Neonatal Acidosis

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Neonatal Acidosis

• Jennifer Camas, MP3
• Baystate Medical Center
• October 29, 2004

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Acid-Base Review

• Acidosis is defined as an abnormally high acidity
  of blood measured by a pH value below normal
  acceptable ranges for age
• Acidosis occurs by three mechanisms
• Increased H ions (increase acid load) that
  overcomes buffering capacity
• Primary loss of HCO3 OR other non-bicarb buffers
  creating a total buffer deficit (- BE)
• Failure of kidney to increase H excretion in
  response to acid load

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Where and How do we buffer?

• ECF compartment contains HCO3 as only substantial
  buffer
• Intracellular mechanisms to maintain pH are
  multiple
• HCO3 buffers but ICF has only ½ amount found in
  ECF
• Proteins, Phosphates, Amino Acids, Bone Carbonate
  make up remaining ½ of ICF buffer system
• Cells also contain H pump that actively
  transports H into/out of cells

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Where and How, cont.

• In someone handling an acid load
• 80-90 of H produced is buffered by consumption
  of HCO3
• 55-60 of H produced is buffered by
  intracellular buffers and bone buffers
• ABGs/Lytes measure buffering in smallest portion
  of ECF compartment

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How do we compensate?

• Use up our available ECF HCO3
• Actively pump H into cells and buffer with
  intracellular buffers
• Increase our overall production of CO2 and
  increase respiratory tidal volume /- respiratory
  rate in order to blow off CO2

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Compensation, cont.

• Increase HCO3 reabsorption by kidney
• Increase renal excretion of H (3-4 times normal
  if kidney fxn ok)
• Increase NH3 production which stimulates increase
  excretion of H
• Increase organic acid uptake
• Increase retention of non-bicarb bases in
  digesting food

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Why do we care?

• Because acidosis is
• BAD

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Why is acidosis bad?

• Neuro Encephalopathy, seizures, IVH, PVL, coma
• Cardio direct depression of myocardium,
  hypotension, arrythmias
• Resp Hyperventilation, RDS, BPD
• Renal Hyperkalemia
• GI NEC
• Optho ROP

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New Studies Show..

• In 2003 a retrospective study published
  evaluating umbilical cord pH and BE (artery and
  vein) with neonatal morbitity in preterm infants
• Perinatal/neonatal database used to obtain pH and
  BE, Apgar scores, adverse outcomes, and
  demographics for singleton live-born infants
  between 1995-2002

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Results in Very Preterm

• Inverse relationship between Apgars scores lt 7 at
  5 minutes and artery/venous pH and BE
• Inverse relationship between venous pH and BE and
  IVH/PVL
• No correlation between artery pH and BE and
  IVH/PVL

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Results in Preterm

• Inverse relationships between umbilical
  artery/venous pH and BE and Apgar scores lt 7 at 5
  minutes
• With progressive acidosis there was increased
  need for assisted ventilation and progression to
  RDS

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A little history of acidosis

• Late 1920s baseline acidosis in otherwise
  healthy term neonates when adult lab values were
  used
• Early 1930s - development of HCO3 and umbilical
  blood gas norms in healthy term infants

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History, cont..

• Early 1940s development of age based norms for
  HCO3 levels as NICU care more specialized and
  premie population increased
• Large studies in neonates over the last 10 yrs
  have shown slightly decreased values for normal
  HCO3 and umbilical artery blood gas values

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Age Based Norms for Umbilical Artery pH

• Age
• Term
• Preterm (lt36 wks)
• Very Preterm (lt30 wks)

• pH
• 7.32-7.38
• 7.30-7.32
• 7.27-7.32

Standard values according to Neonatology texts
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Age Based Norms for Umbilical Artery pH

• Age
• Term
• Preterm
• Post-term

• pH
• 7.28
• 7.26
• 7.24

Standards according to studies completed over
last 10 years
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Age Based Norms for HCO3

