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Intravenous Fluids

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Page 1: INTRAVENOUS FLUIDS FOR PHYSICIANS

Intravenous Fluids

Page 2: INTRAVENOUS FLUIDS FOR PHYSICIANS

Overview

• Body Fluids

• Fluid Regulation

• Intravenous Fluids

• Urine Electrolytes

• Using Intravenous Fluids

Page 3: INTRAVENOUS FLUIDS FOR PHYSICIANS

Total Body Water

• Varies with age, gender, body habitus

• 55% body weight in males

• 45% body weight in females

• 80% body weight in infants

• Less in obese: fat contains little water

• TBW = 0.6 X Weight in kgs

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Body Water Compartments

• Intracellular water: 2/3 of TBW

• Extracellular water: 1/3 TBW

- Extravascular water: 3/4 of extracellular water

- Intravascular water: 1/4 of extracellular water

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Osmolality• Osmolality is a measure of the number of particles present in solution and is independent of the size

or weight of the particles.

• The osmotic pressure is the hydrostatic (or hydraulic) pressure required to oppose the movement of water through a semipermeable membrane in response to an ‘osmotic gradient’ (i.e. differing particle concentrations on the two sides of the membrane).

the solutes present in the solution. The value measured in the laboratory is usually referred to as the ‘osmolality’. The value calculated from the solute concentrations is reported by the laboratory as the ‘osmolarity’. The Osmolar gap is the difference between these two values.

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Osmolality

• Serum osmolality can be measured by use of an osmometer or it can be calculated as the sum of the concentrations of the solutes present in the solution.

• The value measured in the laboratory is usually referred to as the ‘osmolality’.

• The value calculated from the solute concentrations is reported by the laboratory as the ‘osmolarity’.

• The Osmolar gap is the difference between these two values.

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Tonicity

• Tonicity is a measure of the osmotic pressure (as defined by the water potential of the two solutions) of two solutions separated by a semipermeable membrane.

• Tonicity is the effective osmolality and is equal to the sum of the concentrations of the solutes which have the capacity to exert an osmotic force across the membrane.

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Osmolality vs Tonicity

•Two solutions having the same osmolality (exerting the same osmotic pressure) are said to be isosmotic

•When two solutions are separated by a membrane and there is no net transfer of water, the solutions are said to be isotonic

THESE ARE NOT THE SAME!

Page 11: INTRAVENOUS FLUIDS FOR PHYSICIANS

Osmolality vs Tonicity

•Osmolality and Tonicity: Relationship to Membrane

•Osmolality is a property of a particular solution and is independent of any membrane.

•Tonicity is a property of a solution in reference to a particular membrane.

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Osmolality vs Tonicity

• Comparison of Different Definitions of Tonicity

• "Effective" osmolality - The best definition as it accounts for permeant solutes and is quantitative.

• The red cell test - A practical qualitative definition that emphasises the requirement that tonicity is defined in reference to a membrane.

• Comparison with osmolality of plasma - Effectively the same as the definition based on the red cell test.

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Tonicity

• Isotonic

• Hypertonic

• Hypotonic

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Types of Fluids

• Crystalloids

• Colloids

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The IV Fluid Supermarket• Crystalloids

– Dextrose in water

• D5W

• D10W

• D50W

• Saline

• Isotonic (0.9% or “normal”)

•Hypotonic (0.45%, 0.25%)

•Hypertonic

• Combo

•D51/2NS

•D5NS

•D10NS

• Ringer’s lactate “physiologic”.

(K, HCO3, Mg, Ca)

• Colloids– Albumin• 5% in NS• 25% (Salt Poor)

– Dextrans– Hetastarch

• Blood

Page 18: INTRAVENOUS FLUIDS FOR PHYSICIANS

0.45 NS 152 77 77 0

Page 19: INTRAVENOUS FLUIDS FOR PHYSICIANS

Persistence of fluids in Circulation

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Maintenance Fluids• The following factors must be taken into

account:

• Maintenance fluid requirements

• NPO and other deficits: NG suction, bowel prep

• Third space losses

• Replacement of blood loss

• Special additional losses

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Maintenance Fluids

• Who Needs Them?

• What’s Maintenance?

• How Much H20?

• 100 cc/kg/d 1st 10 Kg

• 50 cc/kg/d 2nd 10 Kg

• 20 cc/kg/d for every Kg > 20 Kg

• Na?

• K?

• Dextrose?

