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Pediatric Anatomy, Physiology &
Pharmacology
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IntroductionOf primary importance to the pediatric anesthesia
provider is the realization that infants and childrenare not simply a small adult.
Their anesthetic management depends upon the
appreciation of the physiologic, anatomic andpharmacologic differences between the varying agesand the variable rates of growth.
Also of importance is a general knowledge of thepsychological development of children to enable the
anesthetist to provide measures to reduce fear andapprehension related to anesthesia and surgery.
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Definitions
Preterm or Premature Infant: < 37 weeks
Term Infant: 37-42 weeks gestation
Post Term Infant: > 42 weeks gestation
Newborn: up to 24 hours old
LBW:
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Body Size
The most obvious difference between children & adultsis size
It makes a difference which factor is used forcomparison: a newborn weighing 3kg is 1/3 the size of an adult in length
1/9 the body surface area
1/21 the weight
Body surface area (BSA) most closely parallelsvariations in BMR & for this reason BSA is a bettercriterion than age or weight for calculating fluid &nutritional requirements
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LENGTH
0y.50cm
3m.60 cm
9m.70cm
4y.100cm
Then 5cm per yr till 10y
HC
0y..35cm
3m.40cm
12m.45cm
2y.48cm
12y.52cm
WEIGHT
0 mth 3kg
5mth 6kg
1 y 9kg
2y 12kg
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Fetal Development
The circulatory system is the first to achieve afunctional state in early gestation
The functioning heart grows & develops at thesame time it is working to serve the growing fetus At 2 months gestation the development of the heart and
blood vessels is complete In comparison, the development of the lung begins later
& is not complete until the fetus is near term
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Fetal Circulation Placenta
Gas exchange
Waste elimination
Umbilical Venous Tension is 32-35mmHg
Similar to maternal mixed venous blood
Result: O2 saturation of ~65% in maternal blood, but ~80% in the fetal
umbilical vein (UV)
Low affinity of fetal Hgb (HgF) for 2,3-DPG as comparedwith adult Hgb (HgA)
Low concentration of 2,3-DPG in fetal blood
O2 & 2,3-DPG compete with Hgb for binding, thereduced affinity of HgF for 2,3-DPG causes the Hgb tobind to O2 tighter
Higher fetal O2 saturation
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Fetal Circulatory Flow Starts at the placenta with the umbilical vein
Carries essential nutrients & O2 from the placenta tothe fetus (towards the fetal heart, but with O2 saturated
blood)
The liver is the first major organ to receive blood
from the UV Essential substrates such as O2, glucose & amino acidsare present for protein synthesis
40-60% of the UV flow enters the hepaticmicrocirculation where it mixes with blood draining
from the GI tract via the portal vein
The remaining 40-60% bypasses the liver andflows through the ductus venosus into the upperIVC to the right atrium (RA)
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Fetal Circulatory Flow The fetal heart does not distribute O2 uniformly
Essential organs receive blood that contains more oxygen thannonessential organs
This is accomplished by routing blood through preferred pathways
From the RA the blood is distributed in two directions:
1. To the right ventricle (RV)
2. To the left atrium (LA) Approximately 1/3 of IVC flow deflects off the crista
dividens & passes through the foramen ovale of theintraatrial septum to the LA
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Fetal Circulatory Flow Flow then enters the LV & ascending aorta
This is where blood perfuses the coronary and cerebral arteries The remaining 2/3 of the IVC flow joins the desaturated
SVC (returning from the upper body) mixes in the RAand travels to the RV & main pulmonary artery
Blood then preferentially shunts from the right to the leftacross the ductus arteriosus from the main pulmonaryartery to the descending aorta rather than traversing the
pulmonary vascular bed
The ductus enters the descending aorta distal to the innominateand left carotid artery
It joins the small amount of LV blood that did not perfuse theheart, brain or upper extremities
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Fetal Circulatory Flow The remaining blood (with the lowest sat of 55%)
perfuses the abdominal viscera The blood then returns to the placenta via the
paired umbilical arteries that arise from theinternal iliac arteries
Carries unsaturated blood from the fetal heart The fetal heart is considered a Parallel
circulation with each chamber contributingseparately, but additively to the total ventricular
output Right side contributing 67%
Left side contributing 33%
The adult heart is considered Serial
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Fetal Circulatory Flow
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Fetal Circulatory Flow Summary:
Ductus Venosus shunts blood from the UV to
the IVC bypassing the liver
Foramen Ovale shunts blood from the RA to
the LADuctus Arteriosus shunts blood from the PA to
the descending aorta bypassing the lungs
Fetal circulation is parallel
Blood from the LV perfuses the heart & brain
with well oxygenated blood
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Fetal Pulmonary Circulation
Fetal Lungs
Extract O2 from blood with its main purpose to
provide nutrients for lung growth
Neonatal Lungs
Supply O2 to the blood
Fetal lung growth requires only 7% ofcombined ventricular output
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Transitional & Neonatal
Circulation There are 3 steps to understanding transitional
circulation 1. Foramen Ovale: ductus arteriosus & ductus venosus
close to establish a heart whose chambers pump inseries rather than parallel
Closure is initially reversible in certain circumstances & thepattern of blood flow may revert to fetal pathways
2. Anatomic & Physiologic: Changes in one part of thecirculation affect other parts
3. Decrease in PVR: The principal force causing achange in the direction & path of blood flow in thenewborn
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Transitional & Neonatal
Circulation Changes that establish the newborn
circulation are an series of interrelated
eventsAs soon as the infant is separated from the low
resistance placenta & takes the initial breathcreating a negative pressure (40-60cm H2O),
expanding the lungs, a dramatic decrease inPVR occurs
Exposure of the vessels to alveolar O2increases the pulmonary blood flow
dramatically & oxygenation improves
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Transitional & Neonatal
Circulation Most of the decrease in PVR (80%) occurs in the
first 24 hours & the PAP usually falls below
systemic pressure in normal infants PVR & PAP continue to fall at a moderate rate
throughout the first 5-6 weeks of life then at a
more gradual rate over the next 2-3 years
Babies delivered by C-section have a higher PVR
than those born vaginally & it may take them up to
3 hours after birth to decrease to the normal range
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Transitional & Neonatal
Circulation
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Ductus Arteriosus
Closure occurs in two stages
Functional closure occurs 10-15 hours after birth
This is reversible in the presence of hypoxemia or hypovolemia
Permanent closure occurs in 2-3 weeks
Fibrous connective tissue forms & permanently seals the lumen This becomes the ligamentum arteriosum
{FACTORS FACILITATING CLOSURE OF D.A. ;:: Incr
in pO2,NE,Epi,Ach,Bradykinin.}
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Ductus Venosus
This has no purpose after the fetus is
separated from the placenta at deliveryos
Fnal closure : within frst week
Anat closure:2-3 mths:
{{Patent DV=> Decr delv of drugs to liver, and thrfr may
prolong their elimination t1/2 in first few days of birth}}
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Cardiovascular Differences in the Infant
There are gross structural differences & changes in the
heart during infancy At birth the right & left ventricles are essentially the same in size
& wall thickness
During the 1st month volume load & afterload of the LV
increases whereas there is minimal increase in volume load &decrease in afterload on the RV
By four weeks the LV weighs more than the RV
This continues through infancy & early childhood until the LV istwice as heavy as the RV as it is in the adult
(incr in heart size initially is mainly b coz ofmyocyte hyperplasia, After 6 mnths of age,
DNA disappears from myocyte , and so ventr
grth after 6 mnths is due to hypertrophy)
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Cardiovascular Differences in the Infant Cell structure is also different
The myocardial tissues contain a large number of nuclei& mitochondria with an extensive endoplasmic reticulum
to support cell growth & protein synthesis during infancy
The amount of cellular mass dedicated to contractile
protein in the neonate & infant is less than theadult.30% vs. 60% (primarily cartilagenous)
These differences in the organization, structure &
contractile mass are partly responsible for the decreased
functional capacity of the young heart
Evidence has also been forthcoming to suggest that intra
cellular Ca flu and ca sensitivity of contractile proteins
are decresd in NN myocardium.(Endog Ca stores are less
CO depends on HRxSV
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CO depends on HRxSV
SV dep on: Myocard contrctility
Preload
Afterload.
In PT and FT NNs, HR is the primary determinant of CO.
The low compliance of the ventr myocardium in the NN limits therole of PL in determining SV. In response to hypoxemia, CO incr
via an incr in HR. In response to hypercapnia or lactic acidosis,SV decreases.
Afterload is determined by the resist of the large arterial bld vsls andthe tone of the periph vasc bed. Bcoz sympth tone is poorlydevolped in the NN, afterload is low in the neonate but increasesin parallel with incr in systm BP with aging.
In Summary, CO in the NN depends primarily on rapid HR and toa lesser extent on an adequate PL and adequate myocardcontractility.
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Cardiovascular Differences in the
Infant Both ventricles are relatively noncompliant
& this has two implications for the
anesthesia provider1. Reduced compliance with similar size & wall
thickness makes the interrelationship of theventricular function more intimate
(INTERVENTRICULAR DEPENDANCE)Failure of either ventricle with increasedfilling pressure quickly causes a septal shift& encroachment on stroke volume of the
opposite ventricle
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Cardiovascular Differences in the
Infant2. Decreased compliance makes it less sensitive
to volume overload & their ability to changestroke volume is nearly nonexistent
CO is not rate dependent at low filling pressures butsmall amounts of fluid rapidly change filling
pressures to the plateau of the Frank-Starling lengthtension curve where stroke volume is fixed
This changes the CO to strictly being rate dependent Additional small amounts of fluid can push the filling
pressure to the descending part of the curve & theventricles begin to fail
The normal immature heart is sensitive to volumeoverloading
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Cardiovascular Differences in the
Infant Functional capacity of the neonatal & infant
heart is reduced in proportion to age & as
age increases functional capacity increasesThe time over which growth & development
overcome these limitations is uncertain &variable
When adult levels of systemic artery pressure &PVR are achieved by age of 3 or 4 years theabove limitations probably no longer apply
i l f h
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Autonomic Control of the Heart Sympathetic innervation of the
heart is incomplete at birth with
decreased cardiac catecholamine
stores & it has an increased
sensitivity to exogenous
norepinephrine
It does not mature until 4-6 months of age
Parasympathetic
innervation has been
shown to be complete
at birth therefore we
see an increased
sensitivity to vagalstimulation
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Autonomic Control of the Heart
The imbalance between sympathetic ¶sympathetic tone predisposes the infant
to bradycardiaAnything that activates the parasympathetic
nervous system such as anesthetic overdose,hypoxia or administration of Anectine can lead
to bradycardiaIf bradycardia develops in neonates & infants
always check oxygenation first
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Circulation
The vasomotor reflex arcs are functional in
the newborn as they are in adults
Baroreceptors of the carotid sinus lead toparasympathetic stimulation & sympathetic
inhibition
There are less catecholamine stores & a bluntedresponse to catecholamines
Therefore neonates & infants can show vascular
volume depletion by hypotention without
tachycardia
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Cardiovascular Parameters
Parameters are much different for the infant thanfor the adult Heart rate: higher
Decreasing to adult levels at ~5 years old
Cardiac output: higher Especially when calculated according to body weight & it
parallels O2 consumption
Cardiac index: constant Because of the infants high ratio of surface area to body weight
O2 consumption: depends heavily on temperature There is a 10-13% increase in O2 consumption for each degree
rise in core temperature
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IN TOTO:
*Tendency towrds Biventr Failure
*Sensitive to volume overloading
*Poor tolerance of Incrsd AL
*HR dependant CO
*Greater dep on exogenous Ca &thrfr
incrsd susceptibility to myocarddepression
by inhal agents havin CCB properties.
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Circulation Variables in InFANTS
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CAUSES OF BRADYCARDIA IN
INFANTS:
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CAUSES OF BRADYCARDIA IN
INFANTS HYPOXIA
LARYNGOSCOPY
INTUBATION
HYPOTHERMIA
ENDOTRACHEAL SUCTIONING
TRACTION ON INTRA OC MSLS
VARIOUS DRUGS: HALO, FENTANYL
NEOST
SCHOLINE.
. PASSAGE OF N.G. TUBE
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CAUSES OF TACHYCARDIA IN
INFANTS PAIN
HYPOVOLEMIA
DRUGS:ATR. EPINEPH, LOCAL INFILTRN OF
XYLO-ADR HYPOXEMIA
HYPERCARBIA
ANXIETY
FEVER FULL BLADD
Neonatal and adult myocardium
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Neonatal and adult myocardium
CO: HR dependent
Contractility: decreased
(ratio of contractile tiss to conntiss is 50% act adults, thrfrcontrcn power is less, and sois compliance)
Starling Response:Limited
Compliance: decresd
Ventr Interdpndnce: High
(decrsd complnce+voloverloadNo in SV
chances of CCF.)* NN Purkinje fibres repolarise
faster and APs are faster,thrfrallowing effective HR >200.
* Need of Exo Ca.
HR and SV dependant
Normal
Normal
Normal
Low
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Circulating Blood Volume decreses with
age
PT: 90-100 ml per kg
FT:80 ml per kg
Adult: 70 ml per kg.
Hb F
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30 weeks:95%
40 weeks:80%
6 mnths of birth:5%
Since, 2,3 DPG binds poorly to chains of Hb F, Hb F has edaffinity for O2, i.e. p50 in ODC:
PT=15-18, FT=19.4, 8-12 mnths=31, Adult:27.7
(low p50 optimises uptake of O2 from placenta, but it prevents
release of o2).i.e. left shift of ODC,But this LEFT shift of ODC is compensated by:
Hb
Expanded red cell volume
CO
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RESP
SYSTEM
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Lungs begin to devolp by 4 weeks of gestation:
Lobar airways..5
Segmental Aw..6
Subsegmental aw..7
Trachea/ Bronchus..8 wks of gestn.
Division of Bronchus into 16 branches: shuld finish by 16weeks:otherwise leads to pulmonary hyperplasia.
Gas Exchange function : 16-25 weeks.Surfactant:Starts prod in 2nd TM, but peak at 34-36 weeks.
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During the early years of childhood,development of the lungs continues at arapid paceThis is with respect to the development of new
alveoli(Birth= 20 million) By 12-18 months the number of alveoli
reaches the adult level of 300 million or
moreSubsequent lung growth is associated with anincrease in alveolar size (Adult size by 8 years)
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Functional Residual Capacity (FRC)Determined by the balance between the
outward stretch of the thorax & the inwardrecoil of the lungs. In infants, outward recoil of the thorax is very low
They have cartilaginous chest walls that make their chestwalls very compliant & their respiratory muscles are not
well developed Inward recoil of the lungs is only slightly lower than
that of an adults
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Walls of Bronchi:
NN have incr cartilage, incr conn tissue, and incr
glands, with minimal smooth musclesthrfr minimaleffect of nebulsn.
(Small Aw obstrcn in NN=inflammation and
edema///////act adults= Muscle spasm)
************************************
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1.Oxygen consumption
2. CO2 production
3.Exhaled MV4.Va
5.TV
6.FRC
7.FRC/Va
8.V/Q
6.4 ml/kg/min
6ml/kg/min
210ml/kg/min130ml.kg/min
6ml/kg
30ml/g
.23
.4
3.5
3
9060
7
34
.57
.8
COMPLIANCE
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COMPLIANCE:
Birth: 1.5ml per cm H2O
NN: 5.0
Ad: 200
Cm incr with incr in lung size.
LOW LUNG COMPLIANCE AND HIGH CWCOMPLIANCE
LESS VE INTRA THORACIC PRESSURE IS PROD
SMALL Aw PATENCY
AIRWAY CLOSURE. {CV>> FRC}
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With the first few breaths after delivery, initialresp efforts generate large intra pl pr in order toinflate the fluid filled alveoli. With these efforts ,
alv r recruitd in increasing numbers, with theassistance of ST lowering properties of surfactant.
(Most of the fluid with in the alveoli is cleared rapidly thro the upper Aw,altho any residual fluid is cleard slowly over subsequent 24-72 hrs bytrans cap and trans lymphatic routes)
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Neural & chemical controls of breathing in olderinfants & children are similar to those inadolescents & adults
A major exception to this is found in neonates andyoung infants, especially in premature infants less than40-44 weeks postconception
In these infants, hypoxia is a potent respiratory depressant,rather than a stimulant
This is due either to central mediation or to changes inrespiratory mechanics
These infants tend to develop periodic breathing or centralapnea with or without apparent hypoxia
This is most likely because of immature respiratory control
mechanisms
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CHEMORECPS
Ventilatory resp to hypoxia is complex:
0-3 weeks: vent resp to hypoxia dep on temp.(via perph recps)
{normothermia.decr O2 .incr ventln}
{hypothermia:decr in O2decr in ventln}
After 3 weeks: decr in O2.. Increases ventln irresp of temp.
*********************************** to increase v
Ventltry resp to CO2 is more mature: begin
CO2 resp curve is shifted to left.. i.e.:
Chemorecps begin to incrs ventln at lower CO2 levels.
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MECHANORECPS
Resp centre is affected by reflexes and proprioceptive
informations from CW, muscle spindles., inflation
and deflation.
:::::::: Heads paradoxical resp (insp resp to partial infln
of lungs)
::::::::Hering Breur Reflex (initiation of passiv ehaln
with full infln of lungs)
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Why V/Q is low?
* due to gas trapping
* airway closure
* large physiological shunts
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Breathin pattern of NN, esp PT, is describedas periodic, i.e. normal breathing
punctated by occasional episodes ofapnea(5-15) seconds,
(Apnea episodes dt immature resp centre)
If apnea episodes last more than 15 seconds, itcan cause bradycardia and desatrn. Thesecan occur upto 52 weeks post birth.)
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Breathing Patterns of Infants Less than 6 months of age
Predominantly abdominal (diaphragmatic) and the rib cage(intercostal muscles) contribution to tidal volume is relatively
small (20-40%) After 9 months of age
The rib cage component of tidal volume increases to a level(50%) similar to that of older children & adolescents,reflecting the maturation of the thoracic structure
By 12 months Chest wall compliance decreases
The chest wall becomes stable & can resist the inward recoil ofthe lungs while maintaining FRC
This supports the theory that the stability of the respiratory
system is achieved by 1 year of age
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Resp system is less efficient:
a) Small diam of airways increases resist to airflow
(Resist is inversely prop to radius)a) CW is highly compliant, so ribs provide little support for the
lungs, i.e.the neg intra thor pressure is poorly maintained.,
leading to airway closure with each breath.
b) Oxygen consumption is 2-3 times higher.c) Difference in composition of diaph and intercostal muscles.,
and sole reliance on diaphragmatic function.
d) Increased CV act FRC .with tidal breathing
e) Decreased FRC/Va(i.e. incrsed Va/FRC..thrfore it offsets thefall in PaO2 resulting from low CV)
f) Decrsed surfactant g)Presence of HbF
g) Small and less number of alveoli h)Immature resp control
h) airway closure
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Head is relativly large, occiput is prominent.
i.e. no need of pillow under the head, (infact theymight need a pillow under the shoulders.)
