POSTERIOR CRANIAL FOSSA

ANESTHETIC MANAGEMENT

PRESENTER: DR.DIVYA REKHA KOLLI

PG 3 RD YEAR
MODERATOR: DR.SUDHAKAR
PROFFESSOR
ANATOMY OF POSTERIOR CRANIAL FOSSA
• Formed by portions of the sphenoid, temporal, parietal, and occipital bones.
• It consists of cerebellum, pons, and medulla oblongata.

FEATURES :
1. Median area
2. Squamous part of occipital bone
3. Posterior surface of petrous bone.
Median area:
CLIVUS:
• Formed by the fusion of the posterior part of the body of sphenoid with the
basilar part of the occipital bone.
• It is separated from the petrous temporal bone by petro-occipital fissure which
ends posteriorly at jugular foramen.
FORAMEN MAGNUM:
• Largest foramina of the skull
2. THE SQUAMOUS PART OF THE OCCIPITAL BONE
INTERNAL OCCIPITAL CREST:
• It is a vertical bony ridge, running downward from the internal occipital
protuberance to the foramen magnum.
INTERNAL OCCIPITAL PROTUBERANCE:
• It is located opposite to the external occipital protuberance.
GROOVES FOR THE TRANSVERSE AND SIGMOID SINUSES:
The grooves for the transverse sinus, one on either side, run laterally from the
internal occipital protuberance to the mastoid angle of the parietal bone
where it becomes continuous with the groove for the sigmoid sinus which ends
into the posterior part of the jugular foramen.
CEREBELLA FOSSA
• On each side lies between the transverse and sigmoid grooves and the
foramen magnum.
FOSSAE FOR OCCIPITAL LOBES
• One on each side lie above the groove for the transverse sinus.

POSTERIOR SURFACE OF THE PETROUS BONE :

Internal acoustic (auditory) meatus
Subarcuate fossa
Aqueduct of vestibule
Cochlear canaliculus
STRUCTURES PASSING THROUGH VARIOUS FORAMINA AND CANALS IN
THE POSTERIOR CRANIAL FOSSA
INTERNAL AUDITORY MEATUS
1. Seventh cranial (facial) nerve.
2. Eighth cranial (vestibulo-cochlear) nerve.
3. Nervus intermedius.
4. Internal auditory (labyrinthine) vessels.
JUGULAR FORAMEN
Foramen magnum
CLINICAL PRESENTATION :
• Headache, nausea, or vomiting and papilledema.
• Movement disorders, altered tonicity, and ocular signs such as nystagmus,
strabismus, diplopia, and pupillary abnormality .
• Cranial nerve dysfunction, bulbar palsy, bradycardia, respiratory distress,
and sudden brain stem herniation leading to death.
• The classic triad of symptoms referable to a mass in the posterior fossa is
said to be headache, vomiting, and ataxia.
 PREOPERATIVE EVALUATION
AND PREPARATION

• Patient physical status

• Cardiovascular and pulmonary stability
• Airway
• Documentation of previous operations, cerebrovascular compromise.
• Suitability of vascular access for right atrial catheter placement.
Obese, short neck, poor vasculature.
• Patients with altered limits of cerebral autoregulation
• Impaired cerebral perfusion Chances of
• Abnormal baroreceptor function resulting from hypertension hypotension
in supine
• Cardiovascular disease position
• Cerebrovascular insufficiency
• Prior carotid endarterectomy.
Intravascular volume depletion
• Decreased oral intake
• Supine diuresis
• Vomiting
• Administration of IV contrast agents.
• Administration of intravenous fluids before induction may help limit
hypotension during anesthesia induction and positioning.
• Application of thigh-high compression stockings to the legs limits
venous pooling in the lower extremities
• Echocardiography : to detect patent foramen ovale (PFO) in patients
scheduled for surgery in the head-up position.
• Documentation of dysphagia, cough, gag, and other cranial nerve
dysfunctions; evaluation of cerebellar functions; vision and auditory functions
may be needed in specific types of tumor.
• In patients with bulbar dysfunction, loss of gag and cough reflex increases
the risk of aspiration pneumonitis and extubation failure.

Long stay in ICU, post op ventilation

consent
• Atlantoaxial subluxation and lack of neck movement secondary to
craniocervical fusion.
• Assessment of cervical spine by dynamic flexion and extension views and
doppler study of neck vessels to look out for carotid insufficiency should
be done in all patients where extreme neck flexion is anticipated.

