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| '''Original Editor '''- [[User:Carin Hunter|Carin Hunter]] based on the course by [TUTOR LINK/ TUTOR NAME] | | <div class="editorbox"> '''Original Editor '''- [[User:Carin Hunter|Carin Hunter]] based on the course by ReLab<br> '''Top Contributors''' - {{Special:Contributors/{{FULLPAGENAME}}}}</div> |
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| '''Top Contributors''' - {{Special:Contributors/{{FULLPAGENAME}}}} | |
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| == Rehabilitation Post Burn Injury == | | == Rehabilitation Post Burn Injury == |
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| ∙ The pain and psychological distress of a burn has a massive impact on compliance o An empathetic, encouraging and understanding approach is necessary ∙ The urgency and importance of beginning early rehabilitation should be communicated in a clear but gentle manner (Procter 2010). | | ∙ The pain and psychological distress of a burn has a massive impact on compliance o An empathetic, encouraging and understanding approach is necessary ∙ The urgency and importance of beginning early rehabilitation should be communicated in a clear but gentle manner (Procter 2010). |
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| == Role of the Physiotherapist in the Rehabilitation of the Acute Burn Patient == | | == References == |
| For the purpose of clarity, the following section has been divided into acute, sub acute and chronic rehabilitation. However, rehabilitation is a continuum, and significant crossover may occur. All of the following concepts apply to burns on any part of the body, with specialised treatment addressed for the hand where necessary.
| | [[Category:Course Pages]] |
| | | [[Category:Plus Content]] |
| Depending on the size and the severity of the injury this stage may last from a few days to a few months (Procter 2010)
| | [[Category:Burns]] |
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| Patient
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| ∙ Acute phase of inflammation
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| ∙ Pain
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| ∙ Oedema increasing for up to 36 hours post injury
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| ∙ Hypermetabolic response, peaking at five days post injury
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| ∙ Early synthesis and remodelling of collagen
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| Aims
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| ∙ Reduce risk of complications
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| o Reduce oedema, particularly where it poses a risk for
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| ▪ impinging on peripheral circulation or airways
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| ▪ Predisposition to contractures
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| ∙ Prevent deformities/loss of range
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| ∙ Protect/promote healing
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| Common treatment techniques
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| ∙ Immobilisation
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| o Bed rest
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| o Splinting
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| ∙ Positioning
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| 37
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| 5.11 Immobilisation
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| 5.111 Rationale for Immobilisation
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| {| class="wikitable"
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| |Acute Stage
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| |∙ Prevent deformities
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| ∙ Maintenance of range of motion ∙ Promote Healing
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| ∙ Protection
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| |(Ashe 2001; Kamolz 2009)
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| |-
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| |Sub-acute Stage
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| |∙ Maintenance of range of motion ∙ Regain range of motion
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| |(Kwan 2002; Boscheinen Morrin 2004)
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| |}Table 6: rationale for immobilisation
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| 5.112 Positioning in the Acute Stage
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| <nowiki>*</nowiki>Modify according to burn area, patient pain and medical status.*
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| {| class="wikitable"
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| |Area Of Burn
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| |Common Contracture
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| |Recommended position
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| |-
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| |Anterior neck
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| |Neck flexion: loss of neck contours and extension
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| |Neck in extension. If head needs to be raised, do not use pillows.
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| |-
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| |Posterior neck
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| |Neck extension. Loss of
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| flexion and other movements
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| |Head in flexion. Sitting or lying with a pillow behind the head.
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| |-
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| |Axilla
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| |Limited abduction/ protraction with burn to chest
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| |Lying/ sitting with arms abducted. Slings, pillows, figure of eight bandage around chest for stretch. Prone lying
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| |-
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| |Anterior Elbows
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| |Flexion
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| |Elbow extension
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| |-
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| |Groin
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| |Hip flexion
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| |Prone lying, legs extended, no pillow under knees in supine, limit sitting/side lying
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| |-
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| |Back of knee
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| |Flexion
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| |Long sitting/ supine lying, no pillow beneath knees
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| |-
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| |Feet
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| |Dependent on area
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| |Aim to maintain 90 degrees at ankle: pillows in bed, sitting with feet on floor
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| |-
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| |Face
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| |Variety: inability to
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| open/close mouth/eyelids
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| |Regular change of expression. Soft rolls may be inserted into the mouth
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| |}Table 7 Positions of immobilisation, for pictures, see Procter, 2010
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| 38
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| 5.113 1mmobilisation post skin reconstruction surgery
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| Stopping movement and function of the body parts involved should be enforced after skin reconstruction for a burn has taken place. When a body part must be immobilised, it should be splinted or positioned in an anti-deformity position for the minimum length of time possible (Edgar and Brereton 2004; ANZBA 2007)
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| The following is a table drawn up using current literature on the recommended immobilisation times for the various skin grafts:
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| {| class="wikitable"
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| |Surgical Procedure
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| |Immobilisation Time
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| |-
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| |Biological Dressings
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| |<24hours
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| |-
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| |Autograft (superficial to intermediate)
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| |24-48hours
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| |-
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| |STSG
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| |3-5 days
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| |-
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| |FTSG
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| |5-7 days
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| |}Table 8 Surgical procedure and related immobilisation (ANZBA 2007; Edgar and Brereton 2004)
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| The times frames for mobilisation post-surgery outlined in this booklet are merely a guide taken from an analysis of current literature and are NOT a replacement for the specific time frames directed by the operating surgeon or consultant (ANZBA 2007).
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| For a physiotherapist the most important concepts to grasp are:
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| • What is the minimum timeframe of immobilisation post-surgery
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| • What structures MUST be immobilised
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| • Special considerations for movement, function and ambulation dependent on Donor sites and the structures repaired or excised during surgery.
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| 39
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| 5.114 Immobilisation of the hand
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| Deformity Prevention
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| The most common deformity associated with burns is the ‘claw’ deformity. It involves extension of the MCP joints, flexion of the PIP joints, adduction of the thumb and flexion of the wrist (Kamolz 2009). This position is also referred to as the intrinsic minus position.
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| Figure16a. Dorsal hand burn resulting
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| in claw deformityFigure 16 b: Position of safe
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| immobilisation (Glassey, 2004)
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| Position of Safe Immobilisation
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| The position of safe immobilisation of the burned hand is essentially the opposite of the above claw deformity position. This position involves: 20-30 wrist extension, 80-90 degrees flexion MCP joints, full extension PIP and DIP joints and palmar abduction of the thumb (Boscheinen-Morrin 2004).
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| 5.115 Splinting
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| Physiological rationale for splinting (Kwan 2002)
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| Scar tissue is visco-elastic. It will elongate steadily within a certain range. When this stretching force is released, there is an immediate decrease in the tissue tension but a delay in the retractions of the tissue to a shorter length. These stress relaxation properties of visco elastic scar tissue means it can accommodate to stretching force overtime. Dynamic and static splinting provide this prolonged low stretching force.
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| Categories of Splints
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| 40
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| ∙ Static or Dynamic
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| ∙ Supportive or Corrective
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| ∙ Rigid or soft
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| ∙ Dorsal or Volar
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| ∙ Digit, hand or forearm based (Boscheinen-Morrin 2004) Static Splinting
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| ∙ A serial static splint is a device with no moving parts designed to be remoulded as a contracture improves. The most common serial static splint you will come across is a thermoplastic palmar splint moulded in the position of safe immobilisation.
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| Fig 17: Thermoplastic palmar splints in the position of safe immobilisation (Glassey 2004)
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| ∙ A static progressive splint is a device designed to stretch contractures through the application of incrementally adjusted static force to promote lengthening of contracted tissue (Smiths 2009). There are various types of static progressive splints available depending on the area affected. One such static progressive splint is a finger flexion strap splint. This type of splint is used in the treatment of MCP extension contractures. The flexion straps serially stretch scar bands along the dorsum of hand and wrist causing extension contracture. The stretching force is localised to the MCP joints by applying the straps via a wrist extension splint. This stabilises the wrist providing static support below the MCP joint (Kwan 2002).
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| 41
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| Dynamic Splinting
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| Fig 18: Velcro flexion straps (Glassey 2004)
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| A dynamic splint is one which aids in initiating and performing movements by controlling the plane and range of motion of the injured part. It applies a mobile force in one direction while allowing active motion in the opposite direction. This mobile force is usually applied with rubber bands, elastics and springs (Smith 2009).
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| Dynamic extension splints are most commonly used in the treatment of palmar and / or finger burns (i.e. flexion contractures). All the finger joints including the MCP, PIP and DIP joints are in full extension (Smith 2009).
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| Fig 19 Dynamic Extension Hand Splint
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| (Microsurgeon 2013)
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| Dynamic flexion splints are used in the treatment of dorsal hand burns. During wound healing and subsequent scar maturation, the skin on the dorsal aspect of the hand can markedly contract limiting digit flexion. A dynamic flexion splint in the sub-acute stage of dorsal hand burns can aid in the prevention of MCP joint extension contractures (Kwan 2002).
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| Fig 20 Dynamic flexion hand splint in glove form
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| (Microsurgeon 2013)
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| 42
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| Overview of the Evidence:
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| There is currently no evidence available which identifies the benefit of one hand splint over another in the treatment of the burnt hand. A systematic review carried out in 2006 concluded that there are no studies examining the effectiveness of hand splinting for hand burns, but rather studies describing types of hand splint interventions (Esselman 2006). There are currently no control trials which compares the various types of splints available or which examines the use Vs disuse of splinting the burnt hand. Literature in the area suggests the use of splinting in the initial inflammatory phase to promote a position of safe immobilisation. The use of splinting as an adjunct to treatment in the sub-acute phase is discussed in the literature as an aid to maintain/regain range of motion.
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| Splinting Precautions
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| ∙ Splints need to be cleaned regularly to prevent colonization by microbes which may lead to wound infection (Wright et al 1989; Faoagali et al 1994)
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| ∙ Unnecessary use of splinting may cause venous and lymphatic stasis, which may result in an increase in oedema (Palmada et al 1999)
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| ∙ Precaution must be taken to ensure that splints do not product friction causing unnecessary trauma to the soft tissues (Duncan et al 1989).
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| ∙ Precaution must be taken to ensure that splints do not produce excessive pressure. There is particular risk of pressure injury to skin after burn injuries due to potential skin anaesthesia (Leong 1997).
