desequilibrio hidroelectrolito.pdf

Learning objectives

After reading this article readers should be able to:C recognize the multiple aetiologies of electrolyte abnormalities

of the critically ill

C identify the signs and symptoms of the various electrolyte

INTENSIVE CARE

Electrolyte disorders in thecritically illRaja Palepu

Ross Freebairn

abnormalities

C prescribe appropriate management of abnormalities, in partic-
Abstract
ular the management of different types of dysnatraemia
Electrolyte disorders are extremely common in the critically ill patient.
Competent analysis andmanagement of these is essential in providing qual-

ity intensive care. This article provides a review of and guide to aetiology,

analysis, and management of the major electrolytes in the critically ill.

Keywords Calcium; chloride; critically ill; dysnatraemia; electrolytes;

fluid; magnesium; phosphate; potassium; sodium

Royal College of Anaesthetists CPD Matrix: 1A01, 1A02, 2A05, 2C01, 3C00

Introduction

Electrolyte disorders are extremely common in the critically ill

patient. Competent analysis and management of these is essen-

tial in providing quality intensive care. Electrolyte disorders

represent:

� aids to the diagnosis of the nature of the illness

� markers of disease severity and prognosis

� indications of total body deficit or excess requiring specific

management.

Many electrolyte disturbances can be managed simply; deficits

by increasing intake and excess by reducing intake or encour-

aging loss but generalizing this approach to all electrolyte and

metabolic disturbances is over-simplistic. Fundamental concepts

in understanding electrolyte disorders include the following.

� Serum (or plasma) levels do not always reflect total body

stores of the electrolyte. For example potassium, a princi-

pally intracellular ion, is in a total body deficit in diabetic

ketoacidosis (DKA) yet serum levels are elevated. Simplistic

interpretation would not identify the total body deficit

requiring ongoing replacement.

� An electrolyte abnormality reflects an underlying patho-

logical process that may require definitive treatment.

� ‘Correction’ of a specific electrolyte abnormality may not

improve a patient’s condition, and may even worsen their

outcome, or mask the problem.

Raja Palepu MB ChB is a Registrar in Anaesthesia and Intensive Care

Medicine at Hawke’s Bay Hospital, Hastings, New Zealand. Conflicts of

interest: none declared.

Ross Freebairn MB ChB FANZCA FCICM FRCPE is a Consultant Intensive Care

Physician at Hawke’s Bay Hospital, Hastings, New Zealand and Adjunct

Associate Professor, Chinese University of Hong Kong, Hong Kong,

China. Conflicts of interest: none declared.

ANAESTHESIA AND INTENSIVE CARE MEDICINE 15:2 78

� Established recipes for electrolyte replacement to correct

abnormalities serve as a starting point, but cannot replace

repeated clinical examination and serial measurement of

electrolytes.

� All electrolytes are strong ions or weak acids and electro-

lyte disturbances may alter the acidebase status and vice-

versa. This can be assessed with blood gas data.

Specific electrolytes

The normal values and effects of deficit and excess of common

electrolytes are listed in Table 1.

Sodium

Thirst, vasopressin, and the kidneys control serum levels of the

major extracellular cation, sodium. The prevalence of dysna-

traemias in the intensive care unit (ICU) approaches 30%. They

are an independent risk factor for poor prognosis on admission

and during ICU stay and, not surprisingly, are incorporated into

severity scoring systems such as APACHE II. Sodium has osmotic

and electrostatic activity so measured hypo- or hypernatraemia

needs to be assessed in correlation with the patient’s volume

status and serum and urinary osmolality to determine the likely

cause and appropriate method of correction.

Hypernatraemia

Aetiology: in the outpatient population hypernatraemia is rarely

caused by excess sodium gain, and is usually the result of water

deficit relative to total body sodium. In the ICU population

however, excess total body sodium due to iatrogenic loading of

hypertonic fluid is not uncommon. Multiple factors lead to renal

loss of hypotonic fluid in critically ill patients, which may then be

replaced with a comparatively hypertonic fluid such as 0.9%

saline. Examples of hypotonic fluid loss include sustained diar-

rhoea, vomiting or nasogastric losses, excessive sweating and

central or nephrogenic diabetes insipidus. Sustained hyper-

natraemia can only occur when access to free water is restricted

or when the thirst mechanism is absent e a common situation in

ICU.

Management: as sodium is the major extracellular cation, in

hypernatraemia there will be a fluid shift from intracellular to

extracellular. The brain compensates to this by retaining other

solutes to restore cell volume, although the hypertonic state re-

mains. When correction commences it takes several days for

� 2014 Elsevier Ltd. All rights reserved.

http://dx.doi.org/10.1016/j.mpaic.2013.12.004

Normal physiologic ranges of the common electrolytes and effects of deficit or excess

Electrolyte Normal values (mmol/litre) Effect of excess Effect of deficit

Cations

Sodium 136e145 Cerebral vascular rupture, haemorrhage death Headache, lethargy, irritability, spasticity,

seizures and coma, demyelination syndromes

if corrected too quickly

Potassium 3.5e5.0 Peaked t-waves, can proceed to widened QRS,

heart block, bradycardia, cardiac arrest, muscle

weakness, paraesthesia, loss of tendon reflexes,

ileus, constipation, and palpitations

Depressed ST segments, biphasic t-waves,

prominent u-waves / tachyarrhythmias.

Muscle weakness, paraesthesia, loss of

tendon reflexes, ileus, constipation, and

palpitations

Calcium Total 2.10e2.60, ionized:

1.10e1.35

Neurological (headache, fatigue, apathy,

confusion), gastrointestinal (pain, constipation,

vomiting), renal (polyuria, nephrolithiasis, renal

failure) cardiovascular (arrhythmia’s, short QT

interval and atrioventricular or bundle branch

block) and skeletal (pain, arthralgia)

Tetany, paraesthesia, mental changes,

areflexia, decrease in cardiac output with

hypotension, dehydration via hypercalcaemic

nephrogenic diabetes insipidus

Magnesium 0.6e1.2 Tetany and arrhythmias, atrial dysrhythmias,

reduced cardiac output and death

Muscle weakness, decreased reflexes,

hypotension bradycardia somnolence coma.

Where causes include gastrointestinal

disorders (malabsorption, diarrhoea,

nasogastric losses, pancreatitis, and short

bowel), endocrine disorders, renal losses and

drugs

Anions

Chloride 95e105 Unknown-/related to associated abnormality Unknown-/related to associated abnormality

Phosphate 0.8e1.5 Symptoms of acute hypocalcaemia, acute tubular

necrosis, ectopic calcification

Below 0.32 mmol/litre respiratory muscle

dysfunction, left shift of oxyhaemoglobin

dissociation curve, myocardial dysfunction,

arrhythmia’s, muscle weakness, insulin

resistance, neuropathy, seizures, coma,

haemolytic anaemia

Zinc 10.7e22.9 mmol/litre (serum)

13.8e22.9 mmol/litre (plasma)

Sparse hair, easily pluckable hair, alteration of

taste; reddish dermatitis around nose, mouth and

groin; hair loss, poor wound healing

Copper deficiency resulting in bone marrow

abnormalities

INTENSIVE CARE

these accumulated solutes to disperse. If large volumes of hy-

potonic fluid are delivered rapidly, the resultant cerebral oedema

can lead to irreversible brain damage.

For this reason, correction by less than 0.6 mmol/litre/hour or

10e15 mmol/litre in a 24-hour period is recommended. Hypo-

tonic fluid such as pure water, 5% dextrose, or 0.45% saline in

the lowest volume required to correct the hypertonicty should be

used.

Hyponatraemia

Aetiology: hyponatraemia can occur in the setting of low,

normal, or high total body water as outlined in Table 2. It can

also occur in variable states of tonicity and osmolality depending

on the presence of other solutes. For example, in hyperglycaemia

the excess osmotic load of glucose holds water in the extracel-

lular space, causing a hyponatraemia that is hyperosmolar and

hypertonic.

Differentiating the cause of hyponatraemia requires clinical

examination of fluid status along with simple investigations to

assess serum and urine sodium and osmolality.


Hypervolaemic hyponatraemia is most often related to

impaired water excretion by the kidneys. Hypovolaemic hypo-

natraemia is most often due to renal or extrarenal concurrent

sodium and water loss.

Clinical features: (Table 1) are seen when sodium derangement

(hyper or hypo) is severe and/or occurs rapidly. Signs and

symptoms relate predominantly to central nervous system (CNS)

dysfunction. These are not usually seen until serum sodium falls

below 125 mmol/litre but severity is also related to the speed of

development. Acute hypotonic hyponatraemia is most dangerous

as the entry of water into brain cells results in cerebral oedema

and risk of tentorial herniation.

Management: in mild hypovolaemic hyponatraemia isotonic

saline (0.9% saline) is usually sufficient to correct serum sodium.

In mild hypervolaemic cases fluid restriction may be appropriate.

Convulsions, unconsciousness, self-induced water intoxica-

tion, and hyponatraemia associated with intracranial pathology

are medical emergencies that demand prompt and definitive



Potential causes of the different types ofhyponatraemia

Hypovolaemia Diarrhoea/vomiting

Diuretics

Osmotic diuresis

Aldosterone deficiency

Third space losses e burns,

pancreatitis

Cerebral/renal salt wasting

Euvolaemia SIADH

Stress response: postoperative

pneumonia

Head injury

Positive pressure ventilation

Hypothyroidism

Cortisol deficiency

Hypervolaemia Congestive cardiac failure

Cirrhosis

Nephrotic syndrome

Renal failure

SIADH, syndrome of inappropriate anti-diuretic hormone secretion.

Table 2

INTENSIVE CARE

intervention with hypertonic saline. The aim is a rapid rise in

serum sodium of about 3e7 mmol/litre or return a serum sodium

to approximately 120 mmol/litre. This is best achieved with

bolus infusions of concentrated saline.

If strong saline is unavailable, or there is concern regarding

fluid overload, frusemide can be used to limit volume expansion.

Vasopressin receptor antagonists, which act to increase free

water loss, are another treatment option. Ongoing correction

above 120 mmol/litre should proceed at the slower correction

rate outlined in Box 1.

Priority should then be given to identifying and treating the

underlying cause, for example stopping any medications which

promote fluid loss.

There is significant morbidity and mortality associated with

dysnatraemias and/or their rapid correction. Severe neurological

derangement can occur following correction of hyponatraemia.

Osmotic demyelination syndrome, including central pontine

myelinolysis (CPM) is perhaps the most dangerous and well-

known complication.

Recommended maximum rates of correction ofhyponatraemia

C 6e8 mmol/litre in 24 hours



Box 1


The incidence and precipitating factors of CPM remain poorly

defined. Hyperkalaemia and rapid correction of hyponatraemia

may increase risk, but CPM may still occur following slow

correction. CPM has also been observed to occur after euna-

traemic hyperosmolar hyperglycaemia, suggesting that a hyper-

tonic insult may by the mechanism, in which free water leaves

brain cells leading to cellular dysfunction and demyelination.

Animal studies into drugs that may prevent or reduce the risk of

CPM after correction of hyponatraemia have been promising.

CPM can vary in severity from isolated gait ataxias that

improve significantly post-presentation, through to spastic

quadriparesis, pseudobulbar palsy, and impairment in con-

sciousness with variable reversibility.

Formulae guiding the correction of dysnatraemias generally

consider the patient as a closed system, ignoring the variable

ongoing fluid losses. Studies using these formulae report a wide

discrepancy in serum sodium change and should therefore only

be used as an initial estimate of need. A cornerstone of man-

agement is serial measurement of serum sodium, initially 2e4-

hourly, to avoid correction error. If inadvertent over correction of

hyponatraemia occurs, carefully re-lowering the serum sodium

may be preferred using desmopressin and 5% dextrose in water.

Potassium

Potassium is predominantly intracellular and is the body’s major

cation. Only 2% is normally in serum. In health, 90% of daily

potassium loss is by renal excretion regulated by aldosterone. In

renal failure there is enhanced excretion though the bowel.

Intracellular potassium concentrations are dependent on

active uptake by the Na/K adenosine triphosphate (ATP-ase)

pump, and passive leak along electrochemical gradient. Both of

these are affected by medications, pH changes and osmolarity.

Increased popularity of the renineangiotensinealdosterone axis

medications may influence prevalence of potassium de-

rangements. Causes of hypo- and hyperkalaemia are listed in

Table 3.

Management

Hyperkalaemia: emergency hyperkalaemia management is to

stabilize myocardial membrane with calcium (gluconate or

chloride), then shift potassium intracellularly with either an in-

sulin/glucose or bicarbonate infusion. Loop and thiazide di-

uretics can assist potassium loss. Haemodialysis or filtration may

be required in renal failure.

Hypokalaemia: slow replacement of 10e30 mmol/hour is usu-

ally recommended. Uptake and maintenance of intracellular po-

tassium may be magnesium dependent and this should also be

measured when replacing potassium. Combined deficiency is

common and may potentiate cardiac arrhythmia.

