dr. carlos fernando estrada garzona departamento de...

Dr. Carlos Fernando Estrada Garzona Departamento de Farmacología Universidad de Costa Rica

� � FISIOLOGIA LIQUIDOS CORPORALES

� SOLUCIONES PARENTERALES

� PRINCIPIOS DE FLUIDOTERAPIA

� CRISTALOIDE VS COLOIDE

OBJETIVOS

�

FISIOLOGIA�LIQUIDOS CORPORALES

�

REQUERIMIENTOS FISIOLOGICOS

� Na: 100-150 mmol/d �  6-8 g NaCl

� K: 60-80 mmol/d

� Calorías: 25 kcal/kg/d

!FLUIDS, ELECTROLYTES, & ACID-BASE 15

patients with congestive heart failure (who have increase inboth intravascular and extracellular volumes).

Normally, daily sodium excretion equals intake, so sodiumexcretion varies with dietary or other intake. The average dietcontains 4–8 g of sodium daily, and this quantity must beexcreted. With severe limitation of dietary sodium, normal kid-neys can vigorously reabsorb sodium, so as little as 1–5 meqNa+/L of urine appears, and only 1–2 meq of Na+ is excreteddaily. A daily sodium intake and excretion of approximately40–65 meq (about 1–1.5 g) is sufficient in normal individuals.

" Hypovolemia

ESSENT IALS OF D IAGNOS I S

" Evidence of decreased intravascular volume: hypoten-sion, low central venous or pulmonary artery wedgepressures

" Indirect evidence of decreased effective intravascular vol-ume: tachycardia, oliguria, avid renal sodium reabsorption

" Circumstantial evidence of depleted effective intravas-cular volume: end-organ dysfunction, peripheralvasoconstriction

" Potential source of loss of extracellular volume orevidence of inadequate repletion

General Considerations

A. Definition—Hypovolemia is decreased volume of theintravascular space. Although extracellular volume, of whichthe intravascular space is a part, is often diminished, hypov-olemia can occur even in the presence of normal or increasedextracellular volume (Table 2–2). The assessment of ade-quacy of intravascular volume in the presence of normal orincreased extracellular volume is often difficult, especially incritically ill patients. It is central to the concept of hypov-olemia that total intravascular volume need not be dimin-ished but that effective intravascular volume is low, such thatthere is insufficient volume in the circulation to provide cir-culatory adequacy. The term effective arterial volume is some-times used to characterize the physiologically effective part ofthe intravascular volume.

Some clinicians use the term dehydration as a substitutefor hypovolemia. This is incorrect, and this term should bereserved to mean insufficient water relative to total bodysolute (see below).

B. Pathophysiology—Decreased effective intravascular vol-ume can occur with decreased, normal, or increased extracel-lular volume. Decreased extracellular volume leading todepletion of intravascular volume is most common and canarise from increased loss of extracellular fluid, failure toreplete normal losses, or a combination of both. Bleeding,diarrhea, vomiting, and excessive skin loss of fluid (sweating,burns) can quickly deplete extracellular volume. Abnormallylarge urinary losses of sodium and water from renal disease,adrenal insufficiency, diuretics, or hyperglycemia (osmoticdiuresis) also should be considered as sources of volumedepletion. Decreased extracellular volume also can arise

Table 2–1. Factors affecting body sodium balance.

Increased body sodium content (increased extracellular volume)• Increased sodium intake (in absence of increased sodium excretion)• Decreased sodium excretion by kidneys

Decreased glomerular filtrationIncreased renal tubular sodium reabsorption Increased renin, angiotensin, aldosterone Excessive mineralocorticoid activity

Decreased body sodium content (decreased extracellular volume)• Decreased sodium intake (in presence of normal sodium excretion)• Increased sodium excretion

Renal: Renal failure Salt-losing nephropathy Osmotic diuresis Diuretic drugs Atrial natriuretic peptide Decreased renin, angiotensin, aldosterone, or cortisol

Extrarenal: Diarrhea Vomiting Sweating Surgical drainage

Table 2–2. Hypovolemia (decreased effective intravascularvolume).

With decreased extracellular volume• Increased fluid losses

Gastrointestinal tract (diarrhea, vomiting, fistulas, nasogastric suction)Renal (polyuria with renal sodium wasting, osmotic diuresis)Skin or wound losses (sweating, burns) Hemorrhage (trauma, other bleeding site)

• Decreased intake of sodium and water• Impaired normal capacity to retain sodium and water

Renal sodium wasting (polycystic kidneys, diuretics) Adrenal insufficiency Osmotic diuresis (hyperglycemia)

With increased or normal extracellular volume• Cirrhosis with ascites• Protein-losing enteropathy• Congestive heart failure• Increased vascular permeability (sepsis, shock, trauma, burns)

� SOLUCIONES PARENTERALES

� NaCL AL 0,9%

�  9 g / L NaCl

� 308 mOsm �  154 mmol NaCL por

litro

� Expansor de volumen del LEC

� INDICACIONES:

� Contracción isotónica del LEC

� DEXTROSA AL 5%

�  50 g glucosa por litro

� 277 mOsm � HIPOTONICA

� EXPANSOR LIC Y LEC

� INDICACIONES:

� Contracción hipertónica del LEC

� MIXTA

�  9 g NaCl + 50 g dextrosa por litro

� 585 mOsm � Tonicidad à 308

mOsm

� EXPANSOR DEL LEC

� INDICACIONES:

� APORTE CALÓRICO-REQUERIMIENTO FISIOLOGICO

� NaCL AL 0,45%

� 4,5 g NaCl por litro

� 154 mOsm

� EXPANSOR LIC Y LEC �  66%LEC �  33% LIC

� INDICACIONES:

� Contracción hipertónica del LEC

� DKA-HHS

� SALINA HIPERTONICA

� NaCL al 3%

�  30 g NaCl por litro

�  1026 mOsm

� LIC ààà LEC

� INDICACIONES:

� HIPONATREMIA SINTOMATICA

� < 0,5 mmol/L/h � < 12 mmol/L en 24 h

� DACA

� 5 g NaCl � 10 g glucosa � 1 g KCl � 6,5 g acetato de sodio

� 348 mOsm � Tonicidad à 279

� INDICACIONES:

� Contracción isotónica del LEC

� Diarrea aguda alta tasa

� COLOIDALES

�  Albúmina 5% y 25%

� P oncótica �  25 vs 100 mmHg

� Expansor del IV � < 24 h �  100 vs 500 cc / 100 cc

� INDICACIONES:

� EXPANSOR DE VOLUMEN INTRAVASCULAR

� HIPOALBUMINEMIA SEVERA

! CHAPTER 218

compartments). Although sometimes used to replace extracel-lular volume deficits, Ringer’s lactate (containing Na+, K+, Cl–,Ca2+, and lactate) is no more effective than 0.9% NaCl in mostclinical situations. However, evidence suggests that large vol-umes of NaCl-containing fluids are likely to cause mild hyper-chloremic acidosis, the consequences of which are unclear.Therefore, some practitioners advocate crystalloid replace-ment with Ringer’s lactate, especially in hemorrhagic shockbefore blood replacement is available.

