BURNS

DR. STANLEY KHAINGA

CONSULTANT PLASTIC & RECONSTRUCTIVE SURGEON

10/16/22 1
 SKIN
• One of largest organs in the body
• 0.025m2 – newborn
• 1.8m2 adult
• Consists of
1. Epidermis protective barrier
2. Dermis c.6-1mm in thickness
– Collagen and elastic fibers
– Blood vessels
– Nerve endings
– Sweat glands, sebaceous glands and hair follicles in
deep dermis
– Prevents loss of body fluids and excess heat via micro
circulation and sweat glands
3. Sub cutaneous tissue
– Plexus of capillaries + subdermal layer of fat

10/16/22 2
 FUNCTIONS OF SKIN
1. Protective barrier against environment –
U.V.L. etc
2. Heat loss
3. Fluid and protein loss
4. Protective against infection – stops
micro-organism to penetrate sub dermal
tissues.
5. Protects against body injury via nn
endings.
 Definition of Burns
• Is body injury resulting from cellular
damage due to hyperthermia 95% but very
low To
• A condition similar to burn hypothermia –
5% (frost bite).
• Cellular damage occurs when energetic
portion of electro magnetic field acts on
cells.
 CLASSIFICATION OF BURNS
a) According to cause
1. Electrical
2. Chemical
3. Thermal – 80% of burn injuries

• Flame
• Flash – e.g. explosions To lightening
• Scald – liquids
• Contact/frictional
b) According to depth of burn
 Partial thickness burn
 # 1st degree – Involves epidermis only
 # 2nd degree – Involves epidermis +
dermis
 Superficial
 Deep
 Full thickness burn – 3rd degree
 4th degree – involves skin, subcutaneous
tissues, muscles, tendons and bone.
 c) According to America burn Association
Major burn Mod. Burn Minor burn
Size of partial >25% adults 15-25% adults <15% adults
thickness >20% children 10-20% <10% children
children
Size of full thickness >10% 2-10% <2%
Primary areas Major burn if Not involved Not involved
involved area
Inhalation If present or Not suspected Not suspected
suspected
Associated injury If present Not present Not present
Cormorbid factors Poor risk Patient Not present
patients relatively good
Miscellaneous Electrical - -
Treatment Specialised burn General Out patient
Environment care facility hospital management
10/16/22 8
 PATHOGENESIS OF BURN INJURY
A. Thermal burns:
• Is as a result of heat necrosis of cells.
Depends on:
1) Intensity of heat
2) Conductance of tissues involved determine role
of dissipation of heat or absorption which in
burn depends on:
i. Peripheral circulationcooling effect of circulation
blood
ii. Water content of tissueshavespecific heat and low
thermal conductivity.
iii. Thickness of skin and its pigmentation
iv. Presence of absence of ext. insulating substances
e.g. hair and skin oils.
3) Duration of exposure
• As the rate of tissue absorption exceeds rate of
dissipation varying degrees of injury occur.
• At To <44oc tissue damage occurs only on prolonged
exposure.
• At To>51oc time needed to cause necrosis is very brief.
• at 10 sec. exposure to To 85oc will produce 3o burn.

Note: Depth x BSA = Seriousness of burn

• 1o and 2o burn = Partial thickness burn

• 3o burn = Full thickness burn
• 4o burn = Involves skin, SC tissue, muscle,
tendons and bone
B. Electrical Burns:

• Consists of 3-9% of admissions

• Results from heat produced by the flow of
electrical current through the resistance of
body tissues.
• Causes of injury
Direct cell injury
Heat produced by current
• Determining factors:
1. Type of circuit - AC>DC
2. Voltage - Electro motive force produced by power source
3. Amperage - (intensity) the amount of current flowing per unit time
4. Resistance of tissues involved - dependent on water content
5. Path of current through the body
6. Duration of contact with current source
7. High voltage current involves  volume of tissues
8. Large volumes of necrotic muscle may underly a relatively small
cutenous wound
9.  predisposition to renal failure due to  release of large quantities of
myoglobin into circulation
10.Resistance is  from bone then fat then skin muscle, blood vessels
& nns.
11.Pathway of current depends on contact and exit points of current as
well as resistance of intervening tissues.
12.The path of current determines organs subject to injuries
13.Significant injureis may be encountered in structures far removed
from the entrane and exit points of the current
 C. Chemical Burns
Mechanism of injury
• Chemical reaction
– Coagulation of proteins by reduction
– Corrosion
– Oxidation
– Formation of salts
– Poisoning of protoplasm
• Hyperthermic injury
– Is a product of chemical reaction
– Causes cell necrosis from heat energy

