Posterior Fossa
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
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 :
through vertebrobasilar system ,located mostly anteriorly.
4.
Clinical physiology
Presenceof cerebellum ,mid brain, pons,
medulla and multiple cranial nerves in posterior
cranial fossa provides lesions in this area with a
multitude of possible signs and symptoms.
Mass effects of lesion ,hydrocephalus secondary
to obstruction of CSF flow through aqueduct of
sylvius leads to increased ICP .
5.
Sign and symptoms
Initial non specific symptoms include listlessness, headache,
fatigue, vomitting, anorexia and personality changes
Cerebellar or brainstem signs develop – dysmetria,
hemiparesis and cranial nerve deficits.
More specific clinical syndromes may occur with tumors that
rapidly involve neural structures such as acoustic neuromas,
other CP angle tumors, brainstem glioma, carotid body
tumor.
Sign and symptom due to SOL in posterior fossa are as a
result of elevated ICP due to CSF outflow obstruction.
In infants an enlarged head or bulging fontanelle may
indicate hydrocephalus.
6.
Distinct set ofsigns and symtoms in relation to
location of lesion :
Midline and 4th
ventricle
Truncal ataxia
Wide based gait
Nystagmus
extraocular movement abnormalities
Truncal titubation
Hydrocephalus- early and common
Frequent papilledema
Signs of brainstem lesion are common
7.
Lesion of lateralcerebellar hemisphere :
Hypotonia
Intention tremor
Limb ataxia
Dysmetria
Dysdiadochokinesia
Dysarthria
Ocular abnormalities like nystagmus, gaze paresis, skew
deviation
Hydrocephalus less common and appear later
8.
Herniation ofthe cerebellar tonsils through foramen
magnum (especially in children) appear as :
Meningismus
Head tilt
Muscle spasm
Opisthotonus
Vomiting
Skew deviation of the eyes
Downbeat nystagmus (vertical nystagmus)
Typical ‘posturing’ from tonsillar herniation may be
mistaken for “cerebellar fits”
Bulbar palsies with vocal cord paralysis
9.
Swallowing andgag 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 may result
10.
Brainstem involvement produces:
Ocular problems related to pupil size, ocular mobility, nystagmus
Sensory or motor deficits
Respiratory changes vary depending on brainstem compression :
Hyperventilation
as compression passes caudally
apneustic and ataxic breathing
Multiple cranial nerve problems including bulbar palsies are common
With progressive external compression of the brainstem from midline
or 4th
ventricle lesions, gaze and facial palsies develop with rapid loss
of consciousness, respiratory changes, bradycardia and hypertension
11.
Lesion in theposterior fossa may be neoplastic,
developmental and vascular processes requiring surgical
intervention
Success with surgical intervention has become possible
because of:
Advances in imaging and microsurgical techniques
Improved understanding of physiology
Advances in perioperative care of the patient
Excellent anaesthetic techniques available
13.
Preoperative evaluation
Bonyartefacts are seen in CT scan but MRI scan has greatly
improved diagnosis of posterior fossa pathologic conditions
Imaging allows intraaxial and extraaxial lesions to be
differentiated and allows visualization of the surrounding
anatomic structures and they provide information for
pathologic diagnosis of lesion.
Cerebral Angiography: procedure of choice in diagnosing
and evaluating aneurysms and vascular malformations
Neurophysiologic studies : brainstem auditory evoked
responses and electronystagmography are rarely required for
diagnosis. But they are of some use for diagnosis of acoustic
neurilemmomas and multiple sclerosis
Preoperative audiometry is useful in predicting hearing
preservation after acoustic shwannoma surgery
16.
Anaesthetic considerations
Theposterior fossa is home of brain stem, major
motor and sensory pathways cardiovascular and
respiratory centers , RAS and lower CN nuclei, thus
create challenges to the anaesthesiologists,
whose intraoperative goals are to facilitate
surgical access, minimise nervous tissue trauma
and maintain respiratory and cardiovascular
stability.
17.
Preoperative Evaluation
1) CompleteMedical History
Mainly for function of the heart and the lungs. Most
perioperative morbidity and mortality results from
poor Cardiac or Pulmonary function.
History of CNS Disorders – Seizure disorders need to
be assessed for type and for adequacy of therapy.
Cerebral hemorrhage or prior strokes are noted.
Any residual speech, sensory or motor dysfunction
are recorded.
Obtain the results of any recent intracranial or
diagnostic procedure and consider possibility of
residual pneumocephalus.
18.
2) Review thepatient list of Medications:
Steroid, manitol and diuretics, antihypertensive,
tricyclic antidepressants ,L –dopa, benzodiazepines,
phenothiazines ,which may alter hemodynamics
during surgery.
3 ) Physical Examination :
• Patient physical status, particularly in reference to
cardiovascular and pulmonary stability and airway
manageability, is a determinant of the choice of patient
position for posterior fossa surgery.
