Outline of
Neurosurgery
E. R. Flotte, 2008
Please send comments
and corrections to admin@flotte2.com
·
Cerebral Perfusion Pressure
(CPP) = ICP – MAP (Mean Arterial Pressure)
·
ICP monitoring:
o
ICP Waveform: P1 = percussion wave, systolic contraction, decreased with↑ ↑ ICP, ↓ compliance; P2 = tidal wave; P3 =
aortic valve closure.
o
Lundberg Waves: A (Plateau) = > 50mmHg rise
for > 20min. B = >20mmHg,
lasts 1-2min. C = 4-8Hz.
o
Monitors:
§
Intraventricular Catheter
§
Intraparenchymal Monitor
§
Subarachnoid Bolt: less
accurate
§
Subdural & Epidural
monitors: less accurate
·
General indications:
o
GCS ≤ 8 and abnormal CT or
o
GCS ≤ 8 and normal CT and 2 of: age >40yrs,
posturing, SBP <90
o
Neurologic examinations unavailable (surgery,
pharmacologic paralysis)
·
Signs of increased ICP:
o
Pupilary dilation/ CN3 palsy: 90% ipsilateral mass.
Hemiparesis (cerebral peduncle compression):
70% contralateral mass.
o
Cushings
response: Hypertension, bradycardia, and respiratory irregularity due to increased
ICP and brainstem compression.
Hypertension is due to peripheral vasoconstriction and catecholamine
release; bradycardia is due to medullary
ischemia.
·
Jugular Venous Monitoring
o
Necessary during barbiturate coma. Normal SjO2
>50%.
Raise
head-of bed (HOB) 20-30º
·
Elevation may lower CPP
Sedation/Paralysis
Ventricular
drainage
Mannitol
·
Improves rheology
(decreased blood viscosity) and has osmotic effect on cerebral edema lasting up
to 6 hrs.
·
Prolonged use may distrupt
BBB increasing edema
·
Contraindications: hypotension, renal failure.
·
Common dose: 1mg/kg initially, then 0.25-0.5 mg/kg
q6hrs. Check Serum Na & Osm before giving. Hold if Na > 150-160, or Osm
> 320 (limits can vary depending on the situation).
·
High-dose (1.4g/kg) given
wide open in patients GCS3 & fixed pupils had 33% more
favorable outcome. (JN3/04)
·
Alternatives or adjuncts include Lasix,
hypertonic saline (3% continuous or 9-23% bolus through CVL).
o
3%
saline: 7.5% to 30% boluses Benefit is unclear for continuous infusion of 3%.
Withdraw over 24-48hrs
Hyperventilation:
·
Generally keep CO2 30-35. Avoid prolonged
hyperventilation (PaCO2 <25mmHg).
·
Some suggest avoiding prophylactic hyperventilation
(PaCO2 <35) in the first 24hrs to avoid decreasing CPP, except as a
temporizing measure.
·
Use acutely (CO2 to 25 by manual bagging) only for
acute ICP plateaus
Decompressive craniectomy
·
14cm diameter appears optimal.
·
May be done initially with hematoma removal or within
48 hours of injury due to refractory
increased ICP
·
Hygromas occur, resolve spontaneously in most
(JN4/06)
·
Reconstruction: Timing controversial.
·
Cochrane Database: Only one high quality trial was
identified; which involved 27 pediatric patients who received either DC or conventional
treatment. The results indicate that the risk of death and disability was
moderately reduced when DC was used. No trials investigating the effectiveness
in adults were found. However,
the results of non-randomized trials and controlled trials with historical
controls involving adults, suggest that DC may be a useful option when maximal
medical treatment has failed to control ICP.
·
There
are two ongoing randomized controlled trials of DC (Rescue ICP and DECRAN).
·
Pediactric TBI: Has been used with favorable outcome. See J Jagannathan JN:P4/07
Barbiturate Coma
·
To burst-suppression on EEG. Serum levels are used,
but have poor correlation to clinical benefit.
