Acid-Base DisordersMara Nitu, MD,* GregMontgomery, MD,Howard
Eigen, MDAuthor DisclosureDrs Nitu,Montgomery, andEigen have
disclosedno nancialrelationships relevantto this article.
Thiscommentary does notcontain a discussionof an
unapproved/investigative use of acommercial
product/device.Objectives After completing this article, readers
should be able to:1. Understand the mechanisms for regulating
acid-base physiology.2. Know the differential diagnosis of
metabolic acidosis associated with high anion gapand plan for
initial management.3. Know the differential diagnosis of normal
anion gap metabolic acidosis.4. Describe pulmonary compensatory
changes in metabolic acidosis and alkalosis.5. Understand how
various diuretics can lead to acid-base imbalance.6. Describe renal
compensatory changes in respiratory acidosis and alkalosis.Case
StudyA16-year-oldgirl whohas nosignicantprevious medical
historypresents totheemer-gency department witha4-day history of
nausea, vomiting, fever, chills, diarrhea, legcramps, abdominal
pain, andheadaches. Sheis nishinghermenstrual periodandar-rives
with a tampon in place, which she reports that she inserted
yesterday. Her vital signsinclude a heart rate of 165 beats/min,
respiratory rate of 28 breaths/min, blood pressure65/30 mm Hg, and
oxygen saturation of 100% on 4 L/min of oxygen. The most likely
diag-nosis for this patient is toxic shock syndrome, which was
later conrmed with a positive antibodytest.The initial arterial
blood gas (ABG) values are:pH, 7.24Partial pressure of oxygen
(PO2), 138 mm HgPartial pressure of carbon dioxide (PCO2), 19 mm
HgBicarbonate (HCO3), 8 mEq/L (8 mmol/L)Base excess (BE), 18 mEq/L
(18 mmol/L)Such ndings are suggestive of metabolic acidosis with
respi-ratory compensation.Further laboratory results are:Serum
sodium (Na), 133 mEq/L (133 mmol/L)Potassium (K), 4.2 mEq/L (4.2
mmol/L)Chloride (Cl), 109 mEq/L (109 mmol/L)HCO3, 12 mEq/L (12
mmol/L)Anion gap (AG), 12 mEq/L (12 mmol/L)Blood urea nitrogen
(BUN), 49 mg/dL (17.5 mmol/L)Creatinine, 3.96 mg/dL (350
mol/L)Calcium, 5.2 mg/dL (1.3 mmol/L)Albumin, 2.0 g/dL (20 g/L)The
apparently normal AG is misleading. After correctingthe AG for
hypoalbuminemia, the adjusted AG is 17 mEq/L(17
mmol/L).Lacticacidemiaduetoshock, oneofthelikelycausesfor*Associate
Professor of Clinical Pediatrics, Section of Pediatric Pulmonology,
Critical Care and Allergy; Medical Director, PICU/Riley Hospital
for Children; Medical Co-Director of Lifeline Transport Team,
Indianapolis, IN.Assistant Professor of Clinical Pediatrics,
Section of Pulmonology, Critical Care and Allergy; Medical
Director, PediatricBronchoscopy Laboratory, James Whitcomb Riley
Hospital for Children, Indianapolis, IN.Billie Lou Wood Professor
of Pediatrics, Associate Chairman for Clinical Affairs; Director,
Section of Pediatric Pulmonology,Critical Care and Allergy, James
Whitcomb Riley Hospital for Children, Indianapolis,
IN.AbbreviationsABG: arterial blood gasAG: anion gapBE: base
excessBUN: blood urea nitrogenCa2: calciumCl: chlorideCNS: central
nervous systemDKA: diabetic ketoacidosisGI: gastrointestinalH:
hydrogenHCO3: bicarbonateK: potassiumMg2: magnesiumNa: sodiumNH3:
ammoniaNH4: ammoniumPCO2: partial pressure of carbon dioxidePO2:
partial pressure of oxygenRTA: renal tubular acidosisArticle uids
and electrolytes240Pediatrics in Review Vol.32 No.6 June 2011 at
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increasedAGmetabolicacidosis, is conrmedbyahighserumlactate value
of 6.9 mg/dL (0.8 mmol/L). One hourlater, the ABG values are:pH,
7.06PO2, 63 mm HgPCO2, 47 mm HgHCO3, 13.2 mEq/L (13.2 mmol/L)BE, 16
mEq/L (16 mmol/L)This ABGpanel reveals metabolic acidosis
withoutrespiratory compensationdue to developing
respiratoryfailure.IntroductionThe loss of acid-base balance is an
expression of variousconditions encounteredfrequentlyinclinical
practice.Changes inhydrogenionconcentrationcanleadtounraveling of
the protein tertiary structure, thereby caus-ingenzymedysfunction,
enzymeloss, andcell death.Understandingthe physiology behindvarious
distur-bances in acid-base balance is necessary for determining
acorrect diagnosis and management plan.Maintaining acid-base
homeostasis involves the lungs,kidneys, and a very complex system
of buffers, all aimingto maintain the normal pH (7.35 to 7.45) of
the arterialblood. Lowering the arterial pH below 7.35 is
termedacidosis, and an increase of the arterial pH above
7.45constitutes alkalosis.Metabolic acidosis is associated with a
lowpHand lowHCO3concentration. Metabolic alkalosis is
associatedwith a high pH and high HCO3concentration. Respi-ratory
acidosis is associated with a lowpHand high PCO2.Respiratory
alkalosis is associated with a high pHand lowPCO2 (Fig. 1).Each
acid-base disorder leads to countering respira-toryorrenal
compensatoryresponsesthat attempt
tonormalizethepH.Inmetabolicacidosis,forexample,ventilation is
increased, resulting in a decrease in PCO2,which tends to raise the
pH toward normal. These
com-pensatoryattemptsneverovershootcorrectingthepH(Figs. 2 and
3).The process of acid-base regulation
in-volvestherespiratorysystem(controlsPCO2), kidneys(regulates
plasma HCO3by changes in acid excretion),andaverycomplexsystemof
extracellular andintra-cellular buffers.The Respiratory System in
Acid-Base BalanceThe respiratory system contributes to acid-base
balancevia timely adjustments in alveolar minute ventilation
thatmaintain systemic acid-base equilibrium in response
toalterations in systemic pHand arterial PCO2. Systemic pHis
monitored by central chemoreceptors on the ventro-lateral surface
of the medulla oblongata and arterial PCO2(aswell asarterial
PO2)byperipheral chemoreceptorslocated at the carotid and aortic
bodies. These chemore-ceptors act through central respiratory
control centers inthe pons and medulla to coordinate the
respiratory mus-cle efforts of inhalation and exhalation, leading
to adjust-ments in both components of minute ventilation:
tidalvolume and respiratory cycle frequency. Lung-mediatedchanges
in arterial PCO2 can lead to rapid alteration insystemic
hydrogenions (H) because CO2is lipid-soluble and may readily cross
cell membranes accordingtothe followingequation:
HHCO37H2CO3(carbonicacid)7CO2H2O(water). Undernormalphysiologic
conditions, this process allows for tight con-trol of arterial PCO2
near 40 mm Hg.Figure1.
