Anesthesia for cranioplasty after decompressive craniotomy

Decompressive craniotomy  is  a procedure used in severe intracranial hypertension unresponsive to other measures.

Patients with traumatic brain injury,stroke  or cerebral edema may undergo this procedure.

The removal of the bone flap may  cause by itself neurological deterioration which  follows an initial improvement.

Days or weeks after surgery, a marked concavity  may develop at the craniectomy site associated with a midline shift to the  opposite side.This changes are aggravated by the presence of a VP shunt,dehydration and position changes.

It has been theorized that this " syndrome of the sinking skin flap" ^{1 ,2} (SSSF) is caused by the direct transmission of the atmospheric pressure to the intracranial cavity  aggravated by CSF hypovolemia.

The increased frequency of hydrocephalus in patients after decompressive craniotomy is explained by a disturbance of CSF flow around the convexities.

Severe CSF hypovolemia can produce an herniation syndrome which can be reversed by Trendelemburg position.

The definitive and most effective treatment of the SSSF is cranioplasty ³ .

Cranioplasty  protects the brain,and  provides cosmetic  results but most importantly , improves the neurological deficits by a decrease of local intracranial pressure and correction of CSF dynamics. Also ⁴ the cranioplasty may affect postural blood regulation,cerebrovascular  reserve capacity and cerebral glucose metabolism. Sakamoto ⁵ described a patient after  decompressive craniotomy with a CBF measured in CT perfusion imaging of 23 ml/100g/min and  37 ml/100g/min in the contralateral side which increased to 31 and 41 ml/100g/min respectively after cranioplasty. From this data we learn that the CBF was abnormally low  bilaterally and increased  significantly after cranioplasty. Another conclusion may be that

any intervention which further  reduces CBF like hypotension and hyperventilation has to be avoided  .

The cranioplasty itself may result in complications due to brain dysfunction,risk of fluid  collection and subdural  or intracerebral hematoma.Chun Chih Liao ⁶and coworkers recommend that  if there is a VP shunt ,it has to be occluded  several days before the cranioplasty to allow  the expansion of the depressed area,eliminating the dead space between the bone and the dura,lessening the risk of hematoma.

There is another complication after brain  surgery described by Van Roost ⁷  

This investigator described a severe and sometimes fatal complication after uneventful intracranial surgery.

A postoperative rapid, malignant ,diffuse brain swelling , with a maximum at the level of the basal ganglia and thalamus and  symmetrical distribution. They called it "pseudohypoxic brain swelling" (PBS)

The clinical picture which started 30 to 400 min after the end of surgery,included signs of brain stem dysfunction in some patients , seizures, or persistent coma after the end  of anesthesia.

The CT scans showed hypodensities which resembled an hypoxic incident  (which was ruled out) or severe brain swelling.

TCD-In some patients was normal, other showed accelerated flow or a reberberating flow in fatal cases.

MRI confirmed the CT changes

SPECT- rCBF bilaterally reduced.

ICP- there was a negative correlation between ICP values and survival.

The hypothesis was that excessive CSF loss via wound drainage and subsequent low ICP possibly triggered PBS, due to a massive negative pressure on the brain. Since they stopped removing the vacuum from the suction bottles, and blocking the drains until the patient awakens, no new cases were observed.

Although   they described  one case of this pathology after cranioplasty, based in anecdotic evidence  we think that pseudohypoxic brain swelling  is more frequent after  large cranioplasties .

Anesthetic implications

-Patient scheduled for cranioplasty after decompressive craniotomy and VP shunt should have a temporary occlusion of the shunt several days before surgery.

-Avoid hypotension and provide normoventilation or  mild hypoventilation to avoid further decreases of CBF

-Do not open the drain until the patient is fully awake.

References

1 Han PY et al "Syndrome of the Sinking  Skin Flap" Secondary to the ventriculoperitoneal shunt after craniectomy.J Korean Neurosurg Soc  43 51-53 2008

2 Yamamura A. et al : Cranioplasty following decompressive craniotomy. Analysis of 300 cases. No Shinkei Geka 5:345-353,1977

3 Segal DH et al Neurosurgical recovery after cranioplasty. Neurosurgery 34:729-731,1994.

4 Winkler PA et al Influence of cranioplasty on postural blood flow regulation, cerebrovascular reserve capacity and cerebral glucose metabolism. JNeurosurg 93:53-61,2000

