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UPDATED REVIEW IN NEUROSURGICAL ANESTHESIOLOGY AND NEURO-CRITICAL CARE

UPDATED REVIEW IN NEUROSURGICAL ANESTHESIOLOGY AND NEURO-CRITICAL CARE. RAMSIS F. GHALY, MD, FACS DEPARTMENT OF ANESTHESIOLGY AND PAIN MANAGEMENT, ADVOCATE ILLINOIS MASONIC MEDICAL CENTER GHALY NEUROSURGICAL ASSOCIATES. CBF: METHODOLOGY.

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UPDATED REVIEW IN NEUROSURGICAL ANESTHESIOLOGY AND NEURO-CRITICAL CARE

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  1. UPDATED REVIEW IN NEUROSURGICAL ANESTHESIOLOGY AND NEURO-CRITICAL CARE RAMSIS F. GHALY, MD, FACS DEPARTMENT OF ANESTHESIOLGY AND PAIN MANAGEMENT, ADVOCATE ILLINOIS MASONIC MEDICAL CENTER GHALY NEUROSURGICAL ASSOCIATES

  2. CBF: METHODOLOGY • Methodology: (Kety Schmidt Technique): Consumption of a substance by an organ is the product of blood flow and arteriovenous (arterial and juglar bulb) difference for that substance with knowledge od blood-brain partition coefficient. Indicators: Diffusable substance e.g. N2O, Xe, Ar133, Kr85, Non-diffusable e.g. microsphere. Arteriovenous sampling over 10-14min Or external detection of washout with scintillation detectors post xenon inhalation/injection. Tomographic method: enhancement by stable Xe. PET will require Cyclotron-produced short lived radio isotopes. MRSpectroscopy measures brain substrates like ATP and others.

  3. CEREBRAL METABOLIC RATE • CMR=CBF/ARTERIOVENOUS DIFFERENCE • CMRO2 relatively stable and no change with PaCO2 20-80mmHg • COUPLING: Maintenance of CBF:CMRO2 ratio (14-18) i.e.↑ in acivated areas and ↓ in unstimulated areas) • O2 3.3ML/100G/MIN (brain 20%O2 uptake while <2% body weight) 60% for functional & 40% for neuronal integrity • GLUCOSE 4.5ml/100g/min (substrate for mature brain) 95% Aerobic produces efficient energy & 5% Anaerobic produces lactate and inefficient energy • LACTATE 0.56ml/100g/min • ATP 9umol/g/min

  4. CEREBRAL METABOLIC RATE (CMR) • CMR (CBF / Arterio-venous difference) • O2 3.3 mL/100g/min • Glucose 4.5 mL/100g/min • Lactate 0.56mL/100g/min • ATP 9 umol/g/min • Oxygen requirements: 60% Functional 40% integrity • Glucose, substrate for mature brain 95% Aerobic à efficient energy 5% Anaerobic Lactate à Lactate + inefficient energy • Energy stores are SCANT ATP + ½ ADP Energy Charge ------------------ Normal 0.87-0.96 ATP + ADP + AMP Inadequate O2 Delivery à â O2 – Glucose Index á Lactate –glucose Index Phosphocreatine â • Global CMRO2 relatively stable (but varies with age) No CMRO2 with PaCO2 20-80 mmHg • Coupling Maintenance CBF:CMRO2 Ratio (14-18 normocapnia) Regional á Activated areas and â unstimulated areas

  5. CNS HYPOTHERMIA • Hypothermia ↓neuronal metabolism and cellular hemeostasis • CO2 reactivity is maintained during moderate and deep hypothermia • CBF:CMR coupling is maintained during moderate hypothermia • Hypothermia causes relative pH alkalinity & ↓blood gas solubility • Brain cooling occurs faster during hypercarbia • Prolonged hypothermia is determintal: metabolic acidosis, ↑SVR↓COP, arrythemiacoagulopathy, infection, shivering, irreversible shock in rewarming • Prolonged drug effects by hypothermia

  6. HYPOTHERMIC BRAIN • Q10= ratio of two metabolic rates separated by 10ºC. A ration of 2 means that a 10ºC decrease in temp. result in a 50% decrease in metabolism (animal=2-3, human>2). It is non-expotential: Q10 of 28ºC-18ºC doubled (isolectric EEG) • Tolerance to ischemia: 37ºC→5min 28ºC→12min (2.4/5) 18ºC→60min(5/12) 12ºC-15ºC→>60min * Hypothermia 30ºC+hypoxia→↓rate of energy depletion (1/2 normothermic with unchanged energy stores

  7. HYPOTHERMIC BRAIN • OXYGEN CONSUMPTION & HYPOTHERMIA 30ºC-28ºC→↓50% O2 consumption 25ºC→ ↓75% 20ºC→ ↓85% 18ºC-15ºC→↓90% • Hyperthermia 37ºC-42ºC→↑CBF >42ºC→ ↑CBF (toxic) • EEG & HYPOTHERMIA 37ºC-27ºC→↓EEG frequency (5.7% per 1ºC) ↑amplitude 27ºC-23ºC→ Burst Suppression <21ºC → Isolectric • EVOKED POTENTIAL & HYPOTHERMIA 35ºC-23ºC→ progressive ↑ latency <20ºC-23ºC→potential loss

  8. CEREBRAL TEMPERATURE • SITE BRAIN- TYMPANIC- NASOPHARYNGEAL (32ºC-34ºC) • METHODS OF COOLING ROOM BLANKETS INTRAVENOUS FLUID IRRIGATION OF CENTRAL CAVITY

  9. CEREBRAL DYNAMICS • CVR=CPP/CBF • CPP=MAP-ICP • A-VO2=ARTERIO-VENOUS (JUGLAR BULB OR SAGITTAL SINUS OXYGEN CONTENT DIFFERENCE • CMRO2=CBF/A-VO2

  10. (MAP-ICP) CBF= CVR

  11. FACTORS AFFECTING CBF: AUTOREGULATION • AUTOREGULATION: MYOGENIC INTRINSIC CAPACITY TO MIANTAIN CBF CONSTANT OVER A WIDE RANGE OF CPP (PRODUCT OF CVR AND BP=50-150mmHg in normotensive patients under normal physiologic condition • IMPAIRED IN PATHOLOGICAL CONDITIONS e.g. brain tumors, trauma, hemorrhage, metabolic, infection, encephalopathy, ischemia, hypoxia, pharmacological • HYPERTENSION: normal autoregulation if BP controlled, Subacute increase cause slight shift to the right, chronically untreated causes complete shift to the right. Vascular changes occur 1-2months and tolerance to high BP and higher ischemic threshold. Malignant hypertension may lead to acute hypertensive encephalopathy. • Drug-induced hypotension lower the ischemic threshold & hypovolemic hypotension elevates the ischemic threshold

  12. FACTORS AFFECTING CBF • METABOLIC (CMR)Coupling with CMR status e.g. sleep decrease CMR and CBF & seizure, motor activity and intellectual exercises elevate CMR and CBF • NEUROGENIC:Sympathetic elevate CBF 10-15% & parasympathetic depresses CBF. • CO2(MOST POTENT): Mediated through hydrogen ion in the extracellular fluid of the vascular smooth muscle. Hyperventilation decreases CO2 via vasoconstriction(PaCO2 20mmHg halve CBF) & CO2 retention increases CBF (double CO2 doubles CBF) via vasodilation

  13. FACTORS AFFECTING CBF • O2: hyperoxia >300mmHg decreases CBF & hypoxia <50-60mmHg increases CBF (doubles at PaO2 30mmHg via arteriolar dilation) 1 Atmospheric O2 decrease 10-15% CBF, hyperbaric O2 decreases CBF • TEMPERATURE: Hypothermia reduces CBF For each 1◦C decrease CMRO2 decrease 7% • CEREBRAL DYNAMICS (CPP, CVR, CBV): Cardiac output improves CBF • RHEOLOGIC FACTORS: VISCOSITY IS DETERMINED PRIMARILY BY HCT. HCT 33-45% normal CBF, Anemia increases CBF and decrease CVR, Polycythemia increases CVR and decreases CBF. Optimal O2 delivery at HCT 30-34% • PHARMACOLOGY: Dose-related anesthetic or drug effects can alter vasoactive response just as BP & CO2

