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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. TRAUMATIC BRAIN INJURY AND NEUROANESTHESIA. RECENT UPDATE.

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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. TRAUMATIC BRAIN INJURY AND NEUROANESTHESIA RECENT UPDATE

  3. Primary Brain Injury • Trauma: concussion, contusion, shear injury • Ischemia: global, regional • Inflammation • Compression: tumor, edema, hematoma • Metabolic insults

  4. Pupillary Response • Pupils • Equal • Round • Reactive to Light • Accommodate • Size

  5. TBI: CPP • CPP=MAP-ICP • CBF=CPP/CVR • CMRO2=CBF/A-VDO2 POOR OUTCOME • ICP >20-25mmHg • CPP<50-60mmHg • MAP<80mmHg • SBP<90mmHg

  6. TRAUMATIC BRAIN INJURY: TBI • The only part of brain damage in TBI is at the moment of impact • Numerous secondary insults compund the initial damage in the ensuing hours and days • Extensive management protocols siginificantly reduced TBI morbidity and mortality

  7. CRITICAL THRESHOLDS OF CBF & CPP • Critical CBF and CPP (50-60mmHg) thresholds as determined by the other physiologic indices: • Transcranial dopplar pulsatility index • CO2 responsiveness of MCA • SjO2 and A-VDO2 difference (extraction ratio) • Cerebral microdialysis • CPP <60mmHg on second day died • CPP >80mmHg had better outcome than lower CPP in TBI patients • Elevation of CPP 30mmHg (volume and pressors) has no effect in ICP with intact autoregulation (unpredictable for impaired autoregulation

  8. CPP-CBF THRESHOLDS • Therapy targeting CPP >70mmHg may increase incidence of ARDS and brain swelling • CPP target threshold be set 10mmHg above what is determined to be a critical threshold • Routinely using volume expansion and pressors to maintain CPP>70 is not supported • CBF decrease to 27ml/100gm/min during first 12-24hr post-injury. Hyperventilation could further lower CBF

  9. INTRACRANIAL PRESSURE & CT SCAN • ABNORMAL CT SCAN WITH POTENTIAL HIGH ICP: MIDLINE SHIFT & TRANSFALCINE HERNIATION ABSENT BASAL CISTERN EFFACEMENT OF THE VENTRICULES SULSCI COMPRESSION & EDEMA BRAIN CONTUSION AND ICH GRAY-WHITE MATTER DIFFERENTIATION • FINDINGS ARE NOT PREDICTIVE OF ICP ESPECIALLY EARLY ON • ICP ALONE INADEQUATE TO FOLLOW CTSCAN ABNORMALITIES.

  10. INTRACRANIAL PRESSURE MONITORING • ICP can not be reliably predicted by CT scan alone • ICP monitor predict outcome and guide therapy • There is outcome improvement to ICP reduction and responders • Treatment of presumptive high ICP without monitoring can be deleterious and result in poor outcome

  11. ICP • ICP first indicator of worsening intracranial pathology and surgical mass lesions • Prolonged hyperventilation worsens outcome and significantly reduces CBF • Prophylactic paralysis increase pneumonia and ICU stay • Barbiturates cause siginificant hypotension and prophylactic administration is not recommended.

  12. ICP • EVD IS THE MOST ACCURATE AND USEFUL (CSF DRAN) • MALFUNCTION (6-10%), INFECTION AND HEMORRHAGE (1%) • DAILY ICP DRIFT 0.3mmHg with the device • ICP <15mmHg correlate with good outcome • OPENING ICP >15mmHg one of the risk factor for high mortality

  13. TBI AND ICH • ICH CARRIES POOR PROGNOSIS IN TBI PATIENTS • COMMON IN GROUP OF PATIENTS WITH GCS <9 (50-63%) • ICH DEVELOPS IN 10-15% PATIENTS WITH NORMAL ADMISSION CTSCAN • ICH OCCURRED IN 60% WHEN NORMAL CTSCAN WITH TWO >40Y/O, MOTOR POSTURING, SBP<90mmHg

  14. HYPERVENTILATION • Recommended PaCO2 is 35mmHg • HYPERVENTILATION→ Linear relationship↓CBF +↓CBV→↓ICP • No support for prophylactic hyperventilation (assumption is 40% incidence of high ICP and brain swelling with severe TBI) • PaCO2<25mmHg first 5days had worse outcome • PaCO2 of 29mmHg for 20min no change in SjO2 or PbrO2 • Hyperventilation most common cause of SjO2 desaturation

