FRCS Plastic Surgery > CHAPTER 04: BURNS > Flashcards

CHAPTER 04: BURNS Flashcards

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0
Q

What is Jackson’s burns model?

A

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
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1
Q

Tell me about the epidemiology of burns

How has outcome and mortality rate improved ?

A 
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
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2
Q

Why do blisters form?

A

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

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3
Q

What is the pathophysiology of burn wounds?

A

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
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4
Q

What is eschar and pseudo-eschar?

A

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

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5
Q

Indications for ventilation

A 
history
inc RR, confusion, distressed, tiring
H&N burns
supraglottic oedema
high COHb
Anaesthetic assessment
prophylactic Abx and steroids not indicated
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6
Q

Inhalational injury

a) History
b) Examination
c) Types

A

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

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7
Q

Smoke inhalation pathophysiology

A

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

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8
Q

What cases should be referred to burns unit?

A 
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
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9
Q

Treatment of inhalation injury

A

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

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10
Q

How do you assess depth of burns?

A

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

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11
Q

What do you ask the referring A&E to do before referring to burns unit?

A

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
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12
Q

What investigations may be useful to assess burns?

A

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)
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13
Q

what is an adult and newborn’s skin surface area?

A

adult - 1.5 - 2 m2

newborn - 0.2 - 0.3 m2

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14
Q

What is a child and adult’s circulating blood volume?

A

adult = 60ml/kg

child 80ml/kg

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15
Q

How do you estimate TBSA?

A

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

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16
Q

What is the initial management of burns?

A

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
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17
Q

What is used to measure end points for resuscitation?

A

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
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18
Q

How do you assess volaemic status?

A

initially - UO
after 24hrs - less accurate due to glucose intolerance, SIADH and respy losses
- plasma Na & U
- CVP

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19
Q

What fluid resuscitation formulas can be used after Parkland formula?

What alternative fluid resuscitation formulas are there?

A

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

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20
Q

What other fluids can be used?

Why is Ringer’s Lactate (Hartmanns) better than isotonic saline?

A

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.

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21
Q

What is fluid creep?

A

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.

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22
Q

Explain the colloid vs cystalloid debate.

A

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

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23
Q

How do you classify the timing of burns reconstruction?

