pediatric anesth

8/6/2019 Pediatric Anesth

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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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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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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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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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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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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 &parasympathetic 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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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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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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Respiratory System


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Respiratory System


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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


De elopmental Factors


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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-



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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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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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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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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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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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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



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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



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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



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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



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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.



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Hypernatremia ( Serum Na+ >150 mmol/L )

excessive water loss,

restricted water intake,

inability to respond to thirst



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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.



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Hypocalcemia

Serum calcium < 4.5 meq/L

COMMON CAUSES:

1) Massive blood transfusion .

2) Acute hyperventilation

3) low albumin levels



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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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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


Awake Caudals in Neonates


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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


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



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Spinal Anesthesia

CSF Returns


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Spinal Anesthesia

Injection


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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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pediatric anesth

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