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| ∙ Splinting should not be used in isolation but as an adjunct to a treatment regime Conclusion on Splinting
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| The use of hand splinting does not follow a protocol in the treatment of the burnt hand. It is often common practice to splint the burnt hand in the initially inflammatory phase of healing. Despite the level of evidence available it is important as a physiotherapist to be aware of the role splinting can play as an adjunct to treatment of the burnt hand in the sub-acute phase of healing. The application of hand splinting in the areas of burns must be clinically reasoned for each individual patient. A Physiotherapist must identify the appropriate rather than routine use of splinting. This is to promote patient independence and prevent dependence on splinting devices both by patients and physiotherapists alike.
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| 43
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| [[Management of Burns|Management of Oedema]] | |
| == Role of the Physiotherapist in the Rehabilitation of the Sub Acute Burn Patient ==
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| Beyond the acute stage of immobilisation, inpatient and outpatient rehabilitation typically consists of a variety of interventions including pressure garment therapy, silicone therapy, scar massage, range of motion and mobilisation techniques, strengthening, functional and gait retraining, and balance and fine motor retraining ( Schneider et al, 2012). Interventions should be tailored according to a full patient assessment.
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| As it would be unethical to withhold treatment, physiotherapy intervention as a whole is not well investigated. Schneider et al (2012) found a significant improvement in contractures; balance and hand function with inpatient rehabilitation, through a longitudinal observational study of eleven people. However, in the following section, we will attempt to display the evidence for commonly used modalities.
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| The patient
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| ∙ Primary closure of wound
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| ∙ Scar remodelling
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| ∙ Scar contraction
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| Aims
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| ∙ Optimise scar appearance
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| ∙ Limit effects of scar contraction/prolonged positioning on range of motion and function
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| ∙ Address effects of prolonged bed rest
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| Common modalities
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| ∙ Mobilisation- both mobility and specific joint mobilisation
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| ∙ Scar management adjuncts
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| o Pressure garments, silicone, massage
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| ∙ Continuation of oedema/ positioning management where necessary
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| 46
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| 5.21 Mobilisation
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| The advantages of general mobilisation for a burns patient to counteract the effects of prolonged bed rest are no different to that of a surgical or medical patient. Burns patients should be mobilised as early as possible to avoid deconditioning and possible respiratory complications associated with prolonged bed rest (Esselman 2007).
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| As outlined in the above introduction, due to the ethical issues surrounding withdrawal or modification of treatment the evidence surround the optimal duration, frequency and methods of physiotherapy interventions in the treatment of burn patients is unclear. Despite this lack of clarify surrounding these issues it is clear that both active and passive mobilisation plays a key role throughout the stages of burn recovery. Below is a summary of the recommendations from the currently literature on passive and active mobilisation of burns.
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| 5.211 Active ROM
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| ∙ Depending on the need for immobilisation gentle active ROM exercises is the preferred treatment during the acute stage of injury as it is the most effective means of reducing oedema by means of active muscle contraction (Glassey 2004). If this is not possible due to sedation, surgical intervention etc. then positioning the patient is the next best alternative (see immobilisation and position).
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| 5.212 Passive ROM
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| ∙ Passive ROM exercises in the acute stage are contraindicated as applying passive stretching forces may result in future damage to the burned structures (Boscheinen Morrin 2004). Applying these passive manoeuvres in the acute stage will result in increased oedema, haemorrhage and fibrosis of the burned tissues (Cooper 2007).
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| ∙ The biomechanical principle of creep when passive stretching. A slow sustained stretch is more tolerable for patient and more effective for producing lengthening (Kwan 2002).
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| ∙ Passive joint mobilisations can begin during the scar maturation phase once the scar tissue has adequate tensile strength to tolerate friction caused by mobilisation techniques (Boscheinen-Morrin and Connolly 2001).
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| 47
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| Frequency, Duration Recommendations
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| ∙ Physiotherapy intervention should be twice daily with patients prescribed frequent active exercises in between sessions.
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| ∙ For the sedated patient gentle passive range of motion exercises should be done 3 times a day once indicated (Boscheinen-Morrin and Connolly 2001).
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| ∙ Dependent on the severity of the burn active and very gentle passive range of motion exercises for the hand and fingers are begun from day one of injury.
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| Contraindications
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| ∙ Active or Passive range of motion exercises should not be carried out if there is suspected damage to extensor tendons (common occurrence with deep dermal and full thickness burns). Flexion of the PIP joints should be avoided at all costs to prevent extensor tendon rupture. The hand should be splinted in the position of safe immobilisation or alternatively a volar PIP extension splint until surgical intervention (Boscheinen-Morrin and Connolly 2001) is discussed.
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| ∙ Range of motion exercises are also contraindicated post skin grafting as a period of 3- 5 days immobilisation is required to enable graft healing (Boscheinen-Morrin and Connolly 2001).
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| Evidence for hand mobilisation
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| There is currently limited evidence which examines the effectiveness of hand exercises for the burned hand specifically. Studies in the area of burns generally include subjects who have extensive % TBSA in which their hand/hands may be involved.
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| Okhovation et al (2007) carried out an RCT in which they compared a routine rehabilitation protocol with a burn rehabilitation protocol. This study is particularly relevant form a hand burn rehabilitation perspective as 83% of subjects recruited had partial / full thickness hand burns
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| Subjects: 30 burn admissions to Tehran Hospital in 2005. Matched in pairs based on clinical details (sex, age, TBSA, depth of burn). Randomly assigned into two groups
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| Intervention: The routine rehabilitation protocol included chest physiotherapy and active/passive movements 15-20 minutes daily commenced 2/52 post admission. The burn rehabilitation protocol involved routine protocol plus targeted stretching program to
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| 48
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| contracture risk areas for 30-45min 2-3times daily commenced on day1 of admission. Outcome measures: Outcome measures used were Presence of burn contracture (goniometry) Occurrence of thrombosis Length of Hospital Stay Skin grafting requirement.
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| Results: Development of post burn contractures on discharge from hospital was 6% in the burn rehabilitation group versus 73% in the routine rehabilitation group. No significant difference regarding thrombosis, duration of stay and number of skin grafts
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| Limitations: There were several limitations to the study. The recruitment process was not clearly defined. Information on the group matching and randomised allocation process was not provided. No inclusion/exclusion criterion was defined. Frequency, duration and commencement of the two protocols unequal and appear very bias towards targeted stretching program.
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| Functional Rehabilitation of the Hand
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| Salter and Chesire (2000) suggest that the burnt hand should be used for light self-care activities as soon as tolerated by the patient. This is based on the principle that everyday activities will promote regular movement patterns of the affected hand. Emphasis should be placed on intrinsic flexion of the MCP joints and intrinsic IP joint extension, gross gripping (i.e. composite flexion), maintenance of the web spaces and opposition of the thumb.
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| Practical factors to consider when mobilising
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| ∙ Be aware of dressing clinic/daily dressing changes. Mobilisation should coincide with this as it is important to monitor the wound during AROM frequently.
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| ∙ Timing of pain relief. This should be timed appropriately to ensure maximal benefit during treatment sessions.
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| ∙ Observe the patient carrying out the AROM and PROM exercises prior to beginning treatment. Also observe the patient taking on/off splints.
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| ∙ Always monitor for post exercise pain and wound breakdown.
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| ∙ Avoid blanching for long period as you may compromise vascularity. ∙ The patient may present with a reduced capacity for exercise secondary to increased metabolic rate, altered thermoregulation and increased nutritional demands. ∙ Postural hypotension may be present due to prolonged bed rest and low haemoglobin. (ANZBA 2007)
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| === Massage ===
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| Five principles of scar massage:
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| 1. Prevent adherence
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| 2. Reduce redness
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| 3. Reduce elevation of scar tissue
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| 4. Relieve pruritus
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| 5. Moisturise (Glassey 2004) Scar Massage Techniques
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| ∙ Retrograde massage to aid venous return, increase lymphatic drainage, mobilise fluid ∙ Effleurage to increase circulation
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| ∙ Static pressure to reduce pockets of swelling
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| ∙ Finger and thumb kneading to mobilise the scar and surrounding tissue ∙ Skin rolling to restore mobility to tissue interfaces
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| ∙ Wringing the scar to stretch and promote collagenous remodelling
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| ∙ Frictions to loosen adhesions
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| (Holey and Cook 2003)
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| {| class="wikitable"
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| | colspan="2" |Guidelines for Massage during 3 Stages of healing
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| |-
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| |Inflammatory Phase
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| |gentle massage to decrease oedema and increase blood supply (currently no high level evidence to support this)
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| |-
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| |Proliferative Phase
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| |Massage that applies gentle stress to the healing scar is recommended to ensure collagen is aligned correctly.
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| |-
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| |Remodelling Phase
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| |Massage should be progressed to include prolonged stretching to minimise adhesions. This is proposed to aid in scar tissue breakdown
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| |}Table 10 Guidelines for scar massage during healing stages (Glassey 2004)
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| 58
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| Table 11. Evidence for the use of massage in scar management
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| {| class="wikitable"
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| |Article
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| |Field et al 2000
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| RCT
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| |Morien et al 2008
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| Pilot Study
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| |Shin and Bordeaux, 2012 Lit review
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| |-
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| |Subjects
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| |20 subjects in remodelling phase of wound healing. Randomly assigned into 2 groups
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| Massage Vs Control
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| |8 Children
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| Mean age 13.5 years (10-17years)
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| All thermal burns including hand burns
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| |Not burn specific, though the majority of scars were of this origin
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| 10 articles: n=144 adult and children
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| |-
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| |Intervention
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| |Massage Therapy Group:
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| 30minutes massage with cocoa butter twice weekly for 5 weeks
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| Control Group:
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| Standard Treatment
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| |20-25 minute massage session once daily for 5 days
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| (effleurage,
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| petrissage, friction, lengthening rolling)
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| Session followed by discussion of psychosocial issues
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| |Time to Rx: mean 4.3 months. + variation in protocols. 20 mins/day- 30 mins 2x weekly. 1 Rx-6 months Rx
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| |-
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| |Outcome
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| measures
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| |Itching: VAS
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| Pain: McGill Pain
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| Questionnaire
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| Anxiety: State Trait Anxiety Inventory
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| Mood: Profile of Mood States
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| |Likert pictorial scale
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| Goniometry Range of Motion
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| |Patient and observer scar assessment scale, Vancouver scar scale, thickness, vascularity, colour, pain, pruritus, mood, anxiety, and depression.
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| |-
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| |Results
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| |Massage Therapy Group Reported: decreased itching, pain, anxiety and increased mood
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| Ratings improved from the 1st-last day of the study
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| |Increased ROM in massaged tissue. Decreased ROM in unmassaged tissue
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| No significant difference in mood across time
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| |45.7% improved in at least one of the above parameters. 54.7% had no improvement.
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| Noted massage was more economical than silicone/PGT.
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| |}59
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| {| class="wikitable"
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| |Limitations
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| |Small Sample Size
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| No follow up
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| |Paediatric
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| population. Mood Instrument may have been influenced by other factors. Recruitment and area to be massaged not random
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| Small sample size
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| No follow up
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| |No discussion of quality or statistical tests.
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| |}Conclusion on Scar Massage
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| Evidence suggests that burn patients receive psychological benefits from massage in terms of altered mood (decreased depression, anger), decreased pain, and anxiety (Field et al 1998). Evidence also indicates that massage increases ROM in non-burned patients, but little evidence exist examining the effect of massage on ROM in burn patients (Morien et al 2008).
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| Recommendations for practice and safety considerations.
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| Insufficient consistency in literature with regards to protocols on frequency or duration of treatment. Suggestions for practice include (Shin and Bordeaux, 2012, Morien et al, 2008)
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| ∙ Clean hands essential
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| ∙ Use non irritating lubricant, free of any known sensitisers.
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| ∙ Modify practice according to patient stage of healing, sensitivity and pain levels. Contraindications: Shin and Bordeaux 2012
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| ∙ Compromised integrity of epidermis
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| ∙ Acute infection
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| ∙ Bleeding
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| ∙ Wound dehiscence,
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| ∙ Graft failure
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| ∙ Intolerable discomfort
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| ∙ Hypersensitivity to emollient
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| == The Role of the Physiotherapist in the Rehabilitation of the Chronic Burn Patient. ==
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| The patient
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| ∙ Healing process may continue for up to two years, as scar tissue remodels and matures
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| ∙ May require functional retraining and integration back into the community and activities.
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| It is important to note that though scar management is initiated in the sub-acute phase, it may need to be continued long term, as many patients suffer from continuing limitation to range of motion (Procter 2010).
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| 5.31 Aerobic and Resistance Training Post Burn
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| 5.311 Rationale for Aerobic and Resistance Training
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| ∙ Low cardiorespiratory endurance has been found to be a concern for all (Willis et al 2011)
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| ∙ Aerobic capacity as measured by VO2 peak and time to fatigue has been found to be lower in adults and children of >15% TBSA at one year post burn, compared to age matched healthy controls (Willis et al 2011; McEntine et al 2006)
| |
| | |
| ∙ Muscular strength and lean body mass has been found to be significantly less in patients suffering from burns of >30% TBSA, particularly in exercises requiring a high velocity (Disseldorp et al 2007; Ebid et al 2012). The systemic effects caused by large surface area burns means that weakness may be global, not just local to the site of the injury (Grisbrook et al 2012b)
| |
| | |
| ∙ Reduced lean body mass, endurance and strength has been associated with limited standing/walking tolerance, reduced upper limb function and lower health related QOL and ability to participate in activities (Grisbrook et al 2012b).
| |
| | |
| ∙ This has been found to persist beyond discharge from hospital despite routine physiotherapy and occupational therapy in hospital (Disseldorp et al 2007). Though protein metabolism begins to normalise 9-12 months post burn, patients are still found
| |
| | |
| 61
| |
| | |
| to have significant strength and aerobic related functional impairment at >2 years post burn (Grisbrook et al 2012b).
| |
| | |
| It is proposed that aerobic capacity and muscular strength is diminished by the following factors
| |
| | |
| ∙ Prolonged bed rest necessary in the early recovery process
| |
| | |
| ∙ Hypermetabolisim, which may lead to *
| |
| | |
| o Exhaustion
| |
| | |
| o Protein catabolism
| |
| | |
| o Loss of lean body mass
| |
| | |
| ∙ Impaired thermoregulation **
| |
| | |
| ∙ Inhalation injuries and compromised respiratory function***
| |
| | |
| Recovery of aerobic capacity and strength may also be limited by
| |
| | |
| ∙ Fatigue
| |
| | |
| ∙ Pain
| |
| | |
| ∙ Psychosocial factors
| |
| | |
| (Disseldorp et al 2011; De Lauter et al 2007; Grisbrook et al 2012; Suman and Herndon 2007)
| |
| | |
| <nowiki>*</nowiki>Hyper metabolism, catabolism, loss of lean body mass and exhaustion
| |
| | |
| Hypermetabolisim post burn caused by both second and third degree burns, particularly if sepsis follows. This may begin approximately five days post burn, as the metabolic state is initially suppressed by the effects of acute shock, and can persist for up to two years post injury (Jeschke et al 2007; Herndon and Tomkins 2004). The greater the TBSA, the greater the risk and impact of hyper metabolism (Hurt et al 2000). While it may not be recognised in the acute stages, it may give rise to long term complications and functional impairment, particularly with respect to strength and aerobic capacity (De Lauter et al 2007).
| |
| | |
| A systematic review by Disseldorp et al (2007) found 4 studies involving children with > 40% TBSA
| |
| | |
| 62
| |
| | |
| ∙ All found a decrease of up to 20% in lean muscle mass compared to age matched controls
| |
| | |
| ∙ Adults with a TBSA >30% suffered a significant decrease in torque, work and power in the quadriceps muscles compared to age matched controls. (De Lauter et al 2007)
| |
| | |
| Exercise and Hypermetabolism
| |
| | |
| Though exercise requires an increase in energy expenditure and metabolism for a short period of time no adverse effects have been found with regard to exacerbating hypermetabolism or protein catabolism.
| |
| | |
| o All studies investigating the effects of exercise on lean body mass found it to increase, particularly with resistance training ( Grisbrook et al 2012b; Suman and Herndon 2007; Suman et al 2001; Przkora et al 2007)
| |
| | |
| o Suman et al, 2001, found an increase of 15% in resting energy expenditure in children with burns of >40% TBSA who were not treated with resistance and aerobic exercise, while the REE of those who participated in the intervention remained stable.
| |
| | |
| o Suggested that exercise may have sympathetic nervous system attenuating effects
| |
| | |
| ▪ A balance of resistance and aerobic exercise may cause a decrease in SNS activity, decreasing catabolic effects.
| |
| | |
| o Exercise is required to integrate dietary amino acids into lean muscle mass (Herndon and Tomkins 2004)
| |
| | |
| <nowiki>**</nowiki>Thermoregulation
| |
| | |
| Human skin produces sweat to dissipate heat in response to thermal stress (McEntine et al 2006). A proper sweat response requires functional integrity of the
| |
| | |
| ∙ Sweat glands
| |
| | |
| ∙ Skin circulation
| |
| | |
| ∙ Neural control of the skin (McEntine et al 2006)
| |
| | |
| Full thickness burns damage the dermal appendages including sweat glands. These are not replaced by grafting. There is also a decreased density of sweat glands in the donor site post grafting (Esselman et al 2007).
| |
| | |
| 63
| |
| | |
| However, McEntine et al 2006 found that in 15 children with an average of 55% TBSA there was
| |
| | |
| ∙ No significant difference in core temperature, measured tympanically, pre or post 20 minutes of treadmill exercise at room temperature compared to age matched healthy controls.
| |
| | |
| ∙ No significant difference in average skin temperature between burned and healthy children.
| |
| | |
| ∙ Significantly increased skin temperature in healthy versus burned skin per child.
| |
| | |
| Austin et al, 2003 studied 3 adults with > 60% TBSA, 3 with between 30-40 TBSA and 2 unburned patients post 1 hr cycling at 35 degrees and 60% humidity
| |
| | |
| ∙ None showed significant intolerance for heat as measured by heart rate and core temperature, measured rectally
| |
| | |
| ∙ No significant difference in whole body sweat rate
| |
| | |
| ∙ Overcompensation by healthy skin in the burned patients.
| |
| | |
| ∙ Suggested physical history was a factor in determining patients’ ability to thermoregulate. Therefore adaptations may occur through training.
| |
| | |
| However, studies involving heat loads of 40 degrees have found a significant inability to maintain adequate thermoregulation. Due to the small study numbers of the above, and the controversy surrounding the efficacy of measuring core temperature accurately, it is advised that patients are closely monitored initially during aerobic exercise for signs of heat intolerance.
| |
| | |
| <nowiki>***</nowiki>Inhalation injury and pulmonary insufficiency
| |
| | |
| Long term pulmonary function is compromised in some patients post severe burn
| |
| | |
| ∙ Lasts several years
| |
| | |
| ∙ Documented in both children and adults (Grisbrook et al 2012a)
| |
| | |
| ∙ Caused by
| |
| | |
| o Smoke inhalation
| |
| | |
| o Direct thermal damage to airways
| |
| | |
| o Pulmonary oedema
| |
| | |
| 64
| |
| | |
| o Respiratory tract infection
| |
| | |
| o Complications from intubation
| |
| | |
| o Recurrent infection leading to chronic inflammation
| |
| | |
| Less likely to cause dysfunction in <30% TBSA, no injury over torso, and no inhalation injury
| |
| | |
| (Willis et al 2011)
| |
| | |
| Evidence for impact on aerobic and exercise capacity conflicting (Grisbrook et al 2012a). However Willis et al (2011) studied 8 males post > 15% TBSA burns at one year post injury, and found
| |
| | |
| ∙ Significantly decreased FEV1, peak VO2 and time to fatigue, in the burned patients ∙ No significant decrease in SpO2 at baseline or peak VO2- however, the SpO2 of burned patients took significantly longer to stabilise at baseline post exercise. ∙ No significant difference in participation levels in physical activity, though burn survivors were more likely to participate in work rather than leisure activity. ∙ Burns survivors were less likely to participate in vigorous intensity exercise over 9 METs
| |
| | |
| ∙ Therefore, decreased pulmonary function did not prevent them from participating ∙ The lower relative intensity of their exercise may have caused their decreased aerobic capacity.
| |
| | |
| All of the above factors must be considered as both a contributor to the patients’ loss of strength and aerobic capacity, and a potential limiter of their ability to participate in therapy. Careful monitoring and modification of treatment according to individual response is advised.
| |
| | |
| 65
| |
| | |
| 5.312 Aerobic Training: The Evidence
| |
| {| class="wikitable"
| |
| |Article citation
| |
| |Disseldorp et al, 2011
| |
| |De Lauteur et al, 2007
| |
| |Grisbrook et al, 2012
| |
| |Grisbrook et al, 2012
| |
| |Paratz et al, 2012 (ab)
| |
| |Przkora et al, 2007
| |
| |-
| |
| |Design
| |
| |Systematic
| |
| review
| |
| | |
| Eleven articles included
| |
| | |
| Eight RCTs
| |
| | |
| Pedro 6+
| |
| | |
| 1 RCT<5, 1 non RCT, 2 static group comparison
| |
| |Randomised controlled,
| |
| double
| |
| | |
| blinded trial
| |
| |Non
| |
| randomised
| |
| | |
| controlled trial.
