Managing Agitation in Traumatic TBI

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Transcript Managing Agitation in Traumatic TBI

Managing Agitation in
Traumatic Brain Injury
Jennifer E. Marks, D.O.
Department of PM&R
LSUHSC
TBI

#1 cause of TBI is MVA
 Males at higher risk in all age groups
 Peak risk 18-25 years
TBI
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Severe TBI estimated to be only 6% of all
hospitalized brain injury cases
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However,the health care costs and residual
deficits are much greater than with
mild/moderate TBI
TBI
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Mechanisms of injury:
 PRIMARY: Occur at the moment of impact
 SECONDARY: Triggered by primary
mechanisms, cause more damage to the
brain
Primary Injury MechanismsTBI
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Most brain damage caused
by accelerationdeceleration
Diffuse axonal injury:
Widespread stretching of
axons caused by the
rotation of the brain
around its axis
DAI may be seen on brain
MRI
Diffuse axonal injury
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Aka Shear injury
Occurs in 50% of all head
trauma cases
Characterized clinically by
LOC at time of impact
Multiple b/l focal lesions
throughout white matter
Most commonly seen in
the corpus collosum, brain
stem, and frontal/temporal
lobes
Secondary TBI Injury
Mechanisms
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ICH (ex. SDH)
 Brain edema
 Oxidant injury
 Hypoxia secondary to cerebral perfusion
pressure
 Excitotoxicity: Neuronal damage caused by
accelerated release of excitatory
neurotransmitters by injured neurons
Glasgow Coma Scale
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No direct way to measure the severity of brain
injury
The Glasgow Coma Scale is used to measure TBI
severity
The GCS evaluates the patient’s eye, motor, and
verbal response
The lowest score obtainable is 3, the highest is 15
The lowest post resuscitation score is the preferred
value
GCS Pitfalls
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Score can be affected by intoxication
 Intubation can obscure the difference
between a mild and moderate TBI
 Also unscorable if patient cannot
understand the examiner’s language
Mild TBI
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GCS 13 or greater
 Equivalent to concussion
Moderate TBI
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GCS 9-12
 Follows commands
 Does not answer questions appropriately
Severe TBI
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GCS < or = to 8
 Patient was in a coma
 Permanent neurological sequelae and
functional disability
 At least one year for maximal return to
functioning
 Large majority of patients in rehab units
TBI patient issues
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Spasticity
Hetereotopic ossification
Posttraumatic epilepsy
Postraumatic hydrocephalus
Cranial nerve damage
Sleep disorders
Dysphagia
DVT
Skin breakdown
Post traumatic amnesia/AGITATION
Definition of agitation in TBI
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A consensus at this time has not been reached on
the exact definition of agitation.
 “Subtype of delirium occurring during the period
of post traumatic amnesia, characterized by
excessive behaviors including some combination
of aggression, disinhibition, akathisia, and
emotional lability.”
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A 1996 literature review featured in the Archives of PM&R by Sandel &Mysiw,
77:617-623
Etiology of agitation
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Brain trauma disrupts the
catecholamine/neurotransmitter pathways:
surges of norepinephrine and epinephrine
have been documented in the plasma and
CSF.
 TBI patients can also have hypothalamic
dysfunction affecting temperature, blood
pressure, etc.
Diagnosing agitation
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A diagnosis of exclusion after medical and
neurological conditions have been ruled out
 Must rule out metabolic derangement,
hypothyroidism, infection/sepsis,
hypoglycemia , hypoxemia, medications
such as anticholinergics
 Drug withdrawal (ex. Sedatives, hypnotics)
Diagnosing agitation
continued…
Neurologic complications such as
seizures, hydrocephalus, IC mass lesions,
and migraine are possibilities that must be
investigated
NEVER FORGET THAT THE
PATIENT COULD BE IN PAIN ALSO!!!
Tests suggested to evaluate
the agitated patient
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CMP, Thyroid function, CBC with
differential, UA, B12/folate, tox screen,
Brain CT/MRI, EEG, XR (see if occult
fractures/heterotopic ossification causing
pain)
Agitation Behavior Scale
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Plan for ABS to be instituted at Charity in
the near future
 Patient given a rating of 1(absent) to 4
(severe) on 14 subcategories
 Subcategories include distractibility,
impulsivity, violence, alterations of mood
 High inter-rater reliability
Rancho Los Amigos Scale of
Cognitive Functioning
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Developed at the California Hospital of the
same name
 Rancho I: No response to any stimulation;
appears to be sleeping
 Rancho II: Generalized Response
 Rancho III: Localized response
Rancho Los Amigos scale
(continued)
