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1
Q

How many pairs of nerves are there

A

31
Responsible for motor function, sensory function, and autonomic function

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2
Q

What is the white matter and grey matter function

A

White matter, communication pathway
Gray matter, processing sensory input

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3
Q

What are the dermatomes

A

Cervical shoulders and posterior arms
Thoracic chest and anterior arms
Lumbar anterior legs
Sacral genitals, butt and posterior legs

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4
Q

T/F spinal cord injuries result in decreased life expectancy and increased mortality

A

T

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5
Q

What is a flexion injury

A

Car accident
Ruptured posterior ligaments
Forward buldging or dislocation of disks
Damage to spinal cord

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6
Q

What is a hyperextension injury

A

Chin on table
Compressed ligament
Ruptured anterior ligament

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7
Q

What is a compression fracture

A

Fractured vertebrae in small pieces
Compression of spinal cord

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8
Q

What is a flexion rotation injury

A

Displacement of vertebcae

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9
Q

What is a T6 and L1 injury called

A

Paraplegia

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10
Q

Injuries above C3 are more likely to have what complication

A

Total loss of respiratory muscle function, will arrest within minutes if not intubated

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11
Q

What is a C4 and C6 level of injury called in neurologic terms

A

Tetraplegia

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12
Q

Injuries above C5 are more common to have what complication

A

Can’t protect their airway
Loss of phrenic nerve innervation to diaphragm
Require intubation
*complete injuries

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13
Q

What is the difference between primary injury and secondary injury

A

Primary results from direct physical trauma
Secondary injury is ongoing, progressive damage seen after initial injury

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14
Q

T/F paralysis of the abdominal muscles and often intercostal muscles causing ineffective cough and leading to risk for aspiration, Atelectasis, pneumonia

A

T

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15
Q

Injuries above T6 leads to dysfunction of SNS, what are we assessing

A

We can’t assume fluid status
Leads to neurogenic shock
Bradycardia, hypotension, peripheral vasodilation, relative hypoxemia because of increased capacity of dilated veins
Reduced venous return decreases cardiac output, causing hypotension

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16
Q

What is neurogenic bladder

A

Dysfunction related to abnormal or absent intervention and impaired signal transmission
No reflex contractions—-bladder stretching
Hyperactive reflex (spasticity)—-incontinence
Reflux to kidneys—Inc risk of infection
Catch—inc risk of infection

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17
Q

What is neurogenic bowel

A

Dysfunction related to absent/abnoraml innervation and impaired signal transmission
Above conus medullaris—hyperreflexia
—stool retention and constipation dt inc compliance
Below conus medullaris—areflexia
—impaired peristalsis, damage to reflex, and a relaxed sphincter
—at risk for ileus or toxic megacolon

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18
Q

What are other consequences of a spinal injury

A

Inc risk of skin infection
Poikilothermia —more common with high cervical
—decreased ability to sweat or shiver below injury
Increased metabolism and inc protein breakdown
Higher risk of VTEs
Priapism
Reflexes are exaggerated

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19
Q

What is the difference between nociceptive pain and neuropathic pain

A

Nociceptive pain-dull or aching worsens with movement, tender or cramping in abdomen area
Neuropathic pain—damage to spinal cord or nerve roots located at or below level of injury. Hot, burning shooting pain that may be extremely sensitive to stimuli

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20
Q

What is central cord syndrome

A

Damage to central spinal cord—most commonly cervical region, usually a result of a hyperextension injury
More common in older adults

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21
Q

What are the manifestations of central cord syndrome

A

Motor weakness and altered sensation in upper extremities
Lower extremities are not usually affected
Burning pain in upper extremities

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22
Q

What is anterior cord syndrome

A

Damage to anterior spinal artery casing compromised blood flow
Typically results from flexion injury and compression of anterior spinal cord

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23
Q

What are the manifestions of anterior cord syndrome

A

Motor paralysis and loss of pain and temperature sensation below level of injury
Sensations of touch, position, vibration, and motion remain intact

