Ch 2 - TBI: Pathophysiology Flashcards Preview

Cuccurullo 3rd Edited > Ch 2 - TBI: Pathophysiology > Flashcards

Flashcards in Ch 2 - TBI: Pathophysiology Deck (50)
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1
Q

What is the MCC of head injury in adolescents and adults?

A

Motor vehicle accidents (~50% of cases)

2
Q

What is the single MCC of death and injury in automobile accidents?

A

Ejection of occupant from the vehicle

3
Q

What is the married status of patients with TBI?

A

Single (47%) > married (32%) > divorced (16%) > widowed/separated (5%)

4
Q

What % of TBI etiology involve alcohol?

A

> 50%

5
Q

What is Primary Injury in TBI?

A

Direct disruption of brain parenchyma from shear forces of the impact occurring immediately and not amenable to medical intervention

6
Q

What are types of Primary Injury in TBI?

A

Contusion
Diffuse axonal injury (DAI)
Impact depolarization

7
Q

What is brain contusion?

A

Bruising of the cortical tissue

8
Q

What is Diffuse axonal injury (DAI)?

A

Immediate disruption of the axons due to acceleration–deceleration and rotational forces that cause shearing upon impact

9
Q

What is secondary axotomy in DAI due to?

A

Increased axolemma permeability, calcium influx, and cytoskeletal ABN that propagate after the injury

10
Q

What is the characteristic of DAI on imaging?

A

White matter petechial hemorrhages

11
Q

What is impact depolarization?

A

Massive surge in extracellular K+ and glutamate release (excitatory) occurs after severe head injury and leads to excitotoxicity (secondary injury)

12
Q

What are types of secondary injury in TBI?

A

Ischemia, excitotoxicity, energy failure, and resultant apoptosis
Brain swelling/edema
Axonal injury
Inflammation and regeneration

13
Q

What is excitoxicity?

A

NT (glutamate) causes calcium influx, oxygen-free radical release, lipid peroxidation, mitochondrial failure, and DNA damage > nerve cell death

14
Q

When does brain swelling occur after TBI?

A

w/in 24 hours due to an increase in cerebral blood volume (intravascular blood).

15
Q

How is brain swelling identified on CT?

A

Collapse of ventricular system and loss of CSF cisterns around the midbrain

16
Q

When does brain edema occur after TBI?

A

Later than brain swelling due to an inc in brain volume 2/2 inc brain water content > extravascular fluid

17
Q

What is the pathophysiology of vasogenic brain edema?

A

Outpouring of protein rich fluid through damaged vessels

18
Q

What pathology is vasogenic brain edema related to?

A

Extracellular edema

Cerebral contusion

19
Q

What is the pathophysiology of cryptogenic brain edema?

A

Failing of the cells’ energy supply system > inc cell-wall pumping system> intracellular edema in the dying cells

20
Q

What pathology is cryptogenic brain edema related to?

A

Hypoxic and ischemic brain damage

21
Q

What is focal injury in TBI?

A

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

22
Q

What are types of focal injury in TBI?

A

Cerebral contusions
Focal ischemia
Focal hemorrhages

23
Q

How do cerebral contusions occur?

A

Brain hits the inner table of the skull

24
Q

Where do cerebral contusions typically occur?

A

Inferior frontal lobe and anterior portion of the temporal lobe

25
Q

How does focal ischemia occur (pathophysiology)?

A

2/2 vasospasms after a traumatic SAH or from physical compression of the arteries

26
Q

What are types of focal hemorrhages?

A

Epidural
Subdural
Subarchnoid

27
Q

How do epidural hemorrhages occur?

A

90% temporal bone fx over the middle meningeal artery or veins

28
Q

What is the clinical presentation of epidural hemorrhages?

A

Lucid interval (50%) prior to rapid deterioration

29
Q

What is seen on CT in epidural hemorrhages?

A

Biconvex acute hemorrhagic mass

30
Q

What limits hematoma expansion in epidural hemorrhages?

A

Tight adherence of the dura to the skull

31
Q

How do subdural hematomas occur?

A

Shearing of the bridging veins between the pia-arachnoid and the dura

32
Q

Why are subdural hematomas typically larger in elderly patients?

A

Due to generalized loss of brain parenchyma

33
Q

What is seen on CT in subdural hematomas?

A

High density, crescentic, extracerebral masses

34
Q

When is the presentation of symptoms in subdural hematomas?

A

Acute SDH: Immediate sx
Subacute SDH: 3 days-3 wks
Chronic SDH: > 3 weeks

35
Q

How do subarchnoid hemorrhages occur?

A

Ruptured cerebral aneurysms and AVMs
Leakage from an intraparenchymal hemorrhage
Trauma

36
Q

What is seen on CT in subarchnoid hemorrhages?

A

Blood w/in the cisterns and subarachnoid space ~ 24 hr

37
Q

When does CT sensitivity decrease in subarchnoid hemorrhages?

A

Dec to 30% 2 weeks after the initial bleed

38
Q

What is a grade I DAI?

A

Widespread white matter/axonal damage but no focal abnormalities on imaging

39
Q

What is a grade II DAI?

A

Widespread white matter/axonal damage, and focal findings (MC in the corpus callosum)

40
Q

What is a grade III DAI?

A

Damage involving the brainstem

41
Q

When is DAI initiated?

A

Time of the injury by axonal shearing from acceleration–deceleration rotational forces

42
Q

What is the MCC of unconsciousness during first 24 hours after DAI?

A

Axonal injury

43
Q

Which types of TBI have a higher risk of posttraumtic epilepsy?

A

Penetrating head injuries

44
Q

What is brain plasticity?

A

Capability of the damaged brain to “repair” itself by means of morphologic and physiologic responses

45
Q

What is brain plasticity influenced by?

A

Environment
Complexity of stimulation
Repetition of tasks
Motivation

46
Q

What are the two mechanisms of brain plasticity?

A
  • Neuronal regeneration/neuronal (collateral) sprouting

- Functional reorganization/unmasking neural reorganization

47
Q

What is Diaschisis?

A

Damage to one region of the CNS alter function of uninjured area fiber tracts causing loss of function at both sites

48
Q

How does functional/behavioral substitution help recovery in TBI?

A

New strategies are learned to compensate for deficits and to achieve a particular task

49
Q

How does redundancy help recovery in TBI?

A

Uninjured brain areas normally contribute same function of injured brain

50
Q

How does vicariation help recovery in TBI?

A

Brain areas alter their properties in order to subserve that function

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