Head Trauma Flashcards
DefineTBI
Brain function impairment that results from external force
Classification of TBI
Based on
Severity
Mild-13-15
Moderate-9-12
Severe <8
Morphology
1.Skull fractures
A. Vault-Linear vs stellate
Depressed vs non depressed
B.Basilar-with or without csf leak
With or without 7 th N palsy
2.Intracranial lesions
A.Focal
EDH
SDH
INTRACEREBRAL
B.Diffuse
Concussion
Multiple Contusions
Hypoxic or Ischemic Injury
Axonal injuryWhat is Monro Kellie Doctrine?
Total volume of intracranial contents must remain constant,because the cranium is a rigid non expandable structure.
When normal intracranial volume is exceeded ICP rises.Venous blood and CSF can be pushed out of the container,providing a degree of pressure buffering.
Once limit of displacement reached ICP rises rapidly.
Define cerebral auto regulation
Cerebral auto regulation is a homeostatic process that regulates and maintains cerebral blood flow constant across a range of blood pressures.
Principle of cerebral auto regulation
CPP=MAP-ICP
In healthy adults limits are CPP of 50 to 150 mmHg
Or
MAP of 60 to 160 mmHg
This mechanism ensures that as as MAP or CAP increases ,resistance (vasoconstriction)increases in small cerebral arteries.
This process maintains constant CBF by decreasing cerebrovascular resistance when MAP OR CPP Ddecreases
Cushing reflex
HTN
Bradycardia
Respiratory irregularity
Normal values of ICP in different age group in mmHg
Adults-10-15
Children 3-7
Infants 1.5-6
Volume of different brain compartment in adult
Brain parenchyma-<1300 ml
CSF-100 to 150 ml
Intravascular blood 100 to 150ml
Mechanism of cerebral auto regulation
1.Myogenic-vascular smooth muscles constrict or dilatein response to trans mural pressure
2.Neurogenic-activation of alpha adrenoceptors shifts limits of auto regulation to higher pressure.
3.Metabolic-Changes in pCo2 and H+will cause vasodilation.
R.Endothelial-NO also contributes to auto regulation.
What is primary brain injury
Primary brain injury is caused at the time of impact and is a function of the energy transmitted to the brain by the offending agent
What is secondary brain injury.
Secondary brain injury results from disturbance of brain and systemic physiology by the traumatic event. It is defined as subsequent or progressive brain damage resulting from events developing as a result of primary brain injury Types are Intracranial hematoma Cerebral edema Ischemia Infection Epilepsy Metabolic/Endocrine
Secondary brain injury ( Tintinalli )
A wave of secondary damage is unleashed by the impact that results in a series of deleterious cellular and sub cellular events( secondary neurotoxic cascade)
Secondary neurotoxic cascade causes ongoing damage and poorer neurological outcome than the original mechanism.
Secondary insults
Conditions or circumstances that accelerate neurologic damage Hypotension Hypoxia Hyperglycaemia Hypocarbia Hypercarbia Hyperpyrexia
Brain edema
Extracellular edema-direct damage to or breakdown of the blood brain barrier,ionic shifts and alteration of water exchange mechanisms (aquaporins)
Cytotoxic edema -large ionic shifts and loss of cell membrane integrity from mitochondrial damage (loss of ATP;ion pump productivity and increased free radical production)
Herniation syndromes
Uncal transtentorial
Central transtentorial
Cerebellotonsillar
Upward transtentorial
Uncal transtentorial herniation
Mc clinically significant herniation.
Associated with expanding extraxial lesions in temporal lobe and lateral middle fossa
Uncus of temporal lobe is displaced inferiorly through the medial edge of tentorium.
Causes compression of parasympathetic fivers of 3rd N causing I/L fixed and dilated pupil due to unopposed sympathetic toneFurther herniation compresses the pyramidal tract causing C/L motor paralysis
In some cases pupillary changes are C/L and weakness I/L
Later progresses to direct brain stem compression ;alterations in LOC,respiratory pattern,hemodynamic iinstability ,cardiovascular collapse and death
B/l decerebrate posturing
Kernohans notch syndrome
False localising sign
Uncal herniation causing compression of C/L cerebral peduncle against tentorial hiatus causing I/L hemiplegia
Central transtentorial herniation
Less common
Occurs with midline lesions
Frontal lobe or occipital lobeor vertex
B/L pinpoint pupils,b/l babinskis signs and increased muscle tone are the signs
Fixed midpoint pupils follow along with prolonged hyperventilation and decorticate posturing.
