pediatric anesthesia

1. Yilkal Tadesse (BSc, MSc)
Department of Anaesthesia
Critical Care and Pain Medicine,
School of medicine,
BAHIRDAR UNIVERSITY
destayilkal999@gmail.com
Feburary 2023
Basics of Pediatrics and Neonatal Physiology,
Anatomy and Pharmacology in relation to
Anaesthesia Management

2. By the end of this session you will be able to:
• Explain the fetal circulation and exra-uterine life adaptation of
a neonate.
• Describe normal anatomy of pediatric airway, differences in
pediatric and adult airway, and consideration for evaluation and
management of normal vs. abnormal airway.
• Describe airway management classification of abnormal
pediatric airway and common congenital abnormalities
• Explain the physiologic factors and challenges of pediatric
anesthesia
• Describe relevant aspects of thermoregulation especially in
neonates and infants.
• Explain pediatrics pharmacologic consideration.
2
Learning Objectives

3.  Pediatric patients, especially neonates and infants younger
than 6 months of age, have anatomic and physiologic
differences that place them at higher risk of anesthetic
complications than adults.
 Differences in responses to pharmacologic agents in this
population further add to the complexity of administering
anesthesia to these patients.
 80% of pediatric cardiopulmonary arrest are primarily due to
respiratory distress
 Majority of cardiopulmonary arrest occur at <1 year old
 The challenge of pediatric anesthesia is related to the
ongoing development and maturation of multiple organs.
Introduction

4. • The first year of life is X-zed by an almost
miraculous growth in size and maturity.
•
• The journey down the birth canal is the
most dangerous trip in a person's life.
•
• This change from fetal to extrauterine life is
called the period of transition or
adaptation.
Transition/adaptation period to extrautrine of neonate:

5. o The new born infant is an infant in the first 24hrs of
life.
o The neonatal period is the first 28/30 days of
extrauterine life including the new born.
o An Infant is a child less than 1 year of age
o The most significant part of transition occurs in the 1st
24-72 hrs after birth.
o All systems of the body change during transition, but
the most important to the anesthetists are the
circulatory, pulmonary, hepatic, and renal systems.
Definition of terms;

6. Fetal Circulation

7. • The cardiovascular system exists to efficiently
deliver oxygen and other metabolic nutrients
to tissues throughout the body.
•
• 55% of fetal cardiac output goes to placenta.
• Blood in umbilical vein is 80% saturated with
O2
• Portal and systemic venous blood in fetus 26%
saturated.
• After mixing them – 67% saturated.
Fetal Circulation

8. Umbilical Vessels: carries blood to/from placenta
–2 Umbilical Arteries = bring blood that
contains waste & little O2 from fetus to
placenta
–1 Umbilical Vein = brings blood with O2 and
nutrients to fetus from placenta.

9. • Deoxygenated blood is pumped down the
fetal descending aorta to the umbilical artery
(pair) and then to the placenta; at which it
branches to arterioles, capillaries, and venules
in the intervillous spaces, where oxygen and
nutrient exchange occurs.
• Oxygenated blood returns to the fetus via the
umbilical vein for delivery to all organ systems.

10. • The foramen ovale, ductus arteriosus, and
ductus venosus are the fetal shunts needed
for effective fetal circulation that must close
after birth.
• Blood returning from the placenta in the
umbilical vein has the highest oxygen content.
• Umbilical vein enter the navel of the fetus &
ascends anteriorly.

11. • About one-half of the blood enters the liver &
the rest enter inferior vena cava by shunting
through ductus venousus, this richly
oxygenated umbilical blood flow away from
the liver, to inferior venacava.
• This result in mixing of oxygenated fetal blood
with deoxygenated from lower part the body.
• The newly mixed fetal blood then travel up &
enter right atrium, where it mingles again with
deoxygenated blood from superior vena cava.

12. • Once in the Rt. Atrium most of blood directly to
Lt. atrium through foramen ovale.
• This is because of relatively low pressure in the
left atrium and the high pressure in the right
atrium result in the foramen ovale being open.
• As a result, highly oxygenated blood travels to
the LV and is ejected into the aorta, thereby
feeding primerly the heart and the brain.