Note:
• Avoid neutralisation of acids/alkalis when still present in
concentrated forms
• Wash/extensive irrigation with water
 Pathophysiologic Effects of the burn

Skin
•Has epidermis - Ectoderm
•Dermis - Mesoderm
•Thickness depends on site/age
•Blood supply of epidermis is for dermis
•Epidermis has several layers
•Dermis has upper papilary layer and inner reticular layer. Has
blood vessels, lymphatics, nerves, sweat glands, subaceous
glands, hair follicles.
•Main function is protection against invasion by pathogens,
thermoregulation and checks evaporation of water.
•Rate of water evaporation depends on depth and extent of burn.
•Evaporation – heat loss – compensating hypermetabolism by
patient.
Vascular injury
capillary permeability – loss of fluids electrolytes,
and molecules with most İ125,000
•Capillary permeability is generalised and –
extravasation of fluid into interstitial space.
•Fluid lost is isotonic to plasma.
•Loss of plasma proteins.
•Permeability greatest immediately after burn burn
but returns to normal in 24 hours.
•Results into hypovolaemic – shock.
•Loss of plasma – causes C.O.
•Myocardial depressant factor in plasma of burned
patients – causes C.O.
 8-10% - loss in Red Blood Cells occurs in severe burns
due to:
o Destruction – directly
o Sequestration of injured cells by RES.
o Trapping of RBCs, platelets and white blood cells in
microvascular thrombi of damaged blood vessels.
o Sludging
o T1/2 of red blood cells secondary cirdulating plasma
factor.

• Mild thrombocytopenia in 1st 48-72 hours 2o thrombosis

and mild DIC.
• Return to normal in 3/52.
 General Metabolic Response
• Hypermetabolism
• Negative N2 balance
• Exaggerated stress response
 catecholamine release,  cortisol release

Measures of Severity

• Extend – BSA
• Depth
• Age – extreme of ages
• Associated medical diseases
• Associated injuries
 CRITERIA OF ADMISSION
Must admit
• 10% deep burn
• 10% superficial
• 15% superficial in young healthy adult
• Associated medical problems e.g. HT, CCF,DM
• Special sites/areas
• Inhalational
• Associated injuries e.g. preumothora, head injury,
fractures etc
Admit Burns Unit
1. 20% 0-14 years
2. 30% young healthy aduls
3. Inhalational injuries
History

• Causes – D.M, epilepsy, assault, parasuicide

• Inhalation of smoke or steam
• Hot water, open flame

Exam

• General
• Specific

At site of Burn Injuries 1st Aid

• Stopping the burning process
• Resuscitation
• Relief of pain
• Covering the burn wound
• Transport to hospital
 IN-PATIENT MANAGEMENT
Severe
•Severe ≥15% BSA in adults and ≥10% BSA in <14 years >50 years.
•Stormy course
•Admission time 2-3/12
•Respond poorly to treatment
•Vomit feeds
•Fever is persistent even with antibiotics
•Need catheterisation + IV lines – sources of infection
•Delayed healing
•Eschar delays to separate
•Few donor sites
•Take rate is low
•M.R. is high
•Benefit a lot from treatment

