Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Atls > Head Trauma > Flashcards

Head Trauma Flashcards

1
Q

DefineTBI

A

Brain function impairment that results from external force

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Classification of TBI

A 
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 injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is Monro Kellie Doctrine?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Define cerebral auto regulation

A

Cerebral auto regulation is a homeostatic process that regulates and maintains cerebral blood flow constant across a range of blood pressures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Principle of cerebral auto regulation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Cushing reflex

A

HTN
Bradycardia
Respiratory irregularity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Normal values of ICP in different age group in mmHg

A

Adults-10-15
Children 3-7
Infants 1.5-6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Volume of different brain compartment in adult

A

Brain parenchyma-<1300 ml
CSF-100 to 150 ml
Intravascular blood 100 to 150ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Mechanism of cerebral auto regulation

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is primary brain injury

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is secondary brain injury.

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Secondary brain injury ( Tintinalli )

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Secondary insults

A 
Conditions or circumstances that accelerate neurologic damage
Hypotension
Hypoxia
Hyperglycaemia
Hypocarbia 
Hypercarbia 
Hyperpyrexia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Brain edema

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Herniation syndromes

A

Uncal transtentorial
Central transtentorial
Cerebellotonsillar
Upward transtentorial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Uncal transtentorial herniation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Kernohans notch syndrome

A

False localising sign

Uncal herniation causing compression of C/L cerebral peduncle against tentorial hiatus causing I/L hemiplegia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Central transtentorial herniation

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Cerebellotonsillar herniation

A

Cerebellar tonsils herniate through the foremen magnum.
Due to cerebellAr mass or central vertex mass
Pinpoint pupils,flaccid paralysis and sudden death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Upward tonsillar herniation

A

Expanding posterior fossa lesion
Loc declines rapidly
Pinpoint pupils due to compression against pons
Downward gaze palsy with absent vertical movements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Motor GCS

A

Obeys command -+2
Localises pain -+1
Withdraws to pain or worse-o
Score <2 predict need for ED intubation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Decerebrate posturing

A

Arm extension and IR with finger flex ion and leg extension and IR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Guidelines for CT head in adults in minor tbi

A

New Orleans criteria

Canadian CT head rule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

New Orleans criteria

A 
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

25
Q

Canadian CT head rule

A

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

26
Q

PECARN( Pediatric emergency care applied research Network ) criteria for head CT

A

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
27
Q

Definition of mild traumatic brain injury /concussion

A

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

28
Q

Clinical features of base of skull fracture

A 
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

29
Q

Diffuse axonal injury

A

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

30
Q

PATHOPHYSIOLOGY and CT findings of DAI

A

Cerebral edema can develop rapidly
CT may appear normal
Punctuate hemorrhagic injury along the grey white matter junction of cerebral cortex and brainstem

31
Q

Define Concussion

A

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

32
Q

PATHOPHYSIOLOGY of concussion

A

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

33
Q

Imaging modality that can demonstrate the damage in concussion

A

Diffusion tensor imaging

34
Q

Second impact syndrome

A

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

35
Q

Diagnosis of concussion

A

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

  1. Event history and immediate post event symtoms
  2. Mechanism
  3. key comorbidities(concussion,migraine/,headache,depression history;bleeding disorders or anticoagulant
  4. Current symptom checklist-using Sports concussion assesssment tool or the post Concussion symptom index
  5. Concussion specific neurologic exam
36
Q

What is focused mTBI exam.

A

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.

  1. Cognitive exam-short term memory,encoding or working memory -eg-100-7 more than 4 errors abnormal
  2. 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

37
Q

Io rakers for mTBI

A

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

38
Q

Diagnosis

A

CT -N

Portable EEG

39
Q

Treatment of mTBI

A

Treatable disease

Primary intervention is resting the brain

40
Q

Return to Activity in mTBI

A

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

41
Q

What is post concussive syndrome?

A 
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
42
Q

Chronic traumatic encephalopathy

A

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

43
Q

Definition of mild traumatic brain injury /concussion

A

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

44
Q

Clinical features of base of skull fracture

A 
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

45
Q

Diffuse axonal injury

A

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

46
Q

PATHOPHYSIOLOGY and CT findings of DAI

A

Cerebral edema can develop rapidly
CT may appear normal
Punctuate hemorrhagic injury along the grey white matter junction of cerebral cortex and brainstem

47
Q

Define Concussion

A

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

48
Q

PATHOPHYSIOLOGY of concussion

A

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

49
Q

Imaging modality that can demonstrate the damage in concussion

A

Diffusion tensor imaging

50
Q

Second impact syndrome

A

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

51
Q

Diagnosis of concussion

A

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

  1. Event history and immediate post event symtoms
  2. Mechanism
  3. key comorbidities(concussion,migraine/,headache,depression history;bleeding disorders or anticoagulant
  4. Current symptom checklist-using Sports concussion assesssment tool or the post Concussion symptom index
  5. Concussion specific neurologic exam
52
Q

What is focused mTBI exam.

A

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.

  1. Cognitive exam-short term memory,encoding or working memory -eg-100-7 more than 4 errors abnormal
  2. 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

53
Q

Io rakers for mTBI

A

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

54
Q

Diagnosis

A

CT -N

Portable EEG

55
Q

Treatment of mTBI

A

Treatable disease

Primary intervention is resting the brain

56
Q

Return to Activity in mTBI

A

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

57
Q

What is post concussive syndrome?

A 
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
58
Q

Chronic traumatic encephalopathy

A

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

Atls (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions