Brief anesthesia management for pediatric neurosurgery; Hydrocephalus, Meningomyelocele , craniosynostosis and post op common complication

1. Prepared by:-
Gammachis Akkuma(Ass’t lecturer)
March 2023
3/4/2023 1

2. Outline
• Objectives
• Neurophysiology and development
• Hydrocephalous?
• Meningocele
• Craniosynstosis

3. Learning Objectives:
• At the end of this lesson student will be able
– Identifies clinical features of Hydrocephalus and ↑ICP
– Identifies anesthesia consideration for VP or atrial
shunt placement/hydrocephalus
– Define mengiolcele, craniosynostosis and describe
the underlying pathogenesis and pathophysiology
– Describe the pre-, intra- and postoperative anesthetic
considerations for infants and toddlers requiring
craniofacial surgery and Meningocele

4. Neurophysiology and development
• The skull is a closed box with brain tissue,
blood and CSF as its contents.
• An increase in volume of one of these
components with increase in ICP will result a
compensatory reduction of other components
(Monro–Kellie doctrine).
• Anatomical differences between children and
adults affect CNS physiology, especially ICP.

5. CBF affects the CBV and the intracranial volume,
thereby affecting the ICP, is higher in children
compared to adults (100 vs 50 ml/100g/min).
• CBF is coupled tightly to metabolic demand, increase
proportionally after birth.
• CBF peaked between 2-4 years and settled at 7-8years
• In children the CMRO2 is higher at than the adults (5.2
vs 3.5 ml/100 g/min) and hence, less tolerant to
hypoxia.

6. • The autoregulation range of blood pressure in normal
newborn is narrow between 20 and 60 mmHg.
• The neonate at risk for cerebral ischemia and IVH for
extreme BP
Brain tissue, the largest component of the cranial
contents, may be pathologically enlarged lead to
a gradual increase in ICP.

7. CSF is continuously produced by the choroid
plexus, and after circulating through the
ventricles is absorbed at the arachnoid villi?.
• In children the rate of production of CSF is 0.2-
0.4 ml/min and any given time around 70 ml is
present in the head.
– By Choroid Plexus of ventricles, 0.25% of total
volume replaced every minute
– Extra CSF formation [25%] by glucose oxidation

8. CSF
• Mechanical cushion to brain
• Source of nutrition to brain
• Excretion of metabolic waste products
• Intracerebral transport medium
• Control of chemical environment
• Autoregulation of intracranial pressure

10. • Circulation= circulates from lateral ventricle Foramen
of Monro 3rd ventricle  Aqueduct of Sylvius  4th
ventricle & then to Sub arachnoid space through
foramen of Lushka & Magendie.
• Reabsorption
– By arachnoid villi & arachnoid granulations at dura
walls superior sagittal sinus & venous lacunae.
– 85-90% of CSF reabsorbed in cranium.

11. What is hydrocephalous?
• Hydrocephalus is the medical term for a condition
that is commonly called “water? on the brain.”
– Abnormal accumulation of CSF due to disturbance in
formation, flow or absorption; which may lead to
raised ICP.
– This build-up of CSF causes the brain to swell, and for
pressure to increase inside the skull, resulting in nerve
damage.

12. Epidimology
• The incidence of hydrocephalus is between
0.5-0.8 per 100 live births in the United
States.(Sivagnanam M, Jha Nk, February
2012].)
• The burden of infant hydrocephalus in East
Africa is significant, with more than 6000 new
cases estimated per year (Warf BC;. 2010).

