CHAPTER 04: BURNS Flashcards
What is Jackson’s burns model?
Jackson described the zones of burn injury in 1970
Zone of COAGULATION (NECROSIS)
- centre of burn wound
- cell death immediately following burn injury,
- extracellular proteins denatured,
- circulation ceased.
- can extend into ZOS
Zone of STASIS (OEDEMA)
- local inflammatory mediators damage microcirculation due to sludging and poor oxygen delivery
- can progress to necrosis if patient is hypovolaemic, hypothermic or on inotropes
Zone of HYPERAEMIA (INFLAMMATION)
- can be whole body if 20% TBSA
- vasodilatation: due to inflammatory response
- increased capillary hydrostatic pressure and capillary leak
- increased interstitial osmotic pressure: due to albumin leaking out into extracellular space
Tell me about the epidemiology of burns
How has outcome and mortality rate improved ?
0.5-1% UK pop burnt each yr 10% require admission 10% of admissions are life threatening children - scalds most common adult - flame burns most common
% TBSA associated with death of 1/2 of cohort (LD 50, median lethal dose) age 21
1950 = 45% TBSA
1990 = 85% TBSA
plot of burn size s mortality shows a sigmoid distribution
Due to
- early and effective resus
- better treatment of inhalation injury
- early surgical excision
- control of sepsis
- development of alternative wound closure materials
Why do blisters form?
damage to dermo-epidermal junction → leakage of plasma → separation of dermis from epidermis
blister fluid contains inflammatory mediators and should be regarded as open wound
What is the pathophysiology of burn wounds?
divided into local and systemic effects
Local
- inflammatory mediators (from cap walls, WBC and plts)
- vasodilation, leak, fluid in interstitial space
Systemic
Reduced cardiac output
- decreased myocardial contractility
- decreased VR (hypovolaemia)
- increased SVR and after load
Increased SVR
- catecholamines, ADH, angiotensin II
Pulmonary oedema
- inc pulmonary vasc resistance, cap pressure, cap permeability, LHF, hypoproteinaemia, inhalational injury, ARDS
Renal
dec renal perfusion, inc ADH & aldosterone, inc Na H20 retention
Liver / pancreas
- hyper-metabolic (increased catecholamines and glucagon, decreased sensitivity to insulin, catabolic, poor temp reg)
- immunosuppression (cellular and humoral)
- growth suppression (decreased GH)
GI
- Curling’s ulcer
- gut stasis
- bacterial translocation (gut circ decreased)
- acalculous cholecystitis
What is eschar and pseudo-eschar?
Eschar - considered an open wound and may compromise wound healing, as it is
- medium for bacterial growth
- source of inflammatory mediators and toxins
- consumes clotting factors, fibrinogen and platelets
- protein loss
- if circumferential may compromise blood flow or chest excursion
Pseudo-eschar
- formed when topical antimicrobials e.g. SSD (polypropylene glycol carrier) / flammacerium (cerium nitrate) chelates with wound exudate
Indications for ventilation
history inc RR, confusion, distressed, tiring H&N burns supraglottic oedema high COHb Anaesthetic assessment prophylactic Abx and steroids not indicated
Inhalational injury
a) History
b) Examination
c) Types
a) history - enclosed space, unconscious
symptoms - hoarse voice, carbonaceous sputum, stridor, restlessness, respy difficulty, SOB, wheeze
b) singed nasal hairs, soot in nose and throat, burns in airway, swollen upper airway, inc RR, accessory muscles, hypoxia, pulmonary oedema, ARDS, altered consciousness
c) supraglottic (due to heat)
subglottic - due to products of combustion
systemic - toxic compounds: carbon monoxide, cyanide poisoning
Smoke inhalation pathophysiology
increases mortality by 40%, 70% w pneumonia
inflammatory mediators are released
increased pulmonary artery blood flow
bronchoconstriction TXA2, increased airway resistance
VQ mismatch
decreased pulmonary compliance
interestitial oedema, fibrin casts, infection, distal atelectasis
Late - pseudomembrane, permanent airway fibrosis and stenosis
What cases should be referred to burns unit?
