Fluids and Electrolytes 1 Flashcards

1
Q

What does water loss lead to?

A

Water loss leads to increase in serum sodium and osmolality resulting in a stimulation of thirst and increased release ADH (acts on the kidneys)

In normal people this leads to an increase in water intake and reduced water excretion.

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2
Q

What is the minimum water intake required to maintain homeostasis (assuming normal temp and renal concentrating ability)?

A

500ml/d which would yield 500ml urine

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3
Q

What is the minimal obligatory water intake for normal adults?

A

Normal adults are considered to have a minimal obligatory water intake of 1600 mL/day
Ingested water- 500mL
Water in food- 800mL
Water from oxidation – 300mL

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4
Q

What is normal water loss in healthy adults and where does it come from?

A
Normal healthy individuals have obligatory water loss of 2.5-3L/24hr
Loss from urine 500mL
Skin- 500mL
Respiratory Tract- 400mL
Stool- 200mL
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5
Q

What are the factors affecting fluid requirements?

A

Age
Environmental Factors
Conditions with increased fluid needs
Conditions with decreased fluid need

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6
Q

What are the age factors affecting fluid requirements?

A

Neonates with larger fluid needs

Geriatric patients with smaller fluid needs

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7
Q

What are the environmental factors affecting fluid requirements?

A

Ambient temperature

Neonates- radiant warmers, ultraviolet phototherapy

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8
Q

What are the conditions with increased fluid needs that affect fluid requirements?

A

Burns, diarrhea, dehydration, fever

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9
Q

What are the conditions with decreased fluid needs that affect fluid requirements?

A

CHF, renal failure, iatrogenic fluid overload, mechanical ventilation

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10
Q

What determines the distribution of water between ECF and ICF compartments?

A

To tonicity (osmolality) of ECF

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11
Q

What is tonicity determined by?

A

The concentrations of effective osmoles in the ECF

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12
Q

What are effective osmoles?

A

Solutes that can not move freely across cell membranes (require active transport)

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13
Q

What is the main “effective osmole” in ECF?

A

Sodium

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14
Q

What reflects osmolality of body water?

A

Plasma osmolality

Unless abnormality of sodium and fluid resulting in redistribution between ICF and ECF

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15
Q

Rank the fluid compartments from most to least percentage of body water considering interstitial fluid, plasma, and intracellular fluid.

A

Intracellular fluid > Interstitial fluid > Plasma

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16
Q

What are the low pressure systems and what do they do?

A

Atria and pulmonary vasculature

In response to decreased wall stress (sign of decreased intravascular volume- in the heart and lungs) signal hypothalamus to release antidiuretic hormone (ADH) or vasopressin, while increased stress results in secretion of natriuretic peptide

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17
Q

What are the high pressure systems and what do they do?

A

Baroreceptors in aortic arch, carotid sinus, and juxtaglomerular apparatus
Stimulates the Renin-Angiotensin-Aldosterone system

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18
Q

What is renin released by?

A

Response of juxtaglomerular appraratus to decreased arteriolar wall of tension
Beta-1 innervation of juxtaglomerular apparatus
Tubuloglomerular feedback that senses distal nephron sodium release

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19
Q

What cleaves angiotenson to generate angiotensin I?

A

Renin

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20
Q

What cleaves angiotensin I to generate angiotensin II?

A

Angiotensin I is then cleaved by angiotensin converting enzyme (ACE) to Angiotensin II
Stimulation of Aldosterone secretion by adrenal gland
Increased reabsorption of NaCl from proximal tubule
Central stimulation of thirst and secretion of ADH
Arteriolar vasoconstriction

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21
Q

What type of solution is D5W?

A

Hypotonic

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22
Q

What type of solution is 1/2 NS (0.45%)?

A

Hypotonic

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23
Q

What type of solution is NS (0.9%)?

A

Isotonic

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24
Q

What type of solution is 3% saline?

A

Hypertonic

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25
Q

What type of solution is LR?

A

Isotonic

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26
Q

Dextrose

A
  • Isotonic
  • Small uncharged molecules able to cross capillaries and cell membrane: distributes to intracellular and extracellular compartments
  • 1 liter 670ml ICF + 250ml interstitial + 80ml plasma
  • Poor choice for volume replacement
  • Not affected by osmolality  D5, D10 and D50 distribute to all compartments
  • Metabolized to CO2 + H2O soon after administration; provides calories
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27
Q

Saline- 0.2% (1/4NS) and 0.45% (1/2NS)

A

Distributes to intracellular, plasma and interstitial
1 liter  335ml ICF + 165ml plasma + 500ml interstitial fluid

1 liter distributes to ECF only  250ml plasma + 750ml interstitial
Can cause acidosis in large volumes
Useful in dehydration/hypovolemic state

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28
Q

Saline- 0.9% (NS)

A

Isotonic
1 liter distributes to ECF only  250ml plasma + 750ml interstitial
Can cause acidosis in large volumes
Useful in dehydration/hypovolemic state

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29
Q

Saline- 3%

A

Hypertonic; not commonly used

High solute in extracellular compartment draws water from intracellular compartment

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30
Q

Lactated Ringers

A

More physiologic isotonic solution than NS
Confined to extracellular compartment
1 liter -> 250ml plasma + 750ml interstitial
Safer than NS in large volume replacements

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31
Q

How do you monitor fluids?

A

Measure quantity of all intake and output

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32
Q

What are the sources of intake of fluids?

A

Oral intake from food and beverages

Intravenous intake including maintenance fluids and medications

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33
Q

What are the sources of output of fluids?

A

Urine
Stool
Gastrointestinal (From vomiting or gastric suctioning)
Other losses (chest tubes)

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34
Q

What is involved for the assessment in fluid monitoring?

A

Determine if In and Outs are balanced

May be desirable to have fluid imbalance

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35
Q

What is ins>outs assessed as?

A

Positive fluid balance

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36
Q

What is outs>ins assessed as?

A

Negative fluid balance

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37
Q

What is the goal for correction of dehydration?

A

Input>output

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38
Q

What is the goal for fluid overloaded CHF patient?

A

Output>input

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39
Q

What should be assessed for dehydration/volume depletion?

A
Pulses
Capillary refill
Blood pressure
Urine output
Mucus membranes
HR
Mental Status
Skin tugor
Fontanelle
Skin/Extremities
Tears/eyes
Breathing
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40
Q

What systems should be the primary focus on PE to evaluate fluid overload?

A
Cardiac exam
Abdominal Exam
Extremities
Lung Exam
Blood pressure
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41
Q

What produces osmotic gradient that maintains water distribution between ICF and EFC?

A

Sodium distribution

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42
Q

What is a major determinant of ECG osmolality?

A

sodium is major determinant of ECF osmolality; chloride and bicarbonate also contribute
sodium is activity removed from ICF to ECF

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43
Q

What do sodium disorders result in?

A

Serum toxicity disorders

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44
Q

Do serum sodium concentrations always reflect total body sodium concentrations?

A

Not always
Serum sodium concentrations may be high but the total body sodium concentration may be high, normal or low
Serum sodium concentrations may be low but the total body sodium concentrations may be high, normal, or low

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45
Q

What is the classification of hypernatremia?

A
  • hypervolemic (too much volume and too much sodium)
  • isovolemic (euvolemic)
  • hypovolemic
46
Q

What is the classification of hyponatremia?

A

-hypertonic
-isotonic
-hypotonic
hypervolemic hypotonic
isovolemic (euvolemic) hypotonic
hypovolemic hypotonic

47
Q

What can cause sodium and water abnormalities?

A

Drugs

48
Q

What drug can cause SiADH?

A

Antiepileptic (carbamazepine)

49
Q

What drug can cause Diabetes Insipidus?

A

Antiepileptic (Phenytoin)

50
Q

What is a count of the number of particles in a fluid sample?

A

Osmolality

51
Q

How is the osmolality of plasma regulated?

A
  • The osmolality of plasma is closely regulated by anti-diuretic hormone (ADH).
  • In response to even small increases in plasma osmolality (usually rises in plasma sodium), ADH is released from the pituitary, causing water resorption in the distal tubules and collecting ducts of the kidney and correction of the increased osmolality.
  • The opposite happens in response to a low plasma osmolality with decreased ADH secretion and water loss through the kidneys.
  • Note that ADH is also secreted in response to hypovolaemia and this stimulus will over-ride any response to serum osmolality
52
Q

What is the best measure of urine concentration?

A

The urine osmolality is the best measure of urine concentration with high values indicating maximally concentrated urine and low values very dilute urine.

53
Q

What is the main factor determining urine concentration?

A

The main factor determining urine concentration is the amount of water which is resorbed in the distal tubules and collecting ducts in response to ADH.
In a dehydrated patient with normally functioning pituitary and kidneys, a small volume of highly concentrated urine will be produced.
In a patient with fluid overload the opposite will be an appropriate response. (concentration will be less and fluid will be more dilute)

54
Q

When is serum osmolality used?

A
  • Investigation of hyponatraemia and identification of an osmolar gap (useful with acidosis)
  • Urine osmolality is an important test of renal concentrating ability, for identifying disorders of the ADH mechanism, and identifying causes of hyper-or hyponatraemia. (looking at the function of the kidney)
55
Q

What is hypernatremia?

A

serum Na+ >145 mEq/L
Always associated with hypertonicity
- serum > 295 mOsm

56
Q

What is involved in hypervolemic hypernatremia?

A

Gain of H20 and NA+ (Na+ gain > H2O gain

Due to sodium overload, sodium bicarbonate, albumin, and mineralcorticoid excess

57
Q

What is involved in isovolemic hypernatremia?

A

Loss of H2O

Due to Diabetes insipidus
Osmotic diuretics
Hyperglycemia
No access to water

58
Q

What is involved with hypovolemic hypernatremia?

A

Loss of H2O and NA+ (H2O loss>Na+ Loss)

Due to renal disorders, diuretics, diarrhea, laxative abuse, and excess sweating.

59
Q

What id diabetes insipidus?

A

Isovolemic hypernatremia
Disorder of antidiuretic hormone (ADH-also knowns as vasopressin) release
Binding of ADH to vasopressin receptors (V2 ) in the collecting ducts increases water reabsorption

60
Q

What are the two types of DI?

A

Central and nephrogenic

61
Q

What is involved with central DI?

A

No release of ADH when needed (something is wrong with the pituitary)

62
Q

What is involved with nephrogenic DI?

A

Appropriate release but inadequate response of the collecting duct to ADH (ADH is released by the kidney is not responding to it)

63
Q

What is the clinical presentation of diabetes insipidus-Isovolemic hypernatremia?

A

Dehydration
Volume depletion
Increase in urine output

64
Q

What are the causes of of diabetes insipidus-Isovolemic hypernatremia?

A

CNS tumor, cerebral clots of bleed, head trauma
Renal disease
Infectious diseases- meningitis, syphillis, TB
DRUG-INDUCED- LITHIUM, PHENYTOIN, FOSCARNET, DEMECLOCYCLINE

65
Q

What is the general picture of hypernatremia?

A
  • Rise in plasma sodium concentration and osmolality cause acute water movement from intracellular to extracellular space
  • Decrease in neuronal cell volume
  • Decrease in brain volume can cause rupture of cerebral vein, hemorrhages, and irreversible neurological damage
66
Q

What are the signs and sx of hypernatremia?

A

Initially: lethargy, weakness, confusion, restlessness, irritability
Can progress to: twitching, seizures, coma (serum sodium >160mEq/L
Death (Serum sodium> 180mEq/L

Signs vary depending on volume status

67
Q

What are the laboratory tests for hypernatremia?

A
  • Serum sodium concentrations are generally higher than 145 mEq/L
  • Serum osmolality high
  • Concentrated urine (high specific gravity and osmolality) assuming normally functioning kidney
68
Q

What are the goals of hypernatremia treatment?

A

Resolution of sx
Correction of serum sodium concentrations (at a rate that restores and maintains cell volume as close to normal as possible)
Normalizing the ECF volume if hypo- or hypervolemic
Avoid ADR from too rapid correction
Avoid overcorrection
Prevent recurrence

69
Q

What is the treatment for HYPERVOLEMIC Hypernatremia treatment

A
  • Problem is excess body Na+ > excess of body water
  • Goal- Need to dilute sodium and remove excess sodium and fluid
    • dilute with D5W at 1.5 to 2 mL/kg/hr
    • add loop diuretic (ie furosemide)
  • Decrease serum concentrations slowly to avoid cerebral edema, seizures, permanent neurological -damage
  • Decrease serum sodium by 0.5 to 1 mEq/L/hour
  • Measure serum sodium every 2 to 4 hours initially to guide therapy
70
Q

What is the treatment for ISOVOLEMIC hypernatremia?

A
  • Problem is a “free” water loss, Na+ normal
  • Replace water deficit
  • D5W at rate of 1.5 to 2 mL/kg/hr
  • Treat Diabetes Insipidus if exist
71
Q

What is the treament for ISOVOLEMIC hypernatreamia central diabetes insipidus?

A

-ADH (Vasopressin) analogue: DDAVP (desmopressin acetate), intranasal route preferred, vasopressin (pitressin) for injection, titrate dose to achieve appropriate urine volume and serum sodium.

72
Q

What drugs have antidiuretic properties and are also useful as adjunct or replacement of ADH analogue in the treatment of ISOVOLEMIC hypernatreamia central diabetes insipidus?

A

Hydrochlorothiazide (HCTZ)
Carbamazepine (Tegretol)
Chlorpropamide (Diabinese)

73
Q

What is the treament for ISOVOLEMIC hypernatreamia nephrogenic diabetes insipidus?

A

-Thiazide diuretic and dietary sodium restriction
Thiazides inhibit NA+ reabsorption in distal tubules causing increased excretion of Na+ and water
-Combination can decrease urine volume by 50%
-Increases proximal water absorption and thereby decreasing volume of filtrate delivered to distal nephron
-Use of NSAIDS and amiloride (K-sparing diuretic) also used but may increase serum creatinine

74
Q

What is the problem with HYPOVOLEMIC hypernatremia?

A

Problem is ECF loss>Na+ loss

75
Q

What are the two main parts of treatment for HYPOVOLEMIC hypernatremia?

A
  1. Restore intravascular volume with NS

2. Replace free water deficit

76
Q

Why should the serum concentration in HYPOVOLEMIC hypernatremia be decreased slowly?

A

Decrease serum concentration slowly to avoid cerebral edema, seizures, permanent neurological damage

77
Q

What does the rate of correction for HYPOVOLEMIC hypernatremia depend on?

A

Rate of correction of free water deficit depends on how quickly hypernatremia developed

- acute vs chronic development
- hours vs days
78
Q

How is HYPOVOLEMIC hypernatremia corrrected?

A
  • Correct serum sodium at rate of 1 mEq/L per hour if hypernatremia developed over several hours
  • Correct serum sodium at rate of 0.5 mEq/L per hour if hypernatremia developed over 24 or more hours
  • Monitor serum sodium every 2 to 3 hours for the first 24 hours to assist with therapy
  • After symptoms resolve and serum sodium is less than 148 mEq/L, assess serum sodium every 6 to 12 hours or so
79
Q

What is hyponatremia?

A

Serum sodium < 135 mEq/L

Most common electrolyte abnormality in hospitalized patient

80
Q

What is hypertonic hyponatremia defined as?

A

Plasma mOsm/L >295 (above normal tonicity)

81
Q

What is isotonic hyponatremia defined as?

A

Plasma mOsm/L 280-295 (isotonic)

82
Q

What is hypotonic hyponatremia defined as?

A

Plasma mOsm/L <280 (below normal tonicity)

83
Q

What is hypotonic hyponatremia hypovolemic defined as?