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24
Q

What is brown squard syndrome

A

Damage to one half of the cord
Typically results from a penetrating injury

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25
What are the manifestions of brown sequard syndrome
Ipsilateral (same side) loss of motor function and pressure, position, and vibration sense Contra lateral (opposite) loss of light touch, pain and temperature sensation below sensation
26
What is Cauda Equina syndrome
Results from damage to cuada equina (lumbar and sacral nerve roots)
27
What is the manifestions of cuada equina syndrome
Asymmetrical distal weakness and patchy sensation in lower extremities Flaccid paralysis of lower extremities Complete loss of sensation in saddle area Arefelxic (flaccid) bladder and bowel Severe, radicular, asymmetric pain
28
What is conus medullaris syndrome
Damage to conus medullaris (lowers part of spinal cord) Motor function in legs are varied Decrease loss of sensation in perineal area Arefelxic bowel and bladder Impotence Pain is uncommon “Gray and white matter injury”
29
What s the emergent stabilization of a SCI
Immobilize Maintain norm temp Assess neurological function Determine mechanism of injury Assess musculoskeletal function Assess sensation Place catheter
30
What is spinal shock
Syndrome that can happen shortly after injury, lasts days to weeks Characterized by loss of deep tendon reflexes and sphincter reflexes Flaccid paralysis below level of injury Sensations Cannot know the full extent of neurological deficits until after spinal shock resolves
31
What is neurogenic shock
Lasts for up to 5 weeks after injury Can occur in cervical or high thoracic injury Characterized by unopposed parasympathetic response due to loss of symptachtic nervous system innervation Causes significant hypotension, bradycardia, and temp dysregulation —impacts perfusion
32
What is autonomic dysreflexia
Uncomponenstated cardiovascular response—SNS is in overdrive Can be fatal if not recognized and resolved quickly Small events can trigger this response -severe hypertension Throbbing headache Diaphoretic above level of injury Bradycardia Vision changes
33
How do you manage autonomic dysreflexia
Elevate HOB Straight catheterization —irrigate catheter tube if catherter in place Digital removal of stool Remove tight clothing or shoes Take BP q5min until episode resolves May need to administer vasodilation agents
34
What are the classifications of burns
Superficial (partial thickness) Deep (partial thickness) Full thickness
35
What is first degree burn
It’s damaged epidermis and edema Erythema, blanking, pain, mild swelling No vesicles at risk Sunburn, quick, heat flash
36
What is second degree burns
Damaged epidermis and dermis Fluid filled vesicles Red, shiny, wet Severe pain Mild-moderate edema Flame, chemical, tar, scald, electric, contact burns Healing can be days to years
37
What are full thickness third degree burns
Deep tissue damage Dry, waxy, white, leathery, or hard Insensitivity to pain Involvement of muscle, tendons, bone
38
What are full thickness burns fourth degree
All skin elements and nerve endings destroyed Surgical intervention is required for healing Shivering may occur Sings and symptoms of hypovolemia No barrier against infection and pathogens May need amputation
39
T/F ages <2 and >65 have higher mortality rates
T
40
What is the pros and cons of rule of nines
Used for children or adults Easy to use For use after stabilization But not as accurate 9=head 9-arms 18, front, back, and legs
41
What is classified as severe classification
25% of TBSA on any patients Inhalation of trauma injury Full thickness burns =/>10% TBSA 20% of TBSA in children and adults >40 Burns to face, hands, perineal High voltage burn injury
42
What is the element resuscitative phase
First 72 hours Resolve immediate, life threatening problems Main concern: hypovolemic shock and edema Ends with fluid mobilization and diuresis
43
What is the management of emergency phase
Reevaluate - intubate, escharotomy Vitals, labs Initial fluid resuscitation Pain management Wound care
44
How does hypovolemic shock occur in emergent resuscitative phase
Fluid shifts to extra vascular -Dec BP, inc HR Hemolysis of RBCs—high hematocrit High K Low Na
45
What are the complications of emergent resuscitative phase
Cardio—dysrhythmias, tissue ischemia, hypovolemic shock, VTEs Resp—R distress Urinary—AKI
46
What are escharotomy used for
Restore circulation Incisions in areas with circumferential burns
47
What is parkland formula
LR in 1st 24 hours Colloids in 2nd 24 hours (NS) Time starts at time of injury
48
How do we assess adults fluid resuscitation
Urine output 30-50 ml/hr Map >65 SBP >90 HR <120–cant meet metabolic demand if high
49
What is the forumula for parkland formula
4ml of LR x kg x %TBSA=fluid needs for first 24 ours 50 in 1st 8hours 25 in 2nd 8 hours 25 in 3rd 8 hours Keep urine output 30-50 ml/hr
50
What would an edema out and closed off airway sound like in a burn patient
Stridor
51
What does carbon monoxide poisoning look like
Flu like symptoms, confusion, Dyspnea, headache Red cherry color to skin and mucous membranes Carboxyhemoglobin
52
What is the treatment for carbon monoxide poisoning
100% humidified oxygen Hyperbaric therapy
53
T/F burn patients need increased nutritional needs
T Body is in extreme catabolic state and extreme stress response
54
What is the patho of glucose needs in burn patients
Adults can go in hyperglycemia from teh catabolic state Poor wound healing and worry about kidney function Kids are more likely to go in hypoglycemia because they have higher metabolic rate and their glycogen stores are depleted
