Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

VMCVM SAM 2 > Neurologic Emergencies > Flashcards

Neurologic Emergencies Flashcards

1
Q

most common causes of Traumatic Brain Injury

A

The most common causes of TBI in veterinary patients include motor vehicle accidents, falls, missile injury, and intra/interspecies aggression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

is there much you can do to treat primary injury?

A

nope, initial impact is unchangeable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Definition of primary injury

A

mechanical deformation to the calvarium and intracranial contents. Severity of injury is a function of the degree of impact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

define concussion:

A

microscopic damage, often more widespread, functional problem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

define contusion:

A

macroscopic damage, often more localized, a

bruise, functional and physical problem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

define coup:

A

site of impact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

define countercoup:

A

contralateral site of injury, usually less

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

define laceration:

A

physical disruption of the neuropil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

define fracture:

A

physical disruption of the calvarium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Examples of primary brain injury:

A

Concussion, contusion, laceration, fracture, hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Can you treat secondary injury to the brain?

A

YES this is what we aim to treat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Examples of secondary brain injury

A

ischemia, edema, excitotoxicity, acidosis, free radical production/oxidation - cytotoxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what does ischemia result in?

A

neuronal dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what does edema result in?

A

vasogenic: white matter damage
cytotoxic: white and grey matter
interstitial: csf obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what does excitotoxicity result in?

A

continual firing leading to overstimulation and cellular death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Importance of Increased Intra-cranial pressure

A
  • dec. cerebral blood flow causing hypoxic/ischemic injury

- brain herniation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the Monro-Kellie hypothesis?

A

The cranial vault is incompressible and contains a fixed volume with the intracranial contents at volume equilibrium. An increase in one must be compensated for by a decrease in volume of another.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the Cerebral Perfusion Pressure?

A

CPP is the difference between the mean arterial blood pressure and the intracranial pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What range of MABP (mean arterial blood pressure) do you need to maintain CPP in autoregulation?

A

50-150 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is status epilepticus?

A

a generalized seizure lasting >5 minutes or a series of generalized seizures without intervening periods of normal consciousness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Causes of status epilepticus

A 
Metabolic encephalopathy
Toxins
Intracranial neoplasia
Encephalitis
Vascular incident
Idiopathic epilepsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Metabolic causes of status epilepticus

A 
hypoglycemia
hypocalcemia
hepatic encephalopathy
uremic encephalopathy
hyperlipidemia
DKA/non-ketotic hyperosmolar Diabetes Mellitus
23
Q

Toxic causes of status epilepticus

A

Lead
OPs and Carbamates
Anti-freeze/ethylene glycol

24
Q

Complications of Status Epilepticus

A

Generally complications are a result of ongoing convulsive activity that leads to release of muscle enzymes, consumption of oxygen and glucose without replenishment, and decreased organ perfusion.

  1. Cerebral edema
  2. cortical Necrosis
  3. renal/hepatic failure
  4. hyperthermia
  5. rhabdomyolysis
  6. non-cardiogenic pulmonary edema
  7. cardiac arrythmias
  8. hypoglycemia
25
Q

Is it common for acute encephalopathies to be metabolic in origin? If so, what are they?

A

NO but they certainly can happen:

  1. Hypoglycemia**
  2. Hepatic encephalopathies
  3. Uremic encephalopathy
  4. Hyperlipidemia
  5. E+ disturbance (Hypocalcemia, Hypernatremia [cerebral dehydration], Hyponatremia [cerebral edema]
  6. Inborn errors of metabolism
26
Q

What rate should you NEVER EXCEED when replenishing Na+?

A

NEVER > 0.5mEq/L/hr

27
Q

What is Kussmaul pattern?

A

form of hyperventilation characterized by very DEEP, and LABORED breathing — DKA

28
Q

What is Cheynes-Strokes pattern?

A

ascending then descending respiratory rate followed by apnea — brain stem injury

29
Q

What is hypoventilation?

A

elevated PaCO2, low PaO2, normal Aa gradient, poor chest excursions, myopathy, phrenic nerve damage (C6-C8)

30
Q

Brain injury physical, labwork, imaging examination if suspect:

A
  • Always get TPR
  • Always get BP
  • Complete neuro exam if patient/once patient is stabilized
  • Lab-work Big 5: PCV/TP/Azo/BG/USG
    • if you can, get CBC/Chem/UA
  • Imaging: Skull fracture, Penetrating injury, Concurrent injury
  • Advanced imaging: same + *Not responding to treatment/getting worse and Elevated ICP; Status epilepticus
31
Q

What is the Cushing’s Reflex?