A

Plasma mOsm/L <280 and decreased BP, increased HR, and delayed capillary refill

84
Q

What is hypotonic hyponatremia isovolemic defined as?

A

Plasma mOsm/L <280 but asymptomatic

85
Q

What is hypotonic hyponatremia hypervolemic defined as?

A

Plasma mOsm/L <280 and edema, pulmonary congestion

86
Q

What is the pathophysiology of hypertonic hyponatremia (>295 mOsm/L)?

A
  • Normal amounts of Na+
  • Excess osmols in ECF (including serum)
  • Excess osmols are osmotically active and redistribute water from ICF to ECF
  • Increased ECF dilutes interstitial and serum Na+
  • Serum sodium falls by 1.6 mEq/L for each 100 mg/dL increase in blood glucose
  • Resulting in a rise in serum osmolality of approximately 2mOsm/kgH2O
87
Q

What is the pathophysiology of isotonic hyponatremia (pseudohyponatremia) (280-295 mOsm/L)?

A
  • Normal amount of Na+ and water
  • Primarily a laboratoy artifact resulting from overestimation of volume of serum in sample
  • “Displacement” of sodium-rich fluid with sodium-free non-osmotically active, non-aqueous material (excess lipids, excess proteins)
88
Q

What is the treatment of non-hypotonic hypnatremia?

A

Directed at underlying disorder
Administration of insulin is basis of treatment for uncontrolled diabetes but deficits of water, sodium, and potassium should also be corrected.

89
Q

What is the pathophysiology for hypotonic hyponatremia (<280 mOsmol/L)?

A

Hypotonic (dilutional) hyponatremia represents an excess of water in relation to existing sodium stores
Which can be decreased, essentially normal, or increased Retention of water most commonly reflects the presence of conditions that impair renal excretion of water; in a minority of cases, it is caused by excessive water intake, with a normal or nearly normal excretory capacity
Need to determine ECF volume status
1. hypervolemic
2. isovolemic/euvolemic
3. hypovolemic

90
Q

What is the pathophysiology for hypervolemic hypotonic hyponatremia?

A

Na+ and ECF status
excess of total body Na+
excess of ECF
excess of ECF> Na+

91
Q

What causes hypervolemic hypotonic hyponatremia?

A

Congestive heart failure, cirrhosis, hypoalbiminemia

Decrease in “effective” circulating plasma volume

92
Q

What is the clinical presentation for hypervolemic hypotonic hyponatremia?

A

Edema, acute weight gain, pulmonary congestion

93
Q

What is the pathophysiology for isovolemic hypotonic hyponatremia?

A

Na+ and water status
Normal total body Na+
Small increase in ECF usually insufficient to cause sx

94
Q

What are the causes of isovolemic hypotonic hyponatremia?

A
IMBALANCE OF WATER INTAKE/EXCRETION
SIADH
Excessive ADH activity (SSRI, Ecstasy)
Defective renal diluting mechanism
Altered thirst
Psychiatric disorder
95
Q

What is involved with SiADH in isovolemic hypotonic hyponatremia?

A

Release of ADH when not needed or increased response to ADH

Inappropriate water reabsorption by collecting ducts

96
Q

What is the clinical presentation of SiADH in isovolemic hypotonic hyponatremia?

A
  • some fluid overload however patients usually appear euvolemic
  • hyponatremia from excess fluid
  • minimal water excretion results in decreased urine output and concentrated urine
97
Q

What are the non-drug causes of SiADH in isovolemic hypotonic hyponatremia?

A

Non-drug causes
Many are the same as DI
CNS tumors, cerebral thrombosis or bleed, head trauma
Infectious diseases-meningitis, pneumonias, tuberculosis

98
Q

What are the drug causes of SiADH in isovolemic hypotonic hyponatremia?

A

Drug-induced
NSAIDs, carbamazepine, vincristine
Opioids, phenobarbital, thiazide diuretics
Tricyclic antidepressants, ecstasy

99
Q

What is involved for pathophysiology for hypovolemic hypotonic hyponatremia?

A

Na+ and water status
Deficit of total body sodium and ECF
Na+ deficit>ECF deficit

100
Q

What causes hypovolemic hypotonic hyponatremia?

A
GI losses (vomiting, diarrhea)
Renal losses (diuretics, adrenal insufficiency, salt wasting nephroprathy)
Extrarenal losses (sweating)
Iatrogenic (replacement of sodium-rich losses with sodium- free fluids,
101
Q

How do you diagnose hypovolemic hypotonic hyponatremia?

A

-If loss of sodium is from an extrarenal cause, the urine sodium concentration will be low (20mEq/L)

102
Q

What are the clinical symptoms of hypovolemic hypotonic hyponatremia?

A

-Relate to hypovolemic
signs of intravascular depletion
poor perfusion, low BP, weak pulses
-Related to hyponatremia/hypotonicity (if you see these means the sodium has gotten really low and you don’t want to see these)
signs of cerebral cellular swelling
vomiting, confusion, agitation
if Na+ <120 mEq/L – seizures, coma, death
-Rapid decline in serum sodium may result in more severe signs vs gradual decline

103
Q

What is the goal for hyponatremia treatment?

A
  • Prevent life-threatening signs and symptoms
  • Raise the serum sodium concentration back to normal (or close to normal)
  • Avoid treatment-related adverse events (eg. demylination syndrome)
  • Treat the cause
104
Q

What is osmotic demyelination?

A

Develops several days after aggressive treatment of hyponatremia by any method.
Shrinkage of the brain (due to correction of the sodium) triggers demyelination of pontine and extrapontine neurons that can cause neurologic dysfunction, including quadriplegia, pseudobulbar palsy, seizures, coma, and even death.

105
Q

What increases the risk of osmotic demyelination?

A

Hepatic failure, potassium depletion, and malnutrition increase the risk of this complication.

106
Q

What does treatment for hyponatremia depend on?

A
Cause/classification
Severity of symptoms
Concurrent disease state
ECF volume
Rate of decline of serum sodium concentration
Degree of hyponatremia
107
Q

What is the treatment for hypervolemic hypotonic hyponatremia?

A

-Restrict salt and water
-Fluid restrict to about 1 to 1.2 L/day
-Dietary sodium restriction to 1 to 2 grams per day
one teaspoonful of table salt is equivalent to 2 grams per day
-May need to administer loop diuretics to remove water

108
Q

What is the treatment for hypovolemic hypotonic hyponatremia?

A
  • Goal is to restore vital organ perfusion
  • Replace sodium and volume loss with NS
    • 200 to 400 mL/h depending on severity of symptoms decrease to 100-155 ml/h once hemodynamically stable
    • monitor sodium concentrations
    • do not correct faster that 12 mEq/24 hours (0.5 mEq/L/hr), switch to D5W ½ NS if needed
  • Rapid correction can lead to demyelination
  • Rapid onset < 48h may consider Hypertonic saline
109
Q

What is the treatment for isovolemic hypotonic hyponatremia?

A
  • Correct cause: Hypothyroidism, glucocorticoid deficiency
  • Goal is to induce negative water balance– Outs»Ins by several hundred mLs per day
  • Fluid restrict to about 1 to 1.2 L/day
110
Q

What is the treatment for SiADH isovolemic hypotonic hyponatremia?

A

Treat underlying cause if possible

  • Restrict fluid intake
  • May need to treat hyponatremia with Hypertonic saline
  • May need pharmacotherapy
    • Demeclocycline
      • antibiotic, derivative of tetracycline
      • potent inhibitor of ADH
    • Lithium
      • antidepressant, antimanic agent
      • inhibits ADH action at collecting tubules
    • Phenytoin
      • anticonvulsant
      • inhibits release of ADH
111
Q

What is severe euvolemic hypotonic hyponatremia and how do you treat it?

A

Symptomatic serum Na < 125meq/L
Hypertonic saline
Fluid restriction
Loop diuretic