TEST 4 Flashcards
1
Q
What is central cord syndrome?
A
Incomplete Lesion (injury)-
Motor problems (fine motor)
Upper extremities more affected
Spastic paralysis of upper extremities
Lower extremities less affected
Bowel & Bladder dysfunction variable
2
Q
cause of central cord syndrome?
A
Trauma
Traumatic lesions tend to improve in 1-2 weeks
Tumors
Infections
Surgical decompression may be indicated if r/t spinal stenosis
3
Q
what is anterior cord syndrome?
A
Incomplete Lesion (injury)
Loss below the level of lesion:
Pain
Temperature
Motor function below level of lesion
Retain below level of lesion: (gross sensation)
Light touch
Position
Vibration sensation
4
Q
cause of anterior cord syndrome?
A
Trauma (anterior cord compression)
Association fracture-dislocation of vertebrae
Acute disk herniation
Hyperflexion
Artery infarct
5
Q
what is brown-sequard syndrome?
A
Incomplete cord lesion (Injury)
Lateral cord syndrome
Ipsilateral paralysis/ Ipsilateral paresis
Loss or weakness with movement
Contralateral loss of pain and temperature
6
Q
cause of brown-sequard syndrome?
A
Infection
Inflammation
-MS
-TB
Tumor
Trauma
-Penetrating
-Fracture or dislocation
-Acute disc rupture
7
Q
what is cauda equina syndrome?
A
Progressive compression of nerve roots at base of spinal cord
-Lumbar pain
-Weakness or paralysis of lower extremities
-Saddle anesthesia
-Bowel & bladder incontinence
8
Q
causes of cauda equina syndrome?
A
Usually from herniated disc
9
Q
what is Sciwora?
A
Spinal cord injury without radiographic abnormality
Condition affecting pediatric patients 8 and younger
Objective signs of spinal cord injury from trauma without bony abnormalities or changes on X-ray or CT
Incidence 20-32%
Younger patients may have more severe neuro symptoms
Symptoms may be delayed
Risk related to large blood supply to cord & elasticity of vertebral column
Injuries are usually considered “stable”
Immobilization for 3 months standard treatment
MRI (gold standard)
-Demonstrate: Ligamental injury, disk injury, cord lesions, or hemorrhage
10
Q
T4 is located where?
A
nipple line
11
Q
T10 is located where?
A
base of ribs, roughly point of umbilicus
12
Q
C6, 7, & 8 are located where?
A
hands and fingers
13
Q
T1 is located where?
A
terminate triceps (shrug shoulders)
14
Q
L5-S1 is located where?
A
feet (felx/extend)
15
Q
A in ASIA scale?
A
A = Complete. No sensory or motor function is preserved in the sacral segments S4-S5.
16
Q
B in ASIA scale?
A
B = Sensory Incomplete. Sensory but not motor function is preserved below the neurological level and includes the sacral segments S4-S5 (light touch, pin prick at S4-S5: or deep anal pressure (DAP), AND no motor function is preserved more than three levels below the motor level on either side of the body.
17
Q
C in ASIA Scale?
A
C = Motor Incomplete. Motor function is preserved below the neurological level, and more than half of key muscle functions below neurological level of injury (NLI) have a muscle grade less than 3
18
Q
D in ASIA scale?
A
D = Motor Incomplete. Motor function is preserved below the neurological level, and at least half of key muscle functions below the NLI have a muscle grade of 3 or > 3.
19
Q
E in ASIA scale?
A
normal
20
Q
emergency management of SCI
A
Immobilization!
-Cervical collar
Resuscitation as needed
Move as a unit- avoid additional or worsening injury
Testing
-X-Ray- bony abnormalities
-CT- 3 dimensional view of bone
-MRI- ligament and tissue
Interventions/ Actions
-Initial and continuous assessment
-Frequent vital signs
-Avoid hyperoxia
-Maintain MAP >85mmHg
Pharmacologic treatments
21
Q
respiratory clinical manifestations of SCI
A
C1 – C3: Absence of ability to breathe independently.
C4: poor cough, diaphragmatic breathing, hypoventilation
C5 – T6: decreased respiratory reserve
T6 or T7 – L4: functional respiratory system with adequate reserve
ASSESSMENT q2H AT LEAST
Ascending edema of the spinal cord in the acute phase -Can cause respiratory difficulties requiring immediate intervention
22
Q
non-physical restraints
A
talk down, listen, minimizing stimulation
23
Q
what is STAMP?
A
Staring
Tone (or volume of voice)
Anxiety
Mumbling
Pacing
used for IDing potentially violent pts
24
Q
Restraints
A
reminder to look at restraint doc on canvas
25
what is EMTALA?
emergency medical and active labor act-
duty to treat regardless of inability to pay or insurance coverage
26
EMTALA treatment guidelines
EDs must provide medical screening exam and look for emergency medical conditions, then stabilize if EMC present AND care for pregnant patients with contractions if emergency exists or inadequate time for safe transfer before delivery
27
EMTALA reasons for transfer?
specialized care not available at facility
continuity of care
lack of resources
patient request
28
triage: emergent
life threatening, seen immediately, assess q15min
29
triage: urgent
serious health problem, seen within 1hr, assess q30min
30
triage: non-urgent
episodic illness, seen within 24hrs, assess q1-2h
31
what is ABCDEFGHI assessment?