A

BP ≥ 160mmHg and HR < 60bpm

  • massive sympathetic discharge to keep dying brain alive
  • reflex bradycardia due to sensing of high BP
32
Q

TX of Traumatic Brain Injury

A
  1. Tx the Shock and Hemorrhage – Maintain BP (Colloid and crystalloid Combo best)
  2. Tx elevated ICP
  3. Tx seizures
  4. Sx if depressed skull fracture, penetrating/open/communicating injury
  5. NO STEROIDS EVER
  6. O2 supplementation
33
Q

What TX should you never do if you suspect brain injury?

A

NEVER GIVE STEROIDS

34
Q

How do you tx elevated ICP in traumatic brain injury?

A

Mannitol
Furosemide
Keep the jugular veins intact and no catheter
Head elevation 15-30˚
Slight HYPERventilation PaCO2 25-35mmHg
Sx - if neoplastic but generally not indicated

Last resort: Barbiturate coma

35
Q

When can you give steroids for brain damage?

A

Encephalitis AFTER Definitive DX has been made
Neoplasia - reduces peritumoral edema

NOT for trauma, NOT ischemic injury, NOT metabolic encephalopathy, NOT seizures

36
Q

How do you TX Status Epilepticus?

A

Stop the Seizure!

  • Benzos first! (Hypocalcemia and Hypoglycemia will respond to this initially but should be CHECKED to rule out)
  • If that doesn’t work: Propofol CRI
  • If that doesn’t work: Benzo CRI
  • If that doesn’t work: Pentobarbital

Prevent more seizures! Long-acting anti-convulsants

37
Q

What is refractory pain?

A

refractory to 3 or more medications

38
Q

How is PX if there is concurrent HYPOventilation?

A

terrible

39
Q

How do you assess spinal injury?

A
  • Physical: careful attention to CV status
  • *Intact nociception is the most important prognostic indicator**
  • get RADS or advanced imaging
40
Q

What is the Schiff-Sherington posture:

A

Extensor rigidity in thoracic limbs and pelvic limb paralysis

  • Lesion is at T3-L3
  • is NOT a prognostic indicator, just that there is severe spinal injury present
41
Q

What is spinal shock?

A

Flaccid rear limb paralysis +/- loss of nociception with panniculus a panniculus cut off
- This will resolve

42
Q

What is myelomalacia?

A

Appears same as spinal shock but will not resolve

  • Myelomalacia is progressive hemorrhage and necrosis of the spinal cord secondary to a traumatic lesion, usually a high velocity type I disc herniation.
  • is generally fatal
43
Q

How do you TX spinal cord injury?

A
  • Stabilize CV and Pulmonary ability
  • Pain control after neurologic assessment
  • Spinal stabilization: assess to see if unstable
  • Transport: keep in lateral recumbency
  • Conservative management if stable.

NO STEROIDS

44
Q

What is an unstable spinal cord injury?

A

according to the 3 compartment model: 2 of any 3 compartments damaged and next to each other

45
Q

External coaptation for cervical management

A

from behind eyes to behind scapula

46
Q

External coaptation for T-L injury management

A

from cranial to scapulae to the tail

- same as Lumbar

47
Q

External coaptation for Lumbar injury management

A

from cranial to scapulae to the tail

- same as T-L

48
Q

Indications for conservative management of spinal injury

A

i. Patients with minimal neurologic deficits and minimally
displaced fracture/luxations
ii. May be better for animals with high cervical trauma due to high surgical morbidity associated with lesion here (>40%)
iii. Client constraints

49
Q

Spinal injury PX

A

Sensory positive >80%

Sensory negative poor

50
Q

What can cause emergent motor unit problems?

A
  1. fulminate myasthenia gravis
  2. tick paralysis - dermacentor
  3. botulism
  4. coonhound paralysis
51
Q

What is key when evaluating motor unit neurology?

A
  1. Neurolocalization is key!
  2. Respiratory function!!!!!
  3. check for ticks
  4. Tensilon test - for dx’ing MG
52
Q

What labwork is good for evaluating motor unit issues?

A

Blood gas to assess oxygenation
CK of course to target muscle problems
CBC/Chem/UA

53
Q

What are the indicators for poor ventilation

A

PaCO2 > 60 or PaO2 < 60

EtCO2 50mmHg or SpO2 90%

VMCVM SAM 2 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions