Trauma2 Flashcards
hypoglycemia causes
alcohol intake without food, too little food, too much medication, loss of weight without medication adjustment
signs and symptoms of hypoglycemia
cool, clammy, tachy, HA, tremors, hunger, EKG changes, dizzy
hyperglycemia (DKA)
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
signs and symptoms of hyperglycemia
polyuria, polydipsia, polyphagia
tachy, HTN, kusmal breathing (deep & rapid), fruity smelling breath and urine
Tx for DKA
patent airway, IV fluids (NS), IV insulin (regular), frequent blood glucose checks, IV dextrose to avoid hypoglycemia, monitor serum K+
what is the goal to decrease blood sugar by
50 mg/dl/hr
HHNK
often mistaken for DKA, common in type 2
results from high BG without increase serum ketones
signs and symptoms for HHNK
BG over 600, extremly dehydrated, no significant acidosis, no ketonuria, no kussmauls
tx of HHNK
airway, IV fluids, IV insulin, IV dextrose to avid hypoglycemia monitor serum K+ (EKG changes)
types of burn injury
thermal, chemical, smoke inhaltion, electrical, cold thermal injury
burn management pre hospital care
A, B, C, cool, airway immediately, no ice , no creams/ointments
red shinny appearence, involves epidermis
superficial partial thickness
involves dermis
deep partial thickness
invovles thickness burn
involves fat, muscle, bone
what is burn center referral criteria
2nd degree burn, any age, BSA of 10%
3rd degree burn, any age, any BSA
Emergent (resuscitative) phase
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
what is the goal of fluid resuscitation
prevent shock
parkland formula
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%
patho of fluid & electrolytes shifts
plamsa leakage = increase interstital volume
decrease blood volume, increase HCT, decrease SBP
assessment of burns
rule of 9s, palmer method, lund and browder chart (used at burn centers)
what is the cut off point for recovery of the skin
hair follicle
acute phase
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
complications of burns
infection, cadiovascular arrhythimias, escharotomy, renal (maintain UO of 50/100ml/hr, 100 ml/hr for electrical burns), paralytic ileus
escharotomy
performed on full thickness burns, ideally done in burn center
fasciotomy
release of muscle of fascia
RARE
allograft
cadaver skin * gold standard
xenograft
animal tissue (pig skin)
biobrane
biosynthetic material embedded with collagen (good bc can be done out patient
cultured epithelial autografts
grown from biopsies obtained from pts own skin, used in pts with large BSA burns or with limited skin for harvesting
transcyte
skin cells harvested from newborn foreskin
good for partial thickness wound
integra
artificial skin with dermal layer made of collagen and epidermal layer of silicone
*grow with the pt, so its good for joints
scare management
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
what is the #1 choice for pain management in burns
morphine (high doses bc of increase of metabolism with burn)
opiods, sustained release meds, anxiolytics (xanax), NSAIDS, PCA, sedation
nutrition with burns
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
rehabilitation with burns
protect from sun light for up to 1 year, long term rehab, most common complication is the skin and joint contractures
what are the 3 major goals of TBI
prevention of primary injury, prevention of secondary injury, optimal recovery
what are the #1 reason for TBI in 0-4 and over 75
falls
primary injury
direct tissue damage from trauma
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
MOI
a moving object hits a stationary head
acceleration
*getting hit with bat in the head
a moving head hits a stationary object
deceleration
*in MVC head hits steering wheel
when the head strikes a fixed object, the coup injury occurs at _______, and contracoup injury occurs at ____
coup-contracoup injury
site of impact
opposite side of impact
types of skull fractures
linear, depressed, comminuted, compound, basilar
a crack, clean break in skull
lenear fx
Tx: bedrest
bone is displaced inward, may or may not lacerate the dura or brain tissue
depressed
Tx: surgically elevate bone, repair dura prn, Abx
skull fx or splintering or fragments
comminuted
Tx: surgically remove fragments
skull fx open to outside
compound
linear fx to the base of skull, usually crosses sinus and tears dura (leakage of CSF or blood)
basilar
Tx: if drainage give Abx, bed rest, neuro checks, dont blow nose, hearing test follow up
signs and symptoms of basilar skull fx
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)
meninges in order
Skull Dura arachnoid pia mater brain
most minor type of head trauma is
scalp laceration, highly vascular, profuse bleeding
major complication of lacerations
infection
contusion
bruising of brain tissue, maintains integrity
“talk & die syndrome”, rapidly deteriate and die, bleeding between the dura and inner surface of skull
epidural hematoma
*neurological emergency
can be venous, most likely arterial
*common in temporal region
S/sx of epidural hematoma
ipsilateral pupil changes, contralateral motor changes
Tx for epidural hematoma
surgical removal of clot, if caught early good outcome
bleeding between dura and arachnoid layer, venous bleed, slow onset, change LOC, increase ICP
subdural hematoma
acute subdural hematoma
symptomatic within 24 hours of innjury
Tx: evacuation of clot
subacute subdural hematoma
symptomatic 24-72 hours after injury
chronic subdural hematoma
S/sx show 2 or more weeks after injury, mimic dementia, seen in alcoholics and elderly
*30-60% mortality
bleeding can occur in any area of the brain where there has been tearing of tissue
intracerebral hematoma
what injury can increase risk of abcess
penetrating injury
bleeding into subarachnoid space
subarachnoid hemorrhage
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
concussion
post concussion syndrome
2weeks-2 months after injury, persistant HA, lethargy, personality and behavior changes
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
diffuse axonal injury
S.Sx of diffuse axonal injury
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
Dx for TBI
CT considered best, shows structural changes,
MRI more sensitive for lesions
events (biophysical and biochemical) changes that affect perfusion after the primary injury
secondary injury
cerebral dynamics (metabolism)
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)
what influences the amount of glucose and O2 the brain needs
activity
seizures, hyperthermia, etx.
