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Chapter 8. Treatment ofHand Burns
decrease edema and improve cosmesis, they should be closely
monitored and modified. Silicone sheets may be helpful in
decreasing scar prominence. Use of a moisturizer to facilitate
scar massage usually helps to minimize itching and improve
scar mobility.
207
Long-Term Issues inHand Burns
With proper vigilance, patients with hand burns can regain
full function. Burns that take longer than 10–14days to heal
are often subject to formation of significant scarring; however, thickening of the scar is gradual and not visible for
2–6months after injury. As such, patients with second- and
third-degree hand burns should be followed for at least a
year to detect significant scar formation and contracture
development. Evaluation of range of motion and strength,
as mentioned above, is vital, and referral for hand therapy
and/or to a burn or hand specialist is essential to assure
maintenance of hand function. Pressure garments, specially
fitting gloves that provide scar compression, are often prescribed to minimize hypertrophic scar formation in burned
or grafted hands [24]. Pressure garments should be measured and fitted after burn wounds are healed and edema
resolved. Despite appropriate therapy, patients can develop
scar contractures due to delays in healing, genetic predisposition, or growth (in children). Contractures impeding hand
function generally occur at joints, web spaces, and the palm
in both ungrafted and grafted hand burns. Surgical contracture release is indicated for a hand burn scar that significantly impedes hand function despite appropriate splinting,
stretching, and therapy. Timely release of hand burn scar
contractures prevents loss of hand motion. Surgical burn
scar contracture release, using the reconstructive ladder, is
indicated for contractures that threaten joint function or
hand growth. Waiting for a scar to “mature” (i.e., lose its
pink color) for 6–12months can result in permanent loss of
function. However, early release should be reserved for fail-
208
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T. L. Palmieri
ure of non-operative therapies, severe contractures impeding function, and in patients/families who are committed to
participating in post-operative hand therapy [25].
Another common long-term problem after hand burns is
pruritus, which can be debilitating. Although no single treatment modality successfully treats pruritus in all patients,
application of moisturizer combined with scar massage has
long been used to mitigate itch. Commonly used medications
include oral diphenhydramine, hydroxyzine, chlorpheniramine, gabapentin, and occasionally H2 blockers. Anecdotal
reports of laser use and reduction of pruritus have appeared
in the literature, but prospective trials are sparse [26].
Colloidal oatmeal baths have also been used effectively in the
treatment of burn pruritus [27].
Conclusion
Hand burns are frequent and morbid injuries that have
significant long-term functional implications. Accurate
assessment, treatment, and follow-up or referral are essential
to optimize patient health related quality of life. The anatomy
of the skin is a key factor determining the potential
complications of hand burns. The basic tenets of hand burn
care are to (1) promote a wound healing environment, (2)
maintain circulation, (3) prevent infection, (4) obtain wound
closure, and (5) maintain motion. All care of the burned hand
is based on these principles. Referral to a specialized burn
center is warranted for any second- or third-degree hand
burn; a hand burn that does not heal within 2weeks; or a
hand burn that impacts range of motion or function. Skin
grafting is designed to mitigate scar and prevent scar
contracture and is generally indicated for burns that do not
heal within 2–3weeks. Hand therapy is essential to maintain
function in delayed wound healing situations or after surgery.
In the long term, scarring, itch, and contracture formation are
Chapter 8. Treatment ofHand Burns
209
the primary concerns. Medications, therapy, and specialized
pressure garments may be required. The overall care of the
burned hand is founded in the application of basic principles
and skill sets of multiple team members. With proper initial
care, the patient with a hand burn can have a functional and
cosmetically acceptable outcome.
References
1. Pan BS, Vu AT, Yakuboff KP.Management of the acutely burned
hand. J Hand Surg Am. 2015;40:1477–84.
2. Keyerman PA, Andres LA, Lucas HD, etal. Reconstruction of
the burned hand. Plast Reconstr Surg. 2011;127:752–9.
3. Johnson SP, Sebastin SJ, Rehim SA, Chung KC.The importance
of hand appearance as a patient-reported outcome in hand
surgery. Plast Reconstr Surg Glob Open. 2015;3(11):e552. https://
doi.org/10.1097/GOX.0000000000000550.
4. Palmieri TL, Nelson-Mooney K, Kagan R, Stubbs T, etal. Impact
of hand burns on health-related quality of life in children
younger than 5 years. J Trauma. 2012;73(3):S197–204.
5. Maddern LH, Cadogan JC, Emerson MP. ‘Outlook’: a
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6. Schmidt HM, Lanz U.Chirugische anatomie der hand 2, uberarb,
und aktualisierte aufl. Ed. Stuttgart. G.Thieme; 2003.
7. Pham TN, Hanley C, Palmieri TL, Greenhalgh DG. Results of
early excision and full-thickness grafting of deep palm burns in
children. J Burn Care Rehabil. 2001;22:54–7.
8. Wibbenmeyer L, Gittelman MA, Kluesner K, Liao J, et al.
A multicenter study of preventable contact burns from glass
fronted gas fireplaces. J Burn Care Res. 2015;36(1):240–5.
9. Spauwen PH, Brown IF, Sauer EW, et al. Management of
fingernail deformities after thermal injury. Scand J Plast Reconstr
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10. Simpson RL, Flaherty ME.The burned small finger. Clin Plast
Surg. 1992;19:673–82.
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11. ACS Guidelines. Guidelines for trauma centers caring for burn
patients. In: Resources for optimal care of the injured patient,
Chapter 14; 2014, pp.200–106.
12. Cuttle L, Kempf M, Liu PY, etal. The optimal duration and delay
of first aid treatment for deep partial thickness burn injuries.
Burns. 2010;36(5):673–9.
13. Venter TH, Karpelowsky JS, Rode H.Cooling of the burn wound:
the ideal temperature of the coolant. Burns. 2007;33(7):917–22.
14. Cho YS, Choi YH.Comparison of three cooling methods for burn
patients: a randomized clinical trial. Burns. 2017;43(3):502–8.
15. Rovee DT, Kurowsky CA, Labun J.Local wound environment
and epidermal healing. Mitotic response. Arch Dermatol.
1972;106:330–4.
16. Jan SN, Khan FA, Bashir MM, et al. Comparison of laser
doppler imaging (LDI) and clinical assessment in differentiating
between superficial and deep partial thickness burn wounds.
Burns. 2018;44:405–13.
1 7. Pan SC.Burn blister fluids in the neovascularization stage of
burn wound healing: a comparison between superficial and deep
partial-thickness burn wounds. Burn Trauma. 2013;1:27–31.
18. Smith MA, Munster AM, Spence RJ. Burns of the hand and
upper limb-a review. Burns. 1998;24:493–505.
19. Palmieri TL, Greenhalgh DG. Topical treatment of pediatric
patients with burns: a practical guide. Am J Clin Dermatol.
2002;3:529–34.
20. Sheridan, Salisbury RE, Wright P.Evaluation of early excision of
dorsal burns of the hand. Plast Reconstr Surg. 1982;69:670.
21. Robson MC, Smith DJ Jr, VanderZee AJ, et al. Making the
burned hand functional. Clin Plast Surg. 1992;19:663–71.
22. Greenhalgh DG, Barthel PP, Warden GD.Comparison of back
versus thigh donor sites in pediatric patients with burns. J Burn
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23. Sheridan RL, Baryza MJ, Pessina MA, et al. Acute hand
burn in children: management and long-term outcome based
on a 10-year experience with 698 injured hands. Ann Surg.
1999;229:558–64.
24. Atiyeh BS, El Khatib AM, Dibo SA. Pressure garment therapy
(PGT) of burn scars: evidence-based efficacy. Ann Burns Fire
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Chapter 8. Treatment ofHand Burns
26. Ebid AA, Ibrahim AR, Omar MT, El Baky AMA. Long-term
effects of pulsed high-intensity laser therapy in the treatment
of post-burn pruritus: a double-blind, placebo-controlled,
randomized study. Lasers Med Sci. 2017;32(3):693–701. https://
doi.org/10.1007/s10103- 017- 2172- 3. Epub 2017 Feb 23.
2 7. Reynertson KA, Garay M, Nebus J, Chon S, Kaur S, Mahmood
K, etal. Anti-inflammatory activities of colloidal oatmeal (Avena
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Chapter 9
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Burn Wound Infection
JosephE.Marcus, KevinK.Chung, andDanaM.Blyth
Introduction
Burn wound infections are common complications after a
burn injury. Depending on the burn center, they represent
either the most common or second most common nosocomial
infectious complication [1]. The two greatest risk factors for
bacterial burn wound infection include delayed excision as
well as increased total body surface area (TBSA) of burn
injuries [2]. These skin and soft tissue infections tend to occur
J. E. Marcus
Department of Medicine, Infectious Diseases Service, Brooke
Army Medical Center, Joint Base San Antonio,
Fort Sam Houston, TX, USA
e-mail: Joseph.e.marcus3.mil@health.mil
K. K. Chung (*)
Department of Medicine, Uniformed Services University, Bethesda,
MD, USA
D. M. Blyth
Department of Medicine, Infectious Diseases Service, Walter Reed
National Military Medical Center, Bethesda, MD, USA
e-mail: dana.m.blyth.mil@health.mil
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
J. O. Lee (ed.), Essential Burn Care for Non-Burn Specialists,
https://doi.org/10.1007/978-3-031-28898-2_9
213
214
J. E. Marcus et al.
early in the care of patients with burn injuries, with most
infections occurring in the first week after burn [3]. While less
prevalent, fungal wound infections are also seen, but later in
hospitalizations and associated with older age, greater TBSA
involvement, diabetes, use of total parenteral nutrition, and
longer hospital stays [4]. Infections are not only associated
with damage to the skin and underlying tissue, but can be
associated with sepsis and development of multi- organ dysfunction and death [5].
Several factors work together to predispose a patient to
burn wound infections. After a patient suffers a burn injury,
there is compromise of the integrity of the protective epithelial layers and a devascularized, protein rich eschar is left
behind that can harbor microorganisms. While the initial burn
injury is associated with an immediate pro-inflammatory
response, this response is quickly followed by immunosuppression that affects both the innate and adaptive immune
system with macrophages, neutrophils, and Th-1 cells being
primarily affected [6–8]. The combination of ease of pathogen
entry from the loss of barrier as well as the decreased immunologic function leads to an increase in infectious potential
for burn wounds.
Despite these risks, with modern burn management,
wound infections are becoming less common and have less
associated morbidity. Historically patients were managed
with delayed debridement. After the injury, bacterial growth
was tolerated to break down the eschar with additional passive debridement performed by immersion hydrotherapy and
delaying grafting until there was separation of eschar and
clear granulation tissue covering the wound [9]. Since the late
1980s when the benefits of early excision were shown, there
has been increased use of early excision in the management
of burns, and it is now considered the standard of care [10].
The use of early excision strategies resulted in a drop in burn
wound sepsis from 6% to 1% [11]. With early debridement,
there was a transition to early coverage of wounds which also
reduced subsequent infection [12]. Definitive coverage is performed by application of autograft skin (taken from non-
Chapter 9. Burn Wound Infection
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215
burned areas of the patient’s own skin) or allograft skin
(either fresh or frozen from cadavers). Temporary coverage
can be performed with skin substitutes made from acellular
animal collagen. Of note, with autograft skin, there is also risk
of infection at site of procurement as well as site of engraftment [13]. Additional key advances in the treatment of burn
patients include the use of topical antimicrobials, such as silver sulfadiazine, reducing the rates of burn wound infection
by up to 50% [14, 15].
Diagnosis
The diagnosis of a burn wound infection starts with clinical
suspicion. The most common changes associated with burn
wound infection include erythema over the wound margin,
edema, purulence, graft failure, and pain with systemic signs,
such as fever [1]. These symptoms are generally associated
with more invasive infections and are not sensitive or specific
enough alone to make a diagnosis [16]. Therefore laboratory
measures are usually needed to assist in the diagnosis.
