Studydroid is shutting down on January 1st, 2019

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What is a 1st degree burn?
Limited to epidermis
what is a 2nd degree burn
aka deep or parital-thickness burns

-burns that extend into the dermis
What is a 3rd degree burn?
Full thickness burn

burn that extends into the subcutaneous tissue below the dermis
describe the dermis layer
very vascular, contains numerous blood vessels

contains nerves
When is skin grafting required?
3rd degree (full thickness burns)
What is a 4th degree burn
Burn that involves structures that are burned below the dermis (muscle, fascia, and bone)
Describe the rule of nines
Arms- 9% each
Legs- 18% each
Dorsal trunk- 18%
Ventral trunk- 18%
Head- 10%
What is a major burn? 4 classifications
1. 2nd degree involving more than 10% TBSA in adults or 20% at a extremes
2. 3rd degree involving more than 10% TBSA
3. Any electrical burn
4. A burn complicated by inhalation injury
Where is most tissue damage with electrical burns?
At entry and exit points
What is the concern with electrical burns?
1. Unhidden burn injuries
2. Myoglobinemia d/t muscle damage leading to renal failue caused by myoglobinuria
Massive edema and rapid airway obstruction occur at what temperatures?
1. Steam at 100 C
2. Dry air at 300 C
What causes injury to upper airway structures?
Inhalation of heated air

reflex closure of vocal cords help protect lower airways
What causes injury to lower airway structures?
Inhalation of soot particles and/or chemicals produced by fire

Formation of acidic and alkali substances as result of interaction of inhaled toxins and airway mucosa
What are warning signs of respiratory injury in burn patient? 9
1. hoarsness
2. sore throat
3. dysphagia
4. hemoptysis
5. tachypnea
6. use of accessory muscles
7. wheezing
8. carbonaceous sputum production
9. elevated CO levels
What is the problem when relying on CXR for assessing resp. injury in burn patient?
Normal in early phase of inhalation injury

Abnormal only after pulmonary edema or infiltration develops
What type of intubation is preferred in ped with inhalation injury?
Nasal intubation
- uncuffed one size smaller than expected for age and weight
When should Sch not be given after thermal injury?
more than 24 hours after burn injury is unsafe d/t increased Ach receptors and potential for K release and development of hyperkalemia
What is the cause of increased resistenance to NDMR in burn patients?
1. Increased number of nictonic Ach receptors
2. change in volume and distribution associated with alterations in plasma protein binding

2-3x of normal dose required
How is CO poisining determined? what is the actual determination
CO toxicity measured by carboxyhemoglobin levels

Actual toxicity is determined by tissue CO level
How much more affinity for hemoglobin does CO have than Oxygen?
200 times more affinity
What causes metabolic acidosis d/t CO poisioning?
1. CO binds to hemoglobin and occupies binding sites leading to decreased oxyhemoglobin saturation
2. CO increases stability of oxyhemoglobin molecule causing decrease in the release of oxygen at tissues
3. Decrease in oxygen at tissues causes a disruption in oxidative phosphorylation
4. Disrupted oxidative phosphorylation leads to met. acidosis

What is the treatment for displacing CO from hemoglobin?
100% oxygen via face mask or ETT

Decreases half-life from 250 minutes in RA to 40-60 minutes
What are Clinical manifestations of CO poisioning? 0-5, 5-10, 11-20, 21-40, 41-60, > 60
0-5: none
5-10: mild headache, confusion
11-20: throbbing headache, blurred vision
21-40: disorientation, N/V, irritability, syncope
41-60: Tachycardia, tachypnea, agitation, combative, hallucinating
>60 Death
When is fluid losses greatest in burns? recover?
first 12 hours the greatest, stabilize after 24 hours
What is the cause of fluid losses in burn pt?
1. Direct transudation of plasma and proteins from wound
2. Diffuse capillary leakage from intravascular to interstitial
What is the cause of capillary leak in burn patient?
1. Loss of endothelial integrity
2. Decrease in intravascular oncotic pressure as plasma proteins are lost through wound and incompetent capillary beds
What does the disruption of the capillary barriers cause? 2 things
Hypovolemia and burn-induced edema

