• Share
  • Email
  • Embed
  • Like
  • Save
  • Private Content
Anesthesia for neurosurgery (zuhura)
 

Anesthesia for neurosurgery (zuhura)

on

  • 3,772 views

 

Statistics

Views

Total Views
3,772
Views on SlideShare
3,743
Embed Views
29

Actions

Likes
5
Downloads
0
Comments
1

3 Embeds 29

http://anaesthesiahsnz.wordpress.com 23
http://www.neuropractices.com 5
http://neuropractices.com 1

Accessibility

Categories

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel

11 of 1 previous next

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

    Anesthesia for neurosurgery (zuhura) Anesthesia for neurosurgery (zuhura) Presentation Transcript

    • ANAESTHESIA FOR NEUROSURGERY
      • noor zuhura mohd
    • INTRO
      • Anaesthetic management of neurosurgical patients requires
      • understanding of basic physiology of the CNS
      • understanding the effects of anaesthetic intervention on cerebral function
    • Regulation of Cerebral Blood Flow
    • Cerebral Perfusion Pressure
      • CPP is effective pressure that drives blood flow to the brain
      • CPP = MAP - ICP or CVP (whichever is greater)
      • normal CPP = 80-100 mmHg
      • normal ICP = 5-12mmHg
      • Moderate to severe increases in ICP (>30mmHg) can significantly compromise CPP and CBF even in the presence of normal MAP
    • Autoregulation
      • Intrinsic activity of the organ to maintain a constant blood flow despite changes in perfusion pressure
      • Cerebral vasculature rapidly adapts to changes in CPP
      • ⬇ CPP causing cerebral vasodilation
      • ⬆ CPP causing cerebral vasoconstriction
    • Autoregulation
      • In normal individuals CBF is autoregulated to maintain blood flow between MAP 60-160 mmHg
      • Beyond this limits blood flow becomes pressure dependent
      • Pressure above 150-160mmHg can disrupt BBB causing cerebral edema
    • Autoregulation
      • In normal individuals CBF remains constant between MAP 50-150 mmHg
      • Beyond this limits blood flow becomes pressure dependent
      • Pressure above 150mmHg can disrupt BBB causing cerebral edema
    • Extrinsic Mechanisms
      • Respiratory gas tension
      • CBF directly proportionate to PaCo2 between tension of 20-80mmHg
      • Hypocapnia results in cerebral vasoconstriction and reduction of CSF
      • Hypoxemia PaO2 <50mmHg profoundly increase CBF (not an important determinant)
    • Extrinsic Mechanisms
      • Respiratory gas tension
      • CBF directly proportionate to PaCo2 between tension of 20-80mmHg
      • CO2 cross BBB but H+ does not so acute metabolic acidosis has little effect on CBF
      • Hypoxemia PaO2 <50mmHg profoundly increase CBF
    • Extrinsic Mechanism
      • Temperature
      • Hypothermia decreases both CMR and CBF
      • For every 10 deg C increase in temperature, CMR doubles
      • CMR decreases by 50% if temp of the brain falls by 10 deg C
    • Intracranial Pressure
    • Intracranial Pressure
      • Monroe-Kellie Doctrine
      • The cranial vault as a rigid structure with fixed volume
      • Brain 80%
      • Blood 12%
      • CSF 8%
      • Any increase in one component must be offset by an equivalent decrease in another to prevent rise in ICP
      • ICP normally 10mmHg and less
      • IC compliance determined by measuring the change in ICP in response to change in intracranial volume
      • Initially increases in volume are initially well compensated until it reaches a point which further increase can cause rise in ICP
      • ICP normally 10mmHg and less
      • IC compliance determined by measuring the change in ICP in response to change in intracranial volume
      • Initially increases in volume are initially well compensated until it reaches a point which further increase can cause rise in ICP
      • Compensatory mechanism
      • displacement of CSF from cranial to spinal compartment
      • increase in CSF reabsorption
      • decrease in CSF production
      • decrease in cerebral blood volume
    • AIMS OF ANAESTHETIC MANAGEMENT
      • Provision of optimal operating conditions
      • Maintenance of stable ICP, or reduction of elevated ICP by physical/ pharmacological means
      • Maintenance of stable hemodynamic, oxygenation and ventilation parameters; use of controlled hypotensive anaesthesia
      • Maintenance of an appropriate CPP and cerebral oxygenation, while minimising CMRO2 to protect against ischaemia
      • Early detection and prompt management of intraoperative complications:
      • venous air embolism (VAE) in posterior fossa surgery
      • intracranial bleeding during cerebral aneurysm rupture
      • Controlled but rapid emergence from anesthesia to enable early assessment and monitoring of neurological status
    • COMMON NEUROSURGICAL PROCEDURES
      • Drainage procedures
      • Ventriculo-peritoneal (VP) or Ventriculo-atrial (VA) shunt
      • External ventricular drainage (EVD)
      • Evacuation of EDH/ SDH via Burr hole/ craniotomy
      • Craniotomy for excision / debulking of tumour
      • Frontal, temporal or parietal approach for supratentorial tumour
      • Post. fossa surgery for cerebellar, cerebellopontine (CP) angle tumour
      • Frontal or trans-spenoidal approach for pituitary tumour
      • Cerebrovascular surgery: excision of cerebral aneurysm / AVM
      • Surgery of the spine or spinal cord
      • Laminectomy
      • Excision of myelomeningocele
      • Surgery on the skull : cranioplasty, elevation of depressed fractures
      • Stereotactic surgery
    • ANAESTHESIA FOR CRANIOTOMY
    • Preoperative Assessment
      • Confirm diagnosis, indication and consent
      • Routine preop assessment
      • Airway, CVS and respiratory system
      • Details of concomitant medical illnesses, nature of treatment and compliance to therapy
      • Invenstigations appropriate for age, general status of patient and type of surgery
      • Detailed CNS assessment
      • Level of consciousness, presence and extent of neurological deficit (clear documentation)
      • Observe respiratory effort in terms of tachypnoea, laboured breathing or Cheyne-Stokes pattern of breathing
      • Assess the presence of cough/ gag reflex if bulbar involvement is suspected.
      • Look for clinical manifestation of raised ICP:
      • headache, vomiting, focal neurological signs and papilloedema
      • Late signs: deteriorating GCS, Cushing's reflex, dilated pupils, decorticate then decerebrate posturing and coma
      • Review CT scan or MRI:
      • size and location of the SOL, size of ventricles, presence of midline shift and evidence of generalised/ peri-tumour cerebral oedema
      • Other considerations
      • Assess the fluid status: possibility of dehydration and electrolyte imbalance in patient who has been vomiting, fluid restricted/ receiving diuretic therapy
      • Assess glycaemic status: rule out hyperglycemia in diabetic patient/ patient treated with dexamethasone
      • Rule out endocrine dysfunction esp in pituitary tumours: hypo/ hyperthyroidism, acromegaly, hypo/hyperadrenalism
      • Based on overall assessment, identify patients who would requires postop ventilation in ICU
      • GCS </= 6
      • evidence of raised ICP
      • large or deep seated tumour
      • presence of midline shift and /or significant cerebral oedema
      • Premedication
      • Opiod premedication often avoided : hypercarbia ➡ increased CBF and ICP and possibility of disrupting early postop neurological assessment
      • For patient who is going for spine surgery who is alert, conscious and anxious:
      • Small dose of benzodiazepine may be prescribed
      • Alternatively a small IV dose of benzodiazepine can be administered in OT prior to induction
      • Effect of benzodiazepines are not detrimental as long as hypotension is avoided
      • Other preparation
      • GXM
      • Fasting instruction for the patient
      • Serve the patients medications on the morning of surgery
    • Anaesthetic Management
      • Reassess the patients's neurological status before induction
      • Confirm availability of ICU or HDU
      • Establish venous access w large bore IV cannulae. As the anaesthesiologist is at the foot end, IV cannulae at the saphenous veins avoid extension tubings.
      • Monitors: ECG, non invasive BP, pulse oximetry, and capnography for minor cases (VP shunt, EVD, Burr hole, cranioplasty)
      • Additional monitors: u/o, temperature, neuromascular blockade, invasive BP and CVP monitoring for major cases
      • Preoxygenation with 100% o2 3-5 minutes
      • Common drug at induction:
      • Fentanyl 2-3 mcg/kg
      • Thiopentone 4mg/kg or Propofol 2mg/kg
      • Atracurium 0.6mg/kg, Vecuronium 0.1-0.15 mg/kg or Rocuronium 0.6 mg/kg
      • Lignocaine 1-1.5mg/kg or Esmolol 0.5-1 mg/kg may be used to obtund sympathetic reflex during airway manipulation
      • Suxamethonium transiently increase ICP and best avoided in elective cases (except in difficult intubation) - should not be withheld in emergency cases
      • Monitor the degree of neuromuscular blockade with peripheral nerve stimulator
      • Allow non-depolarising NMB take effect
      • Laryngoscopy and intubation should be attempted when patient is adequately paralysed
      • Use an oral RAE/ flexometallic tube of appropriate size - fasten ETT securely after confirmation of placement
      • Protect the eyes using pads (particularly important if patient is placed prone with head on horseshoe headrest)
      • Allow the surgeon/ assistant to shave the head and position the patient
      • Maintain head-up tilt of 15deg- 20deg and avoid extreme neck flexion or rotation
      • Re-check placement of ETT after positioning
      • Head is often secured in place using Mayfield 3-point fixator
      • An additional dose of Fentanyl before the pins inserted helps to prevent marked hypertension and tachycardia
      • In cases of increase ICP may need to lower ICP by administering mannitol 0.5-1g/kg and/or frusemide 0.5mg/kg
      • Mannitol infusion is best started at the time of skin incision so that the peak effect becomes available upon dural opening
      • Send ABG
      • Maintain PaO2 > 100mmHg and PaCo2 between 30-35 mmHg.
      • Avoid overventilation since hypocarbia may result in cerebral vasoconstriction and reduce cerebral perfusion
      • Maintenance of anesthesia
      • TIVA with propofol, NMB drug, opiod and IPPV with o2-air mixture
      • Inhalation technique with volatile agent, NMB drug, opiod, O2-nitrous or O2-air mixture
      • NMB administered by continuous infusion or intermittent boluses
      • Anesthesia maintained with intermittent boluses of Fentanyl or infusion of Remifentanyl
      • Isoflurane and Sevoflurane are preferred:
      • maintenance of cerebral auto-regulation up to MAC 1.5
      • maintenance of CO2 reactivity of cerebral blood vessels
      • Maintenance of anesthesia
      • Sevoflurane gives smooth induction, rapid onset and offset of action
      • Nitrous oxide causes cerebral vasodilatation, increased CBV and ICP. Also contribute to development of pneumoencephalocele. Should be avoided:
      • in patient with cerebral ischaemia/ reduced intracranial compliance
      • surgery with significant risk of VAE (posterior fossa surgery)
      • Fluid management
      • IV fluid used judiciously and be sufficient to maintain IV volume and hemodynamic stability
      • Dextrose-containing solutions should be avoided unless indicated
      • hypoosmolar causing fluid shift
      • hyperglycemia can cause impaired neurological recovery
      • Ringer's lactate is also hypoosmolar and can cause increase plasma glucose via lactate metabolism
      • 0.9% saline is the preferred crystalloid but may cause hyperchloraemic acidosis when large doses are infused
      • Blood loss maybe torrential. Important to have adequate venous access.
      • Temperature control
      • Controlled hypothermia as a neuroprotective strategy though improved outcome not conclusively demonstrated
      • 'Permissive hypothermia' 33deg-35deg celcius decreases CMRO2 and may increase the period of ischaemia tolerated intraop
      • Normothermia should be achieved before patient awakens to avoid shivering which markedly increases O2 demand
      • Thromboembolic prophylaxis
      • Neurosurgical patients are at risk for DVT and pulmonary embolism
      • Heparin should not be used because of risk of bleeding in confined cavity
      • Mechanical means (graduated compression stockings and intermittent pneumatic leg compression) are used
      • Management of emergence
      • Most patients don't require prolonged intubation and mechanical ventilation after uneventful craniotomy
      • Controlled emergence with early return to consciousness so that full neurological assesssment can be made in earliest time as possible
      • Anaesthetic agents with short action of duration and little hangover effects are preferred
      • The patient should not be allowed to cough through ETT (tachycardia, hypertension and increased ICP)
      • Management of emergance
      • Turn off the volatile agents at the time of bone flap replacement; maintain anaesthesia with nitrous oxide if used and continue infusion of Remifentanil or residual Fentanyl
      • At completion of dressing, reverse the NMB, turn off Remifentanil infusion and administer 100% O2
      • Another longer acting opiod should be administered before discontinuation of Remifentanil to provide subsequent analgesia
    • Post-op Management
      • Decision of post-op ventilatory support depends on:
      • Patients's preop neurological status
      • Intraop events (duration and complexity of surgery, hemodynamic stability, complications, hypovolemia, massive transfusion)
      • Evidence of raised ICP (tense dura / tight brain)
      • Communication with the surgeon is essential to avoid misunderstanding regarding postop plan
      • Regular neurological observations should be recorded.
      • Any neurological deterioration should raise suspicion of ICB/ oedema (urgent CT should be considered)
      • Other aspects:
      • Hemodynamic should be closely monitored to maintain adequate cerebral perfusion pressure
      • Post op pain often not severe and can be managed by intermittent bolus doses or morphine infusion/ other opiods
      • Electrolyte imbalance (esp sodium) should be identified and corrected
      • U/o should be monitored (diabetes insipidus)
    • Posterior Fossa Surgery
    • Anatomy of Posterior Fossa
      • Lies between tentorium cerebelli and foramen magnum
      • Contains cerebellum and brainstem
      • Cranial nerve IX(glossopharyngeal), X(vagus), XI(accessory) , XII(hypoglossal)
      • Emissary veins (valveless veins that drain external veins of skulls into dural venous sinuses)
    • Anatomy of Posterior Fossa
    • The Surgery
      • Indications:
      • resection or biopsy of tumours (glioma, astrocytoma, meningioma, medulloblastoma, acoustic neuroma, hemangioblastoma)
      • resection of vascular lesion (aneurysm, angioma, AVM)
      • abscess, haematoma, congenital lesions
      • Special problems for these reasons:
      • Confined space - not much room for oedema/ bleeding which if uncontrolled can cause coning through foramen magnum
      • Main motor and sensory pathways are in close proximity to op site (lower cranial nerve nuclei and vital centres controlling respiratory and CVS functions in brainstem)
      • Obstruction to CSF flow at the aqueduct /forth ventricle results in hydrocephalus
      • Patient may have altered conscious level with impaired airway reflexes leading to silent aspiration
      • Position:
      • Prone, lateral or semi prone (park-bench). Sitting is rarely adopted.
      • Extreme care must be taken while turning the patient
      • Avoid extreme flexion of the neck which may cause
      • venous and lymphatic obstruction (can cause upper airway oedema)
      • cord hypoperfusion (resulting in quadriparesis) esp in elderly
      • If there is possibility of lower cranial nerve dysfunction with bulbar paresis:
      • Gag reflex, swallowing and laryngeal function may be impaired
      • Insert RT
      • Nitrous oxide should be avoided
      • Increase CMRO2 and CBF
      • Aggravate VAE or pneumocephalus
      • TIVA is preferred
      • Close monitoring of CVS for interference of vital centers
      • arrhythmia or hypertension
      • precipitous decrease in HR often signifies brainstem ischaemia and should be notified to the surgeon
      • resolves spontaneously when surgical retraction is removed
      • atropine is required in severe bradyarrythmias
      • close communication with surgeon is essential
      • Postop ICU with mechanical ventilation is often indicated:
      • In patients with low GCS
      • There is evidence of airway oedema or bulbar paresis
      • The surgical resection is extensive or complicated
      • There are intraop complications
    • VENOUS AIR EMBOLISM
    • INTRO
      • Condition caused by ingress of air into the vascular system
      • Arterial air embolism can occur