Acid-basechangesinmetabolicversusrespiratorydisorders.Figure2.
Primary metabolic acidosis with subsequent
respi-ratoryalkalosiscompensation. Theredarrowdoesnotcrossinto the
alkalosis range, reecting the concept that overcom-pensation never
occurs.uids and electrolytes acid-base disordersPediatrics in
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Downloaded from The Kidneys in Acid-Base BalanceThe kidneys role in
acid-base balance consists of reab-sorbing ltered HCO3and excreting
the daily acid loadderived principally fromthe metabolismof
sulfur-containing amino acids. Ninety percent of lteredHCO3is
reabsorbed in the proximal tubules, primarilyby Na-Hexchange, and
the remaining 10% is reab-sorbedinthedistal nephron, primarilyvia
hydrogensecretion by a proton pump (H-ATPase). Under nor-mal
conditions, no HCO3is present in the nal urine.The excretion of the
daily Hload occurs in the distaltubule. Onceexcretedintheurine,
theHmust bebound to a buffer to avoid excessive urine
acidicationand promote further excretion. The two primary buffersin
the urine are ammonia (NH3), which is excreted andmeasuredas
ammonium(NH4) andphosphate(re-ferred to and measured as titratable
acidity). The kidneyssynthesize and excrete NH3, which combines
with Hexcretedbythecollectingduct cells toformNH4:HNH3NH4.
NH3diffuses freely across mem-branes; NH4does not. Failure to
produce and excretesufcient NH4, therefore, leads to the
development ofmetabolic acidosis.Extracellular and Intracellular
Buffers inAcid-Base
BalanceThemostimportantbufferintheextracellularuidisHCO3,
duebothtoitsrelativelyhighconcentrationand its ability to vary PCO2
via changes in alveolar venti-lation. Chemoreceptor analysis of
arterial pH and PCO2allows for centrally mediated adjustments in
minute ven-tilation to maintain arterial PCO2. The
HCO3interactswithH, as demonstratedinthefollowingformula:H
HCO37H2CO37CO2 H2O. This reactionserves as the basis for the
Henderson-Hasselbalch equa-tion: pH6.1 log (HCO3/0.03 PCO2).
Althoughthis equationdescribes apatients acid-basestatus, itdoes
not provide insight intothe mechanismof theacid-base disorder.The
Henderson-Hasselbalch equation lists PCO2 andHCO3as independent
predictors of acid-base balance,but in reality they are
interdependent (as suggested bythechemical
reactionHHCO3describedprevi-ously). Furthermore, the
Henderson-Hasselbalch equa-tion does not account for other
important nonbicarbon-atebuffers present inthebody, suchas
theprimaryintracellularbuffersofproteins,
organicandinorganicphosphates, andhemoglobin. Inaddition,
boneisanimportant site for buffering of acid and base
loads.Laboratory Assessment of Acid-Base BalanceAcid-base balance
is assessed by blood gas analysis andserummeasurement of several
important electrolytes,leading to the calculation of the AG. Blood
gas analyzersmeasurethepHandthePCO2directly. TheHCO3value is
calculated fromthe Henderson-Hasselbalchequation. The BE value also
is calculated as the amountof base/acid that should be added to a
sample of wholeblood in vitro to restore the pHto 7.40 while the
PCO2isheld at 40 mm Hg. The PCO2 not only points to the typeof
disorder (respiratoryor metabolic) but alsocorre-sponds to the
magnitude of the disorder.The AGmethodwas developedtoinclude
othernonbicarbonatebuffers intheanalysis. Basedontheprincipleof
electroneutrality, thesumof thepositivecharges should equal the sum
of the negative charges asfollows: NaKMg2(magnesium) Ca2(cal-cium)
HClHCO3proteinPO43(phos-phate) OH SO42(sulfate) CO32 conjugatebase.
Sodium, chloride, andHCO3are measuredeasily in the serum.
Therefore, the AGis calculated by theformula AG{Na} {ClHCO3}. A
normal AGis122 mEq/L (12 mmol/L). Some clinicians and somepublished
reports include potassiumas a measured cationin the calculation of
AG, which raises the normal value by4 mEq/L (4 mmol/L).The AGis
denedas the difference betweentheunmeasured plasma anions and the
unmeasured plasmacations. Clinically, an elevated AGis believed to
reect anincreaseofunmeasuredanionsand,therefore,ameta-bolic
acidosis. This concept is explained by the fact
thatunmeasuredcations(Mg2Ca2H)aremoreFigure 3. Primary respiratory
acidosis with subsequent meta-bolic alkalosis compensation. The red
arrow does not cross intothe alkalosis range, reecting the concept
that overcompen-sation never occurs.uids and electrolytes acid-base
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tightlycontrolledandtheunmeasuredanions haveagreater tendency to
uctuate. Theoretically, the AG alsocan increase following a
decrease in serum K, Ca2, orMg2, but the normal concentration of
these cations isso lowthat a reduction does not have a signicant
clinicalimpact on the
AG.Ingeneral,theseprinciplesholdtruefortheprevi-ouslyhealthyindividualwhodevelopsanacuteillness.However,
for the critically ill host whose plasma proteinconcentrations are
greatly reduced, the low protein
val-ueshideanassociatedincreaseinunmeasuredanions.Without the
correction for hypoalbuminemia, it is possi-ble tooverlooka true
highAGacidosis, mistakenlyassuming it to be a normal AG
acidosis.According to the Figge formula, each 1-g/dL reduc-tion in
the serum albumin concentration is expected toreduce the AG by 2.5
mEq/L:Adjusted AGobserved AG (2.5 [normal albumin observed
albumin]Metabolic Acid-Base DisturbanceMetabolic AcidosisMetabolic
acidosis is dened as an acid-base imbalancethat leads to anion
excess (low HCO3concentration)and subsequently to an arterial pH
below 7.35. Severalmechanisms can lead to metabolic acidosis:
excess acidproduction, increased acid intake, decreased renal acid
ex-cretion, increasedHCO3lossfromthegastrointestinal(GI) tract, and
excess HCO3excretion in the kidney.For a patient whohas intact
respiratoryfunction,developing metabolic acidosis leads to
respiratory com-pensation by hyperventilation. Each 1-mEq/L
reductionin plasma HCO3concentration prompts a 1.2-mm
HgcompensatoryfallinthePCO2.Clinically,thepatientsrespiratory rate
increases within the rst hour of the onsetof metabolicacidosis,
andrespiratorycompensationisachieved within 24 hours. Failure of
the respiratory sys-tem to compensate for metabolic acidosis is an
ominoussign that should trigger careful evaluation of the
patientsmental status and cardiorespiratory
function.CalculatingtheAGis a veryuseful initial stepindiagnosing
various causes of metabolic acidosis.Metabolic Acidosis With Normal
Anion GapMetabolic acidosis with normal AG reects an imbalanceof
the measured plasma anions and cations. According tothe formula:
AGNa (Cl HCO3), metabolicacidosis with normal AG can be explained
by excessiveloss of HCO3(inthestool or intheurine) or byinability
to excrete hydrogen ions. Table 1 lists the mostfrequent conditions
leadingtonormal AGmetabolicacidosis.Of particular note is renal
tubular acidosis (RTA), acomplex set of disorders of the kidney
that can lead tonormal AGmetabolic acidosis. One disorder is the
inabil-ity to excrete the daily acid load (type 1 RTA), leading
toprogressiveHionretentionandlowplasmaHCO3concentration(10mEq/L[10mmol/L]).
