Burn Physiotherapy

Original Editor - Carin Hunter based on the course by [TUTOR LINK/ TUTOR NAME]
Top Contributors - Carin Hunter

Rehabilitation Post Burn Injury[edit | edit source]

Significant improvements in the medical and surgical management of burns has occurred  in the last century. Increased survival rates mean that focus is turning to achieving  optimal functional outcomes.

∙ Burn survivors often suffer from

o permanent scarring, reduced range of motion, weakness, and impaired  functional capacity

o psychological and social problems, which significantly affect their ability to  resume their normal activities post discharge  

∙ Rehabilitation requires a prolonged, dedicated and multidisciplinary effort to optimise  patient outcomes, as inpatients and outpatients.

(Schneider et al 2012; Disseldorp et al 2007; Esselman, 2007)

The aims of the multidisciplinary rehabilitation of a burn include:

∙ Prevention of additional/deeper injuries

∙ Rapid wound closure

∙ Preservation of active and passive ROM

∙ Prevention of infection

∙ Prevention of loss of functional structures

∙ Early functional rehabilitation (Kamolz et al 2009) The physiotherapist may only have a role in achieving some of these goals. ∙ Above all cause no harm.  

Early initiation of rehabilitation is essential to maximise functional outcomes for the patient  

∙ 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).

Role of the Physiotherapist in the Rehabilitation of the Acute  Burn Patient[edit | edit source]

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.  

Depending on the size and the severity of the injury this stage may last from a few days to a  few months (Procter 2010)


∙ Acute phase of inflammation

∙ Pain

∙ Oedema increasing for up to 36 hours post injury

∙ Hypermetabolic response, peaking at five days post injury

∙ Early synthesis and remodelling of collagen


∙ Reduce risk of complications

o Reduce oedema, particularly where it poses a risk for

▪ impinging on peripheral circulation or airways

▪ Predisposition to contractures

∙ Prevent deformities/loss of range

∙ Protect/promote healing

Common treatment techniques

∙ Immobilisation

o Bed rest  

o Splinting

∙ Positioning


5.11 Immobilisation

5.111 Rationale for Immobilisation

Acute Stage ∙ Prevent deformities  

∙ Maintenance of range of motion  ∙ Promote Healing

∙ Protection

(Ashe 2001; Kamolz 2009)
Sub-acute Stage ∙ Maintenance of range of motion ∙ Regain range of motion (Kwan 2002; Boscheinen Morrin 2004)

Table 6: rationale for immobilisation

5.112 Positioning in the Acute Stage

*Modify according to burn area, patient pain and medical status.*

Area Of Burn Common Contracture Recommended position
Anterior neck Neck flexion: loss of neck  contours and extension Neck in extension. If head needs to be  raised, do not use pillows.
Posterior neck Neck extension. Loss of  

flexion and other movements

Head in flexion. Sitting or lying with a  pillow behind the head.
Axilla Limited abduction/ protraction  with burn to chest Lying/ sitting with arms abducted. Slings,  pillows, figure of eight bandage around  chest for stretch. Prone lying
Anterior Elbows Flexion Elbow extension
Groin Hip flexion Prone lying, legs extended, no pillow under  knees in supine, limit sitting/side lying
Back of knee Flexion Long sitting/ supine lying, no pillow  beneath knees
Feet Dependent on area Aim to maintain 90 degrees at ankle:  pillows in bed, sitting with feet on floor
Face Variety: inability to  

open/close mouth/eyelids

Regular change of expression. Soft rolls  may be inserted into the mouth

Table 7 Positions of immobilisation, for pictures, see Procter, 2010


5.113 1mmobilisation post skin reconstruction surgery

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)  

The following is a table drawn up using current literature on the recommended  immobilisation times for the various skin grafts:

Surgical Procedure Immobilisation Time
Biological Dressings <24hours
Autograft (superficial to intermediate) 24-48hours
STSG 3-5 days
FTSG 5-7 days

Table 8 Surgical procedure and related immobilisation (ANZBA 2007; Edgar and Brereton 2004)

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).  

For a physiotherapist the most important concepts to grasp are:

• What is the minimum timeframe of immobilisation post-surgery

• What structures MUST be immobilised

• Special considerations for movement, function and ambulation dependent on Donor sites and the structures repaired or excised during surgery.


5.114 Immobilisation of the hand

Deformity Prevention

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.

Figure16a. Dorsal hand burn resulting  

in claw deformityFigure 16 b: Position of safe  

immobilisation (Glassey, 2004)

Position of Safe Immobilisation

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).

