Concussion Flashcards
Mild Traumatic brain injury (TBI)
S/SX
Confusion
Amnesia
Sometimes loss of consciousness
Headache
Dizziness
Nausea/vomiting
Mild TBI
Neurologic assessment
- History with as much detail as possible
Include before and after recollections - Mental status exam
Short term memory
Attention and concentration - Neurologic exam
Cranial nerve exam
Limb strength and reflexes
Coordination and Gait
Pathophysiology of TBI
Axon stretch due to injury
Excitatory neurotransmitters released
K+ efflux and Ca++ influx
This leads to metabolic changes
Hyperglycolysis
Lactate accumulation
Mitocondrial dysfunction/oxidative phosphorylation
Increased energy need/decreased energy production
Globally:
Axonal swelling
Apptosis
Decreased cerebral blood flow
Inflammation
Concussion Recovery Rate
Brain Metabolism
30 days
Concussive Symptoms
15 days
Ion Imbalance
4 days
Second Impact Syndrome
Diffuse cerebral swelling in setting of second concussion
Rare, but can be fatal
May be due to disorder of cerebral autoregulation that causes
Cerebrovascular congestion
Cerebral edema
Increased intracranial pressure
Careful consideration for “return to play”
Post Concussion Syndrome
General
Common sequela of TBI
30-80% of patient with mild/moderate TBI will experience some type of symptom
Female and increased age are risk factors
Post Concussive Syndrome
S/Sx
Headaches
Tension
Migraine
Other
TMJ, occipital neuralgia, trigeminal nerve injury
Dizziness
Lightheadedness, vertigo
Sleep Disturbances
Insomnia usually
Psychological and cognitive symptoms (50% of patients)
Personality change, irritability, anxiety, depression
SKull fracture
most common fracture and causes
Most fractured-> parietal bone, followed by the temporal, occipital, and frontal bones.
Most common fracture-> linear, followed by depressed and basilar skull fractures.
Each year, approximately 2.8 million people suffer head injuries in the US alone.
Most common causes-> Falls, assaults, motor vehicle collisions, penetrating missiles
skull fracture
After injury
-You should assume a skull fracture exists in a any patient who has sustained a significant head injury or other major trauma.
-High kinetic injury is needed to cause injury
-Important to maintain immobilization of the cervical and thoracic spine
-A dressing held in place by a circumferential head bandage
is often not sufficient
skull fracture
patient arrives to the ER..
Identify and stabilize life threatening injuries
Protect and stabilize airway
Note: bleeding wounds from skull fractures can be profuse. Use Direct pressure for approximately 15 minutes as initial treatment
After stabilization, assess for: altered mental status, focal neurologic deficits, scalp lacerations, bony step-off of the skull, or periorbital or retroauricular ecchymosis.
Do NOT probe scalp wounds…
skull fracture
Dx
Non-contrasted CT is the imaging study of choice
There is a specialized study but not much research on it
If there is evidence suggestive of basilar fracture, reasonable to obtain CT angiography to assess for vascular injury
There is little evidence supporting use of CTA for skull fracture. Chat with radiologist to determine next best steps.
MRI is useful if evaluating vascular or ligament injury BUT CT is main choice
No benefit with skull x-rays
If that is the only option depending on practice location, 2 views should be performed
Negative plain radiographs in low risk situation (minor mechanism of injury, normal neuro eval) are reassuring however, they cannot completely rule out injury
skull fracture
don’t miss on Dx
You may need to keep looking.. Per Up to Date 5-15% of patients with skull fracture also suffer fracture of cervical spine.
Essential to perform careful assessment for concurrent injuries
In addition to imaging, may need to consider tox screen if altered mental status
Types of skull frcatures
Linear
Depressed
Basilar
Linear skull frcature
General
A single fracture that often extends through the entire thickness of the skull
Location: most often involving the temporoparietal, frontal, and occipital regions
Fortunately, the majority of linear skull fractures have minimal or no clinical significance
linear skull fracture
There is always a catch…..
If the linear fracture crosses the middle meningeal groove in temporal bone or major venous dural sinuses- could cause significant extra axial bleeding (beneath the skull but outside the brain parenchyma.
linear skull fracture
Presentation
Presentation- if simple and closed- usually no neurologic symptoms.
There may be swelling over fracture site
A minority who develop ICH can have depressed mental status, headache, vomiting, cranial nerve deficit
Depressed Skull Fracture
general
Occur when trauma drives a segment of skull below the level of the adjacent skull
Ex: direct trauma from a bat or a club
Often involve injury to the brain parenchyma
Increased risk of CNS infection, seizures, and death if not early ID and managed appropriately
Mortality is high among patients with depressed fractures with a significant decline in mental status
Closed or Open - majority are open, assume any depressed fracture is open until proven otherwise
depressed skull fracture
Presentation
They can present with report of loss of consciousness
CAREFULLY palpate but this is often limited due to swelling
Bone fragments can easily lacerate adjacent structures such as the dura mater —-which can lead to CNS infection
DO NOT blindly probe wound itself
Basilar skull fracture
general
Involve at least one of the 5 bones that make up the skull base
Cribiform plate of ethmoid bone, orbital plate of the frontal bone, petrous and squamous portion of the temporal bone, and sphenoid and occipital bones.
Most commonly occur through temporal bone, so high risk for extra-axial (outside of the brain but beneath the skull) hematomas
The temporal bone is relatively weak and is right by the middle meningeal artery and vein
basilar skull fractures
Clinical signs
Periorbital ecchymosis– Racoon eyes
Retroauricular ecchymosis (mastoid)- Battle’s sign
These appear 1-3 days later than initial injury
Otorrhea- CSF leak from ear
Rhinorrhea- CSF leak from nose
20% of patients display this. Within hours or up to several days after trauma
Hemotympanum- blood behind the tympanic membrane
Common
Generally appears within hours of injury
Neurologic presentation depends on degree of brain tissue and cranial nerve injury
If close to brainstem, N/V due to vestibular centers
Oculomotor deficits from injury to CN III,IV, or VI as may facial nerve palsies or hearing loss due to injury of CN VII and VIII.
basilar skull fracture
CSF leak
CSF leak occurred in approximately 11-45% of these fractures as noted prior
Most traumatic CSF leaks resolve spontaneously within 7 days but in rare cases, can persist for as long as several months.
lab to check if CSF- Beta 2 transferrin
Elevated skull fracture
Uncommon
Occur when the fracture fragment is elevated above the underlying skull
Impact usually tangential rather than perpendicular
Tangential skull fracutres- gun shot wounds- hemorrhage likely to be noted
Often affect frontal skull
Limited literature but associated with significant intracranial injury
Penetrating skull fracture
Result of gun shot, stab wounds, and blast injuries
Significant brain injury and hemorrhage
Emergent neurosurgical consult
Linear fractures
Tx
No specific intervention is necessary if CT reveals no underlying brain injury or depressed fracture
Emergency neurosurgical consultation ordered for intracranial hemorrhage
Can be admitted for observation for any suspicion or evidence of brain injury
Neuro checks
Patients can also be observed in ER (if no evidence of ICH) for 4-6 hours to detect delated complications.
Confirm adequate supervision for the next 24 hours and clear discharge instructions to return to ER
depressed skull fracture
Tx
Increased risk of infection and seizures—need prophylactic measures
Tetanus status determined
Prophylactic abx for 5-7 days
Anticonvulsants often given to reduce risk of seizures-consult with neurosurgeon or neurologist
Usually admitted to neurosurgery
If depressed more than the thickness of the skull, to OR for elevation (usually any greater than 5mm below adjacent structure)
If open and depressed but NO evidence of dural penetration or complications on CT…can be managed non operatively. Similar is recommended for uncomplicated, closed, depressed skull fractures.
Basilar fracture
Tx
Surgical emergency if ICH
ALL basilar skull fracture patients require admission for observation even if no surgical indications
Be suspicious of epidural hematoma if temporal bone involved…close neuro monitoring
If any noticeable change in neuro status, STAT non contrasted CT of the head should be ordered
CSF can be distinguished from local nasal secretions with beta-2 transferrin
The majority of CSF leaks resolve spontaneously in one week
Recent studies did not support prophylactic antibiotics- consult with neurosurgeon and ID to determine next steps
Incidence of bacterial meningitis rises substantially if leak lasts over 7 days
basilar fractures
Tx for cranial nerve palsy if develops
If cranial nerve palsies develop (usually delated to 2-3 days after injury) can treat with glucocorticoids
If facial nerve palsy appears acutely, poor prognosis of recovery of nerve function. Likely due to transection.
skull fractures
Anticoagulated patients
high risk of ICH
Symptoms of neurologic deterioration may not appear for up to 6 hours following injury
Risk greater in elderly population that are anticoagulated
All patients who are anticoagulated with a skull fracture should be admitted to unit equipped for close neurologic monitoring
Any sign of neuro deterioration -> STAT non contrasted CT of the head (why non contrasted…..??)
