Diagnosis and

Management of
Common Electrolyte
Disorders
Aboubakr. O Aldhib
 Objectives
To discuss diagnostic and
therapeutic strategies for:

1. Hyponatremia
2. Hypernatremia
3. Hyperkalemia
4. Hypokalemia
5. Hypercalcemia
6. Hypocalcemia
2
 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)

3
 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
4
 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
5
 Case 1

• 60 year old man

• “Admit for weakness and
hyponatremia”
• [Na+] 120 mg/dL

6
7
 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 <135 mmol/L

8
 Approach to
hyponatremia
• FIRST, determine tonicity
– Isotonic
• Rare laboratory artifact due to hyperlipidemia or
hyperproteinemia, Multiple myeloma  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

9
 Cont..
• NEXT, if true excess of water relative to
sodium, in other words, hypotonic
hyponatremia, determine volume
status
– Hypovolemic
– Euvolemic
– Hypervolemic

• Vital signs, orthostatics, JVP, skin

tugor, mucous membranes,
peripheral edema, BUN, Cr, uric acid
10
 Hypotonic
hyponatremia
• Three categories:
– Hypovolemic Hypotonic Hyponatremia
– Euvolemic Hypotonic Hyponatremia
– Hypervolemic Hypotonic Hyponatremia

11
 Hypovolemic hypotonic
hyponatremia
• Primary Na loss  secondary H2O 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
12
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
13
 Euvolemic Hypotonic
Hyponatremia
• Primary H2O gain
• Determine whether SIADH or ADH
suppression
– Uosm>100 = SIADH “In patients with
SIADH, urine osmolality is often higher
than serum osmolality.”
– Uosm <100 = psychogenic polydipsia
• >12- 20 L/day

– Uosm variable = ADH physiology reset to14

regulate lower serum Na concentration
 Etiology of SIADH
• Endocrine
– Hypothyroidism.
• Pulmonary
– Pneumonia (which organism?)
• 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

15
16
 Clinical Evaluation
• History
– Symptomatic?
– Predisposed?
– Medications? IVF’s?
• Physical
– Volume status?
• Labs
– Confirm (if unusually abnormal)
– Context
– Additional diagnostic tests

17
 Case 1 (cont’d)
• Nausea, weak, confused x 1 week
• HTN, CHF
• JVD, crackles (rales), edema
– Na+ 120 mEq/L
– BUN 93 mg/dL
– Cr 3 mg/dL
– Glucose 135 mg/dL
– Albumin 2.9 mg/dL
– Plasma osm 252 mOsm/kg
– Urine osm 690 mOsm/kg

18
 “Choose the most
appropriate treatment”
• 3% I.V. NaCl
• 0.9% I.V. NaCl
• 50 mg hydrochlorothiazide daily
• Salt and water restriction
• Demeclocycline

19
Differential diagnosis

20
Hyponatremia usually
reflects excessive H20
 Common Differential Dx
• Decreased Water • Addison’s Disease
Excretion • Malnutrition
GFR • *Pseudohyponatremia
Kidney perfusion • ±Psychogenic (>1 L /
– SIADH hour)

*100mg/dL glucose increase  1.6 mEq/L [Na] decrease

± Urine specific gravity < 1.003

22
23
 COMMON CAUSES of HYPONATREMIA

Volume Status

Low Normal High

SIADH
CHF
GI/Renal Losses Hypothyroidism
Nephrotic Syndrome
Diuretics Adrenal Insufficiency
Cirrhotic
Thiazide

Hypoosmolar (serum osm <270) Hypoosmolar Hypoosmolar

Renal: Urine [Na] > 20 Renal: Urine [Na] > 20

SIADH: Urine Osmolality > 100*)
GI: Urine [Na] < 20 Non-Renal: Urine [Na] <20

1. History: predisposing features

2. Exam: volume status (including orthostatics supine/standing)
3. BMP; Urinalysis; Serum Osmolality; (Urine Sodium; Urine Osmolality)
4. Head C.T. (if symptomatic)
5. Other imaging/labs to evaluate CV, Renal, Endocrine systems as needed 24
 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

25
• 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 
osmotic demyelination syndrome

26
 Complications of
Treating Hyponatremia
• Delayed treatment
– Cerebral edema
– Permanent neurological injury
– Death
• Inappropriately rapid treatment
– Cerebral dehydration/demyelination
– Permanent neurological injury
– Death
• Inappropriate treatment
– Failure to improve  morbidity
– Delayed improvement  morbidity
– Further deterioration

27
• No consensus about the optimal treatment of symptomatic
hyponatremia “Go with your Local policy”