AnotherdisorderarisesfromtheinabilitytoreabsorbHCO3normally in the
proximal tubule (proximal RTAor type 2RTA). HCO3is lost in the
urine despite some reabsorp-tion in the distal nephron, leading to
metabolic acidosisand alkaline urine.Normal
AGmetabolicacidosiscausedbyexcessiveHCO3losses
maybecorrectedbyslowinfusionofsodium bicarbonate-containing
intravenous uids.Elevated Anion Gap Metabolic AcidosisElevated AG
metabolic acidosis results from an excess ofunmeasuredanions.
Various conditions that causeanTable 1. Causes of Normal AnionGap
Metabolic AcidosisDisorders of the Gastrointestinal (GI) Tract
Leading ToExcessive Bicarbonate Loss Diarrhea: the leading cause of
normal anion gapmetabolic acidosis in children Surgical procedures
that lead to an anastomosis of theureter with the GI tract, such as
ureteroenterostomy/ureterosigmoidostomy, due to bicarbonate loss in
theintestine Pancreatic stulaIatrogenic Hyperchloremic Metabolic
Acidosis Result of excessive uid resuscitation with 0.9%sodium
chloride or excessive use of 3% sodiumchloride to correct
hyponatremiaRenal Loss of Bicarbonate Renal tubular acidosis type
II (proximal) Iatrogenic: carbonic anhydrase
inhibitor(acetazolamide) HyperparathyroidismMedications Acidifying
agents: sodium chloride, potassiumchloride, enteral supplements
Magnesium chloride Cholestyramine
SpironolactoneHypoaldosteronismuids and electrolytes acid-base
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accumulation of unmeasured anions, leading to high AGmetabolic
acidosis, are listed in Table 2.When faced with an elevated AG
metabolic acidosis,calculatingthe osmotic gapmay helpdetermine
theunderlying condition. Similar to the AG, the osmotic gapis the
difference between the measured serum
osmolalityandthecalculatedvalue. Thecalculatedserumosmo-lality is:
2[Na] glucose/18BUN/2.8. Anormal osmotic gap should be 122 mOsm/L.
A highosmoticgapis asignof anexcess of
anunmeasuredosmoticactivesubstancesuchasethyleneglycol(anti-freeze),
methanol (wood alcohol), or paraldehyde.KetoacidosisKetoacidosis
describes accumulationof
ketonebodies(beta-hydroxybutyrateandacetoaceticacid)
followingexcessiveintracellularuseoflipidsasametabolicsub-strate.
This metabolic shift occurs during starvation orfasting or as a
reection of a lack of appropriate metabolicsubstratefor
energyproduction(duringspecicdietswherecarbohydratesarereplacedwithlipids).
Hyper-ketotic diets sometimes are employedfor intractableepilepsy
in an effort to decrease the seizure threshold.Diabetic
ketoacidosis (DKA) results from a decreasein insulin production
that leads to an inability to trans-port glucose into the cell. The
cell shifts to lipid metab-olism, despite the surrounding
hyperglycemia (also de-scribed as starvation in the middle of the
plenty). Thediagnosis of DKA is conrmed by the ndings of
hyper-glycemia, a high AG acidosis, ketonuria, and
ketonemia.Theearliest symptoms of DKAarerelatedtohyper-glycemia.
Older children and adolescents typically pres-ent with polyuria
(due to the glucose-induced osmoticdiuresis), polydipsia (due to
the increased urinary losses),fatigue, and weight loss. Hypovolemia
may be severe ifurinarylosses arenot replaced,
withthepresentationof very dry mucous membranes and prolonged
capillaryrell time. As a result of worsening metabolic
acidosis,thepatientdevelopshyperventilationanddeep(Kuss-maul)respirations,
representingrespiratorycompensa-tion for metabolic acidosis.
Hyperpnea develops from anincrease in minute volume (rate tidal
volume) or fromincreased tidal volume alone without an increase in
respi-ratory rate. When DKA is being managed, the patientschest
excursion and respiratory rate should be observedcarefully to
determine if hyperpnea is present. In infants,hyperpnea may be
manifested only by tachypnea.Without prompt medical attention, DKA
can prog-ress to cerebral edema and cardiorespiratory
arrest.Neurologic ndings, ranging from drowsiness, lethargy,and
obtundation to coma, are related to the severity ofhyperosmolality
or to the degree of acidosis. Treatmentof DKA includes sensitive
correction of the underlyinginsulin, volume, and electrolyte
deciencies.Lactic AcidosisLactic acidosis, another cause of an
elevated AG,
occurswhencellsshifttoanaerobicpathwaysforenergypro-ductionas
aresult of tissuehypoxiaduetoinappro-priate tissue perfusion,
inappropriate oxygen supply,
ormitochondrialdysfunction(asseenininbornerrorsofmetabolism or
ingestion of drugs or toxins). The clinicalpresentation may involve
seizures or symptoms consis-tent with the initial disorder that led
to lactic acidosis,such as cyanosis, signs and symptoms suggestive
of tissuehypoperfusion, and hypotension. As lactic acidosis
wors-ens, further hemodynamic compromise occurs. Manage-ment
shouldbetargetedtorestoringadequatetissueperfusion and oxygen
supply by treating the underlyingcause of the lactic
acidosis.Inborn Errors of MetabolismSeveral inbornerrors of
metabolismcanpresent withhigh AG metabolic acidosis. Based on the
affected met-abolic pathway, the increased AG is caused by a
differentchemical substance: urea cycle defects present with
hy-perammonemia; or inborn errors of amino acids, carbo-hydrate, or
organic acid metabolism present either withketoacidosis, lactic
acidosis (as in Krebs cycle defects), orincreased organic acids
production. Symptoms often arenonspecic and include poor feeding,
failure to thrive,seizures, and vomiting.Table 2. Causes of
Elevated AnionGap Metabolic AcidosisKetoacidosis Starvation or
fasting Diabetic ketoacidosisLactic Acidosis Tissue hypoxia
Excessive muscular activity Inborn errors of metabolismIngestions
Methanol Ethylene glycol Salicylates ParaldehydeRenal Failure
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Downloaded from Managing inborn errors of metabolism involves
iden-tifying the defective or decient enzyme and limiting theintake
of the metabolic substrate that requires the use ofthat particular
enzyme. In selected cases, dialysis may bethe appropriate tool for
removing the excess anion.IngestionsIngestions of various chemical
substances areanothercauseofmetabolicacidosiswithanelevatedAG.
