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N202 > Trauma2 > Flashcards

Trauma2 Flashcards

1
Q

hypoglycemia causes

A

alcohol intake without food, too little food, too much medication, loss of weight without medication adjustment

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2
Q

signs and symptoms of hypoglycemia

A

cool, clammy, tachy, HA, tremors, hunger, EKG changes, dizzy

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3
Q

hyperglycemia (DKA)

A

acute, life threatening complication of uncontrolled type 1 DM
metabolic acidosis-characterized by hyperglycemia, and excessive ketones in blood due to breakdown of fats for energy

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4
Q

signs and symptoms of hyperglycemia

A

polyuria, polydipsia, polyphagia

tachy, HTN, kusmal breathing (deep & rapid), fruity smelling breath and urine

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5
Q

Tx for DKA

A

patent airway, IV fluids (NS), IV insulin (regular), frequent blood glucose checks, IV dextrose to avoid hypoglycemia, monitor serum K+

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6
Q

what is the goal to decrease blood sugar by

A

50 mg/dl/hr

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7
Q

HHNK

A

often mistaken for DKA, common in type 2

results from high BG without increase serum ketones

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8
Q

signs and symptoms for HHNK

A

BG over 600, extremly dehydrated, no significant acidosis, no ketonuria, no kussmauls

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9
Q

tx of HHNK

A

airway, IV fluids, IV insulin, IV dextrose to avid hypoglycemia monitor serum K+ (EKG changes)

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10
Q

types of burn injury

A

thermal, chemical, smoke inhaltion, electrical, cold thermal injury

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11
Q

burn management pre hospital care

A

A, B, C, cool, airway immediately, no ice , no creams/ointments

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12
Q

red shinny appearence, involves epidermis

A

superficial partial thickness

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13
Q

involves dermis

A

deep partial thickness

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14
Q

invovles thickness burn

A

involves fat, muscle, bone

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15
Q

what is burn center referral criteria

A

2nd degree burn, any age, BSA of 10%

3rd degree burn, any age, any BSA

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16
Q

Emergent (resuscitative) phase

A

time burned to 1st 48 hours, phase begins with fluid loss & edema formation and continues until fluid mobilization & diuresis begin
airway, maintain body temp., fluid replacement LR

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17
Q

what is the goal of fluid resuscitation

A

prevent shock

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18
Q

parkland formula

A

4ml x body weight (kg) x % of burn = 24 hour total fluid

  • five first 1/2 in 1st 8 hours
  • fluid resusciation begins with BSA more than 10%
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19
Q

patho of fluid & electrolytes shifts

A

plamsa leakage = increase interstital volume

decrease blood volume, increase HCT, decrease SBP

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20
Q

assessment of burns

A

rule of 9s, palmer method, lund and browder chart (used at burn centers)

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21
Q

what is the cut off point for recovery of the skin

A

hair follicle

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22
Q

acute phase

A

after 1st 48 hours to healing, fluid replacement, magangement of complications, PT wound care, excision and grafting, necrotic tissue begins to slough, formation of granulation tissue (heals from edges and goes inward) full thickness burns must be covered with skin grafts

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23
Q

complications of burns

A

infection, cadiovascular arrhythimias, escharotomy, renal (maintain UO of 50/100ml/hr, 100 ml/hr for electrical burns), paralytic ileus

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24
Q

escharotomy

A

performed on full thickness burns, ideally done in burn center

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25
Q

fasciotomy

A

release of muscle of fascia

RARE

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26
Q

allograft

A

cadaver skin * gold standard

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27
Q

xenograft

A

animal tissue (pig skin)

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28
Q

biobrane

A

biosynthetic material embedded with collagen (good bc can be done out patient

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29
Q

cultured epithelial autografts

A

grown from biopsies obtained from pts own skin, used in pts with large BSA burns or with limited skin for harvesting

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30
Q

transcyte

A

skin cells harvested from newborn foreskin

good for partial thickness wound

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31
Q

integra

A

artificial skin with dermal layer made of collagen and epidermal layer of silicone
*grow with the pt, so its good for joints

