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Rosens > 33. Head Trauma > Flashcards

33. Head Trauma Flashcards

1
Q

MC mechanisms of head trauma

A

falls
struck by or against and object
MVC

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2
Q

Head trauma defn

A

broad cateogry ext trauma to craniofacial area from blunt, penetrating, blast, rotational or accel-decel forces

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3
Q

Head injury defn

A

clinically evident injury on PE or presence of ecchymosis, laceration or deformities

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4
Q

Traumatic brain injury

A

injury to brain itself

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5
Q

Mild TBI definition

A

GCS 13-15 within 30min of injury pr preesentation to ED with trauma induced physiologic disruption of brain function manifested by:
1) any period of LOC <30min or decr LOC
2) any memory loss for events pre or post accident
3) alteration of any kind at time of accident
4) neuro deifcit that may or may not be transient

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6
Q

Scalp five tissue layers

A

dermis - thickest
subcut tissue - blood supply, hair follicles
galea - m for wrinkling forehead
Loose areolar tissue
Deepest - pericranium

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7
Q

skull bones

A

frontal
ethmoid
spheoid
occipital
2 parietal
2 temporal

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8
Q

How do contrecoup brain injuries work?

A

may occur on the opposite side of the head impact (coup) as the brain shifts to the uninjured side and strikes against uneven bone surfaces.

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9
Q

What. is the tentorium cerebelli?

A

partitions cerebellum and brainstem from cerebral hemispheres

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10
Q

Brain 3 layers

A

dura
arachnoid
pia

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11
Q

CSF production by?

A

choroid plexus in lateral ventricles primarily

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12
Q

Normal pressure by CSF?

A

65-195mm water or 6-15mmHg

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13
Q

What is the blood brain barrier’s job?

A

maintain microenvironment of brain tissue and CSF

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14
Q

When intact, what does BBB do for neuroactive drugs?

A

to penetrate the brain tissue usually depends on their lipid solubility.

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15
Q

How does TBI disrupt BBB?

A

biome- chanics of a brain injury or posttraumatic cerebral edema can cause a disruption of the BBB for up to several hours after the insult. In severe TBI, prolonged disruption of the BBB further contributes to the development of posttraumatic vasogenic cerebral edema and higher maximum intracranial pressure (ICP

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16
Q

Brain % of o2 consuption of entire body? CO %?

A

20
15

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17
Q

What BP, pH and co2 promote cerebral vasoconstriction related to cerebral brain flow?

A

hypertension
alkalosis
hypocarbia

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18
Q

What BP, pH and co2 promote cerebral vasoDILATION related to cerebral brain flow?

A

hypotension
acidosis
hypercarbia

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19
Q

Cerebral vasoactivity very sn to changes in pp of c02 and o2. Change in pco2 between 20-60mmhg decreases diameter of vessel by ?%

How does this help in concern for ICP?

A

2-3%

why hyperventilation should theoretically work

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20
Q

What is cerebral perfusion pressure?

A

gradient of pressure across the brain

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21
Q

CPP equation: ___ - __

A

MAP - ICP

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22
Q

Cerebral blood flow is relaitvley constant when CPP is __ - __mhg “ie auteoregulation”

A

50-160 (MAP)

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23
Q

If CPP falls below ?mmHg, autoregulation is lost and cerebralblood flow can decline to result in tissue ischemia nd altered cerebral metabolism

Ie why we need to avoid hypoperfusion in brain injury

A

40

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24
Q

Target CPP for brain injury pt

A

60-70

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25
Q

ICP > _ mmHg

A

15

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26
Q

If ICP increases to point where CPP is compromised,then ? occurs and autoregulation becomes dep on ?

A

vasoparalysis

imapired –> MAP

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27
Q

What ICP certainly needs intervention?

A

> 22

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28
Q

Simple techniques to reduce ICP

A

head neutral
HOB >30

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29
Q

Cushing rflex defn

A

hypertension
bradycardia
irreg resp effort

ICP is life thr level

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30
Q

How can incr ICP effect mental status?

A

needs cerebral cortices and intact reticular activating system of brainstem

incr icp can compress brainstem

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31
Q

Severe TBI defn based on GCS

A

</=8 post resus

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32
Q

Mild TBI defn based on GCS

A

13-15

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32
Q

Moderate TBI defn based on GCS

A

gcs 9-12

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33
Q

What factors contribute to degree of brain injury following mTBI?