  15. HYPERVENTILATION • Linear relationship between 20 mmHg and 80mmHg PaCO2 • ↑↓1mmHg PaCO2 →↑↓ 1-2ml/100gm/min CBF (CBV 0.05ML/ 100gm/min). PLATEAEAU RESPONSE >80mmHg PaCO2 • IMMIDIATE EFFECT <CO2/CSF pH CHANGE) BUT NOT SUSTAINED • CSF pH/ CBF NORMALIZES IN 24-36 HOURS by HCO3 EXTRACTION • ACUTE NORMALIZATION OF PACO2 : CSF ACIDOSIS ( POST ↓PaCO2) →↑ CBF and ICP CSF ALKALOSIS (POST↑ PaCO2 )→ ISCHEMIA • PaCO2 < 20mmHg→CEREBRAL ISCHEMIA LEFTWARD SHIT OF HEMOGLOBIN DISSOCIATED CURVE ABNORMAL EEG, INCREASE LACTATE • FOCAL BRAIN ISACHEMIA PARADOXICAL RESPONSE TO PaCO2 (ROBIN HOOD EFFECT)

  16. HYPERVENTILATION • CSF pH get normalized within 12-24hr post hyperventilation • AGGRESSIVE HYPERVENTILATION CAUSES SEVERE CEREBRAL ISCHEMIA • HISTOLOGIC EVIDENCE OF CEREBRAL ISCHEMIA IN THE BRAIN OF THE VICTIMS • Measures to maintain CBF in the first hours post injury • LASER BLOOD FLOW FOR REGIONAL CBF

  17. TBI: CEREBRAL HEMODYNAMIC: HYPOXEMIA • HYPOXEMIA (Apnea cyanosis in the field or PaO2 <60mmHg) • 27% TBI hypoxemic on arrival to ED • Common cause of secondary insult • 22.4% of severe TBI • Mortality rate 50% if O2sat <60% vs 14.3% in non hypoxemic • Duration of hypoxemia O2sat <90% independent factor for severe disability and death • Hypercarbia despite mechanical ventilation

  18. A-VDO2 DIFFERENCE • A-JDO2 juglar bulb difference 5-8 vol% independent predictor of outcome <3.8 vol% severe disability compared to 4.3vol% High Extraction ratio with good outcome Limited improvement of AVDO2 with intervention indicated worse outcome and delay infarction CEREBRAL OXIMETRY: SOMANTICS

  19. BRAIN MICRODIALYSIS • ANALYSIS OF BRAIN METABOLITES: LACTATE, PYRUVATE, GLUTAMATE, GLUCOSE, AND THEIR RATIOS • INCREASED IN GLUCOSE AND DECREASE OF OTHERS WITH INCREASE FiO2 OF 1.0 • BRAIN METABOLITE PATTERN IN TBI

  20. TBI: CEREBRAL HEMODYNAMIC: HYPOTENSION • HYPOTENSION (>90mmHg for adults) • SBP is desirable to be >90mmHg • One of the common avoidable factors correlated with death • SBP <90mmHg is Powerful predictor for poor outcome among age, admission GCS, GCS motor score, pupillary status, intracranial DX, • A single inhospital hypotension double of mortality • Early hypotension increases mortality and worsens prognosis of severe TBI survivors

  21. HYPEROSMOLAR THERAPY • Osmolarity: Osmotic concentration of a solution expressed as osmoles of solute per liter of solution • Osmolality: Osmotic concentration of a solution expressed as osmoles of solute per kg of solution • Osmolality=Nax2+glu/18+(BUN/2.3)(Na in mmol/L glu and BUN in mg/dL) • Osmotic pressure: Pressure exerted by a solution necessary to prevent osmosis=19.3xosmolality • Oncotic pressure: related to protein molecules • Hyperosmolarity: increase osmolarity of a solution above normal plasma concentration • Hypertonicity: ability of a hyperosmolar solution to redistribute fluid from intra- to extracellular compartment • Urea is hyperosmolar but not hypertonic

  22. TBI: HYPEROSMOLAR THERAPY MANNITOL • Mannitol, hyperventilation and CSF drainage effective in reducing high ICP in 78% of TBI patients • Mannitol improves MAP, CPP, CBF and lower ICP by 20min • Brain compliance and V/P response improves after mannitol therapy • Mannitol initial effect is improving rheology (increase plasma volume & erythrocyte deformability, reduce blood viscosity & increase CBF) • After immediate volume expansion, osmotic effect 15-30min. And persist for up to 6hrs • Mannitol side-effects hypotension, sepsis and renal injury • Mannitol intermittent boluses (0.5-1G/KG and rapid infuse 2min is more effective than continuous infusion • Mannitol effect becomes less after multiple doses (3-4 doses /24hrs)

  23. TBI: HYPEROSMOLAR THERAPY: MANNITOL • Mannitol is mostly recognized for short term therapy; single use while intervention is underway. • Mannitol effect most marked in TBI patients with CPP <70 and when autoregulation is intact (suggest rheology effect is more important) • Mannitol is superior to barbiturate to control high ICP and improve CPP (41% vs 77% mortality and CPP 75 vs 45mmHg) • Lack of evidence of mannitol prolonged therapy and regular administration over days. • Rebound phenomenon upon immediate discontinuation.

