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PMR 03 - TBI > Day 1 - Pathophysiology > Flashcards

Day 1 - Pathophysiology Flashcards

1
Q

List 8 Risk factors for ABI

A
  1. Too young <5 years or too old >65 years
  2. Male > Female
  3. Violence/assault
  4. Ethyl alcohol (ETOH) use
  5. Substances abuse
  6. Prior psychiatric history
  7. less likely to participate in preventative measures such as wearing seatbelts
  8. poor stander housing
  9. increased exposure to high risk occupations
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2
Q

Etiology of TBI in Adults

A
  1. MVA: 53%
  2. Falls: 24%
  3. Violence: 13%
  4. Alcohol-related injuries: 46%
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3
Q

Etiology of TBI in Pediatrics

A
  1. Falls (72.8%)
  2. Transportation related (28%)
  3. Sports and recreational activities (17%)
  4. Assault (7%)
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4
Q

Shaken baby syndrome (SBS) Triad

A
  1. Subdural haemorrhage
  2. Retinal bleeding
  3. Hypoxaemic encephalopathy or brain swelling
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5
Q

Age is considered risk factor in ABI with prognosis for couple reasons, mention 2.

A
  1. Decreased balance and syncopal episodes → Falls
  2. Fragile bridging veins → SDH
  3. On anticoagulant → Bleeding
  4. less neuronal plasticity
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6
Q

Open vs Closed TBI

A
  • An open, or penetrating TBI , when head is hit by an object that breaks the skull and enters the brain.
  • A closed TBI occurs when the brain is injured but the skull remains intact.
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7
Q

Non-traumatic causes of ABI include 🔑🔑

A
  1. Focal brain lesions
  2. Anoxia
  3. Vumours
  4. Vascular malformations (aneurysm)
  5. Infections of the brain (Encephalitis, Meningitis)
  6. Stroke
  7. Toxic brain injury
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8
Q

Definition of Primary Injury

A

Direct disruption of the brain tissue from impact which occurs immediately (minutes to hours after the impact) and is not amenable to medical intervention.

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9
Q

Definition of Primary Injury

A

Direct disruption of the brain tissue from impact which occurs immediately (minutes to hours after the impact) and is not amenable to medical intervention.

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10
Q

Mechanisms and location of primary injury

A

1- Contusions

Coup Injury: Contusions under the impact site and result from a rapid change in skull distortion during impact.

Counter Coup Injury: Contusions in the opposite to the impact occur due to negative pressure generated

2- Diffuse axonal injury (DAI)

Result from acceleration–deceleration and rotational forces

Lead to loss of consciousness and coma

MRI: White matter punctate petechial hemorrhages

3- Impact depolarization

Increase in extracellular potassium and glutamate release (excitatory) → excitotoxicity (secondary injury).

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11
Q

Definition of Secondary Injury

A

Cascade of biochemical, cellular, and molecular events, which include both endogenous cerebral damage as well as extracerebral damage that comes with trauma.

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12
Q

Mechanisms of secondary injury include 🔑🔑

A
  1. Secondary cerebral swelling (brain swelling and brain edema)
  2. Ischemia and apoptosis
  3. Axonal injury
  4. Inflammation and regeneration

Swelling results in elevated intracranial pressure (ICP) and decreased cerebral perfusion pressure (CPP). If severe enough, brain swelling can lead to herniation, which has potentially fatal consequences.

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13
Q

Definition of Focal Injury

A

Localized injury in the brain occurring immediately after the injury and easily visualized by CT or MRI

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14
Q

Mechanisms or types of focal injury include

A
  1. Cerebral contusions
  2. Focal hemorrhages
    • Epidural hematoma (EDH) 90%
    • Subdural hematoma (SDH)
    • Subarachnoid hemorrhage (SAH)
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15
Q

Primary Injury vs Secondary Injury. Definition & Types.

A

PRIMARY INJURY

Direct disruption of the brain tissue from impact which occurs immediately (minutes to hours after the impact) and is not amenable to medical intervention.

1- Contusions

Coup Injury: Contusions under the impact site and result from a rapid change in skull distortion during impact.

Counter Coup Injury: Contusions in the opposite to the impact occur due to negative pressure generated

2- Diffuse axonal injury (DAI)

Result from acceleration–deceleration and rotational forces

Lead to loss of consciousness and coma

MRI: White matter punctate petechial hemorrhages

3- Impact depolarization

Increase in extracellular potassium and glutamate release (excitatory) → excitotoxicity (secondary injury).

SECONDARY INJURY

Cascade of biochemical, cellular, and molecular events, which include both endogenous cerebral damage as well as extracerebral damage that comes with trauma.

Mechanisms of secondary injury include 🔑🔑

  1. Ischemia, excitotoxicity, energy failure, and resultant apoptosis
  2. Secondary cerebral swelling (brain swelling and brain edema)
  3. Axonal injury
  4. Inflammation and regeneration
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16
Q

DAI is unique to TBI. Its classification is based on severity 🔑

A

Grade I

  • Widespread white matter/axonal damage
  • No focal abnormalities on imaging

Grade II

  • Widespread white matter/axonal damage
  • Focal findings (most common in the corpus callosum)

Grade III

  • Damage involving the brainstem
17
Q

List 3 cases of DAI

A

DAI is the distinguishing feature of traumatic brain injury due to high-speed accidents.

