Posterior Fossa Procedures

Specific Challenges:

1. Vital structures in the posterior fossa, particularly the brainstem, cranial nerves, and cerebellum.

2. The confined space of the posterior fossa.

3. The awkward position and anatomy of the lesions complicating surgical access.

4. Long duration of surgery in extreme positions.

5. Potential for development of hydrocephalus.

Positioning:

1. Supine with maximal rotation to the contralateral side :

a) Used for access to lateral structures of the posterior fossa.

b) Up to 45 degrees can be achieved by lateral rotation. Beyond that requires elevation of the ipsilateral shoulder. Beware patients with limited neck flexibility.

c) Reverse Trendelenburg positioning facilitates venous drainage from the brain.

d) REMEMBER: for each 2.5 cm increase in vertical height of the head above the heart leads to a 2 mm HG reduction in cerebral perfusion pressure.

e) Associated with decreased venous return from the brain leading to increased ICP.

f) Can cause macroglossia so soft bite block to reduce dental injury.

g) Brachial plexus injury from ipsilateral taped shoulder displacement or inadequate support under shoulder.

2. Lateral Position :

a) Suitable for unilateral procedures of the Posterior fossa.

b) Surgical access is improved by gravitational traction of the cerebellum, drainage of CSF and blood from the operative field optimized by reverse Trendelenburg positioning.

c) VAE incidence is lower than that of sitting position.

d) Better hemodynamic stability than supine or sitting position.

e) Main problems: brachial plexus injuries from ipsilateral stretch, gravitational V/Q mismatch in the dependent lung, pressure induced nerve injuries to the dependent arm.

3. Park Bench :

a) Similar to lateral but resembles the position of a person lying on his/her side on a park bench.

b) Better access to midline structures compared to lateral position.

c) Patient placed semi-prone with head rotated and neck flexed resulting in brow facing the floor. Also known as “sloppy lateral”.

d) Problems: venous engorgement, peripheral nerve injuries and macroglossia.

e) Trendelenburg positioning is used to improve surgical access with resulting hemodynamics being countered by judicious fluid management and vasopressors.

f) The down arm is always a logistics challenge. I find the use of a foam tray positioned in the frame of the Mayfield for an arm holder and secured with a 3 or 4 in gauze wrap useful.

4. Prone position:

a) Facilitates access to the posterior fossa, craniocervical junction and the upper spinal cord.

b) Advantage: low incidence of VAE and optimal surgical access.

c) Disadvantages: problem with patients having restricted neck flexibility, diaphragmatic splinting in obese patients, restricted airway access, incompatibility with effective CPR if necessary.

d) Extreme care and planning must take place for positioning to avoid loss of airway, IV catheters, and invasive monitoring.

e) Mayfield head pinning preferred to horse shoe head holder. Less pressure on the face and orbits.

f) Chest needs to be free with partial support of abdomen and pelvis to help prevent diaphragmatic splinting. Chest rolls or Wilson frame may be used. Head elevation may increase VAE risk although it facilitates venous drainage from the brain.

5. Sitting position:

a) Advantages: Optimal surgical access to the cranial vertebral junction, the midline structures in the posterior fossa and the cerebellopontine angle, promotes venous drainage for blood and CSF, easy airway access, favorable ventilatory mechanics.

b) Life threatening complications: VAE, postural hemodynamics effects compounded by general anesthesia, quadriplegia, pneumocephalus, macroglossia, and peripheral nerve injuries.

c) Contraindicated in patients at risk of right to left shunt (patent foramen ovale with an incidence of 27.3% in autopsy studies), and patients with ventriculoatrial CSF shunts since any air trapped in the ventricles can migrate into the atrium.

d) Physiologic effects:

1) Cardiovascular: reduced venous return and hydrostatic pooling lead to hypotension. GA reduces normal compensatory changes like increased heart rate and peripheral vascular resistance. Effects are accentuated by advanced age and associated co morbidities.

2) Respiratory: Increased FRC but less perfusion negates the effect on oxygenation.

3) Cerebral Perfusion: reduction in global perfusion increasing the risk of ischemia.

e) Venous Air Embolism:

1) Caused by gravity and negative pressure in the venous sinuses and veins of the skull and brain.

2) When defined as a fall in End tidal CO2 incidence is 9.3%. When TEE place incidence approaches 100%.

