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FRCS Plastic Surgery > KEY NOTES CHAPTER 8: BURNS - Epidemiology, Diagnosis, Inhalation Injury, Resuscitation, Nutrition, Sepsis. > Flashcards

KEY NOTES CHAPTER 8: BURNS - Epidemiology, Diagnosis, Inhalation Injury, Resuscitation, Nutrition, Sepsis. Flashcards

0
Q

How do you classify burns?

A

Aetiology

  • Thermal
  • Chemical
  • Electrical
  • Cold Injury
  • Radiation

Depth

  • Superficial
  • SPT
  • DD
  • FT

Resus (>15% adult, 10% child)

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1
Q

What is the incidence of burn injuries in UK?

A 
250,000 injuries
300 deaths
50% TBSA - 10% mortality (50% 25yrs ago)
80-90% TBSA - <50% mortality (90% 10yrs ago)
Improvements attributable to:
- resuscitation.
- surgical techniques.
- sepsis management.
- nutritional and metabolic support.
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2
Q

Thermal burns aetiology

A

scalds - hot liquids or gases
contact
flame
flash

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3
Q

Factors affecting survival in burns

A 
TBSA
Depth
Age
Inhalation injury
Co-existing polytrauma
Co-morbidities
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4
Q

What are the systemic effects of burn injury?

A
  • with >25-30% TBSA, local inflammatory mediators (TNF, IL’s, interferon) overspill into systemic circulation.
  • early excision and closure limits systemic inflammation.
Organ systems affected include
- hypovolaemia
myocardial depression
- pulmonary oedema
- renal impairment
- hepatic dysfunction
- catabolism 
- immunosuppression
- loss of protective gut function
- psychological effects
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5
Q

What are the different methods of estimating TBSA?

A

hand ~ 0.8% TBSA
Wallace’s rule of 9’s
Lund and Browder charts

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6
Q

Escharotomy

A

DD and FT burns are inelastic and can worsen constriction with fluid resuscitation
Escharotomy begin and end in unburnt/SPT skin
Limbs: mid-axial line
Chest: mid-axillary lines, chevron incision parallel to costal margin

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7
Q

Inhalation injury history

A 
confined space
unconscious in fire
hoarse weak voice
brassy cough
restlessness 
SOB
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8
Q

Inhalation injury signs

A 
soot in mouth and nose
singed facial and nasal hairs
deep burns for face, neck, upper body
carbonaceous sputum
swollen upper airway
stridor, dyspnoea, hypoxia, pulmonary oedema
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9
Q

Inhalation injury investigations

A

CXR
ABG
COHb
Fibre-optic bronchoscopy - soot below vocal cords, hyperaemia, mucosal oedema and ulceration.

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10
Q

How do you classify inhalation injuries?

A

Supraglottic - caused by heat.

Subglottic - caused by products of combustion.

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11
Q

What occurs in subglottic inhalation injuries?

A

Bronchospasm, inflammation, increased secretions

  • leading to atelectasis, ARDS, pneumonia
  • VP mismatch
  • decreased lung compliance
  • increased airways resistance
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12
Q

How is respiratory failure treated?

A 
humidified O2
nebulisers
- heparin (prevent cast formation)
- salbutamol
- NAC (mucolytic)
chest physio
non-invasive ventilation with PEEP
intubation, ventilation and bronchial lavage with dilute sodium bicarb
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13
Q

What is the treatment for CO poisoning?

A

100% O2, non-rebreathing mask (1/2 life 40mins, 250mins if breathing room air).
>25-30% - should intubate.
persistent metabolic acidosis - consider cyanide poisoning.

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14
Q

What are the benefits of tracheostomy?

A 
Easier for toileting and lavage
Improved weaning by reducing
- dead space
- airway resistance
- work of breathing
- sedation requirements
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15
Q

What are the complications of tracheostomy?

A 
Bleeding
Accidental decannulation
Swallowing dysfunction
Tracheal ulceration and granulation tissue
T-O fistula
Tracheal stenosis
Tracheomalacia
16
Q

What are the complications of inhalation injury?

A 
Complications of mechanical ventilation: barotrauma and pneumothorax.
Can be avoided by
- pressure controlled ventilation
- high ventilation rate
- small tidal volumes
- inverse ratio ventilation
- physiological PEEP
- lower target O2 sats of 92%
- permissive hypercapnia and respiratory acidosis

Longterm

  • ARDS
  • MODS (multi-organ dysfunction syndrome)
  • fibrosis ->emphysema, bronchiectasis
17
Q

What are the goals of fluid resuscitation?

A
  1. Restore circulating volume.
  2. Preserve tissue perfusion.
  3. Avoid ischaemic extension of burn wound.
18
Q

Parkland formula

A

4ml/kg/TBSA in 1st 24hrs (50% in 1st 8hrs).

Hartmanns solution contains Na, Cl, lactate, K, Ca.

19
Q

What does overuse of crystalloid cause and what crystalloid sparing strategies are there?

A

Burns oedema drives burns shock, increased total body sodium and risk of abdominal compartment syndrome.
Muir and Barclay formula - resus with HAS
0.5ml/kg/% burn per time period.
3x 4hrs, 2x 6hrs, 1x 12hrs.

20
Q

When may more resuscitation fluid be required?

A
  • Paediatric burns
  • Delayed resus
  • Large burns
  • Deep burns
  • Inhalation injury
  • Co-existing polytrauma
  • Electrical burns, myoglobinuria
  • Petrol burns
21
Q

What end-points may be measured to determine adequacy of fluid resuscitation?