A

primary mech
magnitude of injury
secondary insults
pt genetic, molecular response

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34
Q

Primary damage in mTBI caused by?

A

initial impact or force that although not as evi- dent as severe TBI, may lead to smaller contusions, hematomas, axonal damage, and microvascular injury

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35
Q

Repeated mTBI can lead to CTE - what is this?

A

chronic traumatic encephalopathy - term used to describe clinical changes in cognition, mood, personality, behavior, or movement occurring years following concussi

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36
Q

Direct injury to head - what factors are included in resulting damage overall?

A

consistency
mass
surface area
velocity of object strike

vs brain itself: vasoelastic properties of the underlying region of brain tissue, duration of the force applied, magnitude of the force reaching the brain tissue, and surface area of the brain that is affected

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37
Q

Indirect brin injury: ex accel-decl injury which can cause which vessels to shear?

A

subdural heamtoma (bridging vessels)

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38
Q

Name 5 secondary insults causing brain injury?

A

decr o2, E to brain tissue
cascade cytotoci events, mediated by molecular/cellular proceeses:
events include activa- tion of inflammatory responses, imbalances of ion concentrations (e.g., potassium, calcium), an increase in the presence of excitatory amino acids (e.g., glutamate), dysregulation of neurotransmitter synthesis and release, imbalance in mitochondrial functions and energy metabolism, and production of free radicals

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39
Q

Factors of penetrating trauma that lead to more morbidity/mortality

A

high velocity
Projectiles crossing midline and resting in posterior fossa
Large missiles that fragment
Incr Age
Sui attempt
low GCS
Bilateral mydriasis
dural penetration
bihemispheric and multi lobar injury

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40
Q

Wounding capacity of a forearm related to what two aspects?

A

kinetic energy of missile on impact
how much E is dissipated

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41
Q

What are features of clinically significant skull fractures?

A
  1. intracranial air
  2. association with overlying scalp lac (ie open)
  3. depression below level of skull’s inner table
  4. location over major dural venous sinus or middle meningeal artery
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42
Q

Defn of a linear skull fracture

A

single fracture through entire skull thickness

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43
Q

When are linear skull fractures clinically important?

A

cross middle meningeal groove or major venous dural sinuses as can form EDH

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44
Q

Sutural diastasis: what two are often involved in adults?

A

coronal
lambdoid

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45
Q

Where do most depressed skull fractures occur over? (2)

A

parietal
temporal regions

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46
Q

Why are depressed skull fractures clinically important?

A

predispose to sign trauma and complications - infection, seizure

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47
Q

Basilar skull fracture defn

A

linear fractures at base of skull usually occurring through temporal bone

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48
Q

Basilar skull fracture - high risk for what kind of hematoma?

A

extra axial due to proximity to middle cerebral artery

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49
Q

How does a dural tear from a basilar skull fracture present?

A

basilar skull ffracture then communicates with sa space, paranasal sinuses and middle ear so that there is now a route for potential infection

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50
Q

Extra axial vs intra axial IC injury defn

A

extra - in the skull but outside the brain tissue (SAH, SDH, EDH, subdural hygroma)
vs
intra: bleeding within brain itself (TAI, cerebral and cerebellar contusions, cerebral and cerebellar hematomas)

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51
Q

Epidural hematoma cause and where most often?

A

middle meningeal a or vein or dural sinus
temporoparietal region

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52
Q

Subdural hematoma - injury type RF

A

accel-decel injury

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53
Q

Why do SDH tend to occur in pt with brain atrophy?

A

bridfinf veins traverse greater distances and are more likely to rupture with movement of head

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54
Q

Prognosis of SDH - factors

A

degree of brain injury caused by pressure of expanding hematoma on underlying tissue or other IC injuries

GCS 8 or less

ACute herniation syndrome on ED presentation (also bad)

Posterior fossa - bad

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55
Q

Traumatic SAH

A

blood in csf and meningieal intima probably from tear of small subarachnoid vessels

with normal gcs typically no intervention

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56
Q

What is a subdural hygroma?

A

collection of clear, xanthochromic blood tingued fluid in the dural space maybe from tear arachnoid or effusion from injured vessel

typically secondary to trauma

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57
Q

Diffuse axonal injury - diffuse or multifocal in actuality

A

multif

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58
Q

Diffuse axonal injury - preferred term in nontraumatic causes of axial injury? mild vs severe

A

traumatic axonal injury vs diffuse

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59
Q

Diffuse axonal injury - defn

A

prolonged traumatic coma not caused by mass lesion or ischemic insult

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60
Q

How does traumatic axonal injury (TAI) occur?

