First aid burns

1. BURNS
A burn is [a wound in which there is ] coagulative necrosis of
tissue.
-A tissue injury from thermal [heat or cold] application, or from
absorption of physical energy or chemical contact.
-CAUSES include:
1.Dry heat – causing majority of burn injuries. Flame from
Petrol/fuel ignition, Kerosene explosions, house fires etc.
Burn injury – patches of full and partial thickness .
2. Moist heat –-> scald. Hot water, steam. Mostly at home: the
very young, the very old and the very
drunk[alcohol/drugs,epilepsy].
3. Hot fluids/oils, molten metals , hot gases.
4. Electricity – flash burns, deep full thickness burns.
5. Chemical caustics  tissue necrosis.
6. Irradiation – early tissue necrosis; later tissue dysplastic changes

2. 7. Actinic rays – sunburn
8. Friction- heat plus abrasion
9. Cold [e.g. frostbite] – also causes coagulative necrosis.
CLASSIFICATION OF BURN WOUNDS
- According to depth. Two main categories
1. Partial thickness burns
2. Full thickness burns
1. Partial thickness burns – part of skin is affected.
(a) Superficial partial thickness – the depth of skin loss varies.
- First degree: Epidermal burn; red, painful, no blisters.
No tissue loss. Heals rapidly without sequelae.
- Second degree: Superficial dermal burn; total loss of
epidermis and the superficial layers of the dermis. There
is blister formation .May be painful. Heals by
epithelialisation within 14 days.

3. (b) Deep partial thickness/Deep dermal/Deep Second degree
- The skin as far down to the deep dermis is involved.
- Most hair follicles and sebaceous glands are destroyed leaving
deep aspects of sweat glands.
- Re-epithelialisation from these parts of surviving sweat glands
alone is inadequate. There may be scar healing with a thin layer
of epidermis- may become hypertrophic.
2. Full thickness[Deep Burns]- Third degree.
- Whole skin is lost
- Deeper structures may be involved e.g. fat, fascia, muscle or
bone, etc.
Healing is by secondary intention and if unaided may result in a
scar.

4. Extent of Burns
Wallace’s Rule of Nines
- Palm is 1%
- Rapid though not very accurate
- Infants: head > 9%. Lower limbs; much less.
Reverse in adults. Children in between.
-
Lund and Browder’s Chart
More accurate

5. LUND and BROWDER Charts

6. WALLACE’S RULE OF NINES

7. Severity of Injury
1(a) Extent of Body Surface Burnt.
- Superficial Burns: Major injury
10% or more BSA [Body Surface Area] in children
15 – 20% “ “ in adults
- Require intravenous [IV] resuscitation
Large fluid exudation 1st 48 hrs  shock
- Infection  Septicaemia
- Admit
- Deep Burns: Major injury
5% or more BSA in children
10% “ “ “ adults
Minor Injuries : Superficial or deep burns less than stated
above

8. 1(b) Special areas:
• Face
• Hands
• Feet
• External genitalia
• Flexion creases
When any of the above parts is affected, the injury is regarded as serious even
when the surface area affected is small. For example in burns affecting the
face may result in
- metabolic poisoning especially burns in closed environments. The patient
may become dyspnoeic following irritation of the respiratory tract by fumes
and noxious gases.
-Carbon monoxide binds to Hb with an affinity 240 times greater than that
of Oxygen and therefore blocks the transport of Oxygen.
Carboxyhaemoglobin in the blood stream is dangerous if the concentration
rises.CO is the cause of altered consciousness at the scene of fire.
-Hydrogen cyanide is another metabolic toxin produced in house fires. It
causes metabolic acidosis by interfering with mitochondrial respiration.
-Inhalational injury  chemical pneumonitis  bacterial pneumonitis 
increased mortality

9. 2. Depth of Burn and Causative agent
The temperature and the duration of contact will
determine the depth of burn injury. The greater the
temperature and the longer the duration of contact
,the greater the injury.
-Burning clothing, electricity, molten metal – may
cause full thickness injury.
-Flash explosions, scalds [in adults] usually cause
partial thickness injury.
Partial thickness injury – usually appear moist, red,
blistered. Pain sensations generally intact ; nerve
endings not destroyed.
Full thickness injury – appear white or brown[dark].

10. 3. Associated Injuries or Illness.
Concurrent illness increases mortality:
(i)Pre-existing renal, cardiovascular or metabolic
disorders.
(ii) Associated fractures.
4. Age
The burn injury is poorly tolerated by
individuals at extremes of life ; [<2yrs, >65yrs].

11. Inflammation and Circulatory changes.
Burned skin activates a web of inflammatory cascades.
- Release of neuropeptides-
-Activation of complement initiated by the stimulation
of pain fibres and the alterations of proteins by heat.
(i) Local effects – tissue damage
Inflammation;neutrophils/lymphocytes,
macrophages phagocytosis[necrotic cells]
;desloughing by 3 wks.
Infection : bacteraemia, septicaemia.
(ii) Regional effects : eschar
- Compartment syndrome

12. (iii) Systemic changes
(a) Loss of plasma – Hypovolaemia and Burn Oedema
- Injury to vessel walls leads to vasodilatation and increased
permeability leading to extravasation of fluid, electrolytes and
plasma proteins particularly albumin from vessels into tissues and
raw areas leading to oedema formation. Destruction of lymph
vessels prevents drainage of the accumulating fluid.
- Increased protein content of burn oedema fluid leads to increased
osmotic pressure leading to further loss of water and electrolytes
from the circulation.
-The electrolyte composition of the exuded fluid is same as that of
plasma.
- Plasma loss leads to hypovolaemia  shock if severe.
Haemoconcentration, sluggish circulation, stasis and thrombosis may all
occur.
Hypovolaemia inadequate renal perfusion reduced urinary output
/oliguria.
Hypoxia may damage renal cells and cause acute tubular necrosis
and renal failure.
Protein and fluid loss – fastest within 8 hrs of injury.
- reduces in 24 – 48hrs

13. (b)Anaemia
Acute red cell destruction in deep burns – [12-25% of
mass within 12hrs].
Early loss – Direct destruction by heat
- Sludging from haemoconcentration
- Trapping of red cells in vessel thrombosis
- Delayed haemolysis from increased fragility.
Late loss – Multiple changes dressings
- Skin grafting
- Gross infection – reduced bone marrow
production of red cells.

14. (c) Adrenal changes
Medulla - Increased Adrenaline and Noradrenaline.
Cortex - Corticosteroids
(d) Other hormonal effects
- ACTH/Glucagon
Increased lipolysis, proteolysis and
gluconeogenesis.
(e) Renal changes
Hypovolaemia splanchic bed vasoconstriction [early
fluid resuscitation will prevent this]  Renal plasma flow
reduced GFRAcute tubular necrosis[oliguria and anuria].
Haemoglobinuria may damage DCT.
(f)Respiratory Tract changes- Following inhalation of irritant and
noxious gases.
- Resp. distress may result from atelectasis, pulmonary
oedema,tracheo-bronchitis pneumonia or pulmonary
embolism.

15. (g) Metabolic changes: -ve Nitrog. balance & hypermetabolism
- loss in weight
Resistance to Infection
- The burned patient shows increased susceptibility to
infection because of depression of cellular and
immunological defence systems.
-Loss of skin: natural barrier to bacteria protection
-damage to naso-pharyngo-tracheal mucosa
enhance bacterial invasion.
- Damage to the vascular endothelium and micro-circulatory
stasis consequent on the hypovolaemia depress the rapid
transfer of leucocytes and antibodies to sites of invasion.
- Depression of humoral antibodies esp. Ig G and of plasma
cells which produce them.[IgG destroys Gm +ve and Gm-ve
bacteria].

16. MANAGEMENT
First Aid-Prehospital Care
-Principles:(1) Ensure rescuer safety
(2) Stop the burning process; Stop, Drop and Roll
(3) Check for other injuries- ABC etc. of trauma
(4) Cool with water for 10 min. or more
(5) Give Oxygen- enclosed space burn
(6) Elevate – sitting up ;enhances airways
- elevate limbs.
Hospital Care
Order of priorities- A: Airway maintenance
B: Breathing and ventilation
C: Circulation
D: Disability- neurological status
E: Exposure and Environmental control – keep warm
F: Fluid resuscitation

17. History/Examination/Investigation
Airway assessment –History of being trapped in presence of smoke/hot gases.
- Burns of face and neck/palate
- singeing of nasal hairs
- soot in nostrils
- oedema[4-24hrs];subsides after about 48hrs.
1.Quick history- Age
- Cause of burn and site :home,closed environment- cinema, factory,
laboratory, RTA.
- Time of injury.
2.Examination- Remove clothes and quickly estimate total BSA burn and the depth.
-Weigh patient if possible.
Vital signs- BP, Pulse, Respiration.
3. Blood samples:
-Haematocrit [PCV – 8hrly if possible]
-Serum electrolytes and Urea
- Blood grouping and X-matching
Unconscious patient- Arterial samples
- Blood gases :Oxygen ,Carbon dioxide
- pH

18. TREATMENT
(i)IV Fluids/line- Ringer’s lactate /Normal Saline
Fluid estimate for 24 hrs;
Half given within 1st 8hrs
(ii) Analgesics to relieve pain and allay anxiety
IV Morphine, Ketamine
(iii) Catheterize patient- Foley’s catheter
- Hrly urine output
Most reliable parameter in monitoring patient(0.5-
1ml/kg/hr).
(iv) Monitor vital signs every half hour
(v) Prophylactic antibiotic ?
(vi) Antitetanus – T.T. [TIHG-Tetanus Immune Human Globulin]
(vii) Decompression – Prevent tourniquet effect; escharotomies.
(viii) Wound toilet when patient is stable. Splints.

19. (ix) Nourishing Diet – High protein, high energy
vitamins and iron
- Extra feeding within 6hrs to reduce gut mucosal
damage.
- Removal of the burns and achieving healing stops the
catabolic drive.
(x)Physiotherapy- Starts day 1
-Elevation
- Splintage
-Exercise
(xi) Skin grafting-3 weeks.
INHALATIONAL INJURY – CLINICAL FEATURES
- Progressive increase in respiratory effort/rate.
- Increase pulse, anxiety/confusion
- Decreasing Oxygen saturation.
Manifests within 24hrs and any time in the first 5 days.
Burned airway-Early intubation is safest.
- Delay can make intubation very difficult due to swelling.
- Emergency Cricothyroidotomy if intubation delayed.

20. FLUID REPLACEMENT
1. Brooke Formula
(i)”Colloid” Replacement Volume[Blood, Plasma or Plasma
substitutes]
0.5ml/kg b. wt/ % burnt area
(ii) Electrolyte Replacement Volume[Ringer’s lactate, Normal
Saline]
1.5 ml/kg b. wt/% burnt area
(iii)Normal daily requirement added:
Tropics – 1 Litre of Ringer’s lactate
- 2 litres of 5% Dextrose
Temperate – 2 Litres of 5% Dextrose
Half fluid requirement given 1st 8hrs[from time of injury].
Rest “ “ “ over 16 hrs.
2nd 24hrs- half of colloid and electrolyte requirement of previous
day required + Normal daily requirement.