5.115 Splinting

Physiological rationale for splinting (Kwan 2002)

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.

Categories of Splints


∙ Static or Dynamic

∙ Supportive or Corrective

∙ Rigid or soft

∙ Dorsal or Volar

∙ Digit, hand or forearm based (Boscheinen-Morrin 2004)  Static Splinting

∙ 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.

Fig 17: Thermoplastic palmar splints in the position of safe immobilisation (Glassey 2004)

∙ 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).


Dynamic Splinting

Fig 18: Velcro flexion straps  (Glassey 2004)

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).  

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).

Fig 19 Dynamic Extension Hand Splint

(Microsurgeon 2013)

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).

Fig 20 Dynamic flexion hand splint in glove form

(Microsurgeon 2013)


Overview of the Evidence:  

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.

Splinting Precautions

∙ 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)

∙ Unnecessary use of splinting may cause venous and lymphatic stasis, which may  result in an increase in oedema (Palmada et al 1999)

∙ Precaution must be taken to ensure that splints do not product friction causing  unnecessary trauma to the soft tissues (Duncan et al 1989).  

∙ 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).  

∙ Splinting should not be used in isolation but as an adjunct to a treatment regime Conclusion on Splinting

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.


Management of Oedema

Role of the Physiotherapist in the Rehabilitation of the Sub  Acute Burn Patient[edit | edit source]

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.  

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.  

The patient

∙ Primary closure of wound

∙ Scar remodelling

∙ Scar contraction


∙ Optimise scar appearance

∙ Limit effects of scar contraction/prolonged positioning on range of motion and  function

∙ Address effects of prolonged bed rest  

Common modalities

∙ Mobilisation- both mobility and specific joint mobilisation

∙ Scar management adjuncts

o Pressure garments, silicone, massage

∙ Continuation of oedema/ positioning management where necessary


5.21 Mobilisation

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).

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.  

5.211 Active ROM

∙ 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).

5.212 Passive ROM

∙ 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).

∙ 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).

∙ 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).


Frequency, Duration Recommendations

∙ Physiotherapy intervention should be twice daily with patients prescribed frequent  active exercises in between sessions.  

∙ For the sedated patient gentle passive range of motion exercises should be done 3  times a day once indicated (Boscheinen-Morrin and Connolly 2001).

∙ 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.  


∙ 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.  

∙ 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).

Evidence for hand mobilisation

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.  

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

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

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


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.

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

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.

Functional Rehabilitation of the Hand

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.

Practical factors to consider when mobilising

∙ Be aware of dressing clinic/daily dressing changes. Mobilisation should coincide with  this as it is important to monitor the wound during AROM frequently.

∙ Timing of pain relief. This should be timed appropriately to ensure maximal benefit  during treatment sessions.

∙ Observe the patient carrying out the AROM and PROM exercises prior to beginning  treatment. Also observe the patient taking on/off splints.

∙ Always monitor for post exercise pain and wound breakdown.

∙ 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)

Massage[edit | edit source]

Five principles of scar massage:

1. Prevent adherence

2. Reduce redness

3. Reduce elevation of scar tissue

4. Relieve pruritus

5. Moisturise (Glassey 2004) Scar Massage Techniques

∙ Retrograde massage to aid venous return, increase lymphatic drainage, mobilise fluid  ∙ Effleurage to increase circulation

∙ Static pressure to reduce pockets of swelling

∙ Finger and thumb kneading to mobilise the scar and surrounding tissue ∙ Skin rolling to restore mobility to tissue interfaces

∙ Wringing the scar to stretch and promote collagenous remodelling

∙ Frictions to loosen adhesions

(Holey and Cook 2003)

Guidelines for Massage during 3 Stages of healing
Inflammatory Phase gentle massage to decrease oedema and increase blood supply  (currently no high level evidence to support this)
Proliferative Phase Massage that applies gentle stress to the healing scar is recommended  to ensure collagen is aligned correctly.
Remodelling Phase Massage should be progressed to include prolonged stretching to  minimise adhesions. This is proposed to aid in scar tissue breakdown

Table 10 Guidelines for scar massage during healing stages (Glassey 2004)


Table 11. Evidence for the use of massage in scar management

Article Field et al 2000


Morien et al 2008

Pilot Study

Shin and Bordeaux,  2012 Lit review
Subjects 20 subjects in remodelling phase of  wound healing.  Randomly assigned into  2 groups

Massage Vs Control

8 Children  

Mean age 13.5 years  (10-17years)