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Maintenance Fluids

• Insensible losses such as evaporation of water from respiratory tract, sweat, feces, urinary excretion. Occurs continually.

• Adults: approximately 1.5 ml/kg/hr

• “4-2-1 Rule”

- 4 ml/kg/hr for the first 10 kg of body weight

- 2 ml/kg/hr for the second 10 kg body weight

- 1 ml/kg/hr subsequent kg body weight

- Extra fluid for fever, tracheotomy, denuded surfaces

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Dr. Muddassir’s Favourite

•Maintenance Fluid:

•25 - 35 ml / kg Body Weight

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Maintenance Fluids

• NPO deficit = number of hours NPO x maintenance fluid requirement.

• Bowel prep may result in up to 1 L fluid loss.

• Measurable fluid losses, e.g. NG suctioning, vomiting, ostomy output

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Blood Loss

• Replace 3 ml of crystalloid solution per ml of blood loss (crystalloid solutions leave the intravascular space)

• When using blood products or colloids replace blood loss volume per volume

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Other Factors

• Ongoing fluid losses from other sites:

- gastric drainage

- ostomy output

- diarrhea

• Replace volume per volume with crystalloid solutions

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Clinical Evaluation of Fluid Replacement

1.Urine Output: at least 1.0 ml/kg/hr

2. Vital Signs: BP and HR normal (How is the patient doing?)

3. Physical Assessment: Skin and mucous membranes no dry; no thirst in an awake patient

4. Invasive monitoring; CVP or PCWP may be used as a guide

5. Laboratory tests: periodic monitoring of hemoglobin and hematocrit

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DehydrationDehydration

• Elevated plasma sodium concentration and osmolality with loss of intracellular water causing cellular dessication.

• Example

• Elderly with fluid losses in heat and poor access to water

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Volume DepletionVolume Depletion

• Refers to loss of sodium from the extracellular space

• Interstitial fluid

• Intravascular fluid

• Examples

• GI Hemorrhage

• Vomiting

• Diarrhea

• Diuretics

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Concentration of urine

UO = 1-2ml/kg/hr

Sunken eyeballsOliguria

UO = 0.5-1ml/kg/hr

Delayed capillary refill

Acidosis (large base deficit)

UO < 0.5ml/kg/hr

Percent Clinical Dehydration Symptoms

<5%

5-10%

>15%

• Rapid heart rate

• Dry mucous membranes

• Increased severity

• Decreased skin turgor

• Pronounced severity of above signs

• Supine Hypotension

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Orthostatic Hypotension

• Systolic blood pressure decrease of greater than 20mmHg from supine to standing

• Indicates fluid deficit of 6-8% body weight

- Heart rate should increase as a compensatory measure by 10/min

- If no increase in heart rate, may indicate autonomic dysfunction or antihypertensive drug therapy

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Fluid Bolus

• How Much?

• 10-20 ml/kg

• 500ml-1000ml

• How Fast?

• Healthy vs Premorbid Illness

• Of What?

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Fluid Bolus

•Mostly Always Normal Saline!

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Urine Electrolytes

• Na

• K

• Cl

• Osmolality

• No normal values; only normal ranges

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Clinical uses of Urine Chemistries

Parameter Uses

Na+ excretion

•Assessment of volume status•Diagnosis of hyponatremia and acute renal failure•Dietary compliance in patients with hypertension

•Evaluation of calcium and uric acid excretion in stone- formers

Cl- excretion•Similar to that for Na+ excretion•Diagnosis of metabolic alkalosis

•Urine anion gap

K+ excretion Diagnosis of hypokalemia

Osmolality or specific gravity

Diagnosis of hyponatremia, hypernatremia, and acute renal failure

pH •Diagnosis of renal tubular acidosis•Efficacy of treatment of metabolic alkalosis and uric acid stones

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Urine Na

• Effective Intravascular Volume

• Mediated by R-A-A system & ANP

• Represents Excess Dietary Na / Cl

• ~ 10 - 300 mmol/day (normal IV vol)

• < 20 mmol/L ( low IV vol)

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High Output Cardiac Failure

↑ Renin-Angiotensin-Aldosterone System

↑ Vasopressin release

↓ EABV

↓ Cardiac Output↓ PVR

Low Output Cardiac Failure

↑ Sympathetic Nervous System

Renin Sodium andWater Rentention

Forward Hypothesis

Page 39: INTRAVENOUS FLUIDS FOR PHYSICIANS

Urine Na

• Oliguria : Na or Cl constant

• H20 decrease

• Conc of Na / Cl ~ 25 mmol/L

• Appropriate Physiological Response

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Urine Na• Hyponatremia & UNa < 20 =