Chin is retrognathic.. (Diff BMV)
Upper Airway: the nasal airway is the primary
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Upper Airway: the nasal airway is the primarypathway for normal breathing
During quiet breathing the resistance through the nasalpassages accounts for more than 50% of the total airwayresistance (twice that of mouth breathing)
Except when crying, the newborns are consideredobligate nose breathers
This is because the epiglottis is positioned high in the pharynxand almost meets the soft palate, making oral ventilation difficult
If the nasal airway becomes occluded(SECRETIONS/NG TUBE) the infant may not rapidly or
effectively convert to oral ventilation Nasal obstruction usually can be relieved by causing the infant to
cry
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Pharyngeal Airway: is not supported by a
rigid bony or cartilaginous structureIs easily collapsed by:
The posterior displacement of the mandible during
sleep
Flexion of the neck
Compression over the hyoid bone
Chemoreceptor stimuli such as hypercapnia &
hypoxia stimulate the airway dilators
preferentially over the stimulation of the
diaphragm so as to maintain airway patency
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Epigl= SHORT..STUBBY..OMEGA SHAPED
It projects post at angle of 45 degrees to BOT act
15-25 degrees in adults,
Thrfr it has to be lifted during Lx with straight
blade.
The vocal cords of the neonate are slanted so that the
anterior portion is more caudal than the posterior
(Tube might get lodged in ant commisure than
passin into trachea)
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Cricoid Ring: Achilles Heel of upper Aw.(Most
vulnerable str )
*The only circumferential solid cartlg str in Aw.
*Funnel shaped, with caudal aperture being
narrowest.
*Covered with loose pseudostratified columnar
epith., suscpt to both inflammation and edema,
when irritated or traumatised. (2 fold decrease in
radius of lumen increases resist to airflow by 32
fold).
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Classical Teaching tells us:
Ad LX: Cylnd
NN Lx: Funnel shaped.
But, recent studies shows that the narrowest part in
adults(70)% is also subglottic at level of cricoid
ring., But the opening is so large that commonlyused tubes are nearly easy to pass the subglottic
area.
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Cote CJ, Lerman J, Todres ID: A practice of Anesthesia for Infantsand Children, Saunders Elsevier, 2009
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Anatomic Differences in the
Respiratory System Trachea
Infant: the alignment is directed caudally &
posteriorlyAdult: it is directed caudally
Cricoid pressure is more effective in
facilitating passage of the endotracheal tubein the infant
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Anatomic Differences in the
Respiratory System Newborn Trachea
Distance between the bifurcation of the trachea &the vocal cords is 4-5cm
Endotracheal tube (ETT) must be carefully positioned &fixed
Because of the large size of the infants head the tip of thetube can move about 2cm during flexion & extension ofthe head
It is extremely important to check the ETT placementevery time the babys head is moved
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Anatomic Differences in the
Respiratory System Tonsils & Adenoids
Grow markedly during childhood
Reach their largest size at 4-7 years & then recedesgradually
This can make visualization of the larynx more
difficult
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Anatomic Differences in the
Respiratory System
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Anatomic Differences in the
Respiratory System
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Anatomic Differences in the
Respiratory System
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ABG
NN
pO2:35pCO2:65
pH:7.2
After 24 hrs:
pO2:70
pCO2:38
pH:7.36
Why is pH decr IN NN?
*dt incrs CO2* Immature kidneys not
able to retain HCO3-
Oxygen Transport
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Blood volume of a healthy newborn is 70-90ml/kg
(PT=80-110, Adults=70)
Hemoglobin tends to be high (approx. 19g/dl)Consisting primarily of HgF
Hgb rises slightly in the first few days because ofthe decrease in extracellular fluid volume
Thereafter, it declines & is referred to as physiologicanemia of infancy
HgF has a greater affinity for oxygen than HgAAfter birth, the total Hgb level decreases rapidly as
the proportion of HgF diminishes (it can dropbelow 10g/dl at 2-3 months) creating the anemia
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Airway Management
Distance or Depth toTape Tube If older than 2 years
Age2+12
If younger than 2 years 1-2-3-4 kg then it is
taped at 7-8-9-10cmrespectively
Newborn to 6 months =10cm
6 to 12 months = 11cm
1 to 2 years = 12cm
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RENAL SYSTEM
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Renal Differences
Body Fluid
Compartments
Full term infants have
a large % of TBW &
ECF
TBW decreases with
age mainly as a result
of loss of water inextracellular fluid
TOTAL BODY WATER
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ECF ICF NN: 80%of weight: 45% 35%
3 mths :70% " 35% 35%
Infant: 70 % 30% 40%
Ad: 60% 20% 40%
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Significance for Anesthesia Provider
Higher dose of water soluble drug is needed due to
the greater volume of distribution
However, due to the immaturity of clearance &
metabolism the dose given is equal to the dose used in
adults
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Renal Differences
Maturation of the glomerular function
is complete at 5-6 months of age
PHYSIOLOGIC CONSIDERATIONS
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Developmental Factors
RENAL:
immature renal function at birth
GFR
25% of adult level at term
adult level at age of 2 years
concentrating capacity of newborn kidney
term infant : max. 600-700 mOsm/kg
adult :max. 1200 mOsm/kg
PHYSIOLOGIC CONSIDERATIONS
De elopmental Factors
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Developmental Factors
free H2O clearance :
excrete markedly dilute urine up to 50
mOsm / kg vs. 70-100 Osm/kg in adults
Na reabsorption
HCO3
/H exchange
urinary losses of K+ and Cl-
PHYSIOLOGIC CONSIDERATIONS
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Developmental Factors
IMPLICATION:
Newborn kidney has limited
capacity to compensate for volume
excess or volume depletion
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Renal Differences
Creatinine
Normal value is lower in infants than in adults
This is due to the anabolic state of the newborn & the small muscle massrelative to body weight (0.4mg/dl vs. 1mg/dl in the adult)
Bicarbonate (NaHCO3)
Renal tubular threshold is also lower in the newborn (20mmol/Lvs. 25mmol/L in the adult)
Therefore, the infant has a lower pH, of about 7.34
BUN The infants urea production is reduced as a result of growth & so
the immature kidney is able to maintain a normal BUN
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HEPATIC SYSTEM
Glucose from the mother is the main source of energyfor the fetus
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for the fetus Stored as fat & glycogen with storage occurring mostly in
last trimester( PT are hypoglyc)
At 28 weeks gestation the fetus has practically no fatstored, but by term 16% of the body is fat & 35gms ofglycogen is stored
In utero liver function is essential for fetal survival
Maintains glucose regulation, protein / lipid synthesis &drug metabolism
The excretory products go across the placenta & areexcreted by the maternal liver
Liver volume represents 4% of the total body weight in theneonate (2% in adult)
However, the enzyme concentration & activity are lowerin the neonatal liver
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Hypoglycemia
NN/FT
PT(1-3d)
4d (FT/PT)
(Rx: 0.5-1 g/kg i.v. gluc bolus f/b
infusion of 5-6 mg/kg/min as maint )
< 30 mg%
< 20 mg%
< 40 mg%
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Bi f i f d b l i
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Biotransformation of many drugs may b slower in
the NN than in adult. Many enz systems in the
liver r immature at birth.
Activity of phase I cto P450 dependant mixed fn
oxidases is immature in NN, matures by 6 mths.,
{Also the immaturiy is variable, thrfr variability exists in some drugsbeing transformed at fast rates, some slower.}
Activity of phase II rns, are mainly conjugativewhich r immature at birth .{Sulfation is mature at
birth,}... {Decr in phase II results in decr in bil breakdown, thuscausing jaundice and kernicterus}
GIT
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GIT
1st day : pH: alkalotic
2nd
day onwards: normal as adult.
Ability to coordinate swallowing with resprn fully
mature at 4-5 mths of age.
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Structure & Function of the Neuromuscular
System
Incomplete at birth
There are immature myoneural junctions & larger
amount of extrajunctional receptorsThroughout Infancy:
Contractile properties change
The amount of muscle increases
The neuromuscular junction & acetylcholine receptors
mature
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Junctions & ReceptorsThe presence of immature myoneural junctions
might cause a predisposition to sensitivity
A large number of extrajunctional receptors mightresult in resistance
Within a short interval, (< 1 month) this variation
diminishes & the myoneural junction of the infant
behaves almost like that of an adult
Neural mechs resp for perception of noxious
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stim (resp to stress and Sx), are present as early
as 6 wks of gestation
Also Neuro Endocr Axis in PT is also well
devolped.
Thrfore, both PT and FT require complete analgesia and
Ax during and after Sx.
Anatomical Differences:
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1. Soft and pliable cranium
2. Non fused sutures
3. Two open fontanelles(PF= 6-9 mths, AF=18
mths)
4. Incomplete myelination (Until 2 yrs)
5. Poorly devolped cerebral cortex
6. Spinal core ends at L4(act L1) with fragile
sub ependymal vessels.
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BLOOD CHEMISTRY
Sodium 134-152 mmol/L
Potassium 5.0-7.7 mmol/L
Cl 92-114 mmol/L
Gluc (F) 40-90 mg%
TP 5.9-8.5 g%
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TEMP REGULATION
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Temperature Regulation
Body Temperature
Is a result of the balance between the factors
leading to heat loss & gain and the distributionof heat within the body
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Temperature Regulation
Body heat is lost more rapidly by NN :
1. Large BSA relative to Body Wt.
2. Thin layer of insulation.
3. Decreased ability to produce heat.
Central Temperature Control Mech
hi i i i h b b i l
NT CT
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This is intact in the newborn, but, is onlyable to maintain a constant bodytemperature within a narrow range ofenvironmental conditions.
NEUTRAL TEMPERATURE: defined asthe ambient temp which results in the least
O2 consumption.-A deviation in either direction fromthe NTE will increase O2 consumption
CRITICAL TEMP: It is that ambient
temp below which an unanesthetised,unclothed person cannot maintain anormal body temperature.
