The document discusses the posterior fossa, which contains the cerebellar hemispheres, brainstem, and cranial nerves 3-12. It is bounded anteriorly by the clivus and petrous bone, posteriorly by the occipital bone, and laterally by the temporal bone. Lesions in this area can cause a variety of neurological signs and symptoms depending on their location. The document outlines considerations for preoperative evaluation, patient positioning, monitoring, and induction/maintenance of anesthesia for posterior fossa surgeries. Maintaining hemodynamic and respiratory stability is important due to the location of critical brainstem structures in the posterior fossa.

1. By Dr. Basant Kumar Dindor
Under guidance of Dr. C. K. Vyas

2. 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
 Presence of 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 of signs 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 lateral cerebellar 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 of the 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 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 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 the posterior 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
 Bony artefacts 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.

14. EXTRAAXIAL
LESION
INTRAAXIAL
LESION
•Displacement of parenchymal
structures
•Presence of bone erosion
•Well delineated margins
•Contiguity with surrounding
dural or bony structures
•Do not erode bone
•Have indistinct margins

15.  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
 The posterior 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. 1) Complete Medical 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 the patient 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 goals of 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
 Sitting position :
 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 large airway 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 sitting
position
 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 in sitting
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‟s head 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 Park Bench 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 premedication is 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 can be 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 Sequence Induction 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/kg combined 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 volatile agent 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 relaxation is 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
 A balanced 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 should be 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.

39. COMPLICATIONS

40. 1.Brainstem & CN stimulation
 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 into the epidural or dural space sufficient to exert a
mass effect.
 Incidence- 3%
 Sometimes life threatening brain herniation.

43. CAUSES:
 Diminition of brain 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 OF NITROUS 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 flexion of 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 of head on the neck causes streching of the
spinal cord at C5 level, regional cord perfusion may be
compromised if MAP is decreased.

47. References
Manual of NeuroAnaesthesia
Scott L. Mears, M.D., and Richard j. Sperry, M.D.

48. Thanks