13. • The rest of blood left in Rt. Atrium (Superior
vena cava and hepatic venous blood) is directly
flow to Rt.ventricle & then to pulmonary artery.
• Because of the high resistance in the pulmonary
vascular bed and relatively low systemic
resistance due to the placental vasculature,
right ventricular output is shunted away from
the lungs via the ductus arteriosus to enter the
descending aorta.

14. • Small amount of blood 5-10% flows through the
lung and returns to the Lt. atrium via the
pulmonary vein.
• Down stream a common iliac arteries branch
into the external & internal iliac arteries.
•
• The blood in the internal iliac arteries branch
passes in to the umbilical arteries & again flow
back to the placenta to pick up o2 & drop off
waste product.

15. • Most blood from umbilical vein divert directly to
inferior vena cava – via ductus venosus.
• Most blood from inferior vena cava goes to left
atrium – via patent foramen ovale.
• Most blood from superior vena cava goes to right
ventricle then to pulmonary artery.
• Most blood in pulmonary artery pass to aorta – via
ductus arteriosus.
Summary FC …..

17. • Clamping of the umbilical cord and initiation
of ventilation produce enormous circulatory
changes in the newborn.
• As the infants inhales the first time, the
pulmonary vascular resistance falls
dramatically & increases systemic vascular
resistance.
Transition of Circulation

18. a) The sudden increase in the alveolar paO2,
which offsets the hypoxic pulmonary
vasoconstriction.
b) The mechanical increase of lung volume,
which widen the caliber of the extra-alveolar
cell.
• As the pulmonary vascular resistance decreases
, a greater amount of blood flow through lung
 therefore more blood returns to the left
atrium.
These is resulted by two mechanism;

19. - This & the cessation of umbilical flow cause Po
in Lt. atrium Increase close of flap of foramen
ovale with in 3-4 days.
- A few minutes later the smooth muscle of
ductus arteriosus constrict in response to
increased PaO2- 45-50mmHg.
- Final anatomic closure results from thrombosis
and fibrosis over the first few months of life (b/n
3-12months), although the precise mechanisms
of closure are not well elucidated.

20. • Because these shunts are not anatomically
closed immediately after birth, certain
clinical conditions may result in the
persistence of or return foramen ovale &
ductus arteriosus patency.
 Hypoxemia and acidosis are two main
factors known to reverse shunt patency.

21. • Infants who are at high risk for persistent
pulmonary hypertension syndrome ,
formerly known as persistent fetal shunting
includes:
o preterm
o meconium aspiration or sepsis
o Congenital tracheoesophageal
fistula , diaphragmatic hernia
o Neonatal respiratory failure.

22. • Fetal lung fluid is filled.
- At birth the lungs are partially filled with liquid
approximately =newborn`s FRC.
- This fluid is originated from the alveolar cell
during fetal development.
- At birth the fluid is removed from the lung
during the first 24hrs by following mechanism;
1) about 1/3 is squized out of the lung as the fetus
passes through the birth canal.
2) about 1/3 of filuid is absorbed by pul. Capillaries
3) about 1/3 is removed by lymphatic system.
Transition of pulmonary system

23. • As the infant inhales the first breath the lungs
are changed from the fluid filled state into air
filled.
• This is bombarded by a variety of external
sensory stimuli (thermal, tactile, visual…)
 At the time placenta cease function
PO2↓ed,PCO2↑ed & the PH ↓ed
 And the sensitivity of both central and
peripheral chemoreceptor of new born ↑ed
dramatically == in response to this stimuli
infants inhales.

24. Normal blood gas values in new born
subject age PO2
mmHg
PCO2
mmHg
PH
Fetus (Term) Before
laboure
25 40 7.37
Fetus (Term) End of labour 10 - 20 55 7.25
New born
(term)
10 min. 50 48 7.20
‘’ ‘’ ‘’ 1hr 70 35 7.35
‘’ ‘’ ‘’ 1week 75 35 7.4
New born
(preterm)
1week 60 38 7.37

25. • Four anatomic and physiologic differences from
that of mature infants;
 -- Neonates have a high metabolic requirement
for oxygen (7-9 ml/kg/min vs. 3ml/kg/min in
adults)high O2 consumption. So infants more
quickly desaturates in mild airway
obstruction/apnea.
 -- The high closing volume of the neonate’s lungs
are within the lower range of the normal tidal
volume.
ANATOMIC AND PHYSIOLOGIC FACTORS OF THE
PULMONARY SYSTEM IN NEONATE & INFANT

26.  -- The neonate has an increased alveolar
ventilation because of the need to increase to O2
delivery 2o high O2 consumption.
They have = VT with that of adult but three times
greater of respiratory rate. This result in ratio of
high minute ventilation to FRC; 5:1 in neonate &
1.5:1 in older.
The clinical implication of high minute ventilation
to FRC ratio is that there is much more rapid
induction &/ recovery from inhalational
anesthesia.