Surgical Approach:
• Suboccipital (retrosigmoid)
• Midline posterior :subtentorial or transtentorial
• Translabyrinthine, subtemporal/middle cranial fossa-less common.
Anesthetic considerations:

1) To provide optimal patient positioning and surgical access.

2) Maintaining adequate depth of anesthesia while avoiding hemodynamic
instability;
3) Intraoperative neurophysiological monitoring (IONM);
4) Prevention, early identification, and effective management of venous air
embolism (VAE).
5) Smooth emergence with early awakening.
GENERAL MONITORING ISSUES :

• For surgery on the head or neck , placement of central venous catheters in the forearm
or the antecubital fossa, preferably via the basilic vein after induction of anesthesia.
Area or Cranial Nerve Classical Activity Monitor
description
Physical signs

CN V Motor: Jaw jerk EMG

Sensory: Hypertension, Arterial line, ECG
Bradycardia
CN VII Facial twitch EMG
CN VIII BAEP
CN X Hypotension, Bradycardia Arterial line, ECG
CN XI Shoulder jerk EMG
Pons Brain stem compromise BAEP, SSEP
Ectopic cardiac foci ECG
Hypertension, hypotension Arterial Line
Tachycardia/ Bradycardia ECG
Gasp, irregular respiration Respirator trigger
• In patients with small veins, a modified seldinger technique can be used for
specialized right atrial catheters or pulmonary angiography catheters.
• Prolonged head down or rotation avoided as they decrease cerebral blood
perfusion.
• Catheter insertion sites should be sealed with bacteriostatic ointment and
dressing to minimize air entrainment.
• Place and remove these central lines in flat or head down position- vae risk.

CHOICE OF PATIENT POSITION :

• Supine, prone, three-quarter prone, and lateral positions.
SUPINE POSITION:
• Skull secured WITH three-pin head holder;
• Infiltration of the scalp and periosteum at the pin sites reduces the
hypertensive response.
• Arterial pressure transducer is zeroed at the skull base.
• Bony prominences should be well padded.
• The legs placed in thigh-high compression stockings to limit pooling of
blood.
• Elbows supported by pillows or pads to avoid stretch on the brachial
plexus
• Pressure at the common peroneal nerve just distal and lateral to the
head of the fibula IS AVOIDED.
• Prevent cervical cord stretching and obstruction of venous drainage
• Maintenance of at least a 1-inch space between chin and chest.
• Avoid large airways and bite blocks .
• Avoid excessive neck rotation, especially in elderly patients.
• Abdominal compression, lower extremity ischemia, and sciatic nerve injury
are prevented.
• “Lounge chair” modification of the sitting position, with the thoracic cage
raised 30 to 45 degrees, may be used for lateral
lesions .
ADVANTAGES OF SITTING POSITION:

• Lower airway pressures

• Ease of diaphragmatic excursion
• Improved ability for hyperventilation
• Better access to the endotracheal tube and thorax
• Access to the extremities for monitoring, fluid or blood administration and
blood sampling
• Visualization of the face : motor responses during cranial nerve stimulation.
• Improved postoperative cranial nerve function.
 PHYSIOLOGIC CHANGES IN THE
SITTING POSITION
• Head elevation above right atrium reduces dural sinus pressure by 10 mmhg
which decreases the venous bleeding.
• Cvs : increases in pulmonary and systemic vascular resistance
and decreases in cardiac output, venous return, and cpp.
• Dysrhythmias: bradycardia, tachycardia, premature ventricular contractions,
and asystole -- manipulation or retraction of cranial nerves or the brainstem.
• Respiratory system: pulmonary vital capacity and functional residual capacity
are improved .
• Hypovolemia may decrease perfusion of the upper lung, leading to ventilation
or perfusion abnormalities and hypoxemia.
• Increases the size of intravascular air bubbles if air embolism occurs.
Prone position :
• Lower incidence of vae.
• Eye compression can produce blindness from retinal artery thrombosis .
• Visual loss: perioperative ischemic optic neuropathy .

Lateral,three-quarter prone,and park-bench positions :

Unilateral surgical procedures, for easy access of axial structures.
Practical Reasons for use of Sitting Position

