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BR 3rd Ed > Ch 2 - TBI: Medical Management > Flashcards

Ch 2 - TBI: Medical Management Flashcards

1
Q

When is CT head mandatory?

A

Early head CT is mandatory in GCS < 13

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2
Q

When can MRI brain be useful in TBI?

A

Define non-hemorrhagic lesions of the brain (cortical contusions, subcortical gray matter
injury, and brainstem lesions)

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3
Q

What sedating medications can delay neurologic recovery in TBI?

A

Benzodiazepines

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4
Q

What can barbiturates be used for in TBI?

A

Induce coma and dec metabolic requirements of the brain

Control ICP

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5
Q

What is an advantage for using propofol for sedation?

A

Rapid return to consciousness after discontinuation to allow for frequent neuro exams

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6
Q

What is a normal ICP in an adult?

A

Head and trunk elevated to 45° normal ICP is 2-5 mmHg.

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7
Q

What is considered elevated ICP?

A

ICP > 20 mmHg for >5 minutes

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8
Q

What can unchecked inc ICP lead to?

A

Death from deformation of tissue, brain shift, herniation and cerebal ischemia

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9
Q

What happens with ICP >40 mmHg?

A

Neurological dysfunction and impairment of the brain’s electrical activity

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10
Q

What happens with ICP >60 mmHg?

A

Fatal

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11
Q

What can worsen cerebral edema and inc ICP?

A

Fever
Hyperglycemia
Hyponatremia
Seizures

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12
Q

How is cerebral perfusion pressure (CPP) measured?

A

CPP=MAP-ICP

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13
Q

What should cerebral perfusion pressure (CPP) be to ensure cerebral blood flow?

A

> 60 mmHg

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14
Q

What happens to cerebral perfusion pressure (CPP) with increased ICP?

A

Reduced CPP

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15
Q

What are indications for monitoring ICP and for ventilation?

A
  1. GSC <8 and CT findings w/ inc ICP
  2. GSC <6 w/o hematoma
  3. GSC <12 w/ severe chest and facial injuries
  4. GSC <8 prior to IC hematoma evacuation
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16
Q

What are methods to monitor ICP?

A

Papilledema
CT head
LP if no papilledema
Intraventricular ICP monitoring

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17
Q

What are methods to decrease ICP?

A 
Elevated HOB to 30 deg
Intraventricular ICP monitoring
Neurosurgical decompression
Hypothermia
Dec PaCO2 through hyperventilation
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18
Q

What are surgical options for epidural hematoma or SDH?

A

Emergency craniotomy

Emergency burr hold

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19
Q

What does uncal herniation of the medial temporal lobe produce?

A
  1. CN3: ipsi pupil dilation, ptosis, ophthalmoplegia
  2. Ipsi hemiparesis from corticospinal tract on contralateral crus cerebri
  3. Contra hemiparesis from precentral motor cortex or internal capsule
  4. AMS
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20
Q

What is a post traumatic seizure?

A

Single recurrent seizure after TBI

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21
Q

What are types of post traumatic seizures (PTS)?

A

Partial (majority of PTS)

Generalized

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22
Q

What is the time frame for immediate PTS?

A

1st 24 hr post injury

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23
Q

What is the time frame for early PTS?

A

24hr to 7 days post injury

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24
Q

What is the time frame for late PTS?

A

After 1st week post injury

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25
Q

What are risk factors for Late PTS?

A 
Penetrating head injury
Intracranial hematoma
Early PTS
Depressed skull fx
Focal signs (aphasia/ hemiplegia)
Age
Alcohol abuse
Use of TCAs
Dural tearing
Focal signs (aphasia, hemiplegia)
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26
Q

When is the greatest risk for PTS?

A

1st 2 years post injury

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27
Q

What lab finding can indicate posttraumatic epilepsy?

A

Increase prolactin level confirms true seizure activity but normal level does not rule out
seizure activity

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28
Q

What time frame is AED for seizure ppx effective?

A

Phenytoin and valproic acid have been proven effective only during the first week post-injury

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29
Q

Which AED’s are considered drug of choice for treatment of PTS?

A

Carbamazepine (partial seziures) and valproic acid (generalized seizures)

Keppra commonly used 1st line

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30
Q

When are therapeutic anticonvulsant medications are usually started?

A

Once late seizures occur

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31
Q

What is the probability of recurrent late seizures after the first late seizure?

A

Recurrent late PTS is up to 86% within 2 years

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32
Q

Which AEDs should be avoided in TBI PTS?

A

Phenobarbital: cognitive impairment
Phenytoin: cognitive effects and impede brain recovery

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33
Q

Which drug interactions increase the metabolism of carbamazepine?

A

Penobarbital
Phenytoin
Valproic acid

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34
Q

Which drug metabolisms are enhanced by carbamazepine?