Sali-cylateoverdoseis well
knowntocauseincreasedAGmetabolicacidosisbyinterferingwithcellularmetabo-lism(uncouplingof
oxidativephosphorylation). Earlysymptoms of salicylate overdose
include tinnitus, fever,vertigo, nausea, vomiting, anddiarrhea.
Moresevereintoxication can cause altered mental status, coma,
non-cardiac pulmonary edema, anddeath. Most patientsshowsigns of
intoxicationwhentheplasmasalicylateconcentration exceeds 40 mg/dL.
Treatment of salicy-lateingestioninvolves promotingalkalinediuresis
toenhance renal salicylate excretion. In severe cases, dialysismay
be required (generally considered when plasma sa-licylate
concentrations exceed 80 mg/dL in acute intox-ication and 60 mg/dL
in chronic ingestions).Toluene inhalation also can lead to
metabolic acidosiswith an increased AG. In patients who experience
tolu-ene ingestion (glue snifng), the overproduced hippu-rate is
both ltered and secreted by the kidneys, leadingto rapid
elimination in the urine. As a result, the AG maybe near-normal or
normal at the time of presentation andthe patient might be
diagnosed mistakenly as having anormal AG acidosis.Ethylene glycol
(antifreeze), methanol, and paralde-hyde ingestion lead to an
increased AG metabolic acido-sis and an increased osmotic gap. Both
the AG and theacidosis due to methanol and ethylene glycol
ingestionsresult from metabolism of the parent compound. Nei-ther
may be seeninpatients early inthe course ofingestion or when there
is concurrent ingestion of etha-nol. Ethanol combines competitively
with alcohol dehy-drogenase, thereby slowing the metabolism of
methanolor ethylene glycol to their toxic metabolites and
slowingtheappearanceofboththeacidosisandthehighAG.This effect
explains why ethanol administration is used inthe medical
management of methanol and ethylene gly-col ingestions, along with
fomepizole (alcohol
dehydro-genaseinhibitor).Managementofethyleneglycol andmethanol
toxicity also involves hemodialysis, which
re-movesboththeingestedsubstanceandthemetabolicbyproducts from the
serum.Massiveingestions of creams containingpropyleneglycol (eg,
silver sulfadiazine) also can lead to increasedAG metabolic
acidosis.Renal FailureRenal failure causes an increased AG
metabolic acidosisdue to the failure to excrete H. Normally,
eliminationof the serum acid load is achieved by urinary excretion
ofH, both as titratable acidity and as NH4. Titratableacid is a
term used to describe acids such as
phosphoricacidandsulfuricacidpresent intheurine. Thetermexplicitly
excludes NH4as a source of acid and is part ofthe calculation for
net acid excretion. The termtitratableacid was chosen based on the
chemical reaction of titra-tion (neutralization) of those acids in
reaction with so-dium
hydroxide.Asthenumberoffunctioningnephronsdeclinesinchronic kidney
disease and the glomerular ltration ratedecreases to below 25% of
normal, the patient developsprogressive high AG metabolic acidosis
(hyperchloremiamay occur transiently in the initial phases of renal
failure).In addition to the decrease in NH4excretion,
decreasedtitratable acidity (primarily as phosphate) may play a
rolein the pathogenesis of metabolic acidosis in patients
whoexperience advanced kidney disease. Of course, dialysisoften is
employed to correct the severe uid and electro-lyte imbalances
generated by renal failure.Management of Metabolic
AcidosisRegardless of the cause, acidemia, if untreated, can leadto
signicant adverse consequences (Table 3).Useof HCO3therapytoadjust
thepHfor pa-tients who have metabolic acidosis is controversial.
Slowinfusion of sodium bicarbonate-containing intravenousuids
canbeusedincases of normal
AGmetabolicacidosistoreplenishexcessiveHCO3losses(eg,asaresult of
excessive diarrhea). However, infusing
sodiumbicarbonate-containinguids for increasedAGmeta-bolic acidosis
has questionable benet and should not beused clinically.As
discussed, HCO3combines with H, leading toH2CO3that subsequently
dissociates to CO2and H2O.Infusing HCO3decreases serum pH and
raises CO2 andH2O. Neitherthecell membranesnortheblood-brainbarrier
is very permeable to HCO3; CO2diffuses freely tothe intracellular
space, where it combines with H2O, lead-ingtoH2CO3andworseningof
theintracellular pH.Administering intravenous sodiumbicarbonate to
a patientwho has an increased AG metabolic acidosis can lead to
afalse sense of security because the underlying problem ishidden by
an articially improved serum pH.uids and electrolytes acid-base
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bicarbonate once held a prominent positionin the management of
cardiac arrest. Reversing the aci-dosis caused by global
hypoperfusion made physiologicsense because severe acidemia may
worsen tissue perfu-sionbydecreasingcardiaccontractility. However,
themost effective means of correcting the acidosis in cardiacarrest
is torestoreadequateoxygenation, ventilation,and tissue perfusion.