| |
| |Non
| |
| randomised
| |
| | |
| controlled trial.
| |
| |Quasi
| |
| experimental controlled
| |
| | |
| trial
| |
| |Randomised
| |
| controlled trial
| |
| | |
| Oxandrolone, vs osandrolone + exercise, vs exercise + placebo,
| |
| | |
| placebo+no
| |
| | |
| exercise
| |
| |-
| |
| |Subjec
| |
| ts
| |
| |7 different cohorts
| |
| 5 children with exceptionally large TBSA
| |
| |35 adults mean 37.5 days post burn, mean TBSA 19.3%
| |
| | colspan="2" |9 burn injured adults and 9 age matched healthy controls. 20%+ TBSA, 2 yrs post injury, with remaining functional deficit.
| |
| |30 patients, mean age 34.3 years, mean TBSA 42.9%
| |
| |51 children, 7- 17 yrs old, >40% TBSA
| |
| |-
| |
| |Interve
| |
| ntion
| |
| |Aimed to assess physical fitness post burn, and the effectiveness
| |
| of aerobic exercise
| |
| |12 week rehabilitation programme, 3 x weekly 30 mins. Standard
| |
| rehabilitation vs. work to quota and work to tolerance
| |
| | |
| aerobic
| |
| | |
| exercise
| |
| | colspan="2" |12 weeks, 3 x weekly, 80 mins.
| |
| 30 mins of treadmill walking/jogging in intervals (85 vs 65-70 HR max) and resistance exercises.
| |
| |6weeks, 80 % MHR aerobic training, with 70% three RM
| |
| resistance
| |
| | |
| training
| |
| |12 week inpatient
| |
| physiotherapy twice daily for 1 hr. aerobic and resistance
| |
| | |
| exercise
| |
| | |
| Aerobic 5 days per week, 20-40 mins, 70-85% VO2peak
| |
| |-
| |
| |Outco
| |
| me
| |
| | |
| measur
| |
| | |
| e
| |
| |Children and adults after extensive
| |
| burns score worse than non-burned
| |
| | |
| controls in all
| |
| |Max aerobic capacity:
| |
| VO2 max.
| |
| |Spirometry,
| |
| Canadian
| |
| | |
| occupational
| |
| | |
| performance
| |
| | |
| measure, VO2 peak
| |
| |Burn specific health scale, SF 36, quick DASH
| |
| |1RM, VO2 peak, shuttle walk
| |
| distance, LL function
| |
| | |
| score, quick dash, burns
| |
| |Biodex leg extension, 3 RM, VO2 peak, lean body mass,
| |
| |}66
| |
| {| class="wikitable"
| |
| |
| |
| | rowspan="2" |aspects of fitness.
| |
| Burn patients participating in 12 week training
| |
| | |
| programmes
| |
| | |
| improve
| |
| | |
| significantly
| |
| | |
| more than those without.
| |
| |
| |
| |
| |
| |
| |
| |specific
| |
| health scale
| |
| |
| |
| |-
| |
| |Results
| |
| |Work to tolerance and work to quota significantly
| |
| improved
| |
| | |
| aerobic
| |
| | |
| capacity. No significant
| |
| | |
| improvement in control. No significant
| |
| | |
| difference
| |
| | |
| between
| |
| | |
| WTQ and WTT
| |
| |No significant improvement in spirometry values
| |
| (ex/control)
| |
| | |
| Significant
| |
| | |
| improvement in VO2 peak and time to fatigue in both groups.
| |
| | |
| Significant
| |
| | |
| improvement in satisfaction with
| |
| | |
| personalised
| |
| | |
| goals.
| |
| |Burns patients scored lower on HRQOL and quick dash both before and after the intervention
| |
| compared to controls. 5/9 burn patients reached
| |
| | |
| clinically
| |
| | |
| significant
| |
| | |
| improvements in BSHS post intervention. No significant increase in DASH
| |
| |No adverse effects.
| |
| Significant
| |
| | |
| improvement s in functional,
| |
| | |
| physical,
| |
| | |
| psychological measures.
| |
| |LBM increased in all groups except placebo showed average decrease.
| |
| Steroids+
| |
| | |
| exercise=
| |
| | |
| highest relative increase. Both exercise and drug only group showed
| |
| | |
| significant
| |
| | |
| increase in strength.
| |
| | |
| Endurance
| |
| | |
| increased in the exercise groups, but not those with only steroids/placebo
| |
| |-
| |
| |Limitat ions
| |
| |4 studies conducted in children with large TBSA burns. Little variation in the protocols
| |
| being
| |
| | |
| compared, and so no objective evidence of the efficacy of individual
| |
| | |
| components of exercise.
| |
| |Low risk of bias in randomisatio n, no discussion of blinding to initial scores. Unable to blind
| |
| therapists or patients to the
| |
| | |
| intervention. Small patient numbers
| |
| |Small subject numbers, no untreated
| |
| control,
| |
| | |
| blinding not possible
| |
| |Small subject numbers, no untreated
| |
| control,
| |
| | |
| blinding not possible
| |
| |Abstract.
| |
| Unable to identify the methodologic al rigour of this study, and so results should be interpreted
| |
| | |
| with caution.
| |
| |Low risk of bias in
| |
| randomisation, no discussion of blinding which leaves a high risk of bias where a placebo drug is involved.
