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BURNS
Defination : A burn is a wound in which there is
coagulative necrosis of the tissue.
The various types of burns are as follows ;
1 . ORDINARY BURNS – are usually caused by dry heat with fire, open
flame, hot metal or aeroplane crash in civil life and bomb injuries in war
time.
2. SCALDS are caused by moist heat e.g. Hot liquid or steam.
3. ELECTRIC BURNS.— Low-voltage electrical sources produce direct injury
at the point of contact.
- most commonly skin and subcutaneous tissue.
- high voltage not only injury to the point of contact but also damage to
the tissue by tharmal burn.
- Majority of electric bums are caused by high-voltage electric current.
4. CHEMICAL BURN is caused by strong acid or base which comes in contact with skin
or any other tissue.
- severity of the damage concentration of chemical, duration of contact , amount
of chemical
5. RADIATION BURNS are usually caused by X-rays or radium.
- This is in fact a type of inflammation of the skin which can be regarded as burn.
Include in freezing and non freezing.
6. COLD BURNS are caused by exposure to cold
Ex. Chilblain , trench foot
- FROSTBITE results in actual freezing of tissues with the formation of ice crystals.
- Mostly commonly skin and subcutaneous tissue of the hands, feet, ears and nose
are affected.
Pathology:-
• Divided into two parts:-
A. LOCAL CHANGES
B. SYSTEMIC CHANGES
A.Local Changes:-
• These can be described under 4 change:-
1. Severity of burn,
2. The extent of burn,
3. Vascular changes and
4. Infection.
1.Severity of burns:-
• Burns are classified into 3 grades or degrees according to the depth of necrosis.
1. first-degree burn in involved superficial layers of the epidermis , hyperaemia
of the skin with slight oedema of the epidermis.
- healing of the few days. Replace to the epithelium layer , so That is not
scaring.
- avoids further exposure to source of heat
2. Second degree burn in involved superficial layer of epidermis and first part of
dermis layer, hyperaemia of the skin with Blebs or vesicles are formed
between the separating epidermis and dermis.
3. third-degree burn there is complete destruction of the
epidermis and dermis with including the sensory nerves.
• Second and third degree burn in skin grafting required.
• Another type of classification 1. Partial thickness of burn, 2. Full thickness of
burn.
1. Partial thickness of burn – in burn only superficial layer of the skin ,e.g.
The whole of epidermis and sometimes the superficial part of the dermis become
destroy.
Surrounding the hair follicles or sweat glands from which regeneration of
epithelial cell may take place.
-skin grafting is not necessary.
2. Full thickness of burn – in whole superficial layer of epidermis and dermis
layer are complete destroyed.
- Development of scar. Skin grafting is required.
- As sensory nerves are also destroyed in full thickness burn , sensation is lost.
2.Extent of burn:-
• The length and width of the burn wound is expressed as a
percentage of the total surface area displaying either second or
third-degree burn.
• The extent of burn is most commonly estimated by the
‘rule of nines’.
• Rule of nines’ for estimating percentage of body surface involved in bums
are as follows:—
• Anatomic area Percentage of body surface
Head, face and neck 9%
Right upper extremity 9%
Left upper extremity 9%
Right lower extremity (thigh – 9%, leg and foot-9%) 18%
Left lower extremity 18%
Anterior trunk ( chest – 9%, abdomen – 9% ) 18%
Posterior trunk ( upper half – 9%, lower half – 9%) 18%
External genitalia 1%
3.Vascular Changes:-
• There is dilation of large vessels due to direct
injury of vessels wall and local liberation of
histamine that increases the blood flow to the
injured part.
• Due to inflammatory changes in burn area the
capillary permeability increases in great extent so a
large amount of fluid exudate in blisters along with
plasma protein. Body losses a good amount of
plasma protein to cause hypoproteinemia in large
body surface area burn.
• Later on these blisters dried and forms the brown
crust which protects the wound.
Crust
4.Infection:-
• As we know the skin is our first line protection from
infection, so in second and third degree burn skin is
destroyed so these burn always have great risk of
infection.