13. Ethology and classification
• Congenital :-
– Myelomeningocele
– Stenosis of the cerebral
aqueduct
– Arnold-Chiari
malformation
– Arachnoid cysts
– Vascular malformations
– Idiopathic
• Acquired :-
– Infection
– Intraventricular
hemorrhage
– Tumour
– Trauma
– Nutritional deficiencies

15. Clinical presentation
• It depend on underlying pathology, site of
obstruction, speed of onset, its duration and the
patient’s age.
• Acute onset cases usually present with symptoms
of raised ICP and the ventricles may not be
markedly enlarged
• In chronic forms of hydrocephalus, the ventricles
are usually enlarged.
• symptom in infant include poor feeding,
irritability, reduced activity, and vomiting

16. Examination in infants may reveal the
following findings
• Head enlargement
• Dysjunction of sutures
• Dilated scalp veins
• Tense fontanelle
• Setting-sun sign?
• Increased limb tone (spasticity preferentially
affects the lower limbs)

18. Treatment modality
– Relieve hydrocephalus
– Treat complications.
• Surgical correction involves draining fluid from
the ventricular system to one of three places:
peritoneum, atrium, or the pleural cavity.
• As the child grows, the shunts often require
replacement or revision VP ,most common
pediatric neurosurgical procedures

19. • VP shunt is used most commonly. The lateral
ventricle is the usual proximal location.
• A ventriculoatrial (VA) shunt also is called a
"vascular shunt.“
– It shunts the cerebral ventricles through the
jugular vein and SVC into the right cardiac atrium.
– It is used when the patient has abdominal
abnormalities (eg, peritonitis, morbid obesity, or
after extensive abdominal surgery).

20. How a shunt works
All shunts perform two functions.
• They allow CSF to flow in only one direction, to
where it is meant to drain.
• They all have valves, which regulate the amount
of pressure inside the skull.
– When the pressure inside the skull becomes too great
the valve opens, lowering the pressure by allowing
excess CSF to drain out.

21. Shunt Surgery

22. PREOPERATIVE ASSESSMENT
• History-
A. History common to all surgery  GA
– Birth history (premature, birth trauma, forcep
delivery)
– Immunization history
– H/O allergy
– H/O problem with previous anesthesia / surgery
– Fluid status/Last oral intake specially in emergency.
– Underlying cause of hydrocephalus
– Associated congenital anomalies

23. B. History specific to hydrocephalus
– Drug history- anticonvulsant, diuretics acetazolamide
– Associated cong. anomalies (Cardiac, Resp.)
– H/o fever (meningitis)
– H/o recurrent resp. infection due to sensorium &
aspiration.
– H/o nausea, vomiting, headache features ICP
– H/o Convulsion

24. • Examination (general): -
– Pt may have poor GCS.
– Depleted volume status i.e. dehydration &
electrolyte imbalance due to prolonged vomiting and
poor oral feeding.
– Search for the presence of any other congenital

25. • Systemic
– Assessment of Difficult Airway(big head,
edentulous)
– CVS for cong., Cardiac anomaly,
– Resp. system - anomalies like Brovhopulm.
dysplasia,
– kyphoscoliosis, recurrent RTI due to aspiration.
– Assessment of neurological status
• Level of consciousness/irritability, lethargy,
• altered sensorium and cranial nerve palsies.
• Features of  ICP (papilledema), Cushing’s triad
• Features of Brain Stem involvement.
• failure to feed, bulging fontanel and cranial enlargement

26. • CBC- leukocytosis & ESR in presence of infection
• Coagulation profile
• serum electrolytes :- dehydration and electrolyte
imbalances.
• renal and hepatic function test
• CXR, Abdominal U/S
• Special investigations
– X-ray skull (silver bitten appearance)
– CT scan/MRI brain for etiology
– ECG/ECHO-to evaluate/rule out congenital heart disease

27. Anesthesia management
• Goals of Anesthesia
– Maintenance of CPP
– Control of hemodynamics
– Smooth temperature
– Prevent gastric aspiration
• NPO for 6 hours for solids and 2 hrs for clear
fluids.
• Premedication
– Usually not required (lethargic, drowsy)
– Any resultant respiratory depression may cause
hypercapnia and therefore increase ICP.

28. • The method of induction depends upon
– The level of anxiety of the child.
– The child's ability to cooperate and communicate
(because of age or developmental delay)
– The presence or absence of a full stomach
– Intravenous access

29. • IV induction preferred in high ICP
• Ensure venous cannula placement
– Thiopentone (4-7mg/kg)- most commonly used
– Propofol [2-4mg/kg] - can be used
– Except for ketamine?
– Fentanyl (1.5-2 mcg/kg) iv
• children without IV access or with difficult IV
access, inhalational induction sevoflurane
preferred

30. Muscle relaxants :
• Muscle Relaxation –sux?
• NDMR is preferred
– Rocuronium 0.6-1.2 mg/kg iv
• Atracurium - as the surgical procedure is of short
duration
– Can cause histamine release cerebral vasodilatation
 CBF incre ICP
– - Metabolite laudanosine has convulsive effect, but
dose used is too small
• Vecuronium-can cause bradycardia due to its PSN
action-better avoided

31. Maintenance of anesthesia...
• O2 +air+volatile agent
– -Isoflurane preferred, Sevoflurane can be used
– All volatile anesthetics cause an increase in CBF, and
thence the ICP
• N2O avoided:
– Significantly increase CBF  ICP.
– strong emetic effect- it may confuse pt evaluation postop
– chance of air embolism in diploic vein
• Spontaneous ventilation not recommended?
– Risk of air embolism during craniotomy
– Ventilatory depression can cause hypercarbia- raised ICP

32. Intraoperative concerns
• ECG, NIBP, Pulse oximetry, Capnography
• Chance of difficult intubation due to large
head/intubation in lateral position
• To support head a dough nut may be placed
under the head or an assistant may support the
head.
• Positioning and immobility
• Tube should be firmly secured
• Reinforced tube to be used if available

33. • Avoid hypercarbia, hypoxia, hyperglycemia
• Hemodynamic stability- usually dehydrated
– Maintain normovolemia
– H/d changes and arrhythmias during rapid drainage
• Specific issues:-
– hypothermia
– Surgical stimulation during tunnelling- short acting
opioid/ increasing depth of anaesthesia
– Scalp infiltration with LA + adrenaline analgesia &
less bleeding.

34. – Care of ET Tube - as there is chance of accidental
extubation during head manipulation, burr hole &
tunneling.
– Head is turned away from the surgeon with a pad
below operative site.
– Extreme rotation of head-impair venous return
– During shunt placement in abdomen - chance of
visceral injury
– On cannulating ventricle BP may drop abruptly as
Brain Step pressure is suddenly released Patchy
hmrge
– Prophylactic antiemetic 30-60min before extubation?

35. REVERSAL & EXTUBATION
• Neuromuscular blockade is reversed.
• Extubation done once the pt is awake
– avoid hypercarbia
– minimize risk of aspiration
• Mask oxygenation following extubation & suction
• Extubate only if child is awake, return of protective
reflexes and normothermic
• Patients that can be extubated will need
supplemental oxygen and apnea monitoring for 24-
hours

36. POST OPERATIVE MANAGEMENT
• Post-operative care and Monitoring
– Vital parameters to be monitored (pulse, NIBP, Temp.,
Respiration), urine output.
– Positioning -Supine with head up 15 degree.
– Analgesic -PCM, opioids better avoided
– Maintenance of proper hydration- by 4-2-1
– Neurological status : GCS
– Observe for signs of Increased ICP(indicate obstruction of
shunt).
• Assess pupil size
• Abdominal distention
• Respiratory distress or episodes of apnea

37. POSTOP COMPLICATIONS
Immediate postoperative :-
• Respiratory distress
– Pneumothorax
• Massive accumulation of CSF in abdomen
– Increased intra abdominal pressure
– Regurgitation & aspiration
• Deterioration of LOC + neuro deficit due to
– Intraventricular hemorrhage
– Over drainage of CSF-SDH (opposite)
• Seizure

