33. Head Trauma Flashcards
(180 cards)
1
Q
MC mechanisms of head trauma
A
falls
struck by or against and object
MVC
2
Q
Head trauma defn
A
broad cateogry ext trauma to craniofacial area from blunt, penetrating, blast, rotational or accel-decel forces
3
Q
Head injury defn
A
clinically evident injury on PE or presence of ecchymosis, laceration or deformities
4
Q
Traumatic brain injury
A
injury to brain itself
5
Q
Mild TBI definition
A
GCS 13-15 within 30min of injury pr preesentation to ED with trauma induced physiologic disruption of brain function manifested by:
1) any period of LOC <30min or decr LOC
2) any memory loss for events pre or post accident
3) alteration of any kind at time of accident
4) neuro deifcit that may or may not be transient
6
Q
Scalp five tissue layers
A
dermis - thickest
subcut tissue - blood supply, hair follicles
galea - m for wrinkling forehead
Loose areolar tissue
Deepest - pericranium
7
Q
skull bones
A
frontal
ethmoid
spheoid
occipital
2 parietal
2 temporal
8
Q
How do contrecoup brain injuries work?
A
may occur on the opposite side of the head impact (coup) as the brain shifts to the uninjured side and strikes against uneven bone surfaces.
9
Q
What. is the tentorium cerebelli?
A
partitions cerebellum and brainstem from cerebral hemispheres
10
Q
Brain 3 layers
A
dura
arachnoid
pia
11
Q
CSF production by?
A
choroid plexus in lateral ventricles primarily
12
Q
Normal pressure by CSF?
A
65-195mm water or 6-15mmHg
13
Q
What is the blood brain barrier’s job?
A
maintain microenvironment of brain tissue and CSF
14
Q
When intact, what does BBB do for neuroactive drugs?
A
to penetrate the brain tissue usually depends on their lipid solubility.
15
Q
How does TBI disrupt BBB?
A
biome- chanics of a brain injury or posttraumatic cerebral edema can cause a disruption of the BBB for up to several hours after the insult. In severe TBI, prolonged disruption of the BBB further contributes to the development of posttraumatic vasogenic cerebral edema and higher maximum intracranial pressure (ICP
16
Q
Brain % of o2 consuption of entire body? CO %?
A
20
15
17
Q
What BP, pH and co2 promote cerebral vasoconstriction related to cerebral brain flow?
A
hypertension
alkalosis
hypocarbia
18
Q
What BP, pH and co2 promote cerebral vasoDILATION related to cerebral brain flow?
A
hypotension
acidosis
hypercarbia
19
Q
Cerebral vasoactivity very sn to changes in pp of c02 and o2. Change in pco2 between 20-60mmhg decreases diameter of vessel by ?%
How does this help in concern for ICP?
A
2-3%
why hyperventilation should theoretically work
20
Q
What is cerebral perfusion pressure?
A
gradient of pressure across the brain
21
Q
CPP equation: ___ - __
A
MAP - ICP
22
Q
Cerebral blood flow is relaitvley constant when CPP is __ - __mhg “ie auteoregulation”
A
50-160 (MAP)
23
Q
If CPP falls below ?mmHg, autoregulation is lost and cerebralblood flow can decline to result in tissue ischemia nd altered cerebral metabolism
Ie why we need to avoid hypoperfusion in brain injury
A
40
24
Q
Target CPP for brain injury pt
A
60-70
25
ICP > _ mmHg
15
26
If ICP increases to point where CPP is compromised,then ? occurs and autoregulation becomes dep on ?
vasoparalysis
imapired --> MAP
27
What ICP certainly needs intervention?
