Radiation Dosimetry Parameters and Isodose Curves.pptx
Anaesthesia Management of Posterior cranial fossa surgeries
1. Anaesthetic management of posterior
cranial fossa surgeries
21-Apr-14 1
Moderator:
Dr.Uma.B.R
Associate professor,
Department of anaesthesia,
JJMMC,Davangere.
Presenter:
Dr. Naven Kumar .S
PG in Anaesthesia
2. Introduction
The duramater is folded on itself
to form partitions which divide the
cranial cavity into compartments
which lodge different parts of
the brain.
The various folds are falx
cerebri, falx cerebelli,
diaphragm sellae and the
tentorium cerebelli.
Tent shaped fold of dura mater
21-Apr-14 2
4. Posterior Fossa Surgery
Posterior cranial fossa: It is the
deepest and most capacious of the 3
cranial fossae.
It contains the cerebellum, pons, and
medulla oblongata with many vital
centers.
Tumors in the posterior fossa are
considered critical brain lesions.
This is, primarily, because of the
limited space within the posterior
fossa and the potential involvement
of vital brain stem nuclei21-Apr-14 4
6. Anatomy
Boundaries :
Anteriorly : clivus, petrous part
of temporal bone
Posteriorly : occipital bone
Laterally : squamous and
mastoid part of the temporal
bone
Superiorly : tentorium cerebelli
Inferiorly : Foramen magnum
21-Apr-14 6
7. Contents :
Cerebellar hemispheres, large
portion of the brainstem (lower
midbrain, pons and upper medulla)
3rd to 12th cranial nerves nuclei
and many efferent and afferent
fiber tracts that connect the
brain with the rest of the body.
Blood supply :21-Apr-14 7
9. Tumors arising from the
structures above the
tentorium cerebelli are
called supratentorial (80%)
and those arising from below
are called infratentorial
tumors(20%).
Supratentorial are seen more
commonly in adults and
infratentorial are seen more
commonly in children.21-Apr-14 9
13. Cerebellar Herniation Through Foramen Magnum
21-Apr-14 13
Vomiting Opisthotonus
Head tilt Downbeat nystagmus
(vertical nystagmus)
Meningismus Bulbar palsies with
vocal cord paralysis
Muscle spasm
Skew deviation of the
eyes
typical ‘posturing’
from tonsillar
herniation may be
14. Cerebellar herniation:
Swallowing and gag dysfunction
Occipital headache
Neck pain
Coughing may induce paroxysms of
increased symptoms including loss of
consciousness as the tonsils are further
impacted into the foramen magnum
Further herniation compresses the
medulla
irregular respiration and death may21-Apr-14 14
15. Success with surgical intervention
has become possible because of:
1.Advances in imaging and
microsurgical techniques
2.Improved understanding of
physiology
3.Advances in perioperative care
of the patient
4.Excellent anaesthetic
techniques available21-Apr-14 15
17. Goals of Anaesthesia
1.Preserve both injured &
uninjured cerebral territories
by global maintenance of
cerebral homeostasis.
2.Maintain normocarbia,
normotension, normoxia,
euthermia, euglycemia.
3.Avoid secondary brain insults
4.Optimizing operative conditions21-Apr-14 17
18. Anaesthetic implications
Depending on type (vascularity) and location
(supra/ infratentorial) of tumor
Supratentorial
ICP management
Monitoring brain function
Massive intraoperative
hemorrhage
Seizures
Air embolism (if venous
sinuses traversed)
Infratentorial
Positioning
Care during vital
structure handling
Air embolism
Higher mortality
21-Apr-14 18
20. Tumors
Disruption of cerebral
autoregulation
BP fluctuation poorly tolerated
↑BP – Vasogenic edema, ↑ tumor /
aneurysm size, aneurysmal
rupture
↓ BP – Ischemia/ infarction
WHY CONTROL BP ?