PT 34 28
Term 32 23
Adult 28 1
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Temperature Regulation
Important Mechanisms for Heat Production
Metabolic activity
Shivering
Non-shivering thermogenesis
Newborns usually do not shiver
Heat is produced primarily by non-shivering thermogenesis
Shivering does not occur until about 3 months of age
Non-shivering Thermogenesis
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{ Mtb of Brown Fat is stimulated by Nor Epinephrine and
results in TG hydrolysis and thermogenesis }
Exposure to cold leads to production of Norepi
This in turn increases the metabolic activity of brown fat
Brown fat is highly specialized tissue with a great numberof mitochondrial cytochromes (these are what provide the
brown color)
The cells have small vacuoles of fat & are rich in
sympathetic nerve endings
They are mostly in the nape & between the scapulae but some are
found in the mediastinal (around the internal mammary arteries &
the perirenal regions (around the kidneys & adrenals)
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Temperature Regulation
Once released Norepi acts on the alpha & beta
adrenergic receptors on the brown adipocytes
This stimulates the release of lipase, which in turn splits
triglycerides into glycerol & fatty acids, thus increasing
heat production
The increase in brown fat metabolism raises the
proportion of CO diverted through the brown fat
(sometimes as much as 25%), which in turn facilitatesthe direct warming of blood
The increased levels of Norepi also causes
peripheral vasoconstriction & mottling of the skin
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Temperature Regulation
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Temperature Regulation
Heat Loss
The major source of heat loss in the infant is
through the respiratory system A 3kg infant with a MV of 500ml spends 3.5cal/minto raise the temperature of inspired gases
To saturate the gases with water vapor takes an
additional 12cal/min The total represents about 10-20% of the total
oxygen consumption of an infant
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Temperature Regulation
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Heat Exchange Review
1. Conduction: The kinetic energy of the vibratory motion of themolecules at the surface of the skin or other exposedsurfaces is transmitted to the molecules of themedium immediately adjacent to the skin
Rate of transfer is related to temperature differencebetween the skin & this medium
Use warm blankets, Bair huggers & warmed gel pads
2. Convection:
Free movement of air over a surface Air is warmed by exposure to the surface of the body thenrises & is replaced by cooler air from the environment
Increase OR temp, radiant warmers, wrap in saran wrap,cover with blankets and/or OR drapes
Temperature Regulation
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3. Radiation:
Radiation emitted from the body is in the infrared region of
the electromagnetic spectrum The quantity radiated is related to the temperature of the
surrounding objects
Radiation is the major mechanism of heat loss under normalconditions (same techniques to prevent as used in Convection)
4. Evaporation: Under normal conditions ~20% of the total body heat loss is
due to evaporation This occurs both at the skin & lungs
Since the infants skin is thinner & more permeable than the older
childs or adults evaporative heat loss from the skin is greater In the anesthetized infant the MV (relative to body weight) is high
thus increasing evaporative heat loss through the respiratory system
Pharmacological Differences
ith I h l ti A th ti
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with Inhalation Anesthetics Review
Factors that determine uptake & distribution of
inhaled agents
Factors that determine the rate of delivery of gas to
the lungs Inspired concentration
Alveolar ventilation
FRC
Factors that determine the rate of uptake of theanesthetic from the lung
CO
Solubility of the agent
Alveolar-to-venous partial pressure gradient
Pharmacological Differences
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Pharmacological Differences
with Inhalation Anesthetics In children there is a more rapid rise frominspired partial pressure to alveolar partial
pressure than in adultsThis is due to 4 differences between children &
adults
1. The ratio of alveolar ventilation to FRC
This a measure of the rate of wash-in of the anestheticinto the alveoli
In the neonate the ration is 5:1 compared to adults of 1.5:1
Pharmacological Differences
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Pharmacological Differences
with Inhalation Anesthetics 2. There is a higher proportion of CO distributed tothe VRG in the child
In adults an increase in CO slows the rate of rise in
alveolar to inspired partial pressure, but in neonates it
speeds the rate of induction because the CO is
preferentially distributed to the VRG
The VRG constitutes 18% of the body weight of the
neonate as opposed to only 6% in adults
Therefore, the partial pressure in the VRG (whichincludes the brain) equilibrates faster with the alveolar
partial pressure
Pharmacological Differences
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Pharmacological Differences
with Inhalation Anesthetics 3. Neonates have a lower blood/gas solubility ofinhaled anesthetics (the less soluble the greater the
amount that remains in the alveolus
This allows a more rapid rise in the alveolar to inspiredpartial pressure
4. Neonates have a lower tissue/blood solubility of
inhaled anesthetics
Less agent is removed from the blood therefore the partial
pressure of the agent in the blood returning to the lungs
increases
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PERIOPERATIVE FLUID
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MANAGEMENT IN
PAEDIATRICS
Introduction
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Fluid Management in Infants andFluid Management in Infants andchildren can be challenging because ofchildren can be challenging because of
their:their:
Small sizeSmall size
Large surface area to volume ratioLarge surface area to volume ratio Immature homeostatic mechanisms.Immature homeostatic mechanisms.
i
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Introduction contd..
Meticulous fluid management is
required in small pediatric
patients because of extremelylimited margins of error
Perioperative Fluid Management
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ISSUES
1. Developmental and Physiological Considerations
2. Distribution of body fluids and Electrolytes
3. Determining Fluid requirements
4. Preoperative deficit therapy
5. Intraoperative fluid management
6. Post operative fluid management
Developmental
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Developmental
and
Physiological
Considerations
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RENAL
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RENAL
Urine Concentrating Capacity
is limited in neonates
Increased Free Water Clearance
( Diluting Capacity )
RENAL
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RENAL
Thus the ability to handle
free water & solute loads may
be impaired in the neonate.
Its more so in the premature baby
who is less able to conserve Na+
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RENAL
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RENAL
GFR is low at birth
Low systemic arterial BP
High renal vascular resistance and
Low ultra filtration pressure together with
decreased capillary surface area for filtration.
Renal Parameters
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Measurement Premature Term 1-2 wk 6m-1yr 1-3yr adult
GFR{ml/min/ 1.73m2}
143
40.6
14.8
65.8
24.8
7714
9622
12515
RBF{ml/min/ 1.73m2}
40
6
88
4
220
40
352
73
540
118
620
92
Max conc. Ability(mosm/kg) 480 700 900 1200 1400 1400
Sr creatinineclearance (mg/dl) 1.3 1.1 0.4 0.2 0.4 0.8-1.5
Fractionalexcretion of Na+ 2% - 6%
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Infants and neonates aremore sensitive to hypovolemia
Incomplete development
of the myocardium.
Immature sympathetic nervous system.
Cardiac output is very dependent of HR
Cardiovascular
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The hallmark ofintravascular fluid depletion
hypotension without tachycardia.
In the perioperative period.
Maintenance of effective vascular volume
To sustain vital organ perfusion
Di t ib ti f
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Distribution of
Body fluids
and
Electrolytes
Fluid compartments(% of body wt)
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Component
Birth 3mths
Infant Children Adults
Fat 16% 23% 30%
TBW 80 % 70% 70% 70% 55 60%
ECF 45 % 35% 30% 30% 20%
ICF 35% 35% 40% 40% 40%
volume changes with age.
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Determiningfluid
requirements
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D fi it th h th t
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Deficit therapy has three components:
Estimating the
severity of Dehydration
Determination of type of fluid deficit
Repair of the deficit.
Fasting :
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Allowing clear fluids up to two hours
No increase in the risk of aspiration
Prevents dehydration,Keeps the period of starvation short.