For years, colloid solutions have been advocated for moreefficient repletion of intravascular volume, especially in statesof normal or elevated extracellular volume and in hypov-olemic shock. In theory, colloids are restricted at least tran-siently to the intravascular space and thereby exert anintravascular oncotic pressure that draws fluid out of the inter-stitial space and expands the intravascular space by an amountout of proportion to the volume of colloid solution adminis-tered. A theoretical disadvantage is that the interstitial spacewould be depleted of water, leading to an increase in intersti-tial oncotic pressure that would draw water back out.Nevertheless, studies have failed to identify clear-cut advan-tages of colloid-containing solutions over crystalloid solutionsin critically ill patients. This is probably because increased cap-illary permeability in patients with sepsis, shock, and otherproblems negates the potential benefit of retaining colloidwithin the vascular space. Furthermore, some investigatorshave suspected that leakage of colloid into the interstitial spaceof the lungs and other organs can contribute to persistentorgan system dysfunction and edematous states. In hypov-olemia associated with ascites, rapid movement of colloid intothe ascitic fluid may occur, resulting in only a transientincrease in intravascular volume. In patients with nephroticsyndrome or protein-losing enteropathies, albumin and othercolloids may be lost fairly rapidly.

Colloid solutions for intravenous replacement includehuman serum albumin (5% and 25% albumin, heat-treated toreduce infectious risk) and hetastarch (6% hydroxyethylstarch). Albumin is considered nonimmunogenic, but it isexpensive, offers few advantages over other solutions, and hasnot been shown to improve outcome. Hetastarch is a syntheticcolloid solution used for volume expansion. Clinical benefit ofthe use of this solution is unclear. Fresh frozen plasma is anexpensive and inefficient volume expander and should bereserved for correction of coagulation factor deficiencies. Thereis little rationale for the use of whole blood; red blood cells andother blood components should be given for specific indica-tions, along with crystalloid or colloid supplements as needed.

Meta-analyses have found either no difference or a trendtoward increased mortality in critically ill patients givenalbumin. In a large prospective trial comparing albumin orisotonic crystalloid, however, there was no difference in mor-tality. A few clinical conditions have been shown to benefitfrom albumin infusions. Antibiotics and intravenous albu-min, 1.5 g/kg on day 1 and 1 g/kg on day 3, significantlyreduced mortality and renal failure in patients with cirrhosisand spontaneous bacterial peritonitis. Albumin may be help-ful after large-volume paracentesis and to correct dialysis-related hypotension.

D. Complications—Complications of fluid replacementinclude excessive fluid repletion owing to overestimation ofthe hypovolemia or inadvertent excessive fluid administration.Patients with renal and cardiac dysfunction are especiallyprone to fluid overload, and pulmonary edema may be thefirst manifestation. Pulmonary edema is also likely—and mayoccur without excessive fluid repletion—in patients who haveincreased lung permeability or ARDS. During fluid repletion,worsening of peripheral edema or ascites may occur. Large

[Na+] (meq/L) [Cl–] (meq/L) [osm] (mosm/L) Other

Crystalloids

0.9% NaCl (normal saline) 154 154 3085% dextrose in 0.9% NaCl 154 154 560 Glucose, 50 g/L Ringer’s lactate 130 109 273 K+, Ca2+, lactate1

5% dextrose in water2 0 0 252 Glucose, 50 g/L 0.45% NaCl 77 77 1545% dextrose in 0.45% NaCl 77 77 406 Glucose, 50 g/L

Colloids

Albumin (5%) Albumin (25%)6% hetastarch in 0.9% NaCl

1K+ 4 meq/L, Ca2+ 3 meq/L, lactate 28 meq/L.2Not recommended for rapid correction of intravascular or extracellular volume deficit.

Table 2–3. Fluids for intravenous replacement of extracellular volume or water deficit.

� PRINCIPIOS FLUIDOTERAPIA


patients with congestive heart failure (who have increase inboth intravascular and extracellular volumes).

Normally, daily sodium excretion equals intake, so sodiumexcretion varies with dietary or other intake. The average dietcontains 4–8 g of sodium daily, and this quantity must beexcreted. With severe limitation of dietary sodium, normal kid-neys can vigorously reabsorb sodium, so as little as 1–5 meqNa+/L of urine appears, and only 1–2 meq of Na+ is excreteddaily. A daily sodium intake and excretion of approximately40–65 meq (about 1–1.5 g) is sufficient in normal individuals.

" Hypovolemia


" Evidence of decreased intravascular volume: hypoten-sion, low central venous or pulmonary artery wedgepressures

" Indirect evidence of decreased effective intravascular vol-ume: tachycardia, oliguria, avid renal sodium reabsorption

" Circumstantial evidence of depleted effective intravas-cular volume: end-organ dysfunction, peripheralvasoconstriction

" Potential source of loss of extracellular volume orevidence of inadequate repletion


A. Definition—Hypovolemia is decreased volume of theintravascular space. Although extracellular volume, of whichthe intravascular space is a part, is often diminished, hypov-olemia can occur even in the presence of normal or increasedextracellular volume (Table 2–2). The assessment of ade-quacy of intravascular volume in the presence of normal orincreased extracellular volume is often difficult, especially incritically ill patients. It is central to the concept of hypov-olemia that total intravascular volume need not be dimin-ished but that effective intravascular volume is low, such thatthere is insufficient volume in the circulation to provide cir-culatory adequacy. The term effective arterial volume is some-times used to characterize the physiologically effective part ofthe intravascular volume.

Some clinicians use the term dehydration as a substitutefor hypovolemia. This is incorrect, and this term should bereserved to mean insufficient water relative to total bodysolute (see below).

B. Pathophysiology—Decreased effective intravascular vol-ume can occur with decreased, normal, or increased extracel-lular volume. Decreased extracellular volume leading todepletion of intravascular volume is most common and canarise from increased loss of extracellular fluid, failure toreplete normal losses, or a combination of both. Bleeding,diarrhea, vomiting, and excessive skin loss of fluid (sweating,burns) can quickly deplete extracellular volume. Abnormallylarge urinary losses of sodium and water from renal disease,adrenal insufficiency, diuretics, or hyperglycemia (osmoticdiuresis) also should be considered as sources of volumedepletion. Decreased extracellular volume also can arise

Table 2–1. Factors affecting body sodium balance.

