma (80%), hyperplasia (15-20%),
carcinoma (<1%)
– Secondary: response to hypocalcemia
– Tertiary: long standing secondary autonomous nodule
develops
• Malignancy
– Local osteolytic (breast, melanoma)
– Solid tumor secreting PTH-related peptide (SC lung Ca,
RCC)
– Hematologic via ↑1,25-D and cytokines (Bcell lymphomas)
Causes Of Hypercalcemia
• Vitamin D excess (↑1,25-D)
– Granulomatous diseases (TB, sarcoidosis, histo,
cocci, crypto)
– Vitamin D intoxication
• ↑ bone turnover Hyperthyroidism, immobilization,
Paget’s disease
• Others: Thiazides, Vitamin A, Milk-Alkali
Syndrome
Clinical Manifestations of
Hypercalcemia
• “Bones, stones, abdominal groans, and psychic
moans” usually when Ca>12
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Osteopenia and osteitis firbrosa cystica
Neprholithiasis, nephrocalcinosis, nephrogenic DI
Abdominal pain, N/V/C, anorexia
Pancreatitis, PUD
Fatigue, depression, confusion
Decreased DTRs
Short QT intervals
• Hypercalcemia crisis (Ca 13-15)
– Polyuria, dehydration, mental status changes
Treatment of Hypercalcemia
• Aggressive IVF
– NS @ 200-500 cc/hour, depending on the patient’s
cardiovascular status and renal function
• Aggressive calciuresis with loop diuretics, after
normvolemia has been restored
• IV bisphosphonates to inhibit bone reabsorption
– Pamidronate 60 to 90 mg IV over 2 hours
– Zoledronate 4mg IV over 15 minutes
• Treat underlying disease process
Hypocalcemia
• Probably more common than hypercalcemia
• Reported in 15-50% ICU patients
• Severe, symptomatic hypocalcemia may result
in cardiovascular collapse, hypotension
unresponsive to fluids and vasopressors, and
dysrhythmias
• Clinically evident hypocalcemia generally
presents in milder forms and is usually the result
of a chronic disease state
Etiologies of Hypocalcemia
• Hypoparathryoidism
– PGA type I (chronic mucocutaneous candidiasis +hypothyroid +
Addison’s)
– s/p thyroidectomy, hypomagnesiumia
• Pseudo-hypoparathyroidism
– PTH end-organ resistance; normal Ca
– Skeletal abnormalities & retardation
• Vitamin D deficiency
• Renal Failure
– ↓ 1,25- (OH)2D3 production + ↑ PO4  ↑calcium deposition in soft
tissue
• Others
– Pancreatitis, citrate excess (multiple transfusions)
Clinical Manisfestations of
Hypocalcemia
• Neuromuscular irritability
– Chvostek sign
• tapping facial nerve contraction of facial muscles
– Trousseau sign
• inflation of a blood pressure  carpal spasm
– Perioral paresthesias, cramps, laryngospasm
• Irritability, depression, psychosis, ↑ICP, seizures
• EKG: ↑ QT
• Renal osteodystrophy
– ↓ vit D & ↑ PTH in renal failure osteomalacia (↓ bone
mineralization), osteitis fibrosa cystica, osteoporosis
Treatment of Hypocalcemia
• Symptomatic IV Ca gluconate
• Asymptomatic oral Ca and vitamin D
• In renal failure calcitriol (1,25- (OH)2D3)
• In hypoparathyroidism PTH
supplementation not available, therefore give
calcitriol
Magnesium
• 4th most common cation in the body
• A central electrolyte in a large number of cellular
metabolic reactions
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DNA and protein synthesis
Neurotransmission
Hormone-receptor binding
A component of GTPase and a cofactor for Na+/K+–
ATPase, adenylate cyclase, and phosphofructokinase
– Necessary for the production of parathyroid hormone
• Absorbed in the small bowel, mainly in the ileum
• Excreted in stool and urine, but regulation of
serum magnesium is under renal control
Hypomagnesemia
• Etiology
– GI losses
• Malabsorption of magnesium in the ileum results in
GI secretions in large amounts
– Malnutrition
– Renal losses
• Primary renal disorders
• Drugs (diuretics, cisplantin)
• Endocrine disorders (primary aldosteronism,
hypoparathyroidism
Hypomagnesemia
• Symptoms are nonspecific
– <1.8 mEq/L (reference range 1.8-3 mEq/L)
– Weakness, muscle cramping, or rapid heartbeats; AMS
– Less severe cases may result in vertigo, ataxia,
depression, and seizure activity
• Primary clinical findings are neuromuscular
irritability, CNS hyperexcitability, and cardiac
arrhythmias
• Treatment
– Oral for mild; IV for severe
– magnesium oxide, magnesium hydroxide, magnesium
gluconate
Phosphate
• A ubiquitous intracellular anion that is essential
for membrane structure, energy storage and
transport in all cells
– ATP production
– Red blood cells for production of 2,3diphosphoglycerate (2,3-DPG)
• Normal range: 2.5-5 mg/dL
• Hypophosphatemia
– mild (2-2.5 mg/dL)
– moderate (1-2 mg/dL)
– severe (<1 mg/dL or 0.3 mmol/L).
Hypophosphatemia
• Etiology
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–
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Alcohol withdrawal
During treatment of DKA
Chronic alcoholism
Chronic ingestion of phosphate-binding antacids
TPN with inadequate phosphate supplementation
• Symptoms
– Weakness- most common
– Neurologic symptoms vary; ranging from simple
paresthesias to profound alterations in mental status
Hypophosphatemia
• Treatment
– Mild to moderately severe and asymptomatic
• may require oral replacement
• correcting factors that led to the hypophosphatemia usually is
sufficient
– Minimal symptoms or moderate hypophosphatemia
(serum phosphate 1-2 mg/dL)
• po phosphate replacement may be desirable
– Symptomatic or with serum phosphate levels
<1mg/dL
• require IV phosphate replacement
Hyperphosphatemia
• > 5 mg/dL in adults or 7 mg/dL in children or
adolescents
• Phosphorus load (from GI absorption,
exogenous administration, or cellular release)
exceeds renal excretion and tissue uptake
• Majority are ESRD
• ~250,000 persons are affected
• Muscle cramping secondary to low calcium
levels- most common complaint; may progress
to tetany, delirium, and seizures
Hyperphosphatemia
• Etiology
– Renal insufficiency (acute or chronic)
–  catabolism or cellular injury (rhabdomyolysis
,trauma, shock, exhaustive exercise, prolonged
immobilization, massive hemolysis, severe infections)
– Endocrinopathies (hypoparathyroidism, acromegaly,
thyrotoxicosis)
– Poisioning or excessive intake or administration
(bisphosphonate, oral/rectal laxatives, enemas,
hyperalimentation, transfusion of outdated blood)
– Neoplasms (leukemia, lymphoma, bone tumors, tumor
lysis after chemotherapy)
Hyperphosphatemia
• Treatment
– Oral phosphate binders ( the highly efficient GI
absorption of phosphorus)
– Calcium salts are widely used but produce
hypercalcemia
– Aluminum salts are effective binders but induce
aluminum toxicity
– Newer compounds containing iron or bile acid
sequestrants are replacing calcium and aluminum
binders
Remember . . .
• K of 4
• Phosph of 3
• Mg of 2
References
• Adrogue HJ, Madias NE. Hyponatremia. NEJM
2000;342:1581-89.
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