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32
Q

scare management

A

early excision and grafting, position of function, exercise and recondition, may need pressure garments, skin needs to be lubricated (no longer have oil glands), may be hypersensitive to temp. changes

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33
Q

what is the #1 choice for pain management in burns

A

morphine (high doses bc of increase of metabolism with burn)

opiods, sustained release meds, anxiolytics (xanax), NSAIDS, PCA, sedation

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34
Q

nutrition with burns

A 
increase of protein, calories
TPN & PEG tubes
resting metabolic expenditure may be increased by 50-100% above normal 
core temperature is elevated
caloric needs are about 5,000/day
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35
Q

rehabilitation with burns

A

protect from sun light for up to 1 year, long term rehab, most common complication is the skin and joint contractures

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36
Q

what are the 3 major goals of TBI

A

prevention of primary injury, prevention of secondary injury, optimal recovery

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37
Q

what are the #1 reason for TBI in 0-4 and over 75

A

falls

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38
Q

primary injury

A

direct tissue damage from trauma

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39
Q

kinetic forces applied to the cranium and brain produce shearing, sliding, twisting, and compressive strains on the skull and brain, theryby, tearing, and fracturing tissue, vessels, axons, and bone

A

MOI

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40
Q

a moving object hits a stationary head

A

acceleration

*getting hit with bat in the head

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41
Q

a moving head hits a stationary object

A

deceleration

*in MVC head hits steering wheel

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42
Q

when the head strikes a fixed object, the coup injury occurs at _______, and contracoup injury occurs at ____

A

coup-contracoup injury
site of impact
opposite side of impact

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43
Q

types of skull fractures

A

linear, depressed, comminuted, compound, basilar

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44
Q

a crack, clean break in skull

A

lenear fx

Tx: bedrest

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45
Q

bone is displaced inward, may or may not lacerate the dura or brain tissue

A

depressed

Tx: surgically elevate bone, repair dura prn, Abx

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46
Q

skull fx or splintering or fragments

A

comminuted

Tx: surgically remove fragments

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47
Q

skull fx open to outside

A

compound

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48
Q

linear fx to the base of skull, usually crosses sinus and tears dura (leakage of CSF or blood)

A

basilar

Tx: if drainage give Abx, bed rest, neuro checks, dont blow nose, hearing test follow up

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49
Q

signs and symptoms of basilar skull fx

A

bleeding from nose and ears, halo sign, can have facial battle sign/raccoon eyes, paralysis or conjujjated deriation of gaze (location of fx determines s/sx)

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50
Q

meninges in order

A 
Skull
Dura
arachnoid 
pia mater
brain
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51
Q

most minor type of head trauma is

A

scalp laceration, highly vascular, profuse bleeding

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52
Q

major complication of lacerations

A

infection

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53
Q

contusion

A

bruising of brain tissue, maintains integrity

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54
Q

“talk & die syndrome”, rapidly deteriate and die, bleeding between the dura and inner surface of skull

A

epidural hematoma
*neurological emergency
can be venous, most likely arterial
*common in temporal region

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55
Q

S/sx of epidural hematoma

A

ipsilateral pupil changes, contralateral motor changes

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56
Q

Tx for epidural hematoma

A

surgical removal of clot, if caught early good outcome

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57
Q

bleeding between dura and arachnoid layer, venous bleed, slow onset, change LOC, increase ICP

A

subdural hematoma

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58
Q

acute subdural hematoma

A

symptomatic within 24 hours of innjury

Tx: evacuation of clot

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59
Q

subacute subdural hematoma

A

symptomatic 24-72 hours after injury

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60
Q

chronic subdural hematoma

A

S/sx show 2 or more weeks after injury, mimic dementia, seen in alcoholics and elderly
*30-60% mortality

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61
Q

bleeding can occur in any area of the brain where there has been tearing of tissue

