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PMR 03 - TBI > Day 6 - Flash Cards > Flashcards

Day 6 - Flash Cards

1
Q

Describe the flow of cerebrospinal fluid

A
  1. choroid plexus (production of CSF).
  2. lateral ventricles.
  3. foramen of Monroe (intraventricular foramen).
  4. 3rd ventricle.
  5. cerebral aqueduct of silvius.
  6. 4th ventricle.
  7. foramen of luschka x 2 (lateral) & foramen of magendie (midline).
  8. subarachnoid space/cisterna magna/central canal/basal cistern.
  9. arachnoid granulations/villi
  10. jugular vein.
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2
Q

What is the definition of TBI?

A

Craniocerebral trauma arising from blunt or penetrating trauma or from acceleration/deceleration forces

Associated with:

  • skull fracture
  • intracranial lesions
  • decreased level of consciousness
  • amnesia
  • death

Ref: Brain Injury Medicine, p46, quoting CDC definition

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3
Q

What are the usual locations for contusions in TBI?

A

inferior frontal or orbitofrontal areas.

antero-medial temporal lobes.

Ref: http://www.abiebr.com/set/case-study-4/42-multiple-focal-brain-injuries

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4
Q

Who is at risk for TBI?

A
  • M:F 3:1 (ERABI)
  • Highest rate of injury in young men 15-24yo.
  • Trimodal: < 5yrs, 15-24 yrs, and >75 yrs.
  • Previous TBI (3x for 2nd, 8x for third)
  • EtOH (up to 45% of TBI has EtOH involvement).
  • Substance use.

Ref: ABIEBR, Review notes 2012

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5
Q

What are the causes of TBI?

A

Overall: Motor vehicle collision (MVC)

Adults 19-25yo: MVCs, violence

Children <19yo: Abuse, sport-related injuries, falls

Elderly >65yo: Falls

ABIEBR

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6
Q

What is consciousness?

A

A state where a patient is cognitively aware and able to interact with internal and external environmental stimuli in a meaningful way.

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7
Q

What is coma?

A

Coma is state of unconsciousness, where patient is not opening eyes, not obeying commands, and not speaking understandable words.

GCS of 8 or less in acute period is defined as the comatose state.

Ref: Delisa, pg 575.

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8
Q

What is vegetative state?

A

A state that typically follows a period of coma, where there is some evidence of wakefulness (eye opening) without any sustained or reproducible responses to the environment.

Ref: Braddom pg 1144.

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9
Q

What is minimally conscious state?

A

A condition of severely altered consciousness in which there is evidence of self or environmental awareness.

Diagnosis of MCS made on clear evidence of one of the following:

  1. Understandable verbalization.
  2. Simple command following.
  3. Recognizable verbal or gestural ‘yes/no’ responses (accuracy not important).
  4. Emotional responses triggered by relevant environmental stimuli (not reflexive activity).

Ref: BI medicine textbook, pg 424-5.

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10
Q

Describe the basic levels of consciousness, from full alertness to deep coma.

A

Alertness: awake and fully aware of normal external and internal stimuli.

Lethargy: not fully alert and tends to drift off to sleep when not actively stimulated.

Obtundation: difficult to arouse, and when aroused, is confusional.

Stupor and semicoma: respond only to persistent and vigorous stimulation.

Coma: completely unarousable and remain with their eyes closed.

The Mental Status Examination in Neurology p30

Memory aid: the 3 ambiguous ones (lethargy, obtunded, and stuporous) are arranged in alphabetical order.

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11
Q

What is the difference between minimally conscious state and vegetative state?🔑🔑

A

MINIMALLY CONSCIOUS STATE

  • Severely altered consciousness
  • Patient is awake
  • Evidence of awareness of self or environment

VEGETATIVE STATE

  • Severely altered consciousness
  • Evidence sleep-wake cycle
  • No awareness of self or environment.

COMA

  • Severely altered consciousness
  • No sleep-wake cycles
  • No awareness of self or environment.
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12
Q

List 5 negative prognostic factors in TBI outcome.

A

Patient

  1. age (<5 and > 65 worse outcomes).
  2. gender (female – esp post concussive symptoms).
  3. prior brain injury.

Injury

  1. injury etiology. (violent has poor prognosis)
  2. pupillary reaction to light.
  3. doll’s eye sign.
  4. neuroimaging (bilateral brainstem lesions, depth of injury, midline shift, SDH, EDH, SAH, cisternal effacement).
  5. injury severity.
  6. initial GCS score.
  7. length of coma.
  8. duration PTA.
  9. flat EEG (isoelectric activity).
  10. timing of rehab.
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13
Q

List 5 signs of uncal herniation.

