trauma Flashcards
assessment PP: trauma leading cause of death for what age range?
0-30 yrs old
assessment PP: Approx. 75% of hospital mortality from
trauma occurs within how many hours after admission – most commonly from CNS, thoracic, abdominal, retroperitoneal, or vascular injuries.
48 hrs
assessment PP: which 2 types of injury are the most common causes of early mortality?
CNS injury and hemorrhage
assessment PP: most common MOI is what? second? third? which is asso with the highest percentage of death?
MVA 38%;
fall 30%;
GSW 6.6%;
GSW 16%
assessment PP: what are the 2 phases of assessment?
primary and secondary
assessment PP: what are you trying to ascertain in primary assessment? what is the priority assessment?
immediate life-threatening injuries;
ABCDEs
assessment PP: what does ABCDE stand for?
airway, breathing, circulation, disability (MS, GCS), expose
assessment PP: what are you assessing for with airway? breathing?
is it patent;
adequate ventilations, RR, effort, chest wall mvmt, BS;
assessment PP: what are you assessing for with circulation?
pulse RRR, cap refill, BP, bleeding, ECG
assessment PP, circulation: if you can feel a radial pulse, the sbp is at least what? femoral? carotid? less than what sbp is poor cerebral flow?
radial >80;
femoral >70;
carotid >60;
assessment PP, disability: what does AVPU stand for?
alert, responds to verbal stim, responds to painful stim, unresponsive
assessment PP, disability: always intubate with a GCS of what?
assessment PP: what is the goal of resuscitation?
restore tissue oxygenation
assessment PP: anesthesia’s primary concern during assessment of the trauma pt is what (3)?
preserve CNS function, maintain adequate resp gas exchange, and achieve circulatory homeostasis
assessment PP, CNS resuscitation: how do we preserve CNS function?
ensure adequate flow of well-oxygenated arterial blood to the brain and by preventing secondary spinal cord damage due to the mvmt of an unstable spinal fx
assessment PP, resp gas/exchange: do all trauma pts get supp O2?
yes
assessment PP, resp gas/exchange: if resp function inadequate, do what?
intubate
assessment PP, resp gas/exchange: assume what precaution with all trauma pts (2)?
full stomach and cervical spine injury
assessment PP, resp gas/exchange: give MR if unable to ventilate?
no
assessment PP, resp gas/exchange: how are c-spine injuries cleared?
neuro exam AND radiological exam
assessment PP, resp gas/exchange: what is mandatory during intubation?
c-spine stabilization; can take front collar off
assessment PP, resp gas/exchange: when can blind NTT be attempted?
if pt breathing spontaneously
assessment PP, resp gas/exchange: avoid NTT and NGTs in what scenario? why? what lefort fxs would you avoid NTT/NGT?
basilar skull fxs;
tube may enter the cranial vault thru the cribiform plate;
LeFort II/III fxs
assessment PP, resp gas/exchange: when sld an awake intubation be avoided? why?
pt with vascular neck trauma;
gagging and coughing can accelerate bleeding and incr ICP
assessment PP, resp gas/exchange: why avoid blind NTT and OETT with pts with blood in airway and/or maxillo-facial injuries?
bc tissue, bone fragments or teeth may be pushed into the trachea
assessment PP, resp gas/exchange: if intubation is impossible, what is the next option for securing airway?
needle or incisional cricothyroidotomy or tracheotomy, LMA
assessment PP, resp gas/exchange: when is cricothyroidotomy not recommended? why not?
laryngeal fx;
bc in some pts the inominate artery crosses over the trachea
assessment PP, resp gas/exchange: cricothyroidotomy is reserved from which pts?
with severe facial or upper airway obstruction
assessment PP, resp gas/exchange: cricothyroidotomy what equipment is needed (3)? how secure?
scalpel, dilator or curved hemostat, and #7 ETT or trach tube;
sew
assessment PP, resp gas/exchange: with a mandible repair, the surgeon may want what type of ETT?
nasal rae
assessment PP, circ hemostasis: when sld fluids be initiated?
in the field
assessment PP, circ hemostasis: # PIVs
2
assessment PP, circ hemostasis: blood loss replaced with how much blood product? crystalloid?