Pic: Dai yoshihara = drifting, helmet, baby face (Japanese)

  1. High-speed motor vehicle collisions above 15 mph or 24 km/h.
  2. High-speed collisions in sports (i.e. football, hockey, soccer, rugby)
  3. Shaken baby syndrome.
18
Q

Necrosis vs Apoptosis

A

Apoptosis

  • Programmed cell death, is a form of cell death that is generally triggered by normal, healthy processes in the body.

Necrosis

  • Premature death of cells and living tissue. Caused by factors external to the cell or tissue, such as infection, toxins, or trauma
19
Q

Factors help in brain plasticity.

A

Athlete training for competing:

  1. Environment
  2. Motivation.
  3. Complexity of stimulation
  4. Repetition of tasks
20
Q

List 4 Recovery mechanisms 🔑🔑

A
  1. Neuroplasticity
    • Neuronal regeneration and collateral sprouting
    • Functional reorganization
  2. Synaptic Alterations
    • Diaschisis: Initial loss of function secondary to depression of areas of the brain connected to the primary injury site, and resolution is parallel to the recovery of the focal lesion.
  3. Functional Substitution/Behavioral
    • Redundancy: Recovery of function based on uninjured brain areas that normally would contribute to that function
    • Vicariation: Functions taken over by brain areas not originally managing that function.
    • Substitution: Techniques/new strategies are learned to compensate for deficits and to achieve a particular task.
21
Q

What is your initial management of newly admitted TBI patient? 🔑

A
  1. Neuromedical stabilization
  2. Manage bowel and bladder function
  3. Maintain nutrition
  4. Maintain skin integrity
  5. Control spasticity
  6. Prevent contractures
22
Q

List 4 Advantages to use CT 🔑

A
  1. Rapid, reliable & convenience
  2. Relatively low cost
  3. Detects facial and skull fractures
  4. Detect mass lesions requiring immediate surgical intervention.
23
Q

List 4 Advantages to use MRI 🔑

A

Advantages

  1. Good for non Hge lesions
  2. Defining the lesions and extent of injury
  3. Guiding treatment options
  4. Prognostication of lesions in small structures such as the brainstem and for DAI.

Disadvantages

  1. Time consuming
  2. Foreign bodies or implanted devices maybe inside the patient

Sequences

  • T1-weighted maging is preferable to define anatomy
  • T2-weighted sequences highlight edematous, high water content tissue.
24
Q

Canadian CT Head Rule 🔑

A
  1. GCS < 15 at 2 hours after injury
  2. Vomiting > 2 episodes
  3. Age ≥ 65 years old
  4. Basal skull fracture
  5. Open or depressed skull fracture
25
Q

Indication of endotracheal intubation

A
  1. Desaturation to maintain oxygenation
  2. Airway protection is indicated in patients with GCS <9
  3. Correction of hypoxia
26
Q

List 4 Pupillary findings correlate with poor outcomes

A
  1. No pupillary responses
  2. Bilateral fixed dilated pupils
  3. Gaze deviations to the ipsilateral side
  4. Loss of corneal
  5. Loss of oculocephalic reflexes
27
Q

Definition of high ICP 🔑🔑

A
  • Normal ICP is 0 to 10 mm Hg,CP levels up to 15 mmHg are considered harmless
  • Elevated ICP: Defined as ICP >20 mmHg for more than 5 minutes
28
Q

Measurements of Cerebral blood perfusion pressure (CPP)

A

CPP = MAP – ICP.

Mean arterial pressure (MAP) = DP + 1/3(SP – DP) or MAP = DP + 1/3(Pulse pressure)

Recommendations are to maintain a CPP between 60 and 70 mm Hg in adults.

29
Q

What are the goals of lowering ICP?

A
  1. Reducing cerebral edema
  2. Decreasing metabolic demand
  3. Maintaining adequate cerebral blood flow
30
Q

Complication of high ICP

A
  1. Deformation of tissue
  2. Brain shifts
  3. Herniation
  4. Cerebral ischemia.
31
Q

List 4 methods to monitor ICP 🔑🔑

A
  1. Papilledema
  2. Lumbar puncture (LP) if no papilledema (must rule out mass lesion first)
  3. Intraventricular ICP monitoring
  4. CT scan
32
Q

List 4 factors that may increase ICP 🔑

A
  1. Turning head, especially to left side if patient is completely horizontal or head down
  2. Loud noise
  3. Vigorous physical therapy
  4. Chest physical therapy (PT)
  5. Suctioning
  6. Elevated blood pressure
33
Q

List 4 ways to decrease ICP 🔑

A
  1. Decompressive craniectomy
  2. Osmotic agent, diuretics, and hypertonic solutions
  3. CSF drainage
  4. Sedation
  5. Brief hyperventilation → S/E Metabolic acidosis
34
Q

What two osmolar therapies are regularly used in clinical settings, despite mixed evidence on their efficacy?

A
  1. Hypertonic saline
  2. Mannitol
35
Q

List 4 findings that raise the suspension of herniations 🔑

A
  1. Papilledema
  2. LOC (Coma or stupor)
  3. Paresis or posturing.
  4. Cheynes–Stokes pattern of breathing.
  5. Cardiopulmonary arrest.
36
Q

List 3 CT findings in high ICP

A
  1. Midline shift
  2. Sulcal effacement
  3. Ventricular effacement slit like
37
Q

Indication for surgical operation

A
  1. Penetrating injury
  2. Compound depressed skull fracture
  3. Epidural hematoma
  4. Subdural hematoma
  5. Focal contusion or intracerebral hemorrhage

PMR 03 - TBI (8 decks)

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