5 Sakamoto S. et al CT perfusion imaging in the syndrome of the sinking skin flap before and after cranioplasty.Clin Neurol Neurosurg Sep;108(6):583-5

6 Dirk Van Roost et al  Pseudohypoxic brain swelling: a newly defined complication after uneventful brain surgery,probably  related to suction drainage. Neurosurgery 53:1315-1327,2003

Anesthesia for interventional neuroradiology

Introduction


I could not find nothing more appropiate to start this topic  than this blessing (Asher Yatzar) that   jews say several times a day:

The Asher Yatzar blessing was initiated by the holy Amora (Talmudic sage) Abayei, (see tractate Brachot 60b). The Gemara says: "Abayei said, when one comes out of a privy one should say: 

"Blessed is He who has formed man in wisdom and created in him many orifices and many cavities. It is obvious and known before Your throne of glory that if one of them were to be ruptured or one of them obstructed, it would be impossible for a man to survive and stand before You. Blessed are You that heals all flesh and does wonders."

Indications for treatment 

 Most frequent procedures in our hospital are aneurysm coiling, AVM embolization , tumor embolization,carotid stenting, treatment of vasospasm or stenosis, stroke intervention.

 Most procedures are performed under general endotracheal anesthesia for airway control and  immobility.

General goals

Patient immobility

Avoidance of injuries

Physiological stability

Airway control

Hemodynamic manipulation

Management of anticoagulants/antiplatelets

Rapid recovery for neurological assessment

Avoidance of hyperthermia/hypothermia

Good communication with radiologists

Safe intrahospital  transport

Radiation safety

Preoperative assessment

Special emphasis in the following items:

Airway –Difficult airway in a remote location.

Cardiovascular function- Arterial hypertension, SAH related myocardial ischemia, previous function

Renal function.-contrast nephropathy

Respiratory- pulmonary edema (hydrostatic, neurogenic)
Neurologic- SAH, intracerebral hematoma.

Drugs- antiplatelets, anticoagulants,Ca channel blockers.

Accessory examinations: EKG, chest xray ,TCD,CT angio,MRI,MRA.

Laboratory- routine, baseline coagulation screen, platelet  function.

Room preparation

Similar to any  OR

Ideally get help of an anesthesia technician.

Check anesthetic chart, drugs, difficult intubation equipment.

Monitoring

Standard monitoring, urinary catheter.

Arterial line is placed before induction with local anesthesia. Transducer fixed to a pole in the x-ray table.

Intra-intervention laboratory- ABG, ACT.

 IV access-with extension tubes. In TIVA ,dedicated iv cannula.

Induction

Critical in aneurysm because risk of rupture.

Smooth induction with  attenuation of CV response to intubation and maintenance of CPP.

After a small dose of midazolam,  spray lidocaine 10% over tongue,oropharynx.

IV fentanyl 2 mcg/kg.

Hypnosis: Propofol 1-2 mg/kg,or thiopental 3-5 mg/kg or etomidate 0.2 mg/kg.

Muscle relaxant : rocuronium or vecuronium.

Ventilate with O₂ and isoflurane before laryngoscopy.

Available drugs: Nitropruside,labetalol,phenylephrine.

Let BP decrease 20% of baseline.

Trial laryngoscopy- minimal CV response, proceed with intubation. If BP rises, deepen anesthesia with fentanyl, ventilate with more  isoflurane and try again.

Maintenance

Balanced anesthesia with isoflurane at < 1 MAC.

Further doses of fentanyl are generally not needed.

Muscle relaxants: atracurium in continuous infusion or repetitive doses of vecuronium/rocuronium.

TIVA –is another option, propofol/remifentanyl.

Fluids

Patients are generally hypovolemic due to poor intake , contrast media.

Replace fluids with normal saline. Glucose is avoided.

Keep Ht 30-35%

Hetastarch is not recommended due to its interference with coagulation.

Anticoagulation

Routine in intracranial procedures

After measuring a baseline ACT( normal is  90-130 sec) give heparine  2500 to 5000 units to prolong ACT 2-2.5 times.

An adverse effect of heparine administration is induced thrombocytopenia, accompanied by platelets activation and thrombotic complications. In this event it is recommended to shift to a direct thrombin inhibitor like argatoban or lepirudin.
GPIIb/IIIa inhibitors can also produce severe thrombocytopenia. To rule out,check CBC 4 hours after administration.                                     

For acute platelet plugs ,systemic eptifibatide is administered (see table in the angio suite) and/ or intraarterial tissue plasminogen activator (tPA).

Reversal of heparine- protamine, its dose depending on the time elapsed since last dose of heparine.

Reversal of GPIIb/IIIa inhibitors –platelet transfusions

Reversal of Eptifibatide -FFP

Hemodynamic control

Labetalol,α and β blocker, reduces BP and HR.

Nitroprusside-direct vasodilator,  dilates cerebral vessels. May rise ICP in patients with  decreased  cranial elastance.

Phenylephrine- does not influence ICP, is a pure α agonist.

Specific procedures

Aneurysms

The procedure consists in the introduction of coils, or stent and coils which obliterate the aneurysm and promote intraaneurysm clotting.

Complications
-Embolism.

-Rupture of the aneurysm-  extravasation of contrast , Cushing triad.

Treatment- the radiologist  will try to introduce coils to stop bleeding.

-Heparine reversal with protamine

-Lower BP

-Mannitol to reduce ICP.

-Rarely emergency craniotomy for ventriculostomy ,clipping of aneurism.

Occlusion:

Increase BP

Trombolysis-systemic and  intrarterial , mechanical removal of thrombus

AVM  Embolization

AVM  generally requires multiple sessions to occlude AVM nidus or feeding arteries.In some cases, the occlusion of the AVM produce an increase of the CBF in the normal parenquima, which may exceed the autoregulation capacity and cause intraparenquimatous hemorrhages.

It is recommended  to reduce the BP 20% below the patient's  baseline BP.

The obstruction of the draining veins by glue can cause venous outflow obstruction and pulmonary embolism.
Another complication is perforation  with extravasation of contrast media.The treatment is similar to  the rupture of aneurysm.

Stenting for  carotid occlusive disease

Generally done  under monitored anesthesia care,under light sedation, to  assess neurologic function during the procedure.

Drugs :fentanyl, midazolam.

Bradycardia  and asystole from carotid body stimulation can occur. Have atropine ready.
If atropine does not work,chronotropic drugs are as good as external pacing.

Other complications- perforation of the artery ,dissection, spasm, TIA, stroke,

hyperperfusion syndrome

Emergence of general anesthesia

Avoid coughing and bucking.

Treat severe hypertension with labetalol starting at 0.25 mg/k  bolus.
Transfer the patient to neurosurgical intensive care.


I  wish to thank Dr.Yaaqov Amsalem,MD, Director of the Invasive Neuro-Radiology Service
for the revision of this guidelines and for the useful comments and suggestions.

Anesthesia for traumatic brain injury (TBI)

The treatment of TBI is a lesson of humility to the medical profession.

In spite of the advances - in treatment and transport, diagnostic techniques , surgical  procedures ,anesthetic  and  intensive care-,  brain trauma  places an enormous challenge  because of the complexity and  uniqueness of the central nervous system. 

If we resume our present state of the art  of  its treatment, the most we can do is to try to improve the delivery of O₂ and nutrients by  fluid and hemodynamic resuscitation and by treating  increased ICP. We can also evacuate hematomas and  lift  depressed fractures and decompress the brain.

Secondary injury can be minimized .

 But nothing can be done to repair the  nervous tissue.

Almost 100% of persons with  severe TBI  and as many as two thirds of those with moderate head injury will be permanently disabled  and will not return to their previous level of function.

Anesthesiologists participate in almost every  step of the treatment  of the patient with TBI.

In fact  ,one of the best things that can happen to such a patient is to meet an anesthesiologist as early as possible. Anesthesiologists are not only experts in airway management  and in intracranial blood volume but also in the stabilization of vital functions and the  normalization of homeostasis.

I am not going to write about the surgical pathologies and the pathophysiological changes that occur after head trauma,and I'll  go directly to the treatment.

Emergency  assessment (Simultaneously with resuscitation maneuvers) .

-Neurological assessment and spine inmobilization

  GCS(specifying every one of the 3 responses)

  Pupils

-Other organs, specially  internal  bleeding, lung injury, pneumothorax

Any bleeding which causes or may cause instability threatens the perfusion of every organ and specially the brain. Brain perfusion must be ensured  ,even in the presence of  uncontrolled bleeding. Ignoring  this fact can result in the survival of a brain death  patient.

A high degree of suspicion is essential in every step of the treatment.

Internal hemorrhages  previously undetected can suddenly  destabilize the patient.

