Cedars-Sinai Trauma Nursing Conference

Traumatic Brain Injury: The TOP 10

Challenges in Nursing Care

Asma M. Moheet, MD
Neurointensivist, Assistant Professor
Depts. Of Neurology & Neurosurgery
Disclosures

No relevant financial conflicts of interest to report.

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 Outline

10. TBI Epidemiology

09. Mechanisms of Injury

08. Basic Definitions

07. Injury Classification

06. Spine Precautions

05. Sedating the TBI patient

04. Multimodal Monitoring in ICU

03. Brain Arrest and Management of Elevated ICPs

02. Palliative Care, the Donor Patient

01. When Patients Come Back

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 Outline

10. TBI Epidemiology

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10. Epidemiology

Every day 153 people in the US die from injuries that include TBI

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10. Epidemiology

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10. Epidemiology

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10. Epidemiology

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10. Epidemiology

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 Outline

10. TBI Epidemiology

09. Mechanisms of Injury

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09. Mechanisms of Injury

Mechanism Descrip.on Sample of incident

Punched
Accelera(on and impact Direct contact with another object,
accelera(on Hit in the head with a beer bo9le

Sudden stop in an MVC

Decelera(on Decelera(on injury
Follows an impact/accelera(on injury

Accelera(on/Decelera(on High speed MVC with impact

Vic(m bounces o an object

GSW
Penetra(ng Object causes direct parenchymal
injury Other foreign body

GSW
Blast Pressure waves from a device cause
indirect trauma IED, bomb blast

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09. Mechanism of Injury

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09. Mechanism of Injury

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 Outline

10. TBI Epidemiology

09. Mechanisms of Injury

08. Basic Definitions

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08. Basic Definitions

Source: The NCS Pocket Guide: in

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preparation. TBI Chapter, Sivasankar et al.
08. Basic Definitions

Source: The NCS Pocket Guide: in

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preparation. TBI Chapter, Sivasankar et al.
08. Basic Definitions

2nd hit: The risk for further neurologic injury following the initial event due to a
variety of factors such as worsening ischemia, edema, etc.

ICP = INTRACRANIAL PRESSURE

CPP = CEREBRAL PERFUSION PRESSURE

CPP = MAP ICP

PBTO2 = BRAIN TISSUE OXYGEN TENSION

CBF = CEREBRAL BLOOD FLOW

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 Outline

10. TBI Epidemiology

09. Mechanisms of Injury

08. Basic Definitions

07. Injury Classification

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07. Injury Classification

Severity
Mild Moderate Severe
GCS 14-15 GCS 9-13 GCS 8 or less
Duration of loss of consciousness
Mild Moderate Severe
MS change or LOC <30 min LOC 30m-6 h LOC >6h

Primary vs secondary
Primary: the injury due to force at the time of the initial event

Secondary: delayed injury due to worsening perfusion, etc

Focal vs diffuse
Focal: scalp injury, skull fracture, contusions

Diffuse: multiple contusions, tSAH, DAI, hypoxic-ischemic injury

Classification and Complications of Traumatic Brain Injury

Updated: Feb 13, 2017
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Author: Percival H Pangilinan, Jr, MD; Chief Editor: Stephen Kishner, MD, MHA
 Outline

10. TBI Epidemiology

09. Mechanisms of Injury

08. Basic Definitions

07. Injury Classification

06. Spine Precautions

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06. Spine Precautions

Dont forget your ABCs: Airway is the first priority

Cervical cord injuries may result in respiratory insufficiency and need for
intubation.
Intubation should be early, fiberoptic NT or endotracheal with in-line

stabilization.
As a general rule, patients with injuries above C5 need to be intubated.

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06. Spine Precautions

Patients with injuries above T5 are at risk for hemodynamic instability due to
damage of the sympathetic nerve fibers:
NEUROGENIC or SPINAL SHOCK: bradycardia, hypotension, warm and dry skin

Neurogenic shock is a diagnosis of exclusion: always rule out bleeding!

Hypotension should be avoided to prevent a second hit to the spinal cord.