A

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

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24
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
25
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
26
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 ```
27
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
28
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 1. Problems 2. Priorities - pt shopping list 3. Possibilities - what is available? - non-surgicals: injections, physio, psych - surgical - excision and dc, ssg, ftsg, zplasty, local flaps, distant / free flaps 4. Patient perceptions - do they understand what surgery can achieve 5. Plan of action - esp w multiple problems, order of surgery - start with a 'winner'
29
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
30
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
31
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
32
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
33
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 ```
34
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)
35
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 4. Forearm FC transposition flap 5. Reversed lateral / medial arm flaps NB elbow can be affected by heterotopic ossification - excise first / staged
36
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)
37
What are the causes of burn injuries?
Heat Electrical Chemical / extravasation Cold
38
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
39
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)
40
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)
41
What are the delayed complications of electrical burn injuries?
- cardiac arrhythmias - neurological: epilepsy, encephalopathy, brainstem, cord, peripheral progressive demylination, - cataracts
42
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
43
Cold injury symptoms
cold, numb, pain on rewarming
44
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
45
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 ```
46
What are the longterm effects of frostbite?
- residual burning sensation (allodynia?) - cold intolerance, Raynaud;s - permanent sensory loss - hyperhidrosis - osteopenia, joint pain, stiffness
47
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 ```
48
Chemical burns - types, history
Civilian - acids and alkalis Military - white phosphorus (& air bags) Industrial - Acid: plating, fertilising - Alkali: oven cleaners, soap - Phenol: dyes, fertilisers, plastics, explosives - HF: glass etching, petroleum refinement, air conditioner cleaning Hx - conc, time of occurence, exposure, site, 1st aid Management 1st aid - cut clothing off (not over head), lavage, decontamination procedures (industrial) pH ABG emergency debridement (e.g. extravasation of cytotoxics, HF acid)
49
How do you treat burns syndactyly?
z-plasty, jumping man, 4 flap zplasty, V-M plasty
50
How do you classify scalp alopecia?
McCauley classification Type I - single alopecia segment (<15% amenable to serial excision) II - multiple areas amenable to tissue expansion III - not amenable IV - total alopecia
51
Chemical burns Type of necrosis - acid & alkali Specific antedotes
Acid - coagulative necrosis Alkali - liquefactive necrosis Concentrated sulphuric or hydrochloric acid - neutralise with soap first, as direct irrigation with water causes heat. Hydrofluoric acid - hyperkalaemia (F binds to Na/K ATPase -> efflux of K) - hypocalcaemia (F complexes w Ca) Rx - irrigation, 10% calcium gluconate gel, 0.5ml / cm2 of 10% CG sc injection, intrarterial injection, digital fasciotomy, debridement replace Ca & Mg urine alkalinisation, haemodialysis Phenol (carbolic acid) - dermatitis, depigmentation, skin necrosis - 50% polyethylene glycol (antifreeze) Bitumen - cool, dissolve w oils (paraffin, baby) White phosphorus - ignites with air Rx - water, ash, UV light, 0.5% copper sulphate Hydrocarbons (petrol) - lipid solvent action and cell membrane injury, ignite and thermal injury Na, K, Li - ignite with water. Cover with oil first. Diphoterine - amphoteric agent chelating molecule with binding sites for many different compounds including acids, bases, oxidising and reducing agents, vesicants, irritants and solvents.
52
What is heterotrophic ossification?
formation of lamellar bone in soft tissues where it does not norally form 1-3% of burns, usu >20% TBSA, 3/52 - 3/12 Most common b/t olecranon and medial supracondylar ridge calcification increases when wound is open assoc with aggressive passive mobilisation Rx - NSAIDs, bisphosphonates Bone scan - decreased activity = matured can excise, usu does not return
53
How do you treat burns pruritus?
``` 1st line Antihistamines Emollients Pressure garments Silicone (keeps scars moist) Massage Opioids Sedatives Dermacool cream ``` 2nd line - TENS, hypnosis, capsaicin cream ``` 3rd line Topical antihistamines Doxepin (TCA) Gabapentin Dothiepin cream Tacrolimus Topical steroids ```
54
Tell me about extravasation injury