  14. VOLATILE INHALED ANESTHETIC EFFECTS ON BRAIN METABOLISM • HALOTHANE, ISOFLURANE, SEVOFLURANE AND DESFLURANE ↓CMRO2 , ↓CSF PRODUCTION, AND DO NOT ABOLISH CEREBROVASCULAR RESPONISEVENESS TO CO2. HALOTHANE LACK BURST SUPPRESSION • NEUROPROTECTION FOCAL AND INCOMPLETE GLOBAL ISCHEMIA • ↑CBF HALOTHANE>ISO-SEVO OR DESFLURANE • In normocapnic, 0.6MAC cerebral vasodilatation • Biphasic dose dependent effect on CBF:At 0.5MAC ↓CMRO2 counteracts the vasodilatation with no changes on CBF. At >1 MAC→vasodilatation→↑CBF

  15. VOLATILE ANESTHETICS & BRAIN • VOLATILE ANESTHETICS ↑ICP AT DOSES >1MAC AND AUTOREGULATION IS IMPAIRED • ISOFLURANE, DESFLURANE & SEVOFLURANE PRODUCE BURST SUPPRESSION ON EEG AT 1.5-2MAC. ENFLURANE AND SEVOFLURANE PRODUCE EPILEPTOFORM ACTIVITY. • VOLATILE AGENTS PRODUCE LATENCY DELAY AND AMPLITUDE DEPRESSION ON SSEP ARE DOSE-DEPENDENT (0.2-0.5MAC

  16. NITROUS OXIDE AND BRAIN METABOLISM • N2O →↑CMRO2- ↑CBF (Cerebral vasodilation)- ↑ICP. Coadministration of opoids, barbiturate, or propofol • NEUROLOGIC DEFICITS IN B12 DEFICIENT PATIENTS • HYPERHOMOCYSTEINEMIA ASSOCIATED WITH DEMENTIA AND CEREBROVASCULAR DISEASE • NEURODEGENERATION IN NEONATES • SURGICAL WOUND INFECTION • NAUSEA AND VOMITING • INCREASE PRESSURE IN AIR CONTAINING CLOSED SPACES • REGARDLESS, IT IS USED DAILY WITH NO OBVIOUS ILL EFFECT. NO WELL DOCUMENTED DETRIMENTAL OR BENEFICIAL IMPACT ON NEUROLOGIC OR NEUROPSYCHOLOGICAL OUTCOMES.

  17. INTRAVENOUS BARBITURATES & BRAIN METABOLISM • BARBITURATES, IDEAL NEUROANESTHETIC FOR YEARS • Dose-dependent CNS depression, potent vasoconstrictor and ↓CBF, ↓CMRO2,↓ CBV & ↓ICP • MAXIMUM ↓ICP & ↓CMRO2 ACHIEVED WITH BURST SUPPRESSION EEG. • Suppression of seizures • Membrane stabilizer and free radical scavenger • Cerebral edema, CSF secretion • NEUROPROTECTION FOR FOCAL (stroke, surgical retraction, temporary clipping) but not for global (cardiac arrest) ischemia. • Long acting and strong hemodynamic suppressant • METHOHEXITONE activates epileptic foci and used for electroconvulsive therapy. • MAJOR CARDIOVASCULAR AND RESPIRATORY DEPRESSANT ESPECIALLY IN HIGH ANESTHETIC DOSES.

  18. INTRAVENOUS ETOMIDATE & BRAIN METABOLISM • NON-BARBITURATE CARBOXYLATED IMIDAZOLE • POTENT CEREBRAL VASOCONSTRICTOR, ↓CBF, ↓CBV, ↓CMRO2 &↓ICP • PRESERVE CO2 REACTIVITY • FAVORABLE CBF REDISTRIBUTION • MEMBRANE STABLIZER • SHORT DURATION OF ACTION • HEMODYNAMIC STABILITY • NEUROPROTECTIVE (BURST SUPPRESSION EEG), BUT DATA IS LACKING • EXCITATORY SPIKES ON EEG • MYOCLONIC MOVEMENT AND TWITCHING 50% OF PATIENTS WITH SEIZURE LIKE ACTIVITY ON EEG • ADRENOCORTICAL SUPPRESSION

  19. INTRAVENOUS BENZODIAZEPINES & BRAIN METABOLISM • BENZODIAZEPINES ↓CMRO2, ↓CBF (25%-34%) • CEILING EFFECT IN CMRO2 BY NO BURST SUPPRESSION EEG • NO DEMONSTRABLE EFFECT IN ICP • PRESERVE VASOREACTIVITY • NO DEMONSTRABLE NEUROPROTECTIVE EFFECT • POTENT ANTICONVULSANT EFFECT

  20. INTRAVENOUS OPIODS AND LIDOCAINE AND BRAIN METABOLISM • INTRAVENOUS OPIODS: PRODUCE MINIMAL CHANGES IN CMRO2 & CBF • INTRAVENOUS LIDOCAINE ↓CBF & ↓CMRO2 • BRAIN AUTOREGULATION IS PRESERVED

  21. INTRAVENOUS DEXMEDETOMIDINE & BRAIN METABOLISM • SELECTIVE ALPHA 2 ADRENERGIC AGONIST, ↓CBF WITH SIGNIFICANT CHANGES ON CMRO2 OR ICP • TOLERANCE AND DEPENDANCE

  22. INTRAVENOUS KETAMINE & BRAIN METABOLISM • KETAMINE, DISSOCIATIVE ANESTHETIC • CEREBRAL VASODILATOR, ↑CMRO2, CBF, CBV, ICP • NORMOCAPNIA BLUNTS CBF EFFECTS • PRODUCES MYCLONIC MOVEMENT BUT IT IS ANTICONVULSANT

  23. MUSCLE RELAXANTS AND BRAIN METABOLISM • SUCCINYLCHOLINE PRODUCES TRANSIENT ICP AND CAN BE ATTENUATED BY BARBITURATES OR DEFASCICULATING DOSE OF A NONDEPOLARIZING MUSCLE RELAXANT • OTHER MUSCLE RELAXANTS HAVE NO EFFECT

  24. CEREBRAL PERFUSION-RESERVE-STEAL • HYPERPERFUSION AND CIRCULATORY REAKTHROUGH: if CPP exceeds upper limit of autoregulation may lead to arteriolar dilatation and fall in resistance and may result in brain swelling and hemorrhage e.g. postoperative brain swelling and ICH after AVM resection (normal pressure perfusion breakthrough) • HYPOPERFUSION: may lead to ischemia. CBV increases as arterioles dilates until is exhausted and CBF decline passively as CPP decreases. Oxygen extraction increase to maximum as CMRO2 declines. Synaptic transmission and neuronal function shuts down and energy is barely enough for neuronal survival. Then membrane failure (Na, Ca, H2O enter cell and K exit and cytotoxic edema takes place. At such low CBF, irreversible injury and infarction takes place and can not be corrected. Penumbra (almost shadow) area around the infarcted portion that is salvageable if flow restored soon

  25. HYPERPERFUSION • HYPERTENSION AND ↑COP →↑CBF • INDICATIONS: Dysautoregulated ischemic region CBF pressure dependent SAH-induced vasospasm, focal ischemia • METHODS IONOTROPES INCREASE CARDIAC OUTPUT VOLUME EXPANDERS (HYPERVOLEMIA) • Deleterious if used post-injury (HTN-hemorrhage

  26. NEUROPROTECTION RAMSIS F. GHALY, MD, FACS

  27. NEUROPROTECTION • INCREASE TOLERANCE OF NEURAL TISSUE TO ISCHEMIA • IMPROVED OUTCOME AS EVIDENCED BY ELECTROPHYSIOLOGIC, METABOLIC, OR HISTOLOGIC INDICES OF RECOVERY OR ULTIMATELY BY IMPROVED CLINICAL NEUROLOGIC RECOVERY • PROTECTION CAN BE ACHIEVED BY PRETREATMENT (in anticipation of ischemia), DURING or AFTER ISCHEMIA • MAXIMUM COUPLED SUPPRESSION OF CMRO2 & CBF WITH CEILING EFFECT ONCE BURST SUPPRESSION EEG • FOCAL ISCHEMIA PROTECTION ACHIEVED BY OPTIMIZING SUBSTRATE/DEMAND RATIO • GLOBAL ISCHEMIA, NO PROTECTIVE MEASURES IS LIMITED AND AIMED AT SECONDARY PROCESSES (EDEMA, HYPOPERFUSION, MEMBRANE DAMAGE.