As increased ICP causes frequently hypertension, the normotensive or hypotensive patient has to rise our suspicion  of present bleeding.

Airway and Ventilation

Intubation  equals  anesthesia induction, in the ER, the CT scan or in the street.

Once intubated, during transport or in the  OR, the patient will be treated with the same principles of care in every stage ,the most important goals being the optimization of brain perfusion and oxygenation,the avoidance of hypotension and hypoxia, the treatment of increased ICP and the prevention of further neurological  damage.

There are multiple metabolic factors involved in TBI unrelated to this simplistic hydrostatic approach ,many of them still unknown.

Indications  of intubation

To protect the airway from aspiration,to ensure normoxia and normo-hypocapnia.

GCS<8

Ventilatory failure

Irregular respirations

Deterioraring  level of consciousness

Face fractures

Bleeding into mouth

Seizures

Significant lung/chest injury

Shock

Combative

Need of transport

Intubation

When preparing to intubate the patient, take in account:
  -Increased ICP- Drugs are used to blunt the rise of ICP caused by laryngoscopy and intubation.

  -Prediction of difficult intubation-face trauma, laryngeal trauma, and anatomically abnormal airway .

 -Hemodynamic stability-will determine which drugs we are going to use.

 -Cervical spine injury

 -Full stomach

If  there is no predicted difficulty, rapid sequence induction with Sellick' maneuver.

The choice of drugs and its doses will be determinated  by the  hemodynamic  state.

Normovolemic  patients ,(normo or hypertensive) can be intubated with propofol 1-2 mg/kg or thiopental 3-4 mg/kg. 

Muscle relaxant :Succinylcholine 1.5 mg/kg or Rocuronium 1 mg/kg.

If the patient is hypovolemic, Etomidate 0.2-0.3 mg/kg or ketamine 1-1.5 mg/kg .

In predicted difficult intubation in non –cooperative patients the options  include fiberoptic intubation,intubating LMA,light wand,retrograde intubation,cricothiroidotomy .

Please see the excellent site of  difficult intubation in trauma patients  by Tom Trimble.

Cervical spine injury is always suspected- After removing the anterior part of the Philadelphia collar,an assistant  stabilizes the head in a neutral position  without flexion and with minimal extension.Another assistant performs cricoids pressure to avoid passive reflux.

Mechanical  ventilation – After intubation ,patients are ventilated to ensure normoxia and mild hyperventilation.

During the first hours following TBI, unnecessary hyperventilation is  avoided  because aggravates  the already reduced   CBF .

 In the case of asymmetric  neurological signs, hyperventilation is recommended  to reduce ICP ,albeit the risk of ischemia.

PEEP can be used as needed as it has minimal effect on ICP

Cardiovascular resuscitation

Hypotension  or hypoxia increase morbidity and mortality from severe traumatic brain injury.

Hypotension is defined as a systolic BP of 90 mmHg or less.  The CPP  should  be between 60 to 70 mmHg. Higher CPP's  are associated with an increased incidence of ARDS.

Fluid resuscitation (via 2 wide bores peripheral IV's)  is guided by  heart rate,

blood pressure , arterial wave contour , systolic variation (delta down) and capillary refill. Central venous pressure is not routinely monitored and urinary output is affected by mannitol.

Isotonic crystaloids
Assess coagulation function .(PT,PTT,Fibrinogen,TEG)
Early use of blood components.
FFP/PRBC >1:2 ratio reduce mortality
High platelets ratio improved survival in massive transfusion associated with TBI
Consider early use of cryoprecipitate or fibrinogen concentrate as needed
Tranexamic acid has shown to reduce risk of death, less progression of IC hemorrhage.

Serum glucose concentration should be kept between 140-180 mg/dL to avoid neuroglucopenia.Brain metabolism is impaired at levels below 108 mg /dL.

Vasopressors   are used  during fluid resuscitation  to shorten  the occurrence of  hypotension We generally use phenylephrine bolus 1.5 mcg/kg.

Management of increased ICP

Increased ICP over 20 mmHg is a predictor of  worse neurological outcome.

-Posture- Torso up  10-30 degrees.(remember to keep the transducer at ear level) and avoid  lateral deviation of  the head which can compromise venous return.

-Hyperventilation-see above

-Diuretics- Mannitol 1 g/kg  if lateralization signs or trastentorial herniation.Osmolarity kept under 320 mOsm/L. Not to  be used in hemodinamically unstable patients, produces hypotension. May mildly affect coagulation.

