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Paediatric Biochemistry > Neonatal Electrolyte and Acid Base Balance > Flashcards

Neonatal Electrolyte and Acid Base Balance Flashcards

1
Q

What is body fluid distribution in Children?

A

75% Water

  • Intracellular (47%)
  • Extracellular (53%)
    • Intravascular
    • Interstitial
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2
Q

What can fluid imbalance lead to in the neonate after birth?

A
  • Hypovolaemic circulatory failure
  • Hypernatraemia and hyperkalaemia
  • Prerenal ureamia
  • Excessive weight loss
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3
Q

How is fluid balance affected after birth?

A
  • After birth extracellular fluid is lost through diuresis as a result of increased GFR
  • Immature kidneys have a poor response to vasopressin
  • Insensible losses can be significant after birth
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4
Q

What are physical features of a neonate?

A
  • Large surface area relative to body mass
  • Proportionally larger. Brains and more skin so more interstitial fluid
  • Less Body Fat
  • Immature kidneys: unable to conserve or excrete water and electrolytes effectively
  • Thinner Skin
  • Massive diuresis in the first 3-5 days of life
  • Double the metabolic rate of children
  • Change in environmental temperature
  • Proportionally more fluid so greater fluid requirement
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5
Q

What are potential problems encountered in the neonate?

A
  • Those associated with immaturity of systems (Lungs/CNS/Kidney/Liver/Endocrine)
  • Those associated with infection
  • Electrolyte abnormalities (multifactorial)
  • Those associated with neonatal care procedures (Warming/PN)
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6
Q

What are precipitating problems for fluid imbalance among neonates?

A
  • Illness with fever
  • Phototherapy
  • Illness with increased resp rate
  • Illness with vomiting and diarrhoea
  • Renal disease
  • Fistulas
  • Burns
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7
Q

What happens to the cardiorespiratory system after birth?

A
  • Fundamental changes to the cardiorespiratory system occur perinatally.
  • Respiratory gas exchange must be established by the lungs within minutes.
  • The cardiovascular system converts from 2 circulations in parallel to 2 circulations in series.
  • Therefore frequent and serious difficulties to this adaptation can occur
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8
Q

What causes Respiratory Distress syndrome?

A
  • Most commonly caused by hyaline membrane disease in preterm infants.
  • Due to immature sufactant synthesis
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9
Q

What are some other causes of RDS?

A
  • Pneumonia – infected during birth
  • Merconium aspiration
  • Transient tachypnoea of the newborn (Caesarian section, respiratory acidosis)
  • Hypo/hyper thermia
  • Metabolic Acidosis
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10
Q

What are consequences of RDS?

A
  • Neonate develops hypoxia and respiratory acidosis.
  • Hypoxia enhances anaerobic glycolysis which may result in lactic acidosis.
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11
Q

How is Respiratory Distress syndrome treated?

A

Management includes assisted ventilation and surfactant administration.

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12
Q

What are features of Apnoea of Prematurity?

A
  • Cessation of breathing for >20s
  • Occurs in approx 85% infants <1kg
  • Major cause due to immaturity of the central respiratory drive and poor sensitivity to changes in PaCO2.
  • Compounded by suppressed respiratory response to hypoxia
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13
Q

What causes worsening of Apnoea of Prematurity?

A
  • Infection
  • Thermal instability
  • Hypoglycaemia.
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14
Q

How is Apnoea of Prematurity treated?

A

Methylxanthines

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15
Q

What are features of Renal Function in Neonates?

A
  • Nephrons develop from 6 weeks gestation, full complement by 36 weeks.
  • GFR develops more rapidly than tubular function
  • Tubules increase in length, secretory and absorptive function postnatally
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16
Q

How does Renal Biochemistry change in Neonates?

A
  • Functional immaturity characterised by inappropriately high urine sodium for GFR. Preterm infants have a higher sodium requirement per kg. In the first few weeks of life there is a contraction of extra cellular volume leading to natriuresis.
  • Immature response to ADH impairs the concentrating ability of the kidney.
  • Plasma [urea] low in neonates due to increased nitrogen utilisation.
  • Plasma [creat] are initially high (maternal) then fall and gradually rise with muscle mass
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17
Q

What is the Aetiology of Hyponatraemia?

A
  • Maternal Water Excess
  • Iatrogenic Water Excess
  • Excess Vasopressin
  • Retention of water and sodium
  • Renal loss of sodium and chloride
  • CAH
  • Renal loss of sodium and bicarbonate
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18
Q

Describe the Causative Conditions, Presenting Feature, Management in Maternal Water Excess.

A
  • Condition: Reflection of maternal fluid e.g hypotonic IV fluid
  • Presenting Feature: Hyponatraemia for 48 hours
  • Management: Recovers spontaneously
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19
Q

Describe the Causative Conditions, Presenting Feature, Management in Iatrogenic Water Excess

A
  • Condition: Prolonged parenteral admin of dextrose
  • Presenting Feature: Hyponatraemia
  • Management: Add NaCl to fluids and restrict volume
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20
Q

Describe the Causative Conditions, Presenting Feature, Management in Excess Vasopressin

A
  • Condition: Secreted as part of stress response in sick neon
  • Presenting Feature: Weight gain/oedema, ↓plasma osmalality, inappropriately high urine OSM
  • Management: Fluid restrict 40-60ml/kg/24hr
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21
Q

Describe the Causative Conditions, Presenting Feature, Management in Retention of water and sodium

A
  • Conditions: Acute or chronic renal failure, Cardiac failure
  • Presenting Feature: Water retention exceeds sodium retention
  • Management: Fluid restriction
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22
Q

Describe the Causative Conditions, Presenting Feature, Management in Renal loss of sodium and chloride

A
  • Conditions: Immaturity, Congenital renal disease, Osmotic diuresis (hyperglycaemia), Use of loop diuretics
  • Presenting Feature: Hyponatraemia
  • Management: Treat underlying problem, Replace deficit
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23
Q

Describe the Presenting Feature, Management in CAH

A
  • Presenting Feature: Glucocorticoid deficiency, Mineralocorticoid deficiency, Pigmented scrotum, Virilisation – females
  • Management: Treat underlying condition, Add NaCl to feeds
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24
Q

Describe the Causative Conditions, Presenting Feature, Management in Renal loss of sodium and bicarbonate

A
  • Conditions: Proximal renal acidosis
  • Presenting Features: Acidosis, Low/norm K +, High bicarb requlation
  • Management: Confirm diagnosis, Treat with sodium bicarbonate and potassium citrate
25
Q

What is the Aetiology of Hypernatraemia in Neonates?

A
  • Sodium Excess
  • Inadequate fluid Intake
  • Water Loss - Cutaneous
  • Water Loss - GI
  • Water Loss - Renal
26
Q

Describe the Causative Conditions, Presenting Feature, Management in Sodium Excess Hypernatraemia

A
  • Conditions: Administration of sodium bicarbonate/sodium chloride
  • Presenting Features: Oedema, Weight gain
  • Management: Reduce Na intake
27
Q

Describe the Causative Conditions, Presenting Feature, Management in Inadequate Fluid Intake Hypernatraemia in Neonates

A
  • Conditions: Failed breast feeding, Iatrogenic
  • Presenting Features: Dehydration, Hypotension
  • Management: Volume re-expansion with Dextrose and saline
28
Q

Describe the Causative Conditions, Presenting Feature, Management in Cutaneous water Loss Hypernatraemia in Neonates

A
  • Conditions: Prematurity, Heater, Skin damage/disease
  • Presenting Features: Dehydration, Hypotension
  • Management: Humidified environment, Dextrose and saline
29
Q

Describe the Causative Conditions, Presenting Feature, Management in GI Water Loss Hypernatraemia in Neonates

A
  • Conditions: Vomiting, Diarrhoea, Necrotising enterocolitis
  • Presenting Feature: Dehydration, Hypotension
  • Management: Volume re-expansion with Dextrose and saline
30
Q

Describe the Causative Conditions, Presenting Feature, Management in Renal Water Loss Hypernatraemia in Neonates

A
  • Conditions: Diabetes Mellitus, Diabetes Inipidus, Hyperaldosteronism
  • Presenting Features: Polyuria/dehydration, Glucose, Osm Hypokalaemia/ Hypertension
  • Management: Insulin, Diagnose, DDAVP or thiazide, Spironolactone
31
Q

What are Aetiologies of Hypokalaemia?

A
  • Excess Vasopressin
  • GI loss
  • Increased renal loss
  • Primary or secondary hyperaldosteronism
32
Q

Describe the Causative Conditions, Presenting Feature, Management in Excess Vasopression Hypokalaemia in Neonates

A
  • Condition: Secreted as part of stress response in sick neon
  • Presenting Features: Weight gain oedema,↓p.OSM, inappropriately high urine osmolality
  • Management: Fluid restrict 40-60ml/kg/24hr
33
Q

Describe the Presenting Feature, Management in GI Loss Hypokalaemia in Neonates

A
  • Presenting Features: Diarrhoea/Vomiting, Aspiration of gastric fluid
  • Management: Fluid replacement
34
Q

Describe the Causative Conditions, Presenting Feature, Management in Increased Renal Loss Hypokalaemia in Neonates

A
  • Condition: Alkalosis in pyloric stenosis, RTA
  • Presenting Features: Recurrent vomiting, Acidosis
  • Management: Fluid replacement, Bicarbonate
35
Q

Describe the Presenting Features of IPrimary or secondary hyperaldosteronism Hypokalaemia in Neonates

A
  • Presenting Feature: Hypernatremia, Hypokalaemia, Spironolactone drug history
36
Q

What are Aetiologies of Hyperkalaemia in Neonates?