pts at extremes of age & ivi at risk contrast media, hypertonic solns, TPN , cytotoxic drugs (irritants, vesicants) irritants - self-limiting phlebitis vesicants - chemical cellulitis, may progress signs - pain, erythema, skin necrosis, ulceration, damage to deep structures
55
What is the management of extravasation injury?
stop infusion, keep cannula in situ, aspirate contact pharmacist and oncologist for specific antedotes elevation and cooling (warming for vinca alkaloids) saline flushout (Gault method), liposuction topical DMSO (free radical scavenger) injection of GM-CSF, steroids, neutralise w bicarb (controversial)
56
Describe Gault's saline flushout method
BJPS 1993 - aspirate from cannula before removal - inject local + 1500 hyalase diluted in 10ml saline - 10 stab wounds around area - tunnel w blunt needle to connect holes subcut - flush through with saline 2L - milk out excess fluid, bandage, elevate - review
57
What are the intraoperative considerations for patient care?
- monitor pts core temp, keep ambient temp hi - monitor pt volaemic status (UO, CVP, art line) - monitor blood loss, intraop bloods, clotting - blood transfusion, FFP - kaltostat donor dressings - types of grafts: autograft, FTSG, sheet SSG, meshed SSG, sandwich graft, allograft, xenograft, dressings
58
How are paediatric burns different from adult burns?
1. Skin is thinner in children 2. TBSA is calculated using Lund & Browder chart / modified rule of nines (1 yr old = H&N 18%, lower limb 14% each. -1% from H&N each yr and add to LL) 3. Airway - narrower, floppy epiglottis, laryngomalacia 4. Breathing - more diaphragmatic resin 5. Circulation - 80ml/kg (adult 60ml/kg), lower systolic BP, can decompensate rapidly 6. Resus fluids different - 4ml / kg / % TBSA (Hartmann's) plus maintenance (0.45% saline, 100, 50, 20ml/kg), aim for UO 1-2ml/kg/hr beware of hypoglycaemia and natraemia 7. Exposure - less thermoregulation response 8. Longterm - inhibition of growth (?oxandralone Rx post burn) - breast development - joint contractures - psychological problems NAI signs - immersion line, old injuries, inconsistent history, delayed presentation, introverted child, lack of parental bonding
59
What metabolic changes occur in burns injury?
BMR in acute injury phase = up to 180% for >40% TBSA - inc protein, fat and glycogen catabolism - post- receptor insulin resistance - enhanced glucose delivery to cells, increased glucose uptake and gluconeogenesis - protein catabolism, weight loss, impaired wound healing and immunity Changes persist post-injury BMR - 1yr -ve nitrogen balance - 9mths growth delay in children - 2yrs
60
Burns sepsis
``` S. aureus - 75% - collagenases and proteinases, enterotoxins ABC, exotoxins Pseudomonas aeruginosa - toxin pigment pyocyanin, exotoxin A S. pyogenes Coliform bacilli Fungi - Candida and Aspergillus ``` MRSA - Rx: early wound closure (MRSA not contraindication for SSG) - topical mupirocin, SSD - systemic vanc +/- rifampicin, fusidic acid Decolonisation - nasal bactroban, chlohexidine mouthwash, bactrban wound ointment, triclosan skin cleanser
61
What does Herndon's paper in Lancet 2004 recommendations in supporting the metabolic response to burn injury?
``` Reduce hypercatabolic response by: - early wound closure - prevent infection - ambient temp 33degrees Nutrition - enteral route preferred Hormones (hGH, insulin, ILGF-1, Oxandrolone, B-blockade) Exercise ```
62
What other complications are encountered in burns patients?
Acalculous cholecystitis Curlings ulcer Ischaemic enterocolitis Suppurative thrombophlebitis Marjolins ulcer Hypo-pigmentation - due to barrier to melanocyte migration and melanosome transport from melanocyte to keratinocyte Rx - dermabrasion & thin SSG, particularisation (morcelisation of skin graft over dermabraded wound), melanocyte transplant, tattooing / camouflage Heterotopic ossification - formation of lamellar bone where is does not normally form - 1-3% of burns, >20%TBSA more common, medial supracondylar ridge & olecranon Rx - minimise aggressive physio, NSAIDs, bisphosphonates (controversial)
63
What are the principles of burns scar management?
Scar minimisation - early burn excision and wound closure - maintain full P & AROM - splint in POSI early and late Scar treatment - early ambulation and exercise (jts, muscle mass, bone density) - massage, compression, pressure garments - topical Rx: steroid inj, silicone, laser Rx, USS - early scar release to prevent permanent jt changes
64
What is a scar? | DESCRIBE HYPERTROPHIC VS KELOID SCAR
Scars - result when a wound heals by repair and not regeneration - appearance change with time - can be normal or abnormal
65
What are the different options for burns syndactyly?
- most common = 1st web - 'web reversal' occurs = dorsal web more distal and limitation of abduction Rx - jumping man flap, VM -plasty, 4-flap plasty.
66
How are burns to the hand managed?
- high priority, aim to debride within 72hrs, cover with sheet graft or unexpanded mesh - treat palmar burns conservatively or thick SSG, allow non-viable digits to separate - limb elevation, splints - avoid over-aggressive physio (HO) - late scar contracture - full scar excision, extensor tenolysis, thin flaps e.g. lat arm or radial forearm FF
67
How are facial and neck burns managed?
- recon in aesthetic units (FTSG / thick sheet SSG) | - quilting and expose grafting, bd inspection and roll out haematomas
68
How are trunk and genitalia burns managed?
- breast development may be affected - scar contracture release, skin grafts, implants nipple recon, contralateral mastopexy, - new Rx: Integra, FX laser Perineal burns: conservative mx
69
Psychological considerations for burns patients
- Often psychiatric condition preceded burns injury - psychosis, delusions, hallucinations, paranoia - PTSD - self-consciousness, poor self-esteem - phobias, anxiety
70
What is toxic shock syndrome
- originally described in 1978 - may be genetic (antitoxin usu developed by 30yrs of age) - TSST-1 toxin (produced by most S aureus including MRSA) causes overstimulation of immune system Symptoms - pyrexia, rash, D&V, hypotension Rx - antibiotics (clindamycin, penicillin G, vancomycin if penicillin allergic), anti TSST1 immunoglobulin / pooled gammaglobulin / FFP Mortality 50%
71
What is ABA criteria for burn sepsis?
Severe burn injury is accompanied by a systemic inflammatory response, making traditional indicators of sepsis both insensitive and nonspecific. To address this, the American Burn Association (ABA) published diagnostic criteria in 2007 to standardize the definition of sepsis in these patients. These criteria include 1. temperature 39°C+ or less than 36.5 2. tachycardia 110+, 3. progressive tachypnea (>25 breaths per minute not ventilated or minute ventilation >12 L/minute ventilated), 4. thrombocytopenia 200 mg/dl 5. >7 units of insulin/hr intravenous drip, or >25% increase in insulin requirements over 24 hours), and 6. feed intolerance >24 hours (abdominal distension, residuals two times the feeding rate, or diarrhea >2500 ml/day).
72
What is TENS?
Toxic epidermal necrolysis syndrome is a rare, potentially life-threatening medical emergency characterised by wide-spread epidermal sloughing of skin accompanied by mucus membrane involvement Incidence = 0.4-1.3 / million popn / yr Clinical features Prodrome (2 - 3 days) - fever, cough, sore throat, and general malaise Acute phase, (D8 - 12) - Acute macular exanthema, rapidly spreading necrosis of mucus membranes, then - Epidermolysis (dermis not involved) (Nikolsky sign: epidermal separation with gentle rub) - Mucus membranes involvement (conjunctival, pharyngeal, tracheal, oesophageal) Recovery (1-3wks) - Epithelialisation (longer for conjunctiva and mucosal membranes)
73
What drugs commonly cause SJS/TEN?
Antibiotics: Sulfonamides, e.g. cotrimoxizole; beta-lactams i.e. penicillins, cephalosporins Antifungals: Imidazole Antivirals: Nevirapine Allopurinol NSAID (oxicam type mainly) - Naproxen - Ibuprofen Anti-convulsants - Carbamazepine - Phenytoin - Phenobarbital - Valproic acid - Lamotrigine
74
What is the pathophysiology of TENS?
1. Direct “toxic” effect of ingested medication (and/or a metabolite) triggers cell death in epidermal keratinocytes. 2. Immune reaction triggered by drug and activated immunocytes mediate cytopathic effects much like epidermal killing in acute cutaneous graft vs host disease Proposed mechanism Drug specific CD8+ cytotoxic lymphocytes can be detected in the early blister fluid. They have some natural killer cell activity and can probably kill keratinocytes by direct contact. Cytokines implicated include perforin/granzyme, Fas-L and Tumour Necrosis Factor (TNF) alpha. There are probably two major pathways involved: 1. Fas-Fas ligand pathway of apoptosis. The Fas ligand (FasL), a form of tumour necrosis factor, is secreted by blood lymphocytes and can bind to the Fas ‘death’ receptor expressed by keratinocytes. 2. Granule-mediated exocytosis via perforin and granzyme B resulting in cytotoxicity (cell death). Perforin and granzyme B can be detected in early blister fluid and it has been suggested that levels may be associated with disease severity. Drugs that most commonly cause SJS/TEN Antibiotics: Sulfonamides, e.g., cotrimoxizole; beta-lactams i.e., penicillins, cephalosporins Antifungals: Imidazole Antivirals: Nevirapine (non-nucleoside reverse-transcriptase inhibitor) Allopurinol Nonsteroidal anti-inflammatory drugs (NSAID) (oxicam type mainly) Naproxen Ibuprofen ``` Anti-convulsants Carbamazepine Phenytoin Phenobarbital Valproic acid Lamotrigine ```
75
How is SJS and TEN classified?
SJS - Skin detachment less than 10% TBSA - Widespread erythematous or purpuric macules or flat atypical targets Overlap SJS/TEN - 10% - 30% BSA - Widespread purpuric macules or flat atypical targets TEN with spots - 30%+ BSA - Widespread purpuric macules or flat atypical targets TEN without spots - less than 10% of BSA - Large epidermal sheets and no purpuric macules
76
What is the difference b/t EM, SJS and TENS?