27.  The more rapid induction of anesthesia in pedi
also result from a higher percentage of
neonate’s of body weight consists of vessel rich
tissues.
 -- The neonate’s diaphragm is the major
ventilatory muscle.
 The contraction of diaphragm results in
greater intrathoracic pressure.
In mature patients with fixed rib cage, this result
in an increase inward air movement.

28. • However ,with a pliable rib cage, an increase in
intrathoracic pressure result in retraction of
ribs, subcostal & supraclavicular area 
inefficient ventilation and high energy demand.
This is why neonates are fatigue with mild
airway obstruction, pneumonia, …
•
• Normal quiet ventilation in neonate has similar
physical appearance to that of older child.
However, if there is the need of increase minute
ventilation, respiratory rate & tidal volume;
pliable ribs will disadvantageous.

29. Parameter Infant Adult
RR/min 30-50 12-16
Vt. ml/kg 7 7
Dead space 2-2.5 2.2
Alveolar ventilation ml/kg/min 6-9 3
Compliance ml/cmH2O 5 100
Comparison of Normal respiratory values in
infants and Adults
N.B Avoid hypoxia in neonate & small child.

30. • Normal Anatomy
• Airway evaluation
• Management of
normal vs. abnormal
airway
• Difficult airway
The Pediatric Airway

31. • Larynx composed of hyoid
bone and a series of
cartilages
– Single: thyroid, cricoid,
epiglottis
– Paired: arytenoids,
corniculates, and cuneiform
Normal Pediatric Airway Anatomy

32. Laryngeal folds consist of:
– Paired aryepiglottic folds extend from epiglottis posteriorly to
superior surface of arytenoids
– Paired vestibular folds (false vocal cords) extend from thyroid
cartilage posteriorly to superior surface of arytenoids
– Paired vocal folds (true vocal cords) extend from posterior surface of
thyroid plate to anterior part of arytenoids
– Interarytenoid fold bridging the arytenoid cartilages
– Thyrohyoid fold extend from hyoid bone to thyroid cartilage
Sensory Innervation:
Recurrent Laryngeal Nerve-supraglottic larynx
Internal Branch of Superior Laryngeal Nerve-infraglottic larynx
Motor Innervation:
External branch of Superior Laryngeal Nerve-cricothyroid muscle
Recurrent Laryngeal Nerve-all other laryngeal muscles
Blood Supply
Laryngeal branches of the superior and inferior thyroid arteries
Pediatric Anatomy cont.

33. • More rostral larynx
• Relatively larger tongue
• Angled vocal cords
• Differently shaped epiglottis
• Funneled shaped larynx-narrowest part of
pediatric airway is cricoid cartilage
Airway

34. More rostral pediatric larynx
Laryngeal apparatus develops from brachial clefts and descends caudally
Infant’s larynx is higher in neck (C2-3) compared to adult’s (C4-5)

35. Relatively larger tongue
• Obstructs airway
• Obligate nasal breathers
• Difficult to visualize larynx
• Straight laryngoscope blade
completely elevates the epiglottis,
preferred for pediatric
laryngoscopy
Angled vocal cords
• Infant’s vocal cords have more
angled attachment to trachea,
whereas adult vocal cords are
more perpendicular
• Difficulty in nasal intubations
where “blindly” placed ETT may
easily lodge in anterior
commissure rather than in trachea
Image from: http://www.utmb.edu/otoref/Grnds/Pedi-airway-2001-01/Pedi-
airway-2001-01-slides.pdf

36. • Adult epiglottis broader, axis parallel to trachea
• Infant epiglottis ohmega (Ώ) shaped and angled away from
axis of trachea
• More difficult to lift an infant’s epiglottis with
laryngoscope blade
Differently shaped epiglottis