Increased body sodium content (increased extracellular volume)• Increased sodium intake (in absence of increased sodium excretion)• Decreased sodium excretion by kidneys

Decreased glomerular filtrationIncreased renal tubular sodium reabsorption Increased renin, angiotensin, aldosterone Excessive mineralocorticoid activity

Decreased body sodium content (decreased extracellular volume)• Decreased sodium intake (in presence of normal sodium excretion)• Increased sodium excretion

Renal: Renal failure Salt-losing nephropathy Osmotic diuresis Diuretic drugs Atrial natriuretic peptide Decreased renin, angiotensin, aldosterone, or cortisol

Extrarenal: Diarrhea Vomiting Sweating Surgical drainage

Table 2–2. Hypovolemia (decreased effective intravascularvolume).

With decreased extracellular volume• Increased fluid losses

Gastrointestinal tract (diarrhea, vomiting, fistulas, nasogastric suction)Renal (polyuria with renal sodium wasting, osmotic diuresis)Skin or wound losses (sweating, burns) Hemorrhage (trauma, other bleeding site)

• Decreased intake of sodium and water• Impaired normal capacity to retain sodium and water

Renal sodium wasting (polycystic kidneys, diuretics) Adrenal insufficiency Osmotic diuresis (hyperglycemia)

With increased or normal extracellular volume• Cirrhosis with ascites• Protein-losing enteropathy• Congestive heart failure• Increased vascular permeability (sepsis, shock, trauma, burns)


amounts of isotonic saline may contribute to expansionacidosis—a hyperchloremic metabolic acidosis owing largelyto dilution of plasma bicarbonate—but this is uncommon.

E. Maintenance Fluid Requirements—Normal mainte-nance fluids to prevent hypovolemia should provide1.5–2.5 L of water per day for normal-sized adults, adjustedto account for other sources of water intake (eg, medicationsand/or food intake) and the ability of the kidneys to concen-trate and dilute the urine. Sodium intake in the ICU gener-ally should be limited to a total of 50–70 meq/day, but manycritically ill patients avidly retain sodium, and they may havea net positive sodium balance with even a smaller sodiumintake. Patients are frequently given much more sodium thanneeded. For example, 0.9% NaCl has 154 meq/L of sodiumand chloride, and some patients are inadvertently given asmuch as 3–4 L/day. Although it is sometimes necessary,it is difficult to rationalize giving diuretics to a patientsimply to enhance removal of sodium given as part of replace-ment fluids. On the other hand, diuretics are useful whenneeded to facilitate excretion of the sodium ingested froman appropriate diet. In states of ongoing losses of extracellu-lar volume, appropriate fluid replacement in addition tomaintenance water and electrolytes should be given as needed(Table 2–4).

American Thoracic Society Consensus Statement: Evidence-basedcolloid use in the critically ill. Am J Respir Crit Care Med2004;170:1247–59. [PMID: 15563641]

Bellomo R et al: The effects of saline or albumin resuscitation onacid-base status and serum electrolytes. Crit Care Med2006;34:2891–7. [PMID: 16971855]

French J et al: A comparison of albumin and saline for fluid resus-citation in the intensive care unit. N Engl J Med 2004;350:2247–56. [PMID: 15163774]

McGee S et al: Is this patient hypovolemic? JAMA1999;281:1022–9. [PMID: 10086438]

Peixoto AJ. Critical issues in nephrology. Clin Chest Med2003;24:561–81. [PMID: 14710691]

Roberts I et al: Colloids versus crystalloids for fluid resuscitation incritically ill patients. Cochrane Database Syst Rev 2004;4:CD000567. [PMID: 15495001]

SAFE Study Investigators: Effect of baseline serum albumin con-centration on outcome of resuscitation with albumin or salinein patients in intensive care units: Analysis of data from the Salineversus Albumin Fluid Evaluation (SAFE) Study. Br Med J2006;333: 1044. [PMID: 17040925]

Sort P et al: Effect of intravenous albumin on renal impairment andmortality in patients with cirrhosis and spontaneous bacterialperitonitis. N Engl J Med 1999;341:403–9. [PMID: 10432325]

" Hypervolemia


" Edema, ascites, or other evidence of increased extracel-lular volume

" Intravascular volume may be normal, low (hypovolemia),or high

" Potential causes of increased extracellular volume:renal insufficiency, congestive heart failure, liver dis-ease, or other mechanism of sodium retention or exces-sive sodium administration


In contrast to hypovolemia, in which there is always decreasedvolume of the intravascular space, in hypervolemia theintravascular volume may be high, normal, or paradoxicallylow. Peripheral or pulmonary edema, ascites, or pleural effu-sions are the evidence for increased extracellular volume.Increased extracellular volume may not be an emergency inICU patients, but this depends on how much and where theexcess fluid accumulates. If associated with decreased intravas-cular volume (eg, hypovolemia), increased intravascular vol-ume (eg, pulmonary edema), or severe ascites (with respiratorycompromise), rapid intervention may be indicated.

A. Hypervolemia with Decreased IntravascularVolume—Because sodium—along with anions—is the pre-dominant solute in the extracellular space, increased extra-cellular volume is an abnormally increased quantity ofsodium and water. The body normally determines whethersodium and water should be retained by sensing the ade-quacy of intravascular volume, and the nonvascular com-ponent does not play a role in stimulating or inhibitingsodium and water retention. Thus excessive sodium reten-tion resulting in hypervolemia may occur in states of inade-quate effective circulation, such as heart failure, orsuboptimal filling of the vascular space resulting from loss offluid into other compartments, such as occurs with hypoal-buminemia, portal hypertension, or increased vascular per-meability to solute and water.

Table 2–4. Guidelines for replacement of fluid lossesfrom the gastrointestinal tract.

Replace mLper mL with Add

Gastric (vomiting ornasogastric aspiration)

5% dextrose in0.45% NaCl

KCl, 20 meq/L

Small bowel 5% dextrose in0.45% NaCl

KCl, 5 meq/LNaHCO3, 22 meq/L

Biliary 5% dextrose in0.90% NaCl

NaHCO3, 45 meq/L

Large bowel (diarrhea) 5% dextrose in0.45 NaCl


! CHAPTER 224

B. Solute Excretion and Water Excretion Rate—Thequantity of solute excreted also determines the maximumand minimum water excretion rates. In normal subjects,there is an obligate solute loss of about 800 mOsm/day,including sodium, potassium, anions, ammonium, and urea.Urea, from breakdown of amino acids, makes up about 50%of the solute excreted. In the presence of severely limited pro-tein intake, 24-hour urine urea excretion is reduced. Thisdecrease in urine solute excretion limits maximum waterexcretion even if urine is maximally diluted. A fall in the total24-hour urine solute excretion to 300 mOsm/day, for exam-ple, means that even if urine concentration is 50 mOsm/kg,only 6 L of water can be excreted per day. In contrast, if thereis 800 mOsm/day of solute to excrete, 16 L of water per daycould have been excreted with maximum urinary dilution.

" Hyponatremia


" Plasma sodium <135 meq/L" Altered mental status (confusion, lethargy) or new onset

of seizures" Most cases discovered by review of routinely obtained

plasma electrolytes


Hyponatremia is encountered commonly in the ICU. It hasbeen estimated that 2.5% of hospitalized patients have hypona-tremia. Low plasma sodium is associated with a variety ofendocrine, renal, neurologic, and respiratory disorders; medica-tions and other treatment; and other medical conditions. Severehyponatremia is manifested by altered mental status (hypona-tremic encephalopathy), seizures, and high mortality.Hyponatremia is particularly dangerous in patients with acuteneurologic disorders, especially head injury, stroke, and hemor-rhage. Severe hyponatremia must be corrected rapidly, carefully,and in a controlled fashion to avoid further complications.

In the absence of hyponatremia associated with normalor increased tonicity (see below), low plasma sodium indi-cates excess total body water for the amount of solute (dilu-tional hyponatremia). In normal subjects, this conditionwould initiate compensatory mechanisms that facilitate rapidexcretion of water, correcting the imbalance. Therefore, instates of persistent hyponatremia, there is physiologic or patho-logic inability to excrete water normally.

Hyponatremia (dilutional hyponatremia) is seen in threedistinct clinical situations in which extracellular volume is low,high, or normal (Table 2–7).

A. Hyponatremia with Decreased Extracellular Volume—Decreased extracellular volume leads to vigorous waterconservation, primarily mediated by increased ADH release

stimulated by atrial receptors and increased thirst leading toincreased water intake. Generally, urinary sodium excretion isvery low, and water intake and retention lead to increasedTBW relative to the reduced amount of solute. However, inconditions in which the hypovolemic state is due to sodiumand water loss in the urine, such as adrenal insufficiency,diuretic use, and salt-losing nephropathies, urine sodiumexcretion may be normal or high. In adrenal insufficiency,hyponatremia is facilitated because lack of cortisol causes col-lecting ducts to be excessively permeable to water reabsorp-tion, and ADH fails to be suppressed normally by low plasmaosmolality. A frequently seen form of hypovolemic hypona-tremia occurs with thiazide diuretics. Chronic volume deple-tion leading to stimulation of ADH release is an importantfactor. In addition, thiazides impair urinary dilution by block-ing sodium and chloride transport in the diluting segment ofthe distal nephron and potentiate the effect of ADH. Finally,thiazide-induced renal potassium excretion further reducestotal body solute content, also contributing to hyponatremia.

B. Hyponatremia with Increased Extracellular Volume—Hyponatremia in the presence of increased extracellular vol-ume is seen in congestive heart failure, nephrotic syndrome,

Normal plasma osmolality Pseudohyponatremia (hyperlipidemia); rare if measured withion-specific Na+ electrode

Elevated plasma osmolality Hyperglycemia Mannitol, glycerol, radiocontrast agents

Decreased plasma osmolality Urine maximally diluted:1. Decreased solute excretion (low protein intake) 2. Excessive water ingestion or intake Urine not maximally diluted:1. Normal extracellular volume

a. SIADH Lung disease CNS disease Drugs Anxiety

b. Adrenal insufficiency (may also have volume depletion) c. Hypothyroidism

2. Low extracellular volume a. Extrarenal loss b. Renal loss: diuretics, sodium-losing nephropathy

3. Increased extracellular volume a. Congestive heart failure b. Cirrhosis c. Nephrotic syndrome

Table 2–7. Disorders of water balance: Hyponatremia.


Hyponatremic encephalopathy is thought to be due tocerebral edema from water shifts into the brain and increasedintracranial pressure. Decreased cerebral blood flow plays arole. Movement of solute out of brain cells—given sufficienttime—minimizes the effects, probably explaining the lack ofsymptoms of slowly evolving hyponatremia. On the otherhand, evidence has linked a specific neurologic syndrome,osmotic demyelination syndrome (central pontine andextrapontine myelinolysis), with both severe hyponatremiaand rapid correction of hyponatremia. It is speculated thatadaptation to hyponatremia may be the cause of demyelina-tion in susceptible regions of the brain. A firm conclusioncannot be made about whether osmotic demyelination syn-drome is due to the severity of hyponatremia or to exces-sively fast correction. Osmotic demyelination syndrome isreported to occur about 3 days after the start of correction ofhyponatremia, but findings may be seen before, during, orafter plasma sodium has been corrected. Corticospinal andcorticobulbar signs are reported most often, including weak-ness, spastic quadriparesis, dysphonia, and dysphagia, butimpaired level of consciousness is common. Radiolucentareas on CT scan or decreased T1-weighted MRI intensityprovides evidence of myelinolysis in the central pons andelsewhere.

B. Laboratory Findings—Plasma electrolytes; glucose, crea-tinine, and urea nitrogen; plasma osmolality; urine osmolal-ity; urine Na+; and urine creatinine (to calculate fractionalexcretion of Na+) should be measured. Low plasma osmolal-ity (<280 mOsm/kg) confirms hyponatremia owing toincreased water relative to solute. The corrected plasmasodium should be used if there is hyperglycemia. An associa-tion has been found between hyponatremia with hypokalemiaand severe body potassium depletion. Hypokalemia also maypredispose patients with hyponatremia to osmotic demyelina-tion syndromes and encephalopathy. Particularly high mortal-ity has been found when hyponatremia is associated withhypoxemia.

In patients with excessive water intake as the cause ofhyponatremia, urine osmolality will be low (<300mOsm/kg). Patients with hypovolemia will have low urinesodium (<20 meq/L), fractional excretion of sodium (<1%),and fractional excretion of urea (<35%), and these also maybe seen in patients with increased extracellular volume butlow intravascular volume. If, however, hypovolemia is causedby a renal mechanism, urine sodium may not be appropri-ately conserved.

The diagnosis of SIADH is made by finding inappropri-ately high urine osmolality (usually 300–500 mOsm/kg) inthe presence of low plasma osmolality and the absence of lowurinary sodium concentration. It should be noted that inSIADH, urine osmolality may be less than plasma osmolal-ity but not as low as it should be because urine should bemaximally diluted in the presence of severe hypona-tremia. For example, in SIADH, plasma osmolality may be240 mOsm/kg, indicating severe water excess, whereas urine

osmolality is 200 mOsm/kg. Because maximally dilute urinecan be as low as 50 mOsm/kg in young healthy persons, thesefindings are consistent with SIADH. Patients with renal dis-ease may be limited in their maximum urinary diluting abil-ity to 100–200 mOsm/kg.

