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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?
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