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Adult III > Exam 3 - Neuroscience > Flashcards

Exam 3 - Neuroscience Flashcards

LOC, ICP, Spinal cord injury, buillian barre

1
Q

.

A

.

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2
Q

Arousal

A

Brainstem pathways (RAS) governing wakefulness

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3
Q

Awareness (content)

A

Cerebral functions including thought behavior, language, expression

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4
Q

Continuum of Consciousness levels

A 
Alert
Confused
Lethargic
Obtunded
Stuporous
Comatose
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5
Q

Alert (conscious)

A

attends to environment; responds appropriately to commands question with minimal stinulation

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6
Q

Confused

A

Disoriented to surroundings; may have impaired judgment; may need cues to respond to commands

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7
Q

Lethargic

A

Drowsy, needs gentle verbal or touch stimulation to initiate a response

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8
Q

Obtunded

A

Responds slowly to external stimulation; needs repeated stimulation to maintain attention and response to the environment

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9
Q

Stuporous

A

Responds only minimally with vigorous stimulation; may only mutter or moan as verbal response

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10
Q

Comatose

A

No observable response to any external stimuli

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11
Q

Consciousness depends on the

A

Reticular activating System (RAS)

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12
Q

Focused exam for critical/emergent pts

A 
LOC
Motor function
pupils/eyes
respiratory/ airway function
vital signs
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13
Q

Components of the neurological assessment

A
  1. Neurological Hx
  2. Physical Exam
    - LOC
    - Motor function
    - Pupillary changes
    - VS
    - Cranial nerves
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14
Q

Most important and critical indicator of cerebral function

A

LOC

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15
Q

Consciousness is dependent on the ____

A

RAS - Reticulating activating system

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16
Q

LOC assessment

A
  • Consciousness
  • Glascow coma scale
  • stimulus-reaction level scale
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17
Q

Motor function Assessment of Coordination

A

Romberg test
Finger to nose
Rapidly alternating movement (RAM)

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18
Q

Motor Response assessment

A

Decorticate: abnormal flexion (core)
Decerebrate: abnormal extension (E)
Flaccid
Babinski: abnormal in adults (curl=norm, flare=abn)

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19
Q

Cranial Nerve assessment

A
  • Pupils (especially helpful in unconscious client)
  • CN3 (EOM) awake client only
  • CN3: midbrain, one of the first to be compressed
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20
Q

Oculocephalic Reflex

A

“Doll’s eyes”

  • Unconscious pt without spine injury
  • Opposite = Good
  • Same = Bad
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21
Q

Oculovestibular reflex

A

Checks to see if brain stem is intact
-NEED INTACT TYMPANIC MEMBRANE
-unconscious pt
irrigate each ear w/ 30-50mL iced water with pt supine and HOB at 30 degrees
-Normal = eyes move slow toward painful stimulus followed with rapid movement away from stimulus
-Abn=absent reflex, eyes remain midline

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22
Q

Cranial nerves

A

CN IX: gag, cough,

CN XI & XII: must be alert (swallow, shrug shoulders)

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23
Q

Abnormal Respiratory Patterns

A
  • Cheynes-Stokes
  • Central neurogenic hyperventilation
  • Apneustic breathing
  • Cluster breathing
  • Ataxic breathing
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24
Q

Late VS changes

A

BP has increased pulse pressure

HR and rhythm:bradycardia common

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25
Q

ICP

A

Pressure exerted within the cranial vault by brain tissue, CSF, or Blood

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26
Q

Monro-Kellie Doctrine

A

an increase in any one of the contents in the brain is accompanied by a reciprocal change in the volume of one of the others:
blood 10%
CSF 10%
Brain 80%

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27
Q

The compartments BEST able to be manipulated to buffer changes in IICP volume

A

Blood & CSF

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28
Q

Normal ICP Range

A

0-15 mmHg

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29
Q

Indications for ICP monitoring

A
  • GCS of <8 or GCS motor scale +/- 5 (ex: not following commands)
  • Need to assess response to interventions
  • Increased volume of brain, blood, or csf
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30
Q

