Most skull fractures are which type
Linear
How are skull fractures categorized
Location: basilar vs skull convexity
Pattern: linear/depressed/comminuted
Open/closed
Complicated
What would be a complicated skull fxt
One that is open or depressed, involves a sinus or has resulted in air somehow entering the skull (PNEUMOCEPHALUS-slide7)
Clinical significance of linear skull fractures
minimal unless crosses Middel Meningeal groove in temporal bone or a major dural venous sinus (risk of potential bleeding btwn skull and brain parenchyma) (sd 10)
Clinical significance of Depressed skull fxt
- Often involves brain injury with significant risk for CNS INFXN, Seizures and death if not IDd early. 25% have atleast brief LOC.
- High mortality rate in pts with significant decline in mental status.
(sd12-13)
Are most depressed skull fxt open or closed?
Most open, maybe closed but assume open until proven otherwise
Appropriate steps for a depressed skull fxt**
Must explore adjacent wounds, palpate area around wounds.
Tx: admit to neurosurgery, anticonvulsants to reduce seizure risk, ask tetanus status, prophylactic antibiotics for about a week.
If depressed more than thickness of skull OR contaminated wound OR
Basilar skull fxt
fxt of the base of the skull in one/more of 5 bones:
1. cribriform plate of ethmoid bone
2. orbital plate of frontal bone
3. Petrous and squamous portion of temporal bone (MOST COMMON)
4. Sphenoid bone
5. Occipital bone
which skull fxt increases risk for extra axial hematomas, especially subdurals?
Basilar
what other risks/signs are associated with basilar skull fxt?
can easily cause dural tears and leakage of CSF
nausea/vomiting often
CN III palsies, battle sign, raccoon eyes, rhinorrhea, otorrhea, hemotympanum, recurrent meningitis (less common)
(sd 19-21)
Skull X ray for Basilar fxt?
Can miss it! Use the signs, sx!
Tx/management for Basilar fxt*
-Admit for observation!!!
-Bloody drainage from nose or ear on white tissue--> Check for halo sign though can't exclude saliva, other clear fluid
-Most resolve spontaneously in a wk
-If CSF leak >7d, start ANTIBIOTICS
-CN palsies are a DELAYED complicatio
What is Mild BI on on the Glasgow coma scale
13-15
what is Low risk Mild BI on GCS
GCS 15 and NO hx of LOC, amnesia, vomiting or diffuse headache
What is med risk Mild BI
GCS15 and hx of LOC, amnesia, vomiting or diffuse headache. OBTAIN CT since risk of intracranial hematoma.
What is high risk Mild BI
GCS of 14 or 15 w/skull fxt and or neuro deficit.
When must GCS be modified
if child <36 mo
if intubated or
if facial swelling or intoxicated
Which pts with head injury are automatically included in Mild TBI regardless of clinical presentation
pts with coagulopathy, drug or alcohol consumptom, previous neurosurgical procedures, epilepsy or >60 y/o
what % of GCS 13 will have positive CT
40
Concussions
Used interchangeably with Mild TBI (13-15 GCS about 30 min after injury). MC cause is direct injury to head or elsewhere on body with an impulsive force to the head.
Mechanism of concussion
There is a transient electrophysiologic dysfunction of reticular activating system in upper midbrain caused by rotation of cerebral hemispheres on fixed brainstem.
symptoms of mild TBI
Two hallmarks: CONFUSION AND AMNESIA often w/out preceding LOC
other sx:
-dazed after blunt forward impact, dizziness/disorientation, nausea/vomiting/loss of balance, headache is COMMON, lack of motor coordination, light sensitivity, blurred vision, tinni
signs of mild TBI
Vacant stare, delayed verbal response, inability to focus, disorientation, slurred, emotionality out of proportion, uncoordination, memory deficits, any LOC, hx of brief convulsion or autonomic signs.
Imaging in mild TBI
CT and MRI usually normal! but 3% have intracranial hemorrhage of some type.
Sequela in mild TBI
single uncomplicated head injury will cause infrequent permanent neuro changes in previously healthy. Minor memory/concentration problems may be correlated to small shearing/microscopic anatomic lesions.
indications for CT scanning pts with Mild TBI
GCS 13-14
skull fxt or large subgaleal swelling
focal neuro findings
unexplained asymmetric pupils
distracting INJURIES or INTOXICATION
reported LOC/post traumatic seizure
history of coagulopathy
continued diffuse headache
amnesia
vomiting
Post-concussive syndrome
a state of nervous system INSTABILITY that can follow mild or mod. head injury by a few days +/- LOC hx.
Primary features/sx of post-concussive syndrome
fatigues, dizziness, headache, difficulty CONCENTRATING, diff w/ATTENTION, MEMORY, OTHER COGNITIVE DEFICITS
Mechanism of post concussive syndrome
theorized to be secondary to subtle AXONAL SHEARING lesions and/or biochemical changes with or without psychogenic components.
prognosis of post concussive syndrome
seen to some degree in 30-80% of mild to moderate brain injury pts. Scores tend to improve fast during first 6 months then slow down for years.
TX of PCS
Identify and treat depression, sleep problems, anxiety, persistent headache, dizziness.
Clearly explain
avoid habituating drugs
vestibular exercises and w/phenergan if dizzy
serial neuropsych testing to document improvement
evaluate prolonged course for p
contusions and axonal shearing injuries are subdivides into two types
Primary and Secondary brain injuries
Primary brain injury
Happens at the time of trauma. Damage results from multiple focal contusions, hematomas, bleeds, axonal shearing injuries, cerebral edema and swelling. Mechanism: external mechanical forces being transferred to Intracranial contents. Enough trauma to caus
Contusions are often a result of
blunt deceleration impact
Contusion sx/signs
often NO FOCAL neuro deficits
may see HEMIPARESIS or GAZE PREFERENCE in moderately sized ones
Later BILATERAL ones may produce COMA w/extensor posturing
if limited to FRONTAL lobes--> Delirium or aggressive, COMBATIVE SYNDROME
Axonal shearing injuries
axonal rupture m occur at time of impact from shearing forces.
Can be milder (impaired axonal transport)
may cause PERSISTENT COMA when widespread
Axonal shearing injury most common sites
corpus collosum/dorsolateral pons
Axonal shearing injury imaging
want to get PET, SPECT, fxnal MRI since CT may not show the structural changes
Hemorrhages in axonal shearing injuries
shearing in brain can cause hemorrhages in BASAL GANGLIA and other deep structures. may not develop until several days after
Secondary brain injury
Via cascade of molecular injury mechanisms initiated by the first trauma but continue for hours or days.
1. Electrolyte imbalances
2. Mitochondrial dysfunction
3. Inflammatory responses
4. Apoptosis
5. Secondary ischemia from vasospasm
6. Focal microvascu
secondary brain injury tx
no proven tx, avoid further insults such as
1. hypoxia
2. Fever
3. Seizures
4. hyperglycemia
Second impact syndrome
second concussion before first one heals.
often fatal or severely damaging
MOI of second impact syndrome
due to arterioles loosing their ability to auto-regulate following first injury leading to BRAIN EDEMA.
prevention of second impact syndrome
should avoid contact sports for sev days after first concussion and atleast SEVERAL WEEKS after second concussion esp with prolonged neuro sx.
DEMENTIA PUGILISTICA
Repeated concussion in sports associated with mild but CUMULATIVE cognitive deficits can lead to this in the worst case.
Post concussive seizures epidemiology
6% of hospitalized TBI have atleast one seizure. Early seizures occur w/in 1 week. Late occur after 1 week.
early post concussive seizures
provoked by DIRECT trauma (edema, hemorrhage, contusion)
Late post concussive seizures
more epileptic, w/re-wiring of brain leading to a more easily excited state.
management of post concussive seizures
pts with TBI usually given ANTI CONVULSANTS b/c risk of seizures--> brain hypoxia--> release excitatory NTs--> delay healing
Severe Traumatic Brain Injury
GCS of 8 or less. Pts are best cared for in neuro ICUs and Trauma center if head trauma.
Severe traumatic brain injury Prehospital care
1. Prevent HOTN, HYPOXIA (check BP and O2)
2. INTUBATION for GCS<8 or bag mask ventilation
3. IV saline
4. ASSUME cervical spine fractured--> stabilize/immobilize
Severe traumatic brain injury Imaging
CT in ACUTE phase ASAP
Repeat CT for any clinical deterioration
Head CT for any pt GCS <14
Severe traumatic brain injury Labs
continuous re-assessment of GCS esp in initial hours when deterioration is common.
Labs
1. Coagulation parameters
2. Blood alcohol level
3. URINE toxicology screen
Severe traumatic brain injury TX
Must recognize increasing ICP and possible impending HERNIATION (check for fixed pupil, posturing, bradycardia, HTN, resp depression)
Tx with
1. HEAD ELEVATION
2. HYPERVENTILATION
3. OSMOTIC THERAPY (mannitol)
Neurosurgery?
What requires neurosurgery?
1.Epidural hematoma larger than 30 ml
2.Subdural hematoma if acute >10mm in thickness or ass/w midline shift >5mm
3. Intracerebral hemorrhage
4. penetrating injury (debride and close, need antibiotics!)
5. depressed skull fxt- if more than thickness of sk
Neuro ICU principles
i. BP and O2 support
ii. Prevention of DVT
iii. Nutritional support
iv. ICP monitoring
1. Head of bead elevated to 30 DEGREES!
2. Optimize venous drainage from head
3. Monitor CVP and void hypervolemia
v. Hyperventilation avoided for first 2 days
vi. Seda
vegetative state
1. Awake but nonresponsive
2. Yawn, cough, swallow, move but not in response to environment
Akinetic mutism
1. Partially awake state in which pt able to form impressions and think but immobile and mute
2. Frontal lobe injury
Catatonia
Hypomobile and mute state seen in major psychosis
Locked in state
Pt unable to speak, move except for vertical eye movements which can be used to communicate
Most diminished alertness states are due to
widespread cerebral hemisphere abnormalities or due to reduced activity of RETICULAR ACTIVATING SYSTEM.
What can cause coma
any lesions affecting Reticular activating system or widespread cerebral hemispheres. Also Drugs, toxins or metabolic derangements like hypoglycemia, anoxia, uremia, hepatic failure
If pupils enlarged+ loss of light reflex + loss of vertical and adduction movements
location of lesion UPPER BRAINSTEM likely
IF pupillary reactions and eye movements INTACT
probably not upper brainstem but EITHER: Widespread structural lesions or metabolic suppression of cerebral hemispheres
Most common cerebral herniations
from supratentorial to infratentorial through tentorial opening--> TRANSTENTORIAL
types of herniation
Coma due to metabolic disorders
Cause coma by interrupting delivery of ENERGY SUBSTRATES
1. HYPOXIA
2. ISCHEMIA
3. HYPOGLYCEMIA
Or by altering neuronal excitability
1. DRUG/ALCOHOL INTOXICATION
2. ANESTHESIA
3. EPILEPSY
what is a moderate stimulus to test level of arousal
tickling nostrils w/cotton swab.
posturing in response to noxious stimuli indicates--
severe dysfunction of corticospinal system. Can be tested by pressure on knucles or bone prominences or pinprick.
Brainstem reflexes are assessed by testing
a. Pupillary light response
b. Spontaneous and elicited eye movements
c. Corneal responses
d. Respiratory pattern
if brainstem reflexes are preserved in coma, consider___?
Bilateral hemispheral disease.
If Unreactive and enlarged pupil (>6mm), or poorly reactive pupil??
What is a more extreme finding?
compression of CN II from mass.
Extreme finding: Bilaterally fixed dilated pupils? severe midbrain damage often from COMPRESSION BY SUPRATENTORIAL MASS
Must rule out ocular trauma and anticholinergic drugs.
Spontaneous eye movements in coma appear as
conjugate horizontal roving (EXCLUDES midbrain and pons as cause for coma)
Occular movements in coma: Conjugate horizontal ocular deviation to on side?
damage to pons on opposite side OR frontal lobe on SAME side as direction to eyes.
Eyes look to HEMISPHERAL LESION and AWAY from BRAINSTEM lesion!!
Vestibulo-ocular reflex in Coma. What does it indicate about a midbrain lesion?
doll's eyes"
When COMATOSE PT'S HEAD MOVED? normal reflex is EYES REMAIN FIXED where they were before head movement? doll's eyes. Means MIDBRAIN IS INTACT!
Coma prognosis mostly based on?
based on best GCS score w/in first 24 hours after injury.
1. 3-4 after 24 hrs? 87% die or remain vegetative
2. 5-7? 53% die or remain veg, 34% mod disability +/- good recovery
3. 8-10? 27% will die or remain veg
4. 11-15? only 7% will die or remain veg
Other poor coma prognosis factors
pt in vege state for atleast 1 year (unlikely to gain consciousness at all), for 1 month or longer will probably get severe disability. Over 40 y/o, absence of eye opening in first 30 days also leads to poor prognosis.
Epidural hemorrhage. Location and most common cause?
Blood collecting between skull and dura mater.
Most result from BLUNT TRAUMA in temporal or temperoparietal area w/assoc skull fxt disrupting the middle meningeal artery.
Epidural hemorrhage classic presentation
Classic is one of HEAD TRAUMA + LOC followed by lucent period after which pt AGAIN LOSES CONSCIOUSNESS.
But maybe either no LOC or pt never woke up.
Epidural Hemorrhage dx
CT and physical findings
Epidural hemorrhage sequala and tx
i. Arterial bleeding can be HIGH PRESSURE AND LEAD TO BRAIN HERNIATION w/in hours unless vessel ligated (MMA usually)
ii. If neurosurgery unavailable, drilling bilateral BURR HOLES can save pts life and lead to full recovery!
subdural bleeds/SDH location and cause?
i. Form between DURA AND ARACHNOID MEMBRANES
ii. Causes
1. From LINEAR TRANSLATION OR ACCELERATION along diameter of skull in LATERAL direction. This causes injury to VEINS, ARTERIES, OR BRAIN PARENCHYMA? SDH, epidural hematoma or coup-countrecoup contusi
SDH tx
Venous bleeding arrested by rising ICP or by direct compression of CLOT itself
ACUTE SDH sx
most pts drowsy or comatose (50%) after injury. 1/3 have LUCID interval before coma.
Trauma may be minor (or none in older pts and those on anticoagulants)
some pts have UNILATERAL HEADACHE, slightly ENLARGED PUPIL unilaterally.
large subdural hematomas likely to result in
Coma, hemiparesis and obvious pupillary dilation
Subacute SDH sx
some evolve slowly so that sx only obvious after d or weeks.
often pts DROWSY, HEADACHE, CONFUSED
s/t develop HEMIPARESIS
Brain atrophy probably
subacute SDH usually seen in
ALCOHOLICS and OLDER people, often following what seemed to be minor trauma
CHRONIC subdural hematoma sx and signs.
pt +/- have hx of trauma
m develop headache, SLOW THINKING, VAGUE PERSONALITY CHANGES, possible seizures
Headache m be positional
physician may initially suspect STROKE, BRAIN TUMOR, DRUG INTOX, DEPRESSION
Early CT w/out contrast= low density mass over co
Chronic SDH tx
i. Pts w/minimal sx and small chronic subdural ? sometimes just observed clinically w/serial imaging
ii. P w/ a clot thickness greater than 10mm ? surgical evacuation
1. Non comatose pts may not need surgery
iii. Given an acute subdural, ip pt deteriorati
CT assessment SDH
i. DOES cross suture lines
ii. Limited by DURAL ATTACHMENTS
iii. CRESCENT shaped extra-axial lesion
CT assessment epidural hematomas
i. Does NOT cross sutural margins
ii. DOES cross dural attachments since its btwn dura and skull
iii. LENS SHAPED on CT
MC cause of Subarachnoid bleeds
Head trauma is MC cause but others can result in spontaneous SAH
Other causes of spontaneous SAH
Berry aneurysm, Arteriovenuos malformation, Intracerebral hemorrhage extension into subarachnoid space
Clinical manifestations of Berry aneurysms
asymptomatic if unruptured, 50% temporarily LOC due to sudden increase in ICP and wake up later with giant headache.
another 45% will have SUDDEN SEVERE HEADACHE which is generalized and often + Neck stiffness.
Vomiting is common
A small first rupture can
Sentinel bleed
small rupture leaking blood in a Berry aneurysm, often before a SAH.
Grading of SAH based upon
level of severity based on clinical presentation, Grade 4-5 have mortality rate as high as 80%
Delayed neuro deficits of SAH
Rerupture, Hydrocephalus, vasospasm (major cause delayed death via brain ischemia), Hyponatremia.
Lab/imaging in SAH
1. Hallmark--> blood in CSF. Most show this on NON-CONTRAST CT w/in 72 hours, if no blood or mass lesion do LUMBAR PUNCTURE!
2. LP- CSF should be XANTHOCHROMIC. Only do before imaging if noncontrast CT not available
3. X-ray angiography or CT angiography
describe two methods of Aneurysm repair
1. Clipping: metal clip across the neck of aneurysm, preventing rebleed.
2. Coiling: platinum coil placed to block entry to aneurysm from circulation. By catheter via femoral artery