Primary Assessment
A- Airway/ C-spine precautions
B- Breathing
C- Circulation- obvious hemorrhage
D- Deficit- LOC, AVPU, GCS
Secondary Assessment
E- Environmental/ Expose
F- Full set of vital signs/ Family
G- Give comfort
H- History/ Head to toe
I- Inspect Posterior/ Interventions
32
what is blunt trauma?
Physical trauma (closed) body as a result of:
Impact
Injury
Physical Attack
33
biomechanical forces that cause blunt trauma?
compression, stretch, sheer
34
what is compression force?
Impact stops part of the body
Inertia keeps remaining anatomy in motion
35
what is stretch force?
Protein fibers pulled, injured or torn
36
what is sheer force?
Structures under opposing forces are damaged
37
types of blunt trauma?
MVC, falls, assault
38
what are fragile solid organs that damage easily in blunt trauma?
brain, spleen
39
turner sign is where
flank
40
cullen sign is where
umbilical
41
what do turner and cullen signs indicate
retroperitoneal hemorrhage
42
what are hollow organs
Heart
Stomach
Lungs
Bowel
Bladder
Tolerate trauma well
If full of air or fluid may rupture
43
what are solid organs
Kidneys
Liver
Pancreas
Held together with strong tissue
Fracture with injury
44
presentation for blunt trauma to abdomen
Pain
Tenderness
Hemorrhage (no obvious source)
Hypovolemia
turner sign
cullen sign
45
presentation of chest blunt trauma
Pain
Tenderness
Shortness of breath
46
what do you palpate on chest assessment for blunt trauma
sternum, ribs
47
where do you immobilize for a fracture
above and below the joint
48
what do you have to think about every time you splint, wrap, cast, or immobilize
compartment syndrome
49
what are considered major fractures
pelvis, femur
50
what are the types of penetrating trauma?
hgih velocity
low velocity
51
high velocity trauma types
GSW, blast injuries
52
low velocity trauma types
stabbing, impalement
53
penetrating trauma assessment
MOI very important
Never remove an object
-Diagnostic imaging to determine extent of injury
-Removed in OR
-Cheek- exception
--Direct pressure can be applied to both sides of injury
Extent of injury depend on
-Velocity
-Number of projectiles
54
what is crushing trauma?
Body Part caught between 2 objects
-Industrial between machine parts
-Runover by a car between tire and road
55
crushing trauma can cause what complications
Intracellular fluid is released when cells are crushed (think electrolytes)
Myoglobin release due to muscle damage
-Rhabdomyolysis
-Myoglobin causes renal failure
-Clog kidneys
Compartment swelling leads to increased muscle damage
-Compartment syndrome
-Fasciotomy treatment
56
6 P's of compartment syndrome
Pain:
-Earliest
-Progressive
-Disproportionate to injury
Pressure
Pallor (decreased O2)
Paresthesia
Paresis- muscle weakness related to nerve damage
Pulseless
-Late and ominous sign
57
causes of compartment syndrome
Bleeding
Edema
Constricting cast
Constricting dressing
Splinting
Prolonged positioning
Burns
Infections
58
how is compartment syndrome diagnosed?
Presenting symptoms
MOI
Pressure measurement
59
treatment for compartment syndrome?
Identify increased pressure
Release pressure with a fasciotomy
60
treatment priorities for compartment syndrome
Maintain hemodynamic status
-1 Liter crystalloid fluid
-Additional needs- give blood
Keep patient warm
Stop any active bleeding
-Direct pressure
-Tourniquet
Permissive hypotension resuscitation
Stabilize fractures
-Splinting
Disposition
-Admit
-OR
-Transfer
-Discharge
61
what is the trauma triad of death?
hypothermia, coagulopathy, acidosis (and hypocalcemia to make diamond of death)
62
what to do for acidosis in triad of death?
NS or LR
63
what to do for coagulopathy in triad of death
blood products- 1 U PRC to 1 U plasma to 1 U platelets
64
triad of death treatment
Stop the bleeding
Assume your patient’s temp is dropping
Limit patient exposure to environment
Turn up the heat!
Measure lactate levels
Measure end-tidal CO2
Treat hypoventilation
Track & treat coagulation labs
65
frost nip is ___ and ____.
mild and reversible
66
affected locations of frost nip
Earlobes
Cheeks
Nose
Fingers
Toes
67
frost nip presentation
Reddened or blanched skin
Cool/cold to the touch
68
frost nip tx
rewarming
69
frost bite causes ...