the amount of blood passing through brain tissue in one minute
cerebral blood flow
what is the normal CBF
750ml blood/minute
autoregulation
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
the brains ability to accomodate changes in volume (r/t blood flow)
elastance
elastance = pressure/volume
is the inverseof elastance, the expandiability of the brain (r/t brain)
compliance
compliance = volume/pressure
what is ICP influenced by
cerebral blood flow and cerebral edema
normal ICP
0-15 mm Hg
Monro-kellie hypothesis
if there is change in one there has to be a change in the other
(blood 10%, brain 80%, CSF 10%)
normal ICP = what
the pressure exerted by the total volume from the brain, blood and CSF
what are normal compensatory adaptaions for ICP
aleration of CSF absorption or production
displacement of CSF into spinal subarachnoid space
dispensability of the dura
cerebral blood flow is the amount of _____
blood flow/min passing through brain tissue
cerebral blood volume is the amount of ____
blood thats passing though
increase pCO2, decrease pO2, acidosis causes
vasodislation and increase CBF
decrease pCO2, increase pO2 causes
vasoconstriction and decreases CBF
cerebral blood volume is controled by
autoregulation
MAP
MAP = S-D + D
——
3
MAP less 50
cerebral vessels poorly perfused, ischemic changes
MAP greater 170
cerebral vessels cannot vasoconstrict, causes hyperemic state = increase ICP
CPP
the pressure needed to ensure blood flow to the brain
MAP - ICP = CPP
normal CCP
50-150 mmHg (avg. person 80-100)
hyperemic state (increase ICP)
CPP greater 150
ischemia
CPP less 50
CPP incompatible with life
CPP less 30
when MAP = ICP, CPP = ____??
o, and all CBF stops
what happens when ICP is increased
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
early signs of ICP
change of LOC, decreased visual acuity, HA (continuous and worse in AM), elevated temp, vomit, cushings triad
cushings triad
bradcardia
widening pulse pressure
irregular respirations
late signs of ICP
oular signs, decrease motor function, decerebrate (more serious), decorticate posturing
Dx increased ICP
ICP measurements
CT, MRI, cerebral angiography, PET, etc
consciousness has 2 components
arousal component (wakefulness) content component (ability to reason, talk, feel & react to stimuli with purpose & awareness)
abnormal state inwhich the pt is unaware of self or enviornment
unconsciousness
what are characteristics of diminishing LOC
more stimuli to get reponse, thoughts are slower or simpler, reflexes become more slower & primitive
Neuro checks include
neuro assessment, subjective data, pupils, respiratory, motor strength and response, VS including temp
glascow coma scale
motor response
verbal response
eye opening response
what needs to be looked at for the trauma pt
aspiration, skin breakdown, DVT, airway, nutrition
management of TBI
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
enviornmental supprt of TBI
decrease noise, calm enviornment, minimize procedures, gentle movement
temperature control
every one degree of temp increases O2 demand and increases ICP
Tx of any temp aggresivly,
planning care of TBI
DO NOT CLUSTER CARE, can increase ICP, need rest periods
nutritional care of TBI
increase glucose, perfered method is G tube, nutirional intake 140%
a condition that is the consequence of a previous disease or injury
sequela
sequela of ICP
inadequate cerebral perfusion, cerebral herniation
sustained increase of ICP result in brainstem compresion and herniation of the brain from one compartment to another
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
herniation
supratentorial
above the fold of teh tentorium cerebelli
double enfolding of the dura mater under the temporal lobe
infratentorial
below the fold of the tentorium cerebelli
goal of tx of herniation
prevent it
types of herniation
uncal
cingulate
central
infratentorial (upward and downward)
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
uncal (supratentorial)
S.sx of uncal
ipsilateral pupil dilation with contralateral paralysis, contralateral positive babinski
lesion of one hemisphere shifts laterally and forces the cingulated gyrus under the Falx cerebri
cingulate
S.sx of cungulate
LOC decreases
expanding mass midline results in downward displacement of the hemispheres through the tentorial notch
central (transtentorial herniation)
S.sx of central herniation
pupils small fixed, dilated, respiratory changes.
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
upward trantentorial herniation
pressure downward pushes cerebellar tonsils through foramen magnum, compresses the medulla = immediate resp. and cardiac arrest
downward cerebellar herniation
what is something that needs to be initiated with any head injury
sezuire precautions
only Tx for post traumatic epilepsy
bezo (early)
late (after 7 days), same as any other seizure
Tx for stress ulcers
proton pump inhibitors
drainage of CSF from nose or ear denotes presence of what
fistula from subarachnoid through skull to the nose or ear
goal= prevent infection
acute hydrocephalus
problem with reabsorption or blockage of CSF, S/sx are that of ICP, Tx: shunt
the irreversible cessation of all functions of the brain incuding the brain stem
brain death
what tool is used to measure level of awareness, cognition, behavior and interaction with the enviornment
Ranchos Los Amigos Scale
what is the overall nursing management goals for TBI
ICP WNL
adequate ventilation
normal fluid & electrolyte balance
prevention of complications
decreases O2 and glucose demands, limits increases in ICP caused by agitation , restlessness, posturing, asynchrony with mechanical ventilation, and painful procedures
sedative agents
decreases body metabolic neds and controls shivering and posturing that may increase ICP (pt must be sedated, intubated, and on vent with use)
neuromuscular blockades
treats and minimizes pain, prevents iatrogenic increases in ICP
ex: ativan, Versed, Propofol, morphine, haldol
analgesia
Narcan reverses these Rxs
Mannitol
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
CADSCAN Mannitol
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
CADSCAN Lasix
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
used to prevent vomiting, which can increase ICP
antiemetics
used to prevent alcohol S&sx of withdrawal (cause of TBI may have been alcohol related)
Benzodiazepines
usedd but not effective tx
corticosteroids
used to control seizures, DO NOT prophylactically tx all pts , can cause new onset of seizures
anticonvulsants
Dilantin, Phenobarb
refractory high ICP, decreases cerebral metabolism and CBF, but can supress myocardium, hypotension and hypothermia
Barbituates
Ex. pentobarbital, pentothal
aim is to tx or alter pathways associated with ischemia, decreasing secondary injury, needs to be given soon after injury to be affective
neuroprotectants
waxing and wayning of resp. with short period of apnea, have lesion deep inside the cerebral hemipshere & basial ganglia
cheyne stokes
equal, rapid breath, deep, have lesions in the lower midbrain to midpons area
central neurogenic hyperventilation
rapid breaths followed by apnea then rapid breaths followed by apnea, lesions of the upper medulla
cluster breathing
like cluster breathing but hypoventilation is occuring, lesion in medulla
Biots breathing
decrese resp. capacity, and decrease amount of breaths, lesion in medulla
depressed breathing
struggling to breath, medulla lesions
gasping breaths
inhale, period of apnea/puse, exhale, period of apnea/pause, lesions to lower pons
apneustic breathing
SIADH Tx for TBI
IV hypertonic (pulls water out) NSS, Lasix, tends to be self limiting when caused by head trauma
Diabetes insipidus Tx for TBI
replace fluids, vasopressins, tends to be self limiting when caused by head trauma but permanent when following intracrainial surgery
surgeon who specializes in surgery of CNS
neurosurgeon
opening into cranium with removal of bone flap and opening dura to remove lesion, repair a damaged area, drain blood, or relieve increased ICP
craniotomy
excision into the cranium to cut away a bone flap
craniectomy
repair of a cranial defect resulting from trauma, malformation, or previous surgical procedure, artifical material to replace damaged or lost bone
cranioplasty
what are indications for intracranial surgery
intracranial bleeding, skull fractures, relieve refractory ICP
preoperative phase
Dx test, neuro exam to recieve baseline, teach family, scalp preperation
intraop phase
position head rest with tongs, eye care (ointment), anesthesia & Rxs (Abx, mannitol, lasix), monitoring (ICP, EEG, CVP, foley cath
what is the goal during and after surgery
prevent and minimize increase ICP
double fold or dura mater that forms a partition between the cerebrum and brain stem/cerebellum
Tentorium
Supratentorial
above tenrotium, includes cerebrum, incision is made behind hair line
infratentorial
below tentorium, includes brainstem and cerebellum, incison is made above nape of neck
Post op
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
nursing interventions post op
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
HOB for supratentorial incision
elevated 30-45 degrees
HOB for infraentorial incision
FLAT
supratentorial dressing, neck position, OOB, compliations
circles head, neutral position, no twisting/turning, 24-48 hours after surgery, seizures, increase facial edema, ecchymosis around eyes (cant open eyes)
infratentorial dressing, neck position, OOB, compliations
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)
when does increased ICP and cerebral edema peak with surgery
72 hours
are HA common
yes, expected 1st 24-48 hours, very severe
what causes permanent personality changes
cerebral anoxia
extended irreversible decline in the overall cognitive function of the pt
dementia
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
vegatative state
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
locked in syndrome
seen in polio, myasthenia gravis, and some CVA
irreversible severe brain damage, marked by deterioration of cognitive functions and awareness of self and enviornment
brain death
pt appears to be drowsy, lethargic and somnolent, when stimulated, easily aroused and responds approp.
obtundation
pt is very drwosy and lethargiv, only be briefly aroused with repeated vigorous, painful stimuli
stupor