21-Apr-14 20
21. Pre Op Assesment:
HISTORY
Level of consciousness
Seizures - ↑ CMRO2 , ↑ ICP
↑ ICP – headache, vomiting, blurred
vision, ocular palsy (CN 6)
Hydration – fluid intake, NPO status,
diuretics
Focal neurological signs
Paraneoplastic syndromes
Regurgitation of solids and liquids
Disturbances in balance and
21-Apr-14 21
22. •History of drug intake:
I.Diuretics-elecrolyte
disturbances
II.Steroid therapy-hyperglycemia
(cerebral ischemia),HPA
suppression,mucosal effect on the
GIT
III.Antiepiletic drugs-phenytoin,
carbemazapine increase the dose of
NMJ blockers21-Apr-14 22
25. a)Cardiorespiratory status evaluation-)
Respiratory- effect of positioning, resp.
pattern, neurogenic pulm. Edema
Significant for elderly and those with
cardiac disease
Limited cardiorespiratory reserve may
limit the positioning
Risk of orthostatic hypotension
increased in people with uncontrolled
hypotension
CVS – HTN (resets limits of cerebral
autoregulation), BP (cerebral
b)Evaluation for patent foramen ovale-
21-Apr-14 25
26. Investigation:
For surgery:
1. Complete hemogram
2. Blood sugar(hyperglycemia –
cerebral edema , ↑ischemic brain
injury),Electrolytes
3. Renal function tests
4. Coagulation profile
5. ECG – ischemic changes, arrhythmias
6. CXR, Cervical spinal x-ray if planned
for sitting position
21-Apr-14 26
27. For diagnosis of lesion: various
modalites like CT/MRI are used in
imaging of tumour helps in anaesthetic
plan
21-Apr-14 27
Location Silent/Eloquent Area
Size Degree Of Compromise Of
Intracranial Dynamics
Including Auto Regulation
Midline Shift Ventricular
Distortion/Csf
Obstruction
Perilesional Edema Makes Tumor Functionally
Better
Contrast
Enchancement
Degree Of Bbb Disruption
Proximity To Venous
Sinuses
Blood Loss
28. Premedication
Advantage
It can decrease
the stress
ICP
vasogenic edema
Disadvantage
Hypercapnia
Hypoxia
Airway
obstruction ICP
21-Apr-14 28
Midazolam- 0.5mg to 2.0mg i.v
Fentanyl -1-2 μgm/kg
Sufentanil – 0.1- 0.4μgm/kg iv
29. Premedication
Steroids should be started atleast 2-3
days before an elective surgery and
continued upto the day of surgery
In case if HPA axis supression 100mg
methylprednisolone should be given
before surgery
H2 blockers – ranitidine – 50mg iv
Prokinetic agents - metoclopramide
10mg iv
Anticonvulsant therapy – phenytoin –
loading dose 10-15mg/kg iv and the21-Apr-14 29
32. Electrophysiological monitoring during
posterior fossa surgery:
Information about the integrity and
function of spinal cord, brainstem,
cranial nerves and cortex can be
obtained to assist in detecting
intraoperative compromise or to predict
postoperative function.
EEG, Somatosenory evoked potentials
(SSEP), Motor evoked potentials (MEP),
and BAER and cranial nerve monitoring
can be used singly or in combination.
21-Apr-14 32
33. Special monitoring
SSEP useful for detection of
cervical cord ischemia or stretch
injury in sitting position.
Volatile anesthetic agents, N20,
physiologic changes and
temperature may affect the
latency and amplitude of cortical
components.
Also damage to posterior
descending motor tracts may be
21-Apr-14 33
34. Special monitoring
BAER: Brain stem auditory evoked
responses are robust and are
resistant to depressant effects
of anesthetics.
Monitoring of BAER provides a
means of assessing
intraoperative function of eighth
cranial nerve and brainstem.
21-Apr-14 34
35. Special monitoring
Facial nerve potentials: Facial
motor evoked potentials (MEP)
occur when facial nerve is
stretched or stimulated
successful preservation of facial
nerve during resection of CP
angle tumors has been reported
using Facial MEP. Use of muscle
relaxants must be limited during
these procedures.21-Apr-14 35
36. Induction
GOALS – Normotension, Normocarbia,
Normoxia
Preoxygenation
P/M – opioid (fentanyl 1-2 μg/kg )
I/W – Thiopentone (3-5 mg/kg)
Propofol (1.5 – 2.5 mg/kg)
Myorelaxation – Sch (transient ↑ ICP)
Use intermediate acting relaxants
Atracurium – histamine release ( cerebral vasodilatation)
Vecuronium, Rocuronium – commonly used
Only after adequate muscle relaxation achieved, perform quick + gentle laryngoscopy
Intubation – armoured ETT
Tape on opposite side of surgery
Bandaging may ↓cerebral venous return
Controlled ventilation
Lignocaine , Esmolol, 2nd
dose of i.v induction agent
60-90 sec earlier
21-Apr-14 36
37. Positioning
GOAL- Slow and gentle positioning with 15-
20⁰ head up tilt to aid cerebral venous drainage
Verify cautiously – 1. All potential pressure points p
2. Eyes protected & padded
3. Peripheral pulses palpable
4. Nerve compression absent
5. Ventilation adequate ( PEEP, ETT posit
ETT – Kinking in post. Oropharynx
Advancement / extubation
Neck – Extreme rotation / flexion may cause ↑ ICP,
quadriparesis, tongue swelling
Head pins – Adequate plane of anaesthesia
Local infiltration / bolus opioid (fentanyl)
21-Apr-14 37
38. Positioning
It very important in posterior
cranial fossa surgeries as it
causes various hemodynamics
changes
Positioning per se will be
discussed after the anaesthetic
part
21-Apr-14 38
39. Dural opening in presence of high ICP –
- sudden decompression &
transcalvarial herniation
- herniated tissue cannot be
interposed back
- permanent neural damage
ICP to be brought within normal limits
before opening the dura.
Methods – head elevation, mannitol,
Optimization of ICP
21-Apr-14 39
41. Mannitol (20%)
Hyperosmolar agent
Dose : 0.5 – 1g/kg i.v. (0.5-1 g/kg over
15 min just before opening dura)
Action reaches peak at 20-30 min.
Advantages : Draws water from
brain (↓ brain bulk)
↓ Hct (↑CBF , O2 delivery)
Disadvantages: 1. Transiently ↑
intravasular volume
2. Hypokalemia21-Apr-14 41
Management of ICP
42. Furosemide
Loop diuretic (Na K 2Cl channel
blocker)
Dose : 0.5 – 1 mg/kg i.v.
Steroids
Dexamethasone 8mg iv stat followed
by 4mg q6h
21-Apr-14 42
Management of ICP
43. CSF drainage
1. Lumbar subarachnoid drainage
system
2. Ventriculostomy drain (EVD)
(connected by tubing to a CSF
collection device which can be
elevated or lowered)
CSF drainage (↑ICP, aneurysm / ENT
surgeries)
ICP measurement
CSF drainage
– Slow
– bolus ≤ 20-30 ml
Complications
– herniation
– infection
21-Apr-14 43
44. Maintenance OF
Anaesthesia
ANAESTHETIC
AGENT
VOLATILE
ANAESTHETIC
I.V. ANAESTHETIC
PROS 1. Easy
2. Extensively
available
1. Intact CBF – CMRO2
coupling
2. ↓brain bulk
CONS 1. ↑ICP 1. Short acting
RECOMMENDATION 1. Use in short,
uncomplicated
surgeries
2. At < 1.5 MAC
3. Avoid
combination
with N2O
1. Use in cases with
high risk of ↑ICP/
brain bulk
21-Apr-14 44
45. Commonly used technique are opioid-
inhalation anesthetics-NMBA or nitrous
oxide -opioid -NMBA techniques along
with controlled ventillation.
Isoflurane and sevoflurane are the
preferred inhaled anesthetics (do not
increase the CBF upto 1-1.5 MAC.)
Concomittant use nitrous oxide and
volatile agents is avoided due to
increase in the CBF.
21-Apr-14 45
Maintenance OF Anaesthesia
46. Maintenance (cont…)
FLUID THERAPY
Principle – BBB is selectively permeable
Water crosses freely, most ions
(Na+) don't.
If BBB disrupted (ischemia, head injury,
tumors) – hyperosmolar agents may ↑brain
water instead of drawing water out.
21-Apr-14 46
50. Reversal
Most patients undergoing craniotomy
can be extubated if neurological
status is intact.
Extubation as smooth, without coughing
,straining or bucking against the
tracheal tube.
To avoid bucking muscle relaxation
should be reversed after the head
dressing .
Inj lidocaine 1.5mg/kg iv or esmolol
1mg/kg can be given to suppress the
hemodynamic responses.
Neuromuscular blockade reversed with
21-Apr-14 50
51. Emergence
Most important but often neglected
“ A well planned procedure is often
rewarded by a fully awake patient who is
appropriately responding to verbal
commands and neurological
examination.”
Due to pain and shivering, associated with
•↑ catecholamine release
•↑ O2 Consumption
AIMS
To maintain intra + extracranial
homeostasis
(MAP- CPP- CBF- ICP- CMRO2 - PaO2 - PaCO2-
temp)
Avoid intracranial bleed ( coughing,
ventilator fight)
21-Apr-14 51
52. Emergence (cont…)
EARLY AWAKENING LATE AWAKENING
1.Early
neurological
examination &
reintervention
2.Less ↑BP/
catecholamine
burst
3.↓ cost of postop
1.Less risk of
↓O2,↑CO2
associated with
anaesthesia
hangover
2.Better
respiratory &
hemodynamic
control21-Apr-14 52
53. Emergence (cont…)
Checklist for early extubation
1. Good preop GCS (>8)
2. CVS stability + normothermia + normoxia
3. Durationbrain surgery
4. No extensive post fossa manipulation ( CN
9 – 12)
21-Apr-14 53
54. Indication of late extubation
1. Low GCS
2. Inadequate airway control
3. Intraop catastrophe
4. Brain edema/ deranged cerebral
homeostasis
(long duration/ extensive/ repeat
surgery)
5. Surgery around vital areas
Emergence (cont…)
21-Apr-14 54
56. Immediate postoperative concerns (cont….)
2. Post operative care
a) Head end elevation (15-30⁰)
b) Adequate ventilation & oxygenation
c) Monitoring of neurological function
d) Check for serum electrolytes and
osmolarity (mannitol, frusemide to
continue)
e) Seizure prophylaxis (phenytoin /
fosphenytoin)
f) Seizure treatment (thiopentone 50-100
mg, midazolam 2-4 mg , lorazepam 2 mg)
21-Apr-14 56
57. Immediate postoperative concerns (cont….)
g) SIADH
Hyponatremia, S. hyposmolarity,
high U. osmolarity
T/T restrict free water intake
h) DI
After pituitary surgery
Hyponatremia, S. hyposmolarity,
low U. osmolarity
T/T ↑ water intake, vasopressin ,
desmopressin
i) Tension pneumocephalus
Skull X ray / CT
T/T opening the dura
21-Apr-14 57
58. Concerns:
Cranial nerve palsies (IX, X) may
impair gag reflex- aspiration
Hydrocephalus
Cerebellar dysfunction
Edema in floor of fourth ventricle-
damage to resp. centers
Bradycardia and hypertension – due
to V nerve stimulation (resolve with
cessation of stimulus)
Bradycardia, asystole/21-Apr-14 58
60. Sitting Position
Advantages:
– Excellent surgical access
– Facilitates hemostasis (decreased
blood loss)
– Improved venous and CSF drainage
– Exposes face for monitoring
response to cranial nerve
stimulation (though this can also
be done electronically
21-Apr-14 60
62. Physiologic changes in sitting position
CVS-decreased MAP,SBP,SV,CO,CI,PCWP,
reflex tachycardia, and increased
SVR
RS-Increased FRC ,FVC, easier
diaphragmatic excursion, lower
airway pressures.