Because most pediatric cardiac ar-rests are due to respiratory
failure, support of ventilationthrough early intubation is the
primary treatment, fol-lowedby support of the circulationwithuids
andinotropic agents. Currently, the American Heart Associ-ation
recommends that sodium bicarbonate administra-tion be considered
only in children who suffer prolongedcardiac arrest and documented
severe metabolic acidosisandwhofail torespondtooxygenation,
ventilation,intravenous uids, andchest compressions combinedwith
epinephrine in recommended doses.Metabolic AlkalosisMetabolic
alkalosis is dened as an acid-base imbalanceleading to increased
plasma HCO3and an arterial pHabove 7.45. Several mechanisms can
lead to the elevationintheplasmaHCO3: excessivehydrogenloss,
func-tional addition of new HCO3, and volume contractionaround a
relatively constant amount of extracellularHCO3(called a
contraction alkalosis). The kidneysare extremely efcient in
eliminating excess HCO3intheurine.
AconfoundingfactorisrequiredforserumHCO3to accumulate, such as
impaired renal function,Kdepletion, or volume depletion.Ingeneral,
a patient compensates for a metabolicalkalosis by decreasing
ventilation. Respiratory compen-sation by hypoventilation raises
PCO2 by 0.7 mm Hg forevery 1 mEq/L (1 mmol/L) of serum
HCO3increase.Excessive Hlosses can occur either in the urine or
GItract and lead to HCO3accumulation as the result ofthe following
reactions:H2O7HHOHOCO27HCO3Increased loss of gastric content, which
has high con-centrations of hydrogen chloride, as a result of
persistentvomiting (eg, self-induced, pyloric stenosis) or
highnasogastric tube drainage leads to metabolic alkalosis. Ifuid
losses continue unreplaced, dehydration and lacticacidosis
ultimately develop. Of note, infants of motherswho have bulimia
have metabolic alkalosis at birth.HighHloss intheurinecanoccur
inthedistalnephron.Increasedsecretionofaldosteronestimulatesthe
secretory H-ATPase pump, increasing Nareabsorp-tion,
therebymakingthelumenmoreelectronegativeand causing more Hand
Kexcretion, which results inconcurrent metabolic alkalosis and
hypokalemia. Patientswho have primary mineralocorticoid excess
present withhypokalemiaandhypertension. Incontrast,
secondaryhyperaldosteronismduetocongestiveheart failureorcirrhosis
usually does not present with metabolic
alkalosisorhypokalemiabecausetheabove-mentionedmecha-nism is
blunted by decreased distal nephron Nadeliv-ery.
Iatrogenicmetabolicalkalosis
alongwithvolumecontractioncanoccurinpatientstreatedwithlooporthiazidediuretics,
whichcauseCldepletionandin-creaseddeliveryof Natothecollectingduct,
whichenhances Kand Hsecretion.Bartter and Gitelman syndromes
present with meta-bolic alkalosis and hypokalemia due to a genetic
defect inthe transporters in the loop of Henle and distal
tubule,Table3. Consequences ofMetabolic AcidosisCerebral Inhibition
of metabolism Cerebral edema Obtundation and comaCardiovascular
Decreased cardiac contractility Decreased cardiovascular
responsiveness tocatecholamine Decreased threshold for arrhythmias
Reduction of cardiac output, blood pressure, andend-organ perfusion
Pulmonary vasoconstrictionRespiratory Hyperventilation as a result
of respiratorycompensation Decreased respiratory muscle strength
Increased work of breathingHematologic Oxyhemoglobin dissociation
curve shifts to the right(the oxygen is more easily released at the
tissue leveldue to a lower pH)Metabolic Inhibition of anaerobic
glycolysis Insulin resistance Decreased adenosine triphosphate
synthesis Hyperkalemia Increased protein degradationuids and
electrolytes acid-base disorders246Pediatrics in Review Vol.32 No.6
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respectively, thesamelocations as thoseinhibitedbyloop and thiazide
diuretics.In addition to Hloss, metabolic alkalosis also can
beinduced by the shift of Hinto the cells.As discussed previously,
hypokalemia is a frequent nd-ing in patients who have metabolic
alkalosis. Hypokalemiaby itself causes intracellular acidosis and
increased serumalkalosis by the following mechanism: intracellular
Kshifts into the serum to replete the extracellular stores, andto
maintain electroneutrality, Henters the cells. Hydro-gen movement
into the cells lowers the intracellular pHand leaves unbuffered
excess HCO3in the serum. Theintracellularacidosisinrenal
tubularcellspromotesHsecretion and, therefore,
HCO3reabsorption.Metabolic alkalosis due to functional addition
ofnewHCO3canoccurbyseveral mechanisms: de-creased renal excretion
of HCO3, posthypercapnicalkalosis, or excessive intake or
administration of alkali.Decreased Renal Bicarbonate ExcretionRenal
failure can lead to metabolic alkalosis because thekidneys fail to
excrete excess HCO3.Posthypercapnic AlkalosisChronic respiratory
acidosis (retention of CO2) leads to acompensatory increase
inhydrogensecretionandanensuing increase in the plasma
HCO3concentration tocorrect the pH. When the PCO2 is decreased
rapidly bymechanical ventilationof a patient whohas
chronicrespiratoryacidosis, theensuingmetabolicalkalosis isslow to
disappear. Because Clloss often is present inposthypercapnic
alkalosis, repleting the Cldecit maybe essential to correct the
alkalosis.Furthermore, the acute fall in PCO2 in a person whohas
chronic respiratory acidosis raises the cerebral intra-cellular
pHacutely, achangethat caninduceseriousneurologicabnormalities
anddeathbecauseCO2candiffusefreelyacrosstheblood-brainbarrieroutoftheintracellularspace,
leadingtoseverealkalosis. Accord-ingly, the PCO2 must be reduced
gradually in mechani-cally ventilated patients who present
initially with chronichypercapnia.Excessive Intake or
Administration of AlkaliAlkali administration does not induce
metabolic alkalosisin healthy people because the healthy kidney can
excreteHCO3rapidly in the urine. However, metabolic
alka-losiscanoccurif verylargequantitiesof HCO3areadministered
acutely or if the ability to excrete HCO3is impaired.