A

primary insult: torn or stretched so they ball up and screw up sending messages

then secondarily it disrupts the extracellular matrix and influx of inflammatory mediators leads to axonal swelling and axon death (uncoupling of cerebral blood flow, metabolism, apoptosis)

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61
Q

Clinical grading of TAI: I-3

A

(1) grade I (mild)—coma for 6 to 24 hours; (2) grade II (moderate)—coma for longer than 24 hours but not decerebrate; (3) grade III (severe)— coma for longer than 24 hours and decerebrate or flaccid.

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62
Q

Cerebral contusions: layman’s term?

A

bruising on brain tissue - petechail

63
Q

MC Cerebral contusion sites

A

poles and inferior surfaces of frontal and temporal lobes as brain hits bone protuberances here

64
Q

What type of mechanism can cause intracerebral hematomas?

A

shearing/tensile forces that mechanically stretch and tear deep small caliber arterioles at brain

65
Q

What type of mechanism may cause the rare primary traumatic intracerebellar hematoma?

A

direct blow to occiput

66
Q

Primary brain injury - goals of care?

A

fix the issue that caused the injury

67
Q

Secondary brain injury causes:

A

alteration in cell function and propogation of signals:
1. depolarization
2. excitotoxicity
3. BBB disruption
4. ischemic injury
5. edema formation
6. IC hypertension

68
Q

What 4 vital sign abnormalities have been shown to worsen outcomes after TBI? (at least in the paragraph of secondary systemic insults)

A

Hypotension
Hypoxia
Anemia
Hyperpyrexia

69
Q

Why is hypotension bad after TBI?

A

reduces cerebral perfusion so potentiates ischemia and infarction

70
Q

How does hypoxia occur after tbi?

A

po2 <60 due to transient or prolonged apnea by brainstem or injury post vs airway obstruction vs injury preventing normal resps
pulmonary injury reducing effective oxygenation
ineffective airway management

71
Q

What is one of the most potent drivers of cerebral blood flow?

A

paco2

72
Q

Hypocarbia on blood vessels

A

vasodilation

73
Q

Hypercarbia on tbi - what happens to the brain?

A

incr cerebral edema and icp

74
Q

Hypocarbia after tbi - what happens to the brain?

A

reduced cerebral blood flow
transient decr in ICP

75
Q

Why is anemia bad after TBI?

A

reducing o2 carrying capacity of blood

76
Q

Why is hyperpyrexia bad after TBI?

A

core temp >38.5
worse outcomes incr metabolism to injured areas –> resultant incr in ICP

77
Q

What is uncal herniation?

A

transtentorial hernation where CN3 is compressed, then get ipsilateral oculomo nerve then pupil dilatation and nonreactivity, contralateral hemiparesis

78
Q

What is Kernohan notch syndrome in uncal hernation?

A

contralat cerebral peduncle in some small number of TBI pt is forced against opp tentorial hiatus - hemiparesis is then ipsilateral to CN3 findings

79
Q

where does uncal herniation occur?

A

lateral middle fossa or temporal lobe

80
Q

Central trans tentorial herniation: where does this occur?

A

Expanding lesion at the vertex or frontal or occipital pole of the brain

81
Q

Central trans tentorial herniation: how does clinical deterioration occur?

A

Bilateral central pressure exerted on the brain from above: can see a settle, change and mental status or decreased LOC, bilateral motor weakness and pinpoint pupils
As herniation progresses, both pupils become midpoint and lose light responsiveness
Sustained hyperventilation may occur, can also see yawning, size progressing to sustained high respirate, then a regular breaths before respiration arrest
Decorticate positioning by noxious stimuli

82
Q

Cerebellotonsillar herniation: what is this?

A

Cerebellar tonsils, herniate downward through the foramen Magnum, which displaces the entire brainstem

83
Q

Cerebellotonsillar herniation: clinical findings

A

Wrapped in sudden, respiratory and cardiovascular collapses the medulla is compressed.
Pinpoint pupils.
Flaccid quadriplegia is the most common motor presentation

84
Q

Upward transtentorial herniation: what can this occur due to i.e. where is the lesion?

A

Expanding posterior fossa lesion

85
Q

Upward transtentorial herniation: what will you see on exam?