•Hopelessly severly burn ≥80% BSA

•MR is 100% in KNH
Non Severe
•Pass through a steady phase in hospital
•Respond well to treatment
•Sepsis settles down quite well most of them
with antibiotics
•Heal well whether with exposure/dressing
•Eschar separates quite early
•Donor sites are available
•Take rate is high
 FLUID RESUSCITATION
• Most popular fluid formulae used are:
– Evans formula
– Brooke army
– Parklands
• Greatest loss of fluid occurs in 1st 12 hours
postburn
• Protein loss in oedema fluid is approximately
1.2 – 2.8 gm/100ml
• Sign of adequately resuscitated patient is
urinary output of ≥30 – 50ms/hour,
pulse<120/min and a calm patient.
 Clinical monitoring of adequate
fluid resuscitation
• Most fluid loss is in 1st 8 hours.
• Calculate fluid therapy from time of injury and not from time of
admission.
1. Baseline lab invx
– Hb
– HCT
– Bun
– Blood gas in inhalation injury
2. Hourly urinary output 30-50mls/hr is best guide to rate of infusion.
rate of infusion if urine is  20ml/hr and rate of infusion if urine is >
60ml/hr
3. A in BP and urine output suggests need for colloid and a in urine
output and normal BP suggests need for crystalloid.
4. Haemoglobinuria suggest deep burn hence flush renal lobules with
fluid intake or mannitol.
5. Frequent chest auscultation to detect
early pulmonary oedema.
6. Cerebral oedema in burns around face
especially in children must be suspected.
7. CVP line – best guide in avoiding over
infusion.
8. Maintain record of BP and pulse.
9. Evaluate treatment in 3-4 hours.
Evans formula- 2ml/kgBW/BSA
• 1st 24 hours
– Crystalloid: Colloid = 1:1
– Saline: plasma/blood/dextrat/plasma nate +
– 2000ml 5% to replace insensible loss
• 2nd 24 hours
– 1/2 of above vol + 2000mls 5%D
 Brook Army – 2mls/KBW/BSA
• A modification of Evans formula
• Notes that metabolic acidosis is rapidly corrected
by lactated ringers solution rather than saline
solution.
• 1st 24hrs
– 1.5 ml x BSA x KBW: 0.5ml x BSA x KBW
(crystalloid Rogers) (colloid) + 2000ml 5%D
• 2nd 24 hours
– 1/2 of above + 2000ml 5%D
• Note: With both formulae maximum burn
calculated is 50% TBSA
 Parklands formula
• Gives consideration to rapid loss of infused colloid during the
1st 24 hours after injury – calls for administration of crystalloid
(Ringers lactate) with colloid in 1st 24 hours because of its
rapid extravation into interstitial space.

4mls x BSA x KBW

• Note: No addition of 2000mls 5%D

• Total percent burn (TBSA) (rather than 50% BSA in Evans

and Brooke Army) is used to calculate fluid needed.
• Colloid is given in 2nd 24 hours together with glucose and
water.
CVP monitoring
COMPLICATIONS OF BURNS
Outcome:

1. Terminate fatally
2. With stigmata
3. Without stigmata
 TYPES
1. Those related to condition present in a
patient at time of burns injury.
2. Conditions that occur at same time as
burn injury.
3. Conditions occuring as a result of burn
injury.
 Conditions present before burn
1. General state of patient
2. Age – extreme of ages tend to develop
complications
– More infections in children that adults e.g.
parasite, bacterial/malnutrition/anaemia e.t.c
– The aged have D.M, H.T., poor vision, poor
hearing all complicate burn.
3. Pregnancy – abortions are likely
especially in 1st trimester.
 Conditions which occur at same
time with burns

1. Airway obstruction.

2. Bleeding – can be direct cough

 Conditions occuring as a result of
burn
• Instant complications – occur in secs/minutes.
• Involve systems:
– Pulmonary inhalation of hot air/steam
– Dehydration at site of injury – may cause death

• Immediate complications – occur in hours.

– Bleeding
– Airway obstruction
– Circulatory collapse
• Early complications -– occur in days.
– Anaemia
– Electrolyte imbalance
– Infections
• >15% BSA –give prophylatic antibiotic
• <15% BSA – do pus for C/S
• 50 + % BSA – use broad spectrum antibiotics
• Late complications - occur in weeks/months
 EARLY COMPLICATIONS
1. Anaemia
• Direct red blood cells destruction – 1% deep burn – 50mls
blood
  T1/2 rbcs
• 02
• Bone marrow depression
– Direct heat
– Infections
• Surface bleeding
– Dressing method
– Escharectomy/escharotomy
– Skin grafting
• Management
– Transfuse < Hb 10g%
– X2/weekly Hb especially in severe burns
 2. Electrolyte Imbalance
• Severe burns – Na+ in circulation but there’s
whole body impercomplication due to fluid
loss.
• Severe burns – K+ but leakage from cells
causes relative hyperkaelamia in a situation
body conc.
• Above situation occurs in 1st 24-48 hours.
• Situation may change after correcting fluid
loss resulting into diuresis by kidneys – K+
loss hence causing hypokalaemia within
hours.
Treatment
•During shock period solutions given should not
have K+. Start K+ supplements after 48 hours.
•Give Na+ in 1st 48 hours.
•During shock period body is in a state of
hypometabolism (though burn area is
hypermatabolic) hence low calories are given
during shock period, but from day 5 give high
calorie + vitamins.
 3. Infections
• Burn surface is contaminated soon after
burns by pathogens.
• Some multiply to colonise as pathogens.
• > 105 bacteria/gm tissue coincides with fever
and pus.
• Fever may be due to bacteria infx. OR burn
toxaemia (largely) due to proteins going into
circulation – auto immune reactions.
• Fever due to burn toxaemia is in 1st 48 hours.
Common pathogens on burn surface
•Gm –ve and gm +ve (50% of each)
•Staph aureus approx. 50%
 - haemolytic strep – 10%
•Pseudomonas – 10%
•E. coli – 10%
•Kleb – 10%
•1st organism to invade burn wound is strep. Then followed by
staph in 1st 3/7 – 1/52
•Gm –ve in 2nd week
•Fungi and viral later > 3/52
•Burn patients are prone to UTI, pneumonia, ARI, flaring of
malaria, measles in children and thrombophlebitis due to IV
canulas.
Antibiotics
•Give penicillins prophylactically – to control
strept. Pyogenes and cl. Tetani.
•BSA > 15% protect body with antibiotc
•1st 3/7 cloxacillin
•>3/7 aminoglycosides 2ogm-ve
•Do c/s in lab
•BSA > 50% introduce broad spectrum
antibiotics or 2 combined antibiotics during
resuscitation.
 Organal complications
A. GIT
•Has – specialised function (hardly interfered with in mild burns) and
generalised function.
•In severe burns there is vasoconstriction resulting into: e.g. inflammation of gut
cells – fluid exsorption into gut causing vomiting + diarrhoea.
•Acute ulcerative gastroduodenoal disease
– Curling ulcers 2o necrosis of GIT cells
– H2 receptor antagonists + anti acids to have PH ≥ 7.
– Rare in BSA < 15% while in BSA ≥50% occurs in >80% of patients.
– Most are silent.
•Acute gastric dilation, treatment and management + IVFs.
•Fecal impaction treatment
– PR
– IVFs
– Laxities
•Burn reduces body immunity – causing flourishing of gut bacteria and may
cause endotoxic shock especially in liver failure.
B. Kidneys
• Kidney has approximately 1.2 million nephrons and can
function with 30%)
– Pressure in renal aa=100 mmHg
– Afferent arteriole=70 mmHg
– Mean capillary pressure=60 mmHg
– On cotic pressure=25 mmHg
– Therefore outward pressure=35 mmHg
• 50mmHg capillary pressure interferes with filtering effect.
• S.G. of urine approx. 10.20 and of glomerular filtrate 10.10.
• S.G. in burn injury is due to fluid loss 10.50 but is at end of
resuscitation 1008.
• A kidney that can S.G.is still functional.
Causes of anuria
•Glomerular failure – related to shock
(<50mmHg capillary pressure)
•Tubular necrosis
Albumin )
Globulin ) block lobules
RBCS )
•Tubular obstruction – 2o necrosis and
obsstruction
•At BSA of 80-90% renal damage is
irreversible.
Consequences of anuria
1. Urea, NH3, K+ and – lactic, phosphoric
2.Uraemic symptoms are:-
– Headache
– Vomiting
– Confusion
– coma
Management
•Lab results of U/E
•Maintaining urinary output at 30ml/min
•S.G. of urine (not happy when fixed)
•Na+ and K+ in urine (Na+, K+ = 2:1 in normal
function but is reversed in pathology).
Treatment of renal failure
•Prevention
•Flushing of kidney
•Vasodilators – dopamine
•Rest + Bulls regime – restricted fluids (add losses)
– High CHO
– Low protein
– Resins
•Dialysis
– Peritoneal
– Blood
Indication
•Persisting S.G.
•Persisting anuria
•Uraemia
•K+ levels ≥ 7mmol/L
•Failed renal response after flushing +
vasodilator
•Renal cells recover after 1-2/52
C. Liver
• Regulates blood glucose level.
• Formation of protein.
• Formation of blood in infancy.
• Protein Deamination (prot – NH2 + Co2 – Urea)
• Fat metabolism – ketoacidosis
• Filtration of bacteria especially from colon

In severe burns > 50% BSA liver damage

occurs
Management
• Bed rest
• Diet – low protein, high CHO
• Bulls regime in severe liver damage – reduce NH3
formation.
• GIT enema
• Drugs
– Neomycin
– Flagyl
– Manittol – NH3 cause brain oedema
• Fresh blood to supply clotting factors in case of
bleeding.
D. Pulmonary complications
• Pulmonary capillary pressure equal to oncotic
hence nothing in filtered from pulm
capillaries.
• Space between pulm. Capillary and
pulmonary cell is very thin for efficient gas
exchange.
• Alveolar space is dry (in normal state)
• 2 types of hot air
– Hot dry – is cooled along resp. passages
– Hot wet e.g. steam has high specific heat –
resulting into more damage.