38. Postop Complications.....
• Delayed complication:-
– Shunt malfunction- due to obstruction,
disconnection, breakage, migration
– Infection
– Hardware erosion through skin
– Conduit for extra neural metastasis of certain
tumor
– CSF bag formation at the site where shunt is
suture into subcutaneous tunnel

39. Meningomyelocele

40. Thoracolubar 85%
Dorsal 10%
Cervical 5%

41. Etiology
• Genetic
– Females are more affected
– More common in Caucasians and blacks
– Parenteral consanguinity increases incidence
• Environmental- folic acid deficiency
• Teratogenic drugs- valpraote, carbamazapine
• Higher prevalence in lower socio economic
groups

42. Pathophysiology
• Meningocele (20%) - sac containing meninges
bulges through the defect.
– Overlying skin intact.
– Neurological manifestations usually absent
• Meningomyelocele (80%) - contains neural
elements along with meninges.
– Majority of defects occur in lumbosacral area
– Neurological deficits distal to defect are most severe.
• Spina bifida occulta - absence of bony spinous
process. No clinical significance

45. Pathophysiology
• Depending on severity, manifests as neurologic,
motor and sensory deficits
• Associated congenital anomalies may be
present
• Brainstem dysfunction
• Hydrocephalus and ↑ICP

46. Associated anomalies
• Club feet- commonest
• Arnold Chiari malformation (80%-90%)
• Hydrocephalus (80%)
• Neurogenic bladder(90%)
• Musculo skeletal defects
• Urogenital anomalies
• Facial clefts
• Umbilical hernia
• Congenital heart diseases - rare

47. Clinical features
• Fluid filled swelling at back
• Paraparesis with muscle wasting
• Sensory symptoms
• Neurogenic bladder and bowel
• Convulsions/ tonic spasms
• Cranial nerve dysfunctions

48. Complications
• Rupture of sac during birth process
• CSF leak
• Raised ICP- vomiting, convulsions, altered
sensorium, irritability
• Infection - fever, unconsciousness, altered
sensorium (meningitis)

49. Diagnosis
• Prenatal
• Acetyl cholinesterase and alpha fetoprotein in
maternal serum and amniotic fluid in 2nd
trimester)
• Prenatal ultrasound picks up the defect in
100% of the cases
• Many are now scheduled electively before
birth for repair

50. Management
• Management of neural tube defects requires
team approach with cooperation of
pediatrician, neurologist, neurosurgeon and
anesthesiologist
• Surgery is mainstay of treatment and includes
repair of the defect and a VP shunt ( if
associated with hydrocephalus)

51. Management...
• Meningomyelocele is repaired within first day
or two of life. Why it is an emergency?
– Rupture of sac
– Spinal cord vulnerable to infection
– Sepsis commonest cause of death
– Surgery < 24 hours for open defects which
minimizes bacterial contamination and further
neurological damage
– Closed lesions should be operated within 48hrs

54. Pre Anesthetic Evaluation
• Neurological impairment including
– Cranial nerve function and ability to protect airway
– Neurological deficits
– signs of ↑ICP
• Volume status and IV access
• Any drug therapy
– Steroids
– Mannitol, diuretics
– Anti - convulsants

55. Pre Anaesthetic Evaluation
• Investigations
– Hb, Blood Grouping and Cross Matching
– X Ray chest ( if required)
• Pre ор preparation
• Pre ор advice
– Explain NPO to parents
– Adequate hydration to be maintained
– Usually no pre medication is required

57. Induction of anaesthesia
• Intubation is a challenge
– In most cases, Supine position- with sac resting in a
donut shaped cushioned ring and weight of child
supported on pelvis and portions of spine not involved
with the defect
– For large defects, Lateral position- with head held in
midline by an assistant
• Assistant must be available to ensure that no
physical trauma to neuroplaque occurs