• Because of malnutrition, loss of plasma protein,
blood volume and anemia body’s defense mechanism
become week to resist any infection.
• Burn patient should kept in special design burn ward
in sterilized environment to protects from infection.
B.SYSTEMIC CHANGES:-
1. Shock
2. Biochemical Changes
3. Changes in blood
4. Systemic lesions
1.Shock:-
• This is the most important effect of bums.
• Various types of shock are come across in burns such as
1. Oligaemic shock
2. Neurogenic shock
3. Cardiogenic shock
4. Bacteriaemic shock
1. Oligaemic shock:-
• The direct effect of heat as well as liberation of vasoactive materials from the area of
injury increases capillary permeability, which permits loss of fluid and protein from
the intravascular compartment into the extravascular tissue. These volume shifts occur
in direct proportion to the extent of burn and are clinically apparent as oedema and
blebs.
• Owing to the outpouring of fluid there is remarkable concentration of blood as shown
by haemoglobin concentration. This leads to olegaemic shock and oxygen starvation of
the tissues.
• The intense heat destroys the red blood cells and causes haemolysis which may be
massive and accompanied by haemoglobinuria.
• These factors may result in ischaemia of important organs particularly the liver and
kidney, so that acidosis and uraemia may develop.
• This leads to stimulation of adrenal cortex with immediate rise in urinary excretion of
17-Ketosteroids.
2. Neurogenic shock :-due to severe pain and apprehension.
3. Cardiogenic shock:- Cardiac output falls in the early postbum
period initially as a result of marked increase in peripheral
resistance and later on as a result of decreased blood volume and
also increased viscosity. The increase in blood viscosity results from
the combined effect of increased haematocrit and aggregation of
red cells, white cells and platelets.
4. Bacteriaemic shock is mainly due to infection and release of toxic
material absorbed from the burnt area.
2.Biochemical changes:-
1. Electrolyte imbalance becomes obvious in the form of low sodium
and chloride concentration and high potassium level in the blood.
2. Hypoproteinaemia is obvious due to excessive loss of plasma
protein.
3. Hyperglycemia may often develop.
4. There will be rise in blood urea and creatinine level due to
kidney damage in extensive burns.
3.Changes in Blood:-
1.Haemoconcentration is due to outpouring of serum and Haemoglobin
level may rice to 150% in severe burns.
2.Increase number in the Red cell is also due to outpouring of plasma.
3. Sludging of blood may occur due to intravascular agglutination of RBCs
4. There is sudden fall in the Eosinophil count during The first 12 hours is
very characteristics of burn , in the course of 24 hour the count should
begin to rise may give an indication to the prognosis of case.
5. Aggregation of red cell , white cell and platelet is common finding in
burns and it increases blood viscosity.
6. Anemia due to immediate red cell destruction in the early post burn
period and there is also continuous red cell loss during first 5 to 7 postburn
days . And 8 to 12% loss of red cell mass per day is general measurement.
7. Alteration of the coagulation system is also seen in burns and there is
early marked decreased level of platelets and fibrinogen level.
4.Systemic Lesions:-
1. The liver may show numerous area of focal necrosis. In the necrotic areas the cells may
contain intranuclear inclusion which is only bordered by nuclear membrane. In majority of
cases of burns is detected with liver necrosis.
2. Kidney is often involved due to low blood perfusion. In severe cases there may be
haemoglobinuria. Gradually oliguria and Anuria may develop and patient may die of
uraemia.
3. Adrenal glands become slightly enlarged. In severe burns there mat be petechial
haemorrhages and small areas of focal necrosis. In the post mortem examination. there may
find shrunken glands with necrosis and haemorrhage.
4. Gastrointestinal tract also respond to burn injury. Gastric and duodenal mucosal changes
indicative of focal ischamia observed as early as 3 to 5 hours after burns. This is due to less
mucosal blood flow. Acute ulceration of the stomach and duodenum has been noticed as a
common complication of major thermal injury. These ulcer were first described by Curling in
1842. Acute ulceration of the colon has been appeared in severe burns patients.
5. Alteration of pulmonary functions:-The actual changes in pulmonary function
following burns are hyperventilation and pulmonary insufficiency which may e
require of mechanical ventilators support .
