Hyponatremia and Hypernatremia: Disturbances of WATER balance

Elaine M. Kaptein, MD

Professor of Medicine

University of Southern California

Plasma

3.5 L

(25%)

Interstitial

Fluid

10.5L

ECF

14 L ICF

28 L in a 70 kg man

1/3

2/3 TOTAL BODY WATER

(TBW)

60% of lean body mass in men

50% of lean body mass in

women and patients with low

muscle mass

Q: Why does the water

distribute this way?

SODIUM POTASSIUM

NORMAL CONDITIONS

Plasma

ECF

Serum Sodium Concentration

Serum [Na+] =

exchangeable body (sodium+potassium)

total body water

= amount of sodium/volume of ECF water

Normal serum [Na+] is 140 mEq/L of serum

Normal saline is 154 mEq/L of water

Regulation of Total Body

Water and Sodium

Antidiuretic hormone (ADH)

– Stimulates thirst and water reabsorption by the kidney

– Increased by hyperosmolality, hypothalamic

hypoperfusion, nausea, vomiting, stress and narcotics

Renin-Angiotensin-Aldosterone (RAAS)

- Stimulates sodium reabsorption by the kidney

- Increased by renal hypoperfusion

Definition of Hyponatremia

• Serum sodium concentration <134 mEq/L

Diagnostic Approach to

Hyponatremia • Assess serum osmolality (Freezing point depression)

– Isotonic - Hyperlipidemia or hyperproteinemia

– Hypertonic - Glucose, mannitol, contrast

– Hypotonic - Excess free water

• If hypotonic - Assess ECF and IV volume status

– Increased

– Decreased

– Euvolemic

Case Presentation

• A 49 year old male presents with malaise,

tiredness and bone pain.

• Na 128, K 4.4, Cl 95, CO2 28, Creat 1.3,

• Ca 10.9,Total Protein 17.1 g/dL, Triglycerides 60

• WBCc 4.1, Hg 8.6 g/dL

• What test would you order first?

• Serum osmolality 285 mOsm/kg H20 (NORMAL)

ISOTONIC HYPONATREMIA

PSEUDOHYPONATREMIA =

LABORATORY ARTIFACT with HIGH

concentrations of

• Lipids

• Proteins

S[Na+] is underestimated by measurements that

require a specific volume of serum and serum

dilution (Indirect methods).

Normal plasma

80% plasma

water

20% protein/lipid

91% plasma

water

9% protein/lipid

Hyperproteinemic/lipemic plasma

Pseudohyponatremia with flame photometry

Na

154 Na

154

Apparent concentration of Na in serum

154 x 0.91 = 140mEq/L serum 154 x 0.8 = 123 mEq/L

S[Na+] is normal if measured directly with ion-sensitive

electrodes in undiluted PLASMA in the ABG lab in the presence

of excess lipids or protein.

Causes of non-hypotonic hyponatraemia

SETTING:

• Presence of endogenous solutes that cause

pseudohyponatraemia (laboratory artifact)

SERUM OSMOLALITY: Isotonic

EXAMPLES:

• Triglycerides, cholesterol and protein

• Intravenous immunoglobulins

• Monoclonal gammapathies

Treatment of Pseudohyponatremia

• Recognize the problem

• Treat the primary disorder

Hypertonic Hyponatremia

• Glucose, Contrast - low-osmolar non-ionic (3-6 x normal

Osmolality), mannitol, maltose retention with IVIG

• Shift of water from the ICF to the ECF dilutes S[Na+]

• Glucose or mannitol: 2.4 mEq/L reduction in [Na+] for

every 100 mg/dL increase in glucose or mannitol, PLUS

osmotic diuresis which may raise S[Na+] due to loss of

½ NS.

• Glycine - absorption of irrigation fluids during urological

or gynaecological surgery

Hypotonic Hyponatremia

• Increased total body water due to

increased intake PLUS decreased renal excretion

• Most body losses are hypotonic

• Normal subjects can excrete 10 to 20 liters/day of

water if AVP levels can decrease to zero, there

are adequate urine osmoles, and renal function is

normal.

Hypotonic Hyponatremia

• Intake - dextrose and water IV, oral fluids (Except

broth)

• Impaired urine water excretion with excess ADH

or renal failure

• Nonosmotic ADH release - morphine, pain,

nausea, surgery, anesthesia, volume depletion

Case Presentation • A 37 year old female weighing 60 Kg is admitted for

elective knee surgery. Serum sodium was 141 mEq/L.