A

Phenobarbital

Primidone into phenobarbital

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35
Q

What does carbamazepine do to haloperidol?

A

Reduces concentration and effectiveness of haloperidol

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36
Q

Which drugs inhibit the metabolism of carbamazepine?

A

Propoxyphene Erythromycin

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37
Q

What does lamotrigine used with carbamazepine cause?

A

Increase levels of 10,11-epoxide (an active metabolic of carbamazepine)

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38
Q

Which drugs can cause lamotrogine half life to be reduced by 15 hours?

A

Carbamazepine
Phenobarbital
Primidone

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39
Q

Which drug does lamotrogine reduce concentration of when used concurrently?

A

Valproic acid

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40
Q

Which drugs can increase the levels of phenobarbital?

A

Valproic acid increases as much as 40%

Phenyotoin has variable reactions

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41
Q

What drugs can increase phenytoin levels?

A 
Chloramphenicol
Cimetidine
Dicumarol
Disulfiram
Isoniazid
Sulfonamides
Valproic acid Phenylbutazone
Phenobarbital
42
Q

What drugs can decrease phenytoin levels?

A 
Sulfisoxazole
Salicylates
Tolbutamide
Carbamazepine
Phenobarbital
43
Q

What happens when phenytoin and theophylline are taken concurrently?

A

Phenytoin levels may be lowered and theophylline metabolized more rapidly

44
Q

What does phenytoin decrease effectiveness of?

A

Decreases effectiveness to contraceptives

45
Q

What does phenytoin enhance metabolism of?

A

Enhances metabolism of corticosteroids

46
Q

What happens with concurrent use of valproic acid and clonazepam?

A

Rare development of absence status epilepticus

47
Q

When is a reasonable time frame to consider stopping antiepleptic drugs for PTE?

A

After a 2 year seizure free interval

48
Q

What are risk factors for PTE recurrence?

A
  • More frequent recurrence
  • Tx with >1 antiepileptic drug
  • Hx of generalized tonic-clonic seizures
  • ABN or epileptiform discharges on pre-withdrawl EEGs
49
Q

What surgical resections have been shown to reduce seizure recurrence in PTE?

A

Medial temporal and

Neocortical dec 77% and 56% 1 year remission respectively

50
Q

What is FDA approved for adjunctive treatment of intractable partial seizures in patients >12 yo?

A

Vagal nerve simulation (VNS)

51
Q

What time frame does paroxysmal autonomic instability and dystonia occur?

A

Within the first 2 weeks of injury

52
Q

What causes paroxysmal autonomic instability and dystonia to occur?

A

Surge of circulating cathecholamines released from direct trauma to the autoregulatory centers

53
Q

What are signs/symptoms of paroxysmal autonomic instability and dystonia?

A 
Hypertension
Tachycardia
Hyperthermia
Spasticity
Perspiration
54
Q

What can be used for HTN and tachycardia in paroxysmal autonomic instability and dystonia?

A

Lipophilic beta-blockers

55
Q

What can be used for malignant HTN in paroxysmal autonomic instability and dystonia?

A

Dantrolene sodium

56
Q

What are types of dopamine agonist used in paroxysmal autonomic instability and dystonia?

A

Amantadine

Bromocriptine

57
Q

What do dopamine agonist affect in paroxysmal autonomic instability and dystonia?

A

Anterior hypothalamus: temperature sensitive Posterior hypothalamus: heat dissipation center

58
Q

What are non-pharmacologic management options paroxysmal autonomic instability and dystonia? for

A

Cooling blankets

Nasogastric (NG) tube lavage

59
Q

What causes ventriculomegaly after TBI?

A

Cerebral atrophy and focal infarction of brain tissue (ex vacuo changes)

60
Q

What is the MC type of Postraumatic Hydrocephalus after TBI?

A

Communicating or normal-pressure type

61
Q

What is the classic triad of PTH?

A

Incontinence
Ataxia/gait disturbance
Dementia of normal pressure hydrocephalus

62
Q

What are initial symptoms of PTH?

A

Intermittent HA
Vomiting
Mental status changes (confusion, drowsiness).

63
Q

What are findings of PTH on CT head?

A

Periventricular lucency
Sulcal effacement
Uniform ventricular dilation

64
Q

What is the treatment for PTH?

A

LP

Shunt placement

65
Q

What are the most frequently affected CN’s in TBI?

A 
Olfactory nerve (CN I)
Facial nerve (CN VII)
Vestibulocochlear nerve (CN VIII)
66
Q

What is the MC CN damage by blunt head trauma?

A

Olfactory (CNI) due to tearing of the olfactory nerve filaments in or near the cribriform plate through which they traverse

67
Q

What are the symptoms of CNI injury?