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**RANCHO IV: Confused, Agitated, may
be aggressive
 Rancho V: Confused, Inapproriate,
nonagitated
 Rancho VI: Confused, appropriate
 Rancho VII: Automatic, appropriate
 Ranch VIII: Purposeful, appropriate
Management
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Environment
 Educate Staff and Family
 Behavior
 Medication
Environmental Management
Environmental Management
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FIRST REDUCE STIMULI- light, noise,
distractions
 Patient should have a limited number of
visitors at a time
 EVERYONE should speak in a low volume,
one at a time
Environmental Management
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To reduce patient confusion:
 Consistent schedule and staffing
 Don’t move patient to another room
 Reorient person frequently
Behavioral Strategies
Tolerate patient’s restlessness as much as
possible (ex. Allow patient to pace if
ambulatory)
 Mobile patients may need a closed unit or
sensor unit for their safety
 Remove lines tubes ASAP
 Consider Craig bed or Vail bed
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Vail Bed
Environmental Management
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AVOID RESTRAINTS IF AT ALL
POSSIBLE
 Padded hand mittens if necessary
 Soft lap belt in the wheelchair
 Heavy, stable wheelchair that will not tip
over
Medications
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Since 1966, there have only been six
randomized controlled trials concerning
medication management of TBI
agitation!
 Almost all studies evaluating medications
have been on subjects greater than ten years
old.
RCT studies 1966-present
Measurement and Treatment
of Agitation following TBIFugate et al.
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Study of 129 physicians divided into
experts or nonexperts surveyed.
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Experts either had published two or greater
articles on pharmacological interventions
for TBI in the last 5 years, or had > or =
70% of their practice devoted to treating
TBI
Fugate et al. continued
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Experts most frequently prescribed
carbamazepine, beta blockers, TCA’s
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Nonexperts chose Haldol four times more
frequently than experts
Medications
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Most commonly utilized
 Antiepileptics
 Dopamine agonists (amantadine)
 Antidepressants (TCA’S)
 Antipsychotics (Haldol)
 Beta Blockers(Inderal)
Medications for agitation
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Antiepileptics:
 Carbamazepine: Commonly utilized by rehab
facilities. Some promise with agitation but only
case reports have been published
 Phenytoin, Phenobarbitol: Not recommended
secondary to interfering with cognitive function
and causing excessive sedation
Medications
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Benzodiazepines: Not recommended for
long term agitation treatment due to
interference with cognitive function and
sedation
FOR SEVERE AGITATION,
Lorazepam 1-2 mg IM/IV !
Antipsychotics
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Ex. Haldol: The typical agents, in both
human and animal studies, have been shown
to cause a decline in cognitive performance
(verbal ability, memory, learning, attention,
spatial ability…..once the medication was
stopped, cognition improved)
Stanislav et al, Brain Injury 1997, p335-41
Beta blockers
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Two placebo-controlled, blinded studies
with propanolol showed decreased agitation
in patients with TBI.
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Also helps to control tachycardia and
hypertension many TBI patients have
Beta Blockers
Twenty one subjects with TBI
 Treated with propanolol or placebo in a
double-blind study
 In the treatment group the intensity of
agitation was significantly lower, although
the number of episodes was similar. The use
of restraints was also significantly lower.
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Brooke et al., Arch Phys Med Rehabil 73, Oct 1992, 917-921
Beta Blockers
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Starting dose of propanolol at 20 mg BID
 Can use QID dosing
 IN ADULTS can titrate up to 60 mg/day
 Usually max amount 240 mg/day in adults,
but doses as high as 600 mg/day have been
reported
 As patient improves, can taper off
Medication
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Dopamine agonists (amantadine,
bromocriptine) , SSRIs, methyphenidate,
and TCA’s have not been shown to control
agitation successfully, but do improve
alertness/initiation
Conclusion
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More RCT studies need to be done to
determine the optimum pharmacologic
intervention for TBI
Sources
As previously stated, and……
 Randall L. Braddom. Physical Medicine and
Rehabilitation. Second Edition. W. B Saunders Co.
, Pennsylvania. 2000.
 Fleminger S., Greenwood RJ, Oliver D.L.
Pharmacological management for agitation and
aggression in people with acquired brain injury
(Cochrane Review). In: The Cochrane Library,
Issue 3, 2004. Chichester, UK: John Wiley &
Sons, Ltd.
 Thank you to Dr. Kiersta Kurtz-Burke, PM&R
consult service staff at Charity!
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