Intravascular fluid->interstitial compartment
What should be the anesthetists two primary goals of initial therpay for burn patient?
Fluid resuscitation
Airway management
What is the ABA consesus for fluid resuscitation and urine output in burn pt?
Adults: LR 2-4ml x Kg x TBSA burned
Children: LR 3-4ml x Kg x TBSA
*1/2 of Est. volume in first 8 hours,  then remaining half over the next 16 hours

Adults: 0.5 ml/kg/hr
Children <30kg: 1 ml/kg/hr
High voltage injuries: 1-1.5ml/kg/hr
Brooke Formula?
LR 2ml/kg/TBSA (1/2 in 8 hours, 1/2 in 16 hours)

2nd 24 hours: D5W maintenance, and Colloid 0.5ml/kg/TBSA
Parkland formula?
LR 4ml/kg/tbsa (1/2 in 8 hour, 1/2 in 16 hour)
2nd 24 hours: D5W main, Colloid 0.5ml/TBSA/kg
What type of IV fluid should be added to the replacement fluids in a ped burn patient?
D5W to prevent hypoglycemia
When does the hypermetabolic/hyperdynamic phase develop in burn pt?
48 hours after initial surgery, it is caused by a systemic inflammatory syndrome
What causes the hypermetabolic/hyperdynamic phase after burn injury? Findings
1. Increaed blood flow to organs and tissues
1. hyperthermia
2. tachycardia
3. tachypnea
Describe burn shock
1. First 48 hours after burn
2. Low cardiac output is hallmark sign, r/t hypovolemia d/t loss of plasma proteins from intravascular compartment
What happens to the catecholamine response in burn pt?
Catecholamine response is reduced d/t reduced adrenergic-receptor affinity and decreased secondary-messenger production
What happens to FRC and compliance in burn patient?
Decreased FRC
Decreased lung and chest-wall compliance
Ventilation rates increase how much in burn pt?
From 6L/min to 40L/min
What ventilation strategy is best to use in pt with inhalation injury?
High frequency percussive ventilation, helps to decrease risk of barotrauma
What are immune system changes that occur after burn injury?
1. Decrease leukocyte activity
2. Decreased humoral and cellular responses
3. Gram negative bacteria increases mortality
What happens to renal blood flow after burn injury? complications?
1. Decreased renal blood flow, leading to changes in glomerular filtration. Dec RBF d/t hypovolemia, dec CO, and increased circulating catecholamines
2. RAA system and release of ADH are activated, which causes electrolyte disturbances
What medication is given to prevent formation of myoglobin casts in pt at risk of myoglobinuremia?
IV HCO3 to alkanize the urine
What is the most effective nutrition for maintaing body protein in burn pt?
What increases the risk for development of an ileus in burn pt?cause? treatment?
1. Burn pt with TBSA > 20%
2. Ileus develops due to decrease in GI motility
3. Administer H2 blockers and antacids
Describe changes in albumin and alpha 1 acid glycoprotein (AAG) in burn pt
1. Decrease in albumin levels, so albumin bound drugs increase in free concentration
2. Increase in AAG, so basic drugs decrease in free concentration
What are the two main factors that change the volume of distribution in burn pt?
1. Changes in extracellular volume
2. changes in protein binding

Overall, there is significant patient variability based on fluid status and phase of recovery
What happends to drug clearance during the hypermetabolic phase?
CO increase so there is an increase in renal blood flow to kidneys and liver, this increases the rate of drug clearance
What are the 2 surgery end-points during surgical debridement and grafting for burn pt?
1. Limit to 2-3 hours if the patient's core temp decreases to 35 degrees or less
2. Blood loss requiring 10 units or more of PRBC
When should invasive monitoring be used in burn patient?
TBSA greater than 20-30%
Required d/t:
1. rapid blood loss expected
2. hemodynamic swings
3. need to check periop lab values
How should temp be monitored in burn pt during sx? y?
WIth esophageal stethoscope, because burn patients become hypothermic during surgery d/t loss of insulation of the skin, adipose, and muscle
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