Residual gastric volume was lower,
pH higher andDecreased thirst and hunger
Severity of dehydration
Percent of Signs & symptoms Amount of body fluid
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Percent ofbody wt
lost
Signs & symptoms Amount of body fluidlost,ml/kg[%]
Infants Older children &adults
Mild
1 5%
Vomiting, diarrhea
> 12-14hrsDry mouth, urination
50 [ 5%] 30 [ 3%]
Moderate6 10%
Skin tenting, sunken eyes,depressed fontanelles
oliguria, lethargy
100 [10%] 60 [ 6%]
Severe11 15%
CVS instability, mottlinghypotension,tachycardia,anuria, sensorium changes
150 [15%] 90 [ 9%]
20% Coma, shock
Treatment of dehydration
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Goals of preoperative rehydration
Restoration of cardiovascular function
CNS function
Renal perfusion
Treatment of dehydration
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y
The fluid to replace this deficit
Isotonic Fluid
0.9% NaCl or Ringer lactate.
El t l t N S li Ri I l t P D t H t h 6%
Composition of Intravenous fluids
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Electrolytemeq/l
N.Saline Ringers IsolyteP Dextrose5%
Hexastarch 6%
Na+ 154 130 26 - 154
K+ - 4 21 - -
Cl- 154 109 21 - 154
Ca2+ - 3 - - -
Mg2+ - - 3 - -
Acetate - - 24 - -
Lactate - 28 - - -Glucose
(mg/dl)- - - 5 -
Osmolaritymosm/lit
308 274 - 252 310
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IntraoperativeFluid
Management
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Intraoperative fluid requirementNumber of hrs fasting x EFR
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Estimated preoperative fluid deficit
[ EFD]
Number of hrs fasting x EFR
1st hr infuse EFD + EFR 1st hr
2nd hr infuse EFD + EFR 2nd hr
3rd hr infuse EFD + EFR 3rd hr
Intraoperative loses
[ IL]
Minimal incision 3- 5ml/kg/hr
Moderate incision with viscous exposure
5 -10ml/kg/hr
Large incision with bowel exposure
8 - 20ml/kg/hr
Estimated blood loss
[ EBL]
Replace max. allowable blood loss
[ ABL] with crystalloid 3:1
Fluid & dextrose management
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Children at risk of hypoglycemia
if non-dextrose containing fluid is given :
Infants and children on parenteral nutrition
Children of low body weight ( 3hrs )
Children receiving dextrose containing fluids
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Management of Third space losses
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g p
Third space loss is difficult to quantify
1 - 2mL/Kg/Hr given for superficial surgery,
4 - 7mL/Kg/Hr given for thoracotomy and
5 -10mL/Kg/Hr for abdominal surgery
Clinical signs :-
HR, BP and capillary refill time
to ensure adequate replacement
Monitoring of fluid therapy
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Monitoring of fluid therapy
Heart sounds
Breath sounds
ECGHR
BP
SPO2
ETCO
2
Body temperature
Skin color
Urine output
Glucose infusion
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Assessment of blood loss
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Careful assessment of blood loss
Weighing blood-soaked sponges,
Blood and fluid loses using
miniaturized suction bottles
Visual estimation of blood loss
on surgical drapes.
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Blood loss replacement
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Crystalloid :@ 3 times the volume of the blood loss (1:3)
Colloid solution :
(albumin, plasma protein, FFP)
@ (1:1)
Blood loss replacement
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Concept of replacement after 10% blood lossChanged to losses based on hematocrit
Under 10% of blood loss no blood is required. Over 20% loses must be replaced with PRBC
Between 10 - 20% one must consider case by case
Maintenance of 40% hematocrit in neonates and
30% in older children is must.
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Post Operative
Fluid
Management
Post operative fluid management
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Salt and water retention is mainly due to
continued capillary leak,
third space accumulation &
stress induced neuroendocrine activation
Surgery, pain, nausea and vomiting
potent causes of ADH release.
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Post operative fluid management
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Losses from drains or nasogastric tubes
replaced with an isotonic fluid
0.9% NS with or with out added KCl.
Loses should be measured hourly
replaced every 2-4 hrs
All fluid intake to be recorded
When oral intake = hourly maintenance rate
I.V fluids may then be discontinued.
Electrolyte imbalance
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Hyponatremia(Serum Na+
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Treatment:
Symptomatic Hyponatremia
Infusion of 3% NS solution,
serum Na+ should be raised quickly
to a serum Na+ > 125mmol/L
Asymptomatic Hyponatremia
Treated with enteral fluids
If not tolerated, with 0.9%NS solution I.V.
Electrolyte imbalance
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Hypernatremia ( Serum Na+ >150 mmol/L )
excessive water loss,
restricted water intake,
inability to respond to thirst
Electrolyte imbalance
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Hypernatremia : Management
initial volume replacement with 0.9%NS
boluses of 20mL/Kg to restore normovolemia
Complete correction
slowly over atleast 48hrs
prevent cerebral edema,
seizures and brain injury.
Electrolyte imbalance
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Hypocalcemia
Serum calcium < 4.5 meq/L
COMMON CAUSES:
1) Massive blood transfusion .
2) Acute hyperventilation
3) low albumin levels
Electrolyte imbalance
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Symptoms : neuromuscular irritability ,
weakness,
paraesthesia,
cardiac dysrhythmias
prolonged QT interval in ECG
carpopedal spasm
Treatment :
10% calcium gluconate 0.5ml/ kg to
Maximum of 20ml over 10 mins
Conclusion
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Fluid therapy should be tailored
to the needs of the individual child.
There is no replacement
for knowledge of basic physiology
and sound clinical judgment.
Conclusion
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Nothing can replace
a vigilant anaesthesiologist monitoring
the vital functions
close watch of the surgical procedures.
Formulas for fluid therapy are guidelines
that need to be reevaluated
according to the childs response.
Pediatric Regional Anesthesia
C d l A th i
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Caudal Anesthesia
Pediatric Regional Anesthesia
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g
How do children differ from adults?
Why do regional anesthesia and analgesiain children?
Caudal Anesthesia and AnalgesiaTest dose
Single dose local anesthetic or morphine
Continuous Caudal/Epidural Infusion
Spinal Anesthesia (if we have time)
How do children differ from adults?
