Short Answer Questions

Anaesthesia
& Intensive Care
For FCAI, FRCA & EDAIC
Modified by
AYMAN EDAROUS

Part 7: Neuroanaesthesia
Anaesthesia, Pain Management & Intensive Care Medicine Secrets Academy
 For Original Materials and Editors, Please refer to:

North Ireland School of Anaesthesia Website

MODIFIEDhttp://www.nischoolofanaesthesia-finalfrca.org.uk/SAQs/neuro/
BY AYMAN EDAROUS NEURO ANESTHESIA 2
1- Posterior Fossa Craniectomy
A 34 year old man is scheduled for a Posterior Fossa Tumour Excision.
a) List patient positions that might be employed for this operation.(2 marks)
b) What potential intraoperative problems are associated with posterior fossa craniotomy? 5
c) What monitoring techniques can specifically detect the presence of venous air embolism during surgery and
for each method used, give the features that would indicate the diagnosis?8

 The patient positions that might be employed for this operation:

Supine, Prone, Sitting, Lateral, Park bench

 Intraoperative problems are associated with posterior fossa craniotomy:

Cardiovascular instability- related to sitting position, venous pooling in the legs;
direct surgical stimulation of lower pons, upper medulla, floor of 4th ventricle, causing
tachy/brady arrhythmia, associated hypo/hyper tensions
Venous air embolism, site of surgery above the level of the heart entraining air
Pneumocephalus, particularly after closure of cranium, causing raised ICP

 Monitoring Techniques:
Precordial doppler - most sensitive, non-invasive device - change in audio of doppler
Transoesophogeal echocardiography - most sensitive invade device - appearance on echo
End tidal CO2 - set tight alarm limits, a sudden decrease in EtCO 2
End tidal Nitrogen - sudden increase in EtN2
Pulmonary artery catheter to measure pulmonary artery pressure - sudden rise in pressure
Right atrial pressure – increase.
Oesopgeal stethoscope - mill wheel murmur.
ECG - arrythmias, RV strain, ST depression.

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2- Traumatic Brain Injury (TBI)
A 54 year-old patient is admitted to the Emergency Department following a traumatic brain injury. A
CT scan reveals only cerebral oedema.
a) What is secondary brain injury and when is it likely to occur?
b) Outline the main physiological and cellular changes associated with secondary brain injury.
c) How can secondary brain injury be minimised in this patient?

 The secondary brain injury:

Inflammation and release of neurochemical mediators result in vasogenic oedema, contributing to
raised ICP, hypoperfusion and ischaemia. It occurs over hours to days from the initial brain injury.

The main physiological and cellular changes associated with secondary brain injury.

Physiological changes
*Vasogenic oedema causes ongoing hypoperfusion and ischaemia
*Disruption of blood-brain barrier with impaired vasomotor autoregulation leading to dilation of
cerebral blood vessels
*Hydrocephalus due to obstruction in flow and absorption of CSF due to blood in subarachnoid
space

Cellular changes
*Excitatory amino acids e.g. Glutamate are significantly elevated post TBI, causes:
- Cell swelling and neuronal death
- Influx of sodium and chloride into the cell, causing acute neuronal swelling
*Increased metabolism in injured brain stimulated by increase in circulating catecholamines
*TBI induced stimulation of sympatho-adreno-medullary axis and serotonergic system
*Increase in extracellular potassium leading to oedema
*Increase cytokines contributing to inflammation
*Decrease in intracellular Magnesium contributing to Calcium influx, linked to delayed damage

 How can secondary brain injury be minimised in this patient? (11 marks)
Targeted resuscitation and early specialist management beginning in the pre hospital setting and
continuing in tertiary hospital.
Prehospital (Avoid hypotension and hypoxia)
Airway; Early tracheal intubation if GCS <8, hypoxic on supplementary oxygen, hypo/hypercarbic

Breathing; Avoid hypoxia pO2> 11kPa, Maintain pCO2 4.5-5.0kPa

Hyperventilation 4-4.5kPa for impeding herniation- short term option due to normalisation of pH
through bicarbonate buffering

CVS; Avoid hypotension- maintain MAP >90mmHg

Replace intravascular volume- avoiding hypotonic and glucose containing solution
Use blood products as necessary- reverse existing coagulopathy
Vasopressors to maintain CPP > 60mmHg

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Neuro
 ICP monitoring- aim <20mmHg

 Maintain CPP>60 mmHg

 Adequate sedation, analgesia and muscle relaxation
*Propofol, Midazolam
*Opioid infusion
*Cisatracurium infusion –refractory increased ICP
 Hyperosmolar therapy-keep Na <155 mmol-1
*Mannitol/hypertonic saline
* Posm <320 m.mol-1
 CSF drainage (Extraventricular drainage)
 Treatment of seizures e.g. Phenytoin
 Barbituate coma- refractory raised ICP associated with cardiovascular instability
 Head of bed elevated to improve venous drainage
 Endotracheal tube taped, to limit venous congestion
Metabolic
 Strict blood glucose control 6-10 mmol-1
 Avoid hyperthermia, hypothermia for refractory raised ICP

DVT prophylaxis
Surgical: Decompressive Craniectomy.

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3- Raised ICP - Normal And Abnormal Waveforms
(a) What is a normal intracranial pressure (ICP)? (10%)
(b) Describe the normal ICP waveform. (20%)
(c) How does the waveform change with increased ICP? (20%)
(d) What are the anatomical results of a raised ICP? (30%)
(e) What are the symptoms and signs of a raised ICP? (20%)

 Intracranial pressure (ICP):

Intracranial pressure is the pressure within the fixed volume of the skull, and is a balance of
relationship between brain tissue, blood and CSF.
- The normal range estimated at being 7-13mmHg. An ICP above 20mmHg is generally considered as
being raised. There are slight variations in ICP with systolic and diastolic pressures and with
respiratory patterns. There are also variations with posture (slight increase when supine) and on
coughing, straining … etc.

 Normal ICP waveform:

ICP waveform is pulsatile and reflects cardiac and respiratory cycles. The normal ICP waveform is
Triphasic. In normal physiology the first peak is greater in amplitude than the 2nd &3rd

The ICP wave is produced by pressure transmitted from the arterial pulse to the brain. This wave has
3 components:

1. P1 – percussion (systolic) wave – produced by systolic pressure transmitted to choroid plexus

and is the mechanism by which CSF is produced
2. P2 – elastance (tidal) wave – reflects cerebral compliance and because of this is variable
produced by the restriction of ventricular expansion by the rigid dura and scull, like an echo
3. P3 – dicrotic wave – reflects venous pressure and produced by closure of the aortic valve

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LUNDBERG WAVES
Lundberg A (Plateau) waves are periodic, sustained increase in ICP (>50mmHg) for 15 minutes or
more, and is associated with poor intracranial compliance and poor prognosis.

Lundberg B waves are periodic, self-limited increases in ICP (<50mmHg) occuring every 1-2 minutes
and lasting several seconds.

Lundberg C waves are periodic, self-limited increases in ICP (<20mm Hg) occuring every 4-8
minutes. Significance of these waves are unknown.

 The waveform change with increased ICP:

A raised ICP we have stated as being greater than 20mmHg therefore this will be reflected on the
amplitude of the waveform
- The second and third peaks become greater in amplitude in an elevated ICP
- P2 reflects cerebral compliance. If ICP is raised, cerebral compliance is reduced and the second
peak becomes the most prominent
- When observed over a period of time, a pathological ICP trace may show pathological A waves (A
waves sustained < 20mins)
These are also known as plateau waves because of the shape of the waveform, often seen at very
high ICP values (e.g. greater than 50mmHg, 50 – 200mmHg),indicate severe raised ICP and patient
will often show neurological signs of raised ICP

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 The anatomical results of a raised ICP:
Based on Monroe Kellie doctrine, if the volume of
one of the cranium constituents rises, then the
other 2 must compensate to maintain a fixed
volume and pressure
- Vascular anatomical changes include
vasodilatation to maintain CPP.
- Reduction in cranial blood volume
- CSF moves out of cranial vault into thecal sac.
 The Symptoms and Signs of a raised ICP:
Cerebral oedema, causing loss of sulci, reduction in
size of ventricles, from a number of causes;
cytotoxic, in cell death; vasogenic, vasodilatation,
raised BP; transependymal, outflow obstruction of
CSF
- Pressure transmitted along optic nerve causing
papilloedema
- Herniation of brain tissue at extremes of ICP
- UNCAL HERNIATION; temporal lobe herniates below tentorium cerebelli. This inturn may
compress oculomotor cranial nerve (see below)
- TONSILLAR HERNIATION; cerebellar tonsil herniates through foramen magnum
- SUBFALCINE HERNIATION; cingulate gyrus of frontal lobe herniates across midline, across falx
cerebri. May occlude anterior cerebral artery
- UPWARD CEREBELLAR HERNIATION; if primary lesion in posterior fossa

May vary depending on rate of onset, i.e. insidious (e.g. in brain tumour) vs acute (acute bleed,
traumatic brain injury)
- If insidious, or GCS not impaired, symptoms may include headache, particularly postural
in nature (worse supine, on straining etc), visual disturbance (e.g. if cranial nerve
involvement see below).
- Signs, in significantly high ICP and acute onset
include;
NEUROLOGICAL FINDINGS
*Reduced GCS
*Focal neurology and motor posturing
*Seizure activity
*Cranial nerve lesions, e.g. 3rd (oculomotor) cranial nerve compression in uncal herniation causing
ipsilateral mydriasis and movement of eye down and out.
*Papilloedema on fundoscopy
CARDIOVASCULAR SIGNS include;
*Hypertension, physiological response to maintain CPP
*Hypertension and bradycardia, or “cushing’s reflex” seen in brainstem compression in
tonsillar herniation also known as coning
*Arrhythmias, again due to involvement of brainstem
RESPIRATORY; Abnormal respiratory patterns in brainstem herniation, e.g. cheyne stokes.

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4- Acromegaly and Pituitary Surgery
(a) What challenges does a patient with acromegaly present to the anaesthetist? (25%)
(b) What are the advantages and disadvantages of the transphenoidal approach? (35%)
(c) Why might the surgeon request a lumbar drain insertion? (15%)
(d) Describe the possible complications of pituitary surgery (25%)

 Acromegaly Features:
Airway: Nasal polyps, magroglossia, madibular
hypertrophy, difficult BMV, hypertrophy of aryepiglottic
folds, soft palate and epiglottis, difficult intubation;
tracheal compression (1/3) secondary to enlarged
thryroid, subglottic stenosis , recurrent laryngeal nerve
palsy. May need AFOI.

Respiratory: OSA, nasal CPAP impossible as nose packs will

be in post op.

Cardiac: May have cor-pulmonale;

refractory HTN, cardiomyopathy and
IHD bi-ventricular dysfunction heart
block
Endocrine: 25% are diabetics. Secretion
of ACTH, TSH also (as well as GH) or
alternatively compression of tissue and
reduced hormone secretion;
hypoadrenalism results in that situation
-hormonal and antihypertensive
therapy should be continued pre-op
Other: Excess peripheral soft tissue
deposition may make venous
cannulation difficult and increases the
risk -nerve entrapment syndromes;
meticulous attention to theatre
positioning
HDU care post operative:
-Short acting agents such as
Remifentanil are ideal, allowing
intraoperative haemodynamic control
and facilitating rapid recovery; enables
neurological assessment
-NSAIDs linked with post op
haematoma
-N&V prophylaxis
-Steroid replacement therapy needed.

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 Advantages of the Trans-phenoidal approach (Extracranial Approach)

*Safest approach *Shorter hospital stay

*Macro and microadenoma *Minimal surgical trauma
*Minimal blood loss *Direct access to the gland
*Avoidance of the generic hazards of a craniotomy

*Disdvantages of the Trans-phenoidal approach:

* Bifrontal craniotomy needed for giant pituitary tumours or failed transphenoidal approach
persistent CSF rhinorrhoea and the associated risk of postoperative meningitis,
* Panhypopituitarism,
* Transient DI
* Vascular Damage
* Cranial Nerve Injury
* Cerebral Ischaemia, and stroke as a result of vasospasm or thromboembolism.
* Deliberate nasal septum fracture is required for transsphenoidal transnasal approach; to minimize
nasal bleeding, mucosal vasoconstriction is achieved by using a topical anaesthetic & a vasoconstrictor
Co-Phenylcaine (5% lidocaine 0.5% phenylephrine) causes less of a hypertensive response than
adrenaline in pts with Cushings.