Theadministrationof largequantities ofcitrate is known to lead to
metabolic alkalosis. Examplesof large administrations of citrate
are infusion of morethan8units of bankedbloodor
freshfrozenplasmaoradministrationofcitrateasananticoagulantduringdialysis.Contraction
AlkalosisContractionalkalosisoccurswhenrelativelylargevol-umes of
HCO3-free uid are lost, a situation frequentlyseen with
administration of intravenous loop diuretics.Contraction alkalosis
also may occur in other disorders inwhich a high-Cl,
low-HCO3solution is lost, such assweat losses in cystic brosis,
loss of gastric secretions inpatients who have achlorhydria, and
uid loss from fre-quent stooling by patients who have congenital
chlori-dorrhea, a rare congenital secretory diarrhea.Regardlessof
thecause, alkalosis, if untreated, canlead to signicant adverse
consequences (Table 4).Management of Metabolic
AlkalosisThreegeneralprinciplesapplytothetherapyofmeta-bolic
alkalosis: correct true volume depletion, correct Kdepletion, and
correct Cldepletion (in Cl-responsivemetabolic alkalosis). For
patients who have true volumeTable4. Consequences ofUntreated
AlkalosisCerebral Cerebral vasoconstriction with reduction of
cerebralblood ow Tetany, seizures, lethargy, delirium, and
stuporCardiovascular Vasoconstriction of the small arterioles,
includingcoronary arteries Decreased threshold for
arrhythmiasRespiratory Compensatory hypoventilation with
possiblesubsequent hypoxemia and hypercarbia
(respiratoryfailure)Hematologic Oxyhemoglobin dissociation curve
shifts to the left(the oxygen is bound more tightly to
theoxyhemoglobin)Metabolic and Electrolyte Imbalances Stimulation
of anaerobic glycolysis Hypokalemia Decreased plasma ionized
calcium Hypomagnesemia and hypophosphatemiauids and electrolytes
acid-base disordersPediatrics in Review Vol.32 No.6 June 2011 247
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uid administration of normal saline replacesthe Cland free water
decits. Potassium chloride ad-ministration for patients who have
concurrent hypokale-mia is an important component of treatment.
This agentbecomes particularly helpful in patients who are
edema-tous due to heart failure or cirrhosis and cannot
receivesodiumchloridebecauseaninfusioncanincreasethedegree of
edema. Another method for treating metabolicalkalosis in an
edematous patient is to administer acet-azolamide, a carbonic
anhydrase inhibitor, which causesamildincreaseinproductionof
urinethat has highHCO3content, thus reacidifying the
blood.Correcting metabolic alkalosis (usually diuretic-induced)
maybeparticularlyimportant for intubatedpatients who have chronic
respiratory acidosis. Thehigher pHcaused by the metabolic alkalosis
subse-quently impairs the respiratory drive and leads to
hypo-ventilation that exacerbates hypoxemia, delaying wean-ing and
extubation. In these patients, metabolic alkalosisusually is
corrected by enteral supplements of potassiumchloride or sodium
chloride. Very rarely, in the intensivecare unit setting, the
metabolic alkalosis can be so severethat it impairs weaning from
mechanical ventilation. Inthesecircumstances, intravenousinfusionof
hydrogenchloride can correct the alkalosis.Measuring the urinary
Clis the preferred method forassessing the renal response to
Cltherapy. For patientsexperiencingCldepletion(urinaryCl10mEq/L[10
mmol/L]) (eg, GI losses, diuretic therapy, and sweatlosses in
cystic brosis), every attempt should be made tocorrect
hypochloremia. Conditions that cause metabolicalkalosis due to high
aldosterone concentrations are un-responsive to Cland are
associated with high urine
Clconcentrations.Minimizingcontinuingacidandchloridelossesbyexcessivenasogastricuiddrainagewithahistamine2blocker
or proton pump inhibitor also may be helpful.Respiratory Acid-Base
DisturbancesAs noted, chemoreceptor analysis of arterial pHandPCO2
allows for centrally mediated adjustments in min-ute ventilation to
maintain arterial PCO2near 40 mmHg.Primary respiratory disturbances
in acid-base equilibriummay result from different pathologic
scenarios.
ArterialPCO2risesabnormally(respiratoryacidosis)ifsystemicCO2production
exceeds the ventilatory capacity or whenefcient ventilation is
inhibited by intrinsic or acquiredconditions. Conversely, arterial
PCO2decreasesabnor-mally(respiratoryalkalosis)inresponsetophysiologicdisorders
that result in excessive ventilation. Both
respi-ratoryacidosisandalkalosismayappearinassociationwith other
metabolic acid-base disturbances, often mak-ing accurate diagnosis
and treatment of the underlyingdisease difcult to
achieve.Respiratory AcidosisRespiratory acidosis occurs when
arterial PCO2 increasesand arterial pH decreases due to a reduction
in alveolarminuteventilationor,lesscommonly,anexcessivein-crease
inCO2production. Acute respiratory acidosisoccurs
withanacuteelevationinPCO2as aresult ofsuddenlimitationorfailureof
therespiratorysystem.Chronic respiratoryacidosis is
duetomoreindolentincreases in PCO2 as a consequence of systemic
diseaseover thecourseof several days. Reductioninminuteventilation
can result from depression of central nervoussystem (CNS)
respiratory drive, anatomic obstruction ofthe respiratory tract, or
intrinsic or acquired impairmentsof normal thoracic excursion
(Table 5).Table 5. Common Causes ofRespiratory Acidosis
inChildrenCentral Nervous System Depression Medication effects
Sedative: benzodiazepines, barbiturates Analgesic: narcotics
Anesthetic agents: propofol Central nervous system disorders Head
trauma Infection Tumor Congenital central
hypoventilationImpairments of Thoracic Excursion or
VentilatoryEfciency Chest wall/lung disorders Asphyxiating thoracic
dystrophy Progressive thoracic scoliosis Thoracic trauma Acute lung
injury/pneumonia Pneumothorax/parapneumonic effusion Severe obesity
Nerve/muscle disorders Congenital myopathies Spinal cord injury
Toxin exposure: organophosphates, botulism
Guillain-BarresyndromeRespiratory Tract Obstruction Upper airway
obstruction Adenotonsillar hypertrophy Status asthmaticusuids and
electrolytes acid-base disorders248Pediatrics in Review Vol.32 No.6
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compensatory changes inresponse toacute respiratory acidosis
initially are limited to bufferingvia systemically available
cellular HCO3stores. Becauseof this limitation,
serumHCO3concentrations riseacutely by only 1 mEq/L (1 mmol/L) for
every 10-mmHgelevationinarterial PCO2.