Treatment

Severity of hyponatremia ([Na+] <120 meq/L), acuteness ofonset, and the presence of neurologic symptoms (ie, confu-sion, stupor, coma, or seizures) determine how quickly treat-ment should be instituted and how aggressively it should bepursued. If the patient is asymptomatic and hyponatremia ismild and chronic, the need to treat is less emergent, andaggressive treatment is not needed.

A. Estimation of Water Excess—Water excess can be esti-mated by relating current measured [Na+] to TBW and sub-stituting 140 meq/L for normal [Na+]:

For a 70-kg man with a normal TBW of 0.6 L/kg, normalTBW would be 42 L. If [Na+] is 110 meq/L, TBW would beestimated as 42 ! 140 ÷ 110 = 53.5 L. The water excess wouldbe 53.5 L – 42 L = 11.5 L. If it is desired to correct [Na+] to 125meq/L because of concern about too-rapid correction to nor-mal in a patient with chronic hyponatremia, the estimatedwater excess to be corrected would be 53.5 L – (42 ! 125 ÷110) = 5.8 L.

B. Determine Need for Rapid or Aggressive Correction—Patients with hyponatremia who have altered mental statusor seizures attributed to hyponatremia require rapid treat-ment. Most patients with severely reduced [Na+] (<105 meq/L)are also a concern even if asymptomatic. Symptomatichyponatremia is usually associated with severely reduced[Na+], and only rarely do these patients have water intoxica-tion from psychogenic water ingestion, thiazide diuretics,decreased solute excretion, or conditions of hypo- or hyper-volemia. SIADH is the most commonly encountered problemrequiring aggressive and rapid correction of hyponatremia.Patients with neurologic disorders, including stroke, hemor-rhage, and head injury, are at particularly high risk for com-plications of hyponatremia.

C. Correct the Underlying Problem—Of the underlyingproblems leading to hyponatremia, the most straightforwardand easily corrected is hypovolemia. Administration of normalsaline repletes the intravascular volume and inhibits ADHrelease by reducing the hypovolemic stimulus. Water excretionis enhanced by the increased glomerular filtration rate, andurine should become quickly and near maximally dilute, facil-itating water excretion. Patients with psychogenic water intox-ication and those being given large volumes of intravenousfluid already should be maximally excreting water; removing

TBW (L) normal TBW (L)140

[Na ]= ! +


where TBW is the calculated estimate of total body water (seeearlier). This formula is useful for determining how much theplasma [Na+] will change in response to administration of 1 Lof hypertonic or normal saline. It does not take into accountfluid losses, however. To calculate the change for more than 1L of fluid administration, you must calculate for each literincrementally—that is, calculate the change in plasma [Na+]for the first liter and then enter the new value for [Na+] intothe formula to calculate the change for the next liter.

3. Vasopressin antagonism—Conivaptan, an argininevasopressin receptor antagonist, is approved for treatment ofeuvolemic hyponatremia, such as SIADH, in which inappro-priate levels of vasopressin are present. It should not be usedfor hypovolemic hyponatremia. It works by antagonizing theaction of endogenous vasopressin at both V1A and V2 recep-tors. Conivaptan is given as an intravenous loading dose of20 mg followed by a continuous infusion of 20 mg/day for1–3 days. Since the effect will vary among patients, carefulmonitoring of urine output and plasma sodium is indicated.

E. Other Treatment for Chronic Hyponatremia—Patientswith reversible CNS or lung disease generally will respondafter correction or resolution of the underlying problem.Mild to moderate water restriction may be necessary. A fewpatients will need additional help to facilitate water excre-tion; demeclocycline induces a mild nephrogenic diabetesinsipidus–like condition and may be useful in the manage-ment of chronic hypotonic hyponatremia.

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Bhardwaj A, Ulatowski JA: Hypertonic saline solutions in braininjury. Curr Opin Crit Care 2004;10:126–31. [PMID: 15075723]

Ellison DH, Berl T: Clinical practice: The syndrome of inappropri-ate antidiuresis. N Engl J Med 2007;356:2064–72. [PMID:17507705]

Hays RM: Vasopressin antagonists—Progress and promise. N EnglJ Med 2006;355:2146–8. [PMID: 17105758]

Huda MS et al: Investigation and management of severe hypona-traemia in a hospital setting. Postgrad Med J 2006;82:216–9.[PMID: 16517805]

Janicic N, Verbalis JG: Evaluation and management of hypo-osmolality in hospitalized patients. Endocrinol Metab ClinNorth Am 2003;32:459–81. [PMID: 12800541]

Kokko JP: Symptomatic hyponatremia with hypoxia is a medicalemergency. Kidney Int 2006;69:1291–3. [PMID: 16614718]

Oh MS: Management of hyponatremia and clinical use of vaso-pressin antagonists. Am J Med Sci 2007;333:101–5. [PMID:17301588]

Palm C et al: Vasopressin antagonists as aquaretic agents for thetreatment of hyponatremia. Am J Med 2006;119:S87–92.[PMID: 16843091]

Pham PC, Pham PM, Pham PT: Vasopressin excess and hypona-tremia. Am J Kidney Dis 2006;47:727–37. [PMID: 16632011]

Reynolds RM, Padfield PL, Seckl JR: Disorders of sodium balance.Br Med J 2006;332:702–5. [PMID: 16565125]

" Hypernatremia


" Plasma sodium >145 meq/L " Serum osmolality >300 mOsm/kg" Evidence of increased solute administration, polyuria

with dilute urine (diabetes insipidus), or inadequatewater intake

" Altered mental status


In contrast to hyponatremia, for which hypotonicity is oftenbut not always present, hypernatremia, defined as [Na+] greaterthan 145 meq/L, is always associated with hypertonicity,defined as plasma osmolality greater than 300 mOsm/kg.Severe hypernatremia must be treated vigorously but carefullyto avoid excessively rapid correction and further complications.

Hypernatremia indicates a deficit of TBW relative to totalbody solute (Table 2–8). This condition occasionally developswhen a large amount of solute is given in concentrated form,but hypernatremia is much more commonly associated witheither insufficient water intake or excessive water loss.

A. Addition of Solute—Addition of solute to the body with-out a corresponding addition of water results in an increase inplasma osmolality. The source of solute may be exogenous,such as administration of hypertonic saline or sodium bicar-bonate, glucose, mannitol, or other solutes. The only com-mon endogenous mechanism is gluconeogenesis andglycogenolysis causing hyperglycemia. As discussed earlier,hyperglycemia increases plasma osmolality without causinghypernatremia. Increased plasma urea increases plasmaosmolality but does not increase tonicity because urea con-centration also increases within cells. When solute is added,increased plasma osmolality stimulates maximum ADHrelease to minimize water excretion (urine osmolalityincreases). Correction of the hyperosmolal state results whenthe excess solute is disposed of or, in the case of glucose,excreted or taken into the cells as glycogen. However, the obli-gate loss of water needed to excrete solute requires that waterbe given to the patient to achieve appropriate correction.