PT >10% adult, >5% children FT >5% adult burns to specialised areas burn requiring decompression significant chemical or electrical injury ?NAI associated major trauma significant co-morbidities
Treatment of inhalation injury
CO - high affinity for Hb, O2 dissociation curve shifted left
- also binds cytochromes (sick cell syndrome)
CoHb >5% = inhalation injury, >20% toxic symptoms (headache), death >60%
Rx - 100% O2 (reduces 1/2 life of CO from 250mins to 40-60mins)
Cyanide - inhibit cytochrome oxidase, uncouples oxidase phosphorylation
Rx - 100% O2 humidified
hydroxycobalamin
sodium thiosulphate
Treatment of inhalational injury Humidified O2 Intubation early Increase fluid resus Mechanical ventilation, avoid barotrauma, even if PaCO2 is slightly higher (permissive hypercapnia)
ABG, fibreoptic bronchoscopy and BAL, CXR, chest physio, sputum culture, antibiotics, bronchodilators, N-acetyl cysteine, tracheostomy, PPI
How do you assess depth of burns?
Erythema - epidermis intact, no blistering, blanches
Superficial partial thickness - papillary dermis loss, sensate, blanches, blisters, skin appendages intact
Deep dermal - reticular dermis, decreased sensation, fixed staining, poor cap refill
Full thickness - entire dermis and adnexal structures damaged, insensate, leathery, dry
What do you ask the referring A&E to do before referring to burns unit?
EMSB guidelines
- stop the injury (extinguish flames, stop electricity, remove clothing, irrigate chemical)
- cool the burn wound (up to 2hrs, reduces direct thermal trauma, stabilises mast cells, reduce histamine release and other inflammatory mediators), tap water, wet gauzes, hydrogel dressings
ATLS protocol if patient suffered concurrent trauma
- give adequate analgesia
- toilet wound with saline
- photograph
- dress with cling film or jelonet and wrap in gauze
- keep patient warm
- tetanus prophylaxis
- transfer with notes and fluids adminstered thus far
What investigations may be useful to assess burns?
Facial
- fluorescein eye exam
Inhalational injury
- ABG
- COHb
- CXR
- bronchoscopy
Compartment syndrome
- clinical
- 5Ps
- doppler flowmeter
- compartment pressure testing (>30mmHg)
Electrical injuries
- ECG, cardiac monitor
- bloods - U&Es renal func
- urinanalysis - myoglobinuria
Chemical injuries
- pH
Laser Doppler (EG, Chelsmford) Videomicroscopy (Canniesburn)
what is an adult and newborn’s skin surface area?
adult - 1.5 - 2 m2
newborn - 0.2 - 0.3 m2
What is a child and adult’s circulating blood volume?
adult = 60ml/kg
child 80ml/kg
How do you estimate TBSA?
palm = 0.8%, hand ~1%
Lund and Browder charts (adults and children)
Wallaces rule of 9s
Modified for children - 18% head, 14% leg, take away 1% from head and add to legs for each yr
What is the initial management of burns?
EMSB guidelines
ATLS protocol if patient suffered concurrent trauma
Burns resuscitation - adults 15%, child 10%
Fine line b/t adequate resuscitation and fluid overload - frequent adjustments required.
Parkland formula (1st 24hrs) - crystalloid
(Charles Baxter Parkland Hospital Texas 1968)
Adults - 4mls/kg/%/24hrs half given first 8 hrs from burn, Hartmann’s (2mls for kids)
Paeds - Add maintenance (oral/NG/iv) → 4% glucose /saline – oral/NG/i.v. - For 24 hours: o 100ml/kg first 10kg o 50ml/kg next 10kg o 25ml/kg next 10kg
What is used to measure end points for resuscitation?
End Points
- Keep UO 0.5-1ml/hr adults, 1-2ml/kg kids
- Keep Pulse <2.5 deg – a good measure of circulation
- ABG, lactate, haematocrit
- CVP, PAWP
- Swan-Ganz catheter (elderly pts, cardiac)
- ↑ fluids needed for inhalation (30-40%), crush (post escharotomy / fasciotomy) & myoglobinuria (electrical)
- Can use NG tube after resus
How do you assess volaemic status?
initially - UO
after 24hrs - less accurate due to glucose intolerance, SIADH and respy losses
- plasma Na & U
- CVP
What fluid resuscitation formulas can be used after Parkland formula?