All thermal burns  including hand burns

Not burn specific,  though the majority  of scars were of this  origin

10 articles: n=144  adult and children

Intervention Massage Therapy Group:

30minutes massage with  cocoa butter twice  weekly for 5 weeks

Control Group:

Standard Treatment

20-25 minute  massage session  once daily for 5 days


petrissage, friction,  lengthening rolling)

Session followed by  discussion of  psychosocial issues

Time to Rx: mean  4.3 months. +  variation in  protocols. 20  mins/day- 30 mins 2x  weekly. 1 Rx-6  months Rx


Itching: VAS

Pain: McGill Pain


Anxiety: State Trait  Anxiety Inventory

Mood: Profile of Mood  States

Likert pictorial scale  

Goniometry Range of  Motion

Patient and observer  scar assessment  scale, Vancouver  scar scale, thickness,  vascularity, colour,  pain, pruritus, mood,  anxiety, and  depression.
Results Massage Therapy Group  Reported: decreased  itching, pain, anxiety and  increased mood  

Ratings improved from  the 1st-last day of the  study

Increased ROM in  massaged tissue.  Decreased ROM in  unmassaged tissue

No significant  difference in mood  across time

45.7% improved in at  least one of the above  parameters. 54.7%  had no improvement.  

Noted massage was  more economical  than silicone/PGT.


Limitations Small Sample Size

No follow up


population. Mood Instrument may have  been influenced by  other factors.  Recruitment and area  to be massaged not  random

Small sample size

No follow up

No discussion of  quality or statistical  tests.

Conclusion on Scar Massage

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).

Recommendations for practice and safety considerations.

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)  

∙ Clean hands essential

∙ Use non irritating lubricant, free of any known sensitisers.  

∙ Modify practice according to patient stage of healing, sensitivity and pain levels. Contraindications: Shin and Bordeaux 2012

∙ Compromised integrity of epidermis

∙ Acute infection

∙ Bleeding

∙ Wound dehiscence,  

∙ Graft failure

∙ Intolerable discomfort

∙ Hypersensitivity to emollient

The Role of the Physiotherapist in the Rehabilitation of the  Chronic Burn Patient.[edit | edit source]

The patient

∙ Healing process may continue for up to two years, as scar tissue remodels and  matures

∙ May require functional retraining and integration back into the community and  activities.

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).

5.31 Aerobic and Resistance Training Post Burn

5.311 Rationale for Aerobic and Resistance Training

∙ Low cardiorespiratory endurance has been found to be a concern for all (Willis et al  2011)

∙ 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


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)

*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


∙ 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)


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).


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.

***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


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.


5.312 Aerobic Training: The Evidence

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  


Eleven articles  included

Eight RCTs

Pedro 6+

1 RCT<5, 1  non RCT, 2  static group  comparison

Randomised  controlled,  


blinded trial



controlled trial.



controlled trial.


experimental  controlled  



controlled trial

Oxandrolone, vs  osandrolone +  exercise, vs  exercise +  placebo,  





7 different  cohorts

5 children with  exceptionally  large TBSA

35 adults  mean 37.5  days post  burn, mean  TBSA 19.3% 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


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  



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  



12 week  inpatient  

physiotherapy  twice daily for 1  hr. aerobic and  resistance  


Aerobic 5 days  per week, 20-40  mins, 70-85%  VO2peak





Children and  adults after  extensive  

burns score  worse than  non-burned  

controls in all

Max aerobic  capacity:  

VO2 max.





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,


aspects of  fitness.

Burn patients  participating in  12 week  training  




more than  those without.


health scale

Results Work to  tolerance and  work to quota  significantly  



capacity. No  significant  

improvement  in control. No  significant  



WTQ and  WTT

No significant  improvement  in spirometry  values  



improvement  in VO2 peak  and time to  fatigue in both  groups.  


improvement  in satisfaction  with  



Burns patients  scored lower  on HRQOL  and quick dash  both before  and after the  intervention  

compared to  controls. 5/9  burn patients  reached  



improvements  in BSHS post  intervention.  No significant  increase in  DASH

No adverse  effects.  


improvement s in  functional,  


psychological  measures.

LBM increased  in all groups  except placebo showed average  decrease.  



highest relative  increase. Both  exercise and  drug only group  showed  


increase in  strength.  


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  


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  


blinding not  possible

Small subject  numbers, no  untreated  


blinding not  possible


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


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


5.314 Resistance Training: The Evidence



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)


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.