Erythema Multiforme (EM) - hypersensitivity reaction usually triggered by infections (90%), most commonly HSV. - presents with skin eruption characterised by a typical target (iris) lesion. - may be mucous membrane involvement. - acute and self-limiting, usually resolves without complications. - EM is divided into major and minor forms and now regarded as distinct (SJS) and (TEN). Stevens Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) are now believed to be variants of the same condition, distinct from erythema multiforme. SJS/TEN is a very rare, acute, serious, and potentially fatal skin reaction in which there is sheet-like skin and mucosal loss. It is nearly always caused by medications.
77
What blood tests may be helpful?
- elevated levels of serum granulysin - skin biopsy (to exclude Staph scalded skin syndrome and other blistering conditions) Blood tests (not specific but often deranged) - anaemia - leucopenia (esp lymphopenia. neutropenia is a bad prognostic sign) - NO eosinophilia - mild elevation of LFTs - mild proteinuria
78
What blood tests may be helpful in SJS/TEN?
- elevated levels of serum granulysin - skin biopsy (to exclude Staph scalded skin syndrome and other blistering conditions) Blood tests (not specific but often deranged) - anaemia - leucopenia (esp lymphopenia. neutropenia is a bad prognostic sign) - NO eosinophilia - mild elevation of LFTs - mild proteinuria
79
What is the treatment for TENS?
1. Debridement and coverage - Biologic dressings: Allografts, xenografts or collagen-based skin substitutes; or - Acticoat: nanocrystalline silver dressing - reduces infection or 2. No debridement (leave intact blisters) OCULAR - topical lubricants, steroid drops, and regular release of symblepharon Cessation of suspected causative drug(s) Hospital admission Nutritional and fluid replacement (crystalloid) iv / ng Temperature maintenance Pain relief Sterile handling and reverse isolation procedures Skin care: topical antiseptics e.g. silver nitrate or chlorhexidine, (but not silver sulfadiazine as it is a sulfa drug) dressings: jelonet / non-adherent nanocrystalline-containing gauze biosynthetic skin substitutes Eye care: assessment by ophthalmologist, frequent eye drops/ointments (antiseptic, antibiotic, cortisone) Mouth care: mouthwashes, topical oral anaesthetic Lung care: aerosols, bronchial aspiration, physiotherapy Urinary catheter Psychiatric support Physiotherapy Staphylococcal infection common (also gram -ve) - appropriate antibiotic should be given if infection develops prophylactic antibiotics not recommended Case reports/ small patient series of active adjuvant treatments - first 24-48 hours - Ciclosporin 3-5 mg/kg/day, cyclophosphamide, intravenous immunoglobulin (IVIG) 2-3 g/kg, and plasmapheresis. - Systemic corticosteroids (cortisone) - controversial. Short course of high dose corticosteroids at the start of the reaction but may increase the risk of infection, impair wound healing and other complications - infliximab and etanercept (biologic agents) inhibit TNFα (case reports) - S/c heparin Specialised nursing care
80
What are the complications of SJS/TENS?
This condition can be fatal due to complications in the acute phase. The mortality rate is up to 10% for SJS and at least 30% for TEN. During the acute phase, potentially fatal complications include: - Dehydration and acute malnutrition - Infection of skin, mucous membranes, pneumonia, septicaemia - Shock and multiple organ failure - Thromboembolism and DIC Longterm complications include: - Pigment change – hypo and hyper - Skin scarring - Loss of nails, scarring (pterygium), failure to regrow - Joint contractures - Scarred genitalia – phimosis and vaginal synechiae - Dry and/or watery eyes - Conjunctivitis: red, crusted, or ulcerated conjunctiva - Corneal ulcers, opacities and scarring - Symblepharon: adhesion of conjunctiva of eyelid to eyeball - Ectropion or entropion - Trichiasis: inverted eyelashes - Synechiae: iris sticks to cornea
81
What are the complications if the eyes are involved?
Conjunctivitis, corneal ulcers, lid margin keratinization, infections
82
What is the prognosis and mortality of TENS?
Mortality TENS 30-50% SJS 1-3% SCORTEN (severity-of-illness score for TEN) 1. Extent of epidermal detachment >10% 2. Age >40 yr 3. Heart rate >120/min 4. Bicarbonate 20 mg/dl 5. Serum BUN >27 6. Glucose >250 mg/dl 7. History of malignancy ``` Scorten Value Predicted Mortality Rate (%) 0–1 3.2 2 12.1 3 32.4 4 62.2 5 85.5 >6 95 ```
83
What is the prognosis and mortality of TENS?
Mortality - TENS 30-50% - SJS 1-3% SCORTEN (severity-of-illness score for TEN) 'DAHBUGH' 1. Extent of epidermal detachment >10% 2. Age >40 yr 3. Heart rate >120/min 4. Bicarbonate 20 mg/dl 5. Urea >27 6. Glucose >250 mg/dl 7. History of malignancy ``` Scorten Value Predicted Mortality Rate (%) 0–1 3.2 2 12.1 3 32.4 4 62.2 5 85.5 >6 95 ```
84
What is the prognosis and mortality of TENS?
Mortality - TENS 30-50% - SJS 1-3% SCORTEN (severity-of-illness score for TEN) 'DAHBUGH' 1. Epidermal detachment >10% 2. Age >40 3. Heart rate >120 4. Bicarbonate >20 mmol/L 5. Urea >10 mmol/L 6. Glucose >14 mmol/L 7. History of malignancy ``` Scorten Value Predicted Mortality Rate (%) 0–1 3.2 2 12.1 3 32.4 4 62.2 5 85.5 >6 95 ```