  28. NEUROPROTECTION NEUROPROTECTION IS SEEN WITH AGENTS INDUCE CMR DEPRESSION, GABA AGONISM, ADENOSINE A1 RECEPTOR AGONISM, NMDA RECEPTOR ANTAGONISM. For example protective effect of isoflurane (GABA receptor Agonist was reversed by trimethaphan (GABA receptor antagonist) Isolflurane protective effect dose-dependent <1.5MAC and above 0.5MAC Neuroprotective effects being stipulated for Desflurane via CMR depression and enhanced cerebral perfusion, Propofol via mitochondrial swelling and morphine via protien kinase C and NMDA receptors. Ischemic models examined were for focal cerebral ischemia

  29. TEMPORARY FOCAL ISCHEMIA ANTICIPATED TEMPORAY CLIPPING: MAINTAIN BURST SUPPRESSION DURING ISCHEMIC PERIOD THIOPENTAL 3-5mg/kg (5min) 10-15mg/kg (10min) then 3-5mg/kg/hr

  30. CSF REGULATION • CSF (Vf)is formed at a rate 0.4ml/min (500-600cc/day) Total CSF volume is replaced 4 times/day. 60-70% formed actively at the choroid plexus and 30% at extrachoroidal sites across ependyma and pia. CSF reabsorption (Va) via arachnoid villi and granulations. • EQUILIBRIUM: Vf balance with Va /ICP . Vf relatively constant. ICP<7cmH2O minimal Va, ICP>7cmH2O linear ↑Va. Vf↓ when CPP<70mmHg • NEURAL: Choroid plexus richly supplied by adrenergic, cholinergic and peptidergic affecting CSF rate formation. • TEMPERATURE: hypothermia ↓ CSF formation (1C→11%) • CO2: Hypocarbia ↓CSF transiently • METABOLIC ALKALOSIS: ↓CSF formation • OSMOLARITY: ↓CSF formation • ↓CSF formation →↓CPP

  31. PHARMACOLOGICAL ALTERATIONS OF CSF DYNAMICS N2O has no effect ISOFLURANE: ↓Ra and no change to Vf ENFLURANE transiently ↑Vf 80% and Ra(resistance to reabsorption) HALOTHANE ↓Vf and ↑Ra KETAMINE: ↑Ra no change Vf ETOMIDATE and BARBITURATE (HIGH DOSE) ↓Vf and Ra OPOID↓Ra BENZODIAZEPINE↓Vf, ↑Ra DIURETICS ↓Vf. Acetazolamide reduces by 50% (carbonic anhydrase inhibitor)

  32. INTRACRANIAL PRESSURE • ICP is determined by the raltionship of the volume of intracranial contents(brain+blood+CSF=1200-1500cm3) and the volume of the cranial vault (fixed by rigid dura and skull bone). • ELASTANCE is the relationship of pressure and volume (dP/dV). In normal condition a small increase in intracranial volume will not result in ↑ICP. • COMPLIANCE is the relationship of volume and pressure (dV/dP) i.e. inverse of Elastance. • Initially, as intracranial volume increases, no change in ICP occurs (point A, well compensated) until point B where any further increase will cause dramatic increase in ICP (point C).

  33. INTRACRANIAL PRESSURE • CPP=MAP-ICP (zero point at foramen of Monro) • Normal ICP <10-14 mmHg during no stimulation • INTRACRANIAL CONTENTS AND CRANIAL VAULT VOLUME: brain matter and intracellular water (1350-1450g) 80-85%. Cerebral blood volume (CBV) 3-7ml/100g 3-6%. Cerebrospinal fluid (450cc/day) 5-15%. CBV:CBF homogenous changes but not always and inhomogenous in pathological condition. • VPR Pressure change per 1 ml fluid injection (0.7% total CSF) Normal <2mmHg (plateau). Pathological >4-5mmHg (↑ steepness small segment) • VPI (index)=P/V-(logPp/P0). Volume addition required to change ICP by 10 folds (normal 25ml poor<15ml). Surgical intervention before steep portion of VP curve.