The gold standard for diagnosis of a burn wound infection
is histology demonstrating organism invasion into the dermis
[17]. Compared to other methods, histology has the greatest
specificity and is the most correlated with clinical outcome of
any microbiological sampling technique [18]. Biopsy, however, is limited by the significant turn-around time in preparing and analyzing samples as well as the pathology expertise
required to interpret the sample.
With biopsy, quantitative cultures can be performed to
determine the causative organism, however, this is also a
labor-intensive process. In quantitative cultures, a known
weight of sample is collected, so that a determination of
organisms per gram can be calculated. The number of organisms isolated by quantitative cultures is correlated with subsequent risk of sepsis [19]. Quantitative cultures have been
used increasingly, but are generally restricted to large burn
centers [20]. Systematic reviews have shown heterogeneity in
J. E. Marcus et al.
216
T . Denitions of burn infections per American Burn
Association
Wound colonization <105 organisms/gram of tissue, no
evidence of invasion on histology or
biopsy. Asymptomatic
Wound infection >105 organisms/gram of tissue, evidence
of invasion on histology or biopsy.
Symptomatic
Invasive wound
infection
Cellulitis Wound infection+erythema, warmth or
Necrotizing infections Wound infection+deep wound necrosis
Adapted from Greenhalgh etal.
Wound infection+either separation of
eschar, invasion into unburned tissue, or
sepsis
tenderness over wound
the different mechanisms of quantitative cultures from
wounds and caution should be raised when interpreting cultures strictly by bacterial counts [21].
The American Burn Association developed a system to
differentiate wound infection from colonization using quantitative cultures as well as histology. This schema is used in
research and some larger burn centers (Table 9.1) [16]. As
detailed earlier, both biopsy and quantitative culture require
significant investment in clinicians and laboratory skills and
are a challenge to perform even at large burn centers. Due to
this significant investment, and conflicting techniques in the
literature, there is great variability in the practice patterns of
different institutions.
As most centers do not have the capability to perform
biopsy (histopathology) and quantitative culture, the most
widely used method is serial surveillance with superficial
swabs. These swabs are collected after removal of all bandages and creams over a 1 cm area with enough force to
cause minimal bleeding [22]. Other methods such as applying agar plates to wounds and using saline moistened gauze
to collect samples are limited due to reliability and time
Chapter 9. Burn Wound Infection
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217
required, respectively [23]. Superficial cultures may be used
to make semi-quantitative classifications of bacterial inoculum with measurements such as “few organisms” to “many
organisms.” These semi-quantitative counts and the species
of organisms recovered vary across different areas of the
wound and therefore multiple samples from different locations of the wound should be taken at each collection to get
a better representation of the biodiversity of flora and antimicrobial resistance to guide management [24]. The limitations of these cultures include sampling many organisms that
are likely not pathogenic and the frequency of sampling to
understand changes in flora.
In comparison to bacterial wound infections, fungal
infections typically occur later in the course of a burn
recovery. Fungal burn wound infection should be suspected when there is recurrent necrosis after serial debridements, decay seen on the wound edges, rapidly expanding
caseating necrosis, or with graft failure especially in older
patients with higher TBSA burn after spending several
weeks in the hospital [1, 25]. Fungal infections typically are
not diagnosed by quantitative cultures instead by clinical
presentation, histology, and qualitative culture. On histopathology, fungal infections typically have at least 105
organisms per gram of tissues and have evidence of dermal
invasion and is considered invasive when infection affects
deeper tissue or blood vessels [18]. To accurately perform
laboratory testing, two samples must be collected with
each biopsy: one for histology and one for culture. Histology
is used to determine the extent of infection, while culture
is used to identify the causative fungus and to guide antifungals. Close coordination between the surgeon and the
laboratory is essential to ensuring the appropriate tests on
collected samples. Histology that shows fungal elements in
non-viable tissue, such as eschar, is generally considered
fungal wound colonization rather than infection [26].
Unfortunately, indirect markers of fungal invasion such as
serum beta-D- glucan or galactomannan have poor predictive value for infections in patients with burn injuries [27].
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