 Lumbar Drain Insertion:

It is allow descent of tumour into surgical field by injecting small amounts of saline into subarachnoid
space. The same effect can also be achieved by controlled hypercapnoea.
To control post op CSF leak

 Complications of Pituitary Surgery

* Venous or arterial bleeding esp larger tumours
* CSF leak, menigitis
* Airway obstruction
* CN11-V1 damage as close proximity to surgical site
* Postoperative neuroendocrine abnormalities can occur after pituitary surgery. DI (50%) usually
develops within the first 24 h, and resolves spontaneously in about a week. (Polyuria with a urine
specific gravity of < 1.005 and low osmolarity of < 300 mosm)
* Hyponatremia can be caused by excess desmopressin admin
* SIADH (20% occurs 1/52 post op); fluid restriction to 500–1000 ml/ day
* HRT (Hormone Replacement Thearpy) will required in all patients after operation e.g. Steroids
* VAE 10%.

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5- Scoliosis Surgery and Spinal Cord Monitoring
(a) Describe the principles of preoperative assessment in scoliosis surgery. (20%)
(b) What are the potential complications of the prone position - how can these be avoided? (35%)
(c) How is the spinal cord monitored during the procedure? (30%)
(d) What are the options for postoperative analgesia after a spinal procedure? (15%)

 Preoperative assessment in Scoliosis Surgery :

History: Type of scoliosis: idiopathic or secondary.

- Idiopathic usually in fit, healthy patients with no
cardiorespiratory complications. Standard assessment
and history of good exercise tolerance usually sufficient.
- Secondary – elicit primary cause, any other organ
dysfunction eg in muscular dystrophy cardiomyopathy /
restrictive lung defects may be present.

Tests:
- Bloods: including coag screen, Calcium, Phosphate
and Cross match.
- CXR and Spirometry (PFTs).
- If non-idiopathic, ABG if PFTs not possible.
- ECG & Echo for cardiac function, if exercise impossible pharmacological stress Echo useful.

 Complications of the Prone Position :

PROBLEM
Dislodged ETT, monitoring, catheter, cannulae
Pressure damage : Eyes (direct and reduced
venous drainage), Joints and Peripheral nerves
Indirect injury (chest wall, impaired visceral blood
flow)
CVS: IVC compression -> reduced venous return ->
reduced preload -> reduced SV
RS: abdominal compression> higher airway pr.
Chest wall weakness compressing RV
GI: visceral ischaemia incl pancreatitis and hepatic
infarction
PRACTICAL
Sufficient staff (6 recommended), recheck all lines
after turn, reinforced ETT
Turn head to side, padding and tape, check
frequently, nothing tight around neck, care if head
down
Padding, ascertain ROM prior to surgery and do not
exceed
Careful positioning and padding
Avoid direct abdominal pressure (especially in
obese)
Adequate fluid loading, reduce abdominal pressure
with pelvic & chest wedges
Montreal mattress (hole for abdomen), pelvic and
chest wedges

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 Spinal Cord Monitored during Scoliosis Surgery:
- Continuous intraoperative Motor and Somatosensory
evoked potentials.
*Somatosensory: lower limb nerve stimulated and spinal
cord or cortical response monitored.
Not affected by anaesthetic agents (except
local); may be affected by hypothermia
*Motor: cortex stimulated and spinal cord or distal
response monitored.
Sensitive to volatiles so less useful.
Nerve injury indicated by increased latency or reduced
amplitude of response.

* ‘Wake up’ test: If sudden deterioration – stop relaxants and

volatiles and ask patient to move hands and feet. Remifentanil
useful in case this is necessary (responsive without pain).

 Postoperative Analgesia after a Spinal Procedure :

*Systemic: simple analgesics and opioids. NSAIDs usually
avoided for 24hours to avoid bleeding problems and
reduced bone healing.

*Regional: surgically placed paravertebral or epidural

catheters.
Usually a combination used eg simple analgesia,
continuous epidural infusion of local anaesthetic and
continuous or PCA infusion of morphine.

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6- Aneurysmal Subarachnoid Haemorrhage (SAH)
(a) What are the symptoms & signs of SAH (including extra-cranial)?(20%)
(b) What are the complications of SAH? (10%)
(c) Describe specific measures for cerebral protection following a SAH. (30%)
(d) What are the goals of anaesthetic management for neurovascular surgery? (20%)
(e) What are the methods of minimising hypertension during induction of anaesthesia? (10%)

 The symptoms & signs of SAH (including extra-cranial):

-Sudden onset severe headache -Loss of consciousness (transient or prolonged)
-Nausea and vomiting -Seizures
-Focal neurological signs -Neck stiffness
-Photophobia -Papilloedema
-Pyrexia -Reactive hypertension
-Cardiac arrest

 Complications of SAH
-Rebleeding -Raised ICP
-Seizures -Hydrocephalus
-Hyponatraemia -Delayed cerebral ischaemia and vasospasm
-Fevers -Hyperglycaemia
-Cardiac complications – neurogenic stunned myocardium syndrome
-Pulmonary complications – aspiration pneumonitis, ALI/ARDS/pulmonary oedema

 Measures for cerebral protection following a SAH:

- Nimodipine – calcium channel antagonist that reduces incidence of cerebral infarction, give
prophylactically after SAH for 21 days (60 mg PO 4 hourly)
- Triple H therapy - HAEMODILUTION, HYPERTENSION, HYPERVOLAEMIA. Now this is not
recommended.

