This document discusses burns rehabilitation. It covers the management of burns in a burns unit, the pathophysiology of burns including effects on the airway, lungs, metabolism, and circulation. It describes complications like infection, contractures, and how burns are assessed and classified. Treatment involves wound care, skin grafting, splinting and rehabilitation to prevent deformities and promote mobility.

1. BURNS REHABLITATION

2. INTRODUCTION
• BURNS AFFFECT THE SKIN DIRECTLY AND
OTHER SYSTEMS INDIRECTLY
• ACUTE PHASE REHAB AND CHRONIC PHASE
REHAB

4. BURN UNIT
• The management of the major burn injury
represents a significant challenge to every
member of the burns team – burns
doctors,surgeons, anaesthetists, ward and
theatre nurses, physiotherapists, occupational
therapists, dietitians, bacteriologists,
physicians, psychiatrists, psychologists and the
any ancillary staff whose cleaning and supply
services are vital to the successful running of a
burns unit

6. PATHOPHYSIOLOGY OF BURNS
INJURY TO THE AIRWAY AND LUNGS
• Physical burn injury to the airway above the
larynx
• Physical burn injury to the airway below the
larynx--
Steam has a large latent heat of evaporation andcan
cause thermal damage to the lower airway. In
such injuries,the respiratory epithelium rapidly
swells and detaches from the bronchial tree. This
creates casts, which can block the main upper
airway

7. Pathophysiology of burns
• Metabolic poisoning
• Carbon monoxide Carbon monoxide binds to
haemoglobin with an affinity 240 times
greater than that of oxygen and therefore
blocks the transport of oxygen.
• Hydrogen cyanide, which causes a metabolic
acidosis by interfering with mitochondrial
respiration.

8. Inhalational injury
• Chemical pneumonitis causes oedema within the
alveolar sacs and decreasing gaseous exchange
over the ensuing 24 hours, and often gives rise to
a bacterial pneumonia
• This most often decides the mortality of the
patient
Mechanical block on rib movement
• Burned skin is very thick and stiff, and this can
physically stop the ribs moving if there is a large
full-thickness burn across thechest.

10. Inflammation and circulatory changes
The changes occur because burned skin activates a
web of inflammatory cascades.
The release of neuropeptides and the activation of
complement are initiated by the stimulation of
pain fibres and the alteration of proteins by heat.
The activation of Hageman factor initiates a
number of protease driven cascades, altering the
arachidonic acid, thrombin and kallikrein
pathways.

11. Inflammatory and circulatory changes
• At a cellular level, complement causes the degranulation of mast
cells and coats the proteins altered by the burn. This attracts
neutrophils, which also degranulate, with the release of large
quantities of free radicals and proteases. These can, in turn, cause
further damage to the tissue. Mast cells also release primary
cytokines such as tumour necrosis factor alpha (TNF-α). These act
as chemotactic agents to inflammatory cells and cause the
subsequent release of many secondary cytokines. These
inflammatory factors alter the permeability of blood vessels such
that intravascular fluid escapes. The increase in permeability is such
that large protein molecules can also now escape with ease. The
damaged collagen and these extravasated proteins increase the
oncotic pressure within the burned tissue.

12. TBSA
• The overall effect of these changes is to produce a net
flow of water, solutes and proteins from the
intravascular to the extravascular space. This flow
occurs over the first 36 hours after the injury but does
not include red blood cells. As the burn size
approaches 10–15% of total body surface area (TBSA),
the loss of intravascular fluid can cause a level of
circulatory shock. With 25% of TBSA, the inflammatory
reaction causes fluid loss in vessels remote from the
burn injury. This is why such importance is attached to
measuring the TBSA involved in any burn. It dictates
the size of inflammatory reaction and therefore the
amount of fluid needed to control shock

13. • Cell-mediated immunity is significantly
reduced in large burns, leaving them more
susceptible to bacterial and fungal infections.
There are many potential sources of infection,
especially from the burn wound and from the
lung if this is injured, but also from any central
venous lines, tracheostomies or urinary
catheters present.

14. Changes to the intestine
• The inflammatory stimulus and shock can cause
microvascular damage and ischaemia to the gut
mucosa. This reduces gut motility and can prevent the
absorption of food.
• This process also increases the translocation of gut
bacteria, which can become an important source of
infection in large burns.
• Gut mucosal swelling, gastric stasis and peritoneal
oedema can also cause abdominal compartment
syndrome, which splints the diaphragm and increases
the airway pressures needed for respiration

15. • Danger to peripheral circulation In full-
thickness burns, the collagen fibres are
coagulated. The normal elasticity of the skin is
lost. A circumferential full-thickness burn to a
limb acts as a tourniquet as the limb swells. If
untreated, this will progress to limb-
threatening ischaemia and amputation

17. ASSESSMENT
• History
• Type and extent of burns
• Depth of burns –extent of neuro- muscular
and musculoskeletal damage
• Associated medical conditions
• Presence of injuries and medico legal issues