• Serum HCO3
• 24-26
• 22-25
• 19-22

• Age
• Term
• Preterm (lt36 wks)
• Very Preterm (lt30 wks)

Standards according to neonatal texts
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Age Based Norms for HCO3

• AGE
• Term
• Preterm
• Very Preterm

• Serum Bicarb (mEq/L)
• 18-22
• 15-19
• No data

Standards according to studies over the past 10
years
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Causes of Acidosis

• Birth Asphyxia/Hypoperfusion
• Maternal Acidosis
• Sepsis
• RDS/Vent Management
• Diarrhea
• RTA
• Inborn Errors of Metabolism
• Late Metabolic Acidosis

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How do we asses for acidosis?

• Three main measures in neonates
• Umbilical artery blood gas
• Venous blood gas/Capillary blood gas
• pH values slightly lower than arterial
• Electrolytes

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What is the problem with neonates?

• Initial theories proposed a total base deficit in
  newborns when compared to adult counterparts
• Subsequent studies revealed no significant
  difference in average total base values between
  term newborns and adults
• One recent study on total base status in premies
  found lower total base values than adults

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Can we blame the kidneys?

• Fetal kidney makes urine by 8 wks GA
• Glomerulogenesis completed at 34 wks GA
• If you are ON TIME and without oligohydramnios
  issues your GFR is 30 of your adult GFR

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Who to blame, cont..

• Your GFR increases rapidly during first several
  wks of life to reach nearly 80 of your adult
  level
• Important because baseline tubular function is
  immature but GFR and tubular reabsorption
  capability is fairly well matched and
  reabsorption increases along with GFR

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UNLESS..

• If you are a premie your birth GFR is lower than
  30 of your adult GFR
• Your GFR does not begin to increase toward the
  30 level until you reach 34 wks GA
• Tubular reabsorption capacity is less well
  developed and your GFR exceeds your reabsorption
  capacity

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A New Baby

• 34 wk infant born by SVD to a 26 yo G1P0 mom
• Uncomplicated pregnancy, prenatal screens normal
• Meds Prenatal vitamins
• ROM 4 hrs PTD, clear fluid, no maternal temp
• Infant vigorous, good cap refill, no resp distress

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• Voided 14 hrs after delivery, started on Enfamil
  20 on DOL1
• Infant had weight loss (not excessive) in 1st wk
  of life
• Weeks 2-3 showed slower than expected weight
  gain despite adequate feeding, benign physical
  exam, stable vitals
• At 1 month check-up weight was unchanged and
  infant beginning to fall off growth curve

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• Laboratory values as follows
• Initial 138/2.6/116/13/14/0.3 (NL AG)
• Divalents WNL
• CBG 7.20
• Urine pH 7.5

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Renal Tubular Acidosis

• Type II is most common type encountered in
  neonates/children, milder than Type I
• Often found on routine screening or as part of
  FTT w/u
• Lesion in proximal tubule where 85-90 of total
  bicarb reabsorption occurs
• Lowering of renal bicarb threshold
• Renal bicarb threshold is serum conc at which
  bicarb appears in urine

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More RTA.

• Type I is the most common hereditary and more
  severe form of RTA
• Pts often present with FTT, vomiting/lethargy
  and severe acidosis (HCO3 lt10, pH lt 7.1)
• Lesion in the distal tubule
• Defect in the transport of H and/or inability to
  maintain gradient large enough for proper
  excretion of H ion (ie absent or insufficient
  NH3 production)

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Another New Baby..