*New recommendations are aim for:

EUVOLAEMIA (avoid hyper/hypovolaemia).
AVOID HYPOTENSION
NORMAL Hct.
- Control of arterial BP – aim for a systolic BP < 160 mmHg and a MAP < 110 mmHg. Avoid hypotension
(keep systolic BP > 100 mmHg)
- In the situation of a new neurological deficit where medical therapy fails consider aggressive
endovascular treatment e.g. Angioplasty
- Treat fevers with Anti-pyretics and cooling
- Maintain serum blood glucose between 4.5 and 11 mmol/L

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 The goals of anaesthetic management for neurovascular surgery

-Providing optimum operating conditions for surgeon

-Preventing increase in transmural pressure which may cause rupture of aneurysm
-Maintaining adequate cerebral perfusion pressure and cerebral oxygenation

- Prevent rise in MAP especially at laryngoscopy, during placement of head pins & after skull is open
- Uncontrolled hypotension should also be avoided because this may cause cerebral ischaemia
- Maintain normothermia
- Ensure venous drainage is unobstructed: good head
position, head up tilt, avoid tube ties, avoid internal jugular
lines
- Avoid acute drops in ICP as this may risk rupture of
aneurysm by increasing transmural pressure gradient across
aneurysm wall
- Normalise MAP and PaCO2 prior to closure to reveal any
bleeding points
- Smooth and rapid emergence and extubation without
coughing/gagging on ETT
- Use short acting anaesthetic agents and opioids to allow
rapid return to consciousness to assess GCS post op (unless
poor grade SAH and requires continued ventilation on ICU)

 The methods of minimising hypertension during

induction of anaesthesia
- Insert arterial line prior to induction to enable BP control
- Pre-operative beta-blockade
- Captopril 2-3 mg/kg as premed
- Adequate dose of Alfentanil or Remifentanil
- Adequate induction dose of Thiopental or
Propofol
- Bolus dose of induction agent immediately
prior to stimulus
- IV lignocaine (1.5 mg/kg)
- Vasoactive drugs to reduce MAP (Trimetaphan,
Phentolamine)
- Use of nerve stimulator to confirm muscle
paralysis
- Careful intubation technique.

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7- Spinal Cord Injury - Physiology and Effects
A 27 year old man is admitted with a suspected spinal fracture following a fall into water.
(a) Describe the respiratory effects at the different levels of spinal cord injury (20%)
(b) Describe the physiology of spinal shock (20%)
(c) What would be the principles of your management of the airway in a patient with an acute cervical spine
injury? (20%)
(d) What are the complications of hard and semi-rigid collars? (20%)
(e) Why and when may Suxamethonium be contraindicated in a patient with spinal injury? (20%)

 The respiratory effects at the different levels of spinal cord injury:

- C3 and above, denervation of diaphragm  respiratory failure.
- C3-C5 partial diaphragm paralysis  need assisted ventilation
- C5-C8 complete intercostal paralysis,diaphragm intact paradoxical ventilation, ineffective cough
- T1-T7, variable intercostals muscles involvement  poor chest wall movement and poor cough
- Above T7, Neurogenic CVS complication due to traumatic disruption of sympathetic system.
- T1-T4, cardiac sympathetic supply, damage at this level affects chronotropic and inotrpic responses
of heart

 Physiology of Spinal Shock:

Spinal shock describes the initial phase after spinal cord trauma and defined as;
-Temporary interruption of spinal cord function; all reflexes are lost and the cord below the level of
the lesion becomes isolated from centre. (Flaccid paralysis).If there is an evidence of neurological
sparing below the level of lesion it might recover.

Autonomic and reflex activity gradually returns to an injured cord. Loss of descending inhibitory
control causes Autonomic Hyperreflexia and Spasticity.

 Management of the airway in a patient with an acute cervical spine injury :

The initial management of the polytrauma patient follows the ATLS practice of airway and cervical
spine control, breathing and circulation.

-MILS to prevent further spinal cord trauma during laryngoscopy

- Intubation aids (boigie) and The McCoy is an alternative to the Macintosh
- RSI with adequate pre oxygenation
- LMA or intubating laryngeal mask in the failed or difficult intubation. The forces applied during
insertion can cause posterior displacement of the cervical spine but the movement is less than that
seen in direct laryngoscopy.

In the ‘Can’t Intubate, Can’t Ventilate’ scenario there should be early consideration of the
surgical airway or Cricothyroidotomy.
These techniques can produce posterior displacement of the cervical spine but this should not prevent
the use of this life-saving procedure.

Nasal intubation has been superseded by oral intubation for the low success rate and high incidence
of epistaxis and layngospasm .

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Awake fibreoptic intubation : least amount of movement of the cervical spine, in the acute trauma
setting, blood or vomit in the airway may make the technique impossible.
Further disadvantages include a relatively prolonged time to intubation,

 The complications of hard and semi-rigid collars :

Total immobilisation is not achieved
-Increases the chance of difficult laryngoscopy
-Can exacerbate cervical spinal injuries
-Can cause airway obstruction
-Can increase intracranial pressure (ICP)
-Increases risk of aspiration
-Increases risk of deep vein thrombosis (DVT)
-May cause significant decubitus ulcers

 Suxamethonium contraindications in a patient with spinal injury:

-Suxamethonium is safe to use in the first 72 hours and after 9 months following the injury.
In the intervening period there is a risk of suxamethonium-induced hyperkalaemia due to denervation
hypersensitivity and therefore should be avoided.
-After 24 Hours up to a year post burn.

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8- Head Injury and Sodium Disorders
(a) Differentiate between the CT findings of cerebral contusions, diffuse axonal injury, SAH and extra-/sub-dural
haematomas. (20%)
(b) Define primary and secondary brain injury. (20%)
(c) Describe the fluid and electrolyte differences in SIADH, CSWS and CDI (30%)
(d) What are the key principles dictating management of the head injured patient on ICU?(30%)

 Cerebral Contusions:
*Early: Foci of hyperdensity involving grey matter and subcortical white
matter. Later with surrounding oedema. Gradually fade to areas of gliosis.
Can occur anywhere but predilection for anterior cranial fossa, temporal
pole and coup/contrecoup pattern.
*Diffuse axonal injury
*Loss of grey-white matter differentiation

SAH: Hyperdense substance filling normally dark CSF filled subarachnoid

spaces (fissures, sulci, lateral and third ventricle)

EDH: Biconvex/lentiform shaped hyperdense extraaxial collection. Sharply

demarcated. Does not cross sutures. Often beneath temporal bone. Often
causes mass effect.

SDH:
*Acute: Crescent/sickle shaped hyperdense extraaxial collection. Crosses
sutures spreading diffusely over hemisphere.
*Subacute: Isodense with cortex
*Chronic: Hypodense with cortex

 Primary Brain Injury: Damage that occurs at the time of initial insult and may be result of trauma,
mechanical forces applied to the brain (diffuse axonal injury), haemorrhage or tumour

*Secondary Brain Injury:

-Injurious processes after the 1ry injury including ionic, metabolic & inflammatory processes.
-Hypoxaemia, hypercapnia, hypotension, raised intracranial pressure, cerebral arterial spasm and
hypoglycaemia worsen secondary brain injury.

 The fluid and electrolyte differences in SIADH, CSWS and CDI:

SIADH CSWS CDI

Raised plasma volume
Positive/equal sodium balance
Positive water balance
Low serum sodium
Lowered serum osmolality
High urine sodium
High urine osmolality
Lowered plasma volume
Negative sodium balance
Negative water balance
Low serum sodium
High/normal serum osmolality
High urine sodium
Normal/high urine osmolality
Lowered plasma volume
Equal sodium balance
Negative water balance
High serum sodium
High serum osmolality
Normal urine sodium
Reduced urine osmolality

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 Management of the head injured patient on ICU:
Normotension
*Strenuous attempts to maintain blood pressure in normal range.
*Hypotension has negative effect on outcome.
*Impaired cerebral autoregulation in brain injury
*Cerebral perfusion pressure (CPP) = Mean arterial pressure (MAP) - intracranial pressure (ICP).
*Evidence unclear but aim to maintain MAP of at least 70mmHg and to achieve CPP target of over
70mmHg (Rosner protocol) or over 50mmHg (Lund protocol)
*Initially fluid resuscitation and then vasopressors.

Normoxia
*Hypoxia associated with worse outcome
*Cerebral blood flow (CBF) increases when PaO2 falls below 8kPa
*Maintain PaO2 >13kPa
*PEEP to maintain oxygenation (<12-15cmH2O)

Normocapnia
*Aim for PaCO2; 4.5-5.0 kPa
*CBF increases as PaCO2 increases
*Hyperventilation reduces PaCO2 causing vasoconstriction, avoid as it worsens ischaemia

Normothermia
*Avoid hyperthermia which causes increase in CBF and cerebral metabolic oxygen requirement and
increases ICP.

Normoglycaemia
*Hyperglycaemia causes increase in cerebral metabolism and in situation of reduced CBF in trauma
this results in anaerobic metabolism
*Aim for tight blood glucose control 4.0-8.0mmol/l with insulin
*Avoid dextrose

ICP management
*Aim ICP <20mmHg with
sedation/analgesia, maintain CPP,
osmotic therapy if required (mannitol or
hypertonic saline)
*Avoid surges in ICP

General ICU care

*Sedation
*Analgesia
*Nutritional support
*Venous thromboembolism prophylaxis
*Sodium homeostasis

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9- Pre- / Intraoperative Management of Posterior Fossa Surgery
(a) What are the anaesthetic goals in surgery for patients with intracranial pathology? (20%)
(b) What are the features in pre anaesthetic assessment of a patient listed for surgery for a large Glioma (30%)
(c) Describe the intraoperative anaesthetic management of a craniotomy. (30%)
(d) What are the complications of posterior fossa surgery? Why is surgery in the posterior fossa of particular
concern? (20%)

 The anaesthetic Goals in surgery for patients with intracranial pathology :

- Provide optimal operating conditions: may require Osmotherapy if excessive brain swelling
- Avoid secondary injury:
-Maintain cerebral perfusion and oxygenation. With intracranial pathology attention to the
management of ICP and maintenance of adequate MAP to maintain CPP is paramount.
-Avoid increasing venous pressure.
-30o Head up reduces central venous pressure.
-MAP can be manipulated with fluids, vasopressors and inotropes as clinically indicated.
-Avoid hypercarbia and hyperthermia.
-ICP can be reduced with osmotic diruetics.
- Keep patient comfortable and safe: Padding of eyes and other pressure points; monitoring for VAE

 The pre-anaesthetic assessment of a patient listed for surgery for a large Glioma :
- In addition to the normal preoperative assessment specific issues include:
Drug Hx: Diuretic therapy, steroids, antiepileptic drugs with potential effects on glucose, electrolytes
and intravascular volume, QT interval.

Neurology: GCS, focal motor deficits; higher cortical function; seizures

Imaging: size and location, midline shift (>10mm = severe compromise), vascularity or proximity to a
major sinus – risk of bleeding / VAE.

Postoperative plan: level of care required will depend on extent of surgery, likely complications and
potential for airway or respiratory compromise from reduced GCS or other deficit

 Intraoperative Anaesthetic Management of a Craniotomy:

Positioning: avoid extreme neck flexion or rotation, ensure eyes and other pressure points are
protected.
Monitoring: Arterial line, CVP and urinary catheter. Some units may use transcranial doppler, jugular
bulb oximetry and brain tissue oxygenation probes.
Maintenance: Avoid N2O and maintain anaesthesia using volatile or TCI propofol.
Remifentanil is also used. Application of a fixator is highly stimulating and requires bolus analgesia or
anaesthetic.
Cerebral oedema: treatment with diuretics and mild hypocapnia
Fluids: Hypotonic fluids are contraindicated. Saline 0.9% or Hartmann’s are the crystalloids of choice.
Preparing for emergence: closure of the dura, bone flap and scalp takes half an hour. Analgesia should
be added at this point if remifentanil is used. Prepare to treat hypertension with labetalol.

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 The Complications of Posterior Fossa Surgery:

Intraoperative Postoperative Late

Bleeding Raised ICP CSF leak
VAE Cranial nerve palsies Infection
Cardiovascular disturbance Injury to respiratory centre Pseudomeningoocele
Prone positioning Cerebellar mutism (children) Obstructive hydrocephalus
Tumour recurrance

*Monro-Kellie hypothesis:
Is a pressure-volume relationship that aims to
keep a dynamic equilibrium among the
essential non-compressible components inside
the rigid compartment of the skull (Rigid Box).