CNS-decreased CBF&CPP. MAP
decreases by 0.77mmHg for every cm
gradient above the heart
In patients who cannot tolerate an21-Apr-14 62
64. Sitting Position
Patient is semi recumbent
Back increased to 60 degrees
Leg elevated to promote venous return
Knees flexed at level of the heart
Head is fixed in a three point holder
with the neck flexed
Poles have to be attached to the back
of the table (thoracic piece)-easy for
resuscitation
Arms remain at the sides with hands
resting on the lap21-Apr-14 64
65. Optimized sitting position—the legs are elevated to the level of the heart.
Engelhardt M et al. Br. J. Anaesth. 2006;96:467-472
21-Apr-14 65
66. Sitting Position
Measures to avoid hypotension
Pre-positioning hydration
Wrapping of legs with elastic
bandage to counteract
gravitational shifts of blood
Incremental adjustment of
table position
Pressor administration may be
required
21-Apr-14 66
67. Lateral Position
Increased risk of bleeding from the
sinuses(transverse and sigmoid)
Less incidence of air embolism
Shoulder roll-to protect the inferior
shoulder and axillary neurovascular
structures
Lateral popliteal nerve palsy
The superior shoulder in broad
shouldered or short neck patients may
hinder surgeons line of sight21-Apr-14 67
68. Prone Position
Useful for lesions at or near the
midline or near the fourth
ventricle
More commonly used in children
Head is usually elevated to assist
in gravity dependent venous
drainage
Does not avoid problems of
hypotension or air embolism
21-Apr-14 68
69. PARK BENCH POSITION
Allows rapid access to the
cerebellar hemisphere-rapid
positioning
Used for both lateral and midline
lesions
By turning prone, the upper
shoulder is moved out of the
surgeons way
High risk of neck twisting and
venous obstruction
21-Apr-14 69
71. Venous Air Embolism (VAE)
Facilitation of air entry by sub
atmospheric pressure in an opened vein
Presence of non collapsible venous
channels such as diploic veins and dural
sinuses
Children experience greater haemo
dynamic derangements from VAE than
adults
21-Apr-14 71
72. Severity Of VAE
Depends on:
Rate and volume of air entrained
Degree of head elevation
Negative pressure between RA and
surgical site
21-Apr-14 72
73. Pathophysiology Of VAE
Slow continuous entrainment-
mechanical obstruction and local
hypoxemia, reflex vasoconstriction
& pul HTN, decreased venous return
and CO
Release of cytokines &
inflammatory mediators , further
vasoconstriction &
Bronchoconstriction.
Hypoxemia, increase dead space
ventilation, impaired gas exchange,
increased airway pressure.