A
  • Factitious
  • Cell membrane failure
  • Excessive intake
  • Red cell/ tissue, Catabolism
  • Water loss
  • Decreased renal excretion: Acute renal failure
  • Decreased renal excretion: Mineralocorticoid deficiency
37
Q

Describe the Causative Conditions, Presenting Feature, Management in Factitious Hyperkalaemia in Neonates

A
  • Condition: Poor sample (haemolysis, Vaseline, squeezing ankle, alcohol wipes, multiple tubes used)
  • Presenting Features: Unexplained result
  • Management: Repeat
38
Q

Describe the Causative Conditions, Presenting Feature, Management in Cell membrnce failure Hyperkalaemia in Neonates

A
  • Condition: Asphyxia Hypothermia, Sepsis
  • Presenting Features: Sick Infant
  • Management: Treat underlying condition
39
Q

Describe the Causative Conditions, Presenting Feature, Management in Excess intake Hyperkalaemia in Neonates

A
  • Condition: PN nutrition/fluids, Blood transfusion
  • Presenting Features: Hyperkalaemia
  • Management: Reduce intake, Increase fluid input
40
Q

Describe the Causative Conditions, Presenting Feature, Management in Red cell/ tissue catabolism Hyperkalaemia in Neonates

A
  • Condition: Trauma, bruising, haemorrhage
  • Presenting Feature: Hyperkalaemia
  • Management: Increase fluid input
41
Q

Describe the Causative Conditions, Presenting Feature, Management in Water Loss Hyperkalaemia in Neonates

A
  • Condition: Insensible losses
  • Presenting Feature: Dehydration
  • Management: Increase fluid input
42
Q

Describe the Causative Conditions, Presenting Feature, Management in Decreased Renal Excretion Hyperkalaemia in Neonates

A

Acute Renal Failure

  • Condition: Acute Renal Failure
  • Presenting Feature: Oliguria
  • Management: Renal replacement treatment

Mineralocorticoid deficiency

  • Conditions: Mineralocorticoid deficiency
  • Presenting Feature: Hypoglycaemia, Pigmented genitalia, Female virilisation
  • Management: Glucocorticoid, Mineralocorticoid, NaCl
43
Q

How is Hyperkalaemia managed?

A
  • Correct any dehydration and withdraw any potassium supplements
  • Correct any hypocalcaemia with iv 10% calcium gluconate (1ml/kg)
  • Correct any metabolic acidosis with iv sodium bicarbonate (0.3mmol x kg x base deficit)
  • If emergency and arrhythmia iv salbutamol 4µg/kg or infuse glucose and insulin 0.1 unit/kg in 10ml/kg 10% dextrose
  • If due to renal failure, dialysis may be required
44
Q

What are features of Calcium Regulation in the foetus?

A
  • There is active placental transport of calcium and phosphate to the fetus
  • Fetal [plasma] are higher than maternal
  • 3rd trimester this increases 3x – bone mineralisation and growth
  • 25OHD levels reflect maternal level
  • 1,25(OH)2 is synthesised in the placenta and fetal kidney
  • PTH and calcitonin do not cross the placenta and are synthesised by the fetus
45
Q

What are features of calcium metabolism in the neonate?

A
  • Small decreases are frequent and usually asymptomatic in the first few days
  • Premature infants are at risk of osteopenia due to reduced bone mineralisation during the 3rd trimester and delayed rise in PTH
  • Vitamin D deficiency may occur due to maternal deficiency.
  • Birth asphyxia or increased catabolism leading to hyperphosphataemia results in hypocalcaemia
  • Acidosis↑[calcium], Alkalosis↓ [calcium]
46
Q

What are different aetiologies of Hypocalcaemia and their causes?