A

Might have pinpoint pupils due to compression of the ponds, downward, conjugate gaze is accompanied by the absence of vertical eye movements

86
Q

Name four types of brain herniation

A

Uncal
Central transtentorial
Cerebellotonsillar
Upward transtentorial

87
Q

Main history, questions for concern in moderate severe traumatic brain injury

A

Event or mechanism
Circumstances,
Concomitant, drug and alcohol.
Symptoms prior
Past medical history.
Any anticoagulant medication’s?

88
Q

What are the key components of a efficient Neuro exam for emergency medicine?

A

Mental status
GCS
Pupillary and responsiveness.
Motor strength and symmetry

89
Q

List eight characteristics of a Basilar skull fracture

A

Blood and air canal, hemotympanum, rhinorrhea, ottorhea, battle, sign, retro, articular, hematoma, raccoon sign, Peri orbital, ecchymosis, cranial nerve deficits, facial paralysis, decreased, auditory, acuity, dizziness, tinnitus, nystagmus

90
Q

Name the Glasgow coma scale for eyes

A

Four – spontaneous opening, three – to verbal command 2–2 pain one – no eye-opening

91
Q

Name the Glasgow coma scale components for verbal stimuli

A

Five – oriented and converses, four – disoriented and converses, three – inappropriate words, two – incomprehensible, one – no verbal

92
Q

Name the motor response for Glasgow coma scale

A

Six – obeys verbal commands, five – local lies to pain, four – flexion withdrawal, three – abnormal flexion, 2– extension, one – none

93
Q

Strongest predictor of outcome, following moderate and severe TBI

A

Advanced age
Pupillary reactivity.
GCS motors score
External injuries.
CT characteristics, including midline shift and subarachnoid, bleed, hypotension, hypoxia

94
Q

What does abnormal flexion or decorticate posturing imply in terms of where the injury is?

A

Above the midbrain and present as abnormal flexion of the upper extremity and extension of the lower extremity

95
Q

What does decerebrate or abnormal extension tell you about the level of injury?

A

More coddle injury, i.e. below the midbrain

96
Q

What three things in the acute setting assess brain, stem function?

A

Resp pattern
Pupillary size
Eye movements – oculocephalic response and ocular vestibular response using cold water

97
Q

Classic presentation of an epidural haematoma

A

Decreased LOC and then a lucid interval

98
Q

What is the definition of a chronic subdural hematoma?

A

Greater than two weeks

99
Q

What is important in determining consciousness immediately following TBI – i.e. imaging finding

A

Distribution rather than overall extent of axonal pathology

100
Q

What signs and altered LOC point you more towards an intracranial injury

A

Worsening headache.
Focal neural deficit
Confusion,
Lethargy

101
Q

What is the Rotterdam score?

A

Initial non-contrast computed tomography for predicting six month mortality following TBI

102
Q

List the criteria of the Rotterdam score of initial non-contrast CT for predicting six month mortality following TBI

A

One. Basil cistern easement: zero equals none, one partially faced, two completely faced.
Two. Midline shift: zero equals no shift or greater than equal to 5 mm, one equals greater than 5 mm.
Three. Epidural hematoma: zero if ED is present versus one if no ADH.
Four. IVH or SH: zero if neither present, one if either present.

Travel score out of six points from less than equal to one 0% versus six less than equal to 61%

103
Q

What is pneumocephalus?

A

Free air in the brain, if in the setting of TBI should look for an open fracture

104
Q

What is pneumocephalus?

A

Free air in the brain, if in the setting of TBI should look for an open fracture

105
Q

EDH on CT scan

A

Hyperdense, by convex, avoid lenticular. Does not extend beyond the dural attachments of the suture lines.

106
Q

SDH shape on CT scan

A

Follows the contour of the tentorium can be hyper or hypodense

107
Q

What does cerebral oedema look like on a CT scan?

A

Bilateral compression of the ventricles, loss of definition of the cortical sulky or effacement of basal cisterns

108
Q

Emergency department management of acute head injury

A

ATLS: airway, breathing, circulation, disability, if before airway, if possible to get a GCS, exposure
Prevent hypotension and hypoxia
Osmolar therapy if concerned for increased ICP: 3% sodium chloride given 250 ML

109
Q

Peros Enns, what is to Osmo therapies you can use for increased intracranial pressure

A

One. Mandal 0.25 to 1 g per KGQ6H up to a serum osmolarity of 320 Milli Omos per KG.
Two. Hypertonic saline 23.4%, 30–60 ML can be given Q6H up to a maximum serum sodium of 160.