37. Funneled shape larynx
• narrowest part of infant’s
larynx is the undeveloped
cricoid cartilage, whereas in
the adult it is the glottis
opening (vocal cord)
• Tight fitting ETT may cause
edema and trouble upon
extubation
• Uncuffed ETT preferred for
patients < 8 years old
• Fully developed cricoid
cartilage occurs at 10-12 years
of age
INFANT
ADULT

38.  Neonates are obligatory nose breathers
because they can’t coordinates the usual
swallowing & breathing mechanics. Any thing
that obstruct nares will compromise neonate’s
ability to breath.
 The large tongue occupies space in the
neonate’s/infant’s airway and makes it difficult
laryngocopey.
 They have large, floppy, and U-shaped
epiglottis, which is located at high level – C4 in
full term infant and C3 in premature (at level of
C5 in adult)= cephalad location in respect to the
floor of mouth.
Anatomical difference and their clinical significance

39.  The diaphragm is the predominant respiratory
muscle in neonates but is more easily fatigable
than in adults.
Ventilation under anaesthesia should be at least
assisted and infants should not be left to breathe
spontaneously through a tracheal tube.
•
 Gastric distension is common after facemask
ventilation and will splint the diaphragm,
compromise respiration and increase the
possibility of aspiration.
A nasogastric tube should be passed to relieve
gastric distension.

40.  The epiglottis is long and straight and tends
to flop back over the laryngeal inlet, which is
high and anterior; intubation is best achieved
with a straight blade laryngoscope.
The larynx is conical in shape, the narrowest
portion at the level of the cricoid cartilage. An
endotracheal tube that can easily pass
through vocal cord may be trapped in cricoid
ring .
The tight fit endotracheal tube at cricoid ring
may cause either temporary or permanent
damage to cricoid cartilage.

41. • The trachea is short and endobronchial
intubation is not uncommon. The position of the
tracheal tube should always be checked by
auscultation.
• The relatively large occiput result in head being
flexed forward onto the chest when the infant is
lying supine.
Extreme extension can also obstruct airway; so mid
positioning of the head with slight extension is
preferred.
• This is accomplished by placing a small roll at the
base of the neck & shoulder.

42. • The elastic tissue of the lung poorly developed
& result in the decreased lung compliance.
•
• Ribs are horizontal in neonates (vertical in adults)
•
• Control of ventilation is immature and or
hypoxic & hypercapnic ventilatory derives are
not well developed ==the response of hypoxia
& hypercarbia is bradypnea unlike that adult
(tachypinic).

43. • Extrauterine life not possible until 24-25 weeks of gestation
• Two types of pulmonary epithelial cells: Type I and Type II pneumocytes
– Type I pneumocytes are flat and form tight junctions that
interconnect the interstitium
– Type II pneumocytes are more numerous, resistant to oxygen toxicity,
and are capable of cell division to produce Type I pneumocytes
• Pulmonary surfactant produced by Type II pneumocytes
at 24 wks GA
• Sufficient pulmonary surfactant present after 35 wks GA
• Premature infants prone to respiratory distress syndrome
(RDS) because of insufficient surfactant
• Betamethasone can be given to pregnant mothers at 24-35wks GA to
accelerate fetal surfactant production
Pediatric Respiratory Physiology

44. • Work of breathing for each kilogram of body weight is
similar in infants and adult
• Oxygen consumption of infant (6 ml/kg/min) is twice that
of an adult (3 ml/kg/min)
• Greater oxygen consumption = increased respiratory rate
• Tidal volume is relatively fixed due to anatomic structure
• Minute alveolar ventilation is more dependent on
increased respiratory rate than on tidal volume
• Lack Type I muscle fibers, fatigue more easily
• FRC of an awake infant is similar to an adult when
normalized to body weight
• Ratio of alveolar minute ventilation to FRC is doubled,
under circumstances of hypoxia, apnea or under
anesthesia, the infant’s FRC is diminished and
desaturation occurs more precipitously
Pediatric Respiratory Physiology cont.

45. Physiology: Effect Of Edema
Poiseuille’s law
R = 8nl/ πr4
If radius is halved, resistance increases 16 x

46. Normal Inspiration and Expiration
turbulence

47. Obstructed Airways
turbulence &
wheezing

48. • URI predisposes to coughing,
laryngospasm, bronchospasm,
desat during anesthesia
• Snoring or noisy breathing
(adenoidal hypertrophy, upper
airway obstruction, OSA)
• Chronic cough (subglottic
stenosis, previous
tracheoesohageal fistula
repair)
• Productive cough (bronchitis,
pneumonia)
• Sudden onset of new cough
(foreign body aspiration)
• Inspiratory stridor
(macroglossia, laryngeal web,
laryngomalacia, extrathoracic
foreign body)
• Hoarse voice (laryngitis, vocal
cord palsy, papillomatosis)
• Asthma and bronchodilator
therapy (bronchospasm)
• Repeated pneumonias (GERD, CF,
bronchiectasis,
tracheoesophageal fistula,
immune suppression, congenital
heart disease)
• History of foreign body aspiration
• Previous anesthetic problems
(difficulty intubation/extubation
or difficulty with mask
ventilation)
• Atopy, allergy (increased airway
reactivity)
• History of congenital syndrome
(Pierre Robin Sequence, Treacher
Collins, Klippel-Feil, Down’s
Syndrome, Choanal atresia)
Airway Evaluation
Medical History

49. • Increase work of breathing
• Tachypnea/tachycardia
• Nasal flaring
• Drooling
• Grunting
• Wheezing
• Stridor
• Head bobbing
• Use of accessory muscles/retraction of muscles
• Cyanosis despite O2
• Irregular breathing/apnea
• Altered consciousness/agitation
• Inability to lie down
• Diaphoresis
Signs of Impending Respiratory Failure

50. • Facial expression
• Nasal flaring
• Mouth breathing
• Drooling
• Color of mucous membranes
• Retraction of suprasternal,
intercostal or subcostal
• Respiratory rate
• Voice change
• Mouth opening
• Size of mouth
• Mallampati
• Loose/missing teeth
• Size and configuration of palate
• Size and configuration of mandible
• Location of larynx
• Presence of stridor
(inspiratory/expiratory)
• Baseline O2 saturation
• Global appearance (congenital
anomalies)
• Body habitus
Airway Evaluation Physical Exam

51. • Laboratory and radiographic evaluation extremely helpful
with pathologic airway
• AP and lateral films and fluoroscopy may show site and cause
of upper airway obstruction
• MRI/CT more reliable for evaluating neck masses, congenital
anomalies of the lower airway and vascular system
• Perform radiograph exam only when there is no immediate
threat to the child’s safety and in the presence of skilled
personnel with appropriate equipment to manage the airway
• Intubation must not be postponed to obtain radiographic
diagnosis when the patient is severely compromised.
• Blood gases are helpful in assessing the degree of physiologic
compromise; however, performing an arterial puncture on a
stressed child may aggravate the underlying airway
obstruction
Diagnostic Testing

52. Airway Management: Normal Airway
• Challenging because of unique anatomy and
physiology
• Goals: protect the airway, adequately
ventilate, and adequately oxygenate
• Failure to perform any ONE of these tasks will
result in respiratory failure
• Positioning is key!

53. •Clear, plastic mask with inflatable rim
provides atraumatic seal
•Proper area for mask application-bridge of
nose extend to chin
•Maintain airway pressures <20 cm H2O
•Place fingers on mandible to avoid
compressing pharyngeal space
•Hand on ventilating bag at all times to
monitor effectiveness of spontaneous breaths
•Continous postitive pressure when needed to
maintain airway patency
Image from: http://www.hadassah.org.il/NR/rdonlyres/59B531BD-EECC-4FOE-9E81-14B9B29D139B1945/AirwayManagement.ppt
Bag-Mask Ventilation

54. SIZE
PROPER POSITION
Image from: http://www.hadassah.org.il/NR/rdonlyres/59B531BD-EECC-4FOE-9E81-14B9B29D139B1945/AirwayManagement.ppt
Oropharyngeal Airway

55. Oropharyngeal Airway Placement

56. •Distance from nares to angle of mandible approximates the proper length
•Nasopharyngeal airway available in 12F to 36F sizes
•Shortened endotracheal tube may be used in infants or small children
•Avoid placement in cases of hypertrophied adenoids - bleeding and trauma
Nasopharyngeal Airway

57. Sniffing Position
Patient flat on operating table, the oral (o),
pharyngeal (P), and tracheal (T) axis pass through
three divergent planes
A blanket placed under the occiput aligns the
pharyngeal (P) and tracheal (T) axes
Extension of the atlanto-occipital joint
aligns the oral (O), pharyngeal (P), and
tracheal (T) axes