3) Addition of PEEP increases RA pressure can increase the incidence of paradoxical air embolism after VAE.

4) Clinical consequences are dependent on rate of accumulation and the volume of air entrained.

5) Lethal volume in adults thought to be between 200 and 300 mls or 3-5 mls/kg.

6) Air goes to RA> RV> PA> increased PVR > right heart strain and increased alveolar dead space > reduction in EtCO2.

7) If embolism is large, a gas air lock immediately occurs causing cardiac arrest.

8) Signs: tachypnea, tachyarrhythmia, hypoxemia, hypotension, wheezing with decrease in EtCO2 and an increase in arterial CO2.

9) In awake patients signs include continuous coughing, breathlessness, light-headedness, chest pain and a sense of impending doom.

10) PAE occurs in 5-10% of VAEs producing signs of myocardial and cerebral ischemia.

11) Monitoring: right heart ultrasound (Mill Wheel murmur) placed in the 2^nd intercostal space on either side of sternum or between the right scapula and the spine which can detect .05 mls of air/kg, appearance of nitrogen expired air in a nitrogen free anesthetic, a drop in EtCO2 and/or PaO2 or a rise in PA pressure leading to increased risk of PAE, TEE can detect as little as .02 ml/kg.

12) End tidal nitrogen detection is more sensitive than EtCO2 as warning occurs 60 -90 s before the reduction in EtCO2.

13) Pulmonary artery catheter can detect a rise in Right heart pressures but is more invasive and less sensitive than a precordial Doppler.

14) Pulse oximetry, clinical vigilance, esophageal stethoscopes, and ECG changes are late and variable markers of air embolism but continue to be used is some centers.

15) Reduce risk: careful planning, meticulous surgical technique, liberal use of bone wax, vigilance, avoidance of nitrous oxide, maximized intravascular volume.

16) Treatment: Flood the surgical field with saline, Trendelenburg position if possible, jugular venous compression all limit continue entrainment of air.

17) Increase FIO2 to 100%, turn patient to left lateral decubitus if possible to reduce gas lock effect, attempt to aspirate air from right atrium with central line, hemodynamic support with IV fluids, inotropes, and anti-arrhythmic drugs and CPR.

f) Pneumocephalus: air enters the brain of spaces around the brain after dural incision. Can contribute to tension pneumocephalus if air volume is large and accompanied by cerebral edema. Life threatening herniation may occur requiring burr hole evacuation. CT scan is investigation of choice.

g) Macroglossia and airway swelling: caused by extreme neck flexion and obstruction of lymphatic and venous drainage from the head.

h) Other complications: cardiac arrhythmia from damage to vital centers, post op respiratory depression, aspiration from cranial nerve damage, peripheral nerve injury and spinal cord injury.

i) Spinal cord injury from extreme neck flexion and reduction in spinal cord blood flow from hypotension in sitting position.

j) Commonly injured nerves: common peroneal and recurrent laryngeal nerves caused by stretch, compression, or ischemia.

Neurophysiological Monitoring:

1) SSEP and BAER monitor about 20% of brainstem function during surgery especially CP angle and microvascular decompression procedures.

2) Brain stem mapping using a hand held stimulator is used for identification of safe entry zone for the surgeon. Anatomical brain stem nuclei can be identified. Direct mapping of motor nuclei of the cranial nerves in the floor of the 4^th ventricle can be achieved. Can also map cerebral peduncle in the midbrain.

3) Continuous EMG monitoring of CN VI and VII facilitates monitoring during microvascular decompression, surgery for 4^th ventricle tumors and acoustic neuroma surgery.

4) Avoid neuromuscular blocking agents when monitoring EMG.

Induction and Maintenance of Anesthesia

1) Monitoring and anesthetic drug choices are no different than those discussed in previous protocols for management of general anesthesia for intracranial brain tumors. Generally TIVA is preferred but inhalational techniques can be used with the avoidance of nitrous oxide of course.

2) Invasive monitoring including arterial line and central venous line placement for sitting procedures is indicated.

3) As with any case of increased intracranial pressure it is important to avoid systemic hypotension and restricted venous outflow from the head. If using the sitting position, head elevation should be done slowly while bring the feet and legs up simultaneously. Knees should be elevated to approximately heart level to improve venous return and avoid venous pooling.

4) Placement of the precordial Doppler occurs after positioning and tested with a saline flush. Anesthesia techs have our precordial Doppler.