60. • Induction may proceed by mask inhalation or by
IV administration of thiopental, propofol,
glycopyrrolate, and a muscle relaxant.
• Either a NDMR or sux can be used Safely
• Difficult airway-awake intubation with atropine
premedication (20mcg/kg, minimum 0.1 mg)
and preoxygenation
• Intubation with reinforced tracheal tube is
recommended

61. Maintenance of anesthesia
• Patient positioning - prone position
• Abdomen should be free - rolls under chest and
pelvis
• Excessive rotation/flexion of the neck avoided
brainstem compression, rise in ICP
• Extremities relaxed and padded
• Eyes protected with ointment and thick pads

62. Maintenance ....
• Anesthetic agents
– 60% N20 in O2 with Isoflurane/Sevoflurane
– Analgesia maintained with IV Fentanyl. Avoid high
dose opioids- risk of post operative apnea
• Muscle relaxants
– NDMR (Atracurium, Vecuronium)
– Used with caution when nerve stimulation is used to
identify neural structures

63. • Ventilation
– Maintain normocapnia
– Prevent barotrauma
– Avoid prolonged exposure of high FiO2
• Fluid management
– IV fluids - RL is used, IV dextrose solution5% if patient
is hypoglycemic
– High third space losses
– Blood loss is not excessive a bout 30 ml, or 10% of
blood volume??.

65. Latex allergy
• Myelodysplasia patients are at high risk of
developing allergic reactions to latex.
• Due to repeated exposure to latex products
during surgery, or repeated bladder catherization
• To prevent early sensitization, myelomeningocele
patients should be treated as1st if they are latex
allergic
• Manifests as hypotension and wheezing with or
without rash

66. Latex allergy
• Anaphylaxis should always be anticipated
• Treatment - removal of source of latex and
administration of IV fluids and vasopressors
• Post operatively, respiratory status should be
carefully assessed.
• Prone to develop allergic reactions to other
substances later in life

68. Emergence and postop care
• Elimination of anesthetic agents
• Reversal of neuromuscular blockade
• Assessment of airway patency
– Neonates at risk for apnea and extubated fully awake
• Oxygen therapy
• Nursing in prone/ lateral position
• Pain relief by IV fentanyl, PCM suppositories
• Watch for signs of brain stem dysfunction and ↑ICP

69. Anesthetic Considerations for
Craniosynostosis repair

70. Craniosynostosis: Definition
• Premature fusion of one or more cranial sutures,
resulting in abnormal skull development and
head shape and constitutes a diverse group of
deformities
• Growth of skull perpendicular to the affected
suture is restricted
• Compensation in growth occurs parallel to the
affected suture so brain growth can continue

71. Classification
• Overall incidence: ~1 : 2,000 live births
• Simple (non-syndromic: sagittal, coronal,
metopic, lambdoid) – single suture
• Compound/complex: Non-syndromic with
multiple sutures or syndromic

72. •

73. Anatomic Variations
• Trigonocephaly: fusion of the metopic suture that runs
from the top of the head toward the nose (5-15% of
cases)
• Scaphocephaly: The sagittal suture that runs from to
back on top of the skull (40-55% of cases)
• Plagiocephaly: a fusion of either the right or left coronal
suture (20-25% of cases)
• Brachycephaly: fusion of both coronal sutures

76. Pathogenesis
• Exact etiology is unknown
• Intrauterine constraint of fetal head
• Metabolic and hematological disorders (rickets,
hypothyroidism, polycythemia vera, thalassemia)
• Teratogens (nicotine, retinoic acid, valproic acid,
SSRI)
• Genetic defects
• Sporadic in most instances

77. • Potential risk factors :
– White maternal race
– advanced maternal age
– male infant vs female
– maternal smoking
– maternal residence at high altitude
– use of amine containing drugs (e.g. nitrofurantoin,
chlordiazepoxide)
– certain paternal occupations (e.g. agriculture and
forestry, mechanics)
– fertility treatments

