Post-burn healing: quantifying optimal compression

Mrs Rosemary Kendell1, Ms Inge (Hui Ing) Wong2, Dr Sarah McGarry3, W/Prof Fiona  Wood4

1Fiona Stanley Hospital, Perth, Australia, 2Fiona Wood Foundation, Perth, Australia, 3Curtin University of Technology, Perth, Australia, 4Burn Service of Western Australia, Perth, Australia


Pressure garment therapy, has been widely used as the first-line intervention for the prevention and/or reduction of hypertrophic scarring.

The current evidence regarding the effectiveness of pressure garments on hypertrophic scarring is scant, secondly, there is inadequate empirical evidence regarding the actual interface pressure exerted by a garment. Furthermore, there is a failure to acknowledge differing levels of compression based on body site and the effect of movement.

A literature review revealed a single histological study conducted by Li-Tsang et al. (2014) the results of which indicated that pressure therapy elicited an early yet positive change in hypertrophic scarring. The study also indicated that there was an inhibition of proliferation of basal keratinocytes and a correlated reduction in myofibroblasts.

This study, introduced at ANZBA 2018, and now concluded has specifically investigated the impact of compression therapy on scar histopathology, and the link between the level of compression and assessed scar outcomes.

This study has quantified the degree of mmHg compression exerted by different garments on burn injured patients wearing custom-made or ready-to-wear garments, but also the variability of that compression affected by body site and movement factors (using Pico-Press).

Through the utilisation of skin biopsies taken at periodic intervals to analyse scar histology, mmHg compression readings, and clinician assessed and patient perception scar outcome measures, this study seeks to assess the therapeutic efficacy of pressure garment therapy.


Li-Tsang, CWP, Feng B, Huang, L, Liu, X, Shu, B, Chan, YTY & Cheung K 2015, ‘A histological study on the effect of pressure therapy on the activities of myofibroblasts and keratinocytes in hypertrophic scar tissues after burn’, Burns, vol. 41(5), pp. 1008-1016.

The treatment of deep dermal burn wounds with Platelet Rich Fibrin (PRF) after enzymatic debridement

Dr Alexandra Schulz1, Professor Dr Paul Christian Fuchs1, Dr Wolfram Heitzmann1, Dr Jennifer Lynn Schiefer1

1Department of Plastic Surgery, Cologne Merheim Medical Center, University of Witten Herdecke, Cologne, Germany



Enzymatic debridement was found to remove burn eschar selectively. Thus, vital tissue can be preserved and burn wounds can heal spontaneously in many cases. However, healing time can be significantly prolonged depending on burn depth and extend. It is therefore questionable, whether the application of Platelet Rich Fibrin (PRF) can shorten the wound healing time and thus improve long term scar quality.


In a single-centre clinical trial we treated patients with partial thickness to deep dermal burns by enzymatic debridement followed by PRF application. All patients wear compression clothing over 6 months. After 8 and 12 months, the aesthetics and function of the scar were assessed objectively and subjectively.


30 patients (age min16 years, max 70 years; TBSA min 1%, max 35%) with partial thickness to deep dermal burns (among them 10 facial burns) were included in the study.  Between 0.5% and 9% burn surface was treated enzymatically followed by PRF application. PRF preparation and application was easy to learn even for unexperienced users with some device related issues in the early stage of their learning curve. Patients reported minor pain during procedure without additional anaesthesia. No adverse occurred during any treatment. It was found that by adding PRF, wound healing time could be reduced. We found excellent results in scaring after 8 and 12 months.


The treatment of partial thickness to deep dermal burns with PRF following enzymatic debridement might be suitable to improve wound healing, scar quality and the functionality of the hand after burn injury. The treatment is easy to handle and patients tolerate the treatment well.


Dr. Alexandra Schulz is a private lecturer at the University of Witten/Herdecke and a specialist in Plastic Surgery. She is working since many years in burn reserach with a special focus on enzymatic debridement and burn wound treatment.

Wound healing after cultured epithelial autografting in patients with massive burn injury: a cohort study

Mr Cheng Hean Lo1, Dr Shiva  Akbarzadeh1, Professor Catriona McLean2, Mr Andrew Ives1, Dr Eldho Paul3, Professor Wendy Brown4, Ms Heather Cleland1

1Victorian Adult Burns Service, Melbourne, Australia, 2Department of Anatomical Pathology, The Alfred, Melbourne, Australia, 3Department of Epidemiology & Preventive Medicine, Monash University, Melbourne, Australia, 4Monash University, Melbourne, Australia


Background/ Aim

Last century, our laboratory produced Cultured Epithelial Autograft (CEA) for clinical use by the affiliated adult burn service and other burn units across the country. Production of CEA for clinical use was discontinued after several years because of a low success rate and subsequent low demand. Recently at our burns unit, a cell culture program was re-introduced as a direct response to the need for improvement in ongoing deficiencies and clinical requirements in burn wound closure. The aim of this study was to validate the laboratory processes and clinical algorithms established and share our recent clinical experiences involving CEA.


This observational cohort study recruited patients with burns exceeding 35% TBSA admitted to the Victorian Adult Burns Service at The Alfred (December 2013 – December 2016). Autologous keratinocytes were expanded and delivered via sheets of fibrin carrier.


Twelve patients were recruited to participate in the study. Thirty-two sites were treated with CEA. CEA applied in combination with widely meshed SSG led to the highest take rate (90.1%) at 7-10 days. Further debridement and grafting was necessary in sixteen of thirty-two sites treated, all involving wound beds prepared with Cuono method or sites treated with CEA only.


It is important to address the problem of wound bed contamination, either through increased resistance on the part of the construct or wound bed sterilization. Improved understanding of the relative importance of vascularisation, control of cell behaviour, the extracellular matrix, immune function and intrinsic antimicrobial capacity for graft take would then inform a more targeted approach to skin tissue engineering for wound closure in severe burns.


Specialist plastic & reconstructive surgeon with the Victorian Adult Burns Service at The Alfred, Victoria.  He has published more than thirty peer-reviewed journal articles, co-authored a textbook in reconstructive surgery and presented at national and international meetings. He is a senior adjunct lecturer at Monash University and is actively engaged in research.

Utilising mouse models to investigate the link between burn injury and cancer

Dr Lucy Barrett1,2, Dr Jason Waithman1, Dr Vanessa Fear1, Professor Fiona M Wood3,4,5, Dr Mark Fear3,4

1Telethon Kids Institute, Perth, Australia, 2Institute for Respiratory Health, Perth, Australia, 3Burn injury research unit, School of Biomedical Sciences, University of Western Australia, Perth, Australia, 4Fiona Wood Foundation, Perth, Australia, 5Burns Service of Western Australia, WA Department of Health, Perth, Australia


Burn injury is a major public health issue, and while advances in acute care have significantly improved survival and patient outcomes, recent studies using long-term hospital data from burn patients in Western Australia and Scotland with over 30 years follow-up have shown that burns are associated with an increase in rates of cancer. Evidence from our research strongly suggests that immune dysfunction induced by burn injury persists long-term, leading to a chronic suppression of the immune system. The immune system is known to play an important role in cancer control and prevention, and we hypothesise that this sustained immune dysfunction leads to the observed increase in cancer incidence in burn patients.

In order to investigate this link, we tested three different models of tumour development in combination with our established murine model of non-severe burn injury. Whilst no significant difference in primary tumour growth was observed using a B16 melanoma model, an epicutaneous model of tumour growth with limited penetrance demonstrated a significant increase in tumour development in comparison to sham injured control mice. Our results support the population studies suggesting burn injury leads to increased susceptibility to cancer. This model will now be used for future mechanistic studies, in which we aim to gain a better understanding of the mechanisms underlying increased susceptibility to cancer after burn injury.


Dr Barrett is an early-career researcher with a particular interest in understanding how burn injury can have long-term impacts on patient health through disruption of cellular and molecular functions.

Broad immunophenotyping of paediatric burn survivors demonstrates long-term changes to immune profile.

Mr Blair Johnson1, Mr Andrew Stevenson1, Ms Helen McGuire2, Mr Matthew Linden1, Ms Fiona Wood1,3, Mr Mark Fear1

1University Of Western Australia, Crawley, Australia, 2University of Sydny, Sydney, Australia, 3Department of Health, Perth, Australia


Epidemiological studies conducted within Australia have demonstrated that survivors of burn injuries are at a long-term risk of developing a range of morbidities. The personal and social burden is significant, with patients demonstrating a risk of increased lengths of hospitalisation. The mechanisms underlying this pattern of disease is not yet understood; however, many of the post-burn morbidities observed could be the result of immune dysfunction.

Children aged 0-3 are at the greatest risk of a burn injury that results in hospitalisation. Most injuries (84%) are non-severe with a total body surface area (TBSA) involvement of <10%. Plasma and PBMCs were collected >3 years after injury from 38 paediatric burn survivors aged <4yo at the time of injury, and from age/sex-matched controls.

Plasma was assessed using a Luminex assay targeting 13 cytokines. TNFa, IL-2, IL-7 and IFNg were all significantly elevated in the burn cohort.

PBMCs from 22 patients and matched controls were stained with a bespoke panel of 40 metal-conjugated antibodies and measured using a Helios mass cytometer. Unsupervised clustering analysis and hierarchical gating strategies were implemented to identify subpopulations that were altered in the burn survivors. Memory T-regulatory cells, Th17 cells, central memory CD8+ T cells, and central memory CD4+ T cells were all generally elevated (0.05 < p < 0.1) in the burn cohort.

This study has demonstrated a lasting change to the immune profile of burn survivors in both the cellular compartment and circulating cytokines. It suggests new avenues for research into post-burn immune suppression and regulation.


Blair has just begun his PhD at the University of Western Australia investigating changes to the immune system and platelet function following burn injury.



ANZBA is a not for profit organisation and the peak body for health professionals responsible for the care of the burn injured in Australia and New Zealand. ANZBA encourages higher standards of care through education, performance monitoring and research.

Conference Managers

Please contact the team at Conference Design with any questions regarding the conference.

© 2020 Conference Design Pty Ltd