Severe tissue & cell damage
Intracellular water turns to ice
Cold cause decreased blood flow
70
frost bite presentation
Damage depends on depth of freezing
Swelling
Blistering
Pain
Gangrene
Muscle necrosis
71
frost bite tx
External and internal warming
Tepid water emersion
Warm blankets
Warm O2
72
DO NOT what with frost bite
massage areas- causes more damage
73
who is at risk for frost bite
old, young, homeless, beta blockers, alcoholics, malnourished, diabetics, smokers, PVD
74
hypothermia causes
Core temp is 95◦ or less
Result of exposure to cold
Inability to maintain temperature in absence of low ambient temps.
75
what happens when temp <90
-Shivering suppressed
-B/P & P non-palpable
-Vfib
*Defib is ineffective on a cold heart
*Internal and external warming initial treatment
76
causes of heat exhaustion
Excessive heat exposure & dehydration
Very hot environment
Heavy activity
Not enough fluid and salt intake
77
presentation of heat exhaustion
Muscle cramps
Shoulders
Abdomen
Lower extremities
Profound diaphoresis
Thirst
Syncope
Headache
Dizziness
Pale moist skin
Nausea & Vomiting
Temperature 101-102 degrees
Tachycardia
78
tx for heat exhaustion
Move to cool, shady area
PO fluids
Electrolyte containing
IV fluids if necessary
Encourage rest
79
causes of heat stroke
Non-exertional prolonged exposure to high temperatures
Exertional heat stroke: strenuous activity in high temperatures
80
heat stroke presentation
May not have sweat
Weakness
Hot dry skin
Tachypnea
Tachycardia
Hypotension
Temperature 105 or higher
CNS dysfunction:
-Delirious
-Unconscious
-Seizures
-Coma
81
heat stroke tx
Removing clothing
Moving to a cool, shady area; shelters
Active cooling
IV fluids
Medication
-Seizures
-Uncontrollable shivering
Frequent vital signs
Labs
82
meds that alter physiologic response to heat
Phenothiazines
Anticholinergics
Antihistamines
Beta-blockers
Benzodiazepines
Amphetamines
Neuroleptics
Tricyclic antidepressants
Cocaine
Alcohol
83
risk factors for near drowning
Alcohol
Inability to swim
Diving injuries
Hypothermia
Exhaustion
No life jacket
84
what is mammalian dive reflex
Reflex occurs when mammals are submerged in water <70 degrees
Protective mechanism to maintain cardiac and cerebral blood flow
When face submerged:
-Laryngeal spasm starts
-Heart rate slows
-Vasoconstriction
85
near drowning complications
Respiratory
-ARDS
-Hypoxia
-Hypercarbia
-Loss of surfactant (fresh water)
-Pulmonary edema (salt water)
Acidosis
-Respiratory
-Metabolic
Hypothermia
86
drowning morbidity and mortality primarily due to what
anoxic brain injury caused by airway obstruction from laryngospasm or aspirated water
87
chemical ingestion poisoning can be __ or ___.
alkaline or acidic
88
chemical ingestion tx
Identification of substance
Removing toxin
-Gastric lavage
Decrease absorption
-Activated Charcoal
-Dilution
89
symptoms of ingestion poisoning
Early symptoms of may include an intoxicated feeling.
Headache
Fatigue,
Lack of coordination
Grogginess
Slurred speech
Nausea
Vomiting
Continued breakdown causes damage to:
-Kidney
-Lung
-Brain
-Nervous system function.
-Organ damage can occur 24 to 72 hours after
ingestion.
90
button battery ingestion complications
Tracheoesophageal fistula
Esophageal perforation
Vocal cord paralysis
Mediastinitis
Pneumothorax
Pneumoperitoneum
Tracheal Stenosis
Tracheomalacia
Aspiration pneumonia
Empyema
Lung abscess
91
button battery ingestion tx
Endoscopic or surgical removal if lodged
Allow to pass
Honey may help neutralize pH
92
carbon monoxide poisoning
CNS symptoms
Skin color
-Cyanotic
-Pale to pink
-Unreliable sign
93
carbon monoxide poisoning tx
Fresh air
100% O2
Hyperbaric chamber
94
C1, 2, 3, 4, _________; C5 _______
breathe no more; stay alive
95
primary spinal cord injury
Initial insult
Irreversible
Microscopic hemorrhage in gray matter
Edema to white matter
96
secondary spinal cord injury
Contusions
Tears cause nerve fibers swelling & disintegration
Ischemia
Hypoxia
Edema
Hemorrhagic lesions
*Destruction of myelin & axons -potentially reversible if treatment within 4-6 hours
97
SCI MOI: hyperflexion
bending forward
98
SCI MOI: hyperextension
backward
99
SCI MOI: excessive rotation
either flexion- or extension-rotation
100
SCI MOI: compression
downward motion
101
types of spinal fractures
compression, wedge, burst
102
what is a compression spinal fracture
collapsing as a result of pressure or degeneration of the spinal bones
103
what is a wedge spinal fracture?
result from degeneration of the spine or trauma
104
what is a burst spinal fracture?
when a disc/bone in your spine is externally compressed, becoming crushed, spreading fragments throughout your spine
105
what are chance spine fractures?
pediatric seatbelt syndrome- flexion distraction injury of L-spine
106
-plegia
complete lesion
107
paresis
some muscle strength is preserved
108
tetraplegia
Injury of the cervical spinal cord.