Causes of IICP

A
  1. Impaired auto regulation of cerebral blood flow
    - head injury, Reye’s syndrome, Encephalitis, Asphyxia
  2. Cytotoxic Edema
    - Head injury, Toxins, Asphyxia
  3. Mass/Lesion
    - Tumor, bleeding, Abscess
  4. CSF obstruction: hydrocephalus, mass, lesion, or meningitis
  5. Hyperosmoalr states: DKA, HHNS, hypernatremia
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31
Q

Activities that increase ICP

A
  • Valsalva
  • Emotional stress
  • Noxious stimuli
  • Suctioning
  • Fever
  • Pain
  • REM Sleep
  • Cough
  • Sneeze
  • Vomiting
  • Flexion
  • Fart
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32
Q

Normal cerebral blood flow

A

is 15% of cardiac output, consuming 20% of total O2

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33
Q

Cerebral Perfusion Pressure (CPP)

A

CPP= MAP - ICP

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34
Q

Herniation syndromes - Cingulate

A

shift of brain tissue from one cerebral hemisphere to the other

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35
Q

Herniation syndromes - Central

A

Downward shift of cerebral hemispheres thru tentorial notch, compressing vital centers of brain stem

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36
Q

Herniation syndromes - Uncal

A

Uncus of temporal lobe displaced thru tentorial notch, compressing MIDBRAIN
MOST SERIOUS COMPLICATION OF IICP

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37
Q

Early signs of IICP

A

RESTLESSNESS
change in LOC
HA
Pupillary changes (mild, sluggish actually a late sign)
Contralateral motor or sensory loss (opposite side)

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38
Q

Late signs of IICP

A 
Further decrease in LOC
Papiledema
pupillary changes
Changes in VS
Cushings triad
Changes in respiratory pattern
Fever
Projectile vomiting
POSTURING
Loss of reflexes
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39
Q

Cushing’s Triad

A

Increased SBP
Decreased DBP (widened pulse pressure)
Bradycardia

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40
Q

Ventriculostomy - Intraventricular catheter

A

a procedure for measuring ICP by placing an ICP monitor within one of the fluid-filled, hollow, chambers of the brain, called ventricles. These four natural cavities are filled with csf which also surrounds the brain and spinal cord

ICP monitoring, maintained as closed system to avoid infection, maintain transducer at EAR LEVEL, must zero
-NEVER FLUSH

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41
Q

Subarachnoid bolts/Screw

A

ICP monitoring, placed in subaranoid space
Direct measurement for CSF
Access for volume-pressure responses
Access for CSF drainage and sampling

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42
Q

Epidural Sensor

A

Placed between skull and dura
LEAST INVASIVE
ACCURACY UNCERTAIN

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43
Q

Intraventricular catheter

A

Inserted into Anterior horn of lateral ventricle
MOST INVASIVE
MOST ACCURATE
Higher risk for INFECTION & ICH

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44
Q

ICP Monitoring

A

Infection is a serious concern
ICP 20-25 mmHg needs Tx
ICP >60 mmHg is fatal
ICP is measured at END OF EXPIRATION, q2-4hr

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45
Q

Nursing care for ICP Monitors

A
  • Sterile dressing and sterile technique
  • Monitor site for drainage
  • ZERO and maintain at FORAMEN OF MONRO (outer corner of ear)
  • NEVER FLUSH when connected to hemodynamic system
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46
Q

Nursing care for IICP

A
  • Intubation
  • Sedation: Versed/Ativan
  • Elevation of HOB, head midline
  • Meds: mannitol, antiseziure, neuromuscular blockade agents, barbiturate coma
  • TX like “mushrooms” cool dark quiet room
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47
Q

Mannitol

A

Decreases blood viscosity, acts as osmotic agent to decrease brain water with osmotic diuresis

48
Q

Complications of ICP pressure devices

A
  • Hemorrhage
  • Infection
  • CSF leakage
  • Hematoma
49
Q

TBI Primary Injury Patho

A

.

50
Q

TBI Secondary Injury Patho

A

.

51
Q

Primary Injuries - TBI

A
  • Concussion
  • Contusion
  • Laceration
  • Diffuse Axonal Injury (DAI)
52
Q

Concussion

A

mechanical force of short duration applied to skull, results in temporary failure of impulse conduction. Neurological deficits are reversible and general mild.

May lose consciousness for a few seconds at time of injury, lasting effects are not common

53
Q

Contusion

A

Result of a coup and countercoup injury, accompanied by bruising and generalized hemorrhage into brain tissue. S/S are variable.

54
Q

Lacerations

A

Involve actual tearing of the brain tissue and occurs frequently with depressed and compound fractures and penetrating injuries. Tissue damage is severe and surgical repair is impossible because of the texture of brain tissue

55
Q

Diffuse Axonal Injury (DAI)

A

TWISTING AND TURNING OF THE BRAIN TISSUE AT THE TIME OF INJURY

Widespread axonal damage occurring after a mild, moderate ore severe tbi. damage occurs primarily around axons in the subcortical white matter of the cerebral hemispheres, basal ganglia, thalamus and brainstem.

56
Q

DAI Dx tool of choice

A

MRI

57
Q

Secondary injuries - TBI

A
  • Ischemia (resulting from hypoxia and hypotension)

- Infection

58
Q

Skull Fractures - Types

A

-Linear
-Comminuted
-Facial
-Basilar
-Depressed
Compound

59
Q

Linear skull fracture

A

break in continuity of bone without alteration of relationship of parts, caused by low velocity injuries

60
Q

Comminuted skull fracture

A

multiple linear fractures with fragmentation of bone into many pieces (egg shells), direct high momentum impact

61
Q

Facial skull fracture

A

Involve facial bones

62
Q

Basilar skull fracture

A

Fracture in the anterior middle and/or posterior fossa along the floor of the cranial vault. dura is torn

63
Q

Depressed skull fracture

A

Inward indentation of skull caused by powerful blow to head

64
Q

Compound skull fracture

A

depressed skull fracture and scalp laceration with communicating pathway to intracranial cavity, caused by severe head injury.

65
Q

Subdural hematoma (SDH)

A

Bleeding between dura and arachnoid layers, generally VENOUS in nature

66
Q

Acute Subdural hematoma

A

S/S within 24-48hrs

67
Q

Subacute subdural hematoma

A

S/S withing 28hr-2 weeks

68
Q

Chronic subdural hematoma

A

within weeks to months

69
Q

SDH Tx

A

Medical management of IICP
Burr holes
Surgical evacuation

70
Q

Epidural Hematoma

A

Bleeding between dura and skull, generally ARTERIAL in nature

71
Q

EDH Classic sign

A

Brief loss of consciousness followed by lucid interval then coma
Other S/S:
Ipsilateral pupil dilation, contralateral weakness, brainstem compression

MIDDLE MENINGEAL IS USUALLY THE ONE TO BLEED
Pt dies from brainstem compression

72
Q

Intracerebral Hemorrhage (ICH)

A

Bleeding within the cerebral tissue that creates a mass lesion.