Hypovolemia

• Hyponatremia & UNa < 40 = SIADH

• 24 Hr UNa < 100 mEq in HTN = Dietary Compliance with Na

• 24 UNa < 78 mEq = Diuretic-Resistant Asictes

• Spot UNa < UK+ = Diuretic-Resistant Asictes, with maximum tolerable dose of oral diuretics

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Urine Na

• Diuretics:

• Initially UNa & water

• As diuresis increases, Na is reabsorbed both in the proximal as well as the collecting tubules

• Steady achieved within one week

• Drug dose & Dietary Intake constant

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Urine Na•Limitations • Low urine Na+ concentration may be seen in

normovolemic patients who have selective renal or glomerular ischemia due to bilateral renal artery stenosis or acute glomerulonephritis.

• Defect in tubular Na+ reabsorption can lead to a high rate of Na+ excretion, despite the presence of volume depletion e.g. diuretics, in aldosterone deficiency, or in advanced renal failure.

• Rate of water reabsorption. e.g. central diabetes insipidus, can lead to a urine output exceeding 10 L/day. In this setting, the daily excretion of 100 meq of Na+ will be associated with a urine Na+ concentration of 10 meq/L or less, incorrectly suggesting the presence of volume depletion.

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HyponatremiaNormally, the extracellular-fluid and intracellular-fluid compartments make up 40 percent and 60 percent of total body water, respectively (Panel A).

With the syndrome of inappropriate secretion of antidiuretic hormone, the volumes of extracellular fluid and intracellular fluid expand (although a small element of sodium and potassium loss, not shown, occurs during inception of the syndrome) (Panel B).

Water retention can lead to hypotonic hyponatremia without the anticipated hypo-osmolality in patients who have accumulated ineffective osmoles, such as urea (Panel C).

A shift of water from the intracellular-fluid compartment to the extracellular-fluid compartment, driven by solutes confined in the extracellular fluid, results in hypertonic (translocational) hyponatremia (Panel D).

Sodium depletion (and secondary water retention) usually contracts the volume of extracellular fluid but expands the intracellular-fluid compartment. At times, water retention can be sufficient to restore the volume of extracellular fluid to normal or even above-normal levels (Panel E).

Hypotonic hyponatremia in sodium-retentive states involves expansion of both compartments, but predominantly the extracellular-fluid compartment (Panel F).

Gain of sodium and loss of potassium in association with a defect of water excretion, as they occur in congestive heart failure treated with diuretics, lead to expansion of the extracellular-fluid compartment but contraction of the intracellular-fluid compartment (Panel G).

Page 44: INTRAVENOUS FLUIDS FOR PHYSICIANS

Clinical FeaturesSeizures, coma > 160 mmol/L

weakness, lethargy > 150 mmol/L

Normal 137 - 146 mmol/L

no clinical changes expected 125 - 136 mmol/L

nausea, drowsiness < 125 mmol/L

vomiting ,confusion < 120 mmol/L

convulsions, coma < 110 mmol/L

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Formula to calculate the change in serum sodium concentration with 1 L of intravenous fluids, based on the sodium content of the fluid, the current measured serum sodium concentration, a correction factor to help estimate total body water volume, and the patient's weight. This formula applies to the treatment plan for hyponatremia and hypernatremia.

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Algorithm for the recommended management of hyponatremia.

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Effects of transcellular fluid shifts on brain cells in hyponatremia and hypernatremia. Electrolytes and osmolytes shift in response to a hypo-osmolar and hyperosmolar extracellular

environment, respectively,to preserve normal cellular volume. Overly aggressive fluid resuscitation can result in complications, such as osmotic demyelination syndrome and cerebral

edema.

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Extracellular-Fluid and Intracellular-Fluid Compartments under Normal Conditions

and during States of Hypernatremia.

Normally, the extracellular-fluid and intracellular-fluid compartments account for 40 and 60

percent of total body water, respectively (Panel A).

Pure water loss reduces the size of each compartment proportionately (Panel B).

Contrary to common belief, the volume of extracellular fluid in this setting is reduced, not

normal, although the reduction is often not clinically evident. The sodium content of

extracellular fluid remains unaltered, yet 1 of each 2.5 liters of water that is lost is from the

extracellular-fluid compartment.

Hypotonic sodium loss causes a relatively larger loss of volume in the extracellular-fluid

compartment than in the intracellular-fluid compartment (Panel C).

Potassium loss in addition to hypotonic sodium loss further reduces the intracellular-fluid

compartment (Panel D).

Hypertonic sodium gain results in an increase in extracellular fluid but a decrease in intracellular

fluid (Panel E).

Hypernatremia

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Clinical FeaturesSeizures, coma > 160 mmol/L

weakness, lethargy > 150 mmol/L

Normal 137 - 146 mmol/L

no clinical changes expected 125 - 136 mmol/L

nausea, drowsiness < 125 mmol/L

vomiting ,confusion < 120 mmol/L

convulsions, coma < 110 mmol/L

Page 54: INTRAVENOUS FLUIDS FOR PHYSICIANS
Page 55: INTRAVENOUS FLUIDS FOR PHYSICIANS

Formula to calculate the change in serum sodium concentration with 1 L of intravenous fluids, based on the sodium content of the fluid, the current measured serum sodium concentration, a correction factor to help estimate total body water volume, and the patient's weight. This formula applies to the treatment plan for hyponatremia and hypernatremia.

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Effects of transcellular fluid shifts on brain cells in hyponatremia and hypernatremia. Electrolytes and osmolytes shift in response to a hypo-osmolar and hyperosmolar extracellular

environment, respectively,to preserve normal cellular volume. Overly aggressive fluid resuscitation can result in complications, such as osmotic demyelination syndrome and cerebral

edema.

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Urine K

• Depends upon:

• Daily Intake

• Aldosterone

• Direct Effect of Plasma K

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Urine K

• Low K : Decrease K+ Excretion (5 - 25mEq/day)

• Used in Hypokalemia

• Not Helpful in Hyperkalemia

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Hypokalemia

Labs :

BP

TKKG

Acid Base Disorder

Urine K, Cr, Cl

S. Renin

S. Aldosterone

TKKG

Urine K / Cr Ratio

K Shift:

TKKG < 3

Urine K /Cr < 2.5

Paralysis No Paralysis

No Thyroid Family Hx

Sporadic Peroidic Paralysis

Thyrotoxic Periodic Paralysis

Familial Periodic Paralysis

Insulin

Ba Poisoning

Stress Poisoning

TKKG = [ Uk / (Uosm / Posm)]

Pk

Page 62: INTRAVENOUS FLUIDS FOR PHYSICIANS

Hypokalemia

TKKG

Urine K / Cr Ratio

K Deficit:

TKKG > 3

Urine K /Cr > 2.5

Acid Base Disorder

Metabolic Disorder Metabolic alkalosis

Urine Anion Gap

Urine Osmolar Gap

High Low

RTADiarrhea

Toulene Abuse

BP

Normal

Urine Cl

HighLow

Vomiting Diuretics

Gitelman Syndrome

Barter Syndrome

HighSerum Renin

Serum Aldosterone

Low Serum Renin

High Serum Aldosterone

High Serum Renin

High Serum Aldosterone

Primary Aldosterone

Licorice Ingestion

Ectopic Corticotropin

Apparent Mineralocoticoid Excess

Syndrome

Liddle Syndrome

Page 63: INTRAVENOUS FLUIDS FOR PHYSICIANS

Urine Cl-

• Adds to information of Na+ absorption.

• 30 percent of hypovolemic patients have more than a 15-meq/L difference between the urine Na+ and Cl- concentrations. This is due to the excretion of Na+ with another anion (such as HCO3- or carbenicillin) or to the excretion of Cl- with another cation (such as NH4+ in metabolic acidosis).

• Helpful in a patient who seems to be volume depleted, but has a somewhat elevated urine Na+ concentration.

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Urine Cl-

• Metabolic alkalosis, in which acid-base balance can be restored by urinary excretion of the excess HCO3- as NaHCO3. Many of these patients, however, are volume depleted due to vomiting or diuretic use.

• To the degree that the hypovolemic stimulus to Na+ retention predominates, there will be low Na+ and HCO3- levels in the urine and persistence of the alkalosis.

• If, on the other hand, there is a relatively mild volume deficit as compared to the severity of the alkalosis, some NaHCO3 will be excreted, thereby elevating the urine Na+ concentration (in some cases to over 100 meq/L).

• In comparison, the urine Cl- concentration will remain appropriately low (unless some diuretic effect persists), since there is no defect in the reabsorption of NaCl

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Urine Cl-• Normal anion gap metabolic acidosis. In the absence of

renal failure, this problem is most often due to diarrhea or to one of the forms of renal tubular acidosis (RTA).