• Most reported cases of osmotic dymyelination occurred after

corrections of only 9 to 10 mmol/L in 24 hours or 18-19
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

28
 Common Treatment
Options
• Water restriction
• Diuresis (with loop diuretic)
• Volume infusion (with crystalloid)
• Hypertonic saline
• Demeclocycline

29
 What if he had cerebral
edema?
1. Correct [Na+] to 125-130mEq/L
to temporarily relieve edema
2. [Na+] should NOT increase by
more than 10-12 mEq/L in 1st 24
hours
3. Slow/Stop infusion as soon as
symptoms improve
30
 3% NaCl Calculation
[Na+] = 116 mEq/L
Goal [Na+] = 125 mEq/L at 24 hours
Amount of Na+ to be given as 3% infusion:
= [Serum Na+ (desired) – Serum Na+(measured) ]*(TBW)
= [125 – 116] [(0.5)(60kg)]
= 270 mEq Na+
3% saline = 513 mEq sodium/L
270/513 = 0.5 L = 500 ml over 24 hrs.
31
 Case scenario
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?

32
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 the rate of infusion
“Infusion pump”
750cc/24 hour= 31ml/hr
33
Hyponatremia: Key
Points
• Excess water
• If symptomatic,
treat early, but with
• Slowly correct rate
[Na+] *towards*
normal

• Find the underlying

cause and Mx
accordingly 34
 Case 2
• 40 y/o woman s/p hypertensive
brain hemorrhage 2 weeks ago.
• This morning she’s less
responsive.
• What may have caused this new
problem?

35
• Stuporous
• BP 150/70, HR 94
• Dry mouth, poor turgor
• Na 160 mEq/L; K 2.8 mEq/L;
HCO3: 18 mEq/L; Cl 137 mEq/L

36
Differential diagnosis

37
 Hypernatremia usually
reflects insufficient H2O
 Differential Diagnosis
• Lack of water
• Severe diarrhea
• Severe burns
• H2O excretion
–Osmotic diuresis
• H2O conservation
–Diabetes insipidus
39
 Guidelines for
Hypernatremia Rx
• Determine and treat likely cause(s)
• Most common error is
“underguesstimation” of water deficit:
TBW x ([Na+(measured)] – [Na+(desired) ])/[Na+ (desired) ]

• Replace H2O enterally if possible

• Frequent monitoring

40
• 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
41
 Sodium Content of
IVF’s (mEq/L)
• 3% saline: 513
• 0.9% (normal) saline: 154
• Ringer’s Lactate: 130
• Half Normal (0.45%) saline: 77
• 5% Dextrose (D5W): 0

42
Hypernatremia: Key
Points
• [Na+] >145 mEq/L

• Net water loss

• Calculate the water

deficit

43
 Case 3
• 29 y/o man with severe muscle
weakness.
• No vomiting or diarrhea.
• Normal physical exam.

44
• Na = 141 mEq/L
• K = 1.4 mEq/L
• Cl = 116 mEq/L
• HCO3- = 11 mEq/L
• pH = 7.25, pCO2 = 21 mmHg

45
 The most
• Most common electrolyte abnormality in hospitalized pt
“also HypoNa+” > and those are Life-threatening.

• 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

46
 Regulation of
Potassium Balance
• Total body stores (intracellular and extracellular fluid)
are closely regulated by key hormones
– 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

47
48
• 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 > One of manifestations of

Thyrotoxic crisis > HypoK+

• 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

49
50
 Consequences of
Hypokalemia [K] <3
• Neuromuscular manifestations
– Weakness, fatigue, rhabdomyolysis,
myonecrosis, respiratory failure
• GI symptoms
– Constipation, paralytic ileus
• Nephrogenic Diabetes Insipidus
• Dysrhythmias (if heart disease)
• Hypokalemia  the risk of hepatic
encephalopathy in cirrhotic patients.

51
 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

52
 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
53
 Drug Induced
Hypokalemia
• Transcellular Potassium Shift
– Β2-Adrenergic Drugs
– Metabolic Alaklosis

• Increase Renal Potassium Loss

– Diuretics
– Mineralocorticoid/Glucocorticoid Effects
“Conn’s/Cushing syndromes”
– Antibiotics

• Excess Potassium Loss in Stool

54
 Common Causes of
Hypokalemia
• Malnutrition/NPO
• Diarrhea (100 mEq/L)
• Vomiting (volume depletion)
• DRUGS
– Thiazides (stimulate excretion)
– Loop diuretics
– Amphotericin B
– Penicillins
– Gentamicin
– Foscarnet
55
 “Choose the most likely
diagnosis”
• Bartter’s syndrome
• Laxative abuse
• Primary aldosteronism
• Diuretic abuse
• Distal renal tubular acidosis