• 32 wk infant born by SVD to a 26 yo G1P0 mom
• Uncomplicated pregnancy, prenatal screens normal
• Meds Prenatal vitamins
• ROM 4 hrs PTD, clear fluid, no maternal temp
• Infant vigorous, good cap refill, no resp
  distress

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• Voided 14 hrs after delivery, started on EP20 on
  DOL1
• Infant had weight loss (not excessive) in 1st wk
  of life
• Week 2 showed slower than expected weight gain
  despite adequate feeding, benign physical exam,
  stable vitals
• Electrolytes during wk 1-2 were WNL for GA,

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• Infant remained well appearing, had routine
  screening labs on DOL23
• Initial 138/4.9/106/15/14/0.3 (NL AG)
• Divalents WNL
• CBG 7.32
• Urine ph 5.0

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Late Metabolic Acidosis

• Generally develops during wk of life 2-3
• Usually noted because of slow weight gain or on
  routine screening if infant in house
• Majority will spontaneously resolve by 2-3 mo w/o
  treatment but may take as long as 1 yr

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More LMA

• Characterized by
• Well-appearing infants w/o other identifiable
  causes for acidosis
• Slow initiation of weight gain/inadequate weight
  gain despite adequate caloric intake
• Low HCO3 levels (rarely severe) with relatively
  normal pH levels

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LMA cont

• A disproportion between infants daily acid load
  and kidneys capacity to excrete acid
• Once maximum renal acid excretion capacity is
  reached, continued acid loading causes
  development of acidosis
• Acidosis resolves as renal acid excretion
  capacity increases

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Inborn Errors of Metabolism

• List is VERY VERY long
• Generally tend to be the sickest kids with the
  worst acidosis
• May be difficult to diagnose in already sick
  newborns because may be multiple potential
  etiologies for acidosis
• May not present during hospitalization

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High Suspicion if..

• History of unexplained neonatal deaths in the
  family
• Offspring of consanguineous matings
• Infant has lethargy, hypotonia, vomiting,
  seizures and acidosis not immediately explained
  by other etiologies
• Onset of symptoms after period of good health
  (even a few hrs)
• Onset of symptoms with progression of feeds

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Do we treat acidosis?

• Decades of studies on treatment of RTAs show
  significant improvement in growth and development
  and decrease in mortality (type I) using HCO3
  supplements
• Current recommendations
• Oral citrate supplements, titrate dosage to
  achieve HCO3 levels of 20 or higher
• Citrate metabolized to bicarb in the liver

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Do we treat, cont.

• Beyond attempting to correct the underlying
  etiology and providing supportive care should we
  be aggressively treating severe acidosis (pH lt
  7.10) with HCO3?
• NOT SURE

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Any Evidence?

• Current opinions vary for utility of HCO3
  administration in severe acidosis
• In 2002 both Cochrane and American Journal of
  Kidney Disease published lit reviews on use of
  HCO3 for the treatment of severe acidemic states

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Cochrane Review

• Evaluated evidence for rapid correction of
  metabolic acidemia in comparison with placebo, no
  intervention, or slow correction
• Outcome measurements Max O2 requirement and
  length of O2 therapy, need for and length of
  assisted ventilation, IVH/PVL, survival to
  discharge, survival to 24 months

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NO STUDIES
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American Journal of Kidney

• Less rigorous criteria for review
• Multiple studies but conflicting data on benefits
  of bicarb therapy
• Several studies showing good evidence of
  detrimental effects such as paradoxical acidosis,
  sodium load, intracranial bleeds, fluctuations in
  BP

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Alternative agents?

• Tris-hydroxymethyl aminomethane (THAM) inert
  amino alcohol which buffers by its amine group
  (-NH2)
• Potential advantages
• Does not increase NA levels
• Does not produce CO2
• No studies comparing THAM and NaHCO3 or safety of
  THAM

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• Carbicarb equimolar mixture of sodium carbonate
  and sodium bicarbonate
• Has not yet been studied in humans and in dog
  models its use has been correlated with
  increased rates of cardiopulmonary arrest
• Dichloroacetate increases activity of pyruvate
  dehydrogenase which decreases production of
  lactic acid
• One study completed, no improvement in
  hemodynamics or survival

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