A

💡 Herniation into brainstem = cranial nerves, cross symptoms and breathing.

  1. Ipsilateral dilated pupil that is unresponsive to light
  2. Ptosis may occur due to oculomotor nerve palsy
  3. Lateral deviation due to unopposed abducens nerve
  4. Vertical gaze palsy
  5. Contralateral hemiparesis.
  6. LOC (compression of the reticular activating system → lethargy, coma, or death)
  7. Cheyne-stokes respirations (aabnormal breathing patter)
  8. Bilateral decerebration (rarely decorticate).
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14
Q

What are 6 characteristics of frontal lobe dysfunction?

A
  1. Personality changes.
  2. Lack of inhibition (socially inappropriate anger, agitation, aggression).
  3. Apathy/abulia (lack of initiation or motivation).
  4. Impaired concentration.
  5. Frontal eye field involvement – deviation of the eyes to the ipsilateral side
  6. Lack of sacral inhibition → incontinence bowel and bladder.
  7. Reduced fluency of speech (e.g. Broca’s)
  8. Delayed response to questions.
  9. Gait apraxia.
  10. Motor abnormalities (contralateral spastic paralysis, U > L Limbs)
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15
Q

What is an open head injury?

A

Penetrating head injury = open head injury.

Occurs when the DURA MATER IS BREACHED

Ref: Wikipedia, http://en.wikipedia.org/wiki/Penetrating_head_injury, Review notes 2012

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16
Q

List 4 complications of sub-arachnoid hemorrhage.

A
  1. Seizures/epilepsy.
  2. Ischemia
  3. Hydrocephalus
  4. Increase ICP
  5. Brain herniation
  6. CN compression
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17
Q

What are the three structures involved in consciousness?

A
  • RAS (Reticular activating system).
  • Thalamus.
  • Cerebral cortex.
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18
Q

How do you clinically distinguish syncopal episodes from seizures?

A

Syncope

  • Posture (occurs during prolonged standing)
  • provoking factors (e.g., pain, procedure), and
  • prodrome (e.g., sweating, nausea, warmth).

Seizure is suggested by

  • Tongue biting,
  • head turning during loss of consciousness,
  • no recollection of abnormal behavior,
  • prolonged limb jerking (lasting minutes),
  • post-event confusion, and
  • prodromal déjà vu.
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19
Q

Define hydrocephalus ex vacuo.

A
  • Not true hydrocephalus
  • Enlargement of ventricles due to loss brain tissue (most commonly brain atrophy)
  • Usually as a function of normal aging
  • Less likely responsive to shunting
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20
Q

What is the definition of a post-traumatic headache?

A

Secondary headache that develops within 7 days of head trauma (or regaining consciousness after TBI)

Ref: International Classification of Headache Disorders

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21
Q

List 4 brain structures involved in memory.

A
  1. hippocampus
  2. amygdala
  3. mammillary body
  4. parahippocampal gyrus
  5. dentate gyrus
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22
Q

In terms of the locations of where DAI (diffuse axonal injury) occur, what are the clinical implications?

A
  • Corpus callosum – cognitive dysfunction.
  • Cerebral peduncles – hemiparesis or tetraparesis.
  • Grey white matter junction – slow processing.
  • Cerebellar peduncles – ataxia dysmetria and nystagmus and motor impairment.
  • Brainstem – alteration in level of consciousness.
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23
Q

What is Adam’s classification for Grading of DAI?

A

Grade 1: DAI present (white matter, corpus callosum, brainstem, less commonly cerebellum), no hemorrhage in corpus callosum or brainstem

Grade 2: DAI present, also focal lesion in corpus callosum

Grade 3: DAI present, also focal lesions in both corpus callosum or brainstem.

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24
Q

What is the neurotransmitter that is neurotoxic to the brain?

A

Glutamate.

Ref: Brain injury medicine textbook, pg 82.

This occurs by increasing the permeability of the cell membrane that increase the influx of Ca and sodium, causing an increase in free radicals, leading to more increase glutamate and then increase in cell death.

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25
Q

What is the definition of primary injury?

A

The damage that occurs directly and immediately as a result of trauma to the brain.

Ref: Delisa pg 577.

The damage that results directly from the shear forces at impact.

Ref: Brain Injury textbook pg 81.

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26
Q

List 4 types of primary injury after TBI.

A
  1. Cerebral contusion
  2. Cerebral laceration
  3. Intracerebral hemorrhage
  4. Subdural hemorrhage
  5. Subarachnoid hemorrhage
  6. Epidural hemorrhage
  7. Axonal stretch injury
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27
Q

What is the definition of secondary injury?