Usually still move arms using the segments above the injury
Ex. C7 injury, can still flex forearms, using the C5 segment
109
paraplegia
Injury of the thoracic /lumbo-sacral cord ( T1 to S5)
110
hemiplegia
Paralysis of one half of the body usually in brain injuries (e.g., stroke)
111
C1-C4 motor complete injury -tetraplegia
Chronically Ventilator dependent
Require assistance to cough
Dependent on others for self-care
Problems with pressure
Variety of power wheelchairs controlled by the head, chin or mouth for mobility
112
C5 motor complete injury -tetraplegia
Not chronically ventilator dependent
Require assistance to cough
Diaphragmatic breathing only
Dependent on others for self-care
Problems with pressure relief
Variety of power wheelchairs controlled by the head, chin or mouth
113
whats included in post-injury assessment for SCI
Sustain life: ABCs
Prevent further cord damage
-Stabilize fractures
Assessment: Motor status
-Against gravity
-Against resistance
-Both sides of the body
-Ask to move
--Legs
--Hands
--Fingers
--Wrists
--Shrug shoulders
Assessment: Sensory and Vibration
Pinprick starting at toes and working upward
Always have patient close eyes or look away for accurate results
Assess for head injury and increased ICP
114
maintain map of __ for emergency SCI mgmt
>85mmHg
115
C1-C3 SCI respiratory clinical manifestations
Absence of ability to breathe independently
116
C4 SCI resp clinical manifestations
poor cough, diaphragmatic breathing, hypoventilation
117
C5-C6 SCI resp clinical manifestations
decreased respiratory reserve
118
T6 or T7-L4 SCI resp clinical manifestations
functional respiratory system with adequate reserve
119
C1-T5 SCI cardiac clinical manifestations
decreased or absent SNS influence.
Injury above T6 may develop neurogenic shock
120
cardiac interventions for SCI
Perfusion-
Vasopressors to maintain perfusing MAP (85 mmHg)
Neosynephrine/Phenylephrine (IV, Acute treatment)
Midodrine/ProAmatine (PO, chronic treatment)
DVT prophylaxis-
Apply pneumatic compression boots or stockings
Perform ROM at least q8h
Helps prevent muscle contraction
Increases venous return
Thigh and calf measurements daily
Compression stockings
121
urinary clinical manifestations for SCI
Acute
-Atonic bladder with RETENTION in spinal shock
Chronic problems
-Post acute phase
--Irritability causing dribbling
--Frequent urination.
-Neurogenic bladder
--Spastic or flaccid
-Retention and distention
--Urinary infection
--Calculi
Interventions/ Actions
INTERMITTENT CATHETERIZATION!
Sexual function
122
what is crede's crude
maneuver applying pressure over the symphysis pubis to expel the urine when cathing; used to initiate voiding in bladder retention with neurogenic bladder
123
what is poikilothermic?
the adjustment of body temp to room temperature
124
SCI complication: hypercalcemia sx
Dehydration
Fatigue
“lethargy”
Apathy
Abdominal pain
Anorexia
Nausea
Vomiting
Polydipsia
Polyuria
Behavioral changes
Kidney stone- develop over time
125
hypercalcemia tx
Acute Treatment
Hydration first
Monitor for volume overload
Medications to increase Calcium excretion
Pamidronate- slows release of calcium from bones (Biphosphonate) 2-3 days to work
Calcitonin- synthetic hormone that causes decrease blood calcium and increase bone calcium
Loop diuretics can help excrete calcium
Prednisone- (temporary) increases excretion of calcium
Long term
Reduce amount of Vitamin C intake
> 500mg of Ascorbic acid increases oxalate concentration and risk of stones
126
spinal shock presentation
Loss of reflex function below level of injury
A sudden depression of reflex activity in the spinal cord (areflexia)
127
occurence of spinal shock
Immediately after complete cord transection
May begin within 1 hour with incomplete lesions
Lasts upto 6 weeks
Regaining reflexes slowly
128
complications of spinal shock
Blood flow to cord may be compromised
Hypotension can increase cord damage
129
spinal shock assessment findings
Motor/ Sensation
Loss of all spinal reflexes below injury,
Loss of sensation
Absence of visceral and somatic sensations below level of injury
Cardiac
Blood pressure normal to hypotensive
Heart rate normal to bradycardia
Urinary
Decreased bladder function
Abdomen
Bowel distension
Paralytic ileus- begins 2-3 days post injury, resolves by day 7
130
spinal shock interventions
Maintain MAP to perfuse spinal cord
NG tube PRN paralytic ileus
Urinary bladder interventions
Maintain skin integrity
Frequent position changes
Passive ROM to avoid contractures
131
neurogenic shock presentation
Hallmark: Hypotension
due to vasodilation, due to loss of sympathetic tonic input
Bradycardia
Not tachycardia, the usual shock response
Inability to convey the information to the vasomotor centers in spinal cord
132
neurogenic shock occurence
Spinal cord injuries T6 or above
Symptoms begin within 24 hours of injury
Lasts days to weeks
133
neurogenic shock complications