78. Clinical Features and
Complications
• Elevated intracranial pressure (ICP)
• Disturbances in intellectual and neurologic
development
• Brain growth (developmental delay)
• vision (impairment)
• Midface hypoplasia: associated with OSA, airway
complications, exorbitism
• cosmetic appearance

79. INFANT SKULL
• Flexible- to get through the birth canal
• Expansile- to accommodate rapidly growing
brain
• The calvarial sutures serve 2 important functions
– (a) maintenance of head malleability &
– (b) growth sites
• 90% of adult size achieved by age of 1 year
• 96% by the age of 6 years

80. Syndromes Associated with
Craniosynostosis
• Most show an autosomal dominant pattern of
inheritance
• Most commonly associated with
craniosynostosis:
 Apert
 Crouzon
 Pfeiffer
 Others: Saethre-Chotzen, Muekne

81. Apert Syndrome:
Anesthetic Implications
• Airway
 Midface hypoplasia
 Choanal stenosis/atresia
 Tracheal stenosis
 High arched palate
 C5-6 fusion
• Cardiovascular
 10% have congenital heart
disease
 Pulmonary stenosis
 ASD/VSD
 Tetralogy of Fallot
• Genitourinary
10% have renal abnormalities
• Neuromuscular
Possible cognitive delay
Craniosynostosis
Corpus callosum agenesis
May have increased ICP
• Pulmonary
40-50% have OSA
• Syndactyly
 Difficult IV access

82. Crouzon Syndrome:
Anesthetic Implications
– Relative prognathism
 Possible difficult mask ventilation
– Possible difficult intubation secondary to high-
arched palate, retrognathism and other
dysmorphic features
– Over sedation may result in upper airway
obstruction
– Ocular proptosis requires careful attention to eyes
and adequate protection

83. Pfeiffer Syndrome:
Anesthetic Implications
• All major sutures and skull base involved
 Increased ICP more common, as are Chiari malformations
and hydrocephalus
• OSA
- Monitor for airway obstruction
• Difficult airway management rare
• Proptosis requires careful attention to eyes

84. Indications for Surgery
• Increased ICP
• Severe exophthalmos
• OSA
• Craniofacial deformity
• Prevention of neurologic sequelae
• Psychosocial concerns

85. Timing of Surgery
• Emergency surgery required in cases of
raised ICP
• Benefits of early surgery (4-6 months of age)
include softer, more malleable bone and
continued growth of cranial vault
• Disadvantages include risks of anesthesia in a
younger patient, potential for increased
relative blood loss
 Surgery generally performed between 6-12 months of age

86. Surgical Techniques
Strip Craniectomy
• Cranial vault split into multiple segments
• Allows skull to grow with brain
• Requires protective helmet post-op
• Used for children less than 6 months old
• May be done endoscopically

87. Surgical Techniques
Spring Assisted Cranioplasty
• Used in infants 4-6 months
• Midline osteotomy along sagittal suture
 Springs placed to increase dimensions
• Advantages
 Lower transfusion requirement
 Shorter surgery, faster recovery

88. Surgical Techniques
• Removal of plates and
reconstruction
• Longer surgery
• Higher blood loss
• Specific procedures
include:
 Frontal advancement
 Posterior vault
expansion
Total Vault Reconstruction, fronto-orbital
remodeling

89. Preanesthesia assassment
(A) Detailed history:-Birth history, sleeping position
• H/O OSA: daytime somnolence, behavioral
changes, snoring
• 40% to 80% syndromic infants (Zandieh et. al.
2013)
• Cardiac anomaly: h/o sweating with feeds,
cyanosis, and syncope,
• Family history abnormal head shape or multiple
systemic problems

90. DIAGNOSIS: (B) CLINICAL EXAMINATION
• Head Circumference (micro/macrocephaly)
• Head shape (from above, side)
• Palpate suture lines & fontanelles (Look for ridging)
• Ear and facial symmetry, neck, spine, digits, and
toes, hands & feet
• Look for associated anomalies
• Subacute bacterial endocarditis (SBE) prophylaxis?
• Check airway if possible (infant)
• Identifying potential IV and arterial access sites

91. DIAGNOSIS: (C) RADIOLOGICAL EVALUATION
• Plain radiography-AP and lateral views of the
skull- bony bridging across the suture,
straightening and narrowing of the suture
• CT scan Head: more accurate, structural
abnormalities.
• USG: Non invasive, Accuracy depends on a
reliable and experienced operator
• MRI: Complex craniosynostosis, improved
definition of intracranial soft tissue structures
• ICP monitoring

92. PERIOPERATIVE CONSIDRATION.
• Most patients with non-syndromic craniosynostosis
are otherwise healthy
– Preoperative testing for these, should generally include a
CBC and BG and cross
– Coagulation profile routinely performed at some centers
• Syndromic craniosynostosis may be associated with
midface hypoplasia or retrusion resulting in OSA and
other perioperative airway considerations
• Use preoperative sedatives with caution in the
setting of severe obstructive disease

93. PERIOPERATIVE CONCERNS...
• Syndromic concerns- associated systemic anomalies
– Difficult airway, OSA, Bronchospasm, kinking of ET
– Difficult IV access
– Positioning
– Ophthalmologic
– Blood loss
– VAE
– Hypothermia
– Long duration of surgery- facial, tongue edema, pushing
out ET
– Metabolic and electrolyte disturbances

94. MONITORING
• Standard ASA monitors:- ECG, BP, SPO2, TEMP
• Cardiac output monitoring
• Arterial line/ CVP
• Co-oximetry
• ABG/ ROTEM
• Precordial Doppler
• Urine output

95. INDUCTION, AIRWAY MANAGEMENT, &
ANAESTHETIC MAINTENANCE
• Airway management challenging FVFI
• Alternative airway management techniques (e.g.,
LMA, FOB with DA cart, tracheostomy?)
• RAE tube for sphinx position/armored tubes
• Induction: Inhaled commonly performed, if ICP high
go for IV induction propofol, fentanyl..
• In the presence of increased ICP, avoid
– sedative premedication, ketamine, succinylcholine,
hypercapnia, hypoxemia, and arterial hypotension.

96. • POSITIONING :-Supine, Prone, Sphinx (modified
prone)
• Spinal cord injury d/t hyperextended neck
• Proper padding pressure points
• Lifting head for 15sec every 15 mins
(recommended)
• Secure ET / avoid kinking/check airway pressure
• Check eye position/ tarsorrhaphy
– Generally surgeons want eye to be accessible
– Apply eye ointment periodically
– Proptosis may need tarsorrhaphy
• Forced air warming, blanket

98. BLOOD LOSS MANAGEMENT
• Prone to massive blood loss due to:
– duration of the procedure,
– large surface of exposed skin, bone, and dural surfaces, and
– rare complication of injury of large vessels like sagittal sinus
• Nearly 90% to 100% of infants need blood transfusion
• Predictors of excess blood loss:
– surgery time > 5 hours
– age < 18 months
– multi-suture craniosynostosis and syndromic craniosynostosis
• Intraoperative assessment of BVL is difficult

99. REDUCING BLOOD LOSS
• Surgical techniques that minimize blood loss include using
– infiltration of subcutaneous epinephrine
– needle tip cautery
– scalp clips for the scalp flap
– bone wax for the osteotomy edges
– Fibrin sealants or fibrin glue
• Cell saver (reduces blood unit transfusion by 1 unit)
• Preoperative acute normo-volemic hemodilution >6month
• Preoperative autologous donation
• Recombinant human erythropoietin (EPO) given S.C.
weekly for 3-4 weeks prior to surgery

100. Transfusion related concerns:
• Allergic/febrile/hypersenitivity reactions
• Metabolic/electrolyte derangements (hypocalcemia,
hyperkalemia in the setting of massive transfusion)
• Transfusion-associated Lung Injury (TRALI)
• Transfusion-associated circulatory overload (TACO)
Blood Management (continued)

101. FLUID DEBATE
• Lactated Ringer appears unsuitable for pediatric
patients at risk for brain edema (e.g.: neurosurgery,
head trauma, CNS infection), overt or latent Cl-
deficiency (e.g.: vomiting, salt losing renal tubular
disorders, electrolyte disturbances due to diuretics)
• In these two conditions, saline still remains the
solution of choice
• Balanced crystalloids also have higher chloride
than reqd

102. Venous Air Embolism (VAE)
Causes:
 Surgical field above heart with open sinusoids
 CVP decreased due to hypovolemia (bleeding) – air
entrained due to pressure gradient formed between
the surgical site and the right atrium
Diagnosis:
 A precordial doppler may assist in early detection
Hemodynamically significant VAEs rare (resulting from
RV outflow obstruction), and may be heralded by
hypoxemia, hypotension, decreased or absent end-tidal
CO2, cardiac arrest in extreme cases)

103. Prevention:
 Surgeon should apply bone wax to open edges of bone
Limit head down, but remember that even when supine,
children may be at risk due to their larger heads
Treatment
 Notify surgeon to flood surgical field
 Lower surgical field relative to heart
 Increase central venous pressure with crystalloid, colloids, blood
products as indicated
 IV epinephrine may be necessary in the setting of hypotension
 Aspirate air from central venous catheter if placed
Venous Air Embolism (continued)

104. POSTOPERATIVE CARE
• Extubation: Most patients are extubated at the
completion of surgery in OT/ ICU
• Conditions for delay extubation : difficult airway cart
ready when extubating
– prolonged procedure
– marked fluid shifts
– large-volume transfusions
– effects of prolonged prone positioning and
– patient factors such as: preoperative obstructive sleep
apnoea or airway concerns
– Mechanical ventilation/ tracheostomy
– Obstructive sleep apnea/delayed awakening

105. Postoperative Considerations
• Analgesia best achieved with combination of
acetaminophen and IV opioids (PRN or continuous
infusion, such as nurse-controlled analgesia [NCA])
• Local infiltration by the surgeon may be utilized to
supplement
• Adequate pain relief with opiates and PCM
–Monitor for airway obstruction, electrolyte
disturbances (hyponatremia), and anemia/coagulation
abnormalities from blood loss

106. References
• Smith’s Anaesthesia for Infants and Children, 7th Edn.
Philadelphia: Mosby; 2006.
 Miller’s Anesthesia 9th edition volume 2
 Morgan & Mikhail’s Clinical Anesthesiology 6th Edition
• Durham EL, Howie RN, Cray JJ. Gene/environment interactions in
craniosynostosis: a brief review. Orthod Craniofac Res. 2017
• Hughes K, Thomas K, Johnson D et al. Anesthesia for surgery
related to craniosynostosis. Part 2. Pediatr Anesth 2013: 22-7
• Pearson A, Matava CT. Anaesthetic management for
craniosynostosis repair in children. BJA Educ 2016;16

107. • Stricker PA, Goobie SM, Cladis FP et al.
Perioperative Outcomes and Management in
Pediatric Complex Cranial Vault Reconstruction:
2017;(126):276-287
• Thomas K, Hughes C, Johnson D et al. Anesthesia
for surgery related to craniosynostosis. Part 1.
Pediatr Anesth 2012(11): 1033-41
• White N, Bayliss S, Moore D. Systematic review of
interventions for minimising perioperative blood
transfusion for surgery in craniosynostosis. J
Craniofacial Surg, 25 (2015), pp. 126-136