Burn wound management, infection control, and inhalation injury Flashcards
(33 cards)
What are the zones of injury in a burn wound?
Zone of coagulation
Zone of stasis - edema, where inflammatory mediators are released, may progress.
Zone of hyperaemia - vasodilation
What occurs in zone of stasis?
- inflammation
- procoagulation/anti-fibrinolysis
What causes conversion of a wound? occurs in zone of stasis
and
What is the difference between conversion and progression
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.
What is your initial management of a burn injury
- 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
What are 3 principles functions of burn dressings?
- Protective - barrier to microorganisms
- Metabolic - prevents heat evaporation, cold stress
- Comfort - prevents air currents, absorbs secretions
List skin substitutes
Temporary
- Biologic: allograft, xenograft, amnion
- Synthetic: Biobrane, trasncyte
Permanent
- Biologic: Autograft, cultured epidermal cell autograft
- Synthetic: Alloderm, Integra
What are optimal properties of a skin substitute?
- 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)
What are operative indications for Excision and Grafting
- Full thickness burns { larger than 1cm2 in non-critical areas}
- deep partial burns which would take longer than 2-3wks to heal
What are reasons for early E&G?
- improved survival, decrease LOS in hospital
- for hand and foot, less resulting disability
How do you reduce intra-operative blood loss?
- Tumescent solution (1:1 000 000 - 1:500 000 epinephrine)
- Topical epinephrine (1:30 000)
- tourniquet
- staged operations (minimize operative time)
Describe how you would do escharotimies to all critical areas:
- chest/abdo
- neck
- Upper extremity
- Interossei
- Palm
- Digits/toes
- Leg
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
What are risk factors for burn wound infection? and which microorganisms are likely to be responsible?
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
How do you diasnoe and treat a burn wound infection
- Dx: quantitative cultures and signs of infection
- Tx
- prevention: aseptic techqnieu w dressing change
- debriding dressing
How do you treatv pneumonia associated w burn injury/II?
- targeted abx Tx
- chest physio
- coughing
- turning
- pulmonary toileting
How do you manage blood stream/catheter infection
- cleanse site and dress with antmicrobial dressing
- avoid line in burn wound
- change line q3-7days if suspected infection (not prophylactic)
What is inhalational injury
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%
Describe pathogenesis of II in each of the airway locations:
- tracheobronchial mucosa
- alveoli
- pulmonary vasculature
- 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
Describe the products in smoke (combustion products) that are responsible for II in lower tracts
- Ammonia, chloride, sulfur dioxide (furniture/clothing)
- Hydrogen chloride (wall/flooring)
- Cyanide (upholstery, nylon)
- aldehyde, formaldehyde (wall paper, acrylic, cotton)
How do you diagnose and treat cyanide poisoning
- 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
What are 3 effects of CO, signs and symptoms of CO inhalation, 1/2 life of CO and treatment
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
How do you manage a patient with suspected II due to direct thermal damage
- 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
How do you diagnose ARDS
- 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
What are causes of Hypoxia
- 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
What are options for burn wound dressings and their MOA
- 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