55
What is the demobilization phase
Occurs after 48 hours Diuresis Extra vascular fluid shifts into intravascular —hemodilution —edema formation ends
56
What is timeframe stage II acute phase of burns
Mobilization of fluid of diuresis——when graphs are on
57
What do you do in stage II
Diuresis Wound care Debridement
58
What is the difference between open and closed wound care
Open - just cream applied Pros—can visualize and easy wound care Cons—may cause hypothermia and may need heat lamp Closed—cream applied under dressing Pros—prevents webbing, decrease heat loss, increase debridement Cons—bulky and limits assessment ability
59
What is silver sulfadiazene
Poor aschar penetration Water soluble Broad spectrum Side effects—leukopenia, rash
60
What do you need to assess when using silver sulfadiazene
Leukopenia and electrolytes Immune compromised and change in electrolytes
61
What is mafenide acetate
Eschar penetrator Water soluble Broad spectrum Must cover with sterile water or dry gauze Broad spectrum Side effects: stings and metabolic acidosis
62
What are other dressings for burns are there
Aquacel ag—leave on for 3 days Honey Bacitracin—facial burns, non painful, inexpensive Avoid ice and extreme cold
63
What are the biological grafts
Amnion, allograft, xenograft—animal skin
64
Bio synthetic grafts
Biobrane, integra
65
What are considerations for donor site care
Compression dressing for 48 hours Cover with transparent dressing and guzzle Apply topical emollient cream—eucerine, cetaphil May use heat lap
66
What are considerations for autograft care
Remove blood or serum by aspiration Immobilize Mesh graft—cover with wet dressing Assess-color, drainage, reddened edges
67
What are the nutritional needs for burns patients
High protein High carbohydrates Vit ACE, zinc, ferrous sulfate NO TPN
68
How much morphine do we give
2-4 mg/5min-10 min IV
69
What is stage 3
Wounds are healed, almost healed—>self functioning
70
How long do we use pressure garments
Worn 12-18 months 24 hours a day Only remove for bathing
71
What education do we give for burn patients
Use of lotion and vitamin e Avoid sun exposure OTC antihistamines for pruritus
72
What is the monro-Kellie doctrine
3 components must stay at a relatively constant volume within the closed skill to maintain function Brain tissue, blood, CSF
73
What is the normal ICP
5-15
74
What is CCP
Cerebral perfusion pressure Pressure needed to maintain adequate blood flow in the brain
75
What is the equation for CPP
CPP=MAP-ICP Normal is 60-100, ideal is 60-70 Less than 50=tissue death Less than 30=incompatibel with life
76
What happens with there is sustained increased ICP on brain stem
It is irreversible and deadly Cushing’s triad Impaired auto regulation
77
What is cushings triad
Irregular respiration Bradycardia Widened pulse pressure
78
What are manifestions of increased ICP
Changes LOC Change in vitals—Cushings (brain stem compression) Thermodynamic instability Pupil dilation —fixation +dilation = brain steam herniation Headache Vomiting Posturing
79
What is the difference between decorticate or decerebrate posturing
Decorticate— bunny Decerebrate— straight jacket
80
What is dolll’s eyes
Oculocephalic reflex eye movement is opposite direction of movement in a normal brain
81
What is oculovestibular reflex
Eyes should move in response to wold water in ear —must have tympanic membrane intact —must be free of ear wax
82
What do you do to manage increased ICP
Elevate HOB 30 degrees Breathing—-mechanical ventilation, ensure PaO2 >100 Maintain fluid balance —hypertonic solution Maintain systolic arterial pressure between 100-160 Maintain CPP >60 Reduce stress on brain ICP monitoring
83
T/F steroids contraindicate w brain injury
T
84
What meds do you give a increased ICP pt
Mannitol—pulls water out of cells and into plasma Hypertonic saline—water out of edematous swollen brain tissue into blood Corticosteroids generally contraindicated Barbiturates—decrease cerebral metabolism, decrease excess perfusion
85
What is basilar signs
Battle’s sign, raccoon eyes, rhinorrhea/otorrhea (CSF leak)
86
What is the TBI severity using GCS
Mild(GCS 13-15)—often a concussion Moderate (GCS 9-12) Severe (GCS 3-8)—intubate Less than 8 intubate
87
What are the different categories of focal injury
Contusions: bruising of brain tissue, may worsen over time or rebleed Coup-contrecoup injury: injury at impact and opposite side of brain Lacerations: tearing of brain tissue: often with skull fracture
88
What is diffuse axonal injury
Widespread axon damage; decrease LOC, increase ICP, posturing Undetectable on CT
89
What is the management of mild TBIs
Rest Symptom management Gradual return to activity
90
What is the management of moderate-severe TBs
ICP monitoring, seizure prevention, fluid/electrolyte balance Surgery (craniotomy, hematoma evacuation Sedation and ventilation support
91
What is the difference between epidural hematoma and subdural hematoma
Epidural hematoma is bleeding between the durra and inner surface of the skull Subdural hematoma is bleeding between the dura mater and arachnoid (severe causes ipsilateral pupil fixation and dilation
92
What is SIADH-syndrome of inappropriate anti diuretic hormone
Over production of ADH causing fluid retention, concentrated urine, dilutional hyponatremia Problem—-causes cerebral edema Usually temporary in head trauma
93
What is diabetes insipidus
Deficient production or secretion of ADH or a decreased renal response to ADH Polyuria, dilute urine, hypernatremia, polydipsia Problematic—causes profound dehydration

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