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Neuro Review
Cerebral metabolisma. Average adult brain is 1500 gb. CMRO2 = 50 ml/min or 3.5 ml/100g/min 1. Hypocampus and cerebellum most sensitive Cerebral blood flowa. Parallels metabolic activity iv. Flows below 10 ml/100g/min associated with hypoxic injury i. PaCO2 linear correlation with CBF between 20 – 80 ii. PaCO2 < 20 associated with ischemia 1. Hyperoxia causes little change2. Hypoxia acutely raises CBF 1. Vessels receive sympathetic and parasympathetic 3. Pharmacologic control through the ANS very limited vi. Hypertension causes a left shift of autoregulation curve Cerebral perfusion pressurea. CPP = MAP – ICP (or CVP if greater) iii. CPP < 25 = brain damage – worse with hyperglycemia Cerebrospinal Fluida. Found in ventricles, cisterns and subarachnoid spaceb. Formed in choroid plexusc. Absorbed by arachnoid villid. Adults make 400 – 500 mL/day i. CSF production decreased by steroids, acetazolamide, furosemide, isoflurane spironolactone and vasoconstrictors i. Lateral ventricle to foramina of Monroe to 3rd ventricle to cerebral aqueduct to 4th ventricle to foramen of Magendie tocysterna magna to subarachnoid space Sitting Craniotomya. Usually done for lesions in posterior fossab. Increases likelihood of pneumocephalus and excessive CSF lossc. Venous air embolism i. 20 – 40% incidence (highest of all surgeries) ii. Paradoxical embolism can occur with probe-patent foramen iii. Venous air trapped in pulmonary vascular tree 1. Increased PA pressures2. Decreases ETCO23. Hemodynamic manifestations 4. Aspiration via CVP – multiorificed catheter should be a. Notify surgeon – flood surgical field, pack boneb. DC nitrous oxidec. Aspirate CVPd. Increase CVP with volume, PEEPe. Bilateral jugular vein compressionf.
Cerebral aneurysmsa. Aneurysms and AVMs are most common causes of nontraumatic b. Usually occur at arterial bifurcationsc. 10 – 30% have multiple aneurysmsd. 5% of population have aneurysmse. M&M very high from rupture (50%)f.
g. Vasospasm can occur after rupture (30%)h. Vasospasm treated with “triple H” therapy i. Hypervolemia, hemodilution, hypertension Unruptured aneurysms associated with headache, 3rd nerve palsy 1. Both hyper and hypotension can cause rupture – 2. Avoid rapid decrease in ICP prior to opening of dura – 3. “Brain relaxation” or “slack brain” facilitates surgery – mannitol, steroids, hypocapnia, thiopental(?) Seizure disordera. Grand Mal (Tonic-Clonic) seizures ii. Seizures usually benign, secondary injury common iii. Airway reflexes preserved during seizure v. Sudden intraop hemodynamic changes may indicate ii. May be resistant to NMB’s depending on medication ii. Cerebral monitoring – awake patient is best, next is EEG iii. Bradyarrhythmias can occur with carotid sinus manipulation iv. Postop hemodynamic instability common Intracranial hypertension and hydrocephalusa. Intracranial hypertension 1. Brain – 85%2. CSF – 10%3. Blood – 5% 4. ICP > 15 mmHg = intracranial hypertension5. Cushing’s Triad – hypertension, bradycardia, irregular 1. Congenital – aqueductal stenosis, Arnold-Chiari 2. Posttraumatic3. Neoplastic4. Post-inflammatory i. Hyperventilation – most efficient method, but temporary iv. Osmotic diuretic therapy – mannitol, not urea i. Doesn’t work – outcome studies report no change d. Anesthetic management of patients with increased ICP iii. Thiopental, etomidate, propofol, lidocaine all decrease ICP iv. Nitrous, volatile agents, ketamine all are cerebral ii. Dopaminergic failure with cholinergic excess in basal ganglia iii. Bradykinesia, tremor, postural instability 1. L-dopa2. Bromocryptine, lergotrile3. Amantadine4. selegiline5. CNS anticholinergics6. Sterotactic surgery 1. Avoid droperidol, phenothiazines2. Treat nausea with anticholinergics3. May have reduced responsiveness to indirect acting 4. Selegiline a monamine oxidase inhibitor – no 5. May have contracted intravascular volume6. Postop delirium common iv. Patients have often received steroid therapy 1. Avoid hyperthermia2. Spinal anesthetic associated with exacerbation i. Affects 6% over 65, 18% over 75, 50% over 85 ii. Disease of cholinergic neurons in CNS iii. Extensive cerebral atrophy – especially hippocampus iv. Treatment with CNS anticholinesterases i. Seen with spinal cord lesions above T7 1. Stop inciting event2. Nifedipine prophylaxis3. Spinal anesthetic 4. Centrally acting antihypertensives not effective v. With spinal cord trauma initial pathophysiology is lower- 1. After 48 hours avoid succinylcholine2. May use succinylcholine after spasticity ensues Response
Coma implies diffuse cerebralpathology or dysfunctionMany causes including:



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