The average intracranial volume in the adult is

around 1700 mL, composed of brain tissue
(~1400 mL), CSF (~150 mL), and blood (~150
mL). The volume of these three components
remains nearly constant in a state of dynamic
equilibrium. Thus, a decrease in one
component should be compensated by the
increase in other and vice-a-versa.

It is important to note that most of the blood in

the cranial cavity is contained in the low-
pressure venous system, so venous
compression serves as a means of displacing
blood volume.

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10- Awareness - Depth of Anaesthesia Monitoring
(a) What are some of the causes of anaesthetic awareness? (20%)
(b) What is bispectral analysis (BIS)? What is the suggested interpretation of BIS values? (30%)
(c) What other type of depth of anaesthesia monitoring are there? (10%)
(d) What steps would you take if you were informed by the midwives that a patient who had undergone a GA the
previous day was complaining of awareness under anaesthetic? (30%)
(e) Are you aware of any major studies going on at the moment into awareness? (10%)

 Types of Surgery Patient Factors Anaesthetic Factors

*GA caesarean *Haemodynamically unstable
section patient e.g. major
*Cardiac surgery haemorrhage
*Trauma surgery *Difficult airway
*Rigid bronchoscopy *Drugs blunting hypertensive
and tachycardic responses-
beta blockers, Ca channel
blockers
*Chronic opioid or
benzodiazepine use
*Use of neuromuscular blockers
*Failure of monitoring equipment
*Malfunctioning vaporizer
*Empty vaporizer
*Failure of TIVA pump
*Unrecognized tissued IV cannula with
TIVA
*Drug errors (e.g. mixing up thiopentone
and co-amoxiclav)
*Misjudgment of anaesthetic doses
required

 The Bispectral analysis (BIS):

BIS uses EEG monitoring. The machine uses an algorithm to interpret EEG waves and gives a numerical
value from 0 to 100. The target BIS value for general anaesthesia is 40 to 60.

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 The other type of depth of Anaesthesia Monitoring:
*Clinical Assessment for Signs of Sympathetic activity- HR, Blood Pressure, Sweating & Lacrimation
* Monitoring end tidal inhalational agent
*Isolated Forearm Technique
*Forehead Galvanometry
*Oesophageal Motility
* EEG and Auditory evoked potentials

 The steps would be taken if you were informed that a patient who had undergone a GA the
previous day was complaining of awareness under anaesthetic:

*Read patient’s notes- establish details of anaesthetic and circumstances, find out who the
anaesthetist was
*Inform the anaesthetist who was involved and the consultant
responsible if the patient was anaesthetised by a trainee
*Arrange a discussion with the patient with a witness present
*Sympathetic approach to the patient
*Take a detailed history from the patient establishing what she
remembers
*Ask if she felt any pain during surgery
*Apologize to the patient
*Explanation of awareness- why it sometimes occurs
*Document the discussion in the notes
*Write to patient’s GP
*Refer to psychologist if patient wants further support

 NAP 5:
*National audit project undertaken by the Royal College of Anaesthetists and AAGBI
*One year reporting period
*Local reporters in each anaesthetic department report all cases of awareness presenting during that
one year period
*Aims to assess incidence of awareness.

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11- ICP Monitoring and Management of Raised ICP
(a) Which patients with severe head injury should have ICP monitoring? (20%)
(b) List the methods by which the intracranial pressure (ICP) can be measured in ICU. (15%)
(c) Describe two of these in greater detail (30%)
(d) What methods are used to manage or prevent acute rises in the ICP? (20%)
(e) Describe the mechanism of action of Mannitol in head injury(15%)

 ICP Monitoring with Severe Head Injury:

*Severe head injury GCS 3-8 with abnormal admission CT (ie; Haematoma, Contusion, Oedema, or
Compressed Basal Cisterns)
*Severe head injury and normal CT but ≥2 of:
- Age > 40 yrs,
- Unilateral or bilateral motor posturing,
- Systolic BP < 90 mm Hg
- At risk of raised ICP requiring general analgesia.
**Not routinely indicated in patients with mild/moderate head injury however may be appropriate in
certain conscious patients with traumatic mass lesions

 Methods of ICP measurement in ICU

-Intra-ventricular
-Intra-parenchymal
-Subarachnoid
-Subdural
-Epidural
 Intra-ventricular is the ICP measurement
Gold standard.
*Catheter inserted into the ventricle
connected to a column of fluid and a pressure
transducer.
*Wheatstone bridge principle; Change in
pressure causing change in the resistance of
the transducer system, causing change in
electrical current translates to change in
intracranial pressure.
*Can be used for therapeutic CSF drainage.
*High risk of infection, can be used for administration of antibiotics.
*Can get blocked.
Intra-parenchymal
*Uses fibreoptic able with displaceable mirror at the catheter tip, placed in the brain tissue.
*Change in ICP distorts the mirror and reflected light intensity transduced into pressure.
*No saline filled column of fluid and manometer in needed.
*Accuracy comparable to intraventricular catheter but may only
reflect local change in ICP.
*Cannot be calibrated in vivo.
*Prone to drift over time.
*Cannot be used for therapeutic CSF drainage.

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 Management and Prevention of Acute Rises in the ICP:
Physiological
*Head up > 30 degrees, avoid excessive rotation of head
*Loose collar/ ET tube neck tie
*Avoid hypoxaemia, hypercarbia, hyperthermia, vasodilatory drugs, hypotension
*Avoid PEEP, avoid central line in neck.
Pharmacological
*Hypertonic saline 30% up to 20 ml
*Mannitol 1g/kg
*Barbiturate coma
*Hypothermic therapy
*Hyperventilation
*Steroid
Surgical:
*Decompressive craniectomy & Insertion of EVD or ventriculo-peritoneal shunt

 Mechanism of action of Mannitol in head injury:

Immediate: Osmotically active sugar alcohol, expands intravascular volume, increase flow, reduces
viscosity, increase cardiac output, increase cerebral perfusion, increase microvascular oxygenation.
Compensatory regional vasoconstriction where autoregulation is intact causing reduction ICP.
Delayed: Establish osmotic gradient between plasma and brain cells. Draws out extracellular water into
vascular compartment provided blood brain barrier is intact. Reducing oedema.