6. A change in endocrine pattern is seen in burn patient. There is elevated
glucagon , cortisol and catechplamine levels. Insulin and triiodothyronin levels are
depressed. These cause a change in metabolic rate , glucose flow and negative
nitrogen balance.
7. Neurogenic changes are not commonly seen in burn injuries. There may be
some delirium and disorientation due to less blood flow to brain. Specifically
neurological changes are most commonly seen in patient with high voltage
electrical burn.
8. Immunologic impairment is often seen in patient with burns over 50% of total
body surface. And in this condition this patient is having high chances of
infection. There is depression of the immunoglobulin level in the early postburn
period. There is lymphocytes level is also depressed with decreased in T cells and
increased in B cells.
• This is conveniently described under three headings:-
I. Treatment of shock,
II. General treatment and
III. Local treatment of burn wound.
Treatment:-
I. Treatment of Shock:-
• 1. Sedation.—
• Sedative and analgesic medications are required in burn patients.
• Sedatives should be given during the first 4 to 5 days by intravenous
route and at an absolute minimum dosage.
• The dosage should be minimal to prevent depression of cardiopulmonary
function and to allow evaluation of the sense of the patient.
• The dosage is reduced markedly after 48 hours.
• Barbiturates are preferred in the case of children.
• 2. Fluid resuscitation.—
• Indications: -in all adults with burns of 15% or more
-in children with burns above 10%
• Blood transfusion is required when burns involve more than 20% of full thickness
or 40% of partial thickness of total body surface.
• There is conflict of interest for:
use of colloid containing fluid during first 24 hours as it is not retained within the
circulation and exerts greater restorative effect on cardiac output than an equal.
volume of colloid-free electrolyte containing fluid such as Ringer's lactate solution.
• Studies have shown that the colloid solutions not only restore cardiac output more
rapidly but also is more efficient in adequate organ perfusion due to more rapid
replacement of plasma volume deficits.
• Moore’s Formula:
• In 1st 24 hours: Ringer's lactate solution is given 1000 to 4000 ml and
normal saline 1000 ml, 5% dextrose solution 1500 to 5000 ml and colloid-
containing fluid in the form of plasma or plasma substitutes 7.5% of body
weight.
• In 2nd 24 hours: Ringer's lactate solution is given 1000 to 4000 ml and
normal saline 1000 ml, 5% dextrose solution 1500 to 5000 ml and colloid-
containing fluid in the form of plasma or plasma substitutes 2.5% of body
weight.
• Evan’s Formula:
• In 1st 24 hours normal saline is given 1 ml/kg/% burn, 2000 ml of 5%
dextrose and colloid-containing fluid 1 ml/kg/% burn.
• In 2nd 24 hours normal saline is given Vi the amount of 1st 24 hours
requirement, colloid-containing fluid is also given the Vi the requirement
of 1st 24 hours, whereas 5% dextrose is given 2000 ml.
• The rate and amount of transfusion are assessed by:
• -repeated red cell volume and haematocrit estimations
• -hourly monitoring of vital signs
• -general condition
• -urinary output.
• Urinary output is a good reflection of adequacy of resuscitation.
• Patients usually do not require any diuretic except in 4 categories —
(i) high voltage electrical burn
(ii) associated mechanical soft tissue injury
(iii)deep burns involving muscles
(iv) extensive burns
• In first 3 conditions there is chance of heavy loads of haemochromogens
in urine and are prone to develop acute renal failure unless the urine
output is maintained with diuretic.
• Fluid should be infused at the rate needed to achieve an hourly urinary
output of 75 ml to 100 ml.
• 3. Maintenance of airway.—
• Patients with burns exhibit signs and symptoms of hypoxia.
• It ranges from pronounced tachypnoea to respiratory arrest and coma.
• Diagnosis confirmed by analysing the concentration of carbon dioxide in the blood.
• Treatment:
1. Ventilatory support.
2. Endotracheal intubation
3. Tracheostomy
II. General Treatment:-
• These include —
1. Escharotomy and fasciotomy,
2. Tetanus prophylaxis,
3. Antibiotics,
4. Nutritional support,
5. Gastric decompression and
6. Treatment of G.I. complications.
1.Escharotomy and fasciotomy:-
• Eschar: an unyieldingcrust formed due to circumferential third-degree or full thickness burns of the extremities or
thoracicwall.
• It exerts pressure on the blood vessels causingdiminished peripheralpulses and decreased skin temperature with
oedema.
• The clinical signs includes:
- cyanosis
- impaired capillaryrefilling
- progressiveneurologicsigns (paresthesia).
• Indication:Restriction ofchest wall motion to the point at which ventilatory
exchange is impaired.
• Escharotomyis performed as a ward procedure without anaesthesia
• The eschar, which is insensitive,is incised on either midlateral or midmedial line.
• The incision shouldextend alongthe entire length of the burned area and carried down deep through the eschar and
the superficial fascia to a depth sufficient to allowthe cut edges of the eschar to separate.
• The bleedingis usuallyminimal and can be controlled byelectrocoagulation.
• Coveringthe escharotomywound with a topical antimicrobial agent is essential.
• Fasciotomy is indicated when escharotomy may not result in improvement of blood flow
to the peripheral part. In these cases fasciotomy is required.
• Fasciotomy is performed under general anaesthesia and the fascia of all involved
compartments is adequately released.
• It is indicated in severe bums with extensive damage to the underlying fat and muscles.
• Also required in the treatment of electrical bums where there is
extensive muscle injury
2.Tetanus prophylaxis:-
• All burn injuries should be considered contaminated and tetanus
prophylaxis is obligatory. Intramuscular administration of tetanus
toxoid in the dose of 0.5 ml usually provides adequate
prophylaxis.
3.Antibiotics:-
• In burns, microorganisms contaminate the wound. These organisms
will proliferate if topical chemotherapeutic agents are not
applied. Usually gram-positive organisms colonize in the burn
wounds.
• The most common site of involvement in the burn patient is the
lungs. Bronchopneumonia in burn patients is commonly caused by
opportunistic organisms especially gram-negative bacteria.
• Bronchial secretions should be cultured and antibiotic treatment is
begun on the basis of the sensitivity test.
4.Nutritional Support:-
• In case of all major injuries increased metabolism or
hypermetabolism takes place.
• Such hypermetabolism is also manifested by increased oxygen
consumption, elevated cardiac output, increased core
temperature, wasting of body mass and increased urinary nitrogen
excretion.
III. LOCAL TREATMENT:-
1. First aid measure
2. Wound care
• Open method
• Closed method
3. Skin grafting
4. Physiotherapy and Rehabilitation
1. First Aid Measure:-
• The patient should be immediately removed from source of heat.
• Cold clean water should be applied to the burned area
immediately and is continued every 5 minutes.
2. Burn Wound Care:-
• After proper resuscitation, attention should be directed to the
burn wound.
• It should be cleansed with a surgical detergent and all loose
nonviable skin should be trimmed away.
• Silver nitrate must be used soon after injury, before bacteria have
proliferated on the wound.
3.Skin Grafting:-
• The goal of burn wound care is the timely closure of burn wound.
4.Physiotherapy and Rehabilitation:-
• The major local problem of burns is formation of contractures and
deformities.
Complications of Thermal Burn:-
1. Curling Ulcer :-
• Curling’s ulcers are often multiple and are found simultaneously
in the stomach and duodenum.
• Until the burn wound is healed, 30 ml antacid is administered
each hour through nasogastric tube to maintain the gastric pH
above 5.
2. Acute Pancreatitis:-
• The peculiarity is that the abdominal pain is often absent and this
condition is only suggested by increasing fluid requirement and new
onset of hyperglycaemia.
3. Acute acalculous cholecystitis:-
• This complication occurs occasionally in burned patients in two forms.
• In one form, the gallbladder is infected by haematogenous seeding from
a primary source in the septic burn wound.
• The other presentation occurs in critically ill patients with marked
dehydration, ileus, hypematraemia and hyperosmolarity.

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Burns.pdf

  • 2. Defination : A burn is a wound in which there is coagulative necrosis of the tissue. The various types of burns are as follows ; 1 . ORDINARY BURNS – are usually caused by dry heat with fire, open flame, hot metal or aeroplane crash in civil life and bomb injuries in war time. 2. SCALDS are caused by moist heat e.g. Hot liquid or steam. 3. ELECTRIC BURNS.— Low-voltage electrical sources produce direct injury at the point of contact. - most commonly skin and subcutaneous tissue. - high voltage not only injury to the point of contact but also damage to the tissue by tharmal burn. - Majority of electric bums are caused by high-voltage electric current.
  • 3. 4. CHEMICAL BURN is caused by strong acid or base which comes in contact with skin or any other tissue. - severity of the damage concentration of chemical, duration of contact , amount of chemical 5. RADIATION BURNS are usually caused by X-rays or radium. - This is in fact a type of inflammation of the skin which can be regarded as burn. Include in freezing and non freezing. 6. COLD BURNS are caused by exposure to cold Ex. Chilblain , trench foot - FROSTBITE results in actual freezing of tissues with the formation of ice crystals. - Mostly commonly skin and subcutaneous tissue of the hands, feet, ears and nose are affected.
  • 4. Pathology:- • Divided into two parts:- A. LOCAL CHANGES B. SYSTEMIC CHANGES
  • 5. A.Local Changes:- • These can be described under 4 change:- 1. Severity of burn, 2. The extent of burn, 3. Vascular changes and 4. Infection.
  • 6. 1.Severity of burns:- • Burns are classified into 3 grades or degrees according to the depth of necrosis. 1. first-degree burn in involved superficial layers of the epidermis , hyperaemia of the skin with slight oedema of the epidermis. - healing of the few days. Replace to the epithelium layer , so That is not scaring. - avoids further exposure to source of heat 2. Second degree burn in involved superficial layer of epidermis and first part of dermis layer, hyperaemia of the skin with Blebs or vesicles are formed between the separating epidermis and dermis. 3. third-degree burn there is complete destruction of the epidermis and dermis with including the sensory nerves. • Second and third degree burn in skin grafting required.
  • 7. • Another type of classification 1. Partial thickness of burn, 2. Full thickness of burn. 1. Partial thickness of burn – in burn only superficial layer of the skin ,e.g. The whole of epidermis and sometimes the superficial part of the dermis become destroy. Surrounding the hair follicles or sweat glands from which regeneration of epithelial cell may take place. -skin grafting is not necessary. 2. Full thickness of burn – in whole superficial layer of epidermis and dermis layer are complete destroyed. - Development of scar. Skin grafting is required. - As sensory nerves are also destroyed in full thickness burn , sensation is lost.
  • 8. 2.Extent of burn:- • The length and width of the burn wound is expressed as a percentage of the total surface area displaying either second or third-degree burn. • The extent of burn is most commonly estimated by the ‘rule of nines’.
  • 9. • Rule of nines’ for estimating percentage of body surface involved in bums are as follows:— • Anatomic area Percentage of body surface Head, face and neck 9% Right upper extremity 9% Left upper extremity 9% Right lower extremity (thigh – 9%, leg and foot-9%) 18% Left lower extremity 18% Anterior trunk ( chest – 9%, abdomen – 9% ) 18% Posterior trunk ( upper half – 9%, lower half – 9%) 18% External genitalia 1%
  • 10. 3.Vascular Changes:- • There is dilation of large vessels due to direct injury of vessels wall and local liberation of histamine that increases the blood flow to the injured part. • Due to inflammatory changes in burn area the capillary permeability increases in great extent so a large amount of fluid exudate in blisters along with plasma protein. Body losses a good amount of plasma protein to cause hypoproteinemia in large body surface area burn. • Later on these blisters dried and forms the brown crust which protects the wound. Crust
  • 11. 4.Infection:- • As we know the skin is our first line protection from infection, so in second and third degree burn skin is destroyed so these burn always have great risk of infection. • Because of malnutrition, loss of plasma protein, blood volume and anemia body’s defense mechanism become week to resist any infection. • Burn patient should kept in special design burn ward in sterilized environment to protects from infection.
  • 12. B.SYSTEMIC CHANGES:- 1. Shock 2. Biochemical Changes 3. Changes in blood 4. Systemic lesions
  • 13. 1.Shock:- • This is the most important effect of bums. • Various types of shock are come across in burns such as 1. Oligaemic shock 2. Neurogenic shock 3. Cardiogenic shock 4. Bacteriaemic shock
  • 14. 1. Oligaemic shock:- • The direct effect of heat as well as liberation of vasoactive materials from the area of injury increases capillary permeability, which permits loss of fluid and protein from the intravascular compartment into the extravascular tissue. These volume shifts occur in direct proportion to the extent of burn and are clinically apparent as oedema and blebs. • Owing to the outpouring of fluid there is remarkable concentration of blood as shown by haemoglobin concentration. This leads to olegaemic shock and oxygen starvation of the tissues. • The intense heat destroys the red blood cells and causes haemolysis which may be massive and accompanied by haemoglobinuria. • These factors may result in ischaemia of important organs particularly the liver and kidney, so that acidosis and uraemia may develop. • This leads to stimulation of adrenal cortex with immediate rise in urinary excretion of 17-Ketosteroids.
  • 15. 2. Neurogenic shock :-due to severe pain and apprehension. 3. Cardiogenic shock:- Cardiac output falls in the early postbum period initially as a result of marked increase in peripheral resistance and later on as a result of decreased blood volume and also increased viscosity. The increase in blood viscosity results from the combined effect of increased haematocrit and aggregation of red cells, white cells and platelets. 4. Bacteriaemic shock is mainly due to infection and release of toxic material absorbed from the burnt area.
  • 16. 2.Biochemical changes:- 1. Electrolyte imbalance becomes obvious in the form of low sodium and chloride concentration and high potassium level in the blood. 2. Hypoproteinaemia is obvious due to excessive loss of plasma protein. 3. Hyperglycemia may often develop. 4. There will be rise in blood urea and creatinine level due to kidney damage in extensive burns.
  • 17. 3.Changes in Blood:- 1.Haemoconcentration is due to outpouring of serum and Haemoglobin level may rice to 150% in severe burns. 2.Increase number in the Red cell is also due to outpouring of plasma. 3. Sludging of blood may occur due to intravascular agglutination of RBCs 4. There is sudden fall in the Eosinophil count during The first 12 hours is very characteristics of burn , in the course of 24 hour the count should begin to rise may give an indication to the prognosis of case. 5. Aggregation of red cell , white cell and platelet is common finding in burns and it increases blood viscosity. 6. Anemia due to immediate red cell destruction in the early post burn period and there is also continuous red cell loss during first 5 to 7 postburn days . And 8 to 12% loss of red cell mass per day is general measurement. 7. Alteration of the coagulation system is also seen in burns and there is early marked decreased level of platelets and fibrinogen level.
  • 18. 4.Systemic Lesions:- 1. The liver may show numerous area of focal necrosis. In the necrotic areas the cells may contain intranuclear inclusion which is only bordered by nuclear membrane. In majority of cases of burns is detected with liver necrosis. 2. Kidney is often involved due to low blood perfusion. In severe cases there may be haemoglobinuria. Gradually oliguria and Anuria may develop and patient may die of uraemia. 3. Adrenal glands become slightly enlarged. In severe burns there mat be petechial haemorrhages and small areas of focal necrosis. In the post mortem examination. there may find shrunken glands with necrosis and haemorrhage. 4. Gastrointestinal tract also respond to burn injury. Gastric and duodenal mucosal changes indicative of focal ischamia observed as early as 3 to 5 hours after burns. This is due to less mucosal blood flow. Acute ulceration of the stomach and duodenum has been noticed as a common complication of major thermal injury. These ulcer were first described by Curling in 1842. Acute ulceration of the colon has been appeared in severe burns patients.
