UPDATED REVIEW IN NEUROSURGICAL ANESTHESIOLOGY AND NEURO-CRITICAL CARE

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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

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TRAUMATIC BRAIN INJURY AND NEUROANESTHESIA

• RECENT UPDATE

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Primary Brain Injury

• Trauma concussion, contusion, shear injury
• Ischemia global, regional
• Inflammation
• Compression tumor, edema, hematoma
• Metabolic insults

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Pupillary Response

• Pupils
• Equal
• Round
• Reactive to Light
• Accommodate
• Size

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TBI CPP

• CPPMAP-ICP
• CBFCPP/CVR
• CMRO2CBF/A-VDO2
• POOR OUTCOME
• ICP gt20-25mmHg
• CPPlt50-60mmHg
• MAPlt80mmHg
• SBPlt90mmHg

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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

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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 lt60mmHg on second day died
• CPP gt80mmHg 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

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CPP-CBF THRESHOLDS

• Therapy targeting CPP gt70mmHg 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 CPPgt70 is not supported
• CBF decrease to 27ml/100gm/min during first
  12-24hr post-injury. Hyperventilation could
  further lower CBF

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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.

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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

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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.

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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 lt15mmHg correlate with good outcome
• OPENING ICP gt15mmHg one of the risk factor for
  high mortality

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TBI AND ICH

• ICH CARRIES POOR PROGNOSIS IN TBI PATIENTS
• COMMON IN GROUP OF PATIENTS WITH GCS lt9 (50-63)
• ICH DEVELOPS IN 10-15 PATIENTS WITH NORMAL
  ADMISSION CTSCAN
• ICH OCCURRED IN 60 WHEN NORMAL CTSCAN WITH TWO
  gt40Y/O, MOTOR POSTURING, SBPlt90mmHg

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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)
• PaCO2lt25mmHg first 5days had worse outcome
• PaCO2 of 29mmHg for 20min no change in SjO2 or
  PbrO2
• Hyperventilation most common cause of SjO2
  desaturation

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HYPERVENTILATION

• Linear relationship between 20 mmHg and 80mmHg
  PaCO2
• ??1mmHg PaCO2 ??? 1-2ml/100gm/min CBF (CBV
  0.05ML/ 100gm/min). PLATEAEAU RESPONSE gt80mmHg
  PaCO2
• IMMIDIATE EFFECT ltCO2/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 lt 20mmHg?CEREBRAL ISCHEMIA
• LEFTWARD SHIT OF HEMOGLOBIN DISSOCIATED
  CURVE ABNORMAL EEG, INCREASE LACTATE
• FOCAL BRAIN ISACHEMIA PARADOXICAL RESPONSE TO
  PaCO2 (ROBIN HOOD EFFECT)

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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

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TBI CEREBRAL HEMODYNAMIC HYPOXEMIA

• HYPOXEMIA (Apnea cyanosis in the field or PaO2
  lt60mmHg)
• 27 TBI hypoxemic on arrival to ED
• Common cause of secondary insult
• 22.4 of severe TBI
• Mortality rate 50 if O2sat lt60 vs 14.3 in non
  hypoxemic
• Duration of hypoxemia O2sat lt90 independent
  factor for severe disability and death
• Hypercarbia despite mechanical ventilation

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A-VDO2 DIFFERENCE

• A-JDO2 juglar bulb difference 5-8 vol
• independent predictor of outcome
• lt3.8 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

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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

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TBI CEREBRAL HEMODYNAMIC HYPOTENSION

• HYPOTENSION (gt90mmHg for adults)
• SBP is desirable to be gt90mmHg
• One of the common avoidable factors correlated
  with death
• SBP lt90mmHg 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

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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
• OsmolalityNax2glu/18(BUN/2.3)(Na in mmol/L glu
  and BUN in mg/dL)
• Osmotic pressure Pressure exerted by a solution
  necessary to prevent osmosis19.3xosmolality
• 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

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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)

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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 lt70 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.

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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
  3HS) vs intermittent boluses (higher
  concentration)

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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

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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 gt20mmHg

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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

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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

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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.

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SEDATIVE-HYPNOTICS

• COMMON AGENTS USED WITH NO POSITIVE EFFECT ON
  OUTCOME MORPHINE, MIDAZOLAM, FENTANYL,
  SUFENTANYL AND PROPOFOL
• PROPOFOL INFUSION SYNDROME gt5mg/kg/hr or any
  dosagesgt48hr in critically ill adults
• HYPERKALEMIA, HEPATOMEGALY, LIPEMIA,
  METABOLIC ACIDOSIS, MI, RHABDOMYOLYSIS, RENAL
  FAILURE AND DEATH

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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

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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.

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THE END

• THANK YOU
• ?QUESTIONS