·
Pentobarbital: Loading: 10 mg/kg over 60min, then
5mg/kg/hr x3hrs, then 1mg/kg/hr (Thiopental may be substituted).
·
Side-effects: hypotension
Hypothermia: to 95º
is accepted. <95º is controversial.
·
NABIS: Hypothermia study showed reduced ICP but no
difference in 6 month outcomes
Minor Head Injury
·
LOC <1min, normal mental status, no deficits on initial
exam, no skull fracture
·
Guidelines
for children with mild head injury published (Pediatrics, 1999)
·
For LOC (more than seconds), amnesia, vomiting,
lethargy, GCS >13, no focal deficits or seizures, skull fracture (except
across MMA, venous sinuses, or depressed), otherwise normal CT: observed for
2hrs, if GCS 15, no deterioration, able to hold down liquids, and reliable
caretaker, can discharge (JN:P 8/04)
·
New Orleans Criteria and
·
0.3% incidence of deterioration with normal CT
(delayed EDH, diffuse brain swelling)
Sports-concussion
·
See
Cantu RC N6/07
·
Grading:
Cantu or AAN grades
·
Concussion
in sport consensus statements: “National Athletic Trainers’ Association
Position Statement: Sport-Related Concussion,” Journal of AthleticTraining;
·
Guskiewicz KM, The NCAA Concussion Study. JAMA 290:2549, 2005.
·
More
than 90% of athletic concussions do not involve LOC. LOC does not correlate
with the severity of concussion symptoms.
·
Management
must be individualized, determining severity of injury after all symptoms and
signs have resolved. Factors that must be considered include age, sport,
previous history of concussion, specific symptoms associated with the injury.
·
No
athlete with postconcussion signs or symptoms should
be allowed to return to competition while symptomatic.
Traumatic
Brain Injury (TBI)
·
Guidelines for the
Management of Severe Traumatic Brain Injury, 3rd Edition (Journal Of Neurotrauma
24Supp1)
·
Surgical Guidelines: Neurosurgery 3/06
Supplement
o
Keeping ICP<20 improves outcome.
o
Keep CPP >70.
o
There
are no data from randomized controlled trials that can clarify the role of ICP
monitoring in acute coma. (Cochrane Database)
·
Normalize BP (SBP >90mmHg), temperature, oxygen
(SaO2>90%, PaO2>60). Keep mildly hypervolemic (CVP >8). Normalize hematocrit. H2 blocker.
·
Nutrition: paralyzed 100% BME, non-paralyzed 140% BME
·
Imaging: 3view c-spine, CXR, pelvis xrays. CT head (uncontrasted) and
abdomen. Labs: BSB, type & cross, BMP, ABG, coags,
urine toxicology
o
Repeat CT head for new ICP spikes. Delayed hematomas occur in 10-15%
·
AEDs generally
discontinued after 1 week if no seizures occur (and patient is stable)
·
Glascow Coma
Score: Best response used (i.e. best motor if asymmetric)
o
Decorticate posturing: UE flexion, LE extension (damage
above red nucleus)
o
Decerebrate
posturing: UE extension. Brainstem
isolated from higher centers (lateral vestibular nuclei and reticular formation
released from cortical control; red nucleus to spinal cord cut off)
Experimental Treatment:
·
Corticosteroids are not indicated in TBI. (Cochrane Database)
o
CRASH study (Lancet 04) RCT showed worse outcome at 2
weeks for patients receiving steroids
·
Aminosteroids:
There is no evidence to support the routine use of aminosteroids in the
management of traumatic head injury. On the basis of the existing evidence from
randomized trials of aminosteroids in head injury, it is not possible to refute
the possibility of moderate but potentially clinically important benefits or
harms. A further randomized controlled trial of tirilazad
mesylate with 1156 participants has been completed,
the results of which should become available in the near future. (Cochrane Database)
·
Calcium Channel Blockers: The authors found six eligible trials involving 1862 patients.