A

intracerebral hematoma

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62
Q

what injury can increase risk of abcess

A

penetrating injury

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63
Q

bleeding into subarachnoid space

A

subarachnoid hemorrhage

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64
Q

mild TBI, a sudden transient mechanical head injury with disruption of neural activity & change in LOC (NO structural changes)
brief disruption of LOC, amnesia, HA, short duration

A

concussion

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65
Q

post concussion syndrome

A

2weeks-2 months after injury, persistant HA, lethargy, personality and behavior changes

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66
Q

widespread axonal damage occuring after TBI, shows microscopic lessions in the brain, axonal disruption occurs hours following the injury in response to secondary events in the axonal membrane & cytoskeleton

A

diffuse axonal injury

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67
Q

S.Sx of diffuse axonal injury

A

decrease LOC, increase ICP, decerbration or decortication, global cerebral edema
Mild: LOC for 6-12 hours
moderate: prolonged coma
severe: prolonged coma, veg. state, 60% mortality

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68
Q

Dx for TBI

A

CT considered best, shows structural changes,

MRI more sensitive for lesions

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69
Q

events (biophysical and biochemical) changes that affect perfusion after the primary injury

A

secondary injury

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70
Q

cerebral dynamics (metabolism)

A

brain requires 25% of the bodies total O2, and glucose requirements
brain DOES NOT store O2, and little quantities of glycogen (they must have a continuous supply of both)

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71
Q

what influences the amount of glucose and O2 the brain needs

A

activity

seizures, hyperthermia, etx.

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72
Q

the amount of blood passing through brain tissue in one minute

A

cerebral blood flow

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73
Q

what is the normal CBF

A

750ml blood/minute

74
Q

autoregulation

A

this is achieved by the automatic alteration in the the diameter of the cerebral blood vessels to maintain a constant blood flow to the brain

  • arterial pressure decreases with cerebral vasodilation
  • arterial pressure increases with cerebral vasoconstriction
75
Q

the brains ability to accomodate changes in volume (r/t blood flow)

A

elastance

elastance = pressure/volume

76
Q

is the inverseof elastance, the expandiability of the brain (r/t brain)

A

compliance

compliance = volume/pressure

77
Q

what is ICP influenced by

A

cerebral blood flow and cerebral edema

78
Q

normal ICP

A

0-15 mm Hg

79
Q

Monro-kellie hypothesis

A

if there is change in one there has to be a change in the other
(blood 10%, brain 80%, CSF 10%)

80
Q

normal ICP = what

A

the pressure exerted by the total volume from the brain, blood and CSF

81
Q

what are normal compensatory adaptaions for ICP

A

aleration of CSF absorption or production
displacement of CSF into spinal subarachnoid space
dispensability of the dura

82
Q

cerebral blood flow is the amount of _____

A

blood flow/min passing through brain tissue

83
Q

cerebral blood volume is the amount of ____

A

blood thats passing though

84
Q

increase pCO2, decrease pO2, acidosis causes

A

vasodislation and increase CBF

85
Q

decrease pCO2, increase pO2 causes

A

vasoconstriction and decreases CBF

86
Q

cerebral blood volume is controled by

A

autoregulation

87
Q

MAP

A

MAP = S-D + D
——
3

88
Q

MAP less 50

A

cerebral vessels poorly perfused, ischemic changes

89
Q

MAP greater 170

A

cerebral vessels cannot vasoconstrict, causes hyperemic state = increase ICP

90
Q

CPP

A

the pressure needed to ensure blood flow to the brain

MAP - ICP = CPP

91
Q

normal CCP

A

50-150 mmHg (avg. person 80-100)

92
Q

hyperemic state (increase ICP)

A

CPP greater 150

93
Q

ischemia

A

CPP less 50

94
Q

CPP incompatible with life

A

CPP less 30

95
Q

when MAP = ICP, CPP = ____??