110
Q

Why does mannitol work for increased intracranial pressure?

A

Produces an osmotic gradient that reduces brain volume and provides increased space for an expanding haematoma or brain swelling. This peaks about 60 minutes after bolus administration and lasts 6 to 8 hours.

111
Q

What are the benefits of hypertonic saline in increased ICP?

A

Reducing secondary injury through cellular, modulation, decreasing cerebral edema, improving peripheral perfusion, decreasing ICP through vasa, regulatory mechanisms and regulation of pro-inflammatory and prothrombotic mediators

112
Q

Risks of giving mannitol

A

Renal failure, hypotension, can increase bleeding into traumatic lesions by decompressing tampon effect of a haematoma

113
Q

Adverse events associated with hypertonic saline

A

Renal failure, central Pontine, Mylin, lysis, rebound ICP elevation

114
Q

Of note: hyperventilation also reduces cerebral blood flow, which is why it works for reducing ICP, and the brain needs this to meet it’s demands. So don’t really do it.

A
115
Q

What are the neurologic effects of hypocapnia in a TBI patient?

A

Low carbon dioxide leads to increased neuronal, excitability, and basic construction
This can lead to cerebral spinal fluid alkalosis, which further leads to vasoconstriction of vessels (overall decreasing cerebral blood flow and blood volume)
There is a risk of increased amino acid release given low carbon dioxide

Alkalosis of the CSF leads to time buffering and a normal pH with normalization of partial pressure of arterial carbon dioxide, which lead to vasodilation and reperfusion injury

116
Q

What is a decompressive craniectomy

A

Surgical removal of partial of the skull bone for relieving ICP

117
Q

Patients with signs of head trauma, taking warfarin – how to reverse?

A

IV vitamin K, fresh frozen plasma or PCC ( this is preferred over FFP) for a target INR less than 1.5

118
Q

Patients with signs of head trauma, taking more friend – how to reverse?

A

IV vitamin K, fresh frozen plasma or PCC ( this is preferred over FFP) for a target INR less than 1.5

119
Q

Patient with head trauma on dabigatran - recommendations for reversal?

A

Idracuzimab 5g given as 2.5g in infusion over 5-10 mins

120
Q

If your patient lived in the states, and was on a factor 10, a inhibitor, what medication could you give them if they had had trauma?

A

Adnexanet alpha

121
Q

What is the definition of early versus late post traumatic seizures

A

Before seven days versus after of injury

122
Q

Went to start Keppra for early post traumatic seizure?

A

Per Rosens, when the overall benefit is thought to outweigh the risk

123
Q

If there is penetrating, craniocerebral trauma, what antibiotic should you use?

A

Vancomycin 1 g Q 12 H, gentamycin 80 mg Q8H, metronidazole 500 mg Q6H

124
Q

Scalp wound management in the emergency department

A
  1. Haemostasis with direct pressure or stapler.
  2. Prompt irrigation. With removal of any debris from the site.
  3. Hair can delay healing, so make sure it’s not in there.
  4. Large lacerations of the Galia can be repaired with interrupted or vertical mattress sutures of 30 nylon or poly propylene or opposition technique foreclosure
  5. Typically don’t really need antibiotics.
125
Q

Do patients with the linear skull fracture need anything specific for treatment?

A

No, unless they have sides of underlying injury on the CT scan. Simply watch them for 4 to 6 hours.

126
Q

When can patients with the depressed skull fractured not be treated operatively?

A

No clinical or radiographic evidence of dural penetration, significant intracranial, hematoma, depression, greater than 1 cm, front of sinus involvement, gross cosmetic, deformity, wound infection, pneumocephalus, or gross wound contamination

127
Q

When should you give prophylactic antibiotics in a basal skull fracture with a CSF leak?

A

If the leak persists greater than seven days
Treat with Vanco, gentamycin, metronidazole

128
Q

What are urgent indications for EDH evacuation by surgery?

A

EDH larger than 30 cm³ regardless of GCS, as well as comatose patients with an acute EDH and anisocoria on pupillary exam

Per patient who are awake: if they have vocal Neuro deficits, haematoma greater than 30 cm³, thickness of a clot greater than 15 mm, degree of midline shift greater than 5 mm

129
Q

What are surgical indications for surgical evacuation of an acute SDH?