A
  • Urine output (0.5-1ml/kg/hr adults, 1-1.5 children)
  • PR, BP, CRT, RR.
  • Core-peripheral temperature gradient.
  • Urine osmolality.
  • ABG - lactate and base excess.
  • Tranoesophageal doppler to identify patients for inotropes/vasopressors (noradrenaline and dobutamine - but may worsen hypoperfusion and cause extension of burns).
22
Q

What factors need to be considered for paediatric fluid resuscitation?

A

They have different TBSA proportions and reduced physiological reserves.
Maintenance fluids is required (per 24hrs):
- 100ml/kg for 1st 10kg,
- 50ml/kg for 2nd 10kg,
- 20ml /kg for remainder of body weight.

23
Q

What are the complications of under-resuscitation?

A 
Hypovolaemia.
Shock.
Renal failure.
Ischaemia-reperfusion injury.
MODS.
Deepening of burn wounds.
24
Q

What are the complications of over-resuscitation?

A

Generalised oedema.
Pulmonary, cerebral, intestinal oedema.
Compartment syndrome.
Deepening of burn wounds.

25
Q

What is the hyper metabolic response?

A

Cuthbertson: described ‘ebb and flow’ phases of response to major injury.
Ebb: hypo dynamic period for ~48hrs
Flow: for up to 1 year
- hyperdynamic circulation (CO x2)
- hyperthermia (1-2 deg above normal)
- hypermetabolism (increased O2 consumption and CO2 production.

Circulating catecholamines leads to increased glycogenolysis -> hyperglycaemia
Burn wound metabolises glucose anaerobically -> lactate which is metabolised by liver (gluconeogenesis) using amino acids by breaking down muscle protein.

26
Q

What are the complications of lean body mass loss?

A

Impaired immunity, healing, increased infection, weakness, pressure sores, pneumonia.

27
Q

How can hypermetabolic response optimised?

A
  1. Nutrition.
  2. Environment control.
  3. Medication and hormone manipulation.
  4. Prevention of sepsis.
  5. Early wound closure.
28
Q

What are the aims of nutritional support?

A
  • Maintenance of body weight and lean body mass.

- Electrolyte and vitamin homeostasis.

29
Q

What methods of calculating calorie requirements do you know?

A 
Curreri formula (adults):
- 25kcal/kg + 40kcal/% TBSA / day
Galveston formula (children):
- 1500 kcal/m2 BSA (maintenance) + 1500kcal/m2 TBSA
BSA (m2) is calculated using Du Bois formula.
30
Q

What nutritional support is required in burns?

A
  • Enteral feeds for burns patients are high carbohydrate to stimulate endogenous insulin and hence protein synthesis.
  • Exogenous insulin may be required for tight glycaemic control.
  • > 20% TBSA: Vitamins A, C, E, folic acid, copper, zinc, selenium and iron required.
  • Glutamine and arginine (essential amino acids) promote healing.
  • Potassium, calcium magnesium and phosphate may be depleted and require monitoring.
31
Q

What routes of feeding do you know of?

A

Oral, supplementary drinks.
Enteral - NG, NJ (gastric stasis, no need to starve pre-op). (Maintain gut motility, decreased bacterial translocation)
Parenteral - disadvantages: decreased liver function (fatty infiltration), reduced immune function, line sepsis, increased mortality.

32
Q

What medication and hormones are occasionally used in burns patients?

A

Analgesics + anxiolytics

  • opioids
  • benzodiazepines
  • ketamine (larger dressing changes)

Catecholamine antagonists
- Propranolol: decreases HR, CO, lipolysis, resting energy expenditure, thermogenesis, muscle wasting. Titrate to reduce HR by 20%.

Anabolic steroids
- Oxandrolone: decreases protein catabolism and increases synthesis.

Hormones

  • Insulin
  • rhGH (children): controversial. Potential benefits: increased weight, height, lean body mass, bone mineralisation, decreased donor site healing time, REE and CO.
33
Q

Burns sepsis - why is it important?

A

75% deaths attributable to sepsis.

34
Q

What are the sources of wound sepsis?

A
  • Adjacent skin, hair follicles, sweat glands.
  • Gut bacterial translocation.
  • Iatrogenic.
35
Q

What can help minimise sepsis?

A 
Strict barrier nursing, hand washing.
Regular wound toilet (showers/baths) to reduce bacterial count.
Prevention of line sepsis - change intravascular lines and catheters regularly
Antibiotics at induction of operation
Topical antimicrobial agents:
- Flammazine
- Flammacerium (ceruim nitrate - SSD)
- Acticoat (nanocrystalline silver - Ag released into wounds)
- Betadine
- Mupirocin (MRSA)
- Nystatin
- Honey
36
Q

What resistant organisms have you come across on the burns unit?

A 
Pseudomonas - multi-resistant
Acinetobacter
Stenotrophomonas maltophilia
ESBL - extended spectrum beta-lactamase producing Klebsiella
VRE - vanc res enterococcus
MRSA
37
Q

What would you use if a smoke inhalation injury patient is persistently hypoxic and acidotic? Lactate is persistently high?

A

Consider hydroxycobalamin for possible cyanide poisoning.

38
Q

What has been recommended at last BBA about inhalation injury and BAL?

A

Washout with sodium bicarbonate

FRCS Plastic Surgery (63 decks)

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