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12- Anaesthesia for Awake Craniotomy
(a) What are the indications for an awake craniotomy? (20%)
(b) What are the contraindications for an awake craniotomy? (20%)
(c) What local anaesthetic techniques must the surgeon/anaesthetist employ to provide analgesia/anaesthesia?
(d) What is the asleep-awake-asleep technique? (20%)
(e) What complications may be encountered in an awake craniotomy? (20%)

 The Indications for an Awake Craniotomy:

Anatomical
Space occupying lesions in or adjacent to eloquent areas of the cortex.
Excision of tumours in the sensory and motor speech areas in the dominant hemisphere and
sensorimotor cortex in either hemisphere following cortical stimulation mapping.

Physiological
Stimulation or lesion generation of deep brain nuclei (e.g. the subthalamic nucleus) for
intractable movement disorders such as Parkinson’s disease and dystonias.
Pharmacological
Epilepsy surgery when intraoperative electro-corticography (ECoG) is required to define the
resection margins.

 Contraindications for an Awake Craniotomy:

* Confused patient
* Communication difficulties
* Extreme anxiety
* Low occipital tumour (prone position)
* Significant dural involvement (painful)
* Inability to lie still for many hours
*Inexperienced surgeon

 Local Anaesthetic Techniques:

*If Mayfield head fixator is used, adequate local anaesthesia should applied prior to pins application
*Brain Biopsy/Mini-Craniotomy: Infiltration of local anaesthetic into the relevant area of scalp and
pericranium, and later onto the dura, is all that is required.
*Formal Craniotomy:
-The neurosurgeon must perform field blocks of the scalp, using combinations of Lidocaine and
Bupivacaine with Epinephrine.
-Six nerves need to be blocked bilaterally to completely anaesthetise the scalp: the Supratrochlear,
Supraorbital, Zygomaticotemporal, Auriculotemporal, and the Lesser and Greater Occipital nerves.
-The skin, scalp, pericranium and periosteum of the outer table of the skull are all innervated by
cutaneous nerves arising from branches of the trigeminal nerve. Subcutaneous infiltration with local
anaesthesia in the manner of a field block or over specific sensory nerve branches, blocks afferent
input from all layers of the scalp.
-The skull can be drilled and opened without discomfort to the patient (no sensory innervation)

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-The dura is innervated by branches from all three divisions of the trigeminal nerve, the recurrent
meningeal branch of the vagus, and by branches of the upper cervical roots. It must therefore be
adequately anaesthetized with a local anaesthetic nerve block around the nerve trunk running with
the middle meningeal artery, and also by a field block around the edges of the craniotomy.

1. The Supraorbital Nerve is blocked just above the supraorbital notch and local anaesthetic is
deposited just superficial to the periosteum.

2. The temporal branch of the Auriculo-temporal Nerve is blocked immediately posterior to the
superficial temporal artery at the level of the auditory meatus.

3. The main branch of the Zygomatico-temporal Nerve emerges from the temporalis fascia near the
lateral border of the orbit, although many smaller deep branches ramify within the temporalis muscle.
These small branches are especially important to block so as to cover temporally based flap incisions.
Field infiltration above the zygoma through the temporalis muscle and almost down to the periosteum
of the temporal bone will give a good result, without causing a facial nerve block.

4. The Lesser Occipital Nerve can be blocked either deep or superficial to the fascia at the upper,
posterior border of sternocleidomastoid.

5. The Greater Occipital Nerve is blocked subcutaneously by injecting along the middle third of a line
between the mastoid process and the external occipital protuberance along the superior nuchal ridge.
This injection will also reinforce the lesser occipital nerve block as it becomes subcutaneous.

 The asleep-awake-asleep Technique:

Some patients are not able to tolerate craniotomy with sedation alone and general anaesthesia with
intraoperative wake-up is an alternative. The introduction of propofol improved the safety profile of

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the asleep–awake–asleep technique & provided more predictable intraoperative wake-up.

A combination of Propofol and Remifentanil infusion is now the technique of choice because it allows
titratable levels of anaesthesia and fast and reliable wake up.

Bispectral index (BIS) monitoring can be used to guide target-controlled infusions.

 Complications of Awake Craniotomy:

*Seizures
*Nausea and vomiting
*Dysphoric reactions
*Respiratory depression
*Airway obstruction
*Air embolism
*Pulmonary aspiration
*Conversion to general anaesthesia

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13- Sitting Position and Air Embolism
(a) For what types of neurosurgery is the patient positioned sitting?
(b) What are the advantages and disadvantages of the sitting or deckchair position?
(c) Describe the pathophysiological effects of air embolism?
(d) How may an air embolism be detected?
(e) What is the management of a suspected venous air embolism during a craniotomy?

 Types of neurosurgery is the patient positioned sitting:

 Posterior cervical procedures
 Posterior cranial fossa craniotomies

 The advantages and disadvantages of the Sitting or Deckchair Position:

Advantages:
 Better access to the airway
 Reduced facial swelling
 Improved hemodynamic stability
 Reduced blood pooling in the operative field
Disadvantages:
 Venous air embolism
 Hypotension 2ry to venous pooling
 Excessive neck flexion  Cord ischemia

 Pathophysiological effects of air embolism:

*Air enters Rt. Atrium  Rt. Ventricle

*CVS
 Compressive air causes obstruction to Rt. Ventricular Ejections “AIR LOCK” or Pulmonary Outflow Tract.
 Slow ejection of air trapped at pulmonary arterioles  Pulmonary Arterial Hypertension & Rt.
Ventricular failure.
 Micro-emboluses ; obstruct flow
 Neutrophils attracted to fibrin network of RBCs, fat globules and Platelets that build around the
bubbles .
 Ultrastructural damage  Basement Membrane Permeability  Pulmonay Edema.

*Paradoxical Air Embolus:

 Via PFO or transpulmonary gas shunting
 End arteriolar obstruction  Distal Ischaemia.