  • 19. 5. Alteration of pulmonary functions:-The actual changes in pulmonary function following burns are hyperventilation and pulmonary insufficiency which may e require of mechanical ventilators support . 6. A change in endocrine pattern is seen in burn patient. There is elevated glucagon , cortisol and catechplamine levels. Insulin and triiodothyronin levels are depressed. These cause a change in metabolic rate , glucose flow and negative nitrogen balance. 7. Neurogenic changes are not commonly seen in burn injuries. There may be some delirium and disorientation due to less blood flow to brain. Specifically neurological changes are most commonly seen in patient with high voltage electrical burn. 8. Immunologic impairment is often seen in patient with burns over 50% of total body surface. And in this condition this patient is having high chances of infection. There is depression of the immunoglobulin level in the early postburn period. There is lymphocytes level is also depressed with decreased in T cells and increased in B cells.
  • 20. • This is conveniently described under three headings:- I. Treatment of shock, II. General treatment and III. Local treatment of burn wound. Treatment:-
  • 21. I. Treatment of Shock:- • 1. Sedation.— • Sedative and analgesic medications are required in burn patients. • Sedatives should be given during the first 4 to 5 days by intravenous route and at an absolute minimum dosage. • The dosage should be minimal to prevent depression of cardiopulmonary function and to allow evaluation of the sense of the patient. • The dosage is reduced markedly after 48 hours. • Barbiturates are preferred in the case of children.
  • 22. • 2. Fluid resuscitation.— • Indications: -in all adults with burns of 15% or more -in children with burns above 10% • Blood transfusion is required when burns involve more than 20% of full thickness or 40% of partial thickness of total body surface. • There is conflict of interest for: use of colloid containing fluid during first 24 hours as it is not retained within the circulation and exerts greater restorative effect on cardiac output than an equal. volume of colloid-free electrolyte containing fluid such as Ringer's lactate solution. • Studies have shown that the colloid solutions not only restore cardiac output more rapidly but also is more efficient in adequate organ perfusion due to more rapid replacement of plasma volume deficits.
  • 23. • Moore’s Formula: • In 1st 24 hours: Ringer's lactate solution is given 1000 to 4000 ml and normal saline 1000 ml, 5% dextrose solution 1500 to 5000 ml and colloid- containing fluid in the form of plasma or plasma substitutes 7.5% of body weight. • In 2nd 24 hours: Ringer's lactate solution is given 1000 to 4000 ml and normal saline 1000 ml, 5% dextrose solution 1500 to 5000 ml and colloid- containing fluid in the form of plasma or plasma substitutes 2.5% of body weight.
  • 24. • Evan’s Formula: • In 1st 24 hours normal saline is given 1 ml/kg/% burn, 2000 ml of 5% dextrose and colloid-containing fluid 1 ml/kg/% burn. • In 2nd 24 hours normal saline is given Vi the amount of 1st 24 hours requirement, colloid-containing fluid is also given the Vi the requirement of 1st 24 hours, whereas 5% dextrose is given 2000 ml.
  • 25. • The rate and amount of transfusion are assessed by: • -repeated red cell volume and haematocrit estimations • -hourly monitoring of vital signs • -general condition • -urinary output. • Urinary output is a good reflection of adequacy of resuscitation.
  • 26. • Patients usually do not require any diuretic except in 4 categories — (i) high voltage electrical burn (ii) associated mechanical soft tissue injury (iii)deep burns involving muscles (iv) extensive burns • In first 3 conditions there is chance of heavy loads of haemochromogens in urine and are prone to develop acute renal failure unless the urine output is maintained with diuretic. • Fluid should be infused at the rate needed to achieve an hourly urinary output of 75 ml to 100 ml.
  • 27. • 3. Maintenance of airway.— • Patients with burns exhibit signs and symptoms of hypoxia. • It ranges from pronounced tachypnoea to respiratory arrest and coma. • Diagnosis confirmed by analysing the concentration of carbon dioxide in the blood. • Treatment: 1. Ventilatory support. 2. Endotracheal intubation 3. Tracheostomy
  • 28. II. General Treatment:- • These include — 1. Escharotomy and fasciotomy, 2. Tetanus prophylaxis, 3. Antibiotics, 4. Nutritional support, 5. Gastric decompression and 6. Treatment of G.I. complications.