• Pre-op meds included 10 mg of Valium and 6 mg of Morphine. Post-op meds included phenergan for nausea and demerol for pain. She received a total of 2400 ml of “fluids” during this time.

• She was discharged 30 hours after surgery despite some nausea.

• In the evening she was noted to have progressive confusion followed by a seizure. In the ER she was found to be comatose.

Case Presentation

• On admission she was euvolemic with a serum sodium of 106 mEq/L.

• She was started on IV normal saline and 5 hours later following a seizure, her serum sodium was 105 mEq/L.

• Her urinary sodium was 110 mEq/L, and urine potassium was 40 mEq/L. Her urine output over 5 hours was 500 mL.

Treatment of Acute Hyponatremia

• Use of lasix and replacement of ½ of urine

volume with NS if euvolemic

– lasix impairs renal concentrating ability

• Indications for 3% Saline

– Seizures and coma

HYPONATREMIA ONSET

If correction >2 m Eq/hr

give urine water losses

as D5W and/or

DDAVP 2 to 4 ug IV q 8 hrs IV

Increase S[Na] by 1 mEq/L/hr

for 4 to 6 hours or

until seizures stop

Do not increase >4-6mEq/L/24 hours

3% Saline &

Lasix

ACUTE (<48 hr) or

Nausea/vomiting

Confusion

Seizures

Rapid correction =

Demyelination

in 2-6 days (CT/M RI)

Increase S[Na]

<0.5 mEq/L/hr

<6 mEq/L/24 hr

<12 mEq/L/48 hr

Lasix

W ater restrict

Treat cause

CHRONIC (>48 hr) or

M inimal or

No symptoms

Sterns TH: Management of hyponatremia in the ICU Chest 2013: 144(2):672

Goals for Acute Hyponatremia Increase serum [Na+] by

• 5 mEq/L acutely using 100 mL of 3% saline over

20 minutes and repeated X3 as needed (NEJM 2015)

Do not exceed

• >10 mEq/L in the first 24 hours (1D)

• >18 mEq/L in the first 48 hours (1D)

• Consider 1–2 ug i.v. desmopressin with

hypertonic saline

As per new quidelines

Avoid over-rapid [Na+] correction

• Match urinary water losses with D5W

• Administer 2 to 4 ug of parenteral

DDAVP to stop water diuresis (1D)

• If [Na+] rises too rapidly, give D5W to

decrease to the appropriate level (1D)

• Calculate free water required to

decrease [Na+] to desired level with

frequent monitoring

Osmotic Demyelination Syndrome • Occurs 2 to 6 days after rapid correction of

hyponatremia

• Pontine and extrapontine myelinolysis on MRI

• Slowly evolving pseudobulbar palsy and

quadriparesis, movement disorders, behavioral

disturbances or seizures.

• Highest risk: S[Na+]<105 mEq/L, rapid increase

in [Na+], hypokalemia, alcoholism, malnutrition,

liver disease, thiazides or antidepressants.

• Potentially reversible in 1/3 over several weeks

Case Presentation

• A 21 year old HIV positive male who was

admitted with diarrhea and dizziness. One hour

latter he is found unconscious in his bed. Initial

serum sodium was 132 mEq/L. Stat labs show a

serum sodium of 123 mEq/L, potassium of 3.7

mEq/L.

• He had several empty glasses at the bedside and

the 1 liter bag of D5W was empty.

Case Presentation

• What is the most likely diagnosis?

– Acute ?hypovolemic hyponatremia with cerebral

edema

• What is the appropriate treatment?

– Acute reversal of hypo-osmolar state with 3% saline

HIV Associated Hyponatremia

• Incidence in hospitalized HIV-infected patients – 35-55%

• Volume depletion – infectious diarrhea

• Adrenal Insufficiency (up to 15%)

– Adrenalitis due to CMV, Mycobacterium avium intracellulare, cryptococci, or HIV itself.

– Adrenal hemorrhage and infiltration with Kaposi's sarcoma.

– Drugs – ketoconazole blocks synthesis, dilantin and rifampin increase degradation rates

• SIAD - pneumonia (with Pneumocystis carinii or other organisms), malignancy or infection of the central nervous system

HYPOVOLEMIC HYPOTONIC

HYPONATREMIA

• Effective IV volume depletion – vomiting,

diarrhea, diuretics, bleeding, sweating, PLUS

• Free water intake and renal retention due to ADH

• ADH increased due to volume depletion, and

other non-osmotic stimuli for ADH release or

effect (eg. NSAIDs)

• 32 year old female collapses and has a seizure after running a marathon.

• S[Na+] = 102 mEq/L (probable cerebral edema)

• No edema, Bp 100/70, HR 85

• What are the underlying factors?

– Sweating, water intake, NSAIDs

What treatment – NS, 3% saline, lasix if volume overload

HYPERVOLEMIC HYPOTONIC

HYPONATREMIA

• CHF – decreased CO

• Cirrhosis – vasodilation

• Nephrotic syndrome plus diuretics

Decreased pressure sensed by carotid sinus

baroreceptors stimulates ADH release PLUS thirst

Needs assessment of intravascular volume - IVCUS

Case of Hyponatremia

• 66 year old female admitted for cervical spine

surgery for cervical radiculopathy 2 days prior.

• Baseline serum sodium 133 mEq/L

• Given 1/2 normal saline for two days 100 ml/hr

• Current serum sodium 118 mEq/L

Case of Hyponatremia • Sosm 242 mEq/L, urine sodium 190 mEq/L, clinically

euvolemic

• Initial diagnosis was SIADH. Given 3% saline over 24

hours, repeat serum sodium 118 mEq/L

• No CNS or pumonary lesions, no evidence of

malignancy, normal cardiac, hepatic and renal function.

• Meds: Fentanyl patch for pain, Celebrex, compazine for

intractable nausea.

• Prior glucocorticoid therapy for ulcerative colitis

• Currently on hydrocortisone

• History of hypothyroidism on Synthroid

• ASSESSMENT: Increased ADH release with nausea, pain and narcotics.

Increased ADH effect possible with NSAID’s.

• TREATMENT: D/C narcotics, celebrex, treat nausea, lasix and water restriction. Euvolemia

• Followup Serum sodium 130 mEq/L in 24 hours

Syndrome of Inappropriate Antidiuresis

(SIAD)

• Vasopressin secretion is inappropriate because it occurs

independently from effective serum osmolality or

circulating volume.

• May result from increased release by the pituitary gland

or from ectopic production.

• May also result from increased activity of vasopressin in

the collecting duct or from a gain-of-function mutation in

its type 2 receptor.

SIAD

• Euvolaemic hyponatraemia is caused by an

absolute increase in body water, which results

from an excessive fluid intake in the presence of

an impaired free water excretion, either due to

inappropriate release of vasopressin or due to a

low intake of solutes, which impair free water

clearance by the kidney.

SIAD

• Antidiuresis causes progressive

hyponatraemia until the expression of

vasopressin V2 receptors and aquaporin-2

water channels is down-regulated, a process

appropriately called ‘vasopressin escape’

• SIAD is essentially a diagnosis of exclusion

Diagnostic criteria for the syndrome of

inappropriate antidiuresis (SIAD) Essential criteria

• Effective serum osmolality <275 mOsm/kg

• Urine osmolality >100 mOsm/kg at some level of

decreased effective osmolality

• Clinical euvolaemia

• Urine sodium concentration >30 mmol/l with normal

dietary salt and water intake

• No recent use of diuretic agents

• Absence of adrenal, thyroid, pituitary or renal

insufficiency

European Journal of Endocrinology (2014) 170, G1–G47

Non-osmotic stimuli for ADH

• Hypovolemia

• Pharmacological agents

• Nausea and vomiting

• Pain

• Stress - e.g. Surgery and anethesia (lasts 48 hrs)

• Pulmonary disease

• CNS disease

Drugs that enhance antidiuretic

hormone release • Carbamazepine-oxycarbazepine

• Vincristine

• Nicotine

• Narcotics (opioid receptors)

• Antipsychotic/antidepressants, SSRI’s

• Ifosfamide

• Halothane

Drugs that potentiate renal action of

antidiuretic hormone

• Cyclophosphamide

• Nonsteroidal anti-inflammatory drugs

• Acetaminophen

Ectopic ADH Secretion

• Ectopic Hormone Secretion by pumonary

malignancies (bronchogenic Ca)

• Intracranial lesions – stroke, IC hemorrhage,

massive brain destruction

Treatment of Chronic SIAD • Treat underlying cause if possible

• Water restriction

• Increase solute intake with 0.25–0.50 g/kg per day

of urea

• Low-dose loop diuretics and oral sodium chloride

RISK MAY EXCEED BENEFIT: NOT

ADVISED

• ?Demeclocyline – causes a nephrogenic DI (1D)

• ?Vaptans – Conivaptan IV, Tolvaptan po (1C)

European Journal of Endocrinology (2014) 170, G1–G47

Case Presentation

• A 32 year old male presents to ER with

obtundation. He has been drinking nothing but

beer for 10 days. His serum sodium is 92 mEq/L.

He had no edema. He weighs 90 kg.

• He was intubated, give 3% NS but never regained

consciousness.

Potomania • Beer drinkers or malnourished patients have reduced

ability to excrete water due to poor dietary intake.

• Normal osmolar excretion is 600 to 900 mOsmol/kg of solute per day – Na, K, urea

• If min Uosm is 60 mosm/kg H2O, max Uvol is 10 to 15 L/day (900 mOsm per day /60 mOsm/kg H20= 15 L)

• Beer contains no Na, K or protein. CHO load suppresses endogenous protein breakdown.

• Daily solute excretion may fall to <250 mOsm/kg so max Uvol is <4 L/day. If more volume is taken in, hyponatremia develops. Also nausea, volume depletion

Low Solute Excretion • Renal water excretion depends on solute excretion and

hence solute intake and production.

• Depending on renal diluting ability, 50–100 mmol of

solutes, such as urea and salts, are required to remove

one liter of water.

• If solute intake is low relative to water intake, urine

osmoles insufficient to remove water ingested.

• Seen with anorexia (nervosa), beer potomania and ‘tea

and toast’ hyponatraemia.

A case of new onset hyponatremia

• A 64 year old female is admitted to ICU with a S[Na+] of 102 mEq/L. She had a S[Na+] a month earlier of 135. She was given HCTZ for treatment of calcium containing renal stones.

• She is pale with male pattern baldness. Bp 90/60 HR 65, lying in bed mildly confused.

What tests would you order and how would you treat her?

Hyponatremia with Diuretics

• Thiazide diuretics - impair urine dilution and can accentuate hyponatremia without overt hypovolemia

• Loop diuretics – impair urine concentration and can cause overt hypovolemia

64 year old female

• She is given normal saline

• TSH 4.5, cortisol 3

• What is her diagnosis?

• Total and Free T4 very low

• History from daughter – the last born

• Traumatic delivery, no breastfeeding, no

menstruation since, loss of body hair.

Case Presentation How should she be treated?

• Normal saline until euvolemic, then replace water

losses in urine (Do urine [Na+]/154=NS fraction)

• May give 3% saline for CNS symptoms but will

increase volume overload

• Monitor serum sodium concentrations q2 hours

• If rate of S[Na+] rise is too rapid, give D5W to

match water losses in urine

• Give DDAVP to slow rate of water loss in urine

64 year old female

• Diagnosis? Hypopituitarism

• Treatment? Saline, L-T4, hydrocortisone 100 mg

• She makes 5 to 6 liters of urine in the next 24

hours.

• Our recommendation: q2 hour S[Na+] to increase

S[Na+] no more than 1.5 mEq/hour. If too rapid

correction, check urine Na and match UO of H2O

with D5W

64 year old female

• 24 hours later S[Na+] 127 mEq/L because only

NS given and large urinary free water excretion.

Patient more alert and BP normal

• Now what?

• Recommend giving free water and DDAVP to

reverse rapid correction.

• Luckily – No central demyelination

64 year old female Why did the S[Na] rise so rapidly in this patient?

1) Volume depletion corrected and ADH decreased and distal water delivery increased

2) T4 and cortisol increase free water clearance

LESSON: Watch patients with volume depletion very closely to avoid too rapid S[Na+] correction and match water losses with replacement D5W or oral H2O, and give DDAVP q 8 hours IV.

HYPONATREMIA Q. WHAT IS SERUM OSMOLALITY?