  24. TBI: HYPEROSMOLAR THERAPY: HYPERTONIC SALINE • Greatest benefit (survival and hemodynamic stability) in TBI patients compared to non-TBI poly-traumatized hemorrhagic shock • Osmotic mobilization of water across BBB and reduction of brain water content • Improve CBF: endothelial cell dehydration, deformability of erythrocyte, plasma volume expansion, increase blood vessel diameter) • HS concentration used 1.6%, 2%, 3%, 7.2%, 10% • Continous infusion (pediatric TBI 0.1-1cc/kg/hr 3%HS) vs intermittent boluses (higher concentration)

  25. TBI: HYPEROSMOLAR THERAPY: HYPERTONIC SALINE • Rebound phenomenon • Central pontine myelinolysis especially in patiennts with hyponatremia • Acute renal failure if hypovolemia is present • Close blood chemistry and renal profile monitoring needed

  26. TRAUMATIC BRAIN INJURY Furosemide (2mg/kg) and hypertonic saline 1.2gm/kg of 3% saline) caused decrease CSF formation and capillary hydrostatic pressure, inhibition of Na-K ATPase located in brain cells and mediators of cerebral edema formation. Return of Decompressive hemicraniectomy for refractory ICP >20mmHg

  27. Surgical Management of Head Injury • ICP monitor (EVD) insertion • Elevation of depressed skull fracture • Craniotomy with evacuation of Hematoma • Craniotomy with frontal of temporal lobotomy • Burr holes and drainage of chronic subdural Hematoma or hygroma

  28. HYPOTHERMIA AND TBI • HYPOTHERMIA (32c-34c) AND COOLING DURATION 2DAYS AND SLOW REWARMING 1c/HR OR DAY. • Inamasu et al reported that HYPOTHERMIA REDUCED MORTALITY ( 6.7% VS 33.3% AND INCREASED FAVORABLE OUTCOME (27.8% VS 6.7%) AND REDUCED THE INCIDENCE OF UNCONTROLLED ICP (93.3% VS 61%) IN TBI PATIENTS • NO CLEAR REDUCTION IN MORTALITY BY PROPHYLACTIC HYPOTHERMIA • STILL ONGOING DEBATE ABOUT HYPOTHERMIA

  29. PROPHYLACTIC HYPOTHERMIA • Hypothermia associated with fewer seizures but no outcome difference • Hypothermia is associated with higher Pulmonary infection (60.5% vs 32.6%) and thrombocytopenia (62.8% vs 39.5%) compared to normothermia.

  30. SEDATIVE-HYPNOTICS • COMMON AGENTS USED WITH NO POSITIVE EFFECT ON OUTCOME: MORPHINE, MIDAZOLAM, FENTANYL, SUFENTANYL AND PROPOFOL • PROPOFOL INFUSION SYNDROME >5mg/kg/hr or any dosages>48hr in critically ill adults: HYPERKALEMIA, HEPATOMEGALY, LIPEMIA, METABOLIC ACIDOSIS, MI, RHABDOMYOLYSIS, RENAL FAILURE AND DEATH

  31. GLUCOCORTICOIDS • NO EFFFECT IN TBI; OUTCOME OR DECREASE ICP • MOST EFFECTIVE IN PEROPERATIVE PERIOD OF VASOGENIC EDEMA CAUSED BY METASTATIC TUMORS THAN PRIMARY BRAIN GLIOMAS • SPINAL CORD INJURY HIGH DOSE STERIOD WITHIN 8HOURS • RESTORE VASCULAR PERMEABILITY IN BRAIN EDEMA, DECREASE FREE RADICAL PRODUCTION, DECREASE CSF PRODUCTION

  32. FEVER AND COAGULOPATHY AFTER TBISECONDARY BRAIN INJURY FACTORS AFFECTING POOR OUTCOME: HIGH ICP, HYPOXEMIA, HYPOTENSION, FEVER AND COAGULOPATHY FEVER, 68% incidence in TBI (infection, central, drug related) associated with poor outcome perhaps related to glutamate excitotoxicity, BBB alteration, increase CMR (longer ICU 14.7 vs 5.4d and hospital 23.7 vs 12.3d, stay, mortality 12% vs 8.7%, 2.4 fold increase in D/C with low GCS score than 13.

  33. THE END THANK YOU ?QUESTIONS

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