A

Anosmia (complete loss of smell)

Loss of taste

68
Q

What is the only CN neuropathy present in mild TBI?

A

CN I injury

69
Q

How can CN I injury pr present in higher level patients?

A

Dec appetite
Weight loss
Altered feeding pattern

70
Q

When does recovery of CN I injury occur?

A

> 1/3 of cases in first 3 months

71
Q

What are the four components of of CN VII innervation?

A

– Tactile sensation to the parts of the external ear
– Taste sensation to the anterior 2/3 of the tongue
– Muscles of facial expression
– Salivary and lacrimal glands

72
Q

What does damage to CN VIII cause?

A

Loss of hearing

Postural vertigo Nystagmus

73
Q

What does partial damage to CN II cause?

A

Blurring of vision
Homonymous hemianopsia
Scotomas

74
Q

What does complete damage to CN II cause?

A

Complete blindness

Pupil dilated, unreactive to direct light but reactive to light stimulus to the opposite eye [consensual light reflex])

75
Q

What are risk factors for developing HO in TBI?

A
  • Prolonged coma (>2 weeks)
  • Immobility
  • Limb spasticity
  • Long-bone fracture
  • Pressure ulcers
  • Edema
76
Q

What is the period of greater risk to develop HO?

A

3 to 4 months post-injury

77
Q

What are the MC joints involved in for HO in TBI?

A
  1. Hips (most common)
  2. Elbows/shoulders
  3. Knees
78
Q

What are signs/symptoms of HO?

A 
Pain 
Dec ROM
Local swelling
Erythema
Warmth in joint
Muscle guarding
Low-grade fever
79
Q

What lab work can indicate HO?

A

Elevated Serum alkaline phosphatase (SAP) but poor specificity

80
Q

What is the most sensitive method of early detection of HO?

A

Seen within the first 2 to 4 weeks after injury in a triple phase bone scan

81
Q

What are x-rays helpful for in HO?

A

Confirm maturity of HO

Require 3 weeks to 2 months post-injury to reveal HO

82
Q

What are prophylaxis treatment of HO?

A
  • ROM exercises
  • Control of spasticity
  • (NSAIDs)
83
Q

What are treatments to arrest HO?

A

Bisphosphonates
Indomethacin
ROM exercises

84
Q

When can surgical removal of HO be done?

A

Surgical resection usually postponed 12 to 18 months to allow maturation of HO

85
Q

What is the preferred form of feeding when oral feeding is compromised in TBI?

A

Enteral feeding

86
Q

What is the biggest risk with enteral feeding?

A

Aspiration which is inc with GERD and proximal tube placement

87
Q

When should parenteral feeding be utilized?

A

Tempory interruption of GI function or inc metabolic demand

88
Q

When is Total parental nutrition (TPN) is preferred?

A

Segment of GI tract is nonfunctional, or must be free of food for a prolonged amount of time

89
Q

When should TBI patients be screened for endocrine function?

A

3 months and at 1 year post-injury regardless of injury severity

90
Q

What is the recommended endocrine screening labs for TBI?

A 
AM cortisol
Insulin growth factor (IGF)-I
Follicle-stimulating hormone (FSH)
Luteinizing hormone (LH)
Testosterone
Estradiol
Prolactin
Urinary free cortisol
91
Q

What is SIADH?

A

Water retention resulting from excessive antidiuretic hormone (ADH) secretion from the neurohypophysis

92
Q

What medication can cause SIADH?

A

Carbamazepine

93
Q

What are signs of mild SIADH?

A

Na 130-135
Anorexia
N/V

94
Q

What are signs of severe SIADH?

A

Inc body wt

Cerebral edema: restlessness, irritability, confusion, convulsions, coma

95
Q

What are treatments for SIADH?

A

Fluid restriction of 1L/day
3% saline
Do not correct >10 mEq/L over 24 hours until Na reach 125 mEq/L

96
Q

How is chronic SIADH treated?

A

Demeclocycline, which normalizes serum Na+ by inhibiting ADH action in the kidney

97
Q

What is the hallmark of cerebral salt wasting (CSW) syndrome?

A

Dec BV 2/2 Na loss in urine l/t inc ADH secretion which is appropriate

98
Q

What is the treatment for CSW?

A

Hydration/fluid replacement + electrolyte (Na+) correction

99
Q

What can cause diabetes insipidus?

A

A fracture in or near the sella turcica may tear the stalk of the pituitary gland, with resulting DI due to disruption of ADH secretion from post pituitary

100
Q

What are treatments for diabetes insipidus?

A

DDAVP (desmopressin acetate)

Chlorpropamide

101
Q

What does cognitive remediation include?

A

Visuospatial rehabilitation, executive control, self-monitoring, pragmatic interventions, memory retraining, and strategies to improve attention

BR 3rd Ed (92 decks)

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