B. Inadequate Water Intake—Insufficient water intakeresults in hypernatremia because of obligatory renal and non-renal water losses. Daily insensible loss of water amounts toabout 500 mL, increasing somewhat with body temperatureand sweating. Because most insensible loss is through the air-ways, intubation and mechanical ventilation with humidifiedair decrease insensible losses to minimal amounts.

Minimum urine volume is determined by maximumurine concentration and obligate solute excretion. As calcu-lated in Table 2–6, the normal urinary solute excretion of

! CHAPTER 232

should be measured. Plasma sodium greater than 145 meq/Lmakes the diagnosis of hypernatremia, and this will be accom-panied by plasma osmolality greater than 300 mOsm/kg.

1. Hypernatremia without polyuria—In the absence ofrenal disease and with normal ADH response, patients inwhom addition of solute is the cause of hypernatremia willexcrete small amounts of concentrated urine. Urine osmolal-ity is greater than 300 mOsm/kg and usually much higher(up to 1200 mOsm/kg in normal young adults). Patients withdecreased water intake relative to nonrenal water losses withnormal renal function also will have maximum conservationof urine volume with oliguria, plasma urea nitrogen:plasmacreatinine ratio greater than 30, low urine Na+, and low frac-tional excretion of Na+.

2. Hypernatremia with polyuria—In the presence ofhypernatremia, polyuria with dilute urine suggests that themechanism of water loss is inability to concentrate the urineappropriately, but the driving force for polyuria may be eithersolute (osmotic) diuresis or water diuresis. Water diuresis andsolute diuresis can be distinguished by the ratio of urine toplasma osmolality (UOsm/POsm). UOsm/POsm in solute diuresis(osmotic diuresis) is greater than 0.9; UOsm/POsm in water diure-sis is less than 0.9. Thus solute diuresis generally is associatedwith isosthenuria, whereas water diuresis is associated withexcretion of dilute urine. Solute diuresis can be further subdi-vided into electrolyte diuresis or nonelectrolyte diuresis. If 2 !(U[Na+] + U[K+]) >0.6 ! UOsm, then the majority of solute in theurine consists of electrolytes such as sodium and potassium; if itis less than 0.6 ! UOsm, then urea, glucose, mannitol, or othernonelectrolyte solute is the cause of the diuresis. Electrolytediuresis is seen with administration of diuretics and is the nor-mal response to correction of increased extracellular volume.Patients in the ICU who are receiving excessive amounts of nor-mal saline have increased urine output and NaCl diuresis. Urea-induced diuresis occurs after relief of obstructive nephropathyand in the diuretic phase of acute tubular necrosis.

The polyuria with water diuresis may be normal (eg, ifthe patient has hyponatremia) but is abnormal duringhypernatremia, suggesting diabetes insipidus.

3. Diabetes insipidus—Diabetes insipidus is usually charac-terized by hypernatremia, polyuria, and decreased ability toconcentrate urine maximally, but some mild cases may be dif-ficult to identify, and in other cases, earlier treatment mayconfuse the diagnosis. A water deprivation test may be neces-sary. In this test, a patient with normal or near-normal plasmaosmolality is deprived of water for a scheduled interval whileweight, plasma sodium and osmolality, and urine volume andosmolality are measured. If polyuria continues and urine con-centration fails to increase into an appropriately high range(>800 mOsm/kg) despite a plasma osmolality greater than290–300 mOsm/kg, a diagnosis of diabetes insipidus is made.

Water deprivation is allowed to continue until the patient loses3–5% of body weight. For safety when designing the water depri-vation test, patients should be anticipated to continue to maintain

urine output at the starting rate. Thus, for example, if urine vol-ume is initially 600 mL/h, a 60-kg patient could be expected tolose 3% of body weight in just 3 hours; if this urine is maximallydilute (eg, severe central diabetes insipidus), the expectedincrease in plasma osmolality also can be calculated. Actualweight loss and urine volume should be used to make the deci-sion to stop the test. Five units of aqueous vasopressin is admin-istered at the end of the test if urine concentration fails to rise.Lack of response to vasopressin indicates that the cause isnephrogenic rather than failure of release of ADH. Lack ofADH or of response to ADH can be complete or partial.Identification of intermediate response may be important indeciding treatment, and this usually can be concluded from thedegree of urine concentration achieved during the water depri-vation test.

Treatment

A. Calculation of Water Deficit—All patients with hyper-natremia have increased plasma osmolality, and the amountof water needed to correct this state can be calculated fromthe following equation:

If [Na+] is 170 meq/L and normal TBW is 0.6 L/kg, the TBWfor a man whose customary weight is 70 kg is approximately42 L ! 140 ÷ 170 = 35 kg (L), and the water deficit is 42 – 35= 7 L. Note that this is the amount of water needed to correct[Na+] to 140 meq/L. In practice, the patient’s normal bodyweight may not be known, but only the current body weight.Using current weight is acceptable as an estimate, but it ispotentially misleading because the water deficit may con-tribute to the weight difference.

B. Rate of Correction of Hypernatremia—Just as withhyponatremia, too-rapid correction of hypernatremia may beharmful. Cerebral edema with neurologic complications hasoccurred during correction as a result of a compensatorymechanism intended to maintain normal brain cell volume.In response to development of hypertonicity, brain cells fairlyrapidly increase the amount of inorganic ions; this restorescell volume to near normal, but at the expense of disruptedcellular function. With persistence of hypertonicity, braincells generate and take up idiogenic osmoles, sometimescalled organic osmolytes. Since cell volume is determined fromthe amount of solute contained within the cell, organicosmolytes resist the movement of water out of the cells andmaintain brain volume close to normal. Many of the organicosmolytes are taken up from the extracellular space by theformation of specific membrane channels. These channels donot disappear quickly or reverse function when hyperna-tremia is corrected. Therefore, rapid restoration of water tothe body theoretically may cause overexpansion of these cells,resulting in cerebral edema. Although mild controversy exists,

TBW (L) normal TBW (L)140

[Na ]+= !


conservative recommendations are to correct hypernatremiaby no more than 10 meq/L per day to allow elimination oforganic osmolytes and avoid cerebral edema. This slow rate ofcorrection may not be necessary in patients who develophypernatremia over the course of a few hours, however.

The following formula is very helpful in calculating theanticipated changes in plasma [Na+] in the hypernatremicpatient given intravenous fluids. The rate of correction ofplasma [Na+] can be estimated. This formula estimates theamount of change in plasma [Na+] when 1 L of any fluid isadministered:

where TBW is the calculated estimate of total body water(see above). This formula demonstrates how little theplasma [Na+] changes when normal saline ([Na+] = 154meq/L) is given to a hypernatremic patient. In order todetermine how much hypotonic fluid is needed to achieve a10 meq/L decrease in plasma [Na+] in 24 hours, begin bycalculating the change for 1 L of fluid administered, andthen calculate for the next liter, etc., until the desired changeis reached. The total number of liters of fluid divided by24 hours will be the hourly infusion rate. Serial measure-ments of plasma [Na+] are essential because the formuladoes not account for other fluid sources, urinary losses, orinsensible water loss.

C. Hypernatremia Associated with Increased Solute—These patients should have facilitation of solute excretion—if possible, with diuretics and administration of water or 5%dextrose in water. Diuretics will speed removal of sodiumand chloride, but the obligate loss of water with the solutewill increase the amount of water that must be given. Ifpatients have renal insufficiency, removal of solute mayrequire hemodialysis or ultrafiltration with replacement ofwater. A few patients have been treated by hemodialysis withdialysate containing hypotonic solution, facilitating waterreplacement. Peritoneal dialysis using hypotonic solutionsshould be efficacious in removing extracellular solute andincreasing water replenishment.

Patients with hyperosmolality owing to severe hyper-glycemia are treated with intravenous insulin to lower bloodglucose, but normal saline (0.9% NaCl) is the preferred ini-tial fluid replacement. Movement of glucose into cells isaccompanied by movement of water out of the intravascularspace, resulting in severe volume depletion. After adequatenormal saline is given, hypotonic fluid (5% dextrose inwater) is used to correct net water deficits.

D. Hypernatremia with Diminished ExtracellularVolume—These patients have either an extrarenal or renalloss of hypotonic fluid. Therefore, both solute and water haveto be replaced. Extracellular volume should be replaced withnormal saline first, but it should be remembered that even

large volumes of normal saline, despite being hypotonic toplasma in most hypernatremic patients, correct the waterdeficit only very slightly. For example, if [Na+] = 170 meq/Lfor a normally 70-kg patient, 1 L of 0.9% NaCl will add 308mOsm of solute and 1 L of water, predictably decreasing[Na+] to only about 169.5 meq/L. Therefore, if more rapidcorrection of hypernatremia is desired, hypotonic fluid (5%dextrose in water or 0.45% NaCl) should be given as well. Inpractice, volume repletion is generally a higher priority, butafter some correction of the volume deficit, the water deficitshould be addressed directly.

E. Hypernatremia Associated with Diabetes Insipidus—Hypernatremia in diabetes insipidus will respond to admin-istration of water orally or 5% dextrose in waterintravenously, but correction of hypernatremia depends ongiving enough water both to overcome the water deficit andto compensate for continued urine water losses. In severediabetes insipidus, urine volume can exceed 500 mL/h, andwith a severe water deficit, water may have to be given at ratesexceeding 600–700 mL/h.

Central diabetes insipidus should respond to syntheticADH compounds. Aqueous vasopressin (5–10 units two orthree times daily) can be given subcutaneously, or desmo-pressin acetate, which lacks vasopressor effects but retainsADH activity, can be given intravenously or subcutaneously(2–4 µg/day) or by nasal spray. The dose should be adjustedon the basis of plasma [Na+], urine output, and urine osmo-lality. Ideally, urine output should be reduced to 3–4 L/day,an amount that can be replaced readily by oral or intra-venous administration.

Nephrogenic diabetes insipidus is rarely as severe ascomplete central diabetes insipidus, and during water dep-rivation, urine osmolality is sometimes as high as 300–400mOsm/kg. Administration of enough water to maintainnormal plasma [Na+] usually can be achieved. If a reversiblecause such as lithium toxicity is found, the offending agentcan be discontinued, although the effect on renal concen-trating ability may persist for days. Thiazide diureticsinduce mild volume depletion, leading to increased proxi-mal tubular sodium reabsorption and decreased delivery ofsodium and water to the distal diluting segment, so that lesswater is lost.

Boughey JC, Yost MJ, Bynoe RP: Diabetes insipidus in the head-injured patient. Am Surg 2004;70:500–3. [PMID: 15212402]

Chassagne P et al: Clinical presentation of hypernatremia in eld-erly patients: A case-control study. J Am Geriatr Soc 2006;54:1225–30. [PMID: 16913989]

Khanna A: Acquired nephrogenic diabetes insipidus. SeminNephrol 2006;26:244–8. [PMID: 16713497]

Liamis G et al: Therapeutic approach in patients with dysna-traemias. Nephrol Dial Transplant 2006;21:1564–9. [PMID:16449285]

Reynolds RM, Padfield PL, Seckl JR: Disorders of sodium balance.Br Med J 2006;332:702–5. [PMID: 16565125]

!Plasma [Na ]fluid [Na ] plasma[Na ]

TBW+

+ +

= "+ 1


amounts of isotonic saline may contribute to expansionacidosis—a hyperchloremic metabolic acidosis owing largelyto dilution of plasma bicarbonate—but this is uncommon.

E. Maintenance Fluid Requirements—Normal mainte-nance fluids to prevent hypovolemia should provide1.5–2.5 L of water per day for normal-sized adults, adjustedto account for other sources of water intake (eg, medicationsand/or food intake) and the ability of the kidneys to concen-trate and dilute the urine. Sodium intake in the ICU gener-ally should be limited to a total of 50–70 meq/day, but manycritically ill patients avidly retain sodium, and they may havea net positive sodium balance with even a smaller sodiumintake. Patients are frequently given much more sodium thanneeded. For example, 0.9% NaCl has 154 meq/L of sodiumand chloride, and some patients are inadvertently given asmuch as 3–4 L/day. Although it is sometimes necessary,it is difficult to rationalize giving diuretics to a patientsimply to enhance removal of sodium given as part of replace-ment fluids. On the other hand, diuretics are useful whenneeded to facilitate excretion of the sodium ingested froman appropriate diet. In states of ongoing losses of extracellu-lar volume, appropriate fluid replacement in addition tomaintenance water and electrolytes should be given as needed(Table 2–4).