• The normal response to acidemia is to increase urinary acid excretion, primarily as NH4+. When urine NH4+ levels are high, the urine anion gap

•     Urine anion gap   =   ([Na+]  +  [K+])  -  [Cl-]

• will have a negative value, since the Cl- concentration will exceed that of Na+ and K+ by the approximate amount of NH4+ in the urine.

• Urine Cl- concentration high in diarrhea-induced hypovolemia because of the need to maintain electroneutrality as NH4+ excretion is enhanced.

• Urinary acidification is impaired in RTA, leading to a low level of NH4+ excretion and a positive value for the urine anion gap . The urine pH also will be inappropriately high (>5.3) in this setting.

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Metabolic AlkalosisCauses: Low Urine Chloride <10 meq/L Gastrointestinal causes VomitingNasogastric suction Chloride-wasting DiarrheaVillous adenoma of colon Renal Causes Diuretic use (Urine Chloride >10 meq/L) Poorly reabsorbable anion CarbenicillinPenicillinSulfate Phsophate Post-Hypercapnia Exogenous alkali Sodium Bicarbonate (baking soda) Sodium Citrate Lactate Gluconate Acetate Transfusion Antacid Cystic Fibrosis Achlorhydria

Contraction alkalosis

Normal or High Urine Chloride >20 meq/L Hypertensive Patient Adrenal Disease Primary HyperaldosteronismCushing's Syndrome (Pituitary, Adrenal or ectopic) Liddle Syndrome Exogenous steroids Excess mineralocorticoid intake Excess glucocorticoid intake Excessive licorice intake Carbenoxalone Glycyrrhizic acid Chewing TobaccoNormotensive Patient Bartter Syndrome or Gitelman Syndrome HypokalemiaExcessive alkali administration Milk-Alkali Syndrome

Refeeding alkalosis

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Approach to the patient with polyuria due to an osmotic diuresis.

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Approach to the patient with polyuria due to a water diuresis.

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• The major limitation in the use of the FENa is that it is dependent upon the amount of Na+ filtered and therefore the dividing line between volume depletion and normovolemia is not always 1 percent. This can be best appreciated in patients with normal renal function. If the GFR is 180 L/day (125 mL/min) and the plasma Na+ concentration is 150 meq/L, then 27,000 meq of Na+ will be filtered each day. As a result, the FENa will always be under 1 percent as long as daily Na+ intake is in the usual range of 125 to 250 meq. Since patients with relatively normal renal function should be able to lower daily Na+ excretion to less than 20 meq/day in the presence of volume depletion, the FENa should be less than 0.2 percent in this setting. A FENa of 0.5 percent is indicative of normovolemia not volume depletion in such a patient unless there is renal salt wasting. In comparison, a FENa of 0.5 percent does reflect volume depletion in advanced renal failure, a condition in which the GFR and therefore the filtered Na+ load are markedly reduced. If, for example, the GFR is only 10 percent of normal, then the filtered Na+ load is 2700 meq/day; 0.5 percent of this quantity is equal to only 14 meq of Na+ excreted per day.

• The FENa and the UNa are difficult to interpret with concurrent diuretic therapy, since the ensuing natriuresis will raise these values even in patients who are hypovolemic. Although not widely available, measurement of the fractional clearance of endogenous lithium (which is present in trace amounts) may circumvent this problem. Lithium is primarily reabsorbed in the proximal tubule, which has two important consequences: proximal reabsorption is increased and therefore lithium excretion is reduced in hypovolemic states; and lithium excretion is not significantly increased by loop diuretics. The fractional excretion of lithium (FELi) is approximately 20 percent in healthy controls. In one report of patients with acute renal failure, a value below 15 percent (and usually below 10 percent) was highly suggestive of prerenal disease, independent of diuretic therapy [18]. In comparison, the mean FELi was 26 percent in ATN.

• Given the usual lack of ability to measure trace lithium, other markers for proximal function have been evaluated. Uric acid handling occurs almost entirely in the proximal tubule (see page 00) and the fractional excretion of uric acid is not affected by loop diuretic therapy. In the study noted above, values below 12 percent were suggestive of prerenal disease (sensitivity 68 percent, specificity 78 percent), while values above 20 percent were suggestive of ATN (sensitivity 96 percent, specificity only 33 percent) [18]