Inresponsetochronicrespiratory acidosis, the kidney retains
HCO3andsecretesacid, analterationinfunctionthat takessev-eral
(3to5)daystohaveanoticeablephysiologicef-fect. Eventually,
inchronicrespiratoryacidosis, serumHCO3concentrations ultimately
rise by approximately3.5 mEq/L (3.5 mmol/L) for every 10-mm Hg
eleva-tion in arterial PCO2.Respiratoryacidosis canaffect
boththeCNSandcardiovascular system adversely. CNS effects include
in-creasedcerebral bloodowandincreasedintracranialpressure, which
can present clinically as disorientation,acute confusion, headache,
andmental obtundation.Cardiovascular effects include peripheral
vasodilationand tachycardia. Severe hypoventilation leads to
higherarterial PCO2andmoreseverehypoxemia. Hypoxemiamay be
partially compensated by improved tissue extrac-tion of oxygen via
an acute acidosis-mediated rightwardshift in the oxyhemoglobin
dissociation curve and releaseof oxygen to the tissues. However, as
respiratory acidosispersists, areductioninredbloodcell
2,3diphospho-glycerate(anorganophosphatecreatedinerythrocytesduring
glycolysis) results in a shift of the curve to the leftand an
increase of hemoglobin afnity for oxygen.Management of Respiratory
AcidosisTreatment of respiratory acidosis usually focuses on
cor-recting the primary disturbance. Immediate discontinu-ationof
medications that suppress central respiratorydriveor
administrationof appropriatereversal agentsshould be considered.
Noninvasive ventilation or intuba-tionwithmechanical
ventilationmaybenecessarytoachieve adequate alveolar
ventilationandappropriatereduction in arterial PCO2. As arterial
PCO2 is corrected,individuals who experience excessive Cldepletion
maysubsequently suffer poor renal clearance of HCO3,leading to a
concomitant state of metabolic alkalosis.Respiratory
AlkalosisRespiratory alkalosis occurs when there is reduction
inarterial PCO2and elevation in arterial pHdue to excessivealveolar
ventilation. Causes of excessive alveolar ventila-tion include
medication toxicity, CNS disease, intrinsiclung diseases, and
hypoxia (Table 6).Compensatory changes in response to respiratory
al-kalosis involve renal excretion of HCO3. As in respira-tory
acidosis, renal compensation improves as the disor-derpersists.
SerumHCO3concentrationsdeclineby2 mEq/L (2 mmol/L) for every 10-mm
Hg decrease inarterial PCO2inacuterespiratoryalkalosis.
Inchronicrespiratory alkalosis, serum HCO3concentrations
de-clineby4mEq/L(4mmol/L)forevery10-mmHgdecrease in arterial
PCO2.Adverse Effects of Respiratory AlkalosisAdverse systemic
effects of respiratory alkalosis includeCNS and cardiovascular
disturbances. Respiratory alka-losis often provokes increased
neuromuscular irritability,manifested as paresthesias or carpopedal
spasms. In
ad-dition,cerebralbloodvesselsvasoconstrictacutelyandimpede
adequate cerebral blood ow. Myocardial con-tractility may be
diminished and cardiac arrhythmias
mayoccur.Theoxyhemoglobindissociationcurveshiftstothe left in
response to acute respiratory alkalosis, impair-ing peripheral
oxygen delivery.Management of Respiratory AlkalosisTreatment of
respiratory alkalosis centers on correctingthe underlying systemic
cause or disorder. Close assess-ment of oxygenation status and
correction of hypoxemiaviaoxygenadministrationisparamount.
Acutehyper-ventilation syndrome often is treated simply by
havingthepatientbreatheintoapaperbag.Topreventhighaltitude-associatedrespiratoryalkalosis,
slowascent toallowforacclimatizationisrecommended; administra-Table
6. Common Causes ofRespiratory Alkalosis inChildrenMedication
Toxicity Salicylate overdose Central nervous system stimulants
Xanthines (eg, caffeine) Analeptics (eg, doxapram)Central Nervous
System Disorders Central nervous system tumor Head injury/stroke
Hyperventilation syndrome: stress/anxietyRespiratory Disorders
Pneumonia Status asthmaticus Pulmonary edema Excessive mechanical
or noninvasive ventilation Hypoxia/high altitudeuids and
electrolytes acid-base disordersPediatrics in Review Vol.32 No.6
June 2011 249 at Chulalongkorn University on December 8, 2014
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tionofacetazolamidebeforeascentshouldbeconsid-ered. The only cure
for acute mountain sickness, once ithas developed, is either
acclimatization or descent.
How-ever,symptomsofacutemountainsicknesscanbere-duced with
acetazolamide and pain medications forheadaches.Suggested
ReadingBrandis K. Acid-Base Physiology. Accessed March 2011 at:
http://www.anaesthesiamcq.com/AcidBaseBook/ABindex.phpCarrillo-Lopez
H, Chavez A, Jarillo A, Olivar V. Acid-base disor-ders. In:
FuhrmanB, ZimmermanJ, eds. PediatricCriticalCare. 3rd ed.
Philadelphia, PA: Mosby Elsevier; 2005:958989Grogono AW. Acid-Base
Tutorial. 2010. Accessed March 2011
at:http://www.acid-base.comKraut JA, Madias NE. Approach to
patients with acid-base disor-ders. Respiratory Care.
2001;46:392403SummaryA wide array of conditions ultimately can lead
toacid-base imbalance, and interpretation of acid-basedisorders
always involves a mix of art, knowledge,and clinical
experience.Solving the puzzle of acidbase disorders beginswith
accurate diagnosis, a process requiring twotasks. First, acid-base
variables in the blood must bereliably measured to determine the
effect of multipleions and buffers. Second, the data must
beinterpreted in relation to human disease to denethe patients
acidbase status.History, physical examination, and
additionallaboratory testing and imaging help the clinician
toidentify the specic cause of the acid-basedisturbance and to
undertake appropriateintervention.PIR QuizQuiz also available
online at: http://www.pedsinreview.aappublications.org.9. Which of
the following statements best describes the roles of the different
nephron segments inmaintaining acid-base balance?A. The proximal
and distal tubules are equally responsible for acid excretion.B.
The proximal tubule is the primary segment responsible for
bicarbonate reabsorption and acidexcretion.C. The distal tubule is
the primary segment responsible for bicarbonate reabsorption and
acid excretion.D. The proximal tubule is the primary segment
responsible for bicarbonate reabsorption, and the distalnephron
principally promotes acid excretion.E. The proximal tubule and loop
of Henle are primarily responsible for both bicarbonate
reabsorption andacid excretion.10. Which of the following
constellation of choices best describes sequelae of metabolic
acidosis?CardiacOutputRespiratoryRateOxyhemoglobinDissociationCurve
ShiftAdenosineTriphosphateSynthesisA. Increased Decreased To the
left IncreasedB. Decreased Increased To the right DecreasedC.
