KEY NOTES CHAPTER 8: BURNS - Epidemiology, Diagnosis, Inhalation Injury, Resuscitation, Nutrition, Sepsis. Flashcards
How do you classify burns?
Aetiology
- Thermal
- Chemical
- Electrical
- Cold Injury
- Radiation
Depth
- Superficial
- SPT
- DD
- FT
Resus (>15% adult, 10% child)
What is the incidence of burn injuries in UK?
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.
Thermal burns aetiology
scalds - hot liquids or gases
contact
flame
flash
Factors affecting survival in burns
TBSA Depth Age Inhalation injury Co-existing polytrauma Co-morbidities
What are the systemic effects of burn injury?
- 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
What are the different methods of estimating TBSA?
hand ~ 0.8% TBSA
Wallace’s rule of 9’s
Lund and Browder charts
Escharotomy
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
Inhalation injury history
confined space unconscious in fire hoarse weak voice brassy cough restlessness SOB
Inhalation injury signs
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
Inhalation injury investigations
CXR
ABG
COHb
Fibre-optic bronchoscopy - soot below vocal cords, hyperaemia, mucosal oedema and ulceration.
How do you classify inhalation injuries?
Supraglottic - caused by heat.
Subglottic - caused by products of combustion.
What occurs in subglottic inhalation injuries?
Bronchospasm, inflammation, increased secretions
- leading to atelectasis, ARDS, pneumonia
- VP mismatch
- decreased lung compliance
- increased airways resistance
How is respiratory failure treated?
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
What is the treatment for CO poisoning?
100% O2, non-rebreathing mask (1/2 life 40mins, 250mins if breathing room air).
>25-30% - should intubate.
persistent metabolic acidosis - consider cyanide poisoning.
What are the benefits of tracheostomy?
Easier for toileting and lavage Improved weaning by reducing - dead space - airway resistance - work of breathing - sedation requirements
What are the complications of tracheostomy?
Bleeding Accidental decannulation Swallowing dysfunction Tracheal ulceration and granulation tissue T-O fistula Tracheal stenosis Tracheomalacia
What are the complications of inhalation injury?
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
What are the goals of fluid resuscitation?
- Restore circulating volume.
- Preserve tissue perfusion.
- Avoid ischaemic extension of burn wound.
Parkland formula
4ml/kg/TBSA in 1st 24hrs (50% in 1st 8hrs).
Hartmanns solution contains Na, Cl, lactate, K, Ca.
What does overuse of crystalloid cause and what crystalloid sparing strategies are there?
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.
When may more resuscitation fluid be required?
- Paediatric burns
- Delayed resus
- Large burns
- Deep burns
- Inhalation injury
- Co-existing polytrauma
- Electrical burns, myoglobinuria
- Petrol burns
What end-points may be measured to determine adequacy of fluid resuscitation?
- 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).
What factors need to be considered for paediatric fluid resuscitation?
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.
What are the complications of under-resuscitation?
Hypovolaemia. Shock. Renal failure. Ischaemia-reperfusion injury. MODS. Deepening of burn wounds.
What are the complications of over-resuscitation?
Generalised oedema.
Pulmonary, cerebral, intestinal oedema.
Compartment syndrome.
Deepening of burn wounds.
What is the hyper metabolic response?
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.
What are the complications of lean body mass loss?
Impaired immunity, healing, increased infection, weakness, pressure sores, pneumonia.
How can hypermetabolic response optimised?
- Nutrition.
- Environment control.
- Medication and hormone manipulation.
- Prevention of sepsis.
- Early wound closure.
What are the aims of nutritional support?
- Maintenance of body weight and lean body mass.
- Electrolyte and vitamin homeostasis.
What methods of calculating calorie requirements do you know?
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.
What nutritional support is required in burns?
- 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.
What routes of feeding do you know of?
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.
What medication and hormones are occasionally used in burns patients?
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.
Burns sepsis - why is it important?
75% deaths attributable to sepsis.
What are the sources of wound sepsis?
- Adjacent skin, hair follicles, sweat glands.
- Gut bacterial translocation.
- Iatrogenic.
What can help minimise sepsis?
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
What resistant organisms have you come across on the burns unit?
Pseudomonas - multi-resistant Acinetobacter Stenotrophomonas maltophilia ESBL - extended spectrum beta-lactamase producing Klebsiella VRE - vanc res enterococcus MRSA
What would you use if a smoke inhalation injury patient is persistently hypoxic and acidotic? Lactate is persistently high?
Consider hydroxycobalamin for possible cyanide poisoning.
What has been recommended at last BBA about inhalation injury and BAL?
Washout with sodium bicarbonate