21-Apr-14 73
74. Pathophysiology Of VAE
Rapidly entrained air bolus
results in air lock within the right
side of the heart
Volume of 5ml/kg exceeds the
pulmonary arterial capacity
Blockage of RVOT ,acute RV
dilatation and failure, myocardial
and cerebral ischemia,
dysrhythmias and cardio vascular
collapse21-Apr-14 74
75. Diagnosis of VAE
Hypotension
Dysrhythmias
Tachycardia
Drop in etCO2
21-Apr-14 75
77. Detection of VAE
Esophageal stethoscope
– Mill wheel murmur
Precordial Doppler
– Most sensitive noninvasive device
(0.2ml/kg)
– 2.5 MHz continuous ultrasonic signal
– Small volumes of air are detected
as air is a good acoustic reflector
– Place just to the right of sternum
above the xiphoid between second –
fourth intercostal space21-Apr-14 77
78. Detection of VAE
Capnography
– Has a specific role for air embolism
– Detects increased arterial to end-
tidal CO2 gradient
End tidal Nitrogen monitoring
– More specific for air
– Earlier detection than ETCO2
Pulmonary artery catheter
– Detects pulmonary hypertension
resulting from mechanical
obstruction
21-Apr-14 78
79. Detection of VAE
Transesophageal echocardiography
– 3.5 – 5 MHz probe
– Detects even 0.02ml/kg of air when it
is in the right side of the heart
– Used for screening anesthetized
sitting patient for PFO
Transcranial monitoring of MCA
Standard of care – Precordial doppler
and etCO2
21-Apr-14 79
81. Prevention of VAE
No maneuver is 100% effective
Incidence is decreased by
– Adequate hydration
– Avoiding hypovolemia
– Proper wrapping of lower extremities
– Good surgical exposure with careful
dissection
– Liberal use of bone wax
– Avoidance of nitrous oxide
– Minimizing head elevation
21-Apr-14 81
82. Management of VAE
Prevent further air entry
– Notify surgeon
– Pack or flood surgical field
– Jugular compression
Change patient position
–Lower head end
–Lateral position with right
side up (Durant position)
21-Apr-14 82
83. Management of VAE
Treat intravascular air
– Aspirate via right heart catheter
– Discontinue nitrous oxide
– FIO2 of 1
– Pressors or inotrope to support
cardiovascular instability
Chest compressions
21-Apr-14 83
84. Treatment of VAE
Postoperative Goals
– Provide supplemental O2
– Perform ECG, chest X ray
examination
– Measure serial arterial blood
gases
– If arterial air emboli are
suspected, provide hyperbaric
compression if available21-Apr-14 84
85. Paradoxical Air Embolism
Passage of air across the
interatrial septum through a
probe patent foramen ovale
PFO present in 25% of all adults
Incidence of 5-10%
Predisposing factors- significant
increase in pressure in the right
side of the heart and hypovolemia
TEE -more sensitive in picking up PFO
21-Apr-14 85
86. Pathophysiology
Occurs when RA pressure is more than LA
pressure.
Pressure gradient required to open a
PFO is 5 mm of Hg.
Use of PEEP increases the incidence of
PAE.
Consequences of PAE- systemic emboli
(cerebral and coronary emboli)
21-Apr-14 86
87. PNEUMOENCEPHALUS
Presents as delayed awakening or
non awakening in the immediate
post operative period or as severe
headache
Air enters the supratentorial
space in the upright position
Use of nitrous increases the
incidence of Pneumoencephalus
Diagnosis- brow up lateral
radiograph21-Apr-14 87
88. Brainstem Stimulation
Irritation of lower portion of
pons, upper portion of medulla
and extra axial portion of the
5th cranial nerve
Manipulation of 9-12th cranial
nerves
Bradycardia with hypotension
Tachycardia with hypertension
Ventricular dysrhythmias21-Apr-14 88
89. Quadriplegia
Neck flexion resulting in
stretching or compression of the
cord
Patients with degenerative disease
of the spine may need preoperative
radiologic studies
May warrant SSEP monitoring
during positioning
21-Apr-14 89
90. Macroglossia
Swelling of the upper airway
due to edema
Neckflexion also causes
macroglossia due to edema
occurring at the time of
reperfusion
Excessive reduction of
anteroposterior diameterof21-Apr-14 90
91. Conclusion
A thorough knowledge of
Intracranial lesions, adequate
preparation, vigilant monitoring
& post operative care
Results in good patients outcome.
21-Apr-14 91
92. 1. miller’s anesthesia. 7th ed.
2. Stoelting's Anesthesia and Co-Existing
Disease, 5th ed.
3. Handbook of neuroanaesthesia. James
E Cottrell. 4th ed.
4. Clinical anaesthesia procedures of
massachusettes general hospital. 7th
ed.
5. morgan’s clinical anaesthesiology.4th
ed.
6. Wylie 7th edn.
References:
21-Apr-14 92