  • due to closed head injury, aneurysm rupture.
  • Treatment varies related to cause, extent and location of bleeding
73
Q

Basilar skull fractures

A

Raccoon’s eyes and battle’s sign

At risk for MENINGITIS due to communicating pathway

74
Q

Assessment of skull fx

A
  • Neurological deficits and varying LOC

- CSF is positive for glucose, halo sign if blood present

75
Q

Halo sign indicates

A

blood in csf

76
Q

Assessment for meningeal irritation

A
  • Brudzinski (stiff neck when flexed)
  • Positive Kernig’s sign (cannot extend leg when thigh flexed on abdomen
  • Photophobia
  • Headache
  • Fever
77
Q

Interventions for Neuro pt

A
  1. Optimize oxygenation
    - intubate/vent, control CO2 and O2 levels
    - Suction only PRN, consider use of lidocaine to suppress cough
  2. Control/reduce increased ICP
    - icp monitoring & drainage
    - reduce metabolic demands (sedation, seizure control, reg body temp, admin mannitol, lasix, steroid)
  3. Monitor and prevent complications
    - MONITOR I/O, URINE SPECIFIC GRAVITY FOR DI/SIADH
    - ADMIN DVT/GI PROPHYLAXIS
    - maintain bp
    - hourly neuro checks
    - ekg monitoring
78
Q

DI

A

Not enough ADH, fluid volume deficit
Excessive UO, dilute urine
Blood is concentrated

79
Q

SIADH

A

Too much ADG, fluid volume excess
Decreased UO, urine concentrated
Blood is dilute

80
Q

Craniotomy

A
  1. Burr holes; circular openings in skull to evacuate hematomas, or to initiate more invasive brain surgery
  2. Craniotomy; surgical window in the skull made by sawing between multiple burr holes
    - Supratentorial-access to areas above the tentorium
    - Infratentorial- access to areas below the tentorium
81
Q

Craniectomy

A

Surgical removal of a portion of the skull without replacement bone flap

82
Q

Cranioplasty

A

Replacement of missing cranium with bone or plastic insert to restore skull contour and integrity

83
Q

Craniotomy post-op care

A
  • Avoid activities that increase ICP
  • Watch for excessive post op drainage & notify physician at once
  • neuro checks, LOC, pupils, movement and sensation
  • elevate hob, position
  • stool softener, diuretics, steroids, control temp and shivering
84
Q

Subarachnoid Hemorrhage

A

Bleeding into the subarachnoid space between the pica and arachnoid layers of the Meninges.

  • Cerebral aneurysm; weakening and abn dilation of a cerebral blood vessel
  • Arteriovenous malformation (AVM); congenital malformation of cerebral arterial and venous blood vessels that connect directly, bypassing the capillary system; may produce increased ice; HIGHLY SUSCEPTIBLE TO RUPTURE
85
Q

Clinical findings of SAH

A

Before bleed: HA, transient weakness, visual disturbances
After bleed: meningeal irritation, SEVERE HA, nuchal rigidity, N/V, PHOTOPHOBIA, seizures, fever, lethargy, kernig & brudzinski, DECREASED LOC
-neuro deficits
-visual changes due to retinal hemorrhage
-LABILE BP

86
Q

SAH Complications

A
  • Vasospasm (4-14 days after, peaks 7-10)
  • Rebleed (3-11 days after, peaks at 7days)
  • Hydrocephalus (acute or delayed)
87
Q

Complete spinal cord injury (SCI)

A

total loss of sensory and motor function below level of injury

88
Q

Complete quad

A

injuries above C6

89
Q

Incomplete Quad

A

Injuries below C6

90
Q

Paraplegia

A

Injuries in the thoracolumbar region

91
Q

Incomplete SCI

A

mixed loss of voluntary motor activity and sensation below the level of the lesion

92
Q

Central cord syndrome

A

arm paralysis

93
Q

Brown-Sequard syndrome

A

motor loss on one side: pain, temp, touch loss on the opposite side

94
Q

Anterior cord syndrome

A

motor loss, but retains light touch, proprioception and position

95
Q

What is the predictor of complete vs incomplete lesion

A

Rectal tone
normal= squeeze
incomplete = weak squeeze
complete = flaccid

96
Q

Spinal Shock

A

Flaccid paralysis, loss of sensation and reflexes below level of lesion

  • absence of reflex activity; bowel or bladder
  • loss of temp control

May last weeks to months, ends with return of reflexes and muscle spasticity

97
Q

Neurogenic Shock

A

Interruption of descending sympathetic pathways causing vasodilation, resulting in hypotension and bradycardia

98
Q

Potential Complication of SCI

A

Autonomic dysreflexia

hypoxia, dvt/pe, ileus, f&e imbalances, pneumonia

99
Q

SCI Interventions

A 
Vassopressors (dopamine)
TEDs/SCDs (PREVENT DVT/PE)
Fluid replacement
Intubate/vent
pulmonary hygiene
Trach if long term management of airway needed
100
Q

Autonomic Dysreflexia

A

Exaggerated autonomic response to visceral stimulation occurring in its with injuries above T6

101
Q

Precipitating factors for Autonomic dysreflexia

A

Bladder distension, kinked foley
Bowel distension, impaction
Pressure areas, constricting clothing
Pain, spasticity

102
Q

S/Sx of Autonomic Dysreflexia

A
  • Severe Hypertension
  • HA
  • Bradycardia
  • Sweating above level of injury
  • Flushing of face/neck
  • Nausea
  • Nasal congestion
  • Pupil dilation
103
Q

Autonomic dysreflexia interventions

A
  • Elevate HOB to lower BP
  • Check for bowel impaction/bladder distension, foley patency
  • evaluate skin for breakdown
  • Medicate to lower BP (Hyperstat, hydalazine, resperpine)
  • Atropine to increase HR
104
Q

Autonomic dysreflexia meds

A
  • Medicate to lower BP (Hyperstat, hydalazine, resperpine)

- Atropine to increase HR

105
Q

Myasthenia Gravis

A

Autoimmune disease in which antibodies are directed against acteylcholine receptors impairing neuromuscular transmission

106
Q

Myasthenic Crisis

A

Sudden onset of weakness, usually from UNDER MEDICATION, stress or other meds or progression of disease, manifestations include acute respiratory distress and inability speak or swallow

DRY!!!

107
Q

Cholingergic Crisis

A

OVER MEDICATION with cholinergic or anti cholinesterase agents, manifestations include muscle weakness, GI distress (N/V/D), seating, increased salivation and bradycardia

WET!!!

108
Q

Myasthenia Gravis Dx Studies

A
  • Tensilon Test; improved muscular strength following admin of Tensilon (edrophonium) confirms Dx
  • EMG
  • Anti-AChR antibodies in serum
  • MRI thymus gland
  • Thyroid studies
109
Q

Myasthenia Gravis Nursing Dx

A
  • INEFFECTIVE BREATHING PATTERN, INEFFECTIVE AIRWAY CLEARANCE
  • impaired physical mobility
  • risk for aspiration
  • risk for injury
  • anxiety
  • activity intolerance
110
Q

S/S MG

A

Extreme muscle weakness
symmetrical muscle involvement
Ptosis and diplopia
bulbar muscle weakness; impaired chewing/swallowing

111
Q

MG interventions

A

Plasmapheresis

Thymectomy

112
Q

Hypovolemic Shock

A

blood VOLUME problem

Cause: hemorrhage, dehydration

113
Q

Cardiogenic Shock

A

Blood PUMP problem

Cause: LV MI

114
Q

Distributive Shock

A

Blood VESSEL problem
(septic, anaphylactic, neurogenic)

Causes:
neurogenic: cord injuries above T6
Anapgtlactic: type I hypersensitivity
septic: systemic inflammatory response to infection, gram neg toxins (toxic shock)

115
Q

Initial Stage of Shock

A

Tissues are under perfused, decreased CO, increased anaerobic metabolism, lactic acid is building

116
Q

Compensatory Stage of Shock

A

Reversible; SNS activated by low CO, attempting to compensate for the decrease tissue perfusion

117
Q

Irreversible or refractory stage

A

Cellular necrosis and MODs may occur, death is imminent

Adult III (14 decks)

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