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CHAPTER39 Desquamating skin disorders
Introduction todesquamating skin
disorders
Also termed exfoliative and necrotizing diseases of the skin. Desquamation
of the skin literally means shedding of the skin. In normal physiology desquamation of the keratinocytes occurs approximately every 14 days.
Pathological desquamation involving skin and mucous membranes can cause
signicant morbidity and associated complications such as wound infection,
sepsis, poor nutrition and pain, synonymous with a major burns patient.
Classification
• Scalded skin syndrome (SSS). Characterized by skin lesions limited to
one mucosal surface
• Stevens Johnson syndrome (SJS). Two or more mucosal surface
involvement in addition to systemic complications and involving less than
10% body surface area
• Toxic epidermal necrolysis (TEN). Amore severe form of SJS aecting
more than 30% body surface area. Between 10% and 30% the condition
is frequently referred as SJS/ TEN
Aetiology
This is an immunological reaction to a foreign antigen. It is usually iatrogenic,
mainly involving the use of pharmacological agents. Antimicrobials, anticonvulsants, analgesics, NSAIDs, and corticosteroids have all been the culprit
causing TEN. In addition to drugs viral illnesses have also been reported to
cause such an immunological reaction to create SSS and SJS.
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CLINICAL PRESENTATION
Clinical presentation
Signs and symptoms typically seen:
• Apersistent pyrexia
• General malaise
• Cough
• The above may precede dermatological signs by up to 3 weeks
Following general symptoms patients present with generalized tender erythema. These progress to bullous eruptions. As the disease progresses
vesicles and larger bullae emerge from erythematic areas. Erythema is followed by epidermolysis.
Nikolsky’s sign is when the epidermis separates on gentle pressure of
the skin surface: a sign showing the clinician desquamation of the skin.
Sometimes there may be a lag period (1– 3 weeks) from initial immunological insult (ie. administration of a drug) to skin eruption. The dierential
characteristics of SSS, SJS, and TEN are summarized in Table 39.1
Table39.1 Clinical characteristics ofdesquamating skin disorders
SSS SJS TEN
Preceding
symptoms
Skin lesion
distribution
Character of
skin lesions
Biopsy features Dermoepidermal
Mucosal
involvement
Recovery time 4 weeks 6 weeks 6 weeks
Mortality rate 0% 0– 40% 25– 80%
Adapted with permission from Hawkins HK. The burn problem Apathologist ’s perspective. In
Herndon DN (ed.) Total burn care, 4th edn, p.555. Elsevier, Copyright © 2012, Elsevier Inc. All
rights reserved.
None Pyrexia, general
Symmetrical, limbs Variable; <10%
Some target lesions Vesicles;
separation with
a mononuclear
perivascular cell
inltrate with target
lesions
One surface Two or more Two or more and
malaise
TBSA
Nikolsky’s
positive
A more intense
dermal inltrate
than SSS
Pyrexia, general
malaise
Diuse; >30% TBSA
Epidermal
detachment; no
target lesions; large
lesions; Nikolsky’s
positive
Minimal dermal
inammatory
inltrate and large
areas of epidermal
detachment
severely aected
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CHAPTER39 Desquamating skin disorders
Pathology
A skin biopsy is crucial to identify the severity of the desquamation. The
dermal inltrates are made up of immunological cells including cytotoxic
T- cells and T- helper cells. Dendritic lymphoid cells are also seen in addition
to damaged dermal macrophages and necrotic keratinocytes. As seen in
other inammatory skin diseases there is a higher expression of HLA- DR
on the keratinocytes. Immunouorescence microscopy will reveal IgM antibodies and C3 along the dermoepidermal junction in SJS and TEN. The
immune reaction of these disorders is said to be a type II cytotoxic reaction
and type IV delayed hypersensitivity reaction.
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PATHOLOGY
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CHAPTER39 Desquamating skin disorders
Management outline
• TEN is a life threatening disease and thus a surgical emergency
• Admission to the burns unit
• Multidisciplinary team (MDT) approach
The role ofthe MDT
• Dermatology. Two punch biopsies to conrm TENS or SJS
• One biopsy in formalin, second in Michael’s medium for
immunouorescence
• Treatments to skin made collaboratively with plastic surgery and
dermatology
• Ophthalmology review early to assess for ocular therapy
• Anaesthesia and ICU teams to be involved at the time of referral or
admission to assess for requirements of intubation
Initial assessment
• Observations 1– 6 hourly including monitoring of airway. Include
standard set of bloods including full blood count, urea and electrolytes,
albumin, total protein
• Accurate medical and drug history and involve family and the
patient’s GP
• Precipitating symptoms such as fever, sore throat, conjunctival
symptoms, general malaise
• Commence early analgesic regime
• Liaise with dermatology, may proceed with a skin biopsy
• Liaise with dietician and assess for nasogastric feeding
• Stress ulceration prophylaxis should be started and pulmonary support
may require the input of the anaesthetic or intensivist team
• Corneal involvement can be common and should be managed with
regular saline drops and early involvement of the ophthalmology team
• Assess severity using the SCORTEN scale
• As with major burns, these patients require aggressive uid
resuscitation, additional nutritional support, expert wound care, and a
multidisciplinary approach involving physiotherapy, occupational therapy,
dietician for nutritional support, and psychology
• Drugs suspicious of causing the reaction should be discontinued
immediately
Further management
• Medical photography
• Daily multidisciplinary review
• Daily dressings to reduce risk of sepsis
• Clinical isolation
• Fluid and electrolyte balance
• Maintain peripheral IV access
• Anticoagulation prophylaxis
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MANAGEMENT OUTLINE
Wound management
• Swabs for microscopy, culture, and sensitivities
• Do not use prophylactic antibiotics as this may increase the risk of
wound sepsis
• Dressings daily and review by the MDT
Surgical approach tomanagement
• Debridement of necrotic epidermal tissue
• Coverage with a biological or synthetic dressings similar to those used in
major burns. Aparticularly good indication for Biobrane
• Debridement of sloughed tