Burn wound management, infection control, and inhalation injury Flashcards

1
Q

What are the zones of injury in a burn wound?

A

Zone of coagulation

Zone of stasis - edema, where inflammatory mediators are released, may progress.

Zone of hyperaemia - vasodilation

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2
Q

What occurs in zone of stasis?

A
  • inflammation
  • procoagulation/anti-fibrinolysis
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3
Q

What causes conversion of a wound? occurs in zone of stasis

and

What is the difference between conversion and progression

A

Conversion occurs due to an insult such as

  • infection
  • hypoperfusion (over resuscitation, underresuscitation)
  • edema
  • Progression is the timely development of the wound, but cannot be altered, not avoidable
  • conversion is the change due to an additional insult and is avoidable.
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4
Q

What is your initial management of a burn injury

A
  • ABC (life threatening)
  • Escharotomy (limb threatening)
  • Hx: mechanism, comorbidities
  • PE: inhalational injury / burn depth estimation
  • Determination: Severity of injury and need fo rtrasnfer/triage
  • Irrigation and debridement of wounds
  • burn wound dressing and infection control
  • treatment planning: non-op vs op
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5
Q

What are 3 principles functions of burn dressings?

A
  • Protective - barrier to microorganisms
  • Metabolic - prevents heat evaporation, cold stress
  • Comfort - prevents air currents, absorbs secretions
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6
Q

List skin substitutes

A

Temporary

  • Biologic: allograft, xenograft, amnion
  • Synthetic: Biobrane, trasncyte

Permanent

  • Biologic: Autograft, cultured epidermal cell autograft
  • Synthetic: Alloderm, Integra
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7
Q

What are optimal properties of a skin substitute?

A
  • Protective: against heat/vapor loss, barrier to microrganisms
  • Comfort: decrease pain
  • non-immunogenic, non-toxic
  • able to resist shear forces
  • promotes healing and prepares wound bed for autograft (temporary substitutes)
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8
Q

What are operative indications for Excision and Grafting

A
  • Full thickness burns { larger than 1cm2 in non-critical areas}
  • deep partial burns which would take longer than 2-3wks to heal
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9
Q

What are reasons for early E&G?

A
  • improved survival, decrease LOS in hospital
  • for hand and foot, less resulting disability
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10
Q

How do you reduce intra-operative blood loss?

A
  • Tumescent solution (1:1 000 000 - 1:500 000 epinephrine)
  • Topical epinephrine (1:30 000)
  • tourniquet
  • staged operations (minimize operative time)
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11
Q

Describe how you would do escharotimies to all critical areas:

  • chest/abdo
  • neck
  • Upper extremity
  • Interossei
  • Palm
  • Digits/toes
  • Leg
A

In general - beyond the margin of the burn, through to the hypodermis

  • chest/abdo
    • from clavicle, along anterior axillary line, trasnverse across costal margin
  • neck
    • from mastoid to sternal notch, along anterior border of SCM
  • Upper extremity
    • arm in anatomic position
    • medial and lateral arm, anterior to medial epicondyle
  • Interossei
    • longitudinal incision over 2nd and 4th MC
  • Palm
    • along palm crease and at wrist cross ulnar to avoid palmar cut br
  • Digits/toes
    • posterior to mid lateral line on non-tactile surface of each digit
  • Leg
    • midlateral and midmedial incisioncs
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12
Q

What are risk factors for burn wound infection? and which microorganisms are likely to be responsible?

A

RISK FACTORS

  • Large burn
    • burn immunosuppression, hypermetabolism/malnutrition, ileus with altered gut permeability, loss of skin barrier, catheterization
  • Dessicated wounds
  • Pre-burn co-morbidities
  • Age >60 or <16

ORGANISMS

  • Early (within 24hr) endogenous Gr+
  • Late (within 3-7days ) exogenous Gr-
  • Delayed burn closure : yeast, fungi, drug resistant bugs
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13
Q

How do you diasnoe and treat a burn wound infection

A
  • Dx: quantitative cultures and signs of infection
  • Tx
    • prevention: aseptic techqnieu w dressing change
    • debriding dressing
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14
Q

How do you treatv pneumonia associated w burn injury/II?

A
  • targeted abx Tx
  • chest physio
  • coughing
  • turning
  • pulmonary toileting
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15
Q

How do you manage blood stream/catheter infection

A
  • cleanse site and dress with antmicrobial dressing
  • avoid line in burn wound
  • change line q3-7days if suspected infection (not prophylactic)
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16
Q

What is inhalational injury

A

Def; injury to airway and lungs secondary to thermal energy and inhalation of toxins. MANIFESTS 4-12HRS POST BURN.

3 FACTORS:

  • INHALATION OF PRODUCTS OF COMBUSTION
  • INHALATION OF CO
  • DIRECT THERMAL INJURY TO UADT

Increased mortality by 30-40%

17
Q

Describe pathogenesis of II in each of the airway locations:

  • tracheobronchial mucosa
  • alveoli
  • pulmonary vasculature
A
  • Tracheobronchial mucosa
    • vasodilation, increased permeability, edema, trasnudation of fluid into lungs
    • sloughing of mucosa, obstruction
    • decreased ciliary motility
    • PBD3 -> atelectasis and infection
  • Alveoli
    • decerased surfactant, collapse, pulomnary edema
  • Pulmonary vasculature
    • vascoconstriciton due to TXA2
18
Q

Describe the products in smoke (combustion products) that are responsible for II in lower tracts

A
  • Ammonia, chloride, sulfur dioxide (furniture/clothing)
  • Hydrogen chloride (wall/flooring)
  • Cyanide (upholstery, nylon)
  • aldehyde, formaldehyde (wall paper, acrylic, cotton)
19
Q

How do you diagnose and treat cyanide poisoning

A
  • Dx: resistant metabolic acidosis, lactate>10, low A-V stauration, high CN level (above 0.1mg/L, >1mg/L lethal)
  • symptoms, lethargy, N/V, HA

TREATMENT

  • Sodium thiosulphate IV - binds CN and becomes thiocynaide, excreted in urine via osmotic duresis
  • Hydroxycobalamin - chelates CN, renal excretion. 2.5G
  • Sodium nitrate - Met-Hb former by conversion oxyHb to MetHb which binds CN
20
Q

What are 3 effects of CO, signs and symptoms of CO inhalation, 1/2 life of CO and treatment

A

3 EFFECTS of CO

  • high affinity for Hb than O2, displaces O2 from Hb molecule
  • shift Hb-O2 curve to the left reducing O2 offloading at the tissue level
  • inhibit p450 cytochrome, preventing aerobic metbaolism and shifting to anaerobic metabolism

Signs and symptoms

  • HA, hallucinations, cherry red lips coma
  • normal sat on pulse oximetry BUT low SaO2 (hypoxemia) on lab value
  • Based on carboxyhemoglobin % (level)
    • 0-5: normal
    • 15-20: HA, confusion
    • 25-40: nausea, visual changes
    • 40-60: halluciantion, coma
    • >60: 50% mortality

TREATMENT

  • 100% O2 or HBO
    • T1/2 of CO: 5-6hr on RA, 45min on 100% O2, 27mins in HBO at 3atm
21
Q

How do you manage a patient with suspected II due to direct thermal damage

A
  • Hx: LOC, enclosed, space, >10mins exposure
  • PE: singed ahirs, erythema of airway/oral cavity, sout, stridor, voice hoarseness, conjunctivitis
  • Labs
    • Carboxyhemoglobin level >10% significant
    • CN level >0.1mg/L significant
    • ABG (PaO2< SaO2)
    • Metabolic acidosis
  • Investigations
    • Bronchoscopy : edema, erythema of vocal cords, hypopharyn, tracea, ulceration of airway mucosa, sout/char in airway
  • TREATMENT
    • supportive:
    • Endotracheal intubation for 100% O2
    • no barotrauma (VT ?8cc/kg?)
    • HFOV (rescue for ARDS)
    • Pulmonary Toileting (chest physio, percussion/vibration/therpautic bronch, postural drainage)
    • NAC, nebulized heparin (dissolves casts)
    • aerosolized hypertonic saline (to draw out edema)
    • Other
      • change from supine to prone
      • NO (as rescue to vasodilate)
      • no steroids (deleterious)
      • aggresssive treatment of pneumonia
22
Q

How do you diagnose ARDS

A
  • bilateral opacities consistent w pulmonary edema
    • but no other etiology to explain (pleural effusion, cardiac failure, fluid overload)
  • Impaired oxygenation
    • Defined by Hypoxemia (PaO2/FiO2)
    • mild ARDS: PaO2/FiO2 between 200-300mmHg and has PEEP or CPAP on vent
    • moderate ARDS: PaO2/FiO2 between 100-200mmHg and has PEEP >5cm H20
    • severe ARDS: PaO2/FiO2 <100mmHg, less than 200 and has PEEP >5cm H20
  • Symptoms begin wihtin 1wk of insult or with new or worsening symptoms within a week
23
Q

What are causes of Hypoxia

A
  • Hypoxemia (low PaO2)
    • V/Q mismatch
    • hypoventilation
    • impaired diffusion
    • pulmonary shunt
  • Low O2 content in Blod (diffused+bound)
    • low Hb content
    • low PaO2
    • CO poisoning
    • Methemoglobenemia
    • rightward shift in HbO2 curve
  • Low Cardiac Output
    • Arrhtymia, depression
    • high Periphral/pulmonary vascular resistance
    • low coronary perfusion
24
Q

What are options for burn wound dressings and their MOA

A
  • Flamazine (SSD - silver sulfadiazine
    • 1% cream silvernitrate + sodium sulfadiazine
    • MOA: inhibits DNA replication, cytochrome 3a/b activation and alters CM. ALso inhibits folic acid
  • Silver nitrate
    • 0.5% solution of Ag granules
    • MOA: as above - blocks DNA, Cyt 3a/b/CM
  • Sulfamylon (mafenide acetate)
    • 11% cream, 5% solution
    • MOA: unclear
  • Acticoat
    • nylon/polyester sheet coated in silver crytals within polyethylene mesh
    • MOA: slow release of Ag ions when wet - as above w DNA/Cyt/CM
  • Aquacel Ag
    • methycellulose + ionic silver
    • MOA: adheres to wound and separates with healing. same as DNA/cyt 3a/b/CM
25
Q

What is the eschar penetration, spectrum coverage, adv and disadv and S/Es of each of the 5 burn wound dressings?

A
  • Eschar Penetration: Best > intermediate> Poor
    • Sulfamylon > SSD> Acticoat>aquacel Ag> Silver nitrate
  • Spectrum
    • all broad spectrum
    • EXCEPT - sulfamylon has no fungal/MRSAactivity
    • EXCEPT - SSD has reports of resistant pseudomonas and enterobactericeae
  • Advantages
    • PAINLESS: Flamazine, Silver nitrate. Others painful
    • Low frequency of change: acticoat q5d, aquacel q14d
    • Cartialge penetration - Sulfamylon
  • Disadvantage
    • Not for superficial wounds: flamazine, silver nitrate - inhibit fibroblast and keratinocytes
    • Need clean wound base: Aquacel Ag

Side EFFECTS

  • SSD Systemic effect: leukopenia/neutropenia transient, methemoglobunuria, crystalluria, sulfa allergic rxn
  • SSD local effect: rash due to sulfa
  • Silver nitrate: Systemic effect: methemoglobenemia
  • Silver nitrate local effect: staining
  • Sulfamylon systemic effect: CA inhibitor - hyperventilation, hyperchloremic metabolic acidosis, osmotic diuresis
  • Sulfamylon Local: rash
26
Q

Describe the advantages and disadvantages biologic skin substitutes

A
  • Cultured Epithelial autografts
    • can be placed onto of allograft dermis/integra/trasncyte
    • risk of hypertrophic scarring/pigment
  • cultured autologous skin
    • can be expanded in culture then seeded on HA
  • Xenograft
    • no vascularization
    • decreased evaporative loss, early lysis
  • Amnion
    • no vascularization
    • poor evaporative control, early lysis
  • Allograft
    • stimulates angiogenesis, reepitheliazatio and vascularization
    • suppreses bacterial growth
    • rjected in 7-14days
  • Acellular dermal allograft
    • may be left permanent - lyophilized/glycosylized/acellular, NO REJECTION
    • need stsg or CEA
27
Q

List 5 options for synthetic skin substittute

A
  • BIObrane
  • INtegra
  • Trasncryte
  • Dermagraft
  • Apligraf
    *
28
Q

What is biobrane, indications

A

Synthetic skin substitute with top laye rof silicone and bottom layer of porcine type 1 collagen and nylon

  • semipermeable
  • protects against evaporative losses, reduced pain/dressing changes, impermeable to bacteria

INDICATIONS

  • superficial partial dermal burn
  • temporary coverage for excised burn
  • temporary coverage for widely meshed autograft
  • TEN
29
Q

What is integra and indications

A

Synthetic skin substitute bilayered with top silisone an dbottom bovine collage matrix qith shark choidrointin 6 sulfate

  • permanent dermal replacement
  • gradually replaced over 3-6wks
  • requires an ultrathin STSG

INDICATIONS

  • FT or deep partial thikness burns
  • need for reharvesting donor sites
  • chronic/surgical wounds
30
Q

What is transcyte and indications

A
  • Def; synthetic skin substitute silicone + allogeneic human neonatal fibroblasts and bottom layer porcine collage on nylon
  • similar to biobrane in terms of mechanism >removal as burn heals, indications
    *
31
Q

What is dermagraft

A

POlyglactic (vicryl)mesh with allogeneic neonatal fibroblasts

  • permanent dermal template (like interga)
  • requires overlying ultrathin STSG
  • take not as good as interga
    *
32
Q

What is apligraf

A

Synthetic skin substitute

dermal bovine collagen + living neonatal fibroblast and epidermal layer of neonatal keratinocytes

Indications

  • widely meshed autografts to accelrate healing at interstices, chronic venous ulcers, diabetic ulcers
33
Q
A