ROKHAN UNIVERSITY

SURGERY DEPARTMENT

BURN 2

G SURGEON
DR AKHTAR GUL “NASIRI”
YOU TUBE: MEDICALLECTURESINPASHTO
FACEBOOK: GENERAL SURGERY AND UROLOGY SERVES
 EFFECTS OF BURN INJURY
▪ Shock due to hypovolemia.
▪ Renal failure.
▪ Pulmonary oedema, respiratory infection, adult respiratory distress syndrome
(ARDS), respiratory failure.
▪ Infection by Staphylococcus aureus, beta hemolytic Streptococcus, Pseudomonas,
Klebsiella leads to bacteremia, septicemia. Fungal and viral infections of
dangerous types can also occur.
▪ GIT: Hypovolemia, ischemia of mucosa, erosive gastritis—Curling’s ulcer (seen in
burns > 35%).
▪ Fluid and electrolyte imbalance.
▪ Postburn immunosuppression predisposes to severe opportunistic infection.
▪ Eschar formation and its problems like defective circulation, ischemia when it is
circumferential.
▪ Electrical injuries often cause fractures, major internal organ injury, convulsions.
 EFFECTS OF BURN INJURY
▪ Development of contracture is a late problem. It leads to ectropion,
microstomia, disability of different joints, defective hand functions, growth
retardation causing shortening.
▪ Inhalation burn causes pulmonary oedema, respiratory arrest, ARDS.
▪ Chemical injury causes severe GIT disturbances like erosions, perforation,
stricture esophagus (alkali), pyloric stenosis (acid), mediastinal injury.
▪ Other problems commonly seen are DVT, pulmonary embolism, urinary
infection, bed-sores, severe malnutrition with catabolic status, respiratory
infection.
▪ Complications of burns contracture itself like hypertrophic scar, keloid
formation.
▪ Toxic shock syndrome: It is a life-threatening exotoxin mediated disease
caused by Staphylococcus aureus. It is common in children, presents with
rashes, myalgia, diarrhea, vomiting, and multiorgan failure with high
mortality.
 CAUSES OF DEATH IN BURNS
▪ Hypovolemia (refractory and uncontrolled) and shock
▪ Renal failure
▪ Pulmonary oedema and ARDS
▪ Septicemia
▪ Multiorgan failure
▪ Acute airway block in head and neck burns
▪ Indications for admission in burns
▪ Any moderate and severe burns
▪ Airway burns of any type
▪ Burns in extremes of age
▪ All electrical/deep chemical burns
 MANAGEMENT
▪ Initial management
▪ Stop the burning process and keep the patient away from the
burning area.
• Clothing should be removed
• Cooling of the part by running water for 20 minutes
• Cleaning the part to remove dust, mud, etc
• Chemoprophylaxis—tetanus toxoid; antibiotics; local
antiseptics
• Covering with dressings by different methods
• Comforting with sedation and pain killer
 DEFINITIVE MANAGEMENT
▪ Admit the patient.
▪ Maintain airway, breathing, circulation.
▪ Assess the percentage, degree, and type of burn.
▪ Keep the patient in a clean environment.
▪ Sedation and proper analgesia.
▪ Patient should be in burns unit
▪ Fluid resuscitation
▪ Formulas to calculate the fluid replacement:
▪ Parkland regime:
▪ Commonly used: 4 ml/% burn/kg body weight/24 hours.
▪ Maximum percentage considered is 50%. Half the volume is given in first 8
hours, rest given in 16 hours.
 FLUID RESUSCITATION
▪ Fluids used are normal saline, ringer lactate, Hartmann fluid, plasma. Ringer
lactate is the fluid of choice.
▪ Blood is transfused in later period (after 48 hours).
▪ First 24 hours
▪ only crystalloids should be given (Crystalloids are one which can pass
through capillary wall like saline either hypo, iso or hypertonic, dextrose
saline, Ringer lactate).
▪ After 24 hours
▪ up to 30-48 hours, colloids should be given to compensate plasma loss
(colloids are one which are retained in intravascular compartment). Plasma,
haemaccel (gelatin), dextran are used.
▪ Usually at a rate of 0.35-0.5 ml/kg/% burns is used in 24 hours.
 FLUID RESUSCITATION
▪ Urinary catheterization to monitor output; 30-50 ml/hour should be the urine
output.
▪ Tetanus toxoid.
▪ Monitoring the patient: Hourly pulse, BP, PO2, PCO2, electrolyte analysis,
blood urea, nasal oxygen, often intubation is required.
▪ IV ranitidine 50 mg 8th hourly.
▪ Ryle’s tube insertion initially for aspiration purpose later for feeding (Enteral
feeding).
▪ Antibiotics: Penicillins, aminoglycosides, cephalosporins, metronidazole.
▪ Culture of the discharge; total white cell count and platelet count at regular
intervals are essential to identify the sepsis along with fever, tachycardia
and tachypnoea.
▪ In burns of oral cavity tracheostomy may be required to maintain the
airway.
 FLUID RESUSCITATION
▪ Total parenteral nutrition (TPN) is required for faster recovery, using
carbohydrates, lipids, vitamins (through a CVP line).
▪ Tracheostomy/intubation tube may be required in impending respiratory
failure or upper airway block.
▪ Intensive nursing care.
▪ Resuscitation monitoring
▪ The key to monitoring of resuscitation is urine output. Urine output should be
between 0.5 and 1.0 mL/kg body weight per hour.
▪ If the urine output drops and the patient is showing signs of hypoperfusion
(tachycardia, cool peripheries and a high lactate/metabolic acidosis),
▪ Then a bolus of 10 mL/kg body weight should be given. It is important that
patients are not over-resuscitated; urine output in excess of 2 mL/kg body
weight per hour should warrant a decrease in infusion.
 LOCAL MANAGEMENT
▪ Dressing at regular intervals under general anesthesia using paraffin gauze,
Vaseline impregnated gauze or fenestrated silicone sheet ETC
▪ Local agents used commonly are:
▪ Silver sulfadiazine (1%) :
▪ Antiseptic (G +ve and G –ve)
▪ Neutropenia, pseudoeschar
▪ It diffuses poorly through the eschar
▪ Mafenide acetate:
▪ Penetrates very well in to tissues
▪ It is water soluble
▪ It is good antipseudomonal agent
▪ Causes acidosis, by inhibiting the carbonic anhydrase
 LOCAL MANAGEMENT
▪ Method of Dressing
▪ Open method with application of silver sulfadiazine without any dressings,
used commonly in burns of face, head and neck.
▪ Closed method is with dressings done to soothen and to protect the wound,
to reduce the pain, as an absorbent.
▪ Tangential excision of burn wound with skin grafting can be done within 48
hours in patients with less than 25% burns.
▪ It is usually done in deep dermal burn wherein dead dermis is removed
layer by layer until fresh bleeding occurs. Later skin grafting is done.
▪ Slough excision is done regularly.
▪ After cleaning with povidone iodine solution silver sulfadiazine ointment is
used.
 ESCHAR
▪ It is charred, denatured, full thickness, deep burns with contracted dermis. It is
insensitive, with thrombosed superficial veins.
▪ Circumferential eschar in the upper limb, lower limb, neck, thorax can cause more
oedema which initially causes venous compression and later arterial compression
causing ischemia, gangrene of the distal part. So distal area should be monitored
for circulation.
▪ If required deep longitudinal full thickness incisions are made in different areas so as
to prevent collection of oedema fluid and also to prevent compression over the
vessels. This is called as escharotomy.
▪ Escharotomy causes large quantity of blood loss and so blood transfusion is needed
▪ Incision should be of adequate length and depth during escharotomy.
▪ It should be placed in such a way so as to avoid injury to major neurovascular
system.
▪ Eventually eschar should be excised and the area is allowed to granulate and skin
grafting should be done.
▪ Pseudoeschar is thickened burnt skin due to repeated silver sulphadiazine
application.
 CONTRACTURE
▪ Contracture in burns can occur anywhere. It is more common wherein
flexibility and mobility is present like along the joint, eyelids, cheeks, lips,
neck, elbow, knee, etc.
▪ Eyelids must be treated before exposure keratitis arises
▪ Transposition faps and Z-plasties with or without tissue expansion are useful
▪ Full-thickness grafts and free faps may be needed for large or difficult areas
▪ Proper physiotherapy and rehabilitation is essential.
▪ Pressure garments to prevent hypertrophic scars.
▪ Management of itching in the scar using aloe vera, antihistamines and
moisturizing creams.
 ELECTRICAL BURN
▪ Types of Electrical Injury
▪ Low tension injury: Less than 1000 volts.
▪ High tension injury: More than 1000 volts
▪ may be due to current itself causing intense damage on the tissues up to
2000°C
▪ flash injury due to electrical arc up to 4000°C
▪ flame injury by catching of fire to the clothing and body
▪ traumatic injury like fractures and internal organ injuries.
▪ It is always a deep burn (always a major burn).
▪ There is a wound of entry and wound of exit.
▪ Patient may also have major internal organ injuries. GIT, thoracic injuries.
▪ Often convulsions can develop.
 ELECTRICAL BURN
▪ Death may occur due to cardiac arrhythmias (instant death due to ventricular
fibrillation).
▪ Gas gangrene is common after electric injury.
▪ Release of myoglobin can cause renal tubular damage and renal failure.
▪ Acidosis is common and so often bicarbonate infusion is needed.
▪ Patient should always be admitted and should be assessed by ECG, cardiac
monitor, U/S abdomen, chest X-ray, sometimes even CT scan head, cardiac
enzyme analysis.
▪ Depending on the injury it is managed accordingly.
▪ Fractures and dislocations are common in electrical injuries which is treated
accordingly.
▪ Mafenide acetate is better agent as it penetrates well and it is useful against
clostridial infection.
▪ Mannitol is used to prevent myoglobin induced renal failure.
▪ Wound excision, amputation, surgery for internal organ injury, cardiac
monitoring are essential part of the surgical management.
 INHALATION INJURY
▪ It occurs after major fire burns.
▪ It is due to:
▪ Inhalation of heat.
▪ Noxious gases and incomplete products of combustion.
▪ At the site of fire, oxygen concentration is less than 2% which can cause death in 45
seconds due to hypoxia.
▪ Inhaled carbon monoxide binds with Hb immediately to form carboxyhemoglobin
causing severe anoxia and death.
▪ CO has got 240 times more affinity for hemoglobin than oxygen.
Carboxyhemoglobin in blood more than 10% is dangerous; more than 60% is life-
threatening.
▪ Symptoms of carbon monoxide intoxication—headache, disorientation, visual
changes, fatigue, vomiting, hallucinations, shock and cardiac arrest.
▪ Smoke contains hydrocyanide which causes tissue hypoxia and profound acidosis.
▪ Laryngeal oedema and laryngospasm.
▪ Bronchial oedema and bronchospasm.
 INHALATION INJURY
▪ Later Problems
▪ ARDS, pneumonia.
▪ Atelectasis, pulmonary embolism.
▪ Pulmonary oedema, pneumothorax.
▪ Clinical Features
▪ They have low oxygen saturation.
▪ Charring of mouth, oropharynx with facial burns.
▪ Carbon sputum.
▪ Change in the voice, singed facial and nasal hair.
▪ Decreased level of consciousness with stridor or dyspnea.
▪ Acute pulmonary insufficiency with asphyxia, CO poisoning, upper airway
obstruction. After 3 to 5 days, ARDS and hypoxia develops. Bronchopneumonia with
septicemia occurs after 5 days.
 MANAGEMENT
▪ Replacing the patient from the site earliest.
▪ Ventilator support for several weeks.
▪ Antibiotics.
▪ Bronchoscopy, at regular intervals to remove bronchial cast.
▪ Tracheostomy whenever required.
▪ Hyperbaric oxygen.
▪ IV heparin to reduce bronchial cast. Heparin nebulization (10,000 units in 3 ml saline
4th hourly) is also useful.
▪ N-acetylcysteine nebulization—20% in 3 ml saline 4th hourly, bronchodilators like
albuterol 2nd hourly is very useful. Hypertonic saline inhalation induces the effective
coughing to remove casts. Racemic epinephrine is used to reduce mucosal
oedema.
▪ Monitoring the patient with arterial blood gas analysis regularly.
 CHEMICAL BURN
▪ In chemical burns, tissue destruction is more and progressive. It is always a deep
