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Tobias ECVS - Krizia > Ch 81 - Burns > Flashcards

Ch 81 - Burns Flashcards

1
Q

What are the 4 aetiological classifications of burns?

A
  • Thermal
  • Chemical
  • Electrical
  • Radiation
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2
Q

What are the 5 degrees of thermal burns?

A
  • Frist degree - Superficial, only epidermis effected (erytema). No blistering, wounds or scarring
  • Second degree - Full-thickness epidermal necrosis extending into underlying dermis. Results in blistering (rare in dogs/cats)
  • Third degree - Extends through dermis to underlying SQ
  • Fourth degree - extend to underlying muscle or fascia
  • Fifth degree - Extends to bone
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3
Q

What occur when the skin reaches 40-44C, 60C and 70C?

A
  • 40-44C - Failure of cell membrane Na pump
  • 60C - epidermal necrosis within 1 second
  • 70C - full-thickness burns in less than 1 second
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4
Q

What is the rule of 9s?

A

A method of estimating the % surface area effected by a burn
- Head and neck 9%
- Each thoracic limb 9%
- Each pelvic limb 18%
- Dorsal and ventral halves of the trunk 18% each

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5
Q

What are the three zones when evaluating tissue injury secondary to thermal burns?

A
  • Zone of coagulation - no viable tissue remains
  • Zone of stasis - reduced perfusion due to damage to RBC membrane proteins causing reduction in deformability and reduced luminal diameter due to increased interstital pressure from increased capillary permeabiltiy. Tissues in this zone may be saved or may deteriorate
  • Zone of hyperaemia - Primary zone of the inflammatory response
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6
Q

What causes vasodilation as an acute response to a burn injury?

A
  • Postganglionic autonomic stimulation
  • Upregulation of NO synthesis within the burned area and surrounding skin
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7
Q

Why do burns heal slower that usual?

A
  • Only 5% of normal levels of fibroblast growth factor -2 (FGF-2)
  • None of the capillary endothelial chemotactic and proliferative activity seen in normal surgical wounds
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8
Q

List the main toxins associated with smoke inhalation

A
  • Carbon monoxide (preferentially binds Hb)
  • Hydrogen cyanide ( binds mitochondrial cytochrome oxidase, disrupting electron transport and preventing cellular respiration)
  • Inorganic acids (intensely irritating cauding bronchospasm and laryngospasm)
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9
Q

What pathophysiological changes occur in the lungs in response to smoke inhalation?

A
  • Increased pulmonary vasculature permeability
  • Venoconstriction
  • Rapid accumulation of fluid, mucus and neutrophils within the alveoli and airways

Pulmonary oedema

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10
Q

What are the main sources of the cytokines causing the changes resulting in ARDS?

A
  • Smoke damaged lungs
  • Burn-injured tissues
  • GIT
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11
Q

What is the pathophysiology of systemic vascular permeability in response to a major burn injury?

A

Within 10 minutes (burns over 25%), systemic vascular permeability to fluid and albumin increase because of myosin-mediated contraction of vascualr endothelial cells and direct damage to endothelial cells

Mediated by complement, histamine and oxygen free radicals from the burn site

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12
Q

When does generalise oedema and hypovolaemia peak?

A

Within the first 12 hours

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13
Q

What are the main source of fluid loss in burn patients?

A
  • Extravasation
  • Evaporative (3-20 times greater)
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14
Q

What are the main causes of myocardial effects of burn patients?

A
  • Decreased left ventricular contractility (increase of myocyte intracytoplasmic Ca)
  • Myocardial damage and decreased cardiac output secondary to carbon monoxide (decreased ATP production and necrosis)
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15
Q

How is the GIT effected by burns?

A
  • Barrier is compromised leading to translocation of bacteria and endotoxins as well as cytokines leading to septic shock
  • Increases apoptotic rate of gut mucosa
  • Impaired motility (increased expression of inducible NO from myenteric plexus)
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16
Q

What substance may have a protective role against acute renal injury in burn patients?

A

Atrial natriuretic peptide - increases renal blood flow and urine output

17
Q

What is burn anaemia?

A

An immediate and long-lasting reduction in circulating erythrocyte numbers
- Membrane damage increase fragility and decreased deformability
- Intravascular haemolysis
- Decline in protective antioxidants glutathione and alpha-tocopherol
- Reduced erythropoiesis

18
Q

How is the immune system affected in severe burn injuries?

A

Significant negative effects on lymphocyte production and function
- Upregulation of lymphod apoptosis (TNFa)
- Inhibition of chemotactic cytokine production by T-cells leading to an increased susceptibility to sepsis
- Macrophages and neutrophils express a hyperinflammatory phenotype
- Neutrophil migration is suppressed and adhesion is increased leading to vascular damage

19
Q

What is the recommended basic first aid for burns?

A
  • Application of cool to cold running water (2-15C). Can still see a benefit if delayed by up to 3hr after inciting cause
  • Sterile occlusive, nonadhesive dressing
20
Q

What is the main goal of fluid resuscitation?

A

Sufficient to maintain urine output of 1-2ml/kg/h
- This is the best clinical proxy for cardiac output and adequate peripheral perfusion

21
Q

What is the recommended fluid type for resuscitation in burn shock?

A
  • Polyionic crystalloid containing L-lactate only or those based on acetate
  • LRS has been shown to increase the inflammatory cascase and increase neutrophil activation, increase production of reactive oxygen species and increased apoptosis due to it D-lactate content
22
Q

What is bronchial hygiene therapy?

A

Treatment performed to remove accumulated secretions, necrotic material, foreign debris and bacteria from the airways
- Nebulisation and coupage
- Bronchoscopy and saline lavage

23
Q

How does oxygen therapy help with treating smoke inhalation?

A

Speeds removal of carbon monoxide from the blood
Half life of CO on room air is 4 hours, decreased to 1 hr with FiO2 40%

24
Q

What pharmacologic agents may be helpful in treatment of inhalation injury?

A
  • Aerosolized sympathomimetic bronchodilators
  • Aerosolised N-acetylcysteine (resp tract irritant… new N-acetylcysteine-L-lysinate)
  • Low molecular weight dextran to improve mucous rheology (flow)
  • Prophylactic antibiotics
25
Q

What are the three phases of burn pain?

A
  • Acute - Initial 2-3 days
  • Healing phase - weeks or longer
  • Rehabilitation phase - Months to 1yr+
26
Q

What are the three forms of burn pain?

A
  • Procedural pain
  • Background pain
  • Breakthrough pain
27
Q

What can be done to reduce the severity of the stimuli for the hypermetabolic state?

A
  • Keep patient in a warm environment (29 - 33C) and relatively humid
  • Burns kept covered at all times
  • Adequade analgesia
  • Appropriate use of sedatives and provision for adequate sleep
  • Early debridement of burn wound
28
Q

What should be the primary source of energy in burn patients?

A

Carbohydrates - supply energy for maintenance and healing and preserve lean body mass by sparing protein from oxidation for energy needs

29
Q

What are potential pharmacological options to treat the hypermetabolic state due to hormonal imbalances?

A
  • Propanolol (Beta-adrenergic blocade) - titrated to decrease HR by 20%
  • Insulin - normalised glucose conc as well as stimulating protein synthesis and decreasing protein catabolism
  • Growth hormones
  • Synthetic testosterone analogues (oxandrolone) - enhances efficacy of protein synthesis
30
Q

What are the 2 forms of surgical debridement of large burns?

A
  • Tangential debridement
  • Layered debridement
31
Q

What are alternative options to traditonal surgical debridement?

A
  • Hydrosurgical debridement
  • Ultrasonic surgical debridement
  • Autolytic debridement
  • Cerium Nitrate - binds to eschar forming a tough, leathery, impermeable eschar, protecting the underlying wounds and allowing for delayed escharotomy
32
Q

What are the four main classes of chemical which can cause burns?

A
  • Acids - powerful oxidising agents disrupting protein structure and function by inserting oxygen atoms into peptide bonds
  • Alkalis - Reducing agents, denaturing proteins through reduction of amide bonds
  • Hydrocarbons - lipid solvents than disrupt cytoplasmic membranes
  • Vesicants - Cause blistering (doxorubicin)
33
Q

How do electrical burns form?

A

Due to the heat that is generated by the resistance of the tissues to the current flow

34
Q

What is Joule’s law?

A

J = (I^2)RT
Energy delivered to tissue is proportional to the tissue resistance (R), the duration of exposure (T), and the square of the amperage (I)

Therefore, predicts that tissue with a higher resistance will sustain greater damage than those with lower resistance

Bone has a much higher resistance than surrounding soft tissues

35
Q

What temperature water is used for treatment of frostbite?

A

Lukewarm 40-42C

36
Q

What is bronchial hygiene therapy?

A

Treatment performed to remove accumulated secretions, necrotic material, foreign debris and bacteria from the airways
- Nebulisation and coupage
- Bronchoscopy and saline lavage

Tobias ECVS - Krizia (110 decks)

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