A

o, and all CBF stops

96
Q

what happens when ICP is increased

A

ICP is influenced by cerebral blood flow and cerebral edema, these facotrs lead to changes in teh CPP, thus increasing the risk of secondary injury

97
Q

early signs of ICP

A

change of LOC, decreased visual acuity, HA (continuous and worse in AM), elevated temp, vomit, cushings triad

98
Q

cushings triad

A

bradcardia
widening pulse pressure
irregular respirations

99
Q

late signs of ICP

A

oular signs, decrease motor function, decerebrate (more serious), decorticate posturing

100
Q

Dx increased ICP

A

ICP measurements

CT, MRI, cerebral angiography, PET, etc

101
Q

consciousness has 2 components

A 
arousal component (wakefulness)
content component (ability to reason, talk, feel & react to stimuli with purpose & awareness)
102
Q

abnormal state inwhich the pt is unaware of self or enviornment

A

unconsciousness

103
Q

what are characteristics of diminishing LOC

A

more stimuli to get reponse, thoughts are slower or simpler, reflexes become more slower & primitive

104
Q

Neuro checks include

A

neuro assessment, subjective data, pupils, respiratory, motor strength and response, VS including temp

105
Q

glascow coma scale

A

motor response
verbal response
eye opening response

106
Q

what needs to be looked at for the trauma pt

A

aspiration, skin breakdown, DVT, airway, nutrition

107
Q

management of TBI

A

airway (Cspine)
breathing: prevent hypoxia, controled vent. use PEEP (use with caution)
circulation: hypotension, aggresive fluid resusitation (LR or NS), HTN: not aggresivly tx unless systolic is extremly high, if you have to Tx use nimopine (doesnt effect ICP)
positioning (HOB 30-45) slow position changes, suction PRN only hypervent. prior and after

108
Q

enviornmental supprt of TBI

A

decrease noise, calm enviornment, minimize procedures, gentle movement

109
Q

temperature control

A

every one degree of temp increases O2 demand and increases ICP
Tx of any temp aggresivly,

110
Q

planning care of TBI

A

DO NOT CLUSTER CARE, can increase ICP, need rest periods

111
Q

nutritional care of TBI

A

increase glucose, perfered method is G tube, nutirional intake 140%

112
Q

a condition that is the consequence of a previous disease or injury

A

sequela

113
Q

sequela of ICP

A

inadequate cerebral perfusion, cerebral herniation

sustained increase of ICP result in brainstem compresion and herniation of the brain from one compartment to another

114
Q

as pressure increases, it forces shifting or herniation of brain from one compartment of high pressure to one of lesser pressure, the displacement of brain tissue from compressing and displacing adjacent structures

A

herniation

115
Q

supratentorial

A

above the fold of teh tentorium cerebelli

double enfolding of the dura mater under the temporal lobe

116
Q

infratentorial

A

below the fold of the tentorium cerebelli

117
Q

goal of tx of herniation

A

prevent it

118
Q

types of herniation

A

uncal
cingulate
central
infratentorial (upward and downward)

119
Q

most frequent type of herniation, unilateral mass (temporal) increased ICp, tip of temporal lobe displaces laterally and pushes the uncus over the edge of the tentorium

A

uncal (supratentorial)

120
Q

S.sx of uncal

A

ipsilateral pupil dilation with contralateral paralysis, contralateral positive babinski

121
Q

lesion of one hemisphere shifts laterally and forces the cingulated gyrus under the Falx cerebri

A

cingulate

122
Q

S.sx of cungulate

A

LOC decreases

123
Q

expanding mass midline results in downward displacement of the hemispheres through the tentorial notch

A

central (transtentorial herniation)

124
Q

S.sx of central herniation

A

pupils small fixed, dilated, respiratory changes.

125
Q

occurs with expanding lesion of cerebellum, causes protrusion of central part of cerebellum and midbrain up through tentorial notch, compresses 3rd crainal nerve and blocks flow of CSF (hydrocephalus)
Have rapid deterioration

A

upward trantentorial herniation

126
Q

pressure downward pushes cerebellar tonsils through foramen magnum, compresses the medulla = immediate resp. and cardiac arrest

A

downward cerebellar herniation

127
Q

what is something that needs to be initiated with any head injury

A

sezuire precautions

128
Q

only Tx for post traumatic epilepsy

A

bezo (early)

late (after 7 days), same as any other seizure

129
Q

Tx for stress ulcers

A

proton pump inhibitors

130
Q

drainage of CSF from nose or ear denotes presence of what

A

fistula from subarachnoid through skull to the nose or ear

goal= prevent infection

131
Q

acute hydrocephalus

A

problem with reabsorption or blockage of CSF, S/sx are that of ICP, Tx: shunt

132
Q

the irreversible cessation of all functions of the brain incuding the brain stem

A

brain death

133
Q

what tool is used to measure level of awareness, cognition, behavior and interaction with the enviornment

A

Ranchos Los Amigos Scale

134
Q

what is the overall nursing management goals for TBI

A

ICP WNL
adequate ventilation
normal fluid & electrolyte balance
prevention of complications

135
Q

decreases O2 and glucose demands, limits increases in ICP caused by agitation , restlessness, posturing, asynchrony with mechanical ventilation, and painful procedures

A

sedative agents

136
Q

decreases body metabolic neds and controls shivering and posturing that may increase ICP (pt must be sedated, intubated, and on vent with use)

A

neuromuscular blockades

137
Q

treats and minimizes pain, prevents iatrogenic increases in ICP
ex: ativan, Versed, Propofol, morphine, haldol

A

analgesia

Narcan reverses these Rxs

138
Q

Mannitol

A

osmotic diuretic VERY POTENT
not recommended for initial resuscitation dc of diuretic effect (prevent hypotension)
drug of choice in ER when brain herniation is impending

139
Q

CADSCAN Mannitol

A

C: Osmotic diuretic
A: decreases ICP by increasing intravascular to exravascular osmitic gradient (shift of fluids), causes decrease of CSF production
D: IV bolus better 0.25-1.0 gram/kg RAPID IV (to avoid crystallizing)
S: rapid electrolyte changes, decrease BP
N: VS, CVP, electrolytes, assess for fluid volume deficit
caution: rebound phenomenon (need intact BBB), avoid dehydration, onset is 10-20 minutes lasts 6 hours

140
Q

CADSCAN Lasix

A

C: loop diuretic
A: decreases CSF production, deceases H2O in brain tissue by decreasing overall body water
D: 0.5-1 mg/kg IV (usually given with Mannitol)
N: less likely to cause dehydration

141
Q

used to prevent vomiting, which can increase ICP

A

antiemetics

142
Q

used to prevent alcohol S&sx of withdrawal (cause of TBI may have been alcohol related)

A

Benzodiazepines

143
Q

usedd but not effective tx

A

corticosteroids

144
Q

used to control seizures, DO NOT prophylactically tx all pts , can cause new onset of seizures

A

anticonvulsants

Dilantin, Phenobarb

145
Q

refractory high ICP, decreases cerebral metabolism and CBF, but can supress myocardium, hypotension and hypothermia

A

Barbituates

Ex. pentobarbital, pentothal

146
Q

aim is to tx or alter pathways associated with ischemia, decreasing secondary injury, needs to be given soon after injury to be affective

A

neuroprotectants

147
Q

waxing and wayning of resp. with short period of apnea, have lesion deep inside the cerebral hemipshere & basial ganglia

A

cheyne stokes

148
Q

equal, rapid breath, deep, have lesions in the lower midbrain to midpons area

A

central neurogenic hyperventilation

149
Q

rapid breaths followed by apnea then rapid breaths followed by apnea, lesions of the upper medulla

A

cluster breathing

150
Q

like cluster breathing but hypoventilation is occuring, lesion in medulla

A

Biots breathing

151
Q

decrese resp. capacity, and decrease amount of breaths, lesion in medulla

A

depressed breathing

152
Q

struggling to breath, medulla lesions

A

gasping breaths

153
Q

inhale, period of apnea/puse, exhale, period of apnea/pause, lesions to lower pons