DVT due to blood pooling
Orthostatic hypotension due to loss of vascular muscle tone
Unable to regulate temperature, observe close for fever
Fluid resuscitation alone can cause volume overload and pulmonary edema
134
neurogenic shock assessment findings
Cardio/Vascular
Loss of tone: muscle tone in blood vessel walls = pooling of blood
Decrease in: BP, heart rate, cardiac output
Peripheral vasodilation = venous pooling
Postural hypotension
Motor
Loss of ANS function below level of injury
Integumentary
Pt does not perspire in affected areas
Loss of temperature regulation
Venous pooling in extremities
135
neurogenic shock interventions
Transfer or change positions slowly
Monitor for DVT
Monitor vital signs
Vasopressors for hypotension- fluid will not improve
Atropine for severe bradycardia
* A drop in cardiac output and blood pressure can be life threatening*
136
causes of autonomic dysreflexia
Noxious stimuli causes overactivation of ANS
Causes vasospasm
Potentially life threatening medical emergency
Abrupt onset of excessively high blood pressure 200-300
137
occurrence of autonomic dysreflexia
Spinal cord injuries above T6
After recovery from spinal shock
Usually at least 6 months after initial injury
138
complications of autonomic dysreflexia if left untreated
Seizure
Stroke
MI
Death
139
stages of autonomic dysreflexia
Noxious Stimuli
Message sent from affected area to spinal cord
Sympathetic response initiated
Vasoconstriction below injury level
Systemic hypertension
Baroreceptors detect hypertension
Reflex Bradycardia & vasodilation
Signal blocked at injury site
140
autonomic dysreflexia presentation
Cardiovascular
Hypertension > 200/100
Bradycardia
Integumentary
Above injury level
Flushed face
Red blotches on skin
Profuse sweating
Below injury level
Goose Pimples Cold, clammy skin
GI
Nausea
Neuro
Headache
Restlessness
141
autonomic dysreflexia interventions
Immediately place in sitting position
Reduce or eliminate noxious stimuli
-Impaction- digital exam
-Constipation
-Urine retention- straight cath, check foley patency
-Renal stones
-Ejaculation
-Tactile stimulation
-Skin lesions/pressure ulcers- change position
-Ingrown toenail
-Pain
Loosen or remove constricting clothing (TEDS)
Administer antihypertensives as ordered
Educate patient and family about prevention and treatment
142
SCI acute pharmacological tx
vasopressors and high dose solumedrol
143
SCI long term pharmacological tx
GI symptoms- Histamine 2 blockers
Bradycardia- Atropine
Bladder spasticity- anticholinergics
Autonomic dysreflexia- antihypertensives
Hypotension- vasopressors
DVT/ PE prevention- Lovenox, heparin (consider risks)
Spasms- antispasmodics
144
SCI surgical tx
Reduces injury & Stabilizes the spinal cord
Indications
-Cord compression
-Bony fragments or unstable vertebral body
-Bone fragments in the spinal canal
-Compound fracture
-Penetrating trauma to the cord
145
gardner wells tongs are contraindicated for ...
unstable hyperextension injuries
146
what is bipolar I
manic episode with at least one depressive episode
147
what is bipolar II
Recurrent depressive episodes with at least one hypomanic episode
148
what is bipolar mixed
Cycles periods of mania, normal mood, depression
149
what is cyclothymic
Chronic mood disturbance (at least 2 yrs)
No loss of societal/occupational functioning
Exhibits hypomania/depression but never meets above criteria
Never without depression/hypomania for more than two months
150
symptoms of dysthymic disorder
*chronic mood disturbance*
Insomnia
Loss of appetite
Decreased energy
Decreased self-esteem
Trouble concentrating
Sadness
Helplessness
Less severe than major depression
151
what are the 2 types of seasonal affective disorder
winter/fall onset and spring onset
152
winter/fall SAD sx
Increased sleep
Increased appetite – especially carbs
Weight gain
Interpersonal conflicts
Irritability
Heaviness in extremities
153
spring SAD sx
Insomnia
Weight loss
Decreased appetite
154
sx of premenstrual dysphoric disorder
Labile mood
Irritability
Increased interpersonal conflict
Trouble concentrating
Feeling overwhelmed or unable to cope
Anxiety
Tension
Hopelessness
155
what is mania
A distinct period during which mood is abnormally and persistently elevated, expansive, or irritable lasting at least 1 week
156
mania sx
Inflated self-esteem/grandiosity
Decreased need for sleep
Excessive/pressured speech (unrelenting, rapid, often loud without pause)
Flight of ideas -racing, often unconnected thoughts
Distractibility
Increased activity/psychomotor agitation
Excessive pleasure-seeking/risk taking behaviors
Spending money, sexual behaviors
Mood- excessively cheerful, enthusiastic, expansive, irritable
Deny problems, blame others for issues
Can experience delusions & hallucinations when in manic episode
Length of mania varies
157
what is hypomania
Period of abnormal and persistent elevated, expansive, or irritable mood.
