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Neonatal Pathophysiology > Neonatal Fluid and Electrolytes > Flashcards

Neonatal Fluid and Electrolytes Flashcards

1
Q

What is the most abundant component of the human body?

A

water

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2
Q

How is water distributed in the body?

A

into two compartments: intracellular and extracellular fluid

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3
Q

What is extracellular water composed of?

A

interstitial and intravascular spaces; total amount of water outside the cell

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4
Q

what is intracellular water?

A

total amount of water inside the cell

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5
Q

What is the main solute of the ECW?

A

plasma proteins; affects the colloid osmotic pressure

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6
Q

How is total body water affected by GA?

A

total body water decreases over age; over the first trimester, it composes about 90% of total body wt; at 32 wks, 80% of total body wt; by term GA about 78% and by 1 yr of age, it is about 65%: the ratio of ICW:ECW ∆ as well, with ECW gradually decreasing

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7
Q

What determines osmolality?

A

determined by the total # of solute particles in a solution

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8
Q

What is the net result of the fact that cell membranes are completely permeable to H2O, but not to solutes?

A

H2O will shift from one compartment to another until the osmolality on both sides as the membrane is equal

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9
Q

What is the major determinant of osmolality?

A

serum Na concentration

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10
Q

What is the formula to predict the serum osmolality?

A

2(plasma Na) + BUN/ 2.8 + Glucose/ 18

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11
Q

Why do newborns normally lose 5-15% of their birthweight?

A
  • at birth, their is an acute increase in the ECW as H20 and lytes shift from the IC space to the EC space
  • this puts infants in a state of excess ECF
  • this excess ECW is then lost through diuresis as the expanded ECF compartment ctx
  • (can also be r/t circulating levels of hormones)
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12
Q

What is the expected degree of weight loss in a newborn?

A

PT: 15-20%
FT: 5-10%

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13
Q

What is the state of fetal nephrons before 34 weeks GA?

A

functional but immature

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14
Q

What happens to a FT baby’s renal fx after delivery compared with a PT baby?

A

improves more than PT; term and preterm can dilute their urine
- reabsorption of Na, HCO3 and glucose is limited in the newborn

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15
Q

What is characteristic of a PT baby’s renal fx?

A
  • can dilute urine, (but are slower at it); when faced with a rapid fluid load they will have a delayed response resulting in fluid retention
  • difficulty concentrating their urine
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16
Q

What is the effect of antenatal steroids on the renal system?

A
  • a/w decreased insensible H2O losses
  • less frequent incidence of hypernatremia
  • earlier diuresis
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17
Q

What is ADH?

A

hormone released by the posterior pituitary in reponse to a variety of stimuli.

  • ADH influences water balance by stimulating the kidneys to CONSERVE water
  • in the absence of ADH, the distal tubules remain impermeable to water (restricting reabsorption) and fluid is released as urine
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18
Q

Why can’t newborns efficiently concentrate their urine?

A

decreased responsiveness to ADH

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19
Q

What factors stimulate ADH release?

A

1) hypotension

2) hyperosmolality

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20
Q

What is the normal range of UOP in the neonate?

A

1-4mL/Kg/h; highest rate occurs during the physiologic reduction of ECF

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21
Q

What are insensible water losses?

A

defined as the non-measureable losses that occur through the skin and respiratory system; influenced by numerous factors

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22
Q

What is tranepidermal water loss?

A

occurs as body water diffuses through the immature epidermis and is lost to the atmosphere

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23
Q

What influences transepidermal water loss?

A
  • increases with decreasing GA
  • a major source of insensible H2O loss in the VLBW
  • highest on dol 1 and decreases on subsequent days as barrier fx improves
  • closely r/t relative ambient humidity
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24
Q

What skin features predisposed the PT infant to evaporative heat loss?

A
  • poor keratinization
  • high H2O content
  • low subQ fat
  • large surface area
  • high degree of skin vascularity
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25
Q

What is the result of failure to account for TWL?

A

inaccurate calculation/ estimates of TF needs with resultant fluid and electrolyte imbalances

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26
Q

When does skin barrier fx improve?

A

improvement slows with decreasing GA, may take several weeks to allow for full development of the strateum corneum; skin maturation isn’t influenced by antenatal steroids or by gender

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27
Q

what are other sources of fluid loss in the neonate?

A

gastric drainage, enterostomies, surgical wounds, and pleural fluid drainage

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28
Q

What is the estimated amt of fluid loss d/t respiratory?

A

roughly 0-10 mL/kg/d- r/t temp and humidity of inspired gases and to minute ventilation

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29
Q

What is the estimated amt of fluid loss d/t feces?

A

est to be 5mL/kg/d in the first wk of life, then increase to 10mL/kg/d

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30
Q

what are water balance factors affecting loss?

A
  • GA (renal fx, skin, illness)
  • radiant warmer
  • hyperthermia
  • phototherapy
  • tachypnea
  • inadequate humidification
  • diuretics
  • osmotic diuresis
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31
Q

What is the goal of fluid therapy?

A

to permit physiologic, adaptive fluid and electrolyte ∆ to occur appropriately

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32
Q

what is the main guiding principle of fluid therapy?

A

during the first few days of life, fluid intake should be at a level to allow a reasonable weight loss yet avoid intracellular dehydration

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33
Q

What other factors should influence fluid therapy goals?

A
  • extremely PT babies require more fluid relative to boday weight bc of large IWL
  • start at 60-100mL/kg/d and titrate to 150-175mL/kg/d
  • ongoing fluid losses may need replacement
  • individual conditions may factor into TF amt
  • add boluses for hypotension, hypoglycemia and acidemia into daily intake
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34
Q

What conditions might warrant fluid restriction?

A
  • severe cardio/respiratory compromise
  • renal dysfx
  • post asphyxial syndrome
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35
Q

What are possible effects of fluid restriction?

A

1) dehydration
2) hyperosmolality
3) hypoglycemia
4) hyperbilirubinemia

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36
Q

What are possible effects of fluid overload?

A

1) BPD
2) PDA
3) IVH

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37
Q

What are the usual target ranges for TF goals in the first 48h?

A 
* the smaller the baby, usually the greater the fluid need*
< 1000g                110-140mL/Kg/d
1000-1500g          90-120mL/kg/d
1501-2000g          80-110mL/kg/d
FT                         65mL/kg/d
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38
Q

What are the usual target ranges for TF goals at the end of the first week?

A

< 1000g 150-200mL/Kg/d
1000-1500g 120-150mL/kg/d
1501-2000g 110-150mL/kg/d
FT 100-150mL/kg/d

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39
Q

What fluid is most commonly used for initial fluid therapy?

A

D10W

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40
Q

When are electrolytes added to fluid therapy

A

typically not for the first 24-48h of life; serum electrolyte levels and UOP are used to determine when and which lytes to add

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41
Q

When does body weight change with regard to TBW?

A

body weight ∆ alterations of fluid balance only if there is a net ∆ in TBW. internal shifts of TBW may not be detected by weight alone

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42
Q

Why is specific gravity an important indicator of fluid balance assessment?

A

an indirect measure of urine osmolality, unreliable if contaminated with glucose, protein or blood in the urine
- normal range is 1.002-1.0212; this correlates to a normal urine osmolality of 100-300millimoles/L

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43
Q

What assessments may indicate fluid balance in the neonate?

A

1) body weight
2) urine volume
3) Spec grav
4) Lab tests
5) other: skin turgor, mucous membranes, presence of edema, level of AF, pulse quality, BP and perfusion

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44
Q

what is the main extracellular cation?

A

Na; found in varying concentrations in all body fluid compartments

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45
Q

what is the normal range for Na?

A

130-150mEq/L

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46
Q

what is the daily Na requirement for newborns?

A

1-4mEq/kg/d; daily requirement for preemies may be higher

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47
Q

How do electrolytes determine the concentration of fluid compartments?

A

influences the passage of H2O through the vascular and cell membrane, thereby controlling the osmotic equilibirum bw those 2 comparments

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48
Q

What is the result if your baby has a surplus of Na?

A

blood becomes hypertonic–> causes a shift from the IC to EC. this results in cellular dehydration

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49
Q

What is the result if your baby has a deficit of Na?

A

blood becomes hypotonic–> and fluid shifts into the cells. this results in cellular edema.

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50
Q

What is the goal of Na in fluid therapy?

A

ultimately we want a positive Na balance bc that is whats req’d for the growth of new tissue

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51
Q

What is hypoNa?

A

a serum Na < 130 due to retention of H2O relative to serum Na

52
Q

What is occurring physiologically with hypoNa?

A

serum Na decreases, H2o moves into the cells to establish equilibrium in the osmolality

53
Q

what is the clinical presentation of hypoNa?

A

signs are r/t effects on the brain cells: vomiting, lethargy, apnea and coma (coma is a/w level <115)

54
Q

what are the forms of Na supplementation?

A

usually given as NaCl, or NaAcetate of Na HCO3 if the baby also has metabolic acidosis (Na content in 1/2NS is 77mEq/L or 0.77mEq/mL)

55
Q

what is early hypoNa?

A

occurring in the first 2 dol

56
Q

What are the causes of early hypoNa?

A

most common- perinatal asphyxia and SIADH; others: severe RDS, iatrogenic causes: indocin, excessive hypotonic fluids to laboring MOB, diuretics with excessive fluid administration

57
Q

What is the tx for early hypoNa?

