Transcript REVIEW UPDATE IN NEUROSURGICAL ANESTHESIOLOGY

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
Primary Brain Injury
• Trauma:
concussion,
contusion, shear
injury
• Ischemia: global,
regional
• Inflammation
• Compression:
tumor, edema,
hematoma
• Metabolic insults
Pupillary Response
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Pupils
Equal
Round
Reactive to Light
Accommodate
Size
TBI: CPP
• CPP=MAP-ICP
• CBF=CPP/CVR
• CMRO2=CBF/A-VDO2
POOR OUTCOME
• ICP >20-25mmHg
• CPP<50-60mmHg
• MAP<80mmHg
• SBP<90mmHg
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
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
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
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.
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
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.
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
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
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
HYPERVENTILATION
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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)
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
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
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
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
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
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
TBI: HYPEROSMOLAR
THERAPY MANNITOL
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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)
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.
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)
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
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
Surgical Management of
Head Injury
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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
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
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.
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
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
FEVER AND COAGULOPATHY
AFTER TBI
SECONDARY 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.
THE END
THANK YOU
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