  34. ANESTHETIC INDUCTION IN NEUROANESTHESIA: GOALS • Deep anesthetic level with adequate muscle relaxation and blunting response to intubation, pins and craniotomy • No increase ICP, CBV, BP and No decrease in CPP, CBF, BP • No hypoxia • No coughing

  35. ANESTHETIC INDUCTION IN NEUROANESTHESIA • Thiopental (3-7mg/kg, Propofol 2-2.5mg/kg, Midazolam 0.2-0.4mg/kg, Etomidate 0.2-0.4mg/kg, Fentanyl 5-10ug/kg, Lidocaine 1.5mg/kg prior to intubation (Lidocaine oral and laryngeal spray) • Adquate airway ventilation • Non-depolarizing muscle relaxant intubating dose or succinylecholine 1.5mg/kg after defasciculating dose of non-depolarizer

  36. ANESTHETIC INDUCTION IN NEUROANESTHESIA • Thoroughly securing the Airway • Eye protection watertight • Adequate positioning and padding • Avoid head down position • Avoid pressure over the neck or tight tape around • Keep access to the patient and lines • Recheck tubes and lines after positioning • Lidocaine at the Pin sites before head pins placement

  37. ASA TASK FORCE IN POSITIONING 2000 • ASA TASK FORCE ON PREVENTION OF PERIOPERATIVE PERIPHERAL NEUROPATHIES; PRACTICE ADVISORY IN POSITIONING 2000. • LIMIT ARM ABDUCTION TO 90 AND CAREFUL PADDING OF VULNERABLE PRESSURE POINTS • CAREFFULL PAD AND ASSESS AREAS SENSITIVE TO PRESSURE NECROSIS e.g. EYES, EARS, NOSE, GENITALIA AND BREASTS. FEMALE BREASTS DISPLACED MEDIAL AND INFERIOR IN RELATION TO CHEST SUPPORTS • PATIENTS WHO HAVE POSITION-DEPENDENT NEUROLOGIC SYMPTOMS OR EXTREMELY OBESE BENEFIT FROM AWAKE INTUBATION FOLLOWED BY AWAKE POSITIONING

  38. PROBLEMS RELATED TO PRONE POSITION • BRACHIAL PLEXUS INJURY • AIR EMBOLI AND CV COLLAPSE • BLINDNESS • OBSTRUCTION OF FEMORAL VEINS AND IVC→↓VR→↓CVP AND ↓COP • ENGORGEMENT OF PERIVERTEBRAL VENOUS PLEXUSES→DIFFICULT SURGICAL EXPOSURE AND ↑BLOOD LOSS • ABDOMEN HANG FREE→NEGATIVE PRESSURE WITHIN IVC→ PERIVERTEBRAL VENOUS PLEXUSES-→ AIR EMBOLIZATION • FROM SUPINE TO PRONE→↓SV AND↓ CI AND↑ PVR AND ↑SVR. LEAST CHANGES WITH JACKSON SPINE AND LONGITUDINAL BOLSTERS. CARDIAC PATIENTS MAY NOT TOLERATE AND SWAN-GANZ CATHETER MAY BE NEEDED

  39. ROBLEMS RELATED TO PRONE POSITION • CABG PATIENTS MAY OCCLUDE BYPASS GRAFTS • ABDOMINAL PRESSURE → DISPLACE DIAPHRAGM→ REDUCE LUNG COMPLIANCE→ POSITIVE PRESSURE VENTILATION→BAROTRAUMA. • POSITIVE INSPIRATORY EFFECT ON DIAPHRAGM-→ INCREASE FRC AND DESRIABLE EFFECT ON GAS EXCHANGE • VISUAL LOSS 1:100 SPINE SURGERIES DUE TO ISCHEMIC OPTIC NEUROPATHY (↑FLUID, ↑BLOOD LOSS, ↑IOP , ↓PERFUSION PRESSURE) • FACIAL EDEMA