A

fluid restriction

58
Q

What is the mechanism for early hypoNa as it r/t asphyxia?

A

asphyxia at birth results in blood potentially shunting to their adrenals, heart and brain- everything else is deprived. So, if kidneys are not putting out urine, and TF amt isn’t adjusted we can cause a dilution of their serum Na content

59
Q

What is the mechanism for early hypoNa as it r/t RDS and indocin?

A

UOP not normal and giving IVF will cause hemodilution

60
Q

What is late hypoNa?

A

occurring at >1 week of life

61
Q

What are the causes of late hypoNa?

A

common- VLBW babes being fed EBM (naturally low in Na); other: overhydration seen in infants with renal failure, CHF, PDA or SIADH

62
Q

What is the tx for late hypoNa?

A

do not give more Na, restrict fluids

63
Q

When should Na correction be considered?

A

with increased urinary losses in preemies- that is when supplementation beyond maintenance may be req’d

64
Q

How should hypoNa be corrected?

A

slowly (over 12-24h); deficit= 0.6 x weight in kg x (desired Na - actual Na)

65
Q

What is hyperNa?

A

defined as serum Na >150; reflects a deficiency of H2O relative to total body Na content

66
Q

What are causes of hyperNa?

A

excessive IW with insufficient fluid intake, high Na intake or early addition of Na to IVF, BF malnutrition in term infant (occurs with decreased lactation and insufficient amt free H2), and diabetes insipidus

67
Q

What is occurring physiologically with hyperNa?

A

when hyperNa develops, H2O moves out of the cells into the extracellular space to achieve osmotic equillibrium; brain cells can protect themselves by generating new solutes to hold on to their intracellular water

68
Q

What is the clinical presentation with severe hyperNa?

A

high-pitched cry, lethargy, irritability and apnea (can lead to sz and coma)

69
Q

How should hyperNa be corrected?

A

restrict Na in the first few days of life and this may prevent the need for increased IVF; prevention: lower the infused Na concentration for arterial and venous catheters

70
Q

What might be a consequence of too rapid Na repletion?

A

these special brain solutes cannot be metabolized quickly and cerebral edema can occur d/t H2O moving back into the brain cells. Sudden increases in plasma osmolality can also contribute to IVH

71
Q

What is the main intracellular cation?

A

K

72
Q

What are the effects of K on the cell?

A

involved in the regulation of cell membrane potential- variations have important effects; effects on myocardium are the most prominent

73
Q

what is the normal range of K?

A

3.5-5mEg/L

74
Q

what is the daily requirement of K?

A

2-3mEq/kg/d

75
Q

What has an inverse relationship with K?

A

acidosis; causes K to move out of the cell. FOR EVERY 0.1unit decrease in pH, the serum K will increase 0.3-1.3mEq/L

76
Q

What is hypoK?

A

serum K < 3.5mEq/L

77
Q

What are the causes of hypoK?

A
  • decreased intake (not meeting maintenance need)
  • GI losses
  • renal losses
  • poor/hemolyzed stick
  • K wasting drugs (digoxin, lasix, amphotericin B)
  • alkalosis- especially metabolic
78
Q

with a hypoK infant, what EKG ∆ can be seen?

A

ST depression, flattening T wave, widened QRS

79
Q

How should hypoK be treated?

A

K supplementation can begin once UOP has been established (usually 2-3dol). correction must be done cautiously with continuous cardiac monitoring.

80
Q

What can occur with rapid K repletion?

A

fatal arrhythmias

81
Q

What considerations need to be made with a hypoK patient on dig?

A

hypoK can potentiate digitalis toxicity; babies need periodic levels of lytes drawn if on dig long-term

82
Q

what is hyperk?

A

serum K > 6.5mEq/L; must be differentiated from spurious

83
Q

what are the causes of hyperK?

A
  • excessive intake
  • impaired excretion
  • acidosis
  • hemolysis
84
Q

what is the problem with hyperK?

A

cardiac toxicity is the main issue

85
Q

what EKG ∆ can be seen in hyperK pts?

A
  • peaked T wave
  • disappearance of P wave
  • widening of QRS
  • VFib may follow
86
Q

How is hyperK treated?

A
  • treat cause while starting temporary measures*
  • 10% CaGluconate (1mL/kg= 100mg/kg)
  • insulin/ dextrose gtt
  • NaHCO3 (1-2mEq/kg IV)
  • IV lasix
  • K binding kayexalate (1gm/kg)
  • if serum > 8 need exchange transfusion with fresh blood washed PRBCs or FFP
87
Q

How does CaGluconate affect serum K?

A

decreases myocardial contractility

88
Q

How does insulin affect serum K?

A

drives K intracellularly; need to simultaneously increase GIR so as not cause subsequent hypoglycemia

89
Q

How does NaHCO3 affect serum K?