>22
28
Simple techniques to reduce ICP
head neutral
HOB >30
29
Cushing rflex defn
hypertension
bradycardia
irreg resp effort
ICP is life thr level
30
How can incr ICP effect mental status?
needs cerebral cortices and intact reticular activating system of brainstem
incr icp can compress brainstem
31
Severe TBI defn based on GCS
32
Mild TBI defn based on GCS
13-15
32
Moderate TBI defn based on GCS
gcs 9-12
33
What factors contribute to degree of brain injury following mTBI?
primary mech
magnitude of injury
secondary insults
pt genetic, molecular response
34
Primary damage in mTBI caused by?
initial impact or force that although not as evi- dent as severe TBI, may lead to smaller contusions, hematomas, axonal damage, and microvascular injury
35
Repeated mTBI can lead to CTE - what is this?
chronic traumatic encephalopathy - term used to describe clinical changes in cognition, mood, personality, behavior, or movement occurring years following concussi
36
Direct injury to head - what factors are included in resulting damage overall?
consistency
mass
surface area
velocity of object strike
vs brain itself: vasoelastic properties of the underlying region of brain tissue, duration of the force applied, magnitude of the force reaching the brain tissue, and surface area of the brain that is affected
37
Indirect brin injury: ex accel-decl injury which can cause which vessels to shear?
subdural heamtoma (bridging vessels)
38
Name 5 secondary insults causing brain injury?
decr o2, E to brain tissue
cascade cytotoci events, mediated by molecular/cellular proceeses:
events include activa- tion of inflammatory responses, imbalances of ion concentrations (e.g., potassium, calcium), an increase in the presence of excitatory amino acids (e.g., glutamate), dysregulation of neurotransmitter synthesis and release, imbalance in mitochondrial functions and energy metabolism, and production of free radicals
39
Factors of penetrating trauma that lead to more morbidity/mortality
high velocity
Projectiles crossing midline and resting in posterior fossa
Large missiles that fragment
Incr Age
Sui attempt
low GCS
Bilateral mydriasis
dural penetration
bihemispheric and multi lobar injury
40
Wounding capacity of a forearm related to what two aspects?
kinetic energy of missile on impact
how much E is dissipated
41
What are features of clinically significant skull fractures?
1. intracranial air
2. association with overlying scalp lac (ie open)
3. depression below level of skull's inner table
4. location over major dural venous sinus or middle meningeal artery
42
Defn of a linear skull fracture
single fracture through entire skull thickness
43
When are linear skull fractures clinically important?
cross middle meningeal groove or major venous dural sinuses as can form EDH
44
Sutural diastasis: what two are often involved in adults?
coronal
lambdoid
45
Where do most depressed skull fractures occur over? (2)
parietal
temporal regions
46
Why are depressed skull fractures clinically important?
predispose to sign trauma and complications - infection, seizure
47
Basilar skull fracture defn
linear fractures at base of skull usually occurring through temporal bone
48
Basilar skull fracture - high risk for what kind of hematoma?
extra axial due to proximity to middle cerebral artery
49
How does a dural tear from a basilar skull fracture present?
basilar skull ffracture then communicates with sa space, paranasal sinuses and middle ear so that there is now a route for potential infection
50
Extra axial vs intra axial IC injury defn
extra - in the skull but outside the brain tissue (SAH, SDH, EDH, subdural hygroma)
vs
intra: bleeding within brain itself (TAI, cerebral and cerebellar contusions, cerebral and cerebellar hematomas)
51
Epidural hematoma cause and where most often?
middle meningeal a or vein or dural sinus
temporoparietal region
52
Subdural hematoma - injury type RF
accel-decel injury
53
Why do SDH tend to occur in pt with brain atrophy?
bridfinf veins traverse greater distances and are more likely to rupture with movement of head
54
Prognosis of SDH - factors
degree of brain injury caused by pressure of expanding hematoma on underlying tissue or other IC injuries
GCS 8 or less
ACute herniation syndrome on ED presentation (also bad)
Posterior fossa - bad
55
Traumatic SAH
blood in csf and meningieal intima probably from tear of small subarachnoid vessels
with normal gcs typically no intervention
56
What is a subdural hygroma?