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 Air embolism detection:
 The presentation of VAE is dependent upon the rate and volume of air entrained.
 VAE can range from being clinically undetectable to potentially fatal.
 Rapid entrainment of large volumes of air will result in apnoea, hypoxia and cardiovascular
collapse.
 Slower rates of entrainment may result in the patient complaining of light-headedness, breathing
difficulties, shortness of breath, chest pain and a sense of impending death.
 A 10% obstruction to the pulmonary circulation can cause a gasp reflex which, in itself, reduces
right atrial pressure (RAP) further increasing air entrainment.
 Significant embolism leads to tachypnoea, tachycardia, and hypotension. This may be
accompanied by altered mental status, decreased conscious level or focal neurological deficits.

Signs
 Auscultation of the heart might reveal the classical ‘mill wheel’ murmur.
 Pulmonary oedema may develop later.
 End-tidal carbon dioxide falls as a consequence of an increase in physiological dead-space and
intrapulmonary shunting. Arterial oxygen saturation falls.
 ↑ CVP (25%)
 ↑ PA pressure (50%)
 ABG: may reveal hypoxaemia and, less commonly, hypercarbia.
 Chest X-ray is initially normal but signs of non-cardiogenic pulmonary oedema may develop later.

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ECG:
 Tachyarrythmias
 AV block
 Signs of RV strain
 ↑ST/↓ST
Non-specific T wave change

Detector devices:
 ETCO2
 Precordial Doppler
 TOE gold standard
 CVP/PAC
 (ETN2)
 Oesophgeal steothoscope

Differential diagnosis (DD)

When respiratory symptoms and signs predominate, DD
includes pulmonary embolism, pneumothorax,
bronchospasm and pulmonary oedema.

 Management of a suspected VAE during a Craniotomy:

 ABCDE approach.
 Discontinue N2O
 Administer 100% O2
 Flood surgical field with Saline.
 Aspirate air from Rt. atrium via CVC
 Left lateral decubitus position (Durant Maneuver)/ Trendelenburg position
 Inotropic agents
 Cardiopulmonary by-pass
 Thoracotomy.

https://upload.wikimedia.org/wikipedia/commons/d/d4/Echokardiographiebefund_einer_Luftembolie.webm

Notes: Durant’s maneuver consists of placing the patient in the left

lateral decubitus position in order to prevent a venous air embolism
from lodging in the lungs. The air will rise and stay in the right heart
until it slowly absorbs. Similarly, placing a patient in the
Trendelenburg position (head down) helps prevent arterial air
embolism from traveling to the brain causing a stroke.

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Summary of Specific Physiological Changes and Risks and Benefits with Positioning for Neurosurgical Procedures.
Cardiovascular Respiratory Central nervous Benefits Risks
Supine Compared to upright, awake Compared to upright: FRC ↓, TLC ↓ Compared to upright: The easiest position Often needs head flexion/extention/rotation Ulnar and peroneal
and anesthetized: atelectasis of the dependent lung zones; nerve injury
VR ↑, SV ↑, CO ↑ Qs/Qt ↑ JVF ↑ ↔
HR ↓ V/Q mismatch ↑ JVR ↓ ↔
SVR ↓ CPP ↔ ↓
SBP ↔, MAP↓↔ CSF drainage may be
impaired
Lateral Compared to supine, Compared to supine: Compared to supine: Optimal approach to the temporal Brachial plexus injury
anesthetized: lobe
VR ↓, SV ↓, CO↓ FRC ↓, TLC ↓ JVF↑↔ Ear and eye injury
HR↑ ↔ Qs/Qt ↑↑ JVR↓↔ Suprascapular nerve injury (of the dependent shoulder)
SVR↑, PVR↑ V/Q mismatch ↑↑ atelectasis of the with neck flexion:
dependent lung
SBP↓, MAP↓ JVF↓, JVR↑, ICP↑

Prone Compared to supine, awake: Compared to supine: increase in upper Compared to supine: a) Optimal posterior approach to The most difficult position Difficult access to airway Pressure sores
airway resistance (Wilson frame and chest neutral to the heart spine Less risk for VAE (compared of soft tissues Eye injury Blindness Bleeding (compared to sitting)
rolls) to sitting)
VR↓, SV↓
HR↑ ↔ JVF ↑ ↔
SVR↑, PVR↑ FRC↑ ↔, TLC↑ ↔ JVR↓ ↔
SBP↑↔, MAP↑↔ V/Q mismatch ↓ b) lower than heart
In anesthetized patient: less atelectasis in lungs JVF↑, JVR↓, venous
congestion
VR↓, SV↓, CO↓↔ ICP↑
HR↑, SVR↑, PVR↑
SBP↓↔, MAP↓↔
Sitting Compared to supine, awake: Compared to supine: Compared to supine: Optimal approach to posterior fossa Venous air embolism (VAE) Paradoxical air embolism Arterial
Low ICP Hypotension
VR ↓, SV ↓, CO↓ TLC ↑, FRC ↑ JVF ↓, JVR ↑
Qs/Qt↓ ICP↓↓
HR↑, SVR↑, PVR↑ V/Q mismatch ↓ CPP ↔ Minimal bleeding (compared to Pneumocephalus Paraplegia, Quadriplegia Macroglossia
prone) Access to airway
SBP↑↔↓, MAP↓ ↔↑ less atelectasis in lungs Good cerebral venous
and CSF drainage
In anesthetized patient:
VR↓↓, SV↓, CO↓ MAP↓
HR↑, SVR↑, PVR↑ SBP↓,

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Changes of physiologic parameters in cardiovascular, respiratory and central nervous system are presented as observed in anesthetized subjects, changes in
cardiovascular system presented in awake and anesthetized subjects: HR- heart rate, SV-stroke volume, VR – venous return, CO-cardiac output, SBP- systolic
blood pressure, TLC- total lung capacity, FRC- functional residual capacity, Qs/Qt – intrapulmonary shunt, V/Q mismatch- ventilation/perfusion mismatch,
ICP- intracranial pressure, JVF – jugular venous flow, JVR – jugular venous resistance, CPP- cerebral perfusion pressure; ↑- increase, ↓ - decrease, ↔ no
change.

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Anaesthesia, Pain Management & Intensive Care Medicine Secrets Academy [APICSA]
Telegram: https://t.me/joinchat/DRLToA7sXfLoguTCkCxi9w

Reference:
http://www.nischoolofanaesthesia-finalfrca.org.uk/SAQs/neuro/

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