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Psychologically and Parents
Physiology
Pharmacology Anatomy
Physiology
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y gy
Postoperative apnea in former premature
infants
ImplicationsImmature CNS and BBB
Regional alone decreases risk
Pharmacology
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gy
General and Implications Distribution
CSF Volume
Total Body Water
Protein Binding
Clearance Liver
Renal
Local Anesthetics Opioids
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CSF Volume: Implications
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p
Dosage of Drugs
tetracaine 1 mg/kg +
epinephrine for spinal
bupivacaine 0.5-1.0
ml/kg for caudal
Duration of action
e.g. Spinal Tetracaine
with epinephrine
0
5 0
1 0 0
1 5 0
2 0 0
Infants Adults
minutes
Cote, A Practice of Anesthesia for Infants and Children
Total Body Water
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y
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
ICF
ECF
%
of
bodyweight
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g
Protein binding decreased at birth
Albumin and -glycoprotein levels decreased
Adult levels at 1 year of age
Clearance
Liver: Phase I & Phase II decreased
Renal: GFR 30% of adult
Adult levels by 3-5 months of age
Clin Pharm, 14:189, 1988
General Pharmacology Implications
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CSF Volume dose & durationTotal Body Water IV dose,
?
toxicityProtein Binding %drug available toxicity
Clearance t1/2 toxicity
Local Anesthetics
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BE CAREFUL with repeated dosing and infusions
Neurologic symptoms > cardiac symptoms May not be able to illicit early neurologic symptoms in
small children First sign may be a grand mal seizure
Case Reports of Toxicity with Infusion 4 children, 1 neonate
Children all presented with grand mal seizuresNeonate presented with cardiac arrest
Anesth Analg, 75:164, 1992; Anesth Analg, 75:284, 1992; Anesth Analg, 75:287, 1992
Opioids
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Morphine's t1/2
in neonates twice of adults
Approaches adult by 2-4 months
Implications: BE CAREFUL with opioidsand infants
Recommendation for opioidsFor IV,
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Cote, A Practice of Anesthesia for Infants and Children
Why Regional Anesthesia andAnalgesia in Children?
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Regional Anesthesia only
Combined Regional and General Anesthesia
Contraindications
Regional Anesthesia Only!
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Reduce risk of postoperative apnea in formerpremies Regional anesthesia alone will reduce risk of
postoperative apnea
Still need to monitor overnight
Techniques Caudal: 0.25% Bupivacaine (1ml/kg) + Clonidine (1 mcg/kg)
Spinal: Tetracaine, surgical anesthesia for 60-90 minutes
In other age groups, difficult to do regional alone
Anesthesiology 101:A1470, 2004
Combined Regional and General Anesthesia
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Usually regional anesthesia forpostoperative analgesia
TypesSingle dose caudal
Continuous Epidural/Caudal Infusion
Peripheral nerve blocks
Field blocksLocal infiltration
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Contraindications to RegionalAnesthesia in Pediatrics
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Parental refusal
Need for intact sensory system forpostoperative evaluation
Sepsis
Bleeding disorder
Vertebral malformation or previous surgery
Allergy
Pediatric Regional Anesthesia:Neuroaxial Techniques
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Caudal anesthesia and analgesia
Single dose local anesthetic
Morphine
Clonidine
Continuous infusion
Spinal anesthesia
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Caudal Anesthesia
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Caudal Anesthesia
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Needle or Angiocath
Caudal AnesthesiaWhere can it go?
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Caudal in a
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http://www.cvm.okstate.edu/~users/aerrane/mandsagr/www/vms5422/lect22.htm
Single Dose:Local Anesthetic Volume
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Traditional
0.05 ml/seg/kg
0.5 ml/kg T10
1.0 ml/kg T6
For longer duration or lower concentration
1.5 ml/kg T2
Anesthesiology 47:527, 1977Anesthesiology 75:57, 1991
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Single Dose:Caudal Morphine
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30 40 mcg/kg
Provides analgesia for 12-24 hours
No respiratory depression in over 500 children
Nausea incidence similar to general anesthesia
Less labor intensive Does not require special pain service
Side Effects
Nausea
Itching Propofol therapy single dose
Do not need to go to PICU
Anesthesiology 81:A1348, 1994J Clin Anesth 7:640, 1995
Local with Clonidine
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Clonidine in adults as oral sedative or
adjunct to spinal or epidural
Enhances and increases the effect of single
shot bupivacaine caudal
Risk: sedation with > 1mcg/kg
At UTMB, we use for caudal alone forpremies and hernia repair
Anesthesiology 101:A1470, 2004
Awake Caudals in Neonates
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Anesthesiology 101:A1470, 2004
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Anesthesiology 101:A1470, 2004
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Anesthesiology 101:A1470, 2004
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Caudal/Epidural Anesthesia and Analgesia:
Continuous Infusion Rates and Types
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Rates 1 yoa: 0.1-0.4 ml/kg/hr
*less than 0.5 mcg/kg/hr fentanyl to start
Types1 yoa: 0.1% bupivacaine + 3 mcg/ml fentanyl
Anesth Analg, 75:164, 1992
Continuous Caudal/Epidural Infusion:
Side Effects and Treatment
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*If infusion has fentanyl, then turn down infusion& may use naloxone
Itching Diphenhydramine
Nausea Metoclopramide
Urinary Retention Straight Cath prn
Sedation Turn Down Infusion
RespiratoryDepression
avoid sedating drugs
10 mcg/kg
Naloxone*
Naloxone
Naloxone
Naloxone
0.5-2 mcg/kg
Cote, A Practice of Anesthesia for Infants and Children
Pediatric Regional Anesthesia:Goals to Understand
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Identify differences between adults and
infants
When indicated and contraindicated
Techniques
Side Effects and Complications
Spinal Anesthesia
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RARELY done
Technique
IV access
1.5" 22g beveled needle
Dose
Tetracaine 1 mg/kg and "whiff" (0.02 ml)epinephrine
Approximate Distance:Skin to Subarachnoid Space
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0
10
20
30
40
50
1 yr 3 yr 5 yr 10 yr 18 yr
MILLIMETERS
PremieNewborn5 months
Cote, A Practice of Anesthesia for Infants and Children
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Spinal Anesthesia
CSF Returns
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Cote, A Practice of Anesthesia for Infants and Children
Spinal Anesthesia
Injection
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Cote, A Practice of Anesthesia for Infants and Children
Spinal Anesthesia
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Complications
No hypotension seen in children under 6 years of age
If blood encountered, difficult to identify CSF
Limitations
Procedure
Duration 45 minutes
Surgeon
Pearls
Sugar Nipple Do not flex head
Bovie Pad
Spinal Anesthesia
Bovie Pad Placement
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