85
What is the Starling's equation?
- calculates microvascular fluid balance - quantitative measure of fluid transport across capillary wall in physiologic and pathologic states Jv = Kf [ (Pc - Pif) - σ (COPp - COPif) ] ``` Jv = volume of fluid crossing capillary wall Jl = lymphatic drainage ``` ``` Kf = capillary filtration coefficient ↑ (permeability of cap wall due to mediators) Pc = capillary hydrostatic pressure ↑ (vascular dilatation) Pif = interstitial fluid hydrostatic pressure ↓↓ (↓cell-cell adhesion & collagen binding) σ = osmotic reflection coefficient ↓ (osmotic pressure generated by conc gradient of plasma proteins across cap wall) COPp = plasma colloid osmotic pressure ↓ (protein-rich fluid extravasates into burn wound) COPif = interstitial fluid colloid osmotic pressure ↑ ``` Oedema occurs if increased Jl does not keep pace with increased Jv Normal net filtration pressure = 0.5-1mmHg
86
What is burn oedema?
thermal injury ⇉ fluid shift from plasma to interstitial space ⇉ hypovolaemia and oedema of burned skin In >20-30% TBSA, oedema also occurs to non-burned tissue due to circulating inflammatory mediators and stress hormones. ``` Mediators affect: 1. Renal - water and Na retention 2. Cardiac - impaired contractility 3. Peripheral vasoconstriction ⇉ tissue ischaemia ⇉ ↑SVR, ↑CO, end-organ ischaemia, metabolic acidosis ``` Early resus: increase perfusion (but over-resus increases oedema) Early debridement: decrease mediator release
87
What do you know about enzymatic debridement of burn wounds?
Bromelain-based enzymatic debriding agent (Nexobride, Debridase) - 4hr application - selectively removes non-viable tissue preserving zone of stasis and leaves potentially viable dermal remnants behind - wound bed is brushed and SSG then applied, 95% take reported with decreased blood loss
88
What is burn oedema?
Thermal injury ⇉ fluid shift from plasma to interstitial space ⇉ hypovolaemia and oedema of burned skin In >20-30% TBSA, oedema also occurs to non-burned tissue due to circulating inflammatory mediators and stress hormones. ``` Mediators affect: 1. Renal - water and Na retention 2. Cardiac - impaired contractility 3. Peripheral vasoconstriction ⇉ tissue ischaemia ⇉ ↑SVR, ↑CO, end-organ ischaemia, metabolic acidosis ``` Early resus: increase perfusion (but over-resus increases oedema) Early debridement: decrease mediator release
89
What are the different methods of burn wound excision?
Direct excision and closure (small) Tangential excision (Janzekovic) - Watson / Goulian knife / Versajet water dissector Fascial excision - less blood loss, greater morbidity and cosmetically poor Controlling blood loss - tourniquet, temp bandaging after debridement, tumescent infiltration
90
Name some colloid and crystalloid formulas, colloid only and crystalloid only
Colloid only - Muir and Barclay (0.5ml/kg/time period, 4,4,4,6,6,12hrs) Crystalloid only - Parkland (4), modified Brooke (2) Both - Evans (NS:colloid 1:1), Brooke (LR:colloid 1.5:0.5), Slater (FFP) Hypertonic saline formulas
91
What are the different methods of burn wound excision?
- Direct excision and closure (small) - Tangential excision (Janzekovic) - Watson / Goulian knife / Versajet water dissector - Fascial excision - less blood loss, greater morbidity and cosmetically poor Controlling blood loss - tourniquet, temp bandaging after debridement, tumescent infiltration
92
What are the techniques of wound closure?
- FTSG - SSG - meshed, sheet - Alexander technique (widely meshed autograft + narrowly meshed allograft) - cultured epidermal autograft - sheet 2-8 keratinocyte cells thick / suspension - Meek technique - autograft cut to small square, applied to refolded pleated gauze and expanded in 4 directions by 1:3 - 1:9. Gauze is directly applied to wound then allograft sandwich - Dermal replacement - Integra, Matriderm
93
What are the criteria for adequate fluid resuscitation?
``` Normalisation of BP UO 1-2ml/kg/hr Lactate 7.32 CVP Cardiac index 4.5L/min/m2 Oxygen delivery index 600ml/min/m2 ```
94
When is allograft used?
cover extensive wounds where autograft not available cover widely meshed autograft extensive PT burns / epidermal slough (SJS, TENS, SSSS) template for delayed keratinocyte application testing wound bed for later autografting
95
When is allograft used?
- cover extensive wounds where autograft not available - cover widely meshed autograft - extensive PT burns / epidermal slough (SJS, TENS, SSSS) - template for delayed keratinocyte application - testing wound bed for later autografting
96
What is difference between cryopreserved and glycerol preserved allograft?
Harvested within 24hrs of death from cadaver cryopreserved -196deg 95% cell viability can incorporate into recipient site 15% glycerol (ETOH) in phosphate buffer soln with antibiotic preservation - little cell viability Acts as biological dressing
97
What is difference between cryopreserved and glycerol preserved allograft?