  • 29. 1.Escharotomy and fasciotomy:- • Eschar: an unyieldingcrust formed due to circumferential third-degree or full thickness burns of the extremities or thoracicwall. • It exerts pressure on the blood vessels causingdiminished peripheralpulses and decreased skin temperature with oedema. • The clinical signs includes: - cyanosis - impaired capillaryrefilling - progressiveneurologicsigns (paresthesia). • Indication:Restriction ofchest wall motion to the point at which ventilatory exchange is impaired. • Escharotomyis performed as a ward procedure without anaesthesia • The eschar, which is insensitive,is incised on either midlateral or midmedial line. • The incision shouldextend alongthe entire length of the burned area and carried down deep through the eschar and the superficial fascia to a depth sufficient to allowthe cut edges of the eschar to separate. • The bleedingis usuallyminimal and can be controlled byelectrocoagulation. • Coveringthe escharotomywound with a topical antimicrobial agent is essential.
  • 30. • Fasciotomy is indicated when escharotomy may not result in improvement of blood flow to the peripheral part. In these cases fasciotomy is required. • Fasciotomy is performed under general anaesthesia and the fascia of all involved compartments is adequately released. • It is indicated in severe bums with extensive damage to the underlying fat and muscles. • Also required in the treatment of electrical bums where there is extensive muscle injury
  • 31. 2.Tetanus prophylaxis:- • All burn injuries should be considered contaminated and tetanus prophylaxis is obligatory. Intramuscular administration of tetanus toxoid in the dose of 0.5 ml usually provides adequate prophylaxis.
  • 32. 3.Antibiotics:- • In burns, microorganisms contaminate the wound. These organisms will proliferate if topical chemotherapeutic agents are not applied. Usually gram-positive organisms colonize in the burn wounds. • The most common site of involvement in the burn patient is the lungs. Bronchopneumonia in burn patients is commonly caused by opportunistic organisms especially gram-negative bacteria. • Bronchial secretions should be cultured and antibiotic treatment is begun on the basis of the sensitivity test.
  • 33. 4.Nutritional Support:- • In case of all major injuries increased metabolism or hypermetabolism takes place. • Such hypermetabolism is also manifested by increased oxygen consumption, elevated cardiac output, increased core temperature, wasting of body mass and increased urinary nitrogen excretion.
  • 34. III. LOCAL TREATMENT:- 1. First aid measure 2. Wound care • Open method • Closed method 3. Skin grafting 4. Physiotherapy and Rehabilitation
  • 35. 1. First Aid Measure:- • The patient should be immediately removed from source of heat. • Cold clean water should be applied to the burned area immediately and is continued every 5 minutes.
  • 36. 2. Burn Wound Care:- • After proper resuscitation, attention should be directed to the burn wound. • It should be cleansed with a surgical detergent and all loose nonviable skin should be trimmed away. • Silver nitrate must be used soon after injury, before bacteria have proliferated on the wound.
  • 37. 3.Skin Grafting:- • The goal of burn wound care is the timely closure of burn wound.
  • 38. 4.Physiotherapy and Rehabilitation:- • The major local problem of burns is formation of contractures and deformities.
  • 39. Complications of Thermal Burn:- 1. Curling Ulcer :- • Curling’s ulcers are often multiple and are found simultaneously in the stomach and duodenum. • Until the burn wound is healed, 30 ml antacid is administered each hour through nasogastric tube to maintain the gastric pH above 5.
  • 40. 2. Acute Pancreatitis:- • The peculiarity is that the abdominal pain is often absent and this condition is only suggested by increasing fluid requirement and new onset of hyperglycaemia. 3. Acute acalculous cholecystitis:- • This complication occurs occasionally in burned patients in two forms. • In one form, the gallbladder is infected by haematogenous seeding from a primary source in the septic burn wound. • The other presentation occurs in critically ill patients with marked dehydration, ileus, hypematraemia and hyperosmolarity.