A
  1. Cerebral Edema
  2. Raised intracranial pressure
  3. Brain herniation
  4. Ischemia (insufficient blood flow)
  5. Cerebral Hypoxia (insufficient oxygen in the brain)
  6. Hypotension
  7. Impaired metabolism
  8. Free radical formation
  9. Excitotoxicity
  10. Infection
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28
Q

What are the biochemical changes that can occur with TBI?

A
  • High K, Ca, Na, Glutamate, Excitatory neurotransmitters
  • Decrease Serotonin and Dopamine
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29
Q

What are 4 signs of a basal skull fracture?

A
  1. Raccoon eyes (periorbital ecchymosis)
  2. Battle’s sign
  3. CSF otorrhea
  4. CSF rhinorrhea
  5. Hemotympanum
  6. Pneumocephalus

(Zasler, Brain Injury Medicine textbook)

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30
Q

Name two lab tests to distinguish CSF leak versus mucous discharge from the nose of a TBI patient?

A

quantitative glucose (>30 mg% for CSF; < 5 mg% from lacrimal secretions and mucus) - sensitive, not specific (45-75% false positive)

beta-2-transferrin (present in CSF, absent in tears, saliva, nasal fluid, and serum).

Ref: Greenberg – handbook of neurosurgery textbook, pg 175-176.

http://www.utmb.edu/otoref/grnds/CSF-leak-091120/CSF-leak-091120.pdf

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31
Q

List 4 Mechanisms of hypoxic brain injury.

A
  1. Stroke
  2. Cardiac arrhythmia or arrest.
  3. ARDS or Oxygenation failure.
  4. CO poisoning
  5. Attempted hanging.
  6. Near drowning.
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32
Q

List 3 brain structures sensitive to hypoxic/anoxic injury following cardiac arrest and list two impairments patients may sustain as a result.

A

basal ganglia (movement disorder)

Cerebral cortex (cognitive impairments)

hippocampus (memory impairments)

cerebellum (purkinje cells)

Ref: Archives PMR Vol 89, Suppl 1, March 2008, S16-17 (BI study guide supplement).

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33
Q

Name 4 mechanisms of recovery from TBI. 🔑🔑

A

Redundancy وفرة

Recovery of function occurs because a part of the brain that normally contributes to the function takes over the entire function.

Resolution of Diaschisis

Altered function also occurs at a distant area that was not initially injured but is connected to the initial site of injury. The recovery of the injured site then parallels the recovery of the non injured site.

Vicariation النيابة

Function is taken over by a part of the brain that does not usually do that function (unmasking).

Behavioral substitution الاستبدال

New strategies are learned to compensate for the behavioural deficit.

Ref: Secrets, pg 434.

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34
Q

List 3 measures of severity following TBI. 🔑🔑

A
  1. Glasgow Coma Scale (GCS)
  2. Duration of coma (Loss of consciousness)
  3. Duration of Post traumatic amnesia (PTA).

DeLisa

Extra

  • Alteration of consiousness
  • Structural imaging
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35
Q

What durations of loss of consciousness correlate to mild, moderate, severe, and very severe head injury?

A

Mild: < 15 min.

Moderate: 15min - 6 hours.

Severe: 6 – 48 hours.

Very severe: > 48 hours.

ERABI, module 1, pg 3.

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36
Q

Grade TBI severity according to length of coma.

A

Length of coma = amount of time patient unresponsive, eyes closed, no sleep-wake cycle

Mild TBI: up to 30 minutes

Moderate TBI: > 30 min, < 6 hours

Severe TBI: > 6 hours

Ref: Review notes 2012 - Cullen

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37
Q

What length of post-traumatic amnesia would correspond to mild, moderate, severe, and very severe TBI?

A

Mild: < 1 hour.

Moderate: < 1 day.

Severe: < 1 week.

Very severe: < 1 month (actually, 4 weeks).

Extremely severe: > 4 weeks.

Ref: Cuccurullo pg 60; ERABI module 1, pg 3:

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38
Q

List 4 indications for surgery in TBI.

A
  1. GCS < 9 with associated pupillary dilation.
  2. Midline shift > 5mm.
  3. Epidural hemorrhage > 30 cc in volume.
  4. Acute subdural hematoma > 1cm thickness.
  5. Subdural hematoma with neurologic deficits.

Ref: Brain injury medicine textbook pg 272-273.

39
Q

What are the diagnostic criteria for Mild Traumatic Brain Injury (according to the American Congress of Rehabilitation Medicine)?

A

ONE OR MORE

Any period of LOC for up to 30 min

Any loss of memory for events immediately before or after accident for as much as 24 hours

Any alternation of mental state at time of accident (dazed, disoriented, confused)

Focal neurological defecits that may or may not be transient

BUT where severity of injury DOES NOT EXCEED the following:

LOC > 30 min

PTA > 24 hrs

GCS <13 after 30 min

Ref: ACRM, Toronto “Guidelines for mild TBI), adapted from McCrea 2008 and Ruff 2005

40
Q

What are general prognostic indicators following TBI? i.e. threshold values and relation to Glasgow Outcome Scale (GOS)

A
  1. GCS - worse outcomes with lower scores (no threshold values)
  2. Coma duration - worse with longer duration (> 4 weeks)
  3. PTA - longer duration, worse outcomes (>3 months)
  4. Age - 65 yo older associated with worse outcomes
  5. Imaging - brainstem associated with worse outcomes

Ref: Brain Injury Medicine p177-179, Review notes 2012 - Cullen

41
Q

What is the definition of Post traumatic amnesia (PTA)?

A

PTA is the period during which individuals with a TBI “are unable to effectively encode and retain new information and experiences.”

Resolution of PTA clinically correlates with the period when incorporation of ongoing daily events occurs in the working memory.

Ref: ERABI

Brain is unable to form continuous day-to-day memories, also include a state of disorientation to time, place, and person.

42
Q

When is Posttraumatic amnesia (PTA) over?🔑🔑

A

Post traumatic amnesia is complete when the Galveston Orientation and Amnesia Test (GOAT) score of greater than or equal 75 on two consecutive days.

43
Q

List 8 risk factors for late post-traumatic seizures after TBI (late seizures).🔑🔑

A
  1. Prolonged coma or PTA (>24 hours): 35%
  2. Depressed skull fracture: 3% to 70%
  3. Focal signs such as aphasia and hemiplegia
  4. Penetrating head injury: 33% to 50%
  5. Presence of foreign bodies
  6. Intracranial hematoma: 25% to 30%
  7. Early PTS (>24 hours to 7 days): 25%
  8. Age
  9. Alcohol abuse
  10. Use of TCAs
44
Q

Define the following types of post-traumatic seizures & treatment 🔑🔑 Immediate - Early - Late - Post-traumatic epilepsy.

A

💡 Post-traumatic epilepsy: recurrent late seizure episodes not attributable to any other etiology than TBI.

  1. Immediate: < 24 hours after injury (treat for 7 days).
  2. Early: 24 hours to 7 days after injury (treat for 12 months).
  3. Late: > 7 days after injury (treat indefinitely).

Ref: Delisa, Cuccurullo pg 71.

45
Q

What length of time should a TBI pt have seizure prophylaxis? 🔑🔑

A

💡 Seizure prophylaxis not more than 7 days.

L1: anticonvulsants given in first 24 hours (1 day) post ABI reduces occurrence of early seizures.

L1: dilantin/carbamazepine have negative effects on cognitive performance (motor and speed components), which theoretically negatively impact learning during rehabilitation).

L1: Anticonvulsants given immediately post ABI reduce occurrence of seizures only within 1st week.

Ref: ERABI module 10, pg 20.

46
Q

What is second-impact syndrome and why is it important?

A

Occurrence of rapid cerebral edema after a second head injury that is sustained while an individual is still recovering from symptoms caused by a prior concussion.

Occurs when an athlete returns to sport too early after suffering from an initial concussion. The athlete may receive only a minor blow to the head or a hit to the chest or back that snaps the head enough to have the brain rebound inside the skull.

Morbidity = 100%.

Mortality = up to 50%.

47
Q

Name two tests used for assessment of concussion.

A
  1. Standardized Assessment of concussion (SAC)
  2. Sport Concussion Assessment Tool (SCAT)
  3. Maddock’s questions.

Ref: Braddom pg 1020

  1. McGill ACE.
  2. IMPACT (computerized evaluation).
  3. CogSport (computerized evaluation).

Ref: Delisa pg 1419.

48
Q

Athlete post-concussion with normal physical exam. What are the two most notable features in determining readiness to return to play? 🔑

A
  • Asymptomatic with exercise and at rest.
  • Asymptomatic with cognitive stress.

Ref: McRory (2008)

49
Q

At what value of increased ICP should one intervene according to guidelines after TBI?

A

Intervene once ICP > 20 mmHg.

Ref: Delisa pg 579.

50
Q

List four signs that suggest progressive increase in ICP.

A
  • Cushing’s triad (bradycardia, widened pulse pressure, irregular respirations).
  • Altered mental status (LOC, confusion).
  • Papilledema
  • Dilated pupil
  • Ocular palsies (CN 3, 4, 6).
  • Headache.
  • N/V.
  • Decerebrate posturing.
  • Respiratory arrest.

Smith, evaluation and mgmt of elevated ICP in adults – http://www.critical.med.ualberta.ca/en/FileArchive/~/media/criticalcare/Documents/EvaluationandManagementofElevatedIntracranialPressure.pdf.

51
Q

List 5 treatments for increased ICP.

A
  • Head elevated at 30 degrees.
  • Mannitol.
  • hypertonic saline.
  • sedatives (propofol, pentobarbital).
  • hyperventilation.

Ref: DeLisa pg 579.

  • treatment of hyperthermia.

Ref: Braddom pg 1140.

  • craniectomy (uni or bilateral).

Ref: BI medicine textbook, pg 274.

52
Q

What is the formula for calculating CPP (cerebral perfusion pressure)? Range?

A

CPP = MAP – ICP.

Mean arterial pressure; intracranial pressure.

MAP = 1/3rd sBP + 2/3rds dBP

Ref: Brain injury textbook pg 275.

50-70 mmHg.

Ref: DeLisa pg 579.

53
Q

List the features of normal pressure hydrocephalus 🔑🔑

A

💡 In patients with TBI, considered if worsens or fails to progress adequately.

Clinical triad:

dementia.

gait ataxia.

urinary incontinence.

Brain Injury Medicine p584

Gait impairment is the most important diagnostically, and most likely to respond to shunting

54
Q

What is cushing’s triad?

A

💡 Signs opposite of shock. Triad seen in intra-cranial hypertension.

increased BP (HTN).

decreased HR (bradycardia).

decreased/irregular respirations.

Ref: Greenberg textbook pg 649.

55
Q

List the hormones released by the anterior and posterior pituitary.

A

ANTERIOR PITUITARY - Go Find The Adenoma Please:

  1. GH
  2. FSH/LH
  3. TSH
  4. ACTH
  5. prolactin

POSTERIOR PITUITARY:

  1. vasopressin (ADH)
  2. oxytocin.

Ref: Medical physiology textbook, pdf, chapter 32.

56
Q

What time frames should TBI patient do endocrine evaluation? What tests to order? 🔑

A

EVALUATION TIME FRAME:

Hospital/ICU: baseline hormonal work-up and repeat if clinically indicated

3 months and 12 months post TBI: baseline hormonal work-up for all patients

Hint: Day 1 of TBI and 3 months after rehab program and 1 year follow up.

HORMONAL SCREENING:

  1. IGF-1 or growth hormone
  2. Prolactin
  3. FSH, LH → testosterone (men), estrogen – E2 (women).
  4. AM cortisol (9am) → urine free cortisol, density, NA, osmolality
  5. fT3, fT4, TSH.

Ref: Brain injury medicine textbook pg 680; Brain Injury, 20 August 2005; 19(9): 711–724.

57
Q

List 4 endocrine deficiencies in TBI patient. 🔑

A
  1. Growth hormone deficiency.
  2. Diabetes insipidus.
  3. Secondary adrenal insufficiency. (Addison’s disease)
  4. Secondary hypothyroidism.
  5. Secondary hypogonadism.
58
Q

List 3 clinical features of Acromegaly.

A
  1. skeletal overgrowth deformities (large hands/feet, thick heel pad, frontal bossing, prognathism, macroglossia).
  2. HTN.
  3. soft tissue swelling.
  4. peripheral nerve entrapment syndromes.
  5. debilitating H/A.
  6. excessive perspiration (palmar hyperhydrosis).
  7. oily skin.
  8. joint pain.
  9. CV disease (cardiomyopathy).
  10. respiratory disease (OSA).
  11. increased cancer risk (colon CA).
  12. increased risk DM.

Ref: Greenberg textbook pg 441.

59
Q

What is the most common hormonal problem seen in TBI? 🔑🔑

A

Growth hormone deficiency (21.7%) and gonadotropin deficiencies (45.7%)

Other study had more hypogonadism and hypothyroidism (>90%)

Note: evidence slightly conflicting. See reference for more discussion.

Ref: Brain Injury Medicine pg 680.

60
Q

What are risk factors for hypopituitarism in TBI?

A
  • Moderate-severe TBI (with GCS 10 or less)
  • Diffuse brain swelling
  • Hypotensive/hypoxic episode

Ref: Brain Injury Medicine p680

61
Q

State 2 differential diagnoses for hyponatremia in a patient with TBI

A
  • Cerebral salt wasting (CSW): often seen in SAH.
  • Syndrome of inappropriate anti-diuretic hormone secretion (SIADH).
  • psychogenic polydipsia.

Ref: Cuccurullo pg 87-88; Brain injury medicine pg 662.

62
Q

What is the definition of Syndrome of inappropriate anti-diuretic hormone ?

A
  1. Inappropriate release if anti-diuretic hormone, result in
  2. Hyponatremia (<135 mEq/L) and hypo-osmolality (<280 mOsm/L)
  3. Urine osmolality > plasma osmolality, urine Na is usually >25-30 mEq/L
  4. Severe cases: mental confusion, seizures, coma.