SBP should be >90mHg

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06. Spine Precautions

High incidence of spine injury in patients with TBI

Suspected TSCI patients need to be kept in a collar and on log-roll precautions

until cleared

Most patients get an initial CT C spine here if mechanism, signs/symptoms

concerning for spinal injury

Patients need to be clinically evaluated, and may get potential imaging

NEXUS criteria: no signs of intoxication, no focal neurologic deficits, no

painful distracting injuries, normal level of alertness, no posterior midline

tenderness to palpation

Canadian C-spine rules: a bit more complicated. Can clear with posterior C
spine tenderness. Incorporate head turning 45 degrees to the left and right.

Further imaging (MRI to evaluate for ligamentous injury) may be required.

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 Outline

10. TBI Epidemiology

09. Mechanisms of Injury

08. Basic Definitions

07. Injury Classification

06. Spine Precautions

05. Sedating the TBI patient

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05. Sedating the TBI Patient

Sedation should be limited with the exception of the following:

Patient with severe pain or agitation resulting in vent dyssynchrony

Status epilepticus

Storming: excessive paroxysmal sympathetic activity due to hypothalamic

injury

Patient with severe pain or agitation resulting in harm to themselves or others

Patients with ICP elevations

As a general rule we are a bit stingier with our pain meds

Neuro exam is super important

Oddo M et al. Critical Care 2016. Optimizing sedation in Patients with Acute Brain Injury
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05. Sedating the TBI Patient

Oddo M et al. Critical Care 2016. Optimizing sedation in Patients with Acute Brain Injury
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05. Sedating the TBI Patient

Why are these patients so agitated?

Frontal injury with disinhibition

Intoxicated

Detoxing

Baseline personality

No delirium scales have been validated in the acutely brain injured population

No evidence that antipsychotics improve clinical outcomes

Haloperidol can be used but increases risk for seizures

Quetiapine or risperidone can also be used

Benzodiazepines: may obscure exam, cause worsening delirium

Dexmedetomidine has been used (Tang 2011)

1. Oddo M et al. Critical Care 2016. Optimizing sedation in Patients with Acute Brain Injury
2. Tang JF et al. Neurocritical Care 2011. Dexmedetomidine controls agitation and facilitates
reliable, serial neurological examinations in a non-intubated patient with traumatic brain injury.
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05. Sedating the TBI Patient

Some patients may require deep sedation with multiple agents, and even
pentobarbital coma

Target here is to decrease brain metabolism.

EEG burst suppression

Sedation cannot be held for neurologic exams.

Can cause bradycardia, hypotension, ileus
Makes clinical declaration of brain death difficult.

1. Oddo M et al. Critical Care 2016. Optimizing sedation in Patients with Acute Brain Injury
2. Tang JF et al. Neurocritical Care 2011. Dexmedetomidine controls agitation and facilitates
reliable, serial neurological examinations in a non-intubated patient with traumatic brain injury.
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05. Sedating the TBI Patient

When weaning sedation:

Use your PRNs

Consider asking for oral or longer acting narcotics if pain is an issue

Come down on continuous infusions gradually, systematically

Dont treat blood pressure with sedation (at least, not all the time)

Be conscious of how long certain half-lives are (pentobarbital = DAYS)

1. Oddo M et al. Critical Care 2016. Optimizing sedation in Patients with Acute Brain Injury
2. Tang JF et al. Neurocritical Care 2011. Dexmedetomidine controls agitation and facilitates
reliable, serial neurological examinations in a non-intubated patient with traumatic brain injury.
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 Outline

10. TBI Epidemiology

09. Mechanisms of Injury

08. Basic Definitions

07. Injury Classification

06. Spine Precautions

05. Sedating the TBI patient

04. Multimodal Monitoring in ICU

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04. Multimodal Monitoring in the ICU

What are the modes of monitoring the brain here at Cedars?