Difference hypomania do not impair ability to function
No psychotic features
Over time may lead to mania
158
what is mixed episode (mania)
Experiencing both mania and depression nearly every day for at least 1 week
Also called rapid cycling
159
interventions for bipolar
Provide for safety
Must set boundaries and limits for the patient
Meeting physiologic needs (Maslow)
Decrease stimuli
Establish routines
Ringer foods (high protein/high calorie)
Monitor fluids/sleep
Providing therapeutic communication
Use positive communication to avoid perception of judgement or frustration
Use clear, direct, simple sentences
Ask them to repeat brief messages
Accept responsibility for not understanding their speech
Promoting acceptable behaviors
Treat patient with dignity and respect
Remain matter-of-fact and non-judgmental
Use distraction
160
psychopharmacology for bipolar
Lifetime regimen of medication
Antimanic
Lithium
Anticonvulsants
Mood stabilizers
Only psych disorder in which meds can prevent acute exacerbations
Antipsychotic
During acute manic stage (if disordered thinking seen)
Some patients stay on long-term
161
lithium blood levels
0.5 – 1.0 mEq/L Normal
0.8 – 1.5 mEq/L Therapeutic
>1.5 mEq/L Toxicity
162
lithium toxicity sx
N/V/D, drowsiness, muscle weakness, slurred speech
163
challenging side effects of lithium
Tremors
Thirst
Vomiting &/or Diarrhea
Weight gain
Concentration issues
Rebound symptoms if stopped suddenly
Thyroid Issues
164
what is lithium
Salt naturally found in the body
Response rate approx. 70-80%
Stabilizes mood
Avoid extremes of mania/depression
Binds to salt receptor sites
Cleared in kidneys
Need regular bloodwork checks levels
165
alternative meds for bipolar
valproic acid (depakote)
carbamezapine (tegretol)
166
depakote therapeutic level
50-125
167
therapeutic level of carbamezapine
4-12
168
what speeds conduction on a neuron
myelin sheath
169
neurons are unable to ________.
unable to create or store glucose
get glucose by perfusion, adequate blood flow to brain
170
normal glucose level of CSF
40-80 mg/DL
171
what are causes of altered LOC
increased ICP sustained pressure 15 mmHg or more
cerebral infarction
hematoma
intracranial hemorrhage
tumors
infections
demyelinating disorders
hydrocephalus
172
normal adult intracranial pressure
5-15 mmHg
173
why is increased intracranial pressure a life threatening emergency?
Increased ICP causes ↓ cerebral blood flow
-Hypoxemia and hypoxia
-Hypercapnia and ↓pH
-Cerebral vasodilation (↑ blood flow),
-Edema
-Continued Increasing ICP
-Irreversible brain damage, brain herniation, & death
174
clinical manifestations of increased ICP
Changes in cortical function
Irritability, agitation
Behavior, personality changes
Memory,
Impaired judgment
Changes in speech pattern
LOC decreases
175
what is a big difference with pediatric clinical manifestations of increased ICP?
downward deviation of eyes
176
increased ICP interventions
Elevate head of bed to 30-45 degrees
Tight glycemic control (keep in 80-180 range)
Prevent shivering
Avoid hyperthermia
Optimize blood pressure-
Avoid hypo/hypertension
Careful fluid resuscitation-
may need pt to keep PaO2 of 60 and sat of 90
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increased ICP pharmacological interventions
Vasopressors- maintain MAP and CPP
Antihypertensive medications as needed
Pain medications
Anxiety medications
Seizure- preventions and acute treatment
Barbiturates- Cerebral protection, decrease cerebral metabolic needs
Osmotic diuretics- Shift fluids into intravascular (Mannitol, Hypertonic saline)
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TBI primary injury
initial direct damage to tissues and blood vessels-permanent damage
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TBI secondary injury
cascade of complex biochemical responses damaging neurons not involved in initial injury.
Impaired cerebral blood flow regulation
Hypoxia
Hypotension
Ischemia
Seizures
Fever
HYPOPERFUSION
Mortality rate can be higher than Primary Injury
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red flags for TBIs
Sudden acute headache
Nausea & vomiting
Increased restlessness
Agitation
Nuchal rigidity
Motor weakness
Pupil changes
Changes in VS
Decrease in GCS
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types of TBIs
Concussion
-Chronic Traumatic Encephalopathy
Epidural Hematoma
Subdural Hematoma
Intracerebral Hematoma
Basilar Skull Fracture
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cause and result of concussion
Direct blow to head, neck, face or torso
Results
Rapid onset of short-lived impaired neuro function with spontaneous resolution
May or may not involve LOC
Normal Neuroimaging (no structural damage)
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mild concussion
GCS score from 14-15 and less than 30 min
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moderate concussion
GCS score from 9-13 and 30 min to 6 hours
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severe concussion
GCS score below 9 and over 6 hours
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concussion sx
physical- headache, N/V, balance or vision problems, fatigue, photosensitivity, noise sensitivity, being dazed
cognitive- feeling foggy, difficulty w concentrating, forgetting recent info, confusion
emotional- irritability, sadness, over emotional, nervousness
sleep- drowsiness, sleeping more, difficulty falling asleep
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what is cushings triad?
increased systolic BP, decreased pulse, decreased respirations
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what is post concussive syndrome
Can last weeks to months
Risk not necessarily associated w/ severity of injury
Normally within the first 7-10 days
H/A described as tension, dizziness, fatigue, irritability, anxiety, insomnia, decreased concentration/ memory, sensitivity to noise and light
Cumulative threat
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what is concussion secondary impact syndrome
After initial concussion additional trauma to brain (before fully healed) can lead to short and long-term neurologic problems
Additional Brain trauma
May only be minor
Causes neurologic disturbance
Typically with catastrophic results
Signs & Symptoms
Cerebral edema
Cerebral blood flow compromised
Decrease in tissue pH
Hypoxemia and Hypotension
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what is chronic traumatic encephalopathy
Repeated brain trauma cause increased tau release in the brain
Younger (12 & under) athletes sustain more damage with repeated injury
Symptoms can be delayed 8-10 years
Progression is predictable through 4 identified stages
End stage develops into Parkinson’s disease or Alzheimer's like presentation
Postmortem currently only definitive diagnosis
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CTE stage 1
Attentional deficits, headaches, and dizziness
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CTE stage 2
Increased prominence of mood swings or emotional changes, impulsive behavior, or poor judgement. (may include explosive, pathological, intoxicated and morbid paranoia or jealousy)
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CTE stage 3
Memory and cognitive impairment including trouble with executive functioning
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CTE stage 4
Progressive Alzheimer like dementia with motor symptoms, Parkinson's like or lack of coordination, hypomimia (speech abnormalities)
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what is epidural hematoma
Rupture or laceration of artery
Usually by Skull fracture
Arterial bleeding
Blood accumulates between skull & dura mater
Extreme emergency: Rapid Progression
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epidural hematoma sx
Transient LOC then
Lucid intervals
Then rapid deterioration in neuro status
Neurologic deficits
Resulting in coma
Respiratory arrest
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epidural hematoma tx
craniotomy to relieve pressure
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acute subdural hematoma sx
Symptoms within 48 hours
Signs & Symptoms
Altered LOC
S/S of IICP
Hemiparesis
Hemiplegia opposite side from hematoma
Unilateral fixed and dilated pupils on same side
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subacute subdural hematoma sx
Symptoms between 48 hours and 2 weeks
Signs & Symptoms
Altered LOC
S/S of IICP
Hemiparesis
Hemiplegia opposite side from hematoma
unilateral fixed and dilated pupils on same side
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chronic subdural hematoma sx
2 weeks after injury
Seen with alcoholism, anticoagulants
Signs & symptoms
Headache
Progressive personality changes
Decrease in LOC
Ataxia
Incontinence
Seizures
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common causes of intracerebral hematoma
Occurs deep within brain tissue
Common causes
Contusions
Untreated hypertension
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locations of intracerebral hematoma
frontal lobes, temporal lobes
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s/s of intracerebral hematoma
Progressive rapid decline in LOC
Headache
S/S of IICP
Pupil changes
Contralateral hemiplegia
Systemic hypertension,
CVA presentation
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what is basilar skull fracture
Fracture to floor of skull
Laceration to vasculature
Often leads to CSF leakage
High risk for infection
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signs of brain herniation
2 or more of the following:
Movement
Extensor posturing
Lack of motor response to noxious stimuli
Pupils
Asymmetric
Dilated
Non-reactive pupils
Level of Consciousness
Drop in GCS >2 in patient with initial GCS of <9
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pharmacology for increased ICP
Diuretics
Sedation
Paralytics are chemical restraints
Antipyretics
Anticonvulsants
GI prophylaxis
TPN if enteral feeding not possible
IV fluids
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diuretics for increased ICP
Hypertonic Saline
Mannitol (Osmotic) Used for ICP over 15-20mmHg
Draws water out of edematous brain tissue into vasculature
Always use lowest dose possible
Loop Diuretics
Furosemide .
Inhibit Na and Cl reabsorption
Reduce rate of CSF production
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what is persistent vegetativ state
Complete unawareness of self or environment
Loss of all cognitive functions
Death of cerebral hemispheres
Continued function of the brainstem and cerebellum
May have eye opening to external stimuli
Unable to follow commands
Bowel and bladder incontinence
Variable cranial nerve preservation
May retain cough, gag, and swallow reflex
But unable to coordinate actions
Dx 1 month after injury
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what is locked-in-syndrome?
Lesion in pons of the brain
Complete paralysis
Inability to speak
Tetraplegia
Alert & fully aware of environment
Pervasive awareness and cognitive function
Some eye movements
Blinking is the only form of communication
Normal hearing and seeing
No chew, swallow, gag reflexes, or breathing on their own
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prognosis of locked in syndrome varies according to ____.
cause
pathological process
age
condition
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what is brain death
Irreversible loss of function of the entire brain
Absence of brain stem reflexes
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what is a seizure?