American Thoracic Society Consensus Statement: Evidence-basedcolloid use in the critically ill. Am J Respir Crit Care Med2004;170:1247–59. [PMID: 15563641]

Bellomo R et al: The effects of saline or albumin resuscitation onacid-base status and serum electrolytes. Crit Care Med2006;34:2891–7. [PMID: 16971855]

French J et al: A comparison of albumin and saline for fluid resus-citation in the intensive care unit. N Engl J Med 2004;350:2247–56. [PMID: 15163774]

McGee S et al: Is this patient hypovolemic? JAMA1999;281:1022–9. [PMID: 10086438]

Peixoto AJ. Critical issues in nephrology. Clin Chest Med2003;24:561–81. [PMID: 14710691]

Roberts I et al: Colloids versus crystalloids for fluid resuscitation incritically ill patients. Cochrane Database Syst Rev 2004;4:CD000567. [PMID: 15495001]

SAFE Study Investigators: Effect of baseline serum albumin con-centration on outcome of resuscitation with albumin or salinein patients in intensive care units: Analysis of data from the Salineversus Albumin Fluid Evaluation (SAFE) Study. Br Med J2006;333: 1044. [PMID: 17040925]

Sort P et al: Effect of intravenous albumin on renal impairment andmortality in patients with cirrhosis and spontaneous bacterialperitonitis. N Engl J Med 1999;341:403–9. [PMID: 10432325]

" Hypervolemia


" Edema, ascites, or other evidence of increased extracel-lular volume

" Intravascular volume may be normal, low (hypovolemia),or high

" Potential causes of increased extracellular volume:renal insufficiency, congestive heart failure, liver dis-ease, or other mechanism of sodium retention or exces-sive sodium administration


In contrast to hypovolemia, in which there is always decreasedvolume of the intravascular space, in hypervolemia theintravascular volume may be high, normal, or paradoxicallylow. Peripheral or pulmonary edema, ascites, or pleural effu-sions are the evidence for increased extracellular volume.Increased extracellular volume may not be an emergency inICU patients, but this depends on how much and where theexcess fluid accumulates. If associated with decreased intravas-cular volume (eg, hypovolemia), increased intravascular vol-ume (eg, pulmonary edema), or severe ascites (with respiratorycompromise), rapid intervention may be indicated.

A. Hypervolemia with Decreased IntravascularVolume—Because sodium—along with anions—is the pre-dominant solute in the extracellular space, increased extra-cellular volume is an abnormally increased quantity ofsodium and water. The body normally determines whethersodium and water should be retained by sensing the ade-quacy of intravascular volume, and the nonvascular com-ponent does not play a role in stimulating or inhibitingsodium and water retention. Thus excessive sodium reten-tion resulting in hypervolemia may occur in states of inade-quate effective circulation, such as heart failure, orsuboptimal filling of the vascular space resulting from loss offluid into other compartments, such as occurs with hypoal-buminemia, portal hypertension, or increased vascular per-meability to solute and water.

Table 2–4. Guidelines for replacement of fluid lossesfrom the gastrointestinal tract.

Replace mLper mL with Add

Gastric (vomiting ornasogastric aspiration)

5% dextrose in0.45% NaCl

KCl, 20 meq/L

Small bowel 5% dextrose in0.45% NaCl


Biliary 5% dextrose in0.90% NaCl

NaHCO3, 45 meq/L

Large bowel (diarrhea) 5% dextrose in0.45 NaCl


� Coloide vs Cristaloide

� Coloide vs Cristaloide D A T A A N D A N A L Y S E S

Comparison 1. Colloid versus crystalloid (add-on colloid)

Outcome or subgroup titleNo. ofstudies

No. ofparticipants Statistical method Effect size

1 Deaths 52 Risk Ratio (M-H, Fixed, 95% CI) Subtotals only

1.1 Albumin or plasmaprotein fraction

24 9920 Risk Ratio (M-H, Fixed, 95% CI) 1.01 [0.93, 1.10]

1.2 Hydroxyethyl starch 21 1385 Risk Ratio (M-H, Fixed, 95% CI) 1.10 [0.91, 1.32]1.3 Modified gelatin 11 506 Risk Ratio (M-H, Fixed, 95% CI) 0.91 [0.49, 1.72]1.4 Dextran 9 834 Risk Ratio (M-H, Fixed, 95% CI) 1.24 [0.94, 1.65]

Comparison 2. Colloid and hypertonic crystalloid versus isotonic crystalloid







Comparison 3. Colloid versus hypertonic crystalloid







58Colloids versus crystalloids for fluid resuscitation in critically ill patients (Review)

Copyright © 2012 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd.

Perel P, Roberts I. Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database of Systematic Reviews 2012, Issue 6. Art. No.: CD000567. DOI: 10.1002/14651858.CD000567.pub5.

� Coloide vs Cristaloide

(. . . Continued)Study or subgroup Colloid Crystalloid Risk Ratio Risk Ratio

n/N n/N M-H,Fixed,95% CI M-H,Fixed,95% CI

Fries 2004 0/20 0/20 0.0 [ 0.0, 0.0 ]

Ngo 2001 0/56 0/111 0.0 [ 0.0, 0.0 ]

Tollofsrud 1995 0/10 1/10 0.33 [ 0.02, 7.32 ]

Upadhyay 2004 9/29 9/31 1.07 [ 0.49, 2.32 ]

Verheij 2006 1/16 0/16 3.00 [ 0.13, 68.57 ]

Wahba 1996 0/10 0/10 0.0 [ 0.0, 0.0 ]

Wu 2001 2/18 3/16 0.59 [ 0.11, 3.11 ]

Subtotal (95% CI) 224 282 0.91 [ 0.49, 1.72 ]Total events: 13 (Colloid), 15 (Crystalloid)

Heterogeneity: Chi2 = 1.48, df = 4 (P = 0.83); I2 =0.0%

Test for overall effect: Z = 0.28 (P = 0.78)

4 Dextran

Dawidson 1991 1/10 1/10 1.00 [ 0.07, 13.87 ]

Hall 1978 18/86 16/86 1.13 [ 0.62, 2.06 ]

Karanko 1987 0/14 1/18 0.42 [ 0.02, 9.64 ]

Modig 1983 0/14 0/17 0.0 [ 0.0, 0.0 ]

Ngo 2001 0/55 0/111 0.0 [ 0.0, 0.0 ]

Tollofsrud 1995 0/10 1/10 0.33 [ 0.02, 7.32 ]

Vassar 1993a 21/89 11/85 1.82 [ 0.94, 3.55 ]

Vassar 1993b 49/99 20/50 1.24 [ 0.83, 1.83 ]

Younes 1992 7/35 7/35 1.00 [ 0.39, 2.55 ]

Subtotal (95% CI) 412 422 1.24 [ 0.94, 1.65 ]Total events: 96 (Colloid), 57 (Crystalloid)

Heterogeneity: Chi2 = 2.76, df = 6 (P = 0.84); I2 =0.0%

Test for overall effect: Z = 1.53 (P = 0.13)

0.01 0.1 1 10 100

Favours colloid Favours crystalloid

61Colloids versus crystalloids for fluid resuscitation in critically ill patients (Review)

Copyright © 2012 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd.

Perel P, Roberts I. Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database of Systematic Reviews 2012, Issue 6. Art. No.: CD000567. DOI: 10.1002/14651858.CD000567.pub5.

dr. carlos fernando estrada garzona departamento de...

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