Ref: http://www.abiebr.com/set/1-47-year-old-single-male-vehicle-collision-rla-4-and-combative/14-syndrome-inappropriate’; Clin J Am Soc Nephrol 3: 1175–1184, 2008; Brain Injury Medicine p662

63
Q

Describe the mechanisms for CSW, SIADH, and DI.

A

CSW:

salt wasting (inability to resorb Na).

secondary volume depletion (hypovolemia).

resultant release of ADH (appropriate).

SIADH:

inappropriate secretion ADH (plasma iso or hypo-osmolality).

inability to excrete water (water resorbed through aquaporins)

concentrated urine

resultant hyponatremia

DI:

disruption of ADH secretion from posterior pituitary (Fracture near sella turcica, tearing pituitary stalk, etc).

inability to resorb water from kidneys

Ref: cuccurullo pg 87-89; brain injury medicine pg 662; Clin J Am Soc Nephrol 3: 1175–1184, 2008

64
Q

Lab result in SIADH 🔑🔑

A

Euvolemic

Serum Hyponatermia <135 mEq/L

Serum Osm <270 mOsm/kg

Urine Hypernatremia >40 mEq/L

Urine Osm >100 mOsm/kg

65
Q

Give one specific treatment for CSW, SIADH, DI.

A

CSW:

  • hydration (make sure NOT SIADH)
  • electrolyte replacements.

SIADH

  • fluid restriction 1L/day,
  • loop diuretics (furosemide),
  • salt intake
  • In severe cases, slowly increase Na (<10 mEq/day) with hypertonic saline
  • demeclocycline 600-1200 mg/day (for chronic SIADH)

Central DI

  • supplemental ADH (DDAVP – desmopressin acetate).

Ref: Cuccurullo pg 88-89, Lexicomp (for demeclocycline dose)

66
Q

List 8 causes of SIADH

A
  1. Meningitis/brain abscess.
  2. Encephalitis
  3. Trauma (TBI).
  4. SDH
  5. Tumor
  6. CVA/stroke.
  7. SAH..
  8. MS.
  9. Epilepsy.
  10. SAH
  11. Cystic fibrosis
  12. Tuberculosis
  13. Idiopathic
  14. TCA
  15. SSRI
67
Q

SIADH scenario, risk factors for death, what to worry about with treatment.

A

Risk factors:

  • Multifactorial
  • Hospitalized
  • Acute onset
  • Severe hyponatremia

Worry about

  • rapid overcorrection leading to central potine myelinolysis
  • not more than 10-12 mEq per 24 hours

Ref: emedicine.medscape.com/arrticle/246650-overview#aw2aab6b2b6

68
Q

Provide six historical or physical reasons why you wouldn’t give Botox in this situation in a TBI patient with spastic hemiparesis.

A
  1. Known sensitivity to botulinum
  2. Previous botox injection in the last three months.
  3. Concurrent treatment with aminoglycoside or spectinomycin antibiotics
  4. Neuromuscular or motor neuron disease.
  5. Upper eyelid apraxia
  6. Pregnancy and lactation safety unknown
  7. Infection at proposed injection site
  8. Joint contracture
  9. No functional goals or other gains (e.g. would not decrease pain, help with hygiene or caregiver needs).
  10. Weaken muscles and may decrease function.
  11. Previous botox injection in the last three months.
  12. Known antibodies to Botox
69
Q

Patient with TBI 2 weeks ago, now with swollen elbow and decreased ROM. Name 6 investigations you would order.

A

Blood

  1. CBC with differential (infection).
  2. ESR/CRP (Inflammation).
  3. Alkaline phosphatase (Heterotopic Ossification).

Imaging

  1. X-ray elbows AP/lateral
  2. Ultrasound dopplers (DVT).
  3. Ultrasound MSK (Bursitis)
  4. Triple phase bone scan (Heterotopic Ossification).
  5. CT scan.
  6. MRI scan.
70
Q

Treatment of Heterotopic Ossification (HO) in TBI.

A
  1. ROM Exercises
  2. Gentle stretching
  3. Etidronate
  4. Forceful manipulation under anesthesia
  5. Surgical excision

ERABI

Braddom

71
Q

Name 3 complications of Heterotopic Ossification (HO)

A

Bone

  1. Decreased joint range of motion.
  2. Contractures.
  3. Fractures

Connective Tissue

  1. Pain
  2. Pressure ulcers
  3. Spasticity

Vessels & Nerves

  1. Vascular compression.
  2. DVT
  3. Nerve compression.
  4. Lymphatic system compression.
72
Q

TBI scenario. Patient has hip pain, decreased range-of-motion, normal Dopplers, normal x-ray. Bone scan is positive. Diagnosis? Treatment? Three complications.