The results indicate that there is insufficient evidence to support the use of
calcium channel blockers. The authors conclude that there is some evidence that
a calcium channel blocker called nimodipine may be
beneficial for some patients with subarachnoid haemorrhage. (Cochrane Database)
·
Excitatory Amino Acid Inhibitors: The
case for efficacy of excitatory amino acid inhibitor therapy remains unproven.
To date, no product has proven to be efficacious for improving the outcomes of
brain-injured patients. Early termination, unpublished, and underpowered
studies limit a clear appreciation of the merits of this form of intervention.
Additional studies, some of which remain in progress, may more clearly define
the efficacy and effectiveness issues. (Cochrane Database)
·
Hyperbaric Oxygen: In people with traumatic brain injury, the addition of HBOT
significantly reduced the risk of death. Pooled data from the three trials with 327 patients that
reported mortality, showed a significant reduction in the risk of dying when
HBOT was added to the treatment regimen. However, there is little evidence that more survivors have
a good outcome. There
was a trend towards, but no significant increase in, the chance of a favourable outcome when defined as full recovery,
·
Hypothermia:
There is no evidence that hypothermia is beneficial in the treatment of head
injury. The earlier, encouraging, trial results have not been repeated in
larger trials. The reasons for this are unclear. Hypothermia increases the risk
of pneumonia and has other potentially harmful side-effects. Therefore, it
would seem inappropriate to use this intervention outside of controlled trials (Cochrane Database)
·
Magnesium: There is currently no evidence to
support the use of magnesium salts in patients with acute traumatic brain
injury. (Cochrane
Database)
·
Monoaminergic Agonists: The authors found three trials but
none of these looked exclusively at patients with a severe brain injury,
therefore there were no satisfactory studies of the effectiveness of monoaminergic agonists for severe TBI. Consequently, there
is, at present, insufficient evidence to support the routine use of
Sequelae:
·
Agitation/Aggression: The best evidence of effectiveness in the management of agitation
and/or aggression following ABI was for beta-blockers. Two RCTs found propranolol to be effective (one study early and one late
after injury). However, these studies used relatively small numbers, have not
been replicated, used large doses, and did not use a global outcome measure or
long-term follow-up. Comparing early agitation to late aggression, there was no
evidence for a differential drug response. Firm evidence that carbamazepine or valproate is
effective in the management of agitation and/or aggression following ABI is
lacking. (Cochrane
Database)
·
Coma: About
half of people in a coma because of traumatic brain injury will wake within a
year of the accident. Sensory stimulation methods vary greatly, from one or two
hourly sessions of a day, through to shorter sessions every hour for 12 to 14
hours a day. The review found there is no strong evidence to determine whether
sensory stimulation benefits people in comas. (Cochrane Database)
·
Delayed enlargement in 10-30%.
Guidelines:
Indications for Surgery
·
An EDH > 30 cm3 should be surgically
evacuated regardless of the patient’s GCS score.
·
An acute
SDH with a thickness >10 mm or a midline shift greater than 5 mm should be surgically evacuated, regardless of the patient’s
GCS score.
·
All
patients with acute SDH in coma (GCS score less than 9) should undergo
intracranial pressure (ICP) monitoring.
·
A
comatose patient (GCS score less than 9) … should undergo surgical evacuation
of the lesion if the GCS score decreased
between the time of injury and hospital admission by 2 or more points on the GCS and/or the patient presents with
asymmetric or fixed and dilated pupils and/or
the ICP exceeds 20 mm Hg.
Timing
·
It
is strongly recommended that patients with an acute EDH in coma (GCS score
<9) with anisocoria undergo surgical evacuation as
soon as possible.
·
In
patients with acute SDH and indications for surgery, surgical evacuation should
be performed as soon as possible.
Cerebral Contusions/Hematoma
Supratentorial Guidelines:
Indications
·