collection of clear, xanthochromic blood tingued fluid in the dural space maybe from tear arachnoid or effusion from injured vessel
typically secondary to trauma
57
Diffuse axonal injury - diffuse or multifocal in actuality
multif
58
Diffuse axonal injury - preferred term in nontraumatic causes of axial injury? mild vs severe
traumatic axonal injury vs diffuse
59
Diffuse axonal injury - defn
prolonged traumatic coma not caused by mass lesion or ischemic insult
60
How does traumatic axonal injury (TAI) occur?
primary insult: torn or stretched so they ball up and screw up sending messages
then secondarily it disrupts the extracellular matrix and influx of inflammatory mediators leads to axonal swelling and axon death (uncoupling of cerebral blood flow, metabolism, apoptosis)
61
Clinical grading of TAI: I-3
(1) grade I (mild)—coma for 6 to 24 hours; (2) grade II (moderate)—coma for longer than 24 hours but not decerebrate; (3) grade III (severe)— coma for longer than 24 hours and decerebrate or flaccid.
62
Cerebral contusions: layman's term?
bruising on brain tissue - petechail
63
MC Cerebral contusion sites
poles and inferior surfaces of frontal and temporal lobes as brain hits bone protuberances here
64
What type of mechanism can cause intracerebral hematomas?
shearing/tensile forces that mechanically stretch and tear deep small caliber arterioles at brain
65
What type of mechanism may cause the rare primary traumatic intracerebellar hematoma?
direct blow to occiput
66
Primary brain injury - goals of care?
fix the issue that caused the injury
67
Secondary brain injury causes:
alteration in cell function and propogation of signals:
1. depolarization
2. excitotoxicity
3. BBB disruption
4. ischemic injury
5. edema formation
6. IC hypertension
68
What 4 vital sign abnormalities have been shown to worsen outcomes after TBI? (at least in the paragraph of secondary systemic insults)
Hypotension
Hypoxia
Anemia
Hyperpyrexia
69
Why is hypotension bad after TBI?
reduces cerebral perfusion so potentiates ischemia and infarction
70
How does hypoxia occur after tbi?
po2 <60 due to transient or prolonged apnea by brainstem or injury post vs airway obstruction vs injury preventing normal resps
pulmonary injury reducing effective oxygenation
ineffective airway management
71
What is one of the most potent drivers of cerebral blood flow?
paco2
72
Hypocarbia on blood vessels
vasodilation
73
Hypercarbia on tbi - what happens to the brain?
incr cerebral edema and icp
74
Hypocarbia after tbi - what happens to the brain?
reduced cerebral blood flow
transient decr in ICP
75
Why is anemia bad after TBI?
reducing o2 carrying capacity of blood
76
Why is hyperpyrexia bad after TBI?
core temp >38.5
worse outcomes incr metabolism to injured areas --> resultant incr in ICP
77
What is uncal herniation?
transtentorial hernation where CN3 is compressed, then get ipsilateral oculomo nerve then pupil dilatation and nonreactivity, contralateral hemiparesis
78
What is Kernohan notch syndrome in uncal hernation?
contralat cerebral peduncle in some small number of TBI pt is forced against opp tentorial hiatus - hemiparesis is then ipsilateral to CN3 findings
79
where does uncal herniation occur?
lateral middle fossa or temporal lobe
80
Central trans tentorial herniation: where does this occur?
Expanding lesion at the vertex or frontal or occipital pole of the brain
81
Central trans tentorial herniation: how does clinical deterioration occur?
Bilateral central pressure exerted on the brain from above: can see a settle, change and mental status or decreased LOC, bilateral motor weakness and pinpoint pupils
As herniation progresses, both pupils become midpoint and lose light responsiveness
Sustained hyperventilation may occur, can also see yawning, size progressing to sustained high respirate, then a regular breaths before respiration arrest
Decorticate positioning by noxious stimuli
82
Cerebellotonsillar herniation: what is this?