1: 1;
3: 1
assessment PP, circ hemostasis: administer up to how many liters of hetastarch? why limit?
1L;
>1L risk for coagulopathy
assessment PP, circ hemostasis: what is the lethal triad you need to avoid?
acidosis, hypothemria, and coagulopathy
assessment PP, circ hemostasis: if ST (>120bpm) persists after infusion of 2L crystalloid, what suspect?
bleeding and then consider blood transfusion
assessment PP, circ hemostasis: what is an early sign of significant blood loss or pericardial tamponade?
diminished pulse pressure
assessment PP, circ hemostasis: if no type specific blood available, what is next best?
Oneg PRBCs
assessment PP, circ hemostasis: what is the most common cause of coagulopathy in trauma pt?
dilutional thrombocytopenia
assessment PP, circ hemostasis: what blood products have no hemostatic function? what else must you give?
PRBCs-only replacing hgb;
plt, FFP and/or cryo
assessment PP, circ hemostasis: what coagulation factor can administer to improve hemostatic function? what is the caveat for it to work?
Factor VII;
70-90mcg/kg;
need good plt count
assessment PP, circ hemostasis young people: d/t tremendous hemodynamic reserve, HOTN may not develop until what % of blood volume is lost? ST may not occur until what % of blood volume lost?
30-40%;
20-25%
assessment PP, secondary survey: complete head to toe exam with further neuro assessment once what is achieved?
stabilization
assessment PP: in which survey (primary or secondary) would you do CT, c-spine, XRs, U/S, angiography,rectal exam?
secondary
assessment PP, secondary survey: what does SAMPLE stand for?
signs/sxs, allergies, medications, PMH, last oral intake, events and environment r/t injury
burns PP: what are the 3 physiological functions of the skin?
protection from environment, thermoregulation, guards against microbial invasion
burns PP: what are the 3 layers of the skin?
epidermis, dermis, sq
burns PP: what are the 4 classifications of burns?
chemical, thermal, electrical, and inhalation
burns PP: also known as partial-thickness
a. first
b. second
c. third
d. fourth
b
burns PP: muscle, fascia, bone
a. first
b. second
c. third
d. fourth
d
burns PP: grafting necessary
a. first
b. second
c. third
d. fourth
c
burns PP: dry, tissue paper skin
a. first
b. second
c. third
d. fourth
c
burns PP: complete excision required
a. first
b. second
c. third
d. fourth
d
burns PP: sunburn
a. first
b. second
c. third
d. fourth
a
burns PP: 2 types: superficial dermal and deep dermal
a. first
b. second
c. third
d. fourth
b
burns PP: all epidermis and dermis
a. first
b. second
c. third
d. fourth
c
burns PP: heals spontaneously
a. first
b. second
c. third
d. fourth
a
burns PP: limited function
a. first
b. second
c. third
d. fourth
d
burns PP: epidermis destroyed
a. first
b. second
c. third
d. fourth
a
burns PP: full-thickness
a. first
b. second
c. third
d. fourth
c
burns PP: blisters
a. first
b. second
c. third
d. fourth
b
burns PP: second degree, moist, shiny surface
a. superficial dermal
b. deep dermal
a
burns PP: second degree, mottled with white, waxy, dry surface
a. superficial dermal
b. deep dermal
b
burns PP: second degree, red or pale ivory color
a. superficial dermal
b. deep dermal
a
burns PP: second degree, epidermis and deep dermis damage
a. superficial dermal
b. deep dermal
b
burns PP: second degree, blisters may or may not appear
a. superficial dermal
b. deep dermal
b
burns PP: second degree, significant scarring
a. superficial dermal
b. deep dermal
b
burns PP: second degree, immediate blistering
a. superficial dermal
b. deep dermal
a
burns PP, electrical: T/F tissue damage greatly exceeds apparent damage.
true, estimating TBSA% is often difficult
burns PP, electrical: s/sxs of renal insult (3)?
myoglobinuria, hemoglobinuria, and renal failure
burns PP, electrical: UOP goal? give what meds to promote diuresis? what may be given to alkalinize the urine?