21. 2.The Parkland Formula
4 x Wt in Kg x %TBSA
The Parkland Formula calls for 4mls of Ringer’s lactate per Kg
per %TBSA burn to be infused over 24hrs.
-Half of the calculated volume is given 1st 8hrs.
-Remaining half over 16hrs.
3. Muir and Barclay Formula
0.5 x Wt in Kg x %TBSA (mls) = each period
There are 6 periods of 4hrs,4hrs,4hrs,6hrs, 6hrs and 12hrs
measured from time of burn injury.
Colloid solution [e.g. 4.5% human albumin] is infused, and
equal amounts of this fluid are given over six periods of
time. These consist of three periods of 4hrs, then 2 periods
of 6hrs and finally one period of 12hrs. Total 36 hrs –
beginning at the time of injury.
Metabolic needs- 4%D/0.18 Saline (I.5mls/kg/hr)

22. 4. Evan’s Formula
1st 24 hrs - 1ml/Kg x % BSA burn = electrolyte
- “ = colloids
+ Normal daily requirement
2nd 24hrs- Half of calculated fluid
+ Normal daily requirement
CARE OF THE BURN WOUND
Follows resuscitation:
(i) Exposure method – No dressings
Aim – Achieve eschar. Visitors and medical personnel masked.
Suitable for burns of face,perineum.
Contraindicated in ambulant out-patient cases.
(ii) Dressings
(a) Occlusive
(b) Silver Nitrate dressings ; 0.5% solution
- Effective against pseudomonas
-Initial dressing soaked every 3 hrs{If allowed to dry conc.
of silver nitrate rises – healing may be delayed}.

23. Disadvantages of Silver Nitrate dressings:
- Time consuming
-Stains beddings and floor
- May cause hyponatraemia or hypokalaemia from
leaching of Na+, K+ and Cl- from the burn wound.
Serum electrolytes must be checked daily.
(c) Silver sulphadiazine [Flamazine] 1%
Most widely used.
- Effective against pseudomonas and other
infections.
- Causes less electrolyte and allergic disturbances.
- Highly antibacterial, non-toxic, non-painful, non-
staining and penetrates the tissues fairly well.

24. (iii) Excision and skin graft
(a) Initial Excision
- Within 48hrs
-SSG later; few days
(b) Tangential Excision
- About 4th day
- SSG same day simultaneously
(c)Skin grafting
- Between 3rd and 4th week
(d)Homografts
Indications- Extensive burn wounds
- Very ill patient/Septicaemia etc.
(e) Xenografts
(f) Keratinocytes

25. Complications of Burns
1. Hypovolaemic shock
2. Infection
3. GIT problems: paralytic ileus, gastric dilatation,
Curling’s ulcers.
4. Cardio-respiratory problems: respiratory obstructions,
tracheo-bronchitis, pneumonia, atelectasis.
5. Genito-urinary problems: renal failure, Cystitis
Pyelonephritis.
6. Psychiatric problems
7. Vascular problems: thrombophlebitis, DVT
8. Deformities and contractures.
9. Keloid and hypertrophic scars
10. Malignant change in scars – Squamous Ca. Basal[rare].

26. Cause of Death in Burns
1. Hypovolaemic shock- 1st 48 hrs
2. Renal failure: pre-renal, ATN[Acute Tubular
Necrosis] may follow shock.
3. Sepsis: local, septicaemia, tetanus.
4. Pulmonary problems: laryngo-tracheal
bronchitis, laryngeal oedema, pulmonary
oedema,etc
5. Curling’s ulcers; GIT bleeding, perforation

27. Prognosis
• 60-70% burn – 50% probability of survival
• More than 70% - Chances of survival slim
• Respiratory tract injury, concomitant illness worsen prognosis.
• Extremes of age –very young and very old , may tolerate poorly.
Prevention
1. Education- careless handling of matches ,flammable
materials/candles esp by children. Handless pots/non-conducting
handles,etc.
2. Good planning of houses/kitchen
3. Epileptics/Children - away from kitchen.
4. Storage of kerosene, gas, fuel – in safe /secure places.
5. While cooking –frying pan fire should be smothered.
6. Candles put off before sleeping
7. Use of fire extinguishers.
8. Proper use of electrical equipment esp. in rural areas.
9. Etc.