Cerebellar tonsils, herniate downward through the foramen Magnum, which displaces the entire brainstem
83
Cerebellotonsillar herniation: clinical findings
Wrapped in sudden, respiratory and cardiovascular collapses the medulla is compressed.
Pinpoint pupils.
Flaccid quadriplegia is the most common motor presentation
84
Upward transtentorial herniation: what can this occur due to i.e. where is the lesion?
Expanding posterior fossa lesion
85
Upward transtentorial herniation: what will you see on exam?
Might have pinpoint pupils due to compression of the ponds, downward, conjugate gaze is accompanied by the absence of vertical eye movements
86
Name four types of brain herniation
Uncal
Central transtentorial
Cerebellotonsillar
Upward transtentorial
87
Main history, questions for concern in moderate severe traumatic brain injury
Event or mechanism
Circumstances,
Concomitant, drug and alcohol.
Symptoms prior
Past medical history.
Any anticoagulant medication’s?
88
What are the key components of a efficient Neuro exam for emergency medicine?
Mental status
GCS
Pupillary and responsiveness.
Motor strength and symmetry
89
List eight characteristics of a Basilar skull fracture
Blood and air canal, hemotympanum, rhinorrhea, ottorhea, battle, sign, retro, articular, hematoma, raccoon sign, Peri orbital, ecchymosis, cranial nerve deficits, facial paralysis, decreased, auditory, acuity, dizziness, tinnitus, nystagmus
90
Name the Glasgow coma scale for eyes
Four – spontaneous opening, three – to verbal command 2–2 pain one – no eye-opening
91
Name the Glasgow coma scale components for verbal stimuli
Five – oriented and converses, four – disoriented and converses, three – inappropriate words, two – incomprehensible, one – no verbal
92
Name the motor response for Glasgow coma scale
Six – obeys verbal commands, five – local lies to pain, four – flexion withdrawal, three – abnormal flexion, 2– extension, one – none
93
Strongest predictor of outcome, following moderate and severe TBI
Advanced age
Pupillary reactivity.
GCS motors score
External injuries.
CT characteristics, including midline shift and subarachnoid, bleed, hypotension, hypoxia
94
What does abnormal flexion or decorticate posturing imply in terms of where the injury is?
Above the midbrain and present as abnormal flexion of the upper extremity and extension of the lower extremity
95
What does decerebrate or abnormal extension tell you about the level of injury?
More coddle injury, i.e. below the midbrain
96
What three things in the acute setting assess brain, stem function?
Resp pattern
Pupillary size
Eye movements – oculocephalic response and ocular vestibular response using cold water
97
Classic presentation of an epidural haematoma
Decreased LOC and then a lucid interval
98
What is the definition of a chronic subdural hematoma?
Greater than two weeks
99
What is important in determining consciousness immediately following TBI – i.e. imaging finding
Distribution rather than overall extent of axonal pathology
100
What signs and altered LOC point you more towards an intracranial injury
Worsening headache.
Focal neural deficit
Confusion,
Lethargy
101
What is the Rotterdam score?
Initial non-contrast computed tomography for predicting six month mortality following TBI
102
List the criteria of the Rotterdam score of initial non-contrast CT for predicting six month mortality following TBI
One. Basil cistern easement: zero equals none, one partially faced, two completely faced.
Two. Midline shift: zero equals no shift or greater than equal to 5 mm, one equals greater than 5 mm.
Three. Epidural hematoma: zero if ED is present versus one if no ADH.
Four. IVH or SH: zero if neither present, one if either present.
Travel score out of six points from less than equal to one 0% versus six less than equal to 61%
103
What is pneumocephalus?
Free air in the brain, if in the setting of TBI should look for an open fracture
104
What is pneumocephalus?
Free air in the brain, if in the setting of TBI should look for an open fracture
105
EDH on CT scan
Hyperdense, by convex, avoid lenticular. Does not extend beyond the dural attachments of the suture lines.
106
SDH shape on CT scan
Follows the contour of the tentorium can be hyper or hypodense
107
What does cerebral oedema look like on a CT scan?
Bilateral compression of the ventricles, loss of definition of the cortical sulky or effacement of basal cisterns
108
Emergency department management of acute head injury
ATLS: airway, breathing, circulation, disability, if before airway, if possible to get a GCS, exposure
Prevent hypotension and hypoxia
Osmolar therapy if concerned for increased ICP: 3% sodium chloride given 250 ML
109
Peros Enns, what is to Osmo therapies you can use for increased intracranial pressure
One. Mandal 0.25 to 1 g per KGQ6H up to a serum osmolarity of 320 Milli Omos per KG.
Two. Hypertonic saline 23.4%, 30–60 ML can be given Q6H up to a maximum serum sodium of 160.
110
Why does mannitol work for increased intracranial pressure?
Produces an osmotic gradient that reduces brain volume and provides increased space for an expanding haematoma or brain swelling. This peaks about 60 minutes after bolus administration and lasts 6 to 8 hours.
111
What are the benefits of hypertonic saline in increased ICP?
Reducing secondary injury through cellular, modulation, decreasing cerebral edema, improving peripheral perfusion, decreasing ICP through vasa, regulatory mechanisms and regulation of pro-inflammatory and prothrombotic mediators
112
Risks of giving mannitol
Renal failure, hypotension, can increase bleeding into traumatic lesions by decompressing tampon effect of a haematoma
113
Adverse events associated with hypertonic saline
Renal failure, central Pontine, Mylin, lysis, rebound ICP elevation
114
Of note: hyperventilation also reduces cerebral blood flow, which is why it works for reducing ICP, and the brain needs this to meet it’s demands. So don’t really do it.
115
What are the neurologic effects of hypocapnia in a TBI patient?
Low carbon dioxide leads to increased neuronal, excitability, and basic construction
This can lead to cerebral spinal fluid alkalosis, which further leads to vasoconstriction of vessels (overall decreasing cerebral blood flow and blood volume)
There is a risk of increased amino acid release given low carbon dioxide
Alkalosis of the CSF leads to time buffering and a normal pH with normalization of partial pressure of arterial carbon dioxide, which lead to vasodilation and reperfusion injury
116
What is a decompressive craniectomy
Surgical removal of partial of the skull bone for relieving ICP
117
Patients with signs of head trauma, taking warfarin – how to reverse?
IV vitamin K, fresh frozen plasma or PCC ( this is preferred over FFP) for a target INR less than 1.5
118
Patients with signs of head trauma, taking more friend – how to reverse?
IV vitamin K, fresh frozen plasma or PCC ( this is preferred over FFP) for a target INR less than 1.5
119
Patient with head trauma on dabigatran - recommendations for reversal?
Idracuzimab 5g given as 2.5g in infusion over 5-10 mins
120
If your patient lived in the states, and was on a factor 10, a inhibitor, what medication could you give them if they had had trauma?
Adnexanet alpha
121
What is the definition of early versus late post traumatic seizures
Before seven days versus after of injury
122
Went to start Keppra for early post traumatic seizure?
Per Rosens, when the overall benefit is thought to outweigh the risk
123
If there is penetrating, craniocerebral trauma, what antibiotic should you use?
Vancomycin 1 g Q 12 H, gentamycin 80 mg Q8H, metronidazole 500 mg Q6H
124
Scalp wound management in the emergency department
1. Haemostasis with direct pressure or stapler.
2. Prompt irrigation. With removal of any debris from the site.
3. Hair can delay healing, so make sure it’s not in there.
4. Large lacerations of the Galia can be repaired with interrupted or vertical mattress sutures of 30 nylon or poly propylene or opposition technique foreclosure
5. Typically don’t really need antibiotics.
125
Do patients with the linear skull fracture need anything specific for treatment?
No, unless they have sides of underlying injury on the CT scan. Simply watch them for 4 to 6 hours.
126
When can patients with the depressed skull fractured not be treated operatively?
No clinical or radiographic evidence of dural penetration, significant intracranial, hematoma, depression, greater than 1 cm, front of sinus involvement, gross cosmetic, deformity, wound infection, pneumocephalus, or gross wound contamination
127
When should you give prophylactic antibiotics in a basal skull fracture with a CSF leak?
If the leak persists greater than seven days
Treat with Vanco, gentamycin, metronidazole
128
What are urgent indications for EDH evacuation by surgery?
EDH larger than 30 cm³ regardless of GCS, as well as comatose patients with an acute EDH and anisocoria on pupillary exam
Per patient who are awake: if they have vocal Neuro deficits, haematoma greater than 30 cm³, thickness of a clot greater than 15 mm, degree of midline shift greater than 5 mm
129
What are surgical indications for surgical evacuation of an acute SDH?
STH with thickness more than 10 mm or a midline shift of more than 5 mm on a CT scan regardless of the patient’s GCS score, worsening GCS score greater than equal to two points from the time of injury to hospital admission in a comatose patient, asymmetric or fixed or dilated pupil, persistent elevation of ICP
130
What is the most serious complication of a traumatic subarachnoid hemorrhage?
Cerebral Vasos spasm
131
With cerebral contusions, what patients are at high risk for haemorrhagic progression and need for delayed surgical decompression?
Lower GCS score, larger, cerebral contusion
132
When my patients with an intracity haematoma needs surgery?
Emergent intervention or surgery for ICP lowering
If they are unconscious, mortality approaches 45% versus if they are conscious, it is lower
Bleeding into the ventricles or cerebellum carries a high mortality rate
133
Intracerebellar haematoma – what is indicated?
Emergent neurosurgical consultation
134
What are risk factors for an early post-traumatic seizure?
GCS score of 10 or lower, immediate seizure, post traumatic amnesia, lasting longer than 30 minutes, linear, or depressed, skull fracture, penetrating head injury, SDH, ADH, ICH, cortical contusion, age 65 years or younger, chronic alcoholism
135
What are the risk factors for post traumatic epilepsy?
Severe TBI, early post traumatic seizure prior to discharge, acute ICH or cortical contusion, post traumatic amnesia, lasting longer than 24 hours, age older than 65 years and pre-morbid history of depression, higher rates in patience with temporal lobe bleeding
136
Name 3 CNS infections post brain injury
meningitis post basilar skull fracture
brain abscess
cranil OM
137
List 5 medical complications that can occur post TBI
dic
resp complications
cardiac dysr
138
4 main mtbi sx categories
somatic
cognitive
sleep
emotional
139
PE of mTBI
head injury assessment
neuro/cn
MMSE
140
ddx mtbi
intoxication
seizure
hypoglycemia
141
List 7 Canadian CT head rules
High risk 1-5:
GCS <15 2h post injury
suspected open or depr skull fracture
any sign basilarskull fracture
emesis >2 epi
age >65
medium:
amnesia pre impact 3ft
142
NEXUS II crteria for ct head
evidence of sign skull fracture
scalp hematoma
neuro deficit
alt alertness
abn behaviour
coagulopathy
persistent emesis
age >65y
143
What head lesions may show up better/be better dettermined by MRI?
posttrauma ischemic infarct
subac nonhemorrhagic lesions and contusions
axonal shear injury
lesions of brainsteam or posterior fossa
144
When to use Diffusion tensor imaging with mri - head injury?
TAI
145
MTBI d/c home- when?
observe 4-6 hours
anticoag up to 24h and repeat scan possible
146
Warning signs in mtbi
cannot wake up
severe/worsenign h/a
somnolent/confused
restless
unsteady or seizure
difficulty vision
fever or stiff neck
urine/bowel incontinence
weakness or numbness new
147
Post concussive sybdrome - sx
constellation of sx including somatic (h/a, dizzy, vertigo, nausea, fatigue, sn to light and noise)
cogn
affective following mtbi persisting beyond recovery period
148
Postraumatic transient cortical blindness syndrome - what is this?
transient visual loss
n pupils
normal fundoscopy hours following mtbi
returns within 24h max
149
Return to play: step 1:
BEFORE THIS 24H-48H OF REST
sx limited activity - not providing like reintro school
150
Return to play: step 2
light aerobic
walk/stationary bike, no RT to incr HR
151
Return to play: step 3
sport sp exercise
run/skate, no head impact
to add movement
152
Return to play: step 4
noncontact drills training
ie passing or RT
exericse, coordin and incr thinking
153
Return to play: step 5
full contact practice
medically cleared now - N training
to incr confidence
154
Return to play: step 6
return to sport
normal play
155
Return to play length of ea stage
at least 24h
156
TBI key management prehospital
avoid secondary injury: hypoxia >90% - delay defin airway if possible
hypotension
hypercarbia/hypo
ICP raised
157
TBI management in ED
ABCDE
MOVID capnography
Prevent secondary brain injury SBP >110 if 15-49 &70+, target >100 for 50-69y
ICP mangeemnt
Reverseal anticoag adn avoid anemia
avoid hyperthermia
+/- abx, tetanus
seizure prophylaxis+/- tx
158
Decorticate - where is the lesion?
injury above the midbrain
159
Decerebrate - - where is the lesion?
caudal/brainstem injury
160
N ICP
5-15 (really 20 or 22)
161
why is ICP bad?
ischemia
henriation
neuronal injury
162
CPF equation
MAP - ICP
163
List 6 ways to manage early elevation of ICP
head elevation
minimize collar tightness
osmotic agents
avoid large swing in BP - MAP so keep CPP >60
sedation
anti seizure medication consideration
NSx: drains and ICp monitors, surgical decomp
164
Mannitol dose
1g/kg bolus
20% solution in 100ml bag means 100g
165
Mannitol considerations - BP?
hypotension concerns so probably not great if vol resuscitating (use hypertonic saline)
166
Complications of mannitol
hypotension
renal failure
decr tamponade of bleed
167
Hypertonic saline: dose
3-5ml/kg over 20 mins
168
Hypertonic saline 3% ED: how does this work?
augments intrasvacular vol and incr BP in addition to decr ICP - may be preferred agent
169
Goal Na for hypertonic saline?
155-160
170
Complications of hypertonic saline
bleeding secondary to decr plt, aggregation, hypokalemia, hyperchloremia acidosis, central pontine myelinolysis, ICp elevation rebound, renal failure
171
Mod-severe TBI patient benefit from txa?
yes! give within 3h per CRASH 3
172
Theory of why hyperventilation bad
ischemia risk
herniation can incr RR to target 30-35 (within 30s, peak 8 min)
173
Surgical indications EDH
1. >30cm vol
2. comatose
3. anisocira
174
Acute SDH indication for surgery
1. >1cm max thickness
2. >5mm Mid line shift
3. 2+ drop in GCS
4. Asymm or fixed/dilated pupil
175
Aneursymal SAH - what ccb given?
nimodipine
not for trauma
176
High risk factors for mortality penetrating brain injury
incr age
suicide. attempt
lower gcs
bilateral mydriasis
dural penetration
bi hemispheric/multi lobar injury
177
Abx for penetrating injury to brain
vanco
gent
flagyl
178
Skull fracture - manageemnt
if not openL: watch 4-6 hours
prophylacticabx 5-7d for depressed and open - vanco/gent/flagyl
179
If CSF leak > _d needs abx
>7
