Chapter 22 Traumatic Brain Injury Flashcards Preview

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Flashcards in Chapter 22 Traumatic Brain Injury Deck (29):
1

Name 4 leading causes of TBI in order of frequency.

Falls, MVA, Assaults.

2

Name the 4 mechanisms of secondary injury in TBI.

Ischemia, excitotoxicity, energy failure, and cell death

Cerebral swelling

Axonal injury

Inflammation and regeneration

3

Name the 3 Theories of Recovery in TBI.

reversal of diaschisis

compensation

adaptive plasticity

4

What is Diaschisis? How does it relate to functional recovery?

Diaschisis is a temporary reduction in function of structures interconnected with an injured brain. Functional recovery is likely to be related to a gradual reduction in diaschisis.

5

What is compensation?

Compensation is the use of alternative strategies as an individual attempts to supplement lost function.

6

Name 3 underlying mechanisms of adaptive plasticity (neuroplasticity).

A third theory is that functional recovery is largely dependent upon neuroplasticity of intact remaining brain structure. Underlying mechanisms include unmasking of existing connections, long-term potentiation, long-term depression, axonal sprouting, dendritic sprouting, synaptogenesis, and angiogenesis.

7

Describe the Glasgow Outcome Scale.

The Glasgow Outcome Scale (GOS) is a five-level score:

Dead
Vegetative state
Severely disabled
Moderately disabled
Good recovery

8

Severe disability according to the GOS is unlikely when what 2 properties are true?

Time to follow command is less than 2 weeks.
Duration of PTA is less than 2 months.

9

Good recovery according to GOS is unlikely when what 3 properties are true?

Time to follow commands is longer than 1 month.
Duration of PTA is greater than 3 months.
>65 years of age.

10

What is Posttraumatic Amnesia (PTA)?
How is Posttraumatic Amnesia (PTA) assessed? (name the test).
How is the end of Posttraumatic Amnesia (PTA) assessed? (describe the test scenario).

Posttraumatic Amnesia (PTA): the duration during which patients neither encode nor retain any new information and experience and can be assessed by Galveston Orientation Amnesia Test (GOAT). The end of PTA is marked by a score of >75 on GOAT on two consecutive days.

11

Compare the clinical features (consciousness, sleep/wake cycle, motor function) between Coma, VS, and MCS.

Consciousness:
Coma + VS = None.
MCS = partial

Sleep/wake Cycle
Coma = None.
VS + MCS = Present.

Motor function
Coma = Reflexes + Posture responses only.
VS = Posture + Withdrawal responses to noxious stimulus.
MCS = Localizes noxious stimulus.

12

Describe the Glasgow Coma Scale.

Min score is 3.
Max score is 15.
4 Eye opening, 5 Verbal response, 6 Motor response.

13

What is the acute treatment in TBI?

The “ABCs,” airway maintenance, breathing, and circulation, are addressed first.
The spine is immobilized due to a risk of associated cervical spine injury.

14

Intracranial Pressure (ICP) Monitoring in Severe TBI is appropriate if GCS is what value? Describe the Head CT post-TBI for ICP.

Patients with Glasgow Coma Scale scores postresuscitation ≤8.

Head CT showing contusions, hemorrhages, edema, or compressed basilar cisterns.

ICP monitoring may also be appropriate in patients with postresuscitation scores ≤8 with a normal head CT and two of the following: age >40 years, motor posturing, or a systolic pressure of <90 mm Hg.6

15

Name 4 common problems after TBI.

Sleep disturbance, agitation, alertness, dysautonomia, endocrine.

16

Name 3 Pharmacotherapy (drugs) used to induce Arousal and Alertness in TBI.

Dopaminergic agents (amantadine and bromocriptine) and adrenergic agents like methylphenidate are considered in issues related to impaired arousal and alertness.

17


What is post-TBI Agitation?
What scale is used to quantify agitation in the rehabilitation setting?
What is the best medication for TBI related agitation? (Cochrane reviewed)
Name 3 medical reasons for agitation.

Posttraumatic agitation is defined as a delirium present during the period of PTA, manifested by behavioral excesses such as aggression, akathisia, disinhibition, emotional lability, destructiveness, or combativeness.

The Agitated Behavior Scale is commonly used to quantify agitation in the rehabilitation setting. Medical reasons are always considered first (infections, pain, hypoxia, and metabolic abnormalities).

Treatment includes nonpharmacological interventions (quiet room, dim light, limited visitors, Vail bed, and ambulation).

Atypical antipsychotics are considered an option in managing TBI-related agitation.

Cochrane database review reported that the best evidence for medication management in the treatment of TBI-related agitation exists for Propranolol (2003).

18

Name 3 Endocrine Dysfunction after TBI and its treatments.

SIADH, Syndrome of Inappropriate Antidiuretic Hormone is the common TBI endocrinopathy causing hyponatremia and is associated with euvolemia, low BUN, and urine osmolality greater than serum osmolality. The treatment in most cases is fluid restriction and in rare cases hypertonic saline.

A less common cause of hyponatremia is cerebral salt wasting where patients are dehydrated. Hence, treatment includes replacement of fluids and salt.

Diabetes insipidus is rare and usual onset is 5 to 10 days after trauma. Features include polyuria, low urine osmolality, high serum osmolality, and normal to high sodium. Treatment includes hormonal replacement.

Anterior hypopituitarism may present weeks to months after moderate to severe TBI and may have an insidious onset with malaise, hypothermia, bradycardia, hypotension, hyponatremia, or stagnation of rehabilitation progress. Workup includes serum hormonal assays and treatment includes hormonal replacement.

19

Describe the clinical presentation of Dysautonomia. What is the treatment?

tachycardia, increased BP, tachypnea, fever, and sweating.

Treatment options include NSAIDs, β-blockers, and symptomatic treatment.

20

What is Posttraumatic Epilepsy (PTE)? Name 2 drugs used to treat PTE.

a disorder characterized by recurrent late seizure episodes in patients with TBI, not attributable to any other etiology.

Posttraumatic seizures (PTS) refer to a single or recurrent seizure episode after TBI.

PTS have further been classified as early (1 week after TBI).

Carbamazepine and valproic acid are the preferred agents for treatment of PTE, and treatment duration is not clearly established.

21

Describe the clinical presentation of Dysautonomia. What is the treatment?

tachycardia, increased BP, tachypnea, fever, and sweating. Treatment options include NSAIDs, β-blockers, and symptomatic treatment.

22

What is Posttraumatic Epilepsy (PTE)? Name 2 drugs used to treat PTE.

a disorder characterized by recurrent late seizure episodes in patients with TBI, not attributable to any other etiology.

Posttraumatic seizures (PTS) refer to a single or recurrent seizure episode after TBI.

PTS have further been classified as early (1 week after TBI).

Carbamazepine and valproic acid are the preferred agents for treatment of PTE, and treatment duration is not clearly established.

23

Describe the Role of Technology in Rehabilitation of TBI Patients.

Use of virtual reality (for driving simulation and to simulate real-life scenarios), as these sessions have been shown to facilitate neuroplasticity and promote motor recovery. Neuroprosthetics to improve ambulation and robotic trainers to maximize therapy intensity and make mass practice more convenient.
No evidence exists to recommend the use of hyperbaric oxygen therapy in the treatment of TBI.

24

Name 3 Endocrine Dysfunction after TBI and its treatments.

SIADH, Syndrome of Inappropriate Antidiuretic Hormone is the common TBI endocrinopathy causing hyponatremia and is associated with euvolemia, low BUN, and urine osmolality greater than serum osmolality. The treatment in most cases is fluid restriction and in rare cases hypertonic saline.

A less common cause of hyponatremia is cerebral salt wasting where patients are dehydrated. Hence, treatment includes replacement of fluids and salt.

Diabetes insipidus is rare and usual onset is 5 to 10 days after trauma. Features include polyuria, low urine osmolality, high serum osmolality, and normal to high sodium. Treatment includes hormonal replacement.

Anterior hypopituitarism may present weeks to months after moderate to severe TBI and may have an insidious onset with malaise, hypothermia, bradycardia, hypotension, hyponatremia, or stagnation of rehabilitation progress. Workup includes serum hormonal assays and treatment includes hormonal replacement.

25

Describe the clinical presentation of Dysautonomia. What is the treatment?

tachycardia, increased BP, tachypnea, fever, and sweating.

Treatment options include NSAIDs, β-blockers, and symptomatic treatment.

26

What is Posttraumatic Epilepsy (PTE)? Name 2 drugs used to treat PTE.

a disorder characterized by recurrent late seizure episodes in patients with TBI, not attributable to any other etiology.

Posttraumatic seizures (PTS) refer to a single or recurrent seizure episode after TBI.

PTS have further been classified as early (1 week after TBI).

Carbamazepine and valproic acid are the preferred agents for treatment of PTE, and treatment duration is not clearly established.

27

Describe the clinical presentation of Dysautonomia. What is the treatment?

tachycardia, increased BP, tachypnea, fever, and sweating. Treatment options include NSAIDs, β-blockers, and symptomatic treatment.

28

What is Posttraumatic Epilepsy (PTE)? Name 2 drugs used to treat PTE.

a disorder characterized by recurrent late seizure episodes in patients with TBI, not attributable to any other etiology.

Posttraumatic seizures (PTS) refer to a single or recurrent seizure episode after TBI.

PTS have further been classified as early (1 week after TBI).

Carbamazepine and valproic acid are the preferred agents for treatment of PTE, and treatment duration is not clearly established.

29

Describe the Role of Technology in Rehabilitation of TBI Patients.

Use of virtual reality (for driving simulation and to simulate real-life scenarios), as these sessions have been shown to facilitate neuroplasticity and promote motor recovery. Neuroprosthetics to improve ambulation and robotic trainers to maximize therapy intensity and make mass practice more convenient.
No evidence exists to recommend the use of hyperbaric oxygen therapy in the treatment of TBI.