Clinical exam

Pupillometry

EEG

ICP with an EVD or a parenchymal monitor

CBF with a parenchymal monitor

PbTO2 with a parenchymal monitor

Transcranial dopplers

Combining these results in a more complete picture with the ability to target that
exact patients physiology and to avoid the 2nd hit

Other modalities: depth EEG electrodes, cerebral microdialysis, jugular venous

O2, NIRS

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04. Multimodal Monitoring in the ICU

What are indications for invasive neuromonitoring

GCS 8 or less with abnormal CT

GCS 8 or less with normal CT and any of the following: age >40, SBP<90,

posturing
Inability to monitor serial neurologic exams

Goals of neuromonitoring
Identify deterioration

Improve understanding of the pathophysiology

Use data to individualize treatment

Assist in prognostication

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Which type of neuromonitoring?
External ventricular
drain (EVD)
If CSF diversion
required
Drain or monitor ICP
Does not perform both at
the same time
Even is measurements are
obtained Q 15 minutes,
this is dangerous for
patients

Slide courtesy of Tess Slazinski, CCNS

Which type of neuromonitoring?

Fiberoptic ICP (bolt)

ICP
Combination: two channels
ICP
Brain temperature One
catheter
Brain tissue oxygen (Licox)

Slide courtesy of Tess Slazinski, CCNS

 ICP values

Normal ICP: 0 15mmHg

Elevated ICP: > 20mmHg
CPP = MAP ICP
goal=60-80mmHg

Current BTF guidelines recommend

treatment for ICP >22.

Slide courtesy of Tess Slazinski, CCNS

04. Multimodal Monitoring in the ICU

Source: The NCS Pocket Guide: in

preparation. TBI Chapter, Sivasankar et al.
 Volume-Pressure Curve

50 ZONE 3
P1P2
P3

40
I ZONE 2
30
C P1P2P3

20
P ZONE 1
10 P1
P2 P3

0 1 2 3 4 5 6 7

volume
Slide courtesy of Tess Slazinski, CCNS
Which type of neuromonitoring?

PbtO2
Brain tissue oxygen (Licox)
Should be calibrated regularly with 100% FiO2
challenge
Normal is usually 25-30mmHg
Ischemia occurs below 15mmHg
Interventions can improve this number
(transfusion, diuresis and improved gas exchange,
increase FiO2)

Slide courtesy of Tess Slazinski, CCNS

Which type of neuromonitoring?
Cerebral blood flow
(CBF)--Hemedex
Normal values: 50mL/
100g/min

Slide courtesy of Tess Slazinski, CCNS

 Outline

10. TBI Epidemiology

09. Mechanisms of Injury

08. Basic Definitions

07. Injury Classification

06. Spine Precautions

05. Sedating the TBI patient

04. Multimodal Monitoring in ICU

03. Brain Arrest and Management of Elevated ICPs

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03. Brain Arrest and Management of Elevated ICPs

Determinants of ICP Monro-Kellie Principle and the compliance curve

 Clinical Signs and Symptoms
of Increased ICP or Hernia.on
EARLY LATE
Headache Changes in level of consciousness or GCS or
FOUR Score 2 points
Irritability Ipsilesional change in pupillary size, shape and
light-responsiveness
Vomi(ng Contralesional hemiparesis (new or worsening)
Photophobia, Contralesional change in pupillary size and
nystagmus, diploplia ipsilesional hemiparesis (Kernohans
phenomenon)
Lethargy Cushings triad: SBP (widened pulse
pressure), bradycardia, irregular respira(ons
Seizure
03. Brain Arrest and Management of Elevated ICPs

Brain Arrest is an emergency

May be preceded by bradycardia, HTN,

Irregular breathing = Cushings Triad

Common herniation syndromes:

Subfalcine: headache, contralateral leg

Weakness

Transtentorial/uncal: CN III palsy

(ipsilateral dilated pupil, abnormal EOMs),

contralateral hemiparesis

Tonsillar: obtundation

By Brain_herniation_types.svg: User:Delldotderivative work: RupertMillard (talk) -

Brain_herniation_types.svg, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=7825361

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03. Brain Arrest and Management of Elevated ICPs

ENLS advocates a Tiered Approach:

Tier 0: ABCs; HOB > 30; minimize stimuli, ensure adequate sedation; correct
hyponatremia, hyperthermia; keep CPP > 50-70 mm Hg; treat vasogenic
edema

Tier 1: mannitol; HTS; CSF drainage as appropriate and continue to assess

further NS decompression needs

Tier 2: escalate Na goals with hypertonic saline boluses (3%-23.4%), although

levels > 160 mmol/L probable little benefit; sedation increased (rec propofol
CMRO2 and CBF and thus ICP); cont reassess decompressive craniotomy/
craniectomy

Tier 3: pentobarbital bolus and infusion titrated for ICP goal; induce
hypothermia; hyperventilation (PaCO2 25-30 mmHg) if used with cerebral
oxygen monitor

Neurocrit Care. 2015 Dec;23 Suppl 2:S76-82. doi: 10.1007/s12028-015-0168-z.

Emergency Neurological Life Support: Intracranial Hypertension and Herniation.
Stevens RD1, Shoykhet M2, Cadena R3.
03. Brain Arrest and Management of Elevated ICPs

This is where daily (sometimes hourly) updated goals are important:

Serum sodium: normal, mild elevation (135-150), moderate elevation (145-160)?

What IVF are we using? How often are we checking Na?

Serum osmolality: <320. Can the patient get mannitol? How often are we
checking?

ICP goal <20, CPP goal >60:

MAP/SBP goal: Is autoregulation intact? Do we have to worry about an ICH?

pCO2 goal 35-45 or temporary hyperventilation? ETCO2 in place?

pO2 goal: avoid hypoxia

Temperature goal: normal or hypothermic*

Glucose: avoid hypo- or hyper- glycemia

Neurocrit Care. 2015 Dec;23 Suppl 2:S76-82. doi: 10.1007/s12028-015-0168-z.

Emergency Neurological Life Support: Intracranial Hypertension and Herniation.
Stevens RD1, Shoykhet M2, Cadena R3.
03. Brain Arrest and Management of Elevated ICPs

Above all, remember that this is a

potentially reversible process if
caught early enough. You can save a
patients life with a neuro check.

Neurocrit Care. 2015 Dec;23 Suppl 2:S76-82. doi: 10.1007/s12028-015-0168-z.

Emergency Neurological Life Support: Intracranial Hypertension and Herniation.
Stevens RD1, Shoykhet M2, Cadena R3.
 Outline

10. TBI Epidemiology

09. Mechanisms of Injury

08. Basic Definitions

07. Injury Classification

06. Spine Precautions

05. Sedating the TBI patient

04. Multimodal Monitoring in ICU

03. Brain Arrest and Management of Elevated ICPs

02. Palliative Care, the Donor Patient

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02. Palliative Care, the Donor Patient

Donation after Cardiac Death vs Donation after Brain Death

DCD: patient is NOT brain dead, but likely has a poor neurologic

prognosis and is expected to pass away quickly after interventions

are withdrawn. This is done in the OR.

Donation after Brain Death: patient IS brain dead and has been
pronounced. The body remains on supportive protocols of
medication, ventilation, and other interventions through organ
procurement.

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02. Palliative Care, the Donor Patient

Dont be a nihilist, but contact One Legacy early

Avoid mixed messages. Its OK to defer on complicated prognosis

questions. Families may not know the difference between coma and
brain death.

Patients families are different. They need variable amounts of time to

accept prognoses.

What you do is hard. You are on the frontlines with the patient and
family. Take a breath now and then. Decompress.

If a family decides not to donate their loved ones organs, be

respectful.

When a family decides to give the ultimate gift of organ donation, be

grateful.

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 Outline

10. TBI Epidemiology

09. Mechanisms of Injury

08. Basic Definitions

07. Injury Classification

06. Spine Precautions

05. Sedating the TBI patient

04. Multimodal Monitoring in ICU

03. Brain Arrest and Management of Elevated ICPs

02. Palliative Care, the Donor Patient

01. When Patients Come Back

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01- When Patients Come Back

Direct medical costs + indirect costs (lost productivity) =

$60 billion in the US in 2000 (Finkelstein 2006)

After they leave your ICU, they may come back to visit
Recovery can take weeks to months, often up to 2 years

Patients may have persistent motor or cognitive deficits

Patients may have emotional problems

Patients may be completely amnestic for their entire hospitalization

Finkelstein E, Corso P, Miller T and Associates. The Incidence

and Economic Burden of Injuries in the United States. New York 53
(NY): Oxford University Press; 2006.
Thank you!

Special thanks to Tess Slazinski for sharing her slides, and to all of our
amazing nursing staff for taking such good care of our patients!

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