What alternative fluid resuscitation formulas are there?
After Parklands
Brooke formula (colloid)
5% albumin (24hrs) = 0.5ml / kg / %TBSA for 24hrs
Free water (ml/hr) = (25 + percentage burn) X BSA (m2)
ALTERNATIVE FLUID RESUS FORMULAS Muir and Barclay Formula - Colloid (1974 - Mt Vernon) 4.5% albumin %TBSA x wt / 2 = 1 ration 1 ration per 4/4/4/6/6/12 Monitor for hypernatraemia - free water may be needed
Evans - NS at 1 mL/kg per %burn, 2000 mL D5W*, and colloid at 1 mL/kg per %burn
Slater - RL at 2L/24h + FFP at 75 mL/kg/24 h
What other fluids can be used?
Why is Ringer’s Lactate (Hartmanns) better than isotonic saline?
Other fluids = Dextran (Demling), FFP (Slater), bld tx
RL is better than isotonic saline because lower Na conc (130 vs 154mEq/L) and higher pH concentration (6.5 vs 5.0) = more physiologic. RL metabolized lactate also has buffering effect on associated metabolic acidosis.
What is fluid creep?
1st described by Pruitt 2000
Saffle J Burn Care Res 2007
Occurs when pts receive more resus than predicted by Parklands formula, and more than actually required.
Reasons include
1. Parkland not accurate in large burns
2. clinicians are slow/reluctant to reduce ivi when UO is high
3. opioid creep: opiates CVS effects include partial antagonisation of adrenergic stress response
4. influence of goal-directed resus
Deleterious effects of over resuscitation
- increased pulmonary complications ⇉ ARDS
- increased escharotomies of chest or extremities
- abdominal compartment syndrome
- MODS
- cerebral oedema
Aim is to give least amount of fluid to maintain tissue perfusion (prevent burns shock) and avoid complications of over-rescusitation (burn oedema).
Burns e.g. 15-20% TBSA w/o inhalation injury usually doesn’t initiate systemic inflammatory response. These pts may be resuscitated more modestly, via oral route.
Explain the colloid vs cystalloid debate.
Colloid
- Albumin 5% (from pooled plasma product)
- 50% remains intravascularly, (as opposed to 20-30% of crystalloid solns)
Cochrane Injuries Group 1998 - metaanalysis of 30 studies comparing alb vs crys resus in hypovolaemia, burns and hypoproteinaemia.
Showed albumin Rx increased mortality (increased pulmonary oedema and renal dysfunction) - but criticism to report =
- very dissimilar cohorts
- only 3 burns studies (80% survival in paeds >95% TBSA)
Alderson 2004 - Follow-up reports from Cochrane Injuries Group have failed to support earlier claims that albumin administration increases mortality
The SAFE Study Investigators 2004
- double-blind RCT of albumin administration to 6045 ICU pts in Aus & NZ demonstrated the safety of albumin use
- observed that the saline group received 40% more fluid than albumin group
Vincent J-L 2004
- metanalysis concluded that albumin administration significantly reduces morbidity in ill hospitalised patients, including patients with burn injury
How do you classify the timing of burns reconstruction?
Emergency, essential and elective
Emergency - urgent when vital organs exposed e.g. cornea
Essential - significantly improve function and appearance e.g. microstomia, jt contractures, scarring affecting growth
Elective - aesthetics
What is burns oedema?
biphasic (immediate, second phase 12-24h, resolution 48-72h)
mediators - local (histamine, PG, kinins), systemic (catecholamines, angiotensin)
Capillary microcirculation changes
- increased cap hydrostatic pressure (vasodil)
- decreased cap oncotic pressure
- increased tissue oncotic pressure
- decreased tissue hydrostatic pressure
- impaired cell membrane function
What evidence is there for early burns excision?
Papers by Herndon, Tompkins, Muller
- remove devitalized tissue quickly to blunt the systemic inflammatory cascade
- improved survival rate
- decreased hospital stay
- reduced blood loss
- fewer metabolic complications
Dietetics in burns
Calorie requirement
20% protein, 28% fat, 52% carbs
Curreri formula
Adults → 25kcal/kg + 40kcal/% TBSA
Child → 40-60 kcal/kg
Calorie: nitrogen ratio should be 150:1
Hildreth formula
1800kcal/m2 BSA + 2000kcal/m2 TBSA
Other formulae Sutherland - adults - 20kcal/kg +70kcal/%TBSA - children - 60kcal/kg + 35kcal/%TBSA Harris-Benedict (use indirect calorimetry to calculate)
Protein requirement
Davies
children - 3g/kg + 1g/%TBSA
adults - 1g/kg + 3g/%TBSA
thromboprophylaxis vitamin supplementation gastric protection antibiotics if indicated anabolic hormones (oxandrolone) contentious
How do you classify the timing of burns reconstruction?
Emergency, essential and elective
Emergency - urgent when vital organs exposed e.g. cornea
Essential - significantly improve function and appearance e.g. microstomia, jt contractures, scarring affecting growth & ADLs
Elective - aesthetics
What are the principles of burns reconstruction? (Potokar)
Secondary burns reconstruction are often complicated cases
multifactorial
My approach is to 1st take history of burns injury (mechanism etc), assess pt compliance
PMH and social Hx
what Rx have they had
what brought them here now
Potokar’s 5 P’s
- Problems
- Priorities - pt shopping list
- Possibilities - what is available?
- non-surgicals: injections, physio, psych
- surgical - excision and dc, ssg, ftsg, zplasty, local flaps, distant / free flaps - Patient perceptions - do they understand what surgery can achieve
- Plan of action - esp w multiple problems, order of surgery - start with a ‘winner’
How does different scar treatments work?
Pressure therapy (15-40mmHg)
- reduces tissue perfusion and oxygenation, accelerates maturation
Silicone gel sheet
- softens scar
Intralesional triamcinolone
- enhance collagenase, dampens fibroblasts
Massage
Excision (selected scars)
Pulsed dye laser
- Hb absorbs laser energy -> coagulation -> tissue hypoxia -> collagen realignment and remodelling
What are the principles of secondary burns reconstruction?
- prevention of better than cure (of contracture - splints pressure garments and exercises)
- prioritise face and hands
- adhere to aesthetic units
- sheet grafts to face, hands, neck
- thicker grafts - perioral, periorbital, neck
- f/u children until growth complete
What biological skin substitutes are there?
Biobrane - silicone sheet over nylon mesh coated with porcine collagen
Transcyte - similar to Biobrane, but with added neonatal fibroblasts (no proven benefit to biobrane)
Apligraft - cultured allogeneic neonatal keratinoctyes on bovine collagen
gel matrix seeded with neonatal fibroblasts
Dermagraft - cultured fetal fibroblasts on vicryl mesh
Alloderm - ADM human cadaveric skin with epidermis removed and cellular components extracted (dermal template)
Strattice - ADM derived from porcine dermis
Xenograft - porcine skin (EZ Derm)
Integra - dermal matrix of bovine collagen and shark chondroitin 6 sulphate covered with silicone elastomer membrane
MatriDerm® is a 3D matrix construct of native structured collagen fibers with elastin, used for the support of dermal reconstruction.
Collagen is harvested from bovine dermis and contains the dermal collagens I, III and V. Elastin is obtained through the hydrolysis of bovine ligamentum nuchae
Cultured epithelial autografts
What are the principles of burns scar management?
Can be divided into scar minimisation and treatment
Scar minimisation
- early burn excision and wound closure
- splint and physio to prevent contracture
- reduce infection
Scar treatment
- early ambulation, exercise
- massage, compression, pressure garment
- topical Rx - steroid inj, silicone, laser, US
- prevent joint contracture - early scar release
What surgical techniques are there for axillary scar contracture?
incisional vs excisional z-plasty, y-v ssg ftsg dermal template local flap (skin, muscle, FC) regional flaps (RFF, PIA, LD) distant flaps (groin, cross-limb, abdominal) free tissue transfer tissue expansion
How do you classify axillary contractures?
Classification of axillary contractures (Kurtzamn and Stern, 1990).
Type 1A: Injuries involving the anterior axillary fold
Type 1B: Injuries involving posterior axillary fold
Type 2: Injuries involving both anterior and
posterior axillary folds
Type 3: Injuries type 2 plus axillary dome
Treatment
Type 1&2 - Z plasties, Y-V, 5 flap plasty, transposition flap (wider flaps / staged if concerned re: vascularity / tip necrosis)
Type 3 - FC or muscle flaps, medial arm or parascapular, axial bilobed, ascending scapular, thoracodorsal perforator-based flaps
Fishmouth incision & FTSG / SSG (not ideal)
Flaps - can stop night splintage & stretching exercises earlier than skin grafts (6-12mths)
How do you treat an elbow contracture?
Mild contracture
1. Five flap plasty
Moderate contracture / defect
Chevron / fishmouth incisions - above and below antecubital fossa
Release contracture & fill defect with
2. FTSG or Matriderm / Integra & SSG
3. single / multiple bipedicle flap (Prakash)
& SSG of defect
Severe contracture, large defect
- Forearm FC transposition flap
- Reversed lateral / medial arm flaps
NB elbow can be affected by heterotopic ossification - excise first / staged
What is the difference b/t flamazine and flammacerium?
when is it contraindicated?
what potential side effects are there?
Both topical antimicrobials
reacts with wound exudate (?polypropylene glcol carrier)
Flamazine = Silver sulphadiazine
Flammacerium = SSD + cerium nitrate (produces more dry leathery eschar)
Contra - pregnant, nursing mothers, children under 2mths - kernicterus
G6PD deficiency - haemolytic anaemia
face - staining
may cause neutropenia 5-15%
maculopapular rash
methaemoglobinuria (rare)
What are the causes of burn injuries?
Heat
Electrical
Chemical / extravasation
Cold
How do you classify electrical burns?
What can they cause?
Low voltage 1000V
- local tissue necrosis
- AC vs DC
High voltage >1000V
- look for entry exit wounds
- deep muscle injuries, compartment syndrome
- cardiorespy arrest (prolonged CPR recommmended)
- LOC, electrical stunning
- fractures
- bowel perf, paralytic ileus
- spinal cord transection
bone has high resistance, therefore generates greatest heat
Lightning injury types
Electrical burn wound types
- direct strike
- ground splash (hits poor conductor first, then jumps and discharges on person)
- stride potential (current flows thru victims legs when in contact with ground)
Lichtenberg figures
Burn wound types
- entry exit points
- arcing
- thermal burns (clothes set alight)
Treatment of electrical burns
- ABC
- ECG
- haemochromogenuria, compartment syndrome
- debridement
Bailey Em Med J 2007
- cardiac monitoring not required if initial ECG normal and asymptomatic (no LOC, <1000V)
What are the delayed complications of electrical burn injuries?
- cardiac arrhythmias
- neurological: epilepsy, encephalopathy, brainstem, cord, peripheral progressive demylination,
- cataracts
Cold injury classification
Local - frostbite (slow/exposure or fast/dry ice liq N cooling) = focal exposure of body part(s) to cold
Systemic - hypothermia = lowering of core temp
Cold injury symptoms
cold, numb, pain on rewarming
What are the phases of cold injury?
Prefreeze = 3-10 deg - inc vasc permeability
Freeze-thaw = -6 to -15 deg - ice crystals
Vascular stasis = dilation and coagulation, blood shunted away
Late ischaemic = cell death, gangrene
Management of frostbite
avoid rubbing rapid rewarming - 40-42 degrees water, 30mins NSAIDS Thrombolytics leave blisters elevate, splint tetanus, antibiotics allow demarcation and delay amputation
What are the longterm effects of frostbite?
- residual burning sensation (allodynia?)
- cold intolerance, Raynaud;s
- permanent sensory loss
- hyperhidrosis
- osteopenia, joint pain, stiffness
What complications are associated with burns injury?
Burns sepsis Toxic shock syndrome acalculous cholecystitis Curling's ulcer ischaemic enterocolitis suppurative thrombophlebitis heterotopic ossification Marjolin's ulcer
