CNS trauma Flashcards
- Know the peak age groups in which head injuries occur and the mechanisms whereby these injuries are received
The peak age range is 24-35 with small peaks at 0-4 years for child abuse and over 65 years for falls at home. Males > females. Major causes include traffic/transport (highest- 20-50%), violence (20-40%) assaults, homicides, suicides and falls.
Forces responsible for traumatic brain injury
- contact: object striking head leading to fractures, epidural hematomas, cerebral contusions. 2. acceleration/deceleration: shear, tensile and compressive strains. 3. penetrating (knives, etc). 4. secondary injury (hypoxia, hypotension)
Linear skull fractures
Linear skull fractures of the calvarium are identified by radiologic studies and by themselves portend no independent prognosis other than to suggest a high-impact injury
depressed skull fracturs
Depressed skull fractures consist of comminuted bone fragments that may or may not be driven into the brain. Occasionally these injuries require surgical intervention to prevent infection or correct a cosmetic defect.
Basilar skull fracturs
Basilar skull fractures are common with high-velocity blunt injuries. may extend through the cribiform plate or petrous bone and result in CSF leaks (otorrhea or rhinorrhea) that may lead to meningitis
Signs of skull base fracture
CSF rhinorrhoea, Bilateral periorbital haematomas (Racoon eyes), Subconjunctival haemorrhage, Bleeding from external auditory meatus, CSF otorrhoea, Battle’s sign (blood accumulation behind ear, occurs 12 hrs later), Facial nerve palsy
diastatic skull fractures
Diastatic fractures are traumatic separations of the skull at suture lines and have the same significance as linear fractures.
growing skull fractures
Growing fractures of infancy (0-18 months of age) result from dural tears and herniation of the arachnoid into the fracture site. CSF pulsations then cause bone loss over months, often requiring surgical correction
Epidural hematoma cause, location, presentation, treatment, mortality
Epidural hematomas typically result from intracranial, extradural arterial bleeding from skull fractures in the distribution of the middle meningeal artery. Classically they present after an impact injury with a “lucid interval: prior to progressive obtundation and coma as the hematoma expands. Treatment is timely surgical removal of the mass lesion and the prognosis principally depends on the time from injury to evacuation. Mortality is less than 20% with evacuation in less than one hour.
Subdural hematoma cause, location, treatment, mortality
Subdural hematomas result from translational acceleration from high velocity mechanisms. Hemorrhage into the subdural space results from rupture of the bridging veins that connect the cortical surface of the brain with the sagittal sinus. This injury is often associated with underlying cerebral contusions. Associated with elevated intracranial pressure and distant secondary cerebral injury. Treatment includes prompt surgical removal of the blood clot, control of the intracranial pressure, and restoration of adequate cerebral blood flow. Mortality from subdural hematomas is between 40-60%.
cerebral contusion cause, location, presentation, treatment, mortality
High velocity translational and impact injuries result in superficial hemorrhagic contusions of the brain. Characteristic locations include those brain surfaces in contact with the rough bony surface of the anterior cranial fossa (frontal lobe) and the sharp edge of the greater wing of the sphenoid (temporal lobe). Hemorrhage into areas of damaged brain results in mass effect and herniation with secondary brain injury. Treatment involves medical management to prevent brain swelling and occasional surgical evacuation of large hematomas. Mortality is less than 20%.
Coup vs contrecoup
coup: injury at the front of the brain. Contrecoup: injury at the back of the brain
Diffuse Axonal Injury cause, presentation, MRI results, mortality
Diffuse axonal injury results from high velocity rotational acceleration/deceleration injury. The exact pathophysiology remains controversial. Shearing of axons is thought to result in pathologically identifiable “retraction balls” or axonal spheroids on microscopic examination. Clinically the patient is rendered unconscious from the moment of injury, without significant anatomical correlation of injury on CT. MRI studies often show punctuate hemorrhages in large white matter tracts such as the corpus callosum. Patients typically remain in a chronic vegetative state without significant recovery. Mortality is as high as 80%.
Axonal spheroids- when do they appear, how are they detected, where are they most common, how long do they last
Appear when coma exceeds 6hrs. Detectable with light microscopy after 24 hrs. Most common in corpus callosum and brainstem. Last days to weeks. Invisible on CT/MRI
primary vs secondary injury
primary: occurs at the moment of impact, and is largely irreversible injury. Secondary injury: inadequate resuscitation. Mechanisms include hypoxia, altered cerebral blood flow (dysautoregulation), and release of free radical mediators
How do free radials mediate CNS injury
free radical mediators break down the blood brain barrier and result in interstitial (vasogenic) edema. The combination of events results in brain swelling, elevated intracranial pressure (ICP), further hypoxia, dysautoregulation, and herniation
Monroe-Kellie doctrine
CSF volume + cerebral arterial blood volume + cerebral venous blood volume + brain volume + volume of intracranial mass lesion must equal constant volume ( volume of intracranial compartment). An increase in size of mass must be compensated by decrease in volume of another compartment, otherwise compression results.
What is the point of decompensation/critical point on volume pressure curve for brain
The volume of mass where even a small increase in compression results in a large increase in pressure.
Herniation syndromes
forcible displacement of brain tissue across the falx, tentorium, or foramen magnum due to elevated intracranial pressure and mass effect
Common characteristic of most herniation syndromes
progressive lethargy and poor responsiveness (obtundation) - hallmark of acute rise in intracranial pressure and should be recognized as an emergency. Manifest as abrubt changes
Subfalcine herniation
the cingulate gyrus is pushed away from the expanding mass and herniates beneath the falx cerebri. In the process, the anterior cerebral artery is often kinked, and a stroke in the distribution of this vessel is not uncommon
Central herniation
Occurs when there is downward pressure centrally, and can result in bilateral uncal herniation.
Transtentorial (Uncal) herniation
the uncus, a part of the medial temporal lobe, herniates across the tentorial edge, and downward into the posterior fossa. It compresses the midbrain and its ipsilateral cerebral peduncle, usually producing an ipsilateral third nerve palsy and a contralateral hemiparesis or hemiplegia.
Kernohans notch
Rarely, uncal herniation can compress the opposite cerebral peduncle against the tentorial edge, resulting in a hemiparesis that is ipsilateral to the mass lesion and herniated uncus.
Duret hemorrhage
Hemorrhage produced by uncal herniation which which produces devastating neurologic consequences, because of disruption of the ascending reticular activating system
Tonsillar herniation
cerebellar tonsils herniate downward into the foramen magnum, a process also referred to as “coning”. The medulla is compressed, and this can produce abnormal cardiac and respiratory responses, including Cushing’s reflex, which consists of bradycardia and hypertension in the setting of high intracranial pressure. Tonsillar herniation most commonly is encountered in the setting of a mass lesion in the posterior fossa.
Lumbar puncture in setting of intracranial mass lesion?
can precipitate a herniation syndrome, because of the differential pressures this creates between the cranial and spinal subarachnoid space
pathophysiology of traumatic brain injury
Spike in extracellular K,cytotoxic edema, Excitotoxicity, vasogenic edema, increased intracranial pressure causes ischemia
Describe excitotoxicity and vasogenic edema leading to TBI
Excitotoxicity: mechanical forces cause massive neuronal depolarization, with massive neurotransmitter release. Overactivation of NMDA and AMPA receptors by glutamate allows high levels of Ca to enter cell, activating phospholipases, endonucleases and proteases (calpain) which damage cell structures, then damage blood brain barrier. Vasogenic edema results from increased permeability
Describe extracellular K levels and cytotoxic edema leading to TBI
widespread simultaneous neuronal depolarization results in an immediate spike in extracellular K. This causes reversal of glutamate transporters on astrocytes and adds to glutamate toxicity. Also, influx of K into astrocyte causes cell to swell, causing cytotoxic edema and contributing to brain edema. Swelling of astrocyte foot processes causes increased capillary resistance and decreased cerebral blood flow.
Ischemia and TBI
The increased ICP from cytotoxic and vasogenic edema reduces the perfusion of the brain, and the resultant ischemia causes further failure of energy dependent ATPases, further depolarization of neurons (who depend on sodium potassium ATPases to maintain hyperpolarization)
Basic componenets of treatment of elevated intracranial pressure
Minimize ICP and maximize oxygen/metabolite delivery by manipulating the three intracranial compartments: 1) the intravascular space 2) the brain parenchyma, and 3) the cerebrospinal fluid space.
Steps for unconcious patient care
Endotracheal intubation > Controlled ventilation to pCO2 of 35mmHg then reduced to 25mmHg with resultant decrease in blood volume (vasoconstriction) and ICP > elvate head (prevent venous congestion) > IV osmotic diuretics (ie mannitol) reduce interstitial brain edema > ventricular cathether to drain hydrocephalus > drug induced coma w/ barbituates to decrease metabolism and scavenge free radicals
Glasgow coma scale components
- eye opening: spontaneous (4), to speech (3), to pain (2), none (1). 2. BEST motor response: Obeys commands (6), localizes pain (5), flexion (4), abnormal flexion (3), extension (2), none (1). 3. Verbal response: Oriented (5), confused (4), inappropriate words (3), incomprehensible sounds (2), none (1)
Risk of operable intracranial mass lesion in head injured patient using glasgow coma scale
15: 1 in 3615 risk. 9-14: 1 in 51 risk. 3-8: 1 in 7 risk.
Brainstem reflexes used to test location of TBI
Pupillar reflex (CN 2, 3, midbrain), corneal blink reflex (CN 5,7 pons), cold caloric testing “dolls eyes” (CN 8,6,3 pons to midbrain), gag reflex (CN9,10 medulla)
Outcomes 1 year after head injury using glasgow coma scale
Mild severity (GCS 13-15): most have good outcome. Moderate severity (GCS 9-12): Most (38%) have good outcome but 16% are dead/vegetative. Severe (GCS 3-8): most (38%) are dead or vegetative
ranges of ICP pressures
Normal: -3 - 15 mm Hg. Slight increase: 16 - 20, Moderate increase: 21 - 40. Severe increase:> 40
Cerebral perfusion pressure equation
CPP: MAP- ICP. Normal is around 70
Define concussion and its hallmarks
alteration in mental status caused by biomechanical forces which may or may not cause loss of consciousness. The hallmarks of concussion are confusion and amnesia
Common symptoms of concussion
headache, dizziness, poor attention, inability to concentrate, memory problems, fatigue, irritability, depressed mood, intolerance of bright light or loud noise, and sleep disturbance
Post concussive syndrome symptoms
persistent headache, lightheadedness, decreased attention and concentration, poor memory, easy fatigability, irritability, anxiety or depressed, sleep disturbance
signs of concussion
vacant stare, delayed response, inattention, disorientation, slurred or incoherent speech, incoordination, inapropriate emotionality, memory problems, loss of conciousness
definition of of mild loss of consiousness
less than 30 minutes
Pathophys of concussion
differ from that of severe TBI only in degree, and the regions of the brain affected tend to be confined to the junction of the grey and white matter immediately beneath the cortex where gradient echo MRI often detects shearing lesions of DAI
glasgow coma scale for concussions
Mild severity (GCS 13-15)
Which brain lobes are most affected during concussions
frontal and temporal
Which types of forces are more damaging
rotational (angular) are more damaging than translational (linear)
Which forces cause contrecoup contusions
linear (translational) forces will cause contusion on the side opposite of the original injury
Colorado Concussion grading scale
Grade 1 – Confusion without amnesia or LOC. Grade 2 – Confusion and amnesia. Grade 3 – LOC
Second Impact Syndrome
rare but usually fatal consequence of a second concussion while still suffering the effects of an earlier one. Loss of autoregulation of CNS vasculature, cerebral vessels become congested , ICP rises, cerebral perfusion decreases leading to ischemia and vasogenic edema
How long should someone with a concussion be observed closely following the incident?
24 hrs- It is not usually necessary to have the patient awakened multiple times during the night following an acute event unless there had been prolonged amnesia or unconsciousness
When is CT scan indicated for concussions
CT scanning for intracranial bleeding is indicated acutely for anyone with witnessed LOC.
Sleep disturbance and concussions
Sleep disturbance is very common a few days after a concussion and should be treated promptly to avoid the prolongation of symptoms
Recommended treatment for aches/pains from concussion
Acetaminophen should be offered for headaches and associated bodily pain, such as whiplash neck pain, and is considered safe in the acute phase of the injury.