([Na]x2 + glucose /18 + BUN/2.8)

Hyperlidemia

Hyperproteinemia

PSEUDO

NORMAL

Hyperglycemia

Mannitol

Contrast

INCREASED

Saline

GI loss

Renal loss

Third space

Decreased

Treat 1ary cause

H20 restrict

Lasix and Na

Demeclocycline

Hypothyroid

Hypoadrenal

SIADH

Normal

Restrict Na

Diuretics

Restrict H20

CHF

Cirrhosis

Nephrosis

Increased

Q. What is ECF

volume?

DECREASED

HYPONATREMIA Q. WHAT IS SERUM OSMOLALITY?

([Na]x2 + glucose /18 + BUN/2.8)

Hyperlidemia

Hyperproteinemia

PSEUDO

NORMAL

Hyperglycemia

Mannitol

Contrast

INCREASED

Volume expansion

Restrict free water?

Mobilize edema?

GI loss

Renal loss

BLEEDING

THIRD SPACE?

Hypovolemic

Treat primary cause

Restrict free water

Lasix, replace Na losses

Mobilize edema?

Hypothyroid

Hypoadrenal

SIAD

THIRD SPACE?

Normovolemic

Restrict Na

Restrict free water

Loop diuretic

Mobilize edema?

CHF

THIRD SPACE?

Hypervolemic

Q. What is

INTRAVASCULAR

VOLUME?

DECREASED

Treatment of Chronic Hyponatremia • Treat underlying cause if possible

• Water restriction

• Increase solute intake with 0.25–0.50 g/kg per day

of urea

• Low-dose loop diuretics and oral sodium chloride

RISK MAY EXCEED BENEFIT:

• NO Lithium or Demeclocyline – nephrotoxic

(1D)

• NO Vaptans – hepatotoxic, no survival benefit

(1C)

European Journal of Endocrinology (2014) 170, G1–G47

HYPERNATREMIA

S[Na+]>145 mEq/L

Case

A 65 year old male with known liver cirrhosis is

admitted with jaundice and altered mental status.

Serum sodium is 158 mEq/L, BUN 35, Creatinine

2.5.

What is the most likely cause of hypernatremia?

A. Central DI

B. Nephrogenic DI

C. Hepatic encephalopathy

D. Acute renal failure

Case A 65 year old male with known liver cirrhosis is

admitted with jaundice and altered mental status.

Serum sodium is 158 mEq/L, BUN 35, Creatinine

2.5.

Total protein 6.0, albumin 2.1, ABG sodium 154

mEq/L

What is the cause for the difference between BMP

and ABG sodium concentrations?

PseudohypERnatremia

• Low serum protein concentrations increase the

water phase of serum to >93% and can result in

an artifactual increase of [Na+] by indirect

potentiometry compared to direct potentiometry.

• > 4 mEq/L difference in 25% of ICU, 8% of

hospitalized specimens

• 97% with > 4 mEq/L difference were due to low

protein concentrations.

• J Crit Care 27:326.e9-e12, 2012

Normal plasma

95% plasma

water

5% protein/lipid

91% plasma

water

9% protein/lipid

Hypoproteinemic plasma

Pseudohypernatremia with flame photometry

Na

154 Na

154

Apparent concentration of Na in serum

154 x 0.91 = 140mEq/L serum 154 x 0.95 = 146 mEq/L

S[Na+] is normal if measured directly with ion-sensitive electrodes in undiluted

PLASMA in the ABG lab in the presence of low protein and lipids.

Diagnostic Approach to

Hypernatremia Compare serum [Na+] on BMP with VBG/ABG

– Higher on BMP with hypoproteinemia

– Lower with hyperglycemia, mannitol, contrast

• Assess ECF volume status

– Increased

– Decreased

– Euvolemic

• How should this patient be treated?

• Calculate free water deficit

• Estimate ongoing losses

HYPERNATREMIA CLINICAL CIRCUMSTANCES

Elderly/Infants

AMS

Decreased Thirst

Unable to drink

Reset osmostat

Central Nephrogenic

Diabetes Inspidus

Pure Water

Losses

Renal,

GI, lung, skin

Hypotonic

Losses

Increased losses Hypertonic Na

Bicarbonate

3% Saline

TPN

HYPERNATREMIA • CALCULATE FREE WATER DEFICIT

• [Na] x 0.6 (TBwt) = 140 mEq/l x new TBW

• Difference is free water deficit

• S[Na] = 158 mEq/L in a 70 kg male

• 158 x 0.6 x 70 = 140 x new TBW

• New TBW = 47.4 L compared to 42 L

• Free water deficit is 5.4 L

Treatment of Hypernatremia • ½ of free water deficit to decrease serum sodium

no more than 8 mEq/L per 24 hours

• PLUS

• 0.5 to 1 liter of insensible losses

• 50% NG suction or vomitus

• 60%-85% of diarrhea

• 50% urine output to start – if urine sodium 50-70

mEq/L (CHECK urine [Na+])

• GIVE D5W or oral/NG H2O

HYPOTONIC FLUID LOSSES

• RENAL: Osmotic diuresis - glucose, mannitol,

glycerol, urea, sorbitol, contrast, diuretics

Losses = 1/2 normal saline (Ur Na+ 80 mEq/L)

• NONRENAL:

– GI: ?Osmotic diarrhea: sorbital or lactulose, vomiting

– SWEAT

– RESPIRATION

HYPERNATREMIA TREATMENT:

1. Correct underlying problem

2. Replace 1/2 of free water deficit in 24 hours. Do not decrease serum [Na] >0.5 mEq/L per hour to avoid cerebral edema (10 mEq/d)

3. Replace ongoing water losses - insensible losses, ?upper GI, ?diarrhea, 1/2 urine output.

4. Maintain euvolemia.

Assessment of Hypo- and Hypernatremia

1) Assess intravascular volume

2) Make the patient euvolemic

3) Correct free water excess or deficit

REQUIRES

1) Accurate intravascular volume assessment

2) Knowledge of inputs and outputs that contribute

to intravascular volume and total body water

Assessing Intravascular Volume

• Clinical symptoms and signs – difficult to

accurately assess due to comorbidities and

insensitive

• CVP – not always available, not very reliable

• PCWP – frequently not available

• IVC US – readily available and may be useful

IVC Imaging by Ultrasound

The IVC should be visualized in the subcostal view; in the supine

position, probe rotated 90 degrees toward head of patient, measured

2cm from where it enters right atrium.

IVC overload

IVC large, collapsing

• 100 % IVC collapsibility Index

[Na+] mEq/L 050100150200

[Na+] mEq/L 050100150200

Bod

y F

luid

s

BODY FLUID

Gastric

Bile

Pancreatic

Small bowel

Cholera diarrhea

Infectious diarrhea

Non-infectious diarrhea

Osmotic diarrhea sorbitol

Osmotic diarrhea lactulose

Osmotic diarrhea PEG

Secretory diarrhea

Pleural effusion

Ascites

Edema

Hemodialysis Ultrafiltrate

Peritoneal dialysis UF

Sweat

% NS 02550100150

% NS 02550100150

Replacement

NS : Water

1 : 2

1 : 0

1 : 0

1 : 0

1 : 0

1 : 1

1 : 1

1 : 1

1 : 4

0 : 1

1 : 1

1 : 0

1 : 0

1 : 0

1 : 0

1 : 0

Insensible loss

Number

695

248

192

1212

48

63

96

34

72

64

117

8

271

11

46

113

551

Hyponatremic Normal [Na+] Hypernatremic

Hypovolemic • Give volume.

• Don’t replace water

losses unless serum

[Na+] increases too

rapidly

• Give volume.

• Replace ongoing

water and sodium

losses.

• Give volume.

• Replace ½ free

water deficit (<10

mEq/L/day)

• Replace ongoing

Na & water losses.

Euvolemic • Furosemide to impair

urine concentrating

ability

• Replace ½ UOP with

NS

• Replace ongoing

water and sodium

losses

• Replace ½ free

water deficit

• Replace ongoing

sodium and water

losses

Hypervolemic • Furosemide to impair

urine concentrating

ability.

• Do not replace UOP

with NS or free water

• Free water and sodium

restrict

• Furosemide for

volume overload.

• Replace ongoing free

water losses.

• Sodium restrict

• Furosemide for

volume overload.

• Replace ½ free

water deficit

• Replace ongoing

water losses.

• Sodium restrict

Conclusions

• Assessment and management of hypo- and

hypernatremia requires accurate assessment of

intravascular volume and appropriate volume and

water management.

• IVC US may be a valuable tool in assessing

intravascular volume and response to therapy.

• Accurate assessment of water and volume

contributions of inputs and outputs is essential.

• Questions?