-Hypertonic saline- 5ml/kg of a 3% solution.

-Induced moderate hypertension, may produce cerebral vasoconstriction, thus reducing the intracranial blood volume.

-CSF drainage.

-Barbiturates-In refractory cases, needs vasopressor support.

-Decompressive craniotomy.

Temperature  - Treat hyperthermia aggressively. Hypothermia is not recommended.


After the initial resuscitation, the patient is taken to CT scan .Patients with unstable hemodinamics due to bleeding which need emergency extracranial surgery, are taken directly to the OR.
In patients with suspicion of  blunt injury of the neck vessels, a CT angio is performed.The patients at risk are:
neck hematoma,Lefort lll,abnormal neurological examination with normal head CT scan,seat belt injury,massive epistaxis.Although this lesions  are not frequent,can be devastating, and a prompt intervention in the neuroradiology suit can be life saving.

 

Operating room management

As in other stages, keep  goals of treatment.

Remember aggressive treatment of hypotension,hypoxia.

Try to improve operating conditions.

Almost all patients arrive intubated to the OR .Check depth and fixation of tube, lines.

In multiple trauma patients,be aware of sudden hemodynamic or respiratory decompensation  from  previously undiagnosed sources of bleeding , pneumothorax.

Bleeding- Check   frequently : operating field, suctions , CUSA,  monitors. Communication with surgeon is essential.

Bleeding  can be profuse ,so be ready .The main problems are underestimation of blood loss and unreadiness.

Early  blood orders and  available blood in the OR .

In massive bleeding, inform blood bank .

Arterial  wave contour and systolic variation are  the most important parameters for diagnosing hypovolemia and for continuous assessment of  volume  replacement.

In a  second place, pH and bicarbonate. Do fine tuning of the Ht  and other components when bleeding  is stopped and volemia corrected.
Common problems: 

Brain bulging

Causes: the hematoma itself ,brain edema, problems of positioning ,trendelemburg, jugular vein compression , turning of the neck, hypoventilation, PEEP, hypoxemia, hypotension

Iatrogenic use of hypotonic fluids before surgery

Treatment . After correcting  extracranial  factors ,  hyperventilate ,reduce inspiratory time,give another dose of mannitol  or hypertonic saline and /or furosemide

The surgeon may drain CSF from the ventricle.

If it does not help,  deepen the anesthesia with thiopental, which generally demands  the concomitant use of vasopressors

Monitoring

EKG, arterial line, pulse oximetry, esophageal  temperature, ETCO2 and agents, urinary output, TOF.

Brain monitoring in the OR is seldom used in trauma patients in our hospital.
All patients will have a subdural or intraventricular catheter placed for ICP monitoring.

Laboratory- Arterial  blood gases, electrolytes, glucose ,Ht. Coagulation profile, tromboelastogram.

Maintenance.  Balanced anesthesia  . Isoflurane or sevoflurane  are used at concentrations  lower  than 1 MAC. Opioids:fentanyl
TIVA- is another option.It is not associated with improved neurological outcome compared with balanced anesthesia with volatile agents.

Muscle relaxation.  Rocuronium ,vecuronium or atracurium.

Postoperative course-

After the postoperative CT scan , all  severe TBI and craniotomy patients are admitted  to neurosurgical intensive care.

Patients with one or more of these conditions are ventilated after surgery:

Severe traumatic brain injury,multiple trauma patients , massive transfusion, hypothermia, brain swelling, difficult hemostasis.

Please  consult the guidelines of the Brain trauma foundation and the page of Open Anesthesia

I wish to thank  Prof.Jean F.Soustiel, Deputy Director of the Dept.of Neurosurgery, for the revision  of this guidelines  and for his useful  suggestions and comments.

Anesthesia for surgery in the sitting position

I will include in this chapter  posterior fossa surgery, which in our hospital is performed in the sitting position in most of the cases  , and  anesthesia for cervical spine surgery done in this position. I will also include considerations for posterior fossa surgery which are relevant  for any surgical position.

 Preoperative assessment

Increased ICP due to Hydrocephalus-many patients undergo ventriculo-peritoneal shunt  before their definitive surgery.

Assess compromise of cranial nerves and consciousness.

Hydration- due to vomiting, mannitol administration and contrast media,many patients are hypovolemic, which demands correction before sitting the patient.

Planned surgery

Posterior fossa tumors. Due to the presence of neural and vascular structures,the surgical dissection can  stimulate or lesion these structures.As a consequence, cardiovascular reflexes  like hypertension, bradychardia  can suddenly appear  during stimulation of the brain stem ,the trigeminal nerve or the vagus nerve.

Bleeding –from  venous sinuses,from the tumor or arterial.

The sitting position is preferred by most of our surgeons due to excellent exposure, reduced bleeding and bulging albeit the risk of venous air embolism(VAE)

In patients who can be compromised by the hemodynamic instability posed by the sitting position like those with severe cardiac disease, we opt for lateral or park bench position.Patients  known to have PFO or ASD are not operated in this position due to the risk of paradoxical air embolism.

Premedication

Not routine, in anxious patients we give small doses of midazolam just before entering the OR.Patients scheduled for trigeminal nerve decompression or cervical laminectomy are premedicated  as usual.

Goals

Keep adequate CPP and hemodynamic stability
MAP is kept at  least at 70 mmHg at  circle of Willis level.

Adequate positioning, normoventilation.or mild hyperventilation to facilitate exposure.

Minimize VAE  risk

Anesthesia Technique

Monitoring:  EKG ,Pulse oximetry ,non invasive blood pressure, esophageal thermometer,ETCO₂, FIO₂,ET anesthetic agent,Train of four

The capnography is by large the most useful  monitor in VAE diagnosis.

Set  the alarm of low  ETCO₂   2-3 mmHg  below  the baseline in order to have an early warning in case of VAE. Tipically ETCO₂ will decrease in a few respiratory cycles.

Invasive  blood pressure : arterial line, generally Lt.radial ,20G after induction.The  arterial line is placed before induction under local anesthesia and light IV sedation in cardiac and unstable patients.

The transducer is placed at ear level (circle of Willis  level  ) to facilitate the assessment of CPP.

 Volemia is assessed by  the analysis of the arterial wave contour and by measuring   systolic variation (delta down)

Urinary catheter , esophageal  thermometer

1  or 2 wide bore IV's (depending on the vascularity  and site of the tumor ) 

Central venous line : Place a multiorificed ,EKG directed central line.Using an anterior approach of the right internal jugular,and lead l as the sensing lead  the catheter is advanced until  the P wave becomes biphasic, near the superior vena cava-right atrium junction.After fixation, check always patency.

The transducer is placed at the level of the right atrium (fifth intercostal space in the mid –axillary  line) .

In most of the cases of VAE, the amount  of air bubbles aspirated is minimal, as compared to the air that gets to the pulmonary circulation so generally  the central line is another diagnostic device and  is less important as a real retriever of air  from the circulation .

Precordial Doppler-placed after the patient is sitting .Audible heart tones and the typical noise after a rapid injection of saline via central line indicates correct placing of the transducer.The Doppler is affected  by bipolar diathermy  and is a significant noise polluter .Requires continuous listening.

IV induction  After preoxygenation, via  existing IV line

Fentanyl  1-2 mcg/kg

Propofol   2mg/kg or Thiopental or Etomidate until loss of eyelid reflex.

Facilitation of intubation  Rocuronium 0.6 mg/kg.Non depolarizing relaxants are always used during induction,-even when motor responses are monitored- in order to ease the positioning of the patient. Monitoring can be started about  45 min. after induction.

The ET tube is safely fixated and eyes are taped. In sitting position we fixate the tube with a  thin suction catheter.First,pass the catheter through one nostril, and pick it from the mouth with a Magill forceps.Make a knot  over the upper lip ,then knot it around the ET tube.Then fixate it as usual with tape This fixation does not interfere with the surgical field.
 
Maintenance The patient is ventilated with a mixture of O₂/air  to provide normoventilation or mild hyperventilation and normal oxygenation.A potent inhalatory agent , sevoflurane or isoflurane is added at less than  1 MAC.
Analgesia: Fentanyl increments .

If  SSEP are monitored,we use total IV anesthesia with remifentanyl infusion, between 0.1 and 0.25 mcg/kg/min and propofol.Deep TIVA  generaly requires vasopressor support.
Muscle relaxation Generally atracurium, 0.5 mg/kg/h (not in case of EMG monitoring or transcranial motor  evoked potentials)

Positioning

Before sitting the patients  bandage both legs to reduce venous pooling, and administrate a preload of NS.