- Harvested within 24hrs of death from cadaver - cryopreserved -196deg - 95% cell viability - can incorporate into recipient site - 15% glycerol (ETOH) in phosphate buffer soln with antibiotic preservation - little cell viability - Acts as biological dressing
98
What is cadaveric allograft tested for?
HIV Hep B, HepC Syphilis MC&S - S.aureus, GpA haemolytic strep, enerococcus, Gram -ve bacilli, Clostridium sp, fungi
99
Name some temporary and permanent wound covers
Temporary - Human allograft - Biobrane (outer silicone, inner nylon mesh impregnated with collagen) - (Human amnion) Permanent - Cultured epithelial keratinocytes - Strattice (ADM) - Matriderm (synthetic dermal template 1 stage) - Integra (SDM 2 stage)
100
What is the clinical significance of inhalation injury?
``` inc mortality airway closure secondary to oedema haemodynamic instability, ↑ resus fluid req impaired pulmonary gas exchange pneumonia / ARDS SIRS and MOF laryngeal damage chronic pulmonary dysfunction ```
101
What is the clinical significance of inhalation injury?
- inc mortality - airway closure secondary to oedema - haemodynamic instability, ↑ resus fluid req - impaired pulmonary gas exchange - pneumonia / ARDS - SIRS and MOF - laryngeal damage - chronic pulmonary dysfunction
102
What is the treatment protocol of inhalation injury?
- titrate humidified O2 (SaO2>90%) - cough deep breathing exercises every 2hrs - side - side turning 2hrs - chest physio 4hrs - NAC neb 4hrs - bronchodilators - alt heparin and saline nebs 4hrs - nasotracheal suctioning - sputum cultures alt days - early ambulation - pulmonary function tests - patient education - BAL
103
What is the indication for early tracheal intubation?
``` Overt S+S of airway obstruction Extensive burns to H+N Inability to protect airway against aspiration Significant toxicity from CO or cyanide Respiratory failure PaO2 6.5 Extensive burns (>40% TBSA) Haemodynamic instability +2 wks intubation anticipated (Shriners) ```
104
What is the indication for early tracheal intubation?
- Overt S+S of airway obstruction - Extensive burns to H+N - Inability to protect airway against aspiration - Significant toxicity from CO or cyanide - Respiratory failure PaO2 6.5 - Extensive burns (>40% TBSA) - Haemodynamic instability - 2+ wks intubation anticipated (Shriners)
105
What is the treatment?
Mainly supportive - adequate fluid resus - vasoactive drugs - support failing organ systems - excision of necrotic tissue - antibiotics
106
Why does SIRS occur?
In severe burn injury, events that contribute to SIRS include: - ischaemia-reperfusion injury - necrotic tissue - sepsis - poor tissue perfusion due to burn oedema, microthrombosis etc - free radicals and cytokines directly damage tissue and organs
107
What causes the hypermetabolic response in burns?
Hypermetabolism - increased energy expenditure (60-100% of normal) and concomitant protein catabolism. 'Ebb and flow' response to injury - initial (48hrs) reduction in metabolic rate followed by crescendo-decrescendo curve of sustained hypermetabolism that may persist for weeks 1. Sympathetic activation, catecholamine release - increased BMR, glycogenolysis, gluconeogenesis, lipolysis, CO, HR, PVR - increased monocytes, decreased neutrophils 2. Adrenal cortical steroids release - increased energy expenditure, O2 consumption, proteolysis, acute phase protein synthesis, glycogenoylsis, gluconeogenesis - decreased bone formation, T cells, suppressed monocytes and neutrophil activity Catabolic hormones = epinephrine, cortisol and glucagon
108
What mineral and vitamin supplementation are required?
Calcium Magnesium Phosphate Vit A,C,E Zinc & copper (RNA DNA metabolism, signal transduction, gene expression, regulate apoptosis) Selenium (lymphocyte function), chromium (?contribute to insulin resistance), aluminium accumulation
109
How is hypermetabolic response modulated after burn injury?
Response to severe burn injury characterised by 1. Hyperdynamic circulation 2. Altered body temp regulation 3. Glycolysis, proteolysis, lipolysis 4. Inefficient substate cycling Non-pharmacologic 1. Early wound closure 2. Nutritional support 3. Environment support 4. Exercise & adjuncts Pharmacologic 1. Human growth hormone 2. Insulin-like GF 3. Anabolic agents Oxandrolone 4. Propanolol Insulin-resistance Rx - insulin and metformin
110
Who are the assigned burn unit personnel?
``` Burn surgeons Anaesthetists Burn nurses PT, OT, respiratory therapists Dieticians Pharmacists Microbiologists Psychiatrists, psychologists Prosthetist Social worker ``` Renal physicians (haemodialysis)
111
What are the principles of burn scar management?
``` prevent scar contracture - splints, therabites scar massage silicone inserts pressure garments therapeutic exercises ```
112
What is calciphylaxis?
Rare condition characterised by extraskeletal calcifications resulting in tissue necrosis 1. Painful purpuric cutaneous lesions 2. Histology - arterial tunica media calcification ⇉ vascular thrombosis and tissue necrosis ``` Uraemic - 1-4% ESRF pts Non-uraemic causes - primary hyperPTH - breast cancer + chemo - liver cirrhosis - cholangiocarcinoma - Crohn's - RA - SLE ```