18. Pediatric burns vs adult burns
• Body surface area is smaller, hence even
minimal burns will have large systemic
manifestations
• Dehydration is more
• Temperature control is more difficult
• hypertrophic scarring is more severe
• In children mortality rate is high and
rehabilitation is more difficult

19. causes
• Heat—fire ,radiation,steam hot liquids -scalds
and contact with hot objects
• Suicidal attempts with kerosene
• Radiation burns –from nuclear reactors and
ultra violet light
• Light---sunlight burns
• Electrical—household and industry, lightening

21. classification
• First degree - superficial burns --
erythematous white plaque involving only the
epidermis eg sunburns come under this .It is
red and painful but heals spontaneously 3 to 7
days

22. Second degree burns
• Second degree burns( partial thickness burns)—
epidermis and the superficial dermis is involved up to the
deep layer of the dermis is involved—there is blistering of
the skin This blanches with pressure .The pain is due to the
viability of the nerve endings. Spontaneous healing occurs
in 7-21 days. Healing occurs from the edges of he wound.
Deep partial thickness burn heals with hypertrophic
scarring and usually requires grafting of the skin. This is
due to the destruction of the epidermis and the dermal
appendages

23. Third degree
• Third degree burns--- ( full thickness burns)
the entire epidermis is lost, there is damage to
the dermis and subcutaneous tissue, loss of
hair, burns are not painful due to loss of nerve
endings.usually requires grafting

24. 4th degree
• Fourth degree burns—damage to the deeper
tissues like muscles tendons and ligaments
causing charring and later on contractures

25. Complications of burns
• Hypovolemia due to loss of fluid and shock
esp when the degree of burns is more
• When the integrity of the skin is lost body
immunity is compromised
• Bacterial contamination of the wound can
occur leading to septicemia which can be fatal

26. complication contd
• Temperature regulation of the body is lost
• Airway obstruction and pneumonia
• Acute dilatation of the stomach and paralysis
of the intestine
• CONTRACTURES ---POST
BURNS CONTRACTURES
PBC occurs due to the elastic
connective tissue below the skin is replaced by
the thick fibrous tissue

27. CONTRACTURES ---POST BURNS CONTRACTURES
• It happens due the elastic tissue being replaced by the
inelastic fibrous tissue
• Permanent tightening of the skin
• Underlying tissues are resistant to stretching and
affected part can not be moved normally
• It occurs after healing of the scar-ie –healing with
fibrosis , thickening , and tightening
• This even though is normal wound healing it reduces
the range movement of the joints
• Hypertrophy of the scar producing keloids

28. Prevention of contractures
• Prevention
1-- during the healing stage ,pressure dressings are given
to the wound to prevent the hyper trophy of the scars
2 --surgical excision of the wound and skin grafting to
prevent excessive scar formation
* this is usually done 3 days after the burns esp in
full thickness non scald burns
* in children and adults
*in older patients and scald wounds it is better to
wait for 2 weeks before skin grafting
---burn wounds take longer time to heal

29. Management

30. Rule of Nine
* Face and scalp—9%
• Back---18%
• Front of chest—18%
• Front of upper limb---9%
• Back of upper limb----9%
• Front of leg---9%
• Back of leg—9%
• Perineum----1%

31. contd
• This helps to estimate the surface area of invt
and assess the amt of fluid loss—TBSA
• In children Lund and Browder chart is used
for calculation of the burn size
• Goal is to 1.promote wound healing and
prevent infection 2.To correct the fluid and
electrolyte imbalance 3. to prevent swelling
4.To maintain joint and skin mobility with
minimal disfigurement

32. Initial therapy
• Daily wound care---Hydrotherapy
• Protective dressing using ointments like silver
sulfadiazine
• Early excision of he devitalized tissue and
skin grafting
• Auto graft
• Xenograft allograft

33. Rehabilitation
• Control of hypertrophic scarring to minimize
contractures and deformities
• Hypertrophic scars contract and raise above
the skin surface .Stretching and even pressure
dressing will prevent this
• Proper positioning of the patient is essential
to the burns program—using splints pillows
sandbags

34. splinting
• This is done to maintain the desired anatomical
position in the acute stage and to prevent deformity
• Indications
1 To prevent the rupture of the exposed tendons
2 To protect exposed joints
3 to protect a graft after surgery
4 to prevent excessive scarring in areas where
deformity can occur like face and neck by giving
constant pressure
5.diminishes the pain

35. splinting
• Common splints in the acute phase are
footdrop preventing splints
knee extension splint
resting hand splints
cervical collars
facial masks

36. Splinting contd
Body part Predisposition to
contractures
Preventive positioning and
splints
Neck Flexion In extension or
hyperextension
Anterior axillary fold Adducted shoulder Abduction splint
Posterior axillary fold Extended shoulder Splint with shoulder in
flexion
Elbow Flexion Extension
Forearm Pronation Supination
Wrist Flexion extension
MCP Hyper extension MCP flexion
Fingers IP flexion and thumb in
adduction
Ip extended and thumb in
abduction
Hip Flexion adduction and
external rotation
Splint in extension
abduction and neutral
Knee Flexion Extension