When sitting, try to maintain a physiological position, avoiding extreme neck flexion which can compromise the spinal cord perfusion. Check that  the chin to chest distance is at least 4cm. Pad all pressure points.Pay attention to flexion of hips and knees.Do not leave an oral airway in place because of the risk of tongue edema.If motor evoked potentials are monitored, place a gauze roll between the teeth.

Fluids- Normal saline ( mildly hyperosmolar).  Metabolic acidosis is common with this fluid regime

Volume loading  is partially effective in VAE  prevention because it is difficult to rise CVP in patients with normal heart function.

Consequently the venous negative pressure present in the  surgical field cannot be reduced (except by jugular pressure).

 Hypovolemia is to be avoided.

Mannitol is not routinely given because of its hemodynamics effect .

Prophylactic antibiotics  Cefazoline 1g IV .In penicillin allergic patients, clindamycin 600 mg.

Seizure prophylaxis  Phenytoin or  Valproate (loading or maintenance)

In posterior fossa surgery ,some surgeons request them because  of the epileptogenic effect of  pneumocephalus.

Laboratory. In stable patients, Arterial blood gases and Ht are measured at  least   once every 2  hours .In bleeding patients, a full coagulation profile and a CBC is sent  at the beginning of the episode and  then  hourly. In massive bleeding , inform the blood bank which enters in a "massive transfusion mode" providing us  with all the blood components needed.

Intraoperative problems

Hypotension

Due to the change of position,hypotension  is common. Do not start remifentanyl  until the patient is sitting.Treatment: fluids, vasopressors.

If  muscle relaxants are avoided due to monitoring of motor evoked potentials, deeper anesthesia is needed to avoid movements,and a  continuous infusion of phenylephrine is given for hypotension.

Venous air embolism

About 50% incidence  in posterior fossa  . Can occur in any stage of surgery , more frequent during craniotomy.

In cervical laminectomy its incidence is negligible. Generally occurs without serious hemodynamic consequences ,although massive VAE can occur, causing  collapse.

In such cases, the operating table should be placed in the Trendelemburg position to stop VAE and allow resuscitating maneuvers  

Prevention- most probably depends on surgical technique.Avoid hypovolemia. Peep is not used.(may facilitate paradoxical air embolism)

Diagnosis-Typical sounds in precordial  Doppler ; a reduction of ETCO₂ due to an increase in physiological dead space.

Treatment-Inform the surgeon , will flood surgical field with saline

Ventilate with O₂ !00%. Denitrogenation  accelerates the absorption  of the bubbles.(N₂ is less soluble and will stay longer in the circulation)

Jugular pressure- Stops entrance of air and shows the surgeon the open veins responsible for the episode. We  also use this maneuver as a prevention of VAE. When the surgeon performs burr holes  and during the craniotomy, frequent intermittent  application of jugular pressure help the  identification of open veins which otherwise can become a source of VAE.

Aspiration of blood and air via central line.

Wait for a return of the ETCO₂ to baseline values to allow the surgeon to resume surgery.

Cardiovascular reflexes. Inform the surgeon. If repetitive bradycardia occurs,  give atropine to allow the surgeon  complete the dissection or resection of a tumor.

Hypertension. Short bouts of hypertension are generally self limited and are not treated.

Awakening the patient

If possible we  prefer early awakening in the OR

 Goals :patient awake, responds to simple orders, minimal cough,hemodinamically stable,no risk of hypoxia  or hypoventilation

In the following situations do not awaken the patient in the OR, and  transfer him to  the ICU via CT scan:

Patients which are no fully awake before surgery, long procedures, difficult hemostasis, hypothermia, massive transfusion, major hemodynamic instability ,brainstem edema,repiratory failure.

Stop atracurium infusion 30 min before end of procedure

Fentanyl  1.0 -1.5 mcg/kg   and droperidol 1 mg  for PONV prevention   after returning the patient to supine position.

These may cause   hypotension , be ready with ephedrine

After pin removal (on supine position to avoid VAE) and dressing , close inhalatory agent and remifentanyl. Reverse  residual curarization with atropine/neostigmine

The patient will awake in about 10-15 minutes.Emergency hypertension may occur and is treated with Labetalol, beginning with 0.25 mg/kg .

Cough -IV lidocaine  1.5 mg/kg

Extubate when patient is awake, normal Vt ,obeys orders ,no signs of residual curarization.

Transfer the patient to Recovery Room