burn.
▪ Acid burn occurs in skin, soft tissues and GIT.
▪ In GIT, it is common in stomach either due to nitric acid or sulphuric acid which may
lead to severe gastritis or pyloric stenosis.
▪ Acidemia should be corrected by IV sodium bicarbonate.
▪ Hydrofluoric acid is commonly used in industrial areas.
▪ It is strongest inorganic acid that can produce corrosion and dehydration.
▪ It chelates blood calcium causing hypocalcemia and arrhythmias.
▪ It is managed with water irrigation, application of 2.5% calcium gluconate gel at 15
minutes interval, local intradermal and intra-arterial injection of 10% calcium
gluconate.
▪ Continuous cardiac monitoring, IV calcium gluconate or calcium chloride
administration is needed
 CHEMICAL BURN
▪ Alkali burns occur in oral cavity and oesophagus which leads to multiple
esophageal strictures.
▪ Sodium hydroxide, lime, potassium hydroxide and bleach are common alkalis
involved.
▪ They cause saponification of fat, fluid loss, release of alkali proteinates and
hydroxide ions which are toxic.
▪ External chemical burns are always deep and cause extensive disfigurement with
cosmetic problems.
▪ Initial treatment is dilution with water (Hydro therapy). It is done using 15-20 liters
of running tap water.
▪ Neutralization with antidote should never be done at initial phase of treatment as it
creates exothermic reaction which aggravates the tissue damage.
▪ Late neutralization is done, if required by 0.2% acetic acid in alkali burns, sodium
bicarbonate, calcium gluconate 10% gel, topical ziphrin solution in acid burns.
 TREATMENT
▪ Treatment should always be with hospitalization.
▪ Mannitol diuresis, hemodialysis, calcium gluconate IV, pain relief, serum electrolyte
management, TPN, ventilator support are systemic management required.
▪ Late treatment is reconstruction of the face.
▪ Esophageal dilatation or colonic transposition is done for esophageal stricture due
to alkali burn.
▪ Gastrojejunostomy is done for acid induced pyloric stenosis.
▪ Tar burns are treated additionally with neosprin which contains Tween-80 emulsifier
of tar.
▪ Cement is calcium oxide alkali. Its burn is due to hydroxyl ion which is often deep.
▪ Treatment is removal of cloth, irrigation with water, keeping pH below 8. Often it may
form eschar.
 IONIZING RADIATION INJURY
▪ These injuries can be divided into groups depending on whether radiation exposure
was to the whole body or localized.
▪ If this damage have caused an ulcer, then excision and coverage with vascularized
tissue is required.
▪ Whole-body radiation causes a large number of symptoms and may be fatal.
▪ A patient who has suffered whole-body irradiation and has acute desquamation of
the skin has received a lethal dose of radiation causes slow death.
▪ Non-lethal radiation has a number of systemic effects related to the gut mucosa
and immune system dysfunction.
▪ Other than giving iodine tablets, the management of these injuries is supportive.
 COLD INJURY
▪ Cold injuries are principally divided into two types:
▪ acute cold injuries from industrial accidents
▪ frostbite.
▪ Exposure to liquid petroleum gas (LPG), liquid nitrogen and other such liquids will
cause epidermal and dermal destruction.
▪ The tissue is more resistant to cold injury than to heat injury, and the inflammatory
reaction is not as marked.

▪ The assessment of depth of injury is more difficult, so it is rare to make the decision
for surgery early.

▪ Frostbite injuries affect the peripheries in cold climates.

▪ The initial treatment is with rapid rewarming in a bath at 42°C.

▪ The cold injury produces delayed microvascular damage similar to that of
ischemia–reperfusion injury.
▪ The level of damage is difficult to assess, and surgery usually does not play a role in
its management, which is conservative, until there is absolute demarcation of the
level of injury.