58. • Miller blade is preferred for infants and younger
children
• Facilitates lifting of the epiglottis and exposing the
glottic opening
• Care must be taken to avoid using the blade as a
fulcrum with pressure on the teeth and gums
• Macintosh blades are generally used in older children
• Blade size dependent on body mass of the patient
and the preference of the anesthetist
Selection of laryngoscope blade:
Miller vs. Macintosh

59. • Postintubation Croup
– Incidence 0.1-1%
– Risk factors: large ETT, change in patient position introp, patient
position other than supine, multiple attempts at intubation,
traumatic intubation, pts ages 1-4, surgery >1hr, coughing on ETT,
URI, h/o croup
– Tx: humidified mist, nebulized racemic epinephrine, steroid
• Laryngotracheal (Subglottic) Stenosis
– Occurs in 90% of prolonged endotracheal intubation
– Lower incidence in preterm infants and neonates due to relative
immaturity of cricoid cartilage
– Pathogenesis: ischemic injury secondary to lateral wall pressure
from ETT edema, necrosis, and ulceration of mucosa, infx
– Granulation tissues form within 48hrs leads to scarring and
stenosis
Complications of Endotracheal Intubation

60. • Controversial issue
• Traditionally, uncuffed ETT recommended in children < 8 yrs old to
avoid post-extubation stridor and subglottic stenosis
• Arguments against cuffed ETT: smaller size increases airway
resistance, increase work of breathing, poorly designed for pediatric
pts, need to keep cuff pressure < 25 cm H2O
• Arguments against uncuffed ETT: more tube changes for long-term
intubation, leak of anesthetic agent into environment, require more
fresh gas flow > 2L/min, higher risk for aspiration
-Concluding Recommendations-
• For “short” cases when ETT size >4.0, choice of cuff vs uncuffed
probably does not matter
• Cuffed ETT preferable in cases of: high risk of aspiration (ie. Bowel
obstruction), low lung compliance (ie. ARDS, pneumoperitoneum,
CO2 insufflation of the thorax, CABG), precise control of ventilation
and pCO2 (ie. increased intracranial pressure, single ventricle
physiology)
Cuff vs Uncuffed Endotracheal Tube

61. • Rigid bronchoscopy
• Flexible bronchoscopy
• Direct laryngoscopy
• Intubating LMA
• Lighted stylet
• Fiberoptic intubation
• Surgical airway
Difficult Airway Management Techniques

62. • Congenital Neck Masses (Dermoid cysts, cystic teratomas, cystic
hygroma, lymphangiomas, neurofibroma, lymphoma, hemangioma)
• Congenital Anomalies (Choanal atresia,tracheoesophageal fistula,
tracheomalacia, laryngomalacia, laryngeal stenosis, laryngeal web, vascular
ring, tracheal stenosis)
• Congenital Syndromes (Pierre Robin Syndrome, Treacher Collin,
Turner, Down’s, Goldenhar , Apert, Achondroplasia, Hallermann-Streiff,
Crouzan)
• Inflammatory (Epiglottitis, acute tonsillitis, peritonsillar
abscess,retropharyngeal abscess, laryngotracheobronchitis,bacterial
tracheitis,adenoidal hypertrophy,nasal congestion, juvenile rheumatoid
arthritis)
• Traumatic/Foreign Body (burn,laceration,lymphatic/venous
obstruction,fractures/dislocation, inhalational injury, postintubation
croup (edema),swelling of uvula
• Metabolic (Congenital hypothyroidism, mucopolysaccharidosis, Beckwith-
Wiedemann Syndrome,glycogen storage disease, hypocalcemia
laryngospasm)
Airway Management
Classification of Abnormal Pediatric Airway

63. Congenital Neck Masses

64. • Feeding difficulties (coughing, choking and
cyanosis) and breathing problems
• Associated with congenital heart (VSA, PDA, TOF),
VATER, GI, musculoskeletal and urinary tract
defects
• Occurs in 1/ 3000-5000 births
• Most common type is the blind esophageal pouch
with a fistula between the trachea and the distal
esophagus (87%)
Radiograph of a neonate with
suspected esophageal atresia.
Note the nasogastric tube coiled in
the proximal esophageal pouch
(solid arrow). The prominent
gastric bubble indicates a
concurrent tracheoesphageal
fistula (open arrow)
Congenital Anomalies
Tracheoesphageal Fistula

65. • Complete nasal obstruction of
the newborn
• Occurs in 0.82/10 000 births
• During inspiration, tongue
pulled to palate, obstructs oral
airway
• Unilateral nare (right>left)
• Bilateral choanal atresia is
airway emergency
• Death by asphyxia
• Associated with other
congenital defects
Congenital Anomalies Choanal Atresia

66. • Occurs in 1/8500 births
• Autosomal recessive
• Mandibular hypoplasia,
micrognathia, cleft palate,
retraction of inferior dental arch,
glossptosis
• Severe respiratory and feeding
difficulties
• Associated with OSA, otitis media,
hearing loss, speech defect, ocular
anomalies, cardiac defects,
musculoskeletal (syndactyly, club
feet), CNS delay, GU defects)
Congenital Syndromes
Pierre Robin Sequence

67. • Mandibulofacial dysotosis
• Occurs in 1/10 000 births
• Cheek bone and jaw bone
underdeveloped
• External ear anamolies,
drooping lower eyelid,
unilateral absent thumb
• Respiratory difficulties
• Underdeveloped jaw causes
tongue to be positioned
further back in throat
(smaller airway)
• Associated with OSA,
hearing loss, dry eyes
Congenital Syndrome Treacher Collins Syndrome

68. • Trisomy 21
• Occurs in 1/660 births
• Short neck, microcephaly, small
mouth with large protruding
tongue, irregular dentition,
flattened nose, and mental
retardation
• Associated with growth
retardation, congenital heart
disease, subglottic stenosis,
tracheoesophageal fistula,
duodenal atresia, chronic
pulmonary infection, seizures,
and acute lymphocytic
leukemia
• Atlantooccipital dislocation can
occur during intubation due to
congenital laxity of ligaments
Congenital Syndrome
Down’s Syndrome

69. • Etiology: Haemophilus influenzae
type B
• Occurs in children ages 2-6 years
• Disease of adults due to
widespread H. influenza vaccine
• Progresses rapidly from a sore
throat to dysphagia and complete
airway obstruction (within hours)
• Signs of obstruction: stridor,
drooling, hoarseness, tachypnea,
chest retraction, preference for
upright position
• OR intubation/ENT present for
emergency surgical airway
• Do NOT perform laryngoscopy
before induction of anesthesia to
avoid laryngospasm
• Inhalational induction in sitting
position to maintain spontaneous
respiratory drive (Sevo/Halothane)
• Range of ETT one-half to one size
smaller
Inflammatory

70. • Etiology: Parainfluenza virus
• Occurs in children ages 3 months
to 3 years
• Barking cough
• Progresses slowly, rarely requires
intubation
• Medically managed with oxygen
and mist therapy, racemic
epinephrine neb and IV
dexamethasone (0.25-0.5mg/kg)
• Indications for intubation:
progressive intercostal retraction,
obvious respiratory fatigue, and
central cyanosis
Inflammatory

71.  The cardiac muscle is immature at birth.
 There are non contractile tissue which render
the myocardium stiff & non compliant.
 The cardiac stroke volume is relatively fixed
and cardiac output is maintained by a
relatively high resting heart rate (at least 120
beats/min in infants).
 Bradychardia results in a rapid fall in cardiac
output.
The cardiovascular system

72.  Vagal tone (parasympathetic ) is well developed
in infants and they are prone to reflex
bradycardias (intubation, hypoxia, drugs).
=Atropine is useful as a premedication or should
be readily available.
 Neonates are more sensitive to the depressant
effects of anaesthetic agents.
 So avoid bradycardia & vagal stimulation as these
significantly decrease CO; since it is heart rate dependant.
 The major cause of bradycardia in infant is
hypoxia. vagal stimulation is the second cause.

73.  The blood pressure in newborns is 60-
90mmHg and increases with increasing
sympathetic tone to reach adult levels by 10
years of age. In measuring BP in a child, it is
important to use a cuff of the correct width
for the arm or leg.
 Baroreceptor reflex are immature & so
infants may not be able to compensate for
decreased in BP.