Can consider reversal of excess warfarin or DOACs (apixaban, rivaroxaban)
Another random tid-bit for extra fun- idarucizumab for dabigatranreversaland and exanet alfa for apixaban and rivaroxaban reversal
ICH intracranial hemorrhage
general
-Intracerebral hemorrhage is the second most common cause of stroke after ischemic stroke per Up To Date
-Spontaneous or traumatic
-Enlargement of hemorrhage is associated with neurologic decline, increased intracranial pressure
-Edema around focus of hematoma can delay perfusion due to mass effect, local neuronal ischemia, or accumulation or cytotoxic factors
-This can impair cerebral autoregulation and cause acute blood pressure changes-this can then contribute to further ischemia
-Most common causes are hypertension, amyloid angiopathy, and rupture AV malformation
-Also neoplasms, coagulopathy, illicit drugs
ICH
RF
HTN, Non compliance, Smoking, ETOH
Male>female
DOACs
NSAIDs
drugs
trauma
ICH
Presentation
Varies on type of hemorrhage but if sudden and maximal onset of headache= subarachnoid hemorrhage
Can then become obtunded
Blood is an irritant when in the “wrong” place. Due to taking up some space, irritation can be due to traction on meningeal pain fibers, increased ICP in general, or just the blood being present where it should not be.
Elevation of BP
Focal neurologic deficit on exam
Vomiting
If complaining on stiff neck, blood is interventricular and circulating in CSF- meningismus
Nuchal rigidity, photophobia, headache
Stupor or coma are often ominous signs
Seizures may accompany acute ICH
Cardiac abnormalities are commonly associated with spontaneous ICH
EKG prolonged QT interval and ST-T wave changes
May be due to catecholamine-induced cardiac injury that is central mediated release of this due to stress of pressure and autonomic disturbance
ICH
work up
Stable???? Does the patient need intubation and mechanical ventilation, anticoagulation reversal? BP control, neurosurgical consult for intracranial pressure monitoring?
Elevate head of bed >30 degrees
Non contrasted CT of the head is first choice for imaging- mandatory to confirm.
Labs- CBC, CMP, PT, INR, troponin, toxicology screen, urinalysis, pregnancy test
EEG? Later on.
Serial non contrasted CT is warranted to monitor
MRI brain with contrast can help identify the underlying cause of ICH for most patients- ischemia/structural change
Cerebral angiography is gold standard for pre op eval to determine source of bleeding
Can consider LP to assess for presence of blood
Subarachnoid hemorrhage
S/Sx
Thunder clap headache
“The WORST headache of my life!”
Nausea/vomiting
Decreased level of consciousness
Nuchal rigidity
Seizures
SAH
aneurysm
Major cause is rupture of arterial aneurysm
Other causes: AVM, bleeding disorders, trauma, illicit drug use.
With other causes- bleeding is less abrupt and may continue over a longer period of time
Risk factors for aneurysm: smoking, HTN, ETOH, family history of SAH or connective tissue disorder (Marfan’s), or personal previous SAH
Cerebral Amyloid Angiopathy
general
Involves the deposition of amyloid beta-peptide within the cerebral vasculature
Not well understood what leads to this. Genetic factors-autosomal dominant
Can lead to hemorrhage due to deposition in the vascular wall leading to concentric splitting of the vascular wall
Most common clinical manifestation of CAA is acute lobar intracerebral hemorrhage
Lobar = location in cortex and subcortical white matter of a hemispheric lobe of the brain.
Interestingly enough, the depositions favor cortical vessels
Crossing into stroke territory as these lobar hemorrhages can cause hemiparesis and so on
Subdural hematoma
general
Bleeding between the dura and arachnoid membranes
Occurs when bridging vessels between membranes tear during trauma
subdural hematoma
Dx and Tx
conCAVE lesions on CT brain
Can present with headache or confusion
Weightlifter picked up barbell-got headache
Surgical management in severe cases
Can monitor with serial CT scans
Supportive care
Epidural hematoma
General
Dx and Tx
RARE
Occurs when blood pools between dura matter and the skull
conVEX lesions on CT brain
Management similar to subdural hematoma
Surgical if severe
Supportive care and monitoring
ICH
Tx recap
In general, examine patient and obtain history
* Stabilize-intubation, BP management, etc
* CT to determine cause
-If AV malformation- can obliterate these via surgery-neurointerventionalist/vascular
-Treat hydrocephalus and increased ICP-neurosurgery
* Vasospasm after intervention
-Volume expansion and HTN-promotes cerebral perfusion after aneurysm has been obliterated
-CCB of choice by surgeon can be used to dilate vessels and prevent vasospasm. Nimodipine.