A

DDX

Heterotopic ossification (HO) – no fracture because normal XR.

TREATMENT:

conservative (CPM Level 5, force manipulation under anesthesia Level 4).

medications (etirdonate - Level 2)

interventional (PLIMF, radiation therapy, shockwave lithotripsy - not mentioned in ERABI).

surgical resection (Level 4).

COMPLICATIONS:

  1. Decreased joint range of motion.
  2. Contractures.
  3. Vascular compression.
  4. Nerve compression.
  5. Lymphatic system compression.
  6. Pain
  7. Pressure ulcers
  8. Spasticity
  9. Fractures
  10. DVT
73
Q

A case of TBI agitation with normal electrolytes – list 6 other causes.

A

Brain Insult

  1. Seizures
  2. Stroke, TIA, hypoperfusion, hypoxemia
  3. Mood disorders.
  4. Encephalitis, meningitis.
  5. Structural: Hydrocephalus, Intracranial bleeding

Body & Environmental

  1. Noxious stimuli (pain) HO, DVT, ingrown nail, spasticity
  2. UTI, bowel obstruction
  3. Overstimulation

Medical

  1. Medications & drugs
  2. Endocrine: Hypothyroidism, hypo/hypercortisolism
74
Q

Discuss the approach to agitated patient.

A

ETIOLOGY: identify causes (noxious stimuli, fractures, skin, tubes, tracheostomy, medical conditions, drugs, etc).

MONITORING: pt not left alone, one to one monitoring.

BEHAVIOURAL: Tolerate pt behaviours, scheduled voiding/BMs, reward and punishment

RESTRAINTS.

ENVIRONMENT: Decrease stimuli, familiar environment, safe environment (physical restraints).

MEDS: Atypical Anti-psychotics, Beta-blockers, AED (anti-epileptic drugs), Dopaminergic drugs, Stimulants, Anti-depressants, Buspirone (use meds last resort, if ABS > 28, and monitor effect with ABS with clear targets, eg ABS < 21).

target SLEEP WAKE cycle pattern.

Ref: Brain injury textbook, pg 289-90; http://www.abiebr.com/set/1-47-year-old-single-male-vehicle-collision-rla-4-and-combative/16-rancho-los-amigos-level.

75
Q

List 5 classes or specific medications commonly used to treat post-traumatic agitation.

A
  1. benzodiazepines.
  2. anti-convulsants (lamotrigine, carbamazepine, valproic acid, divalproex).
  3. 3.SSRI: sertraline (zoloft).
  4. anti-psychotics (risperidone <4 mg daily, quetiapine, ziprasidone, methotrimeprazine aka |Nozinaan).
  5. buspirone.
  6. amantadine (ERABI module 12 says no evidence).
  7. beta-blockers (pindolol, propranolol – cross BBB).
  8. lithium carbonate.

Ref: Brain Injury textbook, pg 290; specific drugs from - ERABI, module 8, pg 67.

76
Q

What are the recommended maximum doses of propranolol and pindolol for treatment of aggression?

A

propranolol: max dose 420-520 mg/day.
pindolol: max dose 40-100 mg/day.

NOTE: MOA likely from reduction in sympathetic activity.

Ref: http://www.abiebr.com/set/appendix/appx-abikus-guideline-2007

77
Q

Which two classes of medications should be minimized in treatment of aggressive/agitated behaviour because of concerns about slowed brain recovery?

A

benzodiazepines.

neuroleptic antipsychotic agents.

Note: animal studies suggest they slow recovery after brain injury.

Ref: http://www.abiebr.com/set/appendix/appx-abikus-guideline-2007

78
Q

What type of neurogenic bladder is most commonly seen in TBI patients?

A

Injury to frontal micturition centre which is sacral inhibition center → no inhibition.

Uninhibited detrusor reflex (contraction)

Disinhibited bladder with low volume, but empties completely

79
Q

What first line interventions may be helpful for urinary incontinence in TBI?

A

Timed voiding schedule

Anti-cholinergic medications (Oxybutynin)

80
Q

List 4 side effects of amantadine and MOA

A

💡 Amantadine is a weak, non-competitive antagonist of the NMDA receptor, which increases dopamine release and prevents dopamine reuptake. Dosing is 100-400/day total, 1 or 2 divided doses.