74. Systolic
mmHg
Diastolic
mmHg
Neona
te
65 40
1yr 95 65
3yrs 100 70
12yrs 110 70
HR
1yr 100-180
2yrs 80-120
6yrs 70-100
12yrs 60-100
Infants can tolerate Hr up to 200bt/min
Normal values of blood pressure and pulse rate in pediatrics

75. • At birth 75-80% of the neonate’s Hgb is HgbF
which has higher affinity for oxygen than that of
adult HgbA. This is demonstrated by left ward
shift of oxy-Hgb dissociation curve.
•
• The blood volume in relation to body weight is
large compared as adult.
•
• The high blood volume, increased CO & high
Hgb content compenset a decreased O2 to
tissue.

76. • Blood transfusion should be considered when
there is a 10–15% loss in blood volume.
–Circulating blood volume using the formula;
 Newborn 90ml/kg
 Infant 85ml/kg
 Child 80ml/kg
 Adult 70 ml/kg
If an adult lost 200ml of blood it would not be
significant but a child losing that amount would
need a transfusion.

77. • In the newborn the glomerular filtration rate is
only about 25-30% of adult and the renal tubular
transport system is not fully developed.
• By the end of first month after birth 80-90% of
renal function mature & after 9 month kidney
maturation is completed.
• Renal imaturity reduces the ability of neonates
to excrete free water (increase UOP) in case of
fluid over load==over infusion of fluid / blood 
pul.edema & cardiac failure.
Renal system & body fluids

78. • Water conserving mechanisms are poorly
developed  rapid dehydration if kept fasted.
• The decrease in GFR may delay excretion of
some drugs & prolong their effect.
• Neonates have limited glycogen stores and are
prone to hypoglycaemia.
– Added dextrose (5% dextrose in Ringer’s or 0.9%
saline) should be considered for neonates and other
children requiring a dextrose infusion prior to
surgery to maintain blood glucose.

79. • Body fluids constitute the greater proportion of
body weght in infant 85%; 65% adult.
• In neonate most of body water is in the
extracellular compartment.
 So during dehydration initially extracellular is lost &
fluid shift from relatively lower intracellular
compartment to ECF compartment.
===fluid lose in this age should be critically
evaluated.

80. Comparte
ment
prematur
e
Neonate infant adult
ECF 50 40 30 20
plasma 5 5 5 5
ICF 30 35 40 40
Total 85 80 75 65
Distribution of water as percentage of body weight

81.  Neonates and infants body heat is lost more
rapidly because:
-large body surface area relative to body weight
-thin layer of insulating subcutaneous fat
- decreased ability to produce heat
 Shivering is of little significance during heat
production in neonates; instead they use non
shivering thermogenesis mediated by brown fat
metabolism (with the product of heat & fatty
acid ).
Thermoregulation

82.  General anesthesia affects the metabolism of
brown fat.--hypothermia
The dangers of hypothermia include clotting
abnormalities, delayed drug metabolism (opioids,
muscle relaxants), impaired wound healing and
infection.
 So active measures should be taken to minimise
heat loss, at the same time avoiding
hyperthermia.

83.  Pharmacologic responses to drugs may differ
in pediatric patients and adults.
They manifest as differences in anesthetic
requirements, responses to muscle relaxants,
and pharmacokinetics.
 Neonates particularly preterm infants have a
lower plasma concentration of albumin as well
lower qualitative binding ability high plasma
concentration of active drugs.
Pharmacology:

84.  The BBB is immature at birth & more
permeable to drugs. In addition the neonate’s
brain receive large proportion of CO than does
the adult brain brain concentration of drugs
are higher in neonate.
 The neonate and infant have a larger
extracellular fluid volume leading to a larger
volume of distribution and an increased dose
requirement compared with children and adults.

85.  This is significantly seen in succinylcholine; but
in case of non depolarizing muscle relaxant they
are very sensitive this over come delutional
effect & require normal dose as adult in per kg.
 In neonates drugs that are primarly eliminated
through hepatic metabolism (benzodiazepin,
barbiturates,…) may have prolonged action
because of hepatic immaturity.
 Similarly drugs that are eliminated through the
renal system (pancuronium,…) may have the
same effect because of poorly developed
excreting effect of the kidney.

86.  Inhalational inductions are more common in
children than in adult practice with either
halothane or sevoflurane.
 The MAC in a neonate is relatively low and
increases to peak at 6-12 months of age before
decreasing to adult values after a few years.
 MAC of halothane 0.87% in neonate, 1.5% in
infants 1-6 months of age.

87. THANK YOU !!