Cerebellotonsillar herniation
Cerebellar tonsils herniate through the foremen magnum.
Due to cerebellAr mass or central vertex mass
Pinpoint pupils,flaccid paralysis and sudden death
Upward tonsillar herniation
Expanding posterior fossa lesion
Loc declines rapidly
Pinpoint pupils due to compression against pons
Downward gaze palsy with absent vertical movements
Motor GCS
Obeys command -+2
Localises pain -+1
Withdraws to pain or worse-o
Score <2 predict need for ED intubation
Decerebrate posturing
Arm extension and IR with finger flex ion and leg extension and IR
Guidelines for CT head in adults in minor tbi
New Orleans criteria
Canadian CT head rule
New Orleans criteria
Headache Vomiting Seizure Age>60 Intoxication Persistent antegrade amnesia Evidence of trauma above the clavicles
100% sensitive 5%specific for patients with ic lesion and needing neurosurgical intervention
Anyone positive finding needs CT
Canadian CT head rule
For GCS-13-15
GCS<15 at 2hr
Suspected open or depressed skull fracture
>1episode vomiting
Retrograde amnesia>30 min
Dangerous mechanism of fall (>3ft or >5stairs or pedestrian)
Any sign of basilar fracture
Age>=65 years
**Use of anticoagulant present in ATLS
LOC>5 minutes amnesia>30 Minal’s dangerous mechanism put in moderately high risk in ATLS
Ie%sensitive 38%specific for ic lesion
100% sensitive and 37%specific for needing intracranial intervention
PECARN( Pediatric emergency care applied research Network ) criteria for head CT
Age >2 year
GCS =14or other signs of AMS or signs of basilar skull fracture-CT to be done
If no—>h/o loc/vomiting/severe MOI or severe headache ——>CT recommended based on physician experience/parental anxiety/worsening symptoms/multiple or isolated findings
IF YES
Age<2 year
GCS=14 orAMS or palpable skull fracture CT to be done
If NO
occipital or parietal or temporal scalp hematoma/h/o Loc >5 s/severe MOI/or not acting normally as per parent
IF YES SAME AS ABOVEplus age <3 months,
If NO
CT NOT RECOMMENDED
DANGEROUS MOI MVI WITH EJECTION death of another passenger Struck by high impact object Fall >3 feet or >5 feet for age >2 year
Definition of mild traumatic brain injury /concussion
American congress of rehabilitation medicine
Mild tbi is defined in a patient with GCS 13-15 who has a traumatically induced physiological disruption of brain function which may manifest as
1.LOC<30min
2.Post traumatic amnesia(before or after )the event lasting <24 hrs
E.Any alteration in mental state at the time of the event EgFeeling dazed,confused following the event
4.Transient FND
Clinical features of base of skull fracture
Ear bleed Hemotympannum Otorrhoea Rhinorrhoea Battles sign Raccoons eye Cr nerve deficits Facial nerve palsy Decreased auditory acuity Tinnitus Giddiness Nystagmus
Rule out carotid artery and cervical spine injury
Diffuse axonal injury
Disruption of axonal fibers in the white matter and brainstem
Due to shearing force due to sudden deceleration injury
Seen in blunt trauma,shaken baby syndrome in infants
PATHOPHYSIOLOGY and CT findings of DAI
Cerebral edema can develop rapidly
CT may appear normal
Punctuate hemorrhagic injury along the grey white matter junction of cerebral cortex and brainstem
Define Concussion
Impairment of brain function without overt haemorrhage or other gross lesions and is caused by an external force and results in a GCS of 14 or 15
PATHOPHYSIOLOGY of concussion
mTBI represents a spectrum of pathophysiology
mTBI caused an ionic shift that leads to momentary disruption in function .
Symptom recovery is rapid and no obvious structural damage.
Severe forms may lead to long term or permanent structural damage.
Mild insults —->gene regulation——>fupregulation of ion channels along axons.
Increased ion channels—->makes brain vulnerable to overactivation.
Repeated exposure to trauma during this period greatly increases neuronal toxicity and cell death.
Large shifts in ion concentration may cause mitochondrial dysfunction and depletion of intracellular energy.
So neuronal dysfunction persists until recovery.
Metabolic insults,electrochemical imbalances(Ca influx and Na and K shifts ) also damage axonal transport system
Structural abnormalities are not identified on CT but microscopic evidence of injury present on HPE
Imaging modality that can demonstrate the damage in concussion
Diffusion tensor imaging
Second impact syndrome
When a second concussion occurs prior to recovery from first ;rapid onset of cerebral edema and death can occur,particularly in athletes prematurely returning to play
Diagnosis of concussion
Signs and symptoms
OftenNormal physical examination
CT normal
Any blunt force mechanism and/or whiplash type acceleration deceleration event.
Did the event cause any neurologic alteration like dazed,confused,LOC.
Evaluation includes five components
- Event history and immediate post event symtoms
- Mechanism
- key comorbidities(concussion,migraine/,headache,depression history;bleeding disorders or anticoagulant
- Current symptom checklist-using Sports concussion assesssment tool or the post Concussion symptom index
- Concussion specific neurologic exam
What is focused mTBI exam.
Alertness-measured by GCS,a patient with GCS <15 will not be able to cooperate with the rest of the exam and requires ruling out IC pathology.
- Cognitive exam-short term memory,encoding or working memory -eg-100-7 more than 4 errors abnormal
- Evaluate Cspine in all patients..prior to ambulation or movement.Do CT Cspine if needed
4.Vestibulo oculomotor system is highly complex and requires sensory integration among multiple neuronal pathways. Examination includes
1.Near point convergence
2.Near point accommodation.
ESmooth pursuit
R.Saccades
T.Vestibulooccular reflex
5.Rhombergs text and gait to assess balance
Io rakers for mTBI
Glial fibrillaryacid protein(GFAP)
Ubiquitous C terminal hydrolyse L 1(UCH-L1)
FDA approved for need for CT in GCS 9 to 15
S100B not presently approved
Diagnosis
CT -N
Portable EEG
Treatment of mTBI
Treatable disease
Primary intervention is resting the brain
Return to Activity in mTBI
Decisions are based on symptoms and graded evaluation programs
Assessment incorporates serial symptom checklists,neuropsychological tests(memory and reaction time assessment) and balance evaluation
Because this evaluation not practical in the ED Emergency physicians should not provide definite return to activity directions
What is post concussive syndrome?
Physical emotional and cognitive symptoms in the days or weeks after mTBI About 15% have symptoms at 1 year also. MC symptoms are Headache Dizziness Decreased concentration Memory problems Sleep problems Irritability Fatigue Visual disturbances Judgement problems Depression and anxiety When a cluster of symptoms become chronic they are called persistent post concussive or post concussion syndromes Neurophysiological testing and use of symptom checklist are the cornerstone of management. Treatment symptomatic Refer patient to neuropsychologist or mTBI clinic
Chronic traumatic encephalopathy
Early onset of memory loss and depression
Concern in athletes who compete in collision sports
Pathologically large amount of tau protein deposition seen in the brain
Definition of mild traumatic brain injury /concussion
American congress of rehabilitation medicine
Mild tbi is defined in a patient with GCS 13-15 who has a traumatically induced physiological disruption of brain function which may manifest as
1.LOC<30min
2.Post traumatic amnesia(before or after )the event lasting <24 hrs
E.Any alteration in mental state at the time of the event EgFeeling dazed,confused following the event
4.Transient FND
Clinical features of base of skull fracture
Ear bleed Hemotympannum Otorrhoea Rhinorrhoea Battles sign Raccoons eye Cr nerve deficits Facial nerve palsy Decreased auditory acuity Tinnitus Giddiness Nystagmus
Rule out carotid artery and cervical spine injury
Diffuse axonal injury
Disruption of axonal fibers in the white matter and brainstem
Due to shearing force due to sudden deceleration injury
Seen in blunt trauma,shaken baby syndrome in infants
PATHOPHYSIOLOGY and CT findings of DAI
Cerebral edema can develop rapidly
CT may appear normal
Punctuate hemorrhagic injury along the grey white matter junction of cerebral cortex and brainstem
Define Concussion
Impairment of brain function without overt haemorrhage or other gross lesions and is caused by an external force and results in a GCS of 14 or 15
PATHOPHYSIOLOGY of concussion
mTBI represents a spectrum of pathophysiology
mTBI caused an ionic shift that leads to momentary disruption in function .
Symptom recovery is rapid and no obvious structural damage.
Severe forms may lead to long term or permanent structural damage.
Mild insults —->gene regulation——>fupregulation of ion channels along axons.
Increased ion channels—->makes brain vulnerable to overactivation.
Repeated exposure to trauma during this period greatly increases neuronal toxicity and cell death.
Large shifts in ion concentration may cause mitochondrial dysfunction and depletion of intracellular energy.
So neuronal dysfunction persists until recovery.
Metabolic insults,electrochemical imbalances(Ca influx and Na and K shifts ) also damage axonal transport system
Structural abnormalities are not identified on CT but microscopic evidence of injury present on HPE
Imaging modality that can demonstrate the damage in concussion
Diffusion tensor imaging
Second impact syndrome
When a second concussion occurs prior to recovery from first ;rapid onset of cerebral edema and death can occur,particularly in athletes prematurely returning to play
Diagnosis of concussion
Signs and symptoms
OftenNormal physical examination
CT normal
Any blunt force mechanism and/or whiplash type acceleration deceleration event.
Did the event cause any neurologic alteration like dazed,confused,LOC.
Evaluation includes five components
- Event history and immediate post event symtoms
- Mechanism
- key comorbidities(concussion,migraine/,headache,depression history;bleeding disorders or anticoagulant
- Current symptom checklist-using Sports concussion assesssment tool or the post Concussion symptom index
- Concussion specific neurologic exam
What is focused mTBI exam.
Alertness-measured by GCS,a patient with GCS <15 will not be able to cooperate with the rest of the exam and requires ruling out IC pathology.
- Cognitive exam-short term memory,encoding or working memory -eg-100-7 more than 4 errors abnormal
- Evaluate Cspine in all patients..prior to ambulation or movement.Do CT Cspine if needed
4.Vestibulo oculomotor system is highly complex and requires sensory integration among multiple neuronal pathways. Examination includes
1.Near point convergence
2.Near point accommodation.
ESmooth pursuit
R.Saccades
T.Vestibulooccular reflex
5.Rhombergs text and gait to assess balance
Io rakers for mTBI
Glial fibrillaryacid protein(GFAP)
Ubiquitous C terminal hydrolyse L 1(UCH-L1)
FDA approved for need for CT in GCS 9 to 15
S100B not presently approved
Diagnosis
CT -N
Portable EEG
Treatment of mTBI
Treatable disease
Primary intervention is resting the brain
Return to Activity in mTBI
Decisions are based on symptoms and graded evaluation programs
Assessment incorporates serial symptom checklists,neuropsychological tests(memory and reaction time assessment) and balance evaluation
Because this evaluation not practical in the ED Emergency physicians should not provide definite return to activity directions
What is post concussive syndrome?
Physical emotional and cognitive symptoms in the days or weeks after mTBI About 15% have symptoms at 1 year also. MC symptoms are Headache Dizziness Decreased concentration Memory problems Sleep problems Irritability Fatigue Visual disturbances Judgement problems Depression and anxiety When a cluster of symptoms become chronic they are called persistent post concussive or post concussion syndromes Neurophysiological testing and use of symptom checklist are the cornerstone of management. Treatment symptomatic Refer patient to neuropsychologist or mTBI clinic
Chronic traumatic encephalopathy
Early onset of memory loss and depression
Concern in athletes who compete in collision sports
Pathologically large amount of tau protein deposition seen in the brain