  40. PERIPHERAL NERVE INJURY • IMPROPER INTRAOPERATIVE POSITIONINGT • REGIONAL ANESTHETIC TECHNIQUES • INJECTION SITES • DIRECT SURGICAL RETRACTION OR DAMAGE • RISK FACTORS: BODY HABITUS, PREVIOUS H/O NEUROPATHY, SMOKING, DIABETES • ULNAR NERVE INJURY 1/3 OF ASA CLOSED CLAIM ANALYSIS • BRACHIAL PLEXUS AND PERONEAL NERVE FOLLOWED

  41. PERIPHERAL NERVE INJURY • OTHER SITES: MEDIAN AND ULNAR NERVE AT WRIST, RADIAL NERVE AT INNER ARM, VII NERVE AT EXIT SITE COMPRESSED BY MASK AIRWAY • PROLONGED OR IMPROPER LITHOTOMY SCIATIC, FEMORAL, COMMON PERONEAL, SAPHENOUS NERVES • COMPRESSION OR STRETCHING OF NERVE WITH DEMYELINATION • REMYELINATION OCCURS 6-8WEEKS • IMMEDIATE DIAGNOSIS, EARLY NEUROLOGY CONSULTATION AND REHABILITATION ARE CRUCIAL FOR FULL RECOVERY

  42. NEUROANESTHETIC MAINTENANCE ADEQUATE BRAIN RELAXATION • Adequate oxygenation and ventilation (PaCO2 33-35mmHg),, venous return, muscle relaxation, anesthetic depth • Furosmide 10-20mg iv, Mannitol 0.5-1.5g/kg iv, iv thiopental, CSF drainage

  43. NEUROANESTHETIC MAINTENANCE STABLE ANESTHETIC STATE AND RAPID SMOOTH EMERGENCE • Low after the craniotomy (brain is devoid of sensation) • Isoflurane, Sevoflurane or Desflurane 0.5MAC & Propofol 50-150 ug/kg/min and Remifentanil 0.1-0.5ug/kg/min • Muscle relaxant maintaining 2twitches (phenytoin may increase requirment of muscle relaxants)

  44. NEUROANESTHETIC EMERGENCE • AVOID COUGHING STRAINING OR BP INCREASE • Normalize gradually PaCO2 • Full reversal of muscle relaxant • IV Lidocaine • IV labetolol, Nicardpine, NTP, NTG • Brief neurological Assessment before leaving OR

  45. Pre emergence • 1-2 hr before end • Gradual decrease anesth aiming for bis 80 at end • Treat post op htn before hand, I aim for SBP 110 • Maintain solid reversible NMB!!

  46. IMMEDIATE POSTOPERATIVE CARE IN NEUROANESTHESIA • ADEQUATE VENTILATION AND OXYGENATION • HEAD OF BED (10-25C0 • NEUROLOGIC FUNCTION • CEREBRAL DYNAMICS MONITORING AND CONTROL • SERUM ELECTROLYTE: SIADH (↓Na, ↓serum osm, ↑urine osmo) Treatment restrict water intake ‡meds DI (polyuria, ↑Na, ↑serum osmo, ↓urine osmo) Treatment Aqueous vasopressin 5-10USP units sq or 3units iv OR desmporessin 1-2 ug iv sq q6-12hr. Plus adequate fluid replacement • SEIZURE (adequate oxygenation, ventilation and airway protection: midazolam (2-4mg), thiopental (100-150mg), fosphenytoin 15-20mg/kg, 100 mg/min) • POSTOPERATIVE IMAGING (CTScan, MRI, Angiography)

  47. TRANSPORT FROM OPERATING ROOM TRANSPORT FROM OPERATING ROOM TO NEURO-ICU OR PACU: • PRIOR COMPLETE REPORT TO ACCEPTING UNIT WITH SET-UP NEEDED • TRANSPORT ONLY WHEN PATIENT IS STABLE OR AS STABLE AS CAN BE • DIRECT SUPERVISION OF ANESTHETIST • HEMODYNAMIC AND RESPIRATORY SYSTEMS MONITORED AND CONTROLLED • O2 SUPPLEMENT • WORKING IV AND RUNNING INFUSION PUMPS • BLANKETS AND HEAT LOSS PREVENTION • EMERGENCY MEDS AND INTUBATION KIT • ENDORSEMENT IS NOT COMPLETE UNTIL PATIENT IS STABLE AND COMPREHENSIVE REPORT HAS BEEN DELIVERED

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