Better Surgical Exposure

 More complete resection
 Less tissue retraction
 Less cranial nerve Damage
 Less bleeding
Ready Access to Airway, chest and extremities
Major Drawbacks quoted
Higher incidence of Venous Air embolism
 Justification for use of Sitting
 Modern monitoring systems provide early warning
 Serious problems due to VAE uncommon
Brain Stem compromise, ischemia
 Relative Contraindications for operative sitting Position
 Ventriculoperitneal shunt in place and open
 Cerebral ischemia in awake upright
 Left Atrail pressure<Right Atrial Pressure
 Platypnoea
• Preoperative Demonstration of PFO
• known pulmonary arteriovenous
malformations, severe hypovolemia or cachexia
 Complications Position
Sitting Prone Lateral, ¾ Park bench,
prone lounge
Airway
Edema of face, ++ ++ + 0
tongue, neck
Endotracheal
tube migration ++ ++ + +
Pulmonary
Airway pressure↑ 0 ++ 0/+ 0
V/Q abnormality + + + +
Cardiovascular
Hypotension ++ ++ 0 +
Dysrhythmias ++ ++ ± ++
Blood Loss + ++ ± +
 Complications Position

Sitting Prone Lateral, ¾ prone Park bench, lounge

Nervous System
 Cerebral Ischemia ++ + 0 +
 Tension
Pneumocephalus +(100%) + 0/+ 0
 Cervical Spine ++ + 0 +
Ischemia
 Palsies
Cranial nerve + ++ ++ 0
Brachial plexus + ++ +
Sciatic nerve + 0 0 0
Peroneal nerve + 0 ? 0

Eye Compression 0 +++ ++ +

VAE +++ ++ + ++

PAE ++ + ? ?
• First consideration is the question of use of inhalational versus
intravenous.
• Transpulmonary air passage .
• Pentobarbital, fentanyl, and ketamine maintain a higher threshold for
trapping air bubbles in the pulmonary circulation than halothane.
• Second consideration is the maintenance of adequate cpp .
• Before surgical incision, administration of intravenous
anesthetic drugs – lesser effect on cardiovascular function.
• Third issue : preserving cardiovascular responses while brain stem
manipulation.
• Use of n2o – risk of vae still a question.
Premedication :
• Individualised according to patient status, icp status and level of anxiety.
• Antihypertensives are continued.
• Antibiotics, corticosteroids as advised by neurosurgeon.
• Narcotic premedication generally avoided – hypoventilation and co2
retention increases icp.
• Oral benzodiazepines given 60 to 90 minutes before arrival.
Induction of anesthesia :
• Direct arterial blood pressure monitoring established before induction of
anesthesia.
• Low dose (4 to 6 μcg/kg fentanyl) narcotic based.
• Muscle relaxant+0.5 to 1.0 MAC inhalational anesthetic after intravenous
induction with thiopental or propofol .
• This affords adequate analgesia and amnesia, preservation of autonomic
nervous system activity, and rapid awakening after discontinuation of the
inhalational anesthetics.
• Nitrous oxide in oxygen , a propofol infusion (50-100 μcg/kg/min) often
provides better surgical access than inhalational anesthetic alone
• Blood pressure : β-adrenergic blocking drugs and direct-acting vasodilators.
• Verification of appropriate placement of the endotracheal
tube after final positioning.
Maintenance of anesthesia :
Controlled positive-pressure ventilation with paralysis has the following
advantages:
• Maintenance of lighter levels of anesthesia
• Hyperventilation, which diminishes paco2, thereby decreasing both
sympathetic stimulation and blood pressure at any given depth of anesthesia.
• Cerebral vasoconstriction,less bleeding
• Lower icp,less cardiovascular depression because of decreased anesthetic
depth
• Less likelihood of patient movement.
• High levels of iv fluids – due to venous pooling.
• Preop compression stockings.
• Glucose containing solutions are avoided in risk for hyperglycemia on areas
of the brain at risk for cerebral ischemia.
• Administration of osmotic and loop diuretics - electrolyte disturbances or
cardiovascular instability caused by hypovolemia.
• The size of the pneumocephalus may be increased.
• Administration of intravenous colloid is appropriate to maintain cpp.
Emergence from anesthesia:
• Prevent abrupt increase in the blood pressure.
• Minimize coughing and straining on et tube.
• Manipulation of the medullary structures or significant edema :
secured airway should be maintained.
• Persistent postoperative hypertension in a previously normotensive
patient should alert the anesthesiologist to possible brainstem
compression, ischemia, or hematoma.
 VENOUS AIR EMBOLISM

• Incidence: A higher incidence is detected with doppler monitoring is used

(43%) than with ETCO2 monitoring (9%-28%).

• The lethal dose of intravascular air in humans has been estimated to be

greater than 300 ml.
 PATHOPHYSIOLOGY

• During slow, continuous air entrainment, air is dissipated into the

peripheral pulmonary circulation.

• The mechanical obstruction or local hypoxemia produced creates

sympathetic reflex vasoconstriction.