1-1.5cc/kg/hr;
mannitol, lasix;
bicarb
burns PP, electrical: what other 2 systems may have issues d/t the electrical charge?
neuro and CV
burns PP, electrical: dysrhythmias may last how long?
months
burns PP, electrical: what is the typical pattern on the skin after a lightening strike?
ferning
burns PP: what is an escharotomy?
incision thru eschar
burns PP: what complications can turn a 2nd deg burn into a 3rd?
infxn and cellulitis
burns PP, considered a “major burn”:
a. second deg involving >? % TBSA in adults
b. second deg involving >? % TBSA at age extremes
c. any this type of burn
d. burn complicated by what?
a. >10%
b. >20%
c. electrical
d. smoke inhalation
burns PP, mortality: if pt age + %TBSA is > what = mortality >80%
115
burns PP: what are the 3 most common causes of demise?
sepsis, burn shock, and MI (ages >45)
burns PP: how long before revascularization in full thickness burns? partial thickness?
3-4wks;
24-48hrs
burns PP: why is there a reduction of circulating volume?
translocation of fluid from intravascular space to interstitial space
burns PP: when does the major portion of increased cap permeability occur? how long does it persist? what is the cause?
first 12 hrs;
2-3wks;
liberation of vasoactive substances from the area of injury as a direct result of heat
burns PP, cap perm: allows colloidal substances with a MW >what to escape into ECF? if burn is what %, it is present throughout the body?
> 150000;
30%
burns PP: this 3rd spacing results in what 2 things regarding hgb?
hemoconcentration and red cell destruction
burns PP: hemolysis occurs w/in how many hrs of burn?
24hrs
burns PP, hemolysis: RBCs are destroyed but hct increases why?
due to a rapid loss of plasma volume
burns PP hemolysis: large increases in hct reflect what?
poor fluid resuscitation
burns PP hemolysis: burn pts have a markely reduced red cell survival time, about what % of normal?
30%
burns PP plasma proteins: how long do plasma proteins continue to be lost after initial injury? how does this matter to CRNA?
up to 36hrs;
may theoretically alter the responses to highly protein-bound drugs resulting in increased free drug levels
burns PP microbial invasion: intially which type of organisms proliferate? day 5?
gram pos (e.g. staph); gram neg especially pseudomonas
burns PP microbial invasion: which complication can incr TBSA% size of burns?
cellulitis
burns PP microbial invasion: what time period does sepsis occur?
anytime
burns PP, CV: CO up or down?
down
burns PP, CV: CO drop occurs when? why does it decr?
immediately after the burn;
d/t loss of vasc and endothelial integrity and plasma proteins
burns PP, CV: how soon does burn shock happen?
24-36hrs after the burn
burns PP, CV: in large burns CO falls to as much as what % of baseline withing 30min of injury?
50%
burns PP, CV: what are the 3 cardiac related reasons as to why the CO decr?
release of myocardial depressant factor, incr blood viscosity, release of vasoactive substances
burns PP, CV: how long before CO returns to baseline?
within 36hrs post-burn
burns PP, pulm: how soon do early pulm complications occur after injury? delayed with complication example? late with complication example?
0-24hrs-carbon monoxide poisoning
2-5 days-ARDS;
days to weeks-pneumonia, atelectasis, and PE
burns PP, pulm: incr or decr
a. FRC
b. lung and chest wall compliance
c. alveolar/arterial gradient
d. MV and why does it change?
a. decr
b. decr
c. incr
d. incr d/t incr O2 requirements and VQ mistmatch
burns PP, pulm: can compromise occur without inhalation injury? what is the major factor contributing to pulm complications?
yes;
release of mediators
burns PP, pulm: decr COP + impaired vascular/cap permeability + large IVF = what?
pulm edema
burns PP, inhalation injury: when does it occur?
when hot gases, toxic substances, and reactive smoke particles reach the tracheobronchial tree
burns PP, inhalation injury: s/sxs
wheezing, bronchospasm, corrosion, and airway edema
burns PP, inhalation injury: what labs/diagnostic tools? which tool determines the extent of the parenchymal damage?
