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Advanced Anesthesia III > Burns > Flashcards

Burns Flashcards

1
Q

Burns are classified according to

A

1) Depth
2) Extent of skin and tissue destruction
3) Total body surface area involved (TBSA)

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2
Q

Burn Classifications (Degrees)

A

Partial Thickness

1st degree

  • Involve skin and epidermis only
  • These will heal spontaneously

2nd Degree

  • Skin, epidermis, and dermis involved
  • May or may not need grafting

3rd Degree

  • Skin, epidermis, dermis, and SQ tissue involved
  • Definitely needs grafting

4th Degree
- Skin, epidermis, dermis, SQ tissue, and muscle involved

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3
Q

Rule of Nines

A 
Head = 9% TBSA
Upper extremities = 18% TBSA
Trunk = 36% TBSA
Lower extremities = 36% TBSA
Pediatrics are an exception to this rule (look at the image in lecture)
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4
Q

What burns are considered major burns?

A 
Full thickness > 10% TBSA
Partial thickness > 25% TBSA
OR
Partial thickness > 20% in these cases:
- Extremes of age
- Burns of hands, feet, perineum
- Inhalational, chemical, electrical burns
- This is because these burns are associated with co-existing disease
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5
Q

What does the national burn registry say about burns and mortality?

A

If the age of the patient + the TBSA is > 115, the expected mortality is > 80%

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6
Q

In closed-spaced thermal injuries, what are we worried about?

A

Airway injury

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7
Q

In open, accidental burn injuries, what are we worried about?

A

These are often associated with multiple co-existing injuries (like from an MVA where the car caught on fire or something)

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8
Q

Electrocution may lead to

A
  • Severe fracture
  • Skeletal injury
  • Hematoma
  • Visceral injury
  • Cardiac injury
  • Superpowers
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9
Q

Initial treatment of the burn patient should involve

A

The ABCs! Just like any other trauma.

Don’t forget to look for co-existing traumas.

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10
Q

Airway management in the burn patient

A
  • ALWAYS be thinking about upper airway injury if the burn occurred in a closed space or if the patient is unconscious
  • Diagnosis of airway injury is based on H&P –> knowing how the injury occurred and by DVL or fiberoptic bronchoscopy)
  • Damage to soft tissues of the respiratory tract and trachea can make intubation difficult
  • Thermal injury followed by aggressive fluid resuscitation can make glottic edema worse
  • Give 100% O2 via FM
  • ETT is indicated if massive burn, stridor, rest distress, hypoxia/hypercarbia, altered LOC, or pt is likely going to deteriorate
  • AFO under topical anesthesia is safest approach for adults
  • Pediatrics have narrow airways, and thus low threshold for intubation
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11
Q

S/S that would suggest upper airway damage to you

A
  • Facial burns
  • Singed facial hair
  • Hoarseness / dysphonia
  • Cough
  • Soot in mouth or nose
  • Difficulty swallowing
  • CXR (will be normal initially, but later will show pulmonary edema or infiltration)
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12
Q

Lower airway involvement may result in

A

decreased surfactant, decreased mucociliary function, mucosal necrosis and ulceration, tissue sloughing.

Tissue sloughing will result in bronchial obstruction, air trapping, and pneumonia!

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13
Q

When may ARDS, pneumonia, and PE develop post-burn?

A

ARDS = 1-5 days post-burn

Pneumonia and pulmonary edema may occur > 5 days post-burn

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14
Q

What sort of tests should be ordered if inhalation injury is suspected?

A

DVL and bronchoscopic exams, CXR, ABGs, PFTs

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15
Q

How would you treat hypoxia in burn patients?

A 
PEEP
Airway humidification (airways may be dried out from injury --> desiccation leads to poor diffusion across membranes)
Bronchial suctioning / lavage
Bronchodilators
Antibiotics
Chest PT
Nitic oxide (NO)
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16
Q

Smoke inhalation injury

A

This is just damage from the smoke alone. Not thermal injury.

  • Occurs with face/neck burns and fires in closed spaces
  • Chemical pneumonitis occurs –> similar picture to aspiration of gastric contents
  • Pts will have a “honeymoon period” –> CXR looks good for the first 48 hours. Misleading because then they may still develop pneumonitis when you think they’re in the clear.
  • Decreased PaO2 on RA is first sign of smoke inhalation injury
  • Increased sputum production (ciliary cells trying to get that shit out of there)
  • Pt may have rales or wheezing
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17
Q

Hypoxia in burn patients with inhalational injury

A

First 36 hours = high risk of pulmonary edema secondary to pre-intubation bronchial obstruction

Days 2-5 = Expect atelectasis, bronchopneumonia, maximum airway edema 2/2 sloughing of airway mucosa and thick secretions, distal airway obstruction

> 5 days = nosocomial pneumonia, high metabolism respiratory failure, and ARDS

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18
Q

Restrictive disease pattern may result from

A

Circumferential burns of chest and upper abdomen. Restriction begins to occur as eschar contracts and hardens.

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19
Q

This is often found with smoke inhalation

A

CO poisoning

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20
Q

CO has affinity for Hgb __ times more than O2

A

200x more

21
Q

CO causes a shift of the dissociation curve to the

A

LEFT

This impairs the ability of O2 to unload from Hgb to the tissues

22
Q

CO interferes with

A

Mitochondrial function

  • -> Uncouples oxidative phosphoylation
  • -> Reduces ATP production
  • -> Results in metabolic acidosis
23
Q

Effect of CO on the heart

A

May act as a myocardial toxin and prevent the survival of cardiac arrest

24
Q

Management of CO toxicity patients

A
  • O2 sats may look normal, but remember that they can’t unload the O2 to the tissues!
  • Respiratory effort is often normal
  • May have cherry-red coloration of blood, but this may not be present if CO 30% and the pt is hemodynamically and neurologically stable
25
Q

Cough level > ___% is not compatible with life

A

60%

26
Q

Levels of CO toxicity and associated s/s

A

60% = DEATH

27
Q

How do burn patients get cyanide toxicity?

A

CN is often produced as synthetic materials burn

28
Q

CN toxicity and the burn patient

A
  • Pts will get metabolic acidosis
  • Altered LOC with agitation and confusion or coma
  • CV depression / arrhythmia risk
  • Diagnosis is confirmed with blood levels > 0.2mg/L
  • Death occurs with CN levels > 1.0mg/L
  • CN has a half-life of 60 minutes
  • The treatment of choice is O2!
  • Other treatments include amyl nitrate, sodium nitrate, and thiosulfate
29
Q

Systemic results of burns include

A

Immune suppression, hypermetabolism, protein catabolism, sepsis, and MSOF

30
Q

Mediators released locally (from minor burns)

A 
Histamine
Prostaglandins
Bradykinin
NO
Serotonin
Supstance P
31
Q

Mediators released systemically (from major burns)

A

Cytokines (interleukins and TNF)
Endotoxins
NO

32
Q

Metabolism in the burn patient

A
  • Increased metabolic rate proportional to TBSA burned (can double in a TBSA of 50%)
  • Increase in core body temp reflects the increase in metabolic rate
  • Loss of skin results in loss of vasoactivity, piloerection, and insulation functions
  • High evaporative fluid losses (carries heat with it)
  • Increased caloric consumption
33
Q

Daily evaporative fluid loss in burn patients

A

4000mL/m2

34
Q

Effect of anesthesia on body temperature in burn patients

A

Causes vasodilation and decrease in metabolic rate, both of which result in hypothermia

35
Q

CV stressors after burn injury

A
  • Severe decrease in CO for the FIRST 24 hours
  • Circulating LMW myocardial depressant factor
  • Third spacing results in hypovolemia, which intense vasoconstriction as compensation
  • Hemolysis of erythrocytes
  • Increased metabolic demands but decreased O2 supply
  • Hyperdynamic state results AFTER 24 hours –> high output CHF –> see increased BP, HR, and CO 2X normal
  • HTN seen can be SEVERE
36
Q

Other end organ complications seen with severe burn injuries

A

GI
- Ileus, ulceration, and cholecystitis

Renal

  • Decreased GFR, RBF 2/2 hypovolemia and decreased CO
  • Loss of Ca, K, and Mg
  • Retention of Na and H2O (trying to stay euvolemic with all these evaporative losses!)

Endocrine

  • CATECHOLAMINE RELEASE
  • Increased corticotropin, ADH, renin, angiotensin, aldosterone, glucagon, +/- insulin, hyperglycemia (at risk for nonketotic hyperosmolar coma, esp if on TPN)

Blood and Coagulation

  • Increased viscosity (high evaporative loss)
  • Increase in clotting factors (fibrinogen, V, and VIII, fibrin split products
  • At risk for developing DIC
  • Hct usually goes down 2/2 hemolysis
37
Q

Response to catecholamines in burn patients is

A

reduced

38
Q

Hypovolemic shock is often accompanied by

A

cardiogenic shock

39
Q

Edema in burn patients

A

Increased microvascular permeability results in proteins filling the interstitial space

Edema formation stops at 18-24 hours as long as adequate fluid resuscitation has occurred

40
Q

Loss of fluid from the vascular compartment in the first 24 hours =

A

4mL/kg for each 1% of TBSA burned

41
Q

Fluid maintenance for those with TBSA

A

150% of normal maintenance rate

42
Q

Risks associated with overdoing your fluid resuscitation

A

Can worsen airway edema, increase chest wall restriction, and contribute to abdominal compartment syndrome

43
Q

Types of fluids to use

A

First 24 hours = crystalloids only
> 24 hours, consider 5% albumin if plasma proteins are highly diluted.

Remember that edema should correct itself within 18-24 hours if the pt is adequately fluid resuscitated. This is probably d/t repair of the microvasculature. In the first 24 hours, giving albumin will leak out and probably worsen edema. So we wait on albumin until > 24 hours.

44
Q

Doses for fluid resuscitation

A

Albumin 5% (after first 24 hours)
0.3 - 0.5 mL/kg Dose in this range based on extent of burn

Parkland Formulation
4ml / kg / % burned (Give in first 24 hours)

Modified Brooke Formula
2mL/kg/% burned (Give in first 24 hours)

Give 50% of volume in first 8 hours
25% in second 8
Another 25% in the third 8
This is very similar to our fluid deficit replacement!

45
Q

Goals of fluid resuscitation in burns

A

UO 0.5-1 mL/kg/hr
HR 80-140 (consider age)
MAP > 60
Base deficit

46
Q

If perfusion and UO is still poor despite adequate fluids, what else can you do?

A

Low dose dopamine

5mcg/kg/min

47
Q

Electrolyte abnormalities in burn patients

A

Hyper or hyponatremia

Altered iCa, Mg, and K+

48
Q

Anesthesia for echarotomies

A

These are performed multiple times, especially from days 2-14 after burn injury

  • Maintain Hct (often need transfusions)
  • Coagulopathy
  • Temperature (fluid warmer and bair)
  • Fluids and electrolyte correction
  • Hypermetabolic states means higher O2 requirement, ventilation, and nutrition requirements
  • Risk of GI ileum (aspiration risk)

Monitors: May be difficult to place d/t extensive burns providing limited access

  • Need large bore IV access (may need to place in abnormal places)
  • Increase the room temp to 28-32 degrees
  • Minimize blood loss (topical/SQ epi, only address 15-20% TBSA per procedure, use tourniquets
  • Treat complications of massive transfusion (coagulopathy and hypocalcemia)
49
Q

Pharmacology changes in burn patients

A
  • HIGH opioid requirement (ideal anesthetic choice is isoflurane with large dose opioid)
  • Serial debridements calls for ketamine or regional via indwelling catheter

Muscle relaxants

  • In first 24 hours, there is normal response to all paralytics
  • Avoid sux 24 hours to 1 year post-burn injury
  • Resistance to most NDMRs in burns > 30% TBSA

Advanced Anesthesia III (6 decks)

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