• Microvascular bubbles can activate the endothelium, resulting in

complement production, cytokine release, and production of reactive
o2 molecules.
 Causes for VAE with posterior fossa procedures

• Higher in sitting position

• Facilitation of air entry by subatmospheric pressure in an opened vein

• Presence of noncollapsible venous channels, such as diploic veins and dural

sinuses

• Air may enter the venous circulation via burr holes or wounds from the skull
head holder when the head was elevated

• Sites of central venous access- air can be entrained around the site of catheter
entry, from open catheters and may also occur when central catheters are
removed with the patient’s head up.
Presentation :
• Dramatic fall or loss of etco2
• Fall in spo2
• Tachycardia
• Rise in CVP & then fall in CVP
• Mill wheel murmur
• ECG : sinus tachycardia , signs of acute ischaemia , S1Q3T3
pattern
• Pea / emd
 Paradoxical air embolism

• It is less frequent, but complications, such as myocardial or cerebral

ischemia resulting from PAE, may be devastating.

• Mechanism : right-to-left shunting through an intracardiac defect,

patent foramen ovale (incidence of pfo 20-30%) likelihood increased
if the right atrial pressure exceeds left atrial pressure and use of
positive end-expiratory pressure.
Monitor Advantages Disadvantages
Precordial Doppler Non-Invasive Technical Difficulty in obese,
ultrasonography Very Sensitive positions like prone
Early Detection(before air enters False negative result if air may not
PA) pass under the beam,
mannitol, microaggregates of
platelets mimic VAE)
Not quantitative
TEE Most sensitive detector of air Expensive, cumbersome, invasive,
Can detect air in left heart/ aorta not quantitative, needs constant
observation, interferes with
doppler
PA catheter Widely available, minimal Small lumen, less air aspirated
difficulty in experienced hands than RA catheter
Quantitative, more sensitive than Rise in PA pressure not specific
ETCO2 for air
ETCO2 Widely available, Non-invasive, Non-specific for air, Accuracy
sensitive, quantitative affected by low CO, COPD,
tachypnoea
less sensitive than PA catheter
ETN2 Specific for air Less sensitive
Detects earlier than ETCO2 Affected by hypotension
Others-Doppler Monitoring of Carotid and Middle Cerebral Arteries , Brain Electrical Activity: acute
decrements in the bispectral index as a consequence of air embolism
• The right atrial catheter (RAC) is used to aspirate air entering
the right side of the heart
• Disadvantages are that the catheter’s position can change
(especially after patient repositioning) and that it may not
retrieve all intravascular air.
• Multiple-orifice racs are more effective than single-orifice
catheters in aspirating air from the circulation.
• There is greater air recovery with the tip at or 2 cm below the
sinoatrial node.
Location of air Complications
Pulmonary Perfusion defects
Hypercarbia
Hypoxia
Pulmonary Hypertension
Pulmonary edema
Decreased ETCO2
Increased pulmonary dead space
Increased airway pressures
Cardiovascular Hypotension/ hypertension, dysrhythmias
Changes in heart sounds/ mill-wheel
murmur
ECG changes of ischemia
Acute RV failure
Cardiac arrest

Central nervous System Hyperemia, cerebral edema, neurologic

defects, stroke, coma
 Prevention of air embolism

• VAE occurs if a gradient exists between the operative site and the
right atrium, regardless of patient position.

• Hypovolemia has been proposed as a predisposing factor to the

occurrence of pae as well as of vae.

• No manoeuvre is 100% effective in preventing the occurrence of vae.

 The incidence and severity can be decreased by

• The use of controlled positive-pressure ventilation

• Adequate hydration

• Proper wrapping of the lower extremities

• Use minimum required head elevation is

• Meticulous surgical technique with careful dissection and liberal use of

bone wax

• Avoidance of N2O in patients with known intracardiac defects

• Avoidance of drugs that may increase venous capacitance (e.G.,

Nitroglycerin).
 Treatment of venous air embolism

Intraoperative :

intraoperative goals in the treatment of VAE are to stop further air entry, remove
air already present, and correct hypotension, hypoxemia, and hypercapnia.

• Inform surgeon immediately. Apply bone wax to the exposed bone edges

• Discontinue N2O, increase O2 flows.

• Have the surgeon flood the surgical field with fluids.

• Provide jugular vein compression.

• Aspirate the right atrial catheter.

• Provide cardiovascular support.

• Change the patient’s position – head down, left lateral

• Moderate CPAP.

• Hyperbaric oxygen therapy

 Postoperative goals
• Provide supplemental O2.
• Perform electrocardiography, chest radiographs.
• Measure serial arterial blood gas levels.
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