A

Exaggerated physiological fall (1-3days)

  • Prematurity/diabetic mother

Low Intake

  • Inadequate Nutrition

Pathological – PTH

  • Hypoparathyroidism
  • Maternal hyperparathyroidism
  • Di George syndrome/ hypomagnesaemia

Pathological – Vitamin D

  • Maternal Vitamin D Deficiency
  • Fat Malabsorption
  • 1αHydroxylase deficiency

Pathological – multifactorial related to chronic disease or inherited metabolic disease

  • Liver/renal disease
  • Organic acid disorders

Increased losses

  • Loop diuretics

Insoluble calcium salt formation

  • Hyperphosphataemia pathological or iatrogenic, exchange transfusion

Decreased total calcium due to decreased binding

  • Hypoalbuminaemia, Alkalosis
47
Q

Why does hypercalcaemia occur in newborns?

A
  • Inappropriate TPN
  • Immobilisation
  • Malignancy
  • Hyperparathyroidism
  • FHH
  • Thiazide diuretics
  • William’s syndrome (hypersensitive to VitD)
48
Q

What are features of Osteopenia of Prematurity?

A
  • Significant failure of bone mineralisation. Occurs in >50% prem babies <1kg and presents 6-12 weeks postnatally
  • Softening of the rib cage = RDS
  • Multiple non-trauma fractures
  • Inadequate Ca2+ and PO43- in breast milk for pre-term baby with suboptimal mineralisation
  • Exacerbated by inadequate 1,25 OHD activity in immature kidney and limited absorptive capacity of the intestinal tract
49
Q

What are biochemical findings in Osteopenia of Prematurity?

A
  • Alkaline Phosphatase is higher in infants than in adults, up to 6 x ULN
  • In osteopenia of prematurity it increases rapidly to higher than 6 x ULN in high risk infants, then falls rapidly as levels 1/α to growth velocity.
  • Low calcium and phosphate
50
Q

How is Osteopenia of Prematurity treated?

A

Treated with

  • Calcium
  • Phosphate
  • Vitamin D
51
Q

How does glucose change within neonates?

A
  • Glucose, amino acids and FFA’s from mother. FFA’s stored in adipose as triglycerides
  • After birth [glucose] falls resulting in ↓insulin and ↑ glucagon, catecholamines and GH. This stimulates gluconeogenesis and lipolysis
  • Fetal brains have an enhanced capacity to utilise ketones, lactate and a.a’s as fuels
  • Infants produce and require more glucose/kg than adults due to higher brain:body mass
52
Q

What are the main causes of Hypoglycaemia of in neonates?

A
  • Inadequacy of stores (usually accumulated in 3rd trimester) in prem and small for gestational age
  • Asphyxia/sepsis- due to under perfusion of the liver
  • Hyperinsulinism inhibits lipolysis and ketogenesis can occur in IDM, if persistent maybe an IMD.
53
Q

What are features of Hyperglycaemia of Neonates?

A
  • Extremely preterm infants may develop glucose intolerance due to insensitivity to insulin.
  • Often occurs due to fluid replacement with dextrose
  • Insulin may be required if glucose consistently >12 mmol/L
  • Sepsis is a major worry
54
Q

How is Acid-Base Balance affected in Neonates?

A
  • Neonates are vulnerable to acid-base disturbances due to immaturity of organ systems.
  • Maintenance of acid-base balance is dependent on adequate respiration, perfusion and renal function.
  • As the rate of metabolism relative to body mass is higher in infants there is a tendency towards acidosis
55
Q

How can hydrogen ions be altered in neonates?

A
  • In an infant with normal acid base status even premature kidneys can excrete H+ load and generate sufficient buffering capacity.
  • However if H+ increases prem neonates are prone to metabolic acidosis in addition to the respiratory acidosis of respiratory distress
56
Q

What are causes of Metabolic Acidosis in Neonates?

A
  • Hypovolaemia/ Hypoperfusion
  • Renal Impairment
  • Sepsis
  • Hypothermia
  • IEM
  • IV fluids
  • GI losses from stoma/fistulae
57
Q

What are causes of Respiratory Acidosis in Neonates?

A
  • Asphyxia
  • Apnoea
  • Respiratory Distress
  • Obstruction to respiratory tract
  • Pneumonia
  • Pulmonary oedema
58
Q

What are causes of Respiratory and Metabolic Alkalosis in Neonates?

A

Metabolic Alkalosis

  • Diuretics
  • Sodium Bicarbonate
  • Hypokalaemia

Respiratory Alkalosis

  • Over Ventilation
59
Q

How can TPN affect the neonate?

A
  • Premature or very sick neonates often require TPN.
  • This is often because the GI tract is immature and energy reserves are low
  • A very small amount of milk is given (0.5ml/hour) to reduce the risk of infection and necrotising enterocolitis
  • TPN will need to be tailored to the requirements of the baby and may lead to electrolyte abnormalities/fluid imbalance

Paediatric Biochemistry (31 decks)

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