Ch 2 - TBI: Medical Management Flashcards
1
Q
When is CT head mandatory (GCS level)?
A
Early head CT is mandatory in GCS < 13
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)
3
Q
What sedating medications can delay neurologic recovery in TBI?
A
Benzodiazepines
4
Q
What can barbiturates be used for in TBI?
A
Induce coma and dec metabolic requirements of the brain
Control ICP
5
Q
What is an advantage for using propofol for sedation?
A
Rapid return to consciousness after discontinuation to allow for frequent neuro exams
6
Q
What is a normal ICP in an adult?
A
Head and trunk elevated to 45° normal ICP is 2-5 mmHg.
7
Q
What is considered elevated ICP?
A
ICP > 20 mmHg for >5 minutes
8
Q
What can unchecked inc ICP lead to?
A
Death from deformation of tissue, brain shift, herniation and cerebal ischemia
9
Q
What happens with ICP >40 mmHg?
A
Neurological dysfunction and impairment of the brain’s electrical activity
10
Q
What happens with ICP >60 mmHg?
A
Fatal
11
Q
What can worsen cerebral edema and inc ICP?
A
Fever
Hyperglycemia
Hyponatremia
Seizures
12
Q
How is cerebral perfusion pressure (CPP) measured?
A
CPP=MAP-ICP
13
Q
What should cerebral perfusion pressure (CPP) be to ensure cerebral blood flow?
A
> 60 mmHg
14
Q
What happens to cerebral perfusion pressure (CPP) with increased ICP?
A
Reduced CPP
15
Q
What are indications for monitoring ICP and for ventilation (GCS levels)?
A
- GSC <8 and CT findings w/ inc ICP
- GSC <6 w/o hematoma
- GSC <12 w/ severe chest and facial injuries
- GSC <8 prior to IC hematoma evacuation
16
Q
What are methods to monitor ICP?
A
Papilledema
CT head
LP if no papilledema
Intraventricular ICP monitoring
17
Q
What are methods to decrease ICP?
A
Elevated HOB to 30 deg Intraventricular ICP monitoring Neurosurgical decompression Hypothermia Dec PaCO2 through hyperventilation
18
Q
What are surgical options for epidural hematoma or SDH?
A
Emergency craniotomy
Emergency burr hold
19
Q
What does uncal herniation of the medial temporal lobe produce?
A
- CN3: ipsi pupil dilation, ptosis, ophthalmoplegia
- Ipsi hemiparesis from corticospinal tract on contralateral crus cerebri
- Contra hemiparesis from precentral motor cortex or internal capsule
- AMS
20
Q
What is a post traumatic seizure?
A
Single recurrent seizure after TBI
21
Q
What are types of post traumatic seizures (PTS)?
A
Partial (majority of PTS)
Generalized
22
Q
What is the time frame for immediate post traumatic seizures (PTS)?
A
1st 24 hr post injury
23
Q
What is the time frame for early post traumatic seizures (PTS)?
A
24hr to 7 days post injury
24
Q
What is the time frame for late post traumatic seizures (PTS)?
A
After 1st week post injury
25
What are risk factors for Late post traumatic seizures (PTS)?
```
Penetrating head injury
Intracranial hematoma
Early PTS
Depressed skull fx
Age
Alcohol abuse
Use of TCAs
Dural tearing
Focal signs (aphasia, hemiplegia)
```
26
When is the greatest risk for post traumatic seizures (PTS)?
1st 2 years post injury
27
What lab finding can indicate posttraumatic epilepsy?
Increase prolactin level confirms true seizure activity but normal level does not rule out
seizure activity
28
What time frame is AED for seizure ppx effective?
Phenytoin and valproic acid have been proven effective only during the first week post-injury
29
Which AED's are considered drug of choice for treatment of post traumatic seizures (PTS)?
Carbamazepine (partial seziures) and valproic acid (generalized seizures)
Keppra commonly used 1st line
30
When are therapeutic anticonvulsant medications are usually started?
Once late seizures occur
31
What is the probability of recurrent late seizures after the first late seizure?
Recurrent late PTS is up to 86% within 2 years
32
Which AEDs should be avoided in TBI post traumatic seizures (PTS)?
Phenobarbital: cognitive impairment
Phenytoin: cognitive effects and impede brain recovery
33
What does carbamazepine do to haloperidol?
Reduces concentration and effectiveness of haloperidol
34
What does lamotrigine used with carbamazepine cause?
Increase levels of 10,11-epoxide (an active metabolic of carbamazepine)
35
Which drug does lamotrogine reduce concentration of when used concurrently?
Valproic acid
36
What happens when phenytoin and theophylline are taken concurrently?
Phenytoin levels may be lowered and theophylline metabolized more rapidly
37
What does phenytoin decrease effectiveness of?
Decreases effectiveness to contraceptives
38
What does phenytoin enhance metabolism of?
Enhances metabolism of corticosteroids
39
What happens with concurrent use of valproic acid and clonazepam?
Rare development of absence status epilepticus
40
When is a reasonable time frame to consider stopping antiepleptic drugs for post traumatic epilepsy?
After a 2 year seizure free interval
41
What are risk factors for post traumatic epilepsy recurrence?
- More frequent recurrence
- Tx with >1 antiepileptic drug
- Hx of generalized tonic-clonic seizures
- ABN or epileptiform discharges on pre-withdrawl EEGs
42
What surgical resections have been shown to reduce seizure recurrence in post traumatic epilepsy?
Medial temporal and
| Neocortical dec 77% and 56% 1 year remission respectively
43
What is FDA approved for adjunctive treatment of intractable partial seizures in patients >12 yo?
Vagal nerve simulation (VNS)
44
Over what time frame does paroxysmal autonomic instability and dystonia occur (TBI)?
Within the first 2 weeks of injury
45
What causes paroxysmal autonomic instability and dystonia to occur?
Surge of circulating cathecholamines released from direct trauma to the autoregulatory centers
46
What are signs/symptoms of paroxysmal autonomic instability and dystonia?
```
Hypertension
Tachycardia
Hyperthermia
Spasticity
Perspiration
```
47
What can be used for HTN and tachycardia in paroxysmal autonomic instability and dystonia?
Lipophilic beta-blockers
48
What can be used for malignant HTN in paroxysmal autonomic instability and dystonia?
Dantrolene sodium
49
What are types of dopamine agonist used in paroxysmal autonomic instability and dystonia?
Amantadine
| Bromocriptine
50
What do dopamine agonist affect in paroxysmal autonomic instability and dystonia?
Anterior hypothalamus: temperature sensitive
| Posterior hypothalamus: heat dissipation center
51
What are non-pharmacologic management options for paroxysmal autonomic instability and dystonia?
Cooling blankets
| Nasogastric (NG) tube lavage
52
What causes ventriculomegaly after TBI?
Cerebral atrophy and focal infarction of brain tissue (ex vacuo changes)
53
What is the MC type of Postraumatic Hydrocephalus after TBI?
Communicating or normal-pressure type
54
What is the classic triad of Postraumatic Hydrocephalus?
Incontinence
Ataxia/gait disturbance
Dementia of normal pressure hydrocephalus
55
What are initial symptoms of Postraumatic Hydrocephalus?
Intermittent HA
Vomiting
Mental status changes (confusion, drowsiness).
56
What are findings of Postraumatic Hydrocephalus on CT head?
Periventricular lucency
Sulcal effacement
Uniform ventricular dilation
57
What is the treatment for Postraumatic Hydrocephalus?
LP
| Shunt placement
58
What are the most frequently affected CN's in TBI?
```
Olfactory nerve (CN I)
Facial nerve (CN VII)
Vestibulocochlear nerve (CN VIII)
```
59
What is the MC CN damage by blunt head trauma?
Olfactory (CNI) due to tearing of the olfactory nerve filaments in or near the cribriform plate through which they traverse
60
What are the symptoms of CNI injury?
Anosmia (complete loss of smell)
| Loss of taste
61
What is the only CN neuropathy present in mild TBI?
CN I injury
62
How can CN I injury present in higher level patients?
Dec appetite
Weight loss
Altered feeding pattern
63
When does recovery of CN I injury occur?
>1/3 of cases in first 3 months
64
What are the four components of CN VII innervation?
– 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
65
What does damage to CN VIII cause?
Loss of hearing
| Postural vertigo Nystagmus
66
What does partial damage to CN II cause?
Blurring of vision
Homonymous hemianopsia
Scotomas
67
What does complete damage to CN II cause?
Complete blindness
| Pupil dilated, unreactive to direct light but reactive to light stimulus to the opposite eye [consensual light reflex])
68
What are risk factors for developing HO in TBI?
* Prolonged coma (>2 weeks)
* Immobility
* Limb spasticity
* Long-bone fracture
* Pressure ulcers
* Edema
69
What is the period of greater risk to develop HO in TBI?
3 to 4 months post-injury
70
What are the MC joints involved in for HO in TBI?
1. Hips (most common)
2. Elbows/shoulders
3. Knees
71
What are signs/symptoms of HO?
```
Pain
Dec ROM
Local swelling
Erythema
Warmth in joint
Muscle guarding
Low-grade fever
```
72
What lab work can indicate HO?
Elevated Serum alkaline phosphatase (SAP) but poor specificity
73
What is the most sensitive method of early detection of HO?
Seen within the first 2 to 4 weeks after injury in a triple phase bone scan
74
What are x-rays helpful for in HO?
Confirm maturity of HO
| Require 3 weeks to 2 months post-injury to reveal HO
75
What are prophylaxis treatment of HO?
* ROM exercises
* Control of spasticity
* (NSAIDs)
76
What are treatments to arrest HO?
Bisphosphonates
Indomethacin
ROM exercises
77
When can surgical removal of HO be done?
Surgical resection usually postponed 12 to 18 months to allow maturation of HO
78
What is the preferred form of feeding when oral feeding is compromised in TBI?
Enteral feeding
79
What is the biggest risk with enteral feeding?
Aspiration which is inc with GERD and proximal tube placement
80
When should parenteral feeding be utilized?
Tempory interruption of GI function or inc metabolic demand
81
When is Total parental nutrition (TPN) is preferred?
Segment of GI tract is nonfunctional, or must be free of food for a prolonged amount of time
82
When should TBI patients be screened for endocrine function?
3 months and at 1 year post-injury regardless of injury severity
83
What is the recommended endocrine screening labs for TBI?
```
AM cortisol
Insulin growth factor (IGF)-I
Follicle-stimulating hormone (FSH)
Luteinizing hormone (LH)
Testosterone
Estradiol
Prolactin
Urinary free cortisol
```
84
What is SIADH?
Water retention resulting from excessive antidiuretic hormone (ADH) secretion from the neurohypophysis
85
What medication can cause SIADH?
Carbamazepine
86
What are signs of mild SIADH?
Na 130-135
Anorexia
N/V
87
What are signs of severe SIADH?
Inc body wt
| Cerebral edema: restlessness, irritability, confusion, convulsions, coma
88
What are treatments for SIADH?
Fluid restriction of 1L/day
3% saline
Do not correct >10 mEq/L over 24 hours until Na reach 125 mEq/L
89
How is chronic SIADH treated?
Demeclocycline, which normalizes serum Na+ by inhibiting ADH action in the kidney
90
What is the hallmark of cerebral salt wasting (CSW) syndrome?
Dec BV 2/2 Na loss in urine l/t inc ADH secretion which is appropriate
91
What is the treatment for CSW?
Hydration/fluid replacement + electrolyte (Na+) correction
92
What can cause diabetes insipidus?
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
93
What are treatments for diabetes insipidus?
DDAVP (desmopressin acetate)
| Chlorpropamide
94
What does cognitive remediation include?
Visuospatial rehabilitation, executive control, self-monitoring, pragmatic interventions, memory retraining, and strategies to improve attention