ABG, carboxyhemoglobin concentration, xenon scan, FOB;
none, just diagnose inhalation injury
burns PP, inhalation injury: damage to the lung is almost entirely due to what? is steam inhaled frequently? why or why not?
chemical-byproducts of combustion are inhaled and induce a chemical pneumonitis;
rarely bc rarely reaches the carina with high temps
burns PP, inhalation injury: name the 4 pulm responses to inhalation injury.
surfactant production impaired, incr cap perm, resp ciliary action halted, and gas exchange impairment
burns PP, inhalation injury: what is the specific tx?
none, supportive care (e.g. O2, vent with PEEP)
burns PP, inhalation injury: typically gets worse over how many days from time of injury?
first 3 days
burns PP, carbon monoxide poisoning: what is the affinity of CO to hgb compared to O2?
200x stronger
burns PP, carbon monoxide poisoning: what does abg reveal? sao2? pulse ox accurate?
PaO2 is normal but low O2 content;
low SaO2;
no
burns PP, carbon monoxide poisoning: what directional shift on oxyhgb curve?
left
burns PP, carbon monoxide poisoning: why doesn’t the pt become tachypneac?
bc carotid bodies are sensitive to arterial PaO2 and not aterial O2 content.
burns PP, carbon monoxide poisoning: tx? tx with decr LOC? tx for high CO levels or symptomology?
100% O2 NRB;
intubate;
hyperbaric
burns PP, carbon monoxide poisoning: what is the 1/2 life of COhgb on RA? why are preggos more at risk?
3-4hrs;
bc fetal hgb has even higher affinity for CO and takes longer to get rid of it
burns PP, metabolic changes: when does hypermetabolic state occur after the injury/
first few hrs
burns PP, metabolic changes: why does hypermetabolic state occur?
prob d/t incr adrenergic activity, incr catecholamine secretion, endogenous resetting of energy prdxn, and heat loss
burns PP, metabolic changes: results of hypermetabolic state?
incr blood flow to organs/tissues
burns PP, hypermetabolic state s/sxs:
a. protein
b. BGL
c. body temp
d. HR
e. RR
f. O2 consumption
a. protein-incr catabolism and nitrogen waste
b. BGL - hyperglycemia
c. body temp - hyperthermia
d. HR -incr
e. RR- incr
f. O2 consumption - incr
burns PP, hypermetabolic state: tx (3)
incr O2, ventilation, and nutrition
burns PP, renal: what system is activated immediately d/t decr RBF and GFR?
RAAS
burns PP, renal: what hormone is released? results in retention of what (2) and loss of what (3)?
ADH;
Na and water;
loss of Ca, K, and Mg
burns PP, renal: UOP goal initially for adults? kids
.5cc/kg/hr;
1 cc/kg/hr
burns PP, renal: what causes myoblobinemia? tx (2)?
electrical burns can cause extensive areas of devitalized muscle;
fluids, diuretics
burns PP, immune system: how are these effected?
a. neutrophil chemotaxis
b. phagocytosis
c. macrophage activity
d. T-suppressor cells
e. leukocyte function
f. immunoglobulin levels
a. neutrophil chemotaxis - decr
b. phagocytosis - decr
c. macrophage activity - impaired
d. T-suppressor cells - incr
e. leukocyte function - poor
f. immunoglobulin levels - low
burns PP, immune system: tx
abx
burns PP, GI: what complication? what artery is under perfused? tx?
ileus;
splanchnic (leading cause of sepsis);
prophylactic NG, antacids, H2 blockers
burns PP: why does anemia occur with big burns?
erythrocytes are damaged or destroyed by heat and are removed by the spleen in the firs 72hrs
burns PP: what is the parkland formula?
4cc/kg/%TBSA;
1/2 given over 8hrs, 1/4 given next 8hrs, last 1/4 given next 8hrs
burns PP: given colloids in first 24hrs?
not recommeded
burns PP initial fluid resus: what are the 3 factors known to incr the vol of fluid required to resuscitate?
delay in initiation of fluid resus, inhalation injury, and high BAC
burns PP airway mgmt: what size tube?
1 size smaller
burns PP airway mgmt: which nerve blocks helpful/
transtracheal or laryngeal
burns PP: what is the leading cause of death? what will reduce the rate of infxn?
infxn and sepsis;
early excision and grafing
burns PP indxn: preferred sedation?
opioids
burns PP surgery: when is the first surgical excision usually done?
24-48 hrs post-burn after fluid resus
burns PP surgery: what do surgeons use to control bleeding after harvesting grafts that we need to be concerned with? what do they use to make it easier to obtain the grafts?
epi soaked sponges;
phenylephrine to raise skin with pitkin injector
burns PP MRs: burns cause denervation of the muscle membrane and in response, what happens to the muscle membrane receptors? what is the change in response of muscle to depolarizing and NDMR during the first 24hrs after injury?
proliferation of extrajunctional receptors;
no change
burns PP MRs: at what point should sux not be used? why not? what others issues does sux create?
after 24hrs since injury d/t extrajunctional receptors for 1yr;
incr K release with burns exceeding 10% TBSA
burns PP MRs: which type of burn and injury are immediately susceptible to elevated K?
electrical burns and crush injuries
burns PP MRs: there will be resistance to NDMRs in pts with burns >what% TBSA? begins when? peaks when? bc of this, how manage NDMRs?
> 30%;
1wk after injury and peaks 5-6wks;
may need higher dosing or more frequent redosing
burns PP altered drug responses: drugs administered by any route other than IV are faster or slower or same absorption? after how many hrs is the plasma albumin concentration decr?
slower;
48hrs - protein bound meds will have prolonged effect
burns PP altered drug responses: what is the effect of drugs metabolized by the liver by oxidative metabolism (phase I)? conjugation (phase II)?
prolonged;
no change
burns PP altered drug responses: opioid requirements incr or decr?
incr
burns PP altered drug responses: indxn drugs and inhalation agents are likely to cuase HOTN secondary to what?
hypovolemia
intraop mgmt PP: technique to induce?
RSI
intraop mgmt PP: inxn med dosing guidelines?
dose to effect
intraop mgmt PP: MAC?
.3-.5
intraop mgmt PP: hemorrhage and hypovolemia lead to a lower/higher than normal blood concentration of IV agents? decr/incr sensitivity of brain to anesthetics?
higher;
incr
intraop mgmt PP: careful giving opioids to pt in shock bc plasma concentrations of fent and remifent are decr/incr? why?
incr bc of less vol of distribution
intraop mgmt PP: decr vol of distrib increases blood level of prop by what %?
20%
intraop mgmt PP: ketamine okay? which injury is it contraindicated?
yes, but not with TBIs (incr ICP)
intraop mgmt PP: opioids have a lot or little direct effect on CV or baroreflex depressant effect? how do they cause HOTN?
little;
by inhibiting central sympathetic activity
intraop mgmt PP: trauma pts are at high risk of what?
recall
intraop mgmt PP: scopolamine dose with volatile agent
.6mgIV
intraop mgmt PP: nitrous okay?
no
intraop mgmt PP: which gas is the best?
no difference altho des can cause ST
intraop mgmt PP: what MIVF use? glucose containing fluids okay? why or why not?
LR;
no, BGL will be high d/t release of catecholamines
intraop mgmt PP: tx hyperglycemia?
no, bc once problems are corrected, BGL will equilibrate and it is not a priority
intraop mgmt PP: side effect of hyperglycemia that will further aggravate hypovolemia?
osmotic diuresis
intraop mgmt PP: what is the most common complication?
hypothermia
intraop mgmt PP: complications of hypothermia
a. metabolism
b. 1/2 life of drugs
c. platelets
d. oxygen dissociation curve
e. myocardial function
a. metabolism - decr
b. 1/2 life of drugs - incr
c. platelets - sequestration
d. oxygen dissociation curve - shift left
e. myocardial function - decr