The usual maximum recommended intravenous dose is 30

mmol/hour. In unstable life-threatening arrhythmias 2 mmol/

minute for 10 minutes, followed by 10 mmol over 5e10 minutes

can be administered under close cardiac monitoring.

Chloride

Chloride is the body’s major extracellular anion. It is regulated

via the kidneys, gut and skin. In health over 99% of filtered



Causes of potassium disorders

Hypokalaemia

Decreased

intake

Increased loss Transcellular shift

Malnutrition

Alcoholism

Gastrointestinal

C Diarrhoea/

vomiting

C Nasogastric loss

Renal

Drugs

Diuretics, steroids,

amphotericin

Aldosterone and cortisol

excess

Renal tubular acidosis

Alkalosis

Drugs

C Insulin/glucose

C b2 agonists

Hyperkalaemia

Increased intake Decreased loss Transcellular shifts

Oral or IV

Stored RBCs

transfused

Renal failure

Drugs:

Potassium sparing

diuretics

Angiotensin-converting

enzyme inhibitors

Acidosis

Tumour lysis

syndrome

Rhabdomyolysis

Burns

Table 3

INTENSIVE CARE

chloride is reabsorbed in the distal tubule. With increasing in-

terest in Stewart’s approach to acidebase analysis, chloride has

become more important in understanding acid-base physiology.

In Stewart’s approach chloride is one of the major influences on

the strong ion difference (SID), and thus the hydrogen ion

concentration.

Chloride concentration should always be interpreted in rela-

tion to sodium, as concurrent sodium and chloride derangement

(hyperchloraemia with hypernatraemia) will not alter the SID,

and therefore not affect the acidebase balance.

Hyperchloraemia

Aetiology: a number of mechanisms can lead to hyper-

chloraemia in the ICU setting. Chloride loading, through

administration of chloride-rich fluids such as 0.9% saline, or in

total parenteral nutrition (TPN) is one major mechanism. Other

mechanisms include water loss through diarrhoea, fever, burns,

renal losses, and diabetes insipidus or increased renal chloride

reabsorption through early renal failure, renal tubular acidosis

and medications such as acetazolamide.

The significance of hyperchloraemia in the ICU patient re-

mains unclear. Animal studies have shown that in sepsis

elevated serum chloride can contribute more to the total acid

load than lactate. Hyperchloraemic acidosis has also been shown

to be pro-inflammatory and promote cytokine release in animals.

It is still undecided whether hyperchloraemic acidosis contrib-

utes to, or is merely associated with critical illness.

Management: loop diuretics are capable of reducing serum

chloride without reducing sodium. Sodium bicarbonate can also

be used in the correction of hyperchloraemic acidosis. Treatment


of hyperchloraemia and the subsequent outcomes of this are yet

to be studied in published clinical trials.

Hypochloraemia

Aetiology: hypochloraemia can occur through chloride loss, as

seen in vomiting and other gastric loss, diuretic therapy, and

chronic respiratory acidosis, or in excess water gain, such as in

hypotonic fluid replacement, congestive heart failure, and syn-

drome of inappropriate anti-diuretic hormone (SIADH). De-

ficiencies in other electrolytes including sodium, potassium,

calcium, and in albumin often co-exist.

Management: treatment is generally only given when hypo-

chloraemia is a primary disorder rather than a compensatory

mechanism. In the hypovolaemic patient replacement with so-

dium or potassium chloride is recommended.

Calcium

Calcium is an intracellular messenger and cell function regulator.

It is tightly controlled by hormones acting on calcium trans-

porters in the intestine, bone, and kidney. As pH, lactate, and

bicarbonate influence ionized calcium levels, direct measure-

ment of ionized calcium is the gold standard. Calculated

correction of total serum calcium provides a poor alternative to

ionized calcium in ICU.

Aetiology

Calcium disturbance is common in the ICU setting. Causes are

multifactorial, influenced by sepsis, blood transfusions, renal

failure, and renal replacement therapy, particularly when citrate

anticoagulation is used. Rhabdomyolysis can precipitate deposi-

tion of intracellular calcium producing lowered extracellular

ionized and total serum calcium levels.

Management

Management should follow specific protocols where applicable,

for example during continuous renal replacement therapy.

Hypercalcaemia: hypercalcaemia leads to dehydration via

hypercalcaemic nephrogenic diabetes insipidus. Intravenous

rehydration with 0.9% saline provides both volume replacement

and additional sodium to interrupt the resorption of sodium and

calcium. Frusemide can be used to promote calcium excretion

but should only be used in fluid replete patients.

Bisphosphonates are commonly used in the oncology setting

and act by inhibiting osteoclast mediated bone resorption. Given

as a single intravenous infusion, results are seen in 24e48 hours

and the therapeutic effect may last for several weeks. Glucocor-

ticoids are only useful in cases of hypercalcaemia caused by

endogenous overproduction of calcitriol (125-dihydroxyvitamin

D.)

Hypocalcaemia: early identification and correction of co-existing

magnesium, phosphate or vitamin D abnormality are important.

Prolonged critical illness is associated with vitamin D deficiency

that is poorly responsive to replacement. Acute symptomatic

hypocalcaemia is treated with intravenous calcium gluconate

10% 10 ml or calcium chloride 10% 5 ml (3.4 mmol) over 2e3

minutes. In the presence of ongoing symptoms, 1e5 ml/hour of



INTENSIVE CARE

10% calcium chloride should be administered with 4-hourly

monitoring to keep ionized calcium greater than 0.8 mmol/litre.

Hypocalcaemia usually normalizes after a few days in ICU.

Although failure to normalize is associated with increased mor-

tality, calcium replacement appears not to improve normaliza-

tion or mortality.

Magnesium

Magnesium is a primarily intracellular ion that acts as a co-

enzyme in phosphate transfer reactions, and is also required

for protein manufacture and mitochondrial function. Its role can

be described as an intracellular calcium channel blocker.

Serum magnesium undergoes diurnal variation. Routine

regulation is controlled by variable reabsorption of urinary

magnesium in the ascending loop.

Hypermagnesaemia

Aetiology: usually renal failure or grossly excess intake is

required to elevate levels. Lithium poisoning, diabetic ketoaci-

dosis and hypercatabolic states may alter levels.

Management: patients in renal failure may require dialysis to

lower serum magnesium. Patients with normal renal function

should return to normal serum levels when the source of excess

magnesium is stopped.

Hypomagnesaemia

Aetiology: hypomagnesaemia occurs frequently in hospitalized

patients and has a higher prevalence in intensive care. Upper

gastrointestinal secretions contain high concentrations of mag-

nesium. As 99% of total body magnesium is stored intracellularly

and in bone and cannot be readily mobilized, even small ongoing

losses may results in low serum magnesium levels. Hypo-

magnesaemia on admission to ICU has been documented in 61%

of patients and is associated with a doubling of mortality in pa-

tients with equivalent APACHE II scores.

Management: hypomagnesaemia in high risk or symptomatic

patients should be corrected with intravenous magnesium

sulphate 10 mmol over 15 minutes and in repeated doses or

infusion (20e60 mmol/24 hours) to keep serum magnesium 1.0

e1.5 mmol/litre.

Phosphate

Phosphate is an intracellular anion, and a vital part of the ATP

pathway. It acts as a buffer and is also a component of several

important cellular molecules. Normal clearance is predominantly

renal. Urinary phosphate measurement is useful in determining

the cause of derangement.

Hyperphosphataemia

Aetiology: hyperphosphataemia occurs when either the phos-

phate load exceeds the kidneys’ rate of filtration or when there is

increased resorption of filtered phosphate in the proximal


tubules. Tissue breakdown (e.g. rhabdomyolysis) or cellular

shift, as seen in lactic and ketoacidosis, can lead to excess

phosphate load in the ICU setting. Oral phosphate bowel prepa-

rations have also been implicated in severe and sometime fatal

electrolyte disturbances.

Management: with normal renal function hyperphosphataemia

is self-correcting within 24 hours. Severe or symptomatic

hyperphosphataemia in the setting of renal failure requires

dialysis. Hypertonic glucose can be used to drive phosphate (and

potassium) into cells.

Hypophosphataemia

Aetiology: hypophosphataemia be due to total body depletion, as

in renal wasting or large gastrointestinal losses, or compartment

shift. It is seen postoperatively, particularly post-cardiac pro-

cedures, and in sepsis.

Management: Phosphate should be replaced either orally or

intravenously at 2e20 mmol/hour, up to 100 mmol/day to keep

serum phosphate levels greater than 0.8 mmol/litre. A

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