Burns, Shock, Sepsis Flashcards
1
Q
Epidemiology of Burns?
A
- mortality in pts over 65
- highest risk is 18-35 yo and 2:1 male to female in both injury and death
- in kids highest incidence is scalding injuries from hot drinks to bath
2
Q
Fxn of the skin?
PP of burns - cell changes?
A
- skin: dermis and epidermis
- various thickness
- thickness varies w/ age
- skin is semi-permeable barrier for evaporative loss
- skin also responsible for control of body temp
cellular changes seen in burns:
- intracellular influx of Na/H2O
- extracellular migration of K
- disruption of cell membrane fxn
- failure of Na pump
- Burn shock w/ depression of myocardium and metabolic acidosis
3
Q
Heme changes in burns? Local progressive injury?
A
heme changes:
- increase in hematocrit
- increase in blood viscosity
- anemia due to RBC destruction
local progressive injury:
- liberation of vasoactive substances
- disruption of cellular fxn
- edema formation
4
Q
At what temp does cell damage occur? Diff zones?
A
- occurs when above 113F due to denaturation of protein
- zone of coag: irreversibly destroyed
- zone of stasis: stagnation of microcirculation, can/will extend if not tx appropriately
- zone of hyperemia: increase blood flow
5
Q
How is burn size quantified?
A
- as % of BSA burned
- rapid method based on area of back of pt’s hand 1% of BSA
- Rule of 9’s
6
Q
Characteristics of 1st degree burn?
A
- erythema of skin
- possibly minimal surrounding edema
- minimal pain
7
Q
Characteristics of 2nd degree burn?
A
- deeper than 1st degree
- involve partial thickness
- ex: deep sunburn, contact w/ hot liquids, flash burns from gas flames
- usually much more painful than 3rd degree
- skin appears: red or mottled, blisters w/ broken epidermis, considerable swelling, wet/weeping surfaces, painful, sensitive to air
8
Q
Characteristics of 3rd degree?
A
- damage to all skin layers, subq tissues, and nerve endings
- skin appears: pale white or charred appearance, leathery, broken skin w/ fat exposes, dry surface, painless to pinprick, edema
9
Q
Signs of airway damage in burn pt? Tx?
A
- carbon around nose
- burns involving mouth
- sig resp problems
- fire in enclosed areas
- remember CO exposure
- toxic gases from combustion (house fires)
- intubate early
10
Q
What are chemical burns? Tx?
A
- alkali or acids can cause burns
- alkali burns more serious than acid burns b/c alkalis penetrate deeper
- Don’t try to neutralize, soln to poln is dilution - Irrigate!!
11
Q
What can occur w/ electrical burns? Tx?
A
- always more serious than they appear
- skin has more resistance than bone, muscle, blood vessels or nerves, therefore deeper structures have more damage
- occult destruction of muscle can cause rhabdomylosis which causes the release of myoglobin and can lead to acute renal failure
tx: - if urine dark - assume myoglobin and increase fluids to achieve a urine output of 100ml/hr
- if urine doesn’t clear: mannitol to ensure cont diuresis
- control metabolic acidosis by perfusion and add Na bicarb as needed to alkalinize urine to solubilize myoglobin
12
Q
ED management of burns?
A
- major burn pts are mult injury trauma pts: ABCDE
- check for evidence of airway involvement and if present - consider endotracheal intubation
early - start 2 large bore IVs ASAP: place in non-burned areas if practical (if no access - IO)
- do secondrary survey and look closey at eyes for evidence of corneal burns
- est depth and extent of burn and record
- any pt w/ greater than 20% BSA partial thickness burn needs NG tube placed as ileus is likely
- remove any jewelry: closely monitor distal pulses in extremities w/ circumferential burns - escharotomy PRN
- pain control: esp in pts w/ widespread 2nd degree burns
13
Q
What tests, labs are needed in burn pt? What does q pt w/ sig burns need?
A
- CBC, lytes, BUN, Cr, glucose (chem 7) should be obtained
- ABGs, carboxyhemaglobin level, CXR and EKG on any suspected inhalation injury
- urine for myoglobin and CPK
- check tetanus status and when in doubt, give
- q pt w/ sig burns gets a Foley catheter:
criticla in monitoring resuscitation, until Swan-Ganz or CVP line placed- only way to ensure adequate renal perfusion
14
Q
Fluid resuscitation in burn pts?
A
- adults: NS or RL
- half of above over the first 8h from time of burn
- other half over next 16 hrs
15
Q
Dressings for burn pts w/ minimal burns or burns that are being tx as an oupt?
A
- 1% silver sulfadiazine (silvadene)
- re-evaluate q 24 hrs until full extent is known
- dressing changes BID until burn stops weeping
- commercial preps containing honey shown to be of benefit
16
Q
Transfer guidelines for Burn pts?
A
- partial thickness burns of more than 10% BSA
- burns involving face, hands, feet, genitalia, perineum or major jts
- 3rd degree burns in any age group
- electrical burns, especially lightening injuries
- burns w/ preexisting complicating medical disorders
- kids w/ significant burns that aren’t in a children’s hosp
- when in doubt call referral burn center
17
Q
Definition of shock?
A
inadequate tissue/organ perfusion:
- pump failure
- decreased peripheral resistance
- hemorrhage
18
Q
Cardiac, renal, and neuroendocrine response?
A
cardiac response:
- tachycardia
- increased myocardial contractility/O2 demand
- constriction of peripheral blood vessels
renal response:
- stimulating an increase in renin secretion
- vasoconstriction of arteriolar smooth muscle
- stimulation of aldosterone secretion by adrenal cortex
neuroendocrine response:
- increase in circulating ADH
19
Q
Progression of shock?
A
- inadequate perfusion
- cell hypoxia
- energy deficit
- lactic acid accum and fall in ph - leads to anaerobic metabolism
- metabolic acidosis - leads to vasoconstriction and failure of pre-capillary sphincters - and then to peripheral pooling of blood
- cell membrane dysfxn and failure of Na pump
- intracellular lysosomes release digestive enzymes lead to efflux of K and influx of Na and H2O
- toxic substances enter circulation
- capillary endothelium damaged
- further destruction, dysfxn, and cell death
20
Q
Diff types of shock?
A
- hypovolemic: decreased vascular volume, hemorrhagic
- septic: systemic infections lead to hypotension, decreased vascular volume
- cardiogenic: shock resulting from some abnormal cardiac fxn
- neurogenic: due to failure of vasomotor regulation and pooling of blood in dilated capacitance vessels - suddenly tank is too big
21
Q
What are the signs of shock?
A
- tachycardia (earliest manifestation)
- hypotension
- decreased urine output
- altered mental status
22
Q
Tx of shock?
A
- fluids: fluid repletion w/ isotonic saline
- clinical signs, including BP, urine output, mental status, and peripheral perfusion are often adequate to guide resuscitation
- development of peripheral edema is often due to acute dilutional hypoalbuminemia and shouldn’t be used as marker for adequate fluid resuscitation or fluid overload
- colloids: albumin, hespan for bleeding (but saline solns are still generally preferred)
23
Q
Physiological responses to blood loss?
A
physiological responses to blood loss:
- HR increases
- cardiac contractility increases
- blood shunted to vital organs: causes pale extremities
- conservation of H2O and Na: decreased urine output
24
Q
Physiological effects at site loss in hemorrhagic shock?
A
- local activation of coagulation system
- affected blood vessels contract
- activated platelets adhere to damaged vessels
- activated platelets release thromboxane A2
- thromboxane A2 causes increased vessel contraction – stimulates wound healing