56
 Less Common Causes
• Hormonal
– Primary hyperaldosteronism
• Adenomas, hyperplasia, ectopic ACTH, ectopic
mineralocorticoid (licorice, chaw)
– Secondary hyperaldosteronism
• Renal hypoperfusion (CHF, RAS, severe HTN)
• Renin-secreting tumor
• Renal tubular disease
– Type 1 or 2 RTA
– Bartter’s syndrome (metabolic alkalosis, polyuria)
– Chronic magnesium depletion
• Laxative abuse (metabolic alkalosis)
57
 Non-Drug Causes Due
to Transcellular Shifts
• Hyperthyroidism • Familial Hypokalemic
Periodic Paralysis
– Severe <3.0 mmol/L
– autosomal dominant
 sudden onset of
– Mutations of gene
severe muscle
encoding the
weakness and dihydropyridine receptor
paralysis
– Sudden attacks of
– 2 to 8% of patients muscle paralysis, K+ <
with hyperthyroidism 2.5 mmol/L
in Asian countries – Provoked by high
intake of CHO, sodium,
or by exertion
– Subside < 24 hours

58
• Severe pernicious
anemia
– Treatment with
vitamin B12 rapid
uptake of K+ by
new cells formed
– Transfusion with
frozen washed red
cells

59
 Hypokalemia Rx
• Recognize likely total body depletion
– 1 mEq/L decrease = 150-400mEq total
deficiency
• Gradual oral replacement
• I.V. replacement if serum level less
than 3 mEq/L
• Check & Replace magnesium

60
Hypokalemia: Key Points
• [K+] < 3.5: review
medications, review
health status
• [K+] < 3: start
intervention
• Recognize Mg+ is
cofactor
• Renal/CV monitoring

61
 Case 4

• 59 y/o man with 3-days malaise,

decreased mental acuity and
responsiveness, slurred speech.
• ESRD on hemodialysis; HTN, DM,
Hypothyroidism

62
• Disoriented and lethargic
• BP (supine) 148/79mmHg, HR
101/min (supine) RR 26/min, T
37.7oC.
• Mucous membranes are moist, neck
veins are distended. Bilateral
crackles and wheezes. Loud S4.
3+ peripheral edema.

63
64
65
• 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 Mild

6.1 - 7.0 mEq/L Moderate
7.0 mEq/L and greater Severe

66
 Common 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

67
 Clinical manifestations
• Hyperkalemia frequently discovered as an incidental laboratory finding

• However may experience:

– Generalized fatigue
– Weakness
– Paresthesias
– Paralysis
– Palpitations

• EKG findings
– Early: peaked T waves, shortened QT interval, and ST segment
depression or elevation!

– Later: bundle branch block, resulting in widened QRS, increases in

the PR interval, and decreased amplitude of the P wave

68
 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?

71
 Cont…
• 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
72
 Cont…
• 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 73
Emergency Treatment
[K] > 6 mEq/L

• “STAT” ECG
• “STAT” repeat [K+]
• Give IV Calcium

74
 Additional Rx
• More IV Calcium
• Glucose and Insulin
• Bicarbonate
• Inhaled Beta-2 agonists
• Sodium polystyrene sulfonate
(Kayexalate®)

75
Severe hyperkalemia is
usually preceded by
moderate, uncorrected
hyperkalemia
 Differential Dx

• Renal Failure (GFR < 10 ml/min)

• Extra Renal Causes
– Metabolic acidosis
– Cell lysis (chemotherapy, trauma)
– Salt substitutes, ACE-I/ARB,
– Addison’s Disease
– Pseudo (coagulated RBC’s/platelets)

77
Hyperkalemia: Key Points
• K>4.5: caution
with medications,
& monitor
• K>5.5: intervene
• Calcium (not
kayexalate) is 1st
line
• Check ECG

78
 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
79
 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

80
 Common causes
• 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) 81
 Clinical manifestation
• “Bones, stones, abdominal groans, and
psychic moans” usually when Ca>12
– 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
82
 Management of
hypercalcemia
• Aggressive IVF “main Rx”
– 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 resorbtion

– Pamidronate 60 to 90 mg IV over 2 hours
– Zoledronate 4mg IV over 15 minutes

• Treat underlying disease process

83
 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

84
 Causes
• 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)
85
Clinical manifestations
• 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

86
 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

87
 SUMMARY
• Construct your differential
• Know the complications of therapy
• Know the implications of lack of therapy
• Calculate water/electrolyte needs
• … But repeated and frequent monitoring
is most important.
• Electrolyte disorders may be a
diagnostic clue or an expected
consequence of therapy
88