19.
4) Neurological Examination:
Level of consciousness
Document any focal motor or sensory deficit.
Examination of sign and symptom of increased ICP.
5) Routine Investigations:
CBC
Blood Chemistry
Coagulation profile
ECG and CXR
20.
Monitoring
The goalsof monitoring are to ensure adequate CNS perfusion
maintain cardiovascular stability and detect and treat VAE
( venous air embolism )
Five lead ECG
Pulse oximetry
NIBP
EtCO2 monitoring
Capnography
Temperature
Precordial stethoscope
Central venous catheter
Precordial doppler probe
Esophageal stethoscope
TEE
21.
Patient position
Sittingposition :
Patient head secured in a three pin head holder. Infiltration
of the scalp and periosteum at pin site reduces hypertensive
response
Bony prominences are padded
Legs placed in thigh high compression stockings to limit
pooling of blood
Elbows supported by pillows or pads to avoid contact with
table or stretch on brachial plexus and the legs freed of
pressure at the level of common peroneal nerve just distal
and lateral to the head of fibula
Maintain 1 inch space between the chin and chest to prevent
cervical cord stretching and obstruction of venous drainage
from the face and tongue
22.
Avoid largeairway and bite block placements
Avoidance of excessive neck rotation
Avoid excessive flexion of knees towards the chest to
prevent abdominal compression, lower extremity ischemia
and sciatic nerve injury
24.
Advantages of sitting
position
Lower airway pressure
Easy of diaphragmatic excursion
Improved ability for hyperventilation
Increased access to ETT and thorax for monitoring
Access to extremities for monitoring fluid or blood
administration and blood sampling
Visualisation of the face for observation of motor responses
during cranial nerve stimuation
Number of blood transfusion are less in sitting position as
compared to supine position
Better surgical exposure, less tissue retraction, less cranial
nerve damage and more complete resection of tumor
possible.
25.
Contraindications for sittingposition
Intracardiac defects
Severe hypovolemia
Cachexia
Severe hydrocephalus
Lesion vascularity
extremes of age / impaired cardiac function
Degenerative diseases of cervical spine
Significant CVD.
26.
Physiologic changes insitting
position
Head elevation above the rt. atrium
decrease in dural sinus pressure upto 10 mm Hg
Increased risk of VAE decreases venous bleeding
(45 % in sitting position)
27.
Prone position
Patient’shead elevated to decrease venous bleeding
Face compression is prevented by keeping head elevated and
shoulders at or above the edge of the operating table
Lower incidence of VAE
Disadvantages :
Surgical field is not as clear as in sitting
Eye compression can produce blindness from retinal artery
thrombosis
Conjunctival edema.
Venous pooling in the lower extremities sufficient to impair
venous return and hypotension especially in elderly, debilitated
patients
29.
Lateral Or ParkBench Position
Can be used for access to the post parietal &
occipital lobes & lat. post fossa, including tumors
at the cerebellopntine angle & aneurysms of the
vertebral & basilar arteries.
30.
Premedication
Preoperative premedicationis individualized by patients’
Physical status
Evidence of increased ICP
Level of patient anxiety
Continue antihypertensives
Corticosteroids
Antibiotics
Oral benzodiazepines 60 minutes prior are effective in
reducing anxiety and do not have sufficient effect on ICP
Narcotic premedication to be avoided in pts with SOL or
hydrocephalous from 4th
ventricle occlusion because
resultant hypoventilation and CO2 retention may increase
ICP
31.
Induction
It canbe performed by various agent. The best induction agent
is Barbiturates because its administration provides a profound
reduction in CMRO2 , CBF and ICP.
Smooth and gentle induction of general anaesthesia is more
important. An acceptable induction sequence combines four
steps –
1.) Preoxygenation and self hyperventilation
2.) Thiopentone 3-4 mg/kg IV followed by mask ventilation to
assure airway patency.
3.) Vecuronium 0.1 mg/kg IV and mask hyperventilation with
oxygen and N2O (50:50) until neuromuscular blockade
achieved.
If there is C/I to use of N2O, add small concentration of
isoflurane to the O2.
4.) Lidocaine 1.5 mg/kg IV and additional thiopentone 2 mg/kg IV
just before ET Intubation.
32.
Rapid SequenceInduction can be performed with the
same combination of drugs as a routine induction.
However, cricoids pressure is applied, mask ventilation
is not delivered.
Vecuronium 0.15 mg/kg used for intubation.
In a patient with full stomach and a difficult airway,
awake intubation should be performed.
Heavy topical anaesthesia and minimal IV sedation
with subsequent oral endrotracheal intubation using a
lighted stylet is extremely effective in these patient.
If Narcotics are to be used as a part of anaesthesia
administer slowly during induction. Fentanyl or
sufentanil make induction and ET intubation very
smooth.
33.
Maintenance of Anaesthesia
It can be accomplished in a number of ways.
These technique generally fall in to two categories –
1.) Primarily Volatile agent and
2.) Narcotics
Either technique can be used.
In Narcotics based anaesthetic technique with either
N2O or low dose (< 1%) isoflurane in O2 is optimum .
Fentanyl or sufentanil may be used.
34.
Fentanyl 5µg/kgcombined with < 1% isoflurane in
O2 is an acceptable technique for anaesthetic
maintenance.
Alternatively, sufentanil 0.5 to 1 µg/kg loading dose,
followed by either incremental bolus (not to be
exceed 0.5 µg/kg/hr) or IV infusion of 0.25 to 0.5
µg/kg/hr in combination with < 1% isoflurane in O2
may be used.
The sufentanil must be discontinued approximately
1 hr before the end of surgery.
If the patient has HT or tachycardia near the end of
surgery, it is best to treat with either Labetalol or
Esmolol.
35.
A volatileagent preferably isoflurane with little or
no narcotic supplementation can also be used.
Hyperventilation combination with < 1% isoflurane
generally results in stable intracranial dynamics.
N2O may be used in anaesthetic regimen but it is
contraindicated if the patient is suspected to have
pneumocephalus (recent intracranial surgery or
trauma) or if there is potential for air embolism N2O
expand both the pneumocephalus and the air
embolus.
36.
Muscle relaxationis also important during
neurosurgery relaxation prevent patient movement
at inappropriate time,
it may decrease ICP by relaxing the chest wall with
decrease intrathoracic pressure and encourage
venous drainage.
37.
Fluid Management
Abalanced salt solution is the fluid of choice for
neurosurgical procedures. The volume of fluid
administered should be minimized during the
induction of anaesthesia and then kept as low as
hemodynamic stability and urine output will allow.
Use no dextrose containing solution.
Maintain hematocrit at 30 to 35 %.
Patients who present for tumor surgery should be kept
on the dry side of normal. Excess fluid administered to
these patients may cause brain edema at the sites of
blood brain barrier disruption. Thus a dry but stable
patient is optimum for tumor surgery.
38.
Emergence
It shouldbe smooth and gentle.
Lidocaine 1.5 mg/kg IV decrease cough and strain.
If surgery is superficial and performed without much
traction on the brain stem, it is assumed safe to extubate.
If lesion is deep seated with frequent traction on the brain
stem there may be danger of apnea or decrease
sensorium with diminish airway reflexes,
Such patient should remain intubated and be allowed to
awaken slowly in the ICU after a period of monitoring and
continued ventilation.
1.Brainstem & CNstimulation
Hypertension results from stimulation of Vth CN,
periventricular gray area, reticular formation, or
nucleus of tractus solitarius.
Bradycardia and escape rhythms results from vagus N
stimulation,
Hypotension can results from pontine or medullary
compression.
Ventricular and supraventricula arrhythmias can occur
from brain stem stimulation.
Close attention to cardiovascular parameters during
critical periods of surgery is essential and surgeon
may inform of brainstem encroachment
41.
2.Venous Air Embolism
Most Feared Complication associated with sitting
position.
CAUSES:
open veins & non collapsible venous channels
gravitational effects of low CVP
neg. I.v. pressure relative to atm. Pressure
poor surgical technique
Incidence- 25-50%
42.
3.Pneumocephalus
Air intothe epidural or dural space sufficient to
exert a mass effect.
Incidence- 3%
Sometimes life threatening brain herniation.
43.
CAUSES:
Diminition ofbrain volume secondary to
mannitol
hyperventillation
removal of SOL
contraction of intravascular blood vol. associated with acute
hemorrhage
Gravitational effect of sitting position
Intraop drainage of CSF
“Inverted Pop Bottle Analogy” as CSF pours out, air bubbles to
the top of the container(cranium)
So that is why slow cont. gravitational drainage of CSF in
sitting position can result in accumulation of air in subdural
space
44.
ROLE OFNITROUS OXIDE:
major contributing factor
avoidance would not eliminate the risk
it increases the size of air filled space
S/S:
Confusion
Headache
Convulsions
Neurological deficits
Failure to regain conciousness
CT scan confirms the diagnosis and localisation of intracranial
air, if untreated Brain herniation and death.
T/T:
IMMEDIATE twist drill aspiration of air through burr holes on
either side of the vertex.
45.
4.MACROGLOSSIA
CAUSES:
Extreme flexionof head with chin resting on the
chest
Prolong presence of an oral airway
Obstruction of its venous and lymphatic drainage
Airway obstruction
hypoxemia
hypercapnia postop
46.
4.QUADRIPLEGIA
CAUSES:
Flexion ofhead on the neck causes streching of
the spinal cord at C5 level, regional cord
perfusion may be compromised if MAP is
decreased.