| |
| |}Table 12 Evidence for Aerobic Training Post Burn
| |
| | |
| 67
| |
| | |
| 5.313 Aerobic Training Summary and Recommendations for Practice Exercise prescription:
| |
| | |
| Frequency: The majority of papers which investigated an aerobic intervention used 3 times per week as their frequency (De Lauteur et al 2007; Grisbrook et al 2012). These obtained significant improvements. However, Przkora et al (2007) used a frequency of 5 times per week with children. There have been no studies investigating optimal frequency.
| |
| | |
| Intensity: All studies used between 65 and 85% predicted heart rate max, with one study using interval training of 120 seconds 85% HRM and 120 seconds of 65-70 HRM. All studies obtained positive effect, with none directly comparing intensities to determine the optimum. De Lauteur et al (2007), concluded that whether the patient gradually increased their intensity by working to a specific quota each week, or if they simply worked at their target heart rate for as long as they could tolerate, there was no significant difference in gains in aerobic capacity.
| |
| | |
| Type: All interventions used treadmill training, whether walking or running.
| |
| | |
| Time: All studies recommended the duration of treatment be 12 weeks, with the exception of Paratz et al, 2012, who investigated a high intensity six week programme. However, the specific results of this are unknown. Sessions were 20-40 minutes in length, with the majority using 30 minutes (Grisbrook et al 2012; De Lauteur et al 2007; Przkora et al 2007)
| |
| | |
| Please note safety considerations Pg 72
| |
| | |
| 68
| |
| | |
| 5.314 Resistance Training: The Evidence
| |
| | |
| 69
| |
| | |
| 70
| |
| | |
| 5.314 Resistance Training Summary and Recommendations for Practice
| |
| | |
| Exercise prescription: Post two years, Grisbrook et al (2012b) found that burned patients responded to resistance exercise similarly to controls. Therefore, normal guidelines may be adequate.
| |
| | |
| Frequency: All studies investigating the effects of resistance training used a frequency of three times per week. There have been no studies to investigate the optimum frequency for resistance training in this population. Suman et al (2001), suggested that a break of more than 48 hrs must be given between bouts of resistance training.
| |
| | |
| o Resistance exercise causes microtrauma to muscles already in a compromised state. o Resistance exercise in burned patients stimulates protein synthesis as in unburned subjects- However; a longer period of recovery may be required for optimum results.
| |
| | |
| Type/ Intensity: Children: using free weights or resistive machines: 1 set of 50-60% of the patients 3 RM week 1, followed by a progression to 70-75% for week 2-6 (4-10 repetitions), and 80-85% week 7-12, (8-12 repetitions) (Suman et al 2001; Suman and Herndon 2007).
| |
| | |
| Isokinetic training: 10 reps at 150 degrees per second, using 1-5 sets for the 1st-5th session,6 sets for the 6th-24th session, and 10 sets from 25th to 36th session, with three minute rests between sets. (Ebid et al 2012).
| |
| | |
| Mixed and functional strength training: Grisbrook et al (2012b) commenced on the biodex, targeting specific muscle groups for the desired functional goal, and progressed to resistive machine and finally free weight training using functional items. Intensity was 50- 60% of 1 RM initially, for 10-15 reps, adjusting as 1 RM increased. While no studies have compared the optimum type/intensity of exercise, this may be the optimum approach. Providing functional exercises may also increase motivation and compliance.
| |
| | |
| Time: All the studies used a protocol of 12 weeks. There were no studies comparing the efficacy of shorter or longer time frames, however, given that loss of lean body mass is a possible cause of strength loss post burn, an exercise programme of longer than eight weeks is probably required to ensure hypertrophy and optimum gains in the burn patient (Suman et al 2001)
| |
| | |
| 71
| |
| | |
| 5.316 Safety Considerations for Strength and Aerobic Training:
| |
| | |
| Initiating aerobic and strength training:
| |
| | |
| ∙ studies stipulated a minimum of six months to two years post burn before initiation of programmes, though many subjects were included who had been burned many years before. These participants all benefited from the interventions.
| |
| | |
| ∙ Suman and Herndon (2007) suggested that the time frame of 6 months post burn was chosen based on clinical experience because by this time paediatric patients with >40% TBSA burns were
| |
| | |
| o 95% healed
| |
| | |
| o ambulatory
| |
| | |
| o had had the opportunity to return home
| |
| | |
| ▪ Therefore, more favourable psychological status
| |
| | |
| ∙ There were no studies investigating early training
| |
| | |
| o With extensive burns, adequate healing of wounds and medical stability required before initiating aerobic/strength exercise
| |
| | |
| Other safety considerations:
| |
| | |
| ∙ Though exercise has been shown to increase lean body mass, liaison with doctors concerning anabolic steroids and medication and with dieticians regarding optimal nutrition is recommended in order to ensure correct management of hypermetabolisim.
| |
| | |
| ∙ Caution should be used with regard to impaired thermoregulation. Monitoring of heart rate and blood pressure may be advisable, particularly on initiation of exercise and when exercising with additional thermal stress. Manage the environment to minimise thermal stress initially in particular.
| |
| | |
| ∙ Particularly those at risk of reduced pulmonary function post burn (i.e., >30% TBSA, injury to torso, or inhalation injury), monitor SpO2 and RPE during exercise. Allow additional rest periods to allow SpO2 to return to normal levels post exercise, as this has been shown to be delayed.
| |