A

HCO3 causes K to move into the cell

90
Q

How does lasix affect serum K?

A

K wasting; effective short term but can be used in combo with NaHCO3 or insulin)

91
Q

How does K binding Kayexalate affect serum K?

A

decreases K slowly, 1g moves 1mEq of K

92
Q

What is the main inorganic anion in the ECF?

A

Cl

93
Q

What does Cl have an inverse relationship with?

A

HCO3; if a baby retains Cl, their HCO3 will decrease leading to metabolic acidosis; if Cl is over excreted (ex: lasix wasting), HCO3 will rise leading to metabolic alkalosis.

94
Q

Why is Cl important?

A

essential to maintain plasma volume with Na; plays an important role in acid base balance

95
Q

What is the normal range of Cl?

A

90-112mEq/L

96
Q

What is hypoCl?

A

serum Cl < 90 mEq/L

97
Q

What are causes of hypoCl?

A

inadequate intake of increased losses (GI or renal)

98
Q

How should hypoCl be treated?

A

treatment depends on the cause

99
Q

What is hyperCl?

A

serum Cl > 115 mEq/L

100
Q

What are the causes of hyperCl?

A

usually a/w metabolic acidosis, excessive intake, or HCO3 depletion

101
Q

How should hyperCl be tx?

A

treatment depends on the cause

102
Q

What is the most abundant mineral in the body?

A

Ca

103
Q

What is the role of Ca in the body?

A

essential component of the skeleton and plays an important role in muscle contraction, blood coagulation and neural transmission

104
Q

What is the most common of Ca disorders?

A

hypoCa; early onset : birth to 72h; late onset: >72h

105
Q

what is hypoCa?

A

serum Ca < 7

106
Q

What are causes of hypoCa?

A
  • early onset (r/t MOB)
  • prolonged poor enteral intake
  • maternal DM (decrease glucose & increase calcitonin which inhibits Ca mobilization from the bone)
  • perinatal stress (thought to be d/t corticosteroids and catecholamines
  • alkalosis (inverse relationship bw pH and Ca)
  • blood transfusions
  • diuretic therapy
  • congenital hypoparathyroidism
107
Q

What are signs of acute hypoCa?

A
  • apnea
  • irritability
  • slight tremors
  • profound tetany
  • sz
  • prolonged QT intervals
  • cardiac dysfunction
108
Q

What are signs of chronic hypoCa?

A
  • bone demineralization
  • elevated alkaline phosphate levels
  • rib and long bone fractures
109
Q

How should hypoCa be treated?

A

supplemental Ca, determine and tx the underlying etiology

110
Q

In what form can Ca supps be given?

A

bolus or as a cont gtt; Ca is very caustic- consider a central line

111
Q

What can occur if Ca repletion occurs too rapidly?

A

bradycardia, even asystole

112
Q

What is hyperCa?

A

serum Ca > 11mEq/L

113
Q

What are signs and symptoms of hyperCa?

A

constipation, polyuria and bradycardia

signs: poor feeding, poor weight gain, depressed tone, lethargy, sz, shortened QT interval

114
Q

What causes hyperCa?

A

usually iatrogenic; too much in TPN, on HMF for too long- have built up stores and we continue to give more

115
Q

How is hyperCa diagnosed?

A

total and ionized Ca levels

- calculation of Ca, vitamin D and phosphate intake

116
Q

How is hyperCa treated?

A

dependent on cause

  • dc thiazide diuretics
  • acute causes: give lasix
117
Q

Why is magnesium important?

A

required to maintain calcium homeostasis; implicated in energy production, cell membrane fx, mitochondrial fx and protein synthesis

118
Q

What is hypoMg?

A

< 1.5mg/dL

119
Q

What is hyperMg?

A

> 2.3mg/dL

120
Q

What causes hypoMg?

A
  • hypoCa (usually p/w hypoCa that doesn’t respond to tx)

- inadequate intake

121
Q

How is hypoMg diagnosed?

A

lab values; may require supplemental MgSO4

122
Q

What is the effect of hyperMg on the neonate?

A

excessive levels depress the CNS and decrease skeletal muscle activity

123
Q

What are the causes of hyperMg?

A
  • maternal MgSO4

- administration of Mg containing antacids- especially when UOP is low

124
Q

What are signs of hyperMg?

A
  • poor feeding
  • lethargy
  • decreased tone
  • apnea
  • decreased GI motility with distension
  • hyporeflexia
125
Q

How should hyperMg be treated?

A

may need respiratory support, provide adequate Ca intake

126
Q

What is hypoPhos?

A

< 4mg/dL

127
Q

What is hyperPhos?

A

> 7mg/dL

Neonatal Pathophysiology (17 decks)

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