Abnormal discharge of energy & subsequent spread through cerebral cortex.
Disrupts neurologic functioning.
Result in generalized or localized motor activity
*key piece of information is the patient's hx or not of seizures
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causes of seizures
TOXINS/POISONING
DRUGS
METABOLIC DISTURBANCES/ ELECTROLYETS
HYPOGLYCEMIA
KIDNEY FAILURE
INFECTION
SHOCK
Bleeding in the brain
TRAUMATIC BRAIN INJURY
STROKE
TUMORS/ CANCERS
FEVER
ALCOHOL
HYPOXIA
ECLAMPSIA
MEDICATION NON-COMPLIANCE
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generalized seizures
occurs in both hemispheres
may begin with an aura
tonic clonic and absence
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what is tonic-clonic seizure
muscle hypertonic state to clonic or ridged contractions
rhythmic
recurrent jerking
possible airway compromise
followed by post-ictal state
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what is petite mal seizure
absence
loss of awareness
no change in muscle tone
common in children
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what is a partial seizure
limited to a discrete part of brain
rare post ictal state because only one area
sx dependent on location
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what is a simple seizure
remain conscious
sudden unexplained feelings
sense something aren't real
may have language impairment
may have muscle involvement
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what is a complex seizure
may have an aura
amnesia before and after
impairment of awareness with typical movements (lip smacking, picking at clothing)
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what is status epilepticus
prolonged continuous seizure activity or multiple seizures in a short period of time without full recovery
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precipitating seizure events
AURAS
-LIGHTS
-SOUNDS
-SMELLS
SPECIFIC COMPLAINTS
-WEAKNESS
-PAIN
UNUSUAL BEHAVIORS
RECENT INFECTION
HEADACHE/RECENT TRAUMA TO THE HEAD
HISTORY OF SUBSTANCE ABUSE
MEDICATION CHANGES
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DO for seizure interventions
Keep them safe
Monitor Airway
Place in side-lying position
Move objects away
Time the seizure
Observe characteristics
Have suction ready
Pad siderails
Ask family about precipitating factors
-Medication compliance
-Trauma
-Toxic ingestion
-Infection
-Hypoglycemia
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DONT for seizure interventions
Restrain the patient
Put anything in their mouth
Leave the patient
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brief seizure
less than 5 minutes
225
prolonged seizure
over 30 minutes
226
goal of therapy for status epilepticus
rapid termination of both clinical and electrical seizure activity
Airway control
Midazolam (Versed) IV/IN if IV not established
Diazepam (Valium) & Lorazepam (Ativan) given IV
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acute complications for status epilepticus
Hyperthermia
Pulmonary Edema
Cardiac Arrhythmias
Cardiovascular Collapse
Death
228
long term complications for status epilepticus
Epilepsy
Encephalopathy
Local Neurologic deficits
229
clinical presentation of New Onset Refractory Status Epilepticus
Patients suddenly develop a prolonged seizure or a flurry of seizures that do not respond to at least two standard anti-convulsant medications and for which cause for the seizures remains unidentifiable beyond 72 hours.
230
What is NORSE?
defined as refractory status epilepticus without an obvious cause after initial investigations
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seizure medications
anticonvulsants- levetiracetam (keppra), carbamezapine (tegretol), phenytoin (dilantin)
barbiturates- phenobarbital
benzodiazepines- diazepam (valium), lorazepam (ativan)
232
what is tegretol first choice for?
partial, generalized tonic clonic and mixed seizures
233
common adverse effects of tegretol
fatigue, vision changes, nausea, dizziness, rash, serious blood disorders
234
risk factors for dilantin toxicity
Advanced age
Concurrent use of medications
-Other seizure medications
-Antibiotics
-Antiarrhythmics
-Alcohol
-Tuberculosis medications
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symptoms of dilantin toxicity
Fast, uncontrollable eye movements or double vision
Dizziness, drowsiness, or confusion
Lack of coordination of fingers, hands, arms, legs, or body
Slurred speech
Nausea or vomiting, Decreased appetite
Decreased activity
Abdominal bloating
Irregular jerky movements in children or the elderly
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public health
reminder to look at public health pictures- lyme
237
required documentation for non-behavioral restraints
* Verification of restraint order
* Modification in plan of care
* Alternatives tried prior to restraints
* Individual assessment and reassessment related to restraints
* Clinical justification for restraints
* Type of restraint used
* Education provided to patient or family about restraints
* Monitoring results
* Care provided while in restraints
* Staff concerns related to safety that led to restraints
* Any injuries sustained by patient (if applicable)
238
required documentation for behavioral restraints
* Verification of restraint order
* Modification in plan of care
* Alternatives used or considered prior to restraints
* Individual assessment and reassessment related to restraints
* Clinical justification for restraints
* Type of restraint used
* Education provided to patient or family about restraints
* Monitoring results
* Care provided while in restraints
* Staff concerns related to safety that led to restraints
* Any injuries sustained by patient (if applicable)
* Participants in restraint application