Increased Increased To the left IncreasedD. Increased Decreased To
the right IncreasedE. Decreased Decreased To the right
Decreaseduids and electrolytes acid-base disorders250Pediatrics in
Review Vol.32 No.6 June 2011 at Chulalongkorn University on
December 8, 2014 http://pedsinreview.aappublications.org/
Downloaded from 11. Among the following, the most common mechanism
leading to metabolic alkalosis is:A. Chronic diarrhea.B. Secondary
hypoaldosteronism.C. Hypokalemia.D. Hypoventilation.E. Primary
hyperaldosteronism.12. The most common sequelae of early acute
respiratory acidosis are:IntracranialPressure Heart
RateOxyhemoglobinDissociationCurve ShiftRenal
BicarbonateReabsorptionA. Increased Decreased To the right
IncreasedB. Decreased Increased To the right DecreasedC. Increased
Increased To the left IncreasedD. Increased Increased To the right
IncreasedE. Decreased Decreased To the left Decreased13. The most
accurate statement about respiratory alkalosis is that:A. Cardiac
arrhythmias are never observed.B. It occurs when there is a
reduction in PCO2.C. It results in decreased renal excretion of
alkali.D. It results in vasodilation of cerebral blood vessels.E.
Oxygen delivery is generally unaffected.uids and electrolytes
acid-base disordersPediatrics in Review Vol.32 No.6 June 2011 251
at Chulalongkorn University on December 8, 2014
http://pedsinreview.aappublications.org/ Downloaded from DOI:
10.1542/pir.32-6-2402011;32;240 Pediatrics in ReviewMara Nitu, Greg
Montgomery and Howard EigenAcid-Base DisordersServicesUpdated
Information
&http://pedsinreview.aappublications.org/content/32/6/240including
high resolution figures, can be found at:
Referenceshttp://pedsinreview.aappublications.org/content/32/6/240#BIBLThis
article cites 1 articles, 0 of which you can access for free at:
Subspecialty
Collections_subhttp://pedsinreview.aappublications.org/cgi/collection/endocrinologyEndocrinologyfollowing
collection(s): This article, along with others on similar topics,
appears in thePermissions &
Licensinghttp://pedsinreview.aappublications.org/site/misc/Permissions.xhtmlin
its entirety can be found online at: Information about reproducing
this article in parts (figures, tables)
orReprintshttp://pedsinreview.aappublications.org/site/misc/reprints.xhtmlInformation
about ordering reprints can be found online: at Chulalongkorn
University on December 8, 2014
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is the result of the col-lateral ventilation through the poresof
Kohn, the bronchoalveolar chan-nels of Lambert, or
interbronchiolarchannels. Given that collateral circu-lation may
not be developed until thesecond 6 months after birth,
hyper-ination may not be apparent in theperinatal period.
Alternatively, hy-perinationmayoccurshortlyafterbirthwiththe start
of respiration,becausetheproposedpathwaysforcollateral ventilation
favor the move-ment of air into the obstructed
seg-mentbyacheck-valvetypemecha-nism. At the root of the
involvedtissue, a mucus-lled cystic structure(the mucocele) with
nger-like pro-jectionsrepresentstheatreticbron-chus, which is
isolated fromthe prox-imal bronchial tree and is dilated
bytheaccumulatedmucus. Thebron-chial patterndistal
tothemucoceleusually is normal.The only physical nding may
bedecreased breath sounds over the af-fected area. When a major
bronchusis atretic, the affected distal lobe
maybesignicantlyhyperinated, caus-ing compression of
surroundinghealthy lung and shift of the medias-tinum to the
opposite side. In suchpatients, symptoms of reduced exer-cise
tolerance and possibly wheezingand shortness of breath may
beprominent. CTor, less commonly,MRI is used to conrmthe
diagnosis.Bronchoscopymaybeusedtoruleout other causes.ManagementIn
many cases, bronchial atresia war-rants no intervention. Surgical
exci-sion is indicated when overdistentionof the affected lung
segment or lobeleads to compromise of
surroundingnormallung(asincongenitallobaremphysema) and the patient
has sig-nicant complications, such as recur-rent infections.Lessons
for the ClinicianWhen a teenager presents with lo-bar or segmental
hyperination ofthelung,bronchialatresiashouldbe considered in the
differential di-agnosis.Congenital bronchial atresia is a rareand
benign entity that might occa-sionally resemble serious
underlyingdiseases onradiographic examina-tion. There are occasions
when in-fectionmight result andantibiotictreatment might be
necessary.CT scan of the chest is the proce-dureof choicefor
thediagnosis,but indoubtful cases, bronchos-copy may be useful to
excludeother conditions and infection.(Muhammad Adeel Rishi,
MD,Rashid Nadeem, MD, RosalindFranklinUniversity of Science
andMedicine, Chicago Medical School,Chicago, IL.)References1.
Rennie G. Exophthalmic goiter com-binedwithmyastheniagravis.
RevNeurolPsychiatry. 1908;6:2292332. Ramsay BH, Byron FX. Mucocele,
con-genital bronchiectasis, andbronchiogeniccyst. J Thorac Surg.
1953;26:2130To view Suggested Reading lists forthe cases, visit
pedsinreview.aappublications.org and click onIndex of
Suspicion.ClaricationThe article entitled Acid-Base Disorders in
the June issue (Pediatr Rev. 2011;32:240251) contains this
statement: Lowering the arterial pHbelow7.35 is termed acidosis,
andan increase of the arterial pH above 7.45 constitutes alkalosis.
This terminology is indeedused in common clinical parlance with
which readers are familiar. Technically, acidosis andalkalosis
refer to the physiologic processes that affect the pH of the blood,
with the termsacidemia and alkalemia designating abnormalities of
the blood pH specically.CorrectionIn the In Brief article entitled
Growth in the September issue (Pediatr Rev. 2011;32:404406), the
formula for estimating height based on parental measurements for
girlsshould read as follows: For girls: [fathers height (cm) 13
mothers height (cm)]/2 or[fathers height (in) 5 mothers height
(in)]/2. The journal regrets the error.index of suspicionPediatrics
in Review Vol.32 No.11 November 2011 501DOI:
10.1542/pir.32-6-2402011;32;240 Pediatrics in ReviewMara Nitu, Greg
Montgomery and Howard EigenAcid-Base
Disordershttp://pedsinreview.aappublications.org/content/32/6/240located
on the World Wide Web at: The online version of this article, along
with updated information and services,
isl.pdfhttp://pedsinreview.aappublications.org/http://pedsinreview.aappublications.org/content/32/11/501.1.fulAn
erratum has been published regarding this article. Please see the
attached page for:
http://pedsinreview.aappublications.org/content/suppl/2011/09/01/32.6.240.DC1.htmlData
Supplement at: Pediatrics. All rights reserved. Print ISSN:
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2011 by the American Academy of published, and trademarked by the
American Academy of Pediatrics, 141 Northwest Pointpublication, it
has been published continuously since 1979. Pediatrics in Review is
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