A

apneustic breathing

154
Q

SIADH Tx for TBI

A

IV hypertonic (pulls water out) NSS, Lasix, tends to be self limiting when caused by head trauma

155
Q

Diabetes insipidus Tx for TBI

A

replace fluids, vasopressins, tends to be self limiting when caused by head trauma but permanent when following intracrainial surgery

156
Q

surgeon who specializes in surgery of CNS

A

neurosurgeon

157
Q

opening into cranium with removal of bone flap and opening dura to remove lesion, repair a damaged area, drain blood, or relieve increased ICP

A

craniotomy

158
Q

excision into the cranium to cut away a bone flap

A

craniectomy

159
Q

repair of a cranial defect resulting from trauma, malformation, or previous surgical procedure, artifical material to replace damaged or lost bone

A

cranioplasty

160
Q

what are indications for intracranial surgery

A

intracranial bleeding, skull fractures, relieve refractory ICP

161
Q

preoperative phase

A

Dx test, neuro exam to recieve baseline, teach family, scalp preperation

162
Q

intraop phase

A

position head rest with tongs, eye care (ointment), anesthesia & Rxs (Abx, mannitol, lasix), monitoring (ICP, EEG, CVP, foley cath

163
Q

what is the goal during and after surgery

A

prevent and minimize increase ICP

164
Q

double fold or dura mater that forms a partition between the cerebrum and brain stem/cerebellum

A

Tentorium

165
Q

Supratentorial

A

above tenrotium, includes cerebrum, incision is made behind hair line

166
Q

infratentorial

A

below tentorium, includes brainstem and cerebellum, incison is made above nape of neck

167
Q

Post op

A

assessments (esp. 1st 48 hours), neuro status, ICP, I&O, stools for OB, watch for Diabetes insipidus (common),
NO couching, deep breathing, suctioning, vomiting, straining

168
Q

nursing interventions post op

A

aseptic technique for dressing, bedrest 24hours, HA (ice on and off 30 minutes, loosen dressing), periocular edema (alternate warm/cold compress)
positioning: HPB depends on type of incision

169
Q

HOB for supratentorial incision

A

elevated 30-45 degrees

170
Q

HOB for infraentorial incision

A

FLAT

171
Q

supratentorial dressing, neck position, OOB, compliations

A

circles head, neutral position, no twisting/turning, 24-48 hours after surgery, seizures, increase facial edema, ecchymosis around eyes (cant open eyes)

172
Q

infratentorial dressing, neck position, OOB, compliations

A

circles head with neck support, turned on either side, neck completly straight, OOB 3-5 days, resp. & temp issues, 9th/10th crainal nerve (tounge/gag reflex)

173
Q

when does increased ICP and cerebral edema peak with surgery

A

72 hours

174
Q

are HA common

A

yes, expected 1st 24-48 hours, very severe

175
Q

what causes permanent personality changes

A

cerebral anoxia

176
Q

extended irreversible decline in the overall cognitive function of the pt

A

dementia

177
Q

chronic condition that occurs after severe cerebral injury
*intact autonomic functions, intact reflexes, presence of a sleep-wakefullness cycle, spontaneous eye opening, absense of local motor response to stimuli, absence of intact cognitive functions or awareness of self or the enviornment

A

vegatative state

178
Q

complete paralysis of all 4 extremities, but maintain full consciousnes, are unable to move or speak, only voluntary movement is vertical eye movement and blinking

A

locked in syndrome

seen in polio, myasthenia gravis, and some CVA

179
Q

irreversible severe brain damage, marked by deterioration of cognitive functions and awareness of self and enviornment

A

brain death

180
Q

pt appears to be drowsy, lethargic and somnolent, when stimulated, easily aroused and responds approp.

A

obtundation

181
Q

pt is very drwosy and lethargiv, only be briefly aroused with repeated vigorous, painful stimuli

A

stupor

N202 (8 decks)

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