A

STH with thickness more than 10 mm or a midline shift of more than 5 mm on a CT scan regardless of the patient’s GCS score, worsening GCS score greater than equal to two points from the time of injury to hospital admission in a comatose patient, asymmetric or fixed or dilated pupil, persistent elevation of ICP

130
Q

What is the most serious complication of a traumatic subarachnoid hemorrhage?

A

Cerebral Vasos spasm

131
Q

With cerebral contusions, what patients are at high risk for haemorrhagic progression and need for delayed surgical decompression?

A

Lower GCS score, larger, cerebral contusion

132
Q

When my patients with an intracity haematoma needs surgery?

A

Emergent intervention or surgery for ICP lowering
If they are unconscious, mortality approaches 45% versus if they are conscious, it is lower
Bleeding into the ventricles or cerebellum carries a high mortality rate

133
Q

Intracerebellar haematoma – what is indicated?

A

Emergent neurosurgical consultation

134
Q

What are risk factors for an early post-traumatic seizure?

A

GCS score of 10 or lower, immediate seizure, post traumatic amnesia, lasting longer than 30 minutes, linear, or depressed, skull fracture, penetrating head injury, SDH, ADH, ICH, cortical contusion, age 65 years or younger, chronic alcoholism

135
Q

What are the risk factors for post traumatic epilepsy?

A

Severe TBI, early post traumatic seizure prior to discharge, acute ICH or cortical contusion, post traumatic amnesia, lasting longer than 24 hours, age older than 65 years and pre-morbid history of depression, higher rates in patience with temporal lobe bleeding

136
Q

Name 3 CNS infections post brain injury

A

meningitis post basilar skull fracture
brain abscess
cranil OM

137
Q

List 5 medical complications that can occur post TBI

A

dic
resp complications
cardiac dysr

138
Q

4 main mtbi sx categories

A

somatic
cognitive
sleep
emotional

139
Q

PE of mTBI

A

head injury assessment
neuro/cn
MMSE

140
Q

ddx mtbi

A

intoxication
seizure
hypoglycemia

141
Q

List 7 Canadian CT head rules

A

High risk 1-5:
GCS <15 2h post injury
suspected open or depr skull fracture
any sign basilarskull fracture
emesis >2 epi
age >65

medium:
amnesia pre impact </=30 min
dangerous mech: ped struck by vehicle, occup ejected from vehicle, fall from elevation >3ft

142
Q

NEXUS II crteria for ct head

A

evidence of sign skull fracture
scalp hematoma
neuro deficit
alt alertness
abn behaviour
coagulopathy
persistent emesis
age >65y

143
Q

What head lesions may show up better/be better dettermined by MRI?

A

posttrauma ischemic infarct
subac nonhemorrhagic lesions and contusions
axonal shear injury
lesions of brainsteam or posterior fossa

144
Q

When to use Diffusion tensor imaging with mri - head injury?

A

TAI

145
Q

MTBI d/c home- when?

A

observe 4-6 hours
anticoag up to 24h and repeat scan possible

146
Q

Warning signs in mtbi

A

cannot wake up
severe/worsenign h/a
somnolent/confused
restless
unsteady or seizure
difficulty vision
fever or stiff neck
urine/bowel incontinence
weakness or numbness new

147
Q

Post concussive sybdrome - sx

A

constellation of sx including somatic (h/a, dizzy, vertigo, nausea, fatigue, sn to light and noise)

cogn

affective following mtbi persisting beyond recovery period

148
Q

Postraumatic transient cortical blindness syndrome - what is this?

A

transient visual loss
n pupils
normal fundoscopy hours following mtbi

returns within 24h max

149
Q

Return to play: step 1:

A

BEFORE THIS 24H-48H OF REST
sx limited activity - not providing like reintro school

150
Q

Return to play: step 2

A

light aerobic
walk/stationary bike, no RT to incr HR

151
Q

Return to play: step 3

A

sport sp exercise
run/skate, no head impact
to add movement

152
Q

Return to play: step 4

A

noncontact drills training
ie passing or RT
exericse, coordin and incr thinking

153
Q

Return to play: step 5

A

full contact practice
medically cleared now - N training
to incr confidence

154
Q

Return to play: step 6

A

return to sport
normal play

155
Q
A
156
Q

Return to play length of ea stage

A

at least 24h

Rosens (40 decks)

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