      • paradoxical air embolism via heart defect
      • direct arterial cannulation during cardiac surgery or angiography
      • Classically a/w sitting craniotomy
      • Also potential complication of laparascopic, pelvic and orthopaedic procedures
    • Pathophysiology
      • 2 conditions must exist for venous air embolism to occur
      • direct communication between source of air and vasculature
      • pressure gradient favouring passage of air into ciculation
      • Estimated of 5ml/kg of air displaced into IV space is required for significant injury
      • The closer of vein entrainment to heart the smaller the lethal volume is
      • Large volume of air in systemic venous circulation
      • Strain to right ventricle
      • Significant rise in pulmonary artery pressure
      • Right ventricular outflow obstruction
      • Compromise pulmonary venous return to the heart
      • Decrease ventricular preload, CO
      • CVS collapse
      • Activation of complement and mediators
      • Injury to the lungs
      • Capillary leakage
      • Non cardiogenic pulmonary edema
      • Alteration in resistance of lung vessels
      • V/Q mismatch
      • Intrapulmonary right to left shunting
      • Increased alveolar dead space
      • atrerial hypoxia and hypercapnea
      • Caused by
      • Entrainment of air into the venous system when the venous pressure is sub atmospheric
      • Surgical field above level of the heart
      • Central venous cannulation during spontaneous respiration
      • Infusion of air or other gas under pressure into the venous system
      • Insufflation of CO2 in laparascopic surgery
      • Venturi jet ventilation
      • Pressurised IV infusion set
      • Major cause of fatality is attributed to circulatory obstruction and ultimately arrest d/t air trapped in right ventricular outflow
      • The severity determined by rate and volume of air entrained and position of patient at the time VAE occurs
      • Entry of air in arterial system may present as acute cerebrovascular or coronary event
    • Clinical Manifestation
      • Decrease ETCO2 d/t reduction in pulmonary circulation
      • Fall in SaO2 with hypercarbia d/t reduced pulmonary blood flow and V/Q mismatch
      • CVS changes
      • Millwheel murmur via esophageal/precordial sthetescope
      • loud course continuous murmur that may obliterate s1 s2
      • insensitive but indicates massive air embolism with imminent collapse
      • Hypotension
      • CVS changes
      • Non specific ECG changes
      • tachy/brady arrhythmia
      • right heart strained pattern with peaked P waves
      • ST segment elevation or depression non specific T wave
      • sudden increase in CVP with reduced cardiac output and increase pulmonary vascular resistance
      • Circulatory collapse with EMD
      • Neurological signs
      • occur secondary to paradoxical air embolism across patent foramen ovale
      • delayed emergance
      • cerebral irritation
      • convulsions
      • localizing neurological signs
    • ANAESTHESIA FOR CEREBROVASCULAR SURGERY
    • INTRO
      • Intracranial aneurysm, AVM, atheromateous plaque at the branches of extracranial/ intracranial vessels
      • AVM
      • dilated arteries and veins with no intervening capillaries
      • presentation: SAH, ICB, headache/seizure
      • high blood flow through shunts may cause ischaemia and loss of vascular reactivity in the underlying brain tissue
      • treated by:
      • excision or devascularisation by neuroradiology
      • surgery is not urgent unless hemorrhage causing hematoma and increase ICP
      • Prevalance of unruptured intracranial aneurysm is 2-5%
      • Majority of aneurysms are saccular (berry) aneurysm
      • 90% occur at the anterior part of circle of willis (ant. communicating and ant. cerebral arteries)
    •  
      • May present with SAH
      • sudden onset of unusually severe headache
      • followed by period of unconsciousness
      • May cause compression to adjacent neural structures
      • headache
      • cranial nerve palsies
      • Some patients are asymptomatic and diagnosis is made by incidental CT scan findings
      • Optimal timing of surgery after SAH is controversial
      • Early surgery <48H maybe a/w suboptimal surgical conditions but may reduce the incidence of re-bleeding and vasospasm
      • Worst outcome is a/w surgery between 7-10 days after SAH (carries greater risks of angiographic and clinical vasospams)
      • Delayed surgery provides times for oedema to subside
      • Technically easier
      • Increase risk of re-bleeding and prolonged bed rest
      • Anaesthetic concerns include:
      • Problems common to neurosurgical procedures
      • Problems a/w ruptured intracranial aneurysm
      • Control of intracranial hypertension
      • Prevention and treatment of cerebral vasospams
      • Problems during intraoperative management
      • Stringent control of intraop BP within narrow limits
      • Intraop rupture of aneurysm may cause rapid and massive blood loss
    • Pre-Op Assessment
      • Assess clinical manifestation of SAH (headache, vomiting, neck stiffness, or seizures)
      • CVS
      • Hypertension (preexisting/ Cushing,s reflex/ use of inotropes in triple-H therapy [vide infra])
      • ECG changes following SAH (peaked P, short PR intervals, long QT intervals, pathological Q waves, ST-T wave abnormalities, prominent U waves, cardiac arrythmia)
      • May mimic myocardial injury
      • Respiratory system
      • basal atelectasis in patients with prolonged bed rest
      • aspiration pneumonia in comatose patients
      • neurologic pulmonary oedema
      • Fluid and electrolytes
      • dehydration secondary to vomiting/ reduce oral intake
      • Fluid and electrolyte imbalance secondary to inappropriate ADH secetion or salt wasting syndrome (must be corrected before surgery)
      • Management of SAH
      • to maintain normal CPP
      • avoidance of extreme hypertension
      • maintenance of normal fluid balance
      • Triple-H therapy (Hypertension, Hypervolemia, Haemodilution) in attempt to improve CPP and prevent ischaemic neurological deficit caused by vasospasm.
      • Oral nimodipine, a CCB with vasodilating effect in cerebral vessels is often used in treating cerebral vasopspasm
      • IV nimodipine may cause hypotension
    • Anaesthetic Management
      • Good communication between surgeon and anaesthesiologist concerning surgical conditions and hemodynamic parameters is essential
      • IABP and CVP before commencement of anesthesia
      • Pulmonary artery catheter indicated in the presence of significant myocardial damage and ventricular dysfunction
      • Prevent wide fluctuations of BP:
      • Smooth induction (prevent hypertension during intubation and hypotension post induction)
      • Intraoperative BP should be maintained within 10-20% of baseline BP
      • Hyperetension risks aneurysm rupture while hypotension risks cebral ischaemia
      • Large bore IV cannula - potential of catastrophic haemorrhage
      • Rapid transfusion devices should be primed and ready for volume resuscitation
      • Induced hypotension in excision of AVM:
      • reduce intraop blood loss
      • systolic BP 60-80mmHg should be adequate achieved by:
      • volatile anaesthetic
      • beta blockers and/or
      • sodium nitropurasside
      • when AVM is excised reperfusion of surrounding tissue may cause cerebral edema and increase ICP
      • Induced hypotension is used with caution
      • hypotension may increase risk of cerebral ischaemia in patients with vasospasm and impaired autoregulation
      • indicated in complex cases or if intraop aneurysm rupture occurs
      • Other neuroprotective measures (e:g in difficult aneurysm surgery/ intraop aneurysm rupture)
      • hypothermia to 32deg celcius
      • thiopentone infusion to reduce CMRO2
      • All patients should be admitted to ICU for hemodynamic and neurological status monitoring
      • Prolonged surgery or intraop complications may necessitate sedation and ventilation postop
      • Close attention of hemodynamic and fluid resuscitation
      • Vasoactive drugs
      • Judicious use of fluids
      • Neurological status should be assessed as soon as feasible and regular assessment should be made thereafter
      • Decrease in GCS or development of new neurological deficit indicate:
      • vasospasm
      • intracranial bleed
      • hydrocephalus
      • Urgent CT may be needed for definitive diagnosis and further mangement plan
    • THANK YOU