Anesthesia for neurosurgery (zuhura)

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Anesthesia for neurosurgery (zuhura)

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

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