113
What is ALI and ARDS?
ALI = PaO2 / FiO2 >30 + 200
114
What is reperfusion injury?
Results as flow is re-established to a zone of stasis, providing oxygen to drive renewed free radical production through - phospholipase A2 - acts on free phospholipids released on cell injury, and converts them via arachadonic acid pathways to chemotactic agents to neutrophils. More free radicals are formed etc - xanthine oxidase - converts hypoxanthine to xanthine and free radicals as byproducts
115
What do you know about heterotopic calcification?
1-3% of burn population, elbow>shoulder>knee lamellar bone deposition in ectopic sites factors associated with HO >20% TBSA delayed healing prolonged immobility prolonged hypermetabolic state Treatment NSAIDs - indomethacin Controlled & assisted AROM and terminal resistance Bisphosphonates - no proven benefit Excision in plateau phase, may recur, joint orthopaedic, may require capsulotomy / tendon excision
116
How do burns in children differ from adults?
Epidemiology - Scalds (2/3) more than burns - Different premorbid conditions Physiological - Skin is thinner - Surface area different (head proportionally larger and limbs smaller) - Airway narrower, T+A larger, short neck, floppy epiglottis, more like to bronchospasm - Breathing: diaphragmatic resp, may require escharotomy in non-circumferential thoracoabdominal burns - Circulation: resus fluids + maintenance, UO 1ml/kg/hr+ (less concentrating ability of kidneys) - More prone to hypoglycaemia (less glycogen stores), hyponatraemia (leads to cerebral oedema) hypophosphataemia Pain relief - Paracetamol, ibuprofen, oromorph, Intranasal diamorph, entonox Thermoregulation less developed, prone to hypothermia Long term - Inhibition of growth - Breast development - Joint contractures - Psychosocial Vulnerable to NAI
117
What are the criteria for discussion and referral to a specialised burns care service?
Discuss with specialised burn care services if  A child with a partial thickness burn greater than 2% TBSA  An adult with a partial thickness burn greater than 3% TBSA  Inhalation injury is defined as visual evidence of suspected upper airway smoke inhalation, laryngoscopic and/or bronchoscopic evidence of tracheal or more distal contamination / injury or suspicion of inhalation of non soluble toxic gases.  A full thickness burn greater than 1% TBSA  Burns to special areas (hands, face, neck, feet, perineum)  Burns to an area involving a joint which may adversely affect mobility and function  Electrical burns  Chemical burns  Suspected non-accidental injury (NAI). (expert assessment within 24 hours)  A burn associated with major trauma  A burn associated with significant co-morbidities  Circumferential burns to the trunk or limbs  Any burn not healed in 2 weeks
118
What burns referral guidance is there?
National Network for Burn Care (NNBC) National Burn Care Referral Guidance Version 1, Approved February 2012 The guidance uses 5 criteria to guide referral decisions: • TBSA • Depth • Site (anatomical) • Mechanism / etiology • Other Factors (Parameters that may impact on the severity/complexity of burn injury) Thresholds are divided into 'refer' or 'discuss'
119
What are the suggested minimum threshold for referral into specialised burn care services?
- All burns ≥2% TBSA in children or ≥3% in adults - All full thickness burns - All circumferential burns - Any burn not healed in 2 weeks - Any burn with suspicion of NAI should be referred to a Burn Unit/Centre for expert assessment within 24 hours Discuss with Consultant in a specialised burn care service and consideration given to referral: - All burns to hands, feet, face, perineum or genitalia - Any chemical, electrical or friction burn - Any cold injury - Any unwell/febrile child with a burn - Any concerns regarding burn injuries and co-morbidities that may affect treatment or healing of the burn * If the above criteria/threshold is not met then continue with local care and dressings as required * If burn wound changes in appearance / signs of infection or there are concerns regarding healing then discuss with a specialised burn service * If there is any suspicion of Toxic shock syndrome (TSS) then refer early
120
What are the 3 levels of Specialised Burn Services?
Following the recommendations of the National Burn Care Review 2001, Specialised Burn Services were stratified into three levels of service: Burn Centres – This level of in-patient burn care is for the highest level of injury complexity and offers a separately staffed, geographically discrete ward. The service is skilled to the highest level of critical care and has immediate operating theatre access. Burn Units – This level of in-patient care is for the moderate level of injury complexity and offers a separately staffed, discrete ward. Burn Facilities – This level of in-patient care equates to a standard plastic surgical ward for the care of non- complex burn injuries
FRCS Plastic Surgery
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