  1. Over-stimulation.
  2. Insomnia
  3. Hallucinations.
  4. Anxiety
  5. Agitation
  6. Lowering of seizure threshold (esp doses > 300 mg/day).

https://www.drugs.com/sfx/amantadine-side-effects.html

81
Q

List 4 side effects of methylphenidate and MOA

A

💡 Methylphenidate is norepinephrine and dopamine reuptake inhibitor (NDRI). Dosing 5-10 mg am/lunch, max 60 mg/day

  1. Headache
  2. Insomnia
  3. Irritability
  4. Decreased appetite
  5. Hallucinations
  6. Seizures

https://www.drugs.com/methylphenidate.html

82
Q

List 4 neurotransmitter and their function.

A
  1. Memory (Recall) → Acetylcholine
  2. Attention (To light) → Norepinephrine
  3. Mood (هرمون السعادة) → Serotonin
  4. Arousal (إثارة) → Dopamine
83
Q

What percentage of TBI pts with anosmia will recover in first 3 months?

A

50%. Ref: textbook Rehab of people with TBI.

84
Q

How to treat poor memory?

A

NON-PHARMACOLOGICAL:

Education for family and patient

Memory aids: computer, pager, diaries, agendas, calendars, family members, photos.

Verbal and visual cuing

Memory training: learning to ‘chunk’ information, memory games, mnemonics.

visual imagery.

didactic lessons, homework assignments.

PHARMACOLOGICAL:

Aricept -ie. donepezil (acetylcholinesterase inhibitor) - memory.

Improve attention: amantadine, methylphenidate.

physostigmine: memory in men with TBI.

Ref: EBRSR module 12 pg 34; ERABI module 12 pg 96.

85
Q

List 2 medications to improve attention

A

Donepezil (Level 1).

Amantadine (Level 4).

Ref: ERABI module 12.

86
Q

Following TBI, what medication may be helpful to treat insomnia?

A

Zoplicone or lorazepam equally effective (Level 1 ERABI)

1 RCT (7 day study) by Li Pi Shan!

87
Q

50 year old male, 2 weeks on rehabilitation unit, SAH 6 weeks ago. General decline x 3 days (incontinent, increasing difficulty with transfers, decrease LOC).

What is your differential diagnosis?

A

normal pressure hydrocephalus (non-obstructive/communicating hydro).

sepsis.

re-hemorrhage.

SIADH & other electrolyte abnormalities.

subclinical seizure activity.

medication and drug effects (eg. Overuse of opioids).

Ref: GL thoughts.

88
Q

A patient develops LOC after brain surgery (ventricle surgery). List 4 causes of LOC.

A
  1. infectious: meningitis, encephalitis.
  2. drugs: benzodiazepines, antidepressants.
  3. structural: hydrocephalus, increased ICP.
  4. vascular: anemia (blood loss).
  5. metabolic: electrolyte imbalance, hypo/hyperglycemia.
  6. neurologic:, hemorrhage, seizures, stroke, migraine.
  7. cardiopulmonary: cardiac arrest, DVT/PE, CHF.

Ref: GL thoughts.

89
Q

TBI pt, 2-3 months post injury. Marked swelling entire L upper extremity. No evidence lymphadenopathy. No evidence of infection on labs or physical exam. What is the most likely diagnosis? Give 3 differentials?

A
  • Most likely diagnosis : CRPS type 1 (RSD)
  • HO.
  • DVT.
  • trauma/fracture.

Ref: EK/GL thoughts.

90
Q

23 year old male involved in MVC 3 months ago, presenting with “mild TBI” symptoms. List three DDx.

A
  1. Mood disorder: Anxiety, depression, PTSD
  2. Malingering
  3. Alcohol and drug use
  4. Medication side effect

Ref: Review notes 2012

91
Q

Mild TBI: list 8 clinical factors that should lead clinical to further neuro-imaging (ie CT).

A
  1. Headache.
  2. Vomiting
  3. Sign of basal skull fracture
  4. Age > 60 years.
  5. Failure to reach GCS 15 within 2 hours.
  6. Short-term memory loss
  7. Seizure
  8. Drug or alcohol intoxication.

Ref: Haydel MJ, Preston CA, Mills TJ, et al. Indications for computed tomography in patients with minor head injury. N Engl J Med 2000; 343: 100–105.

Ref: Stiell IG,Wells GA, Vandemheen K, et al. The Canadian CT Head Rule for patients with minor head injury. Lancet 2001; 357: 1391–1396.

92
Q

What are the Canadian CT head rules?

A

age >/=65

any sign of basal skull fracture

vomiting >/=2 episodes

GCS <15 at 2hrs post injury

suspected open or depressed skull fracture

93
Q

With a TBI and shearing of the pituitary stalk, which part of the pituitary will be affected – anterior pituitary or posterior, and why?

A

Anterior pituitary will be affected as blood supply travels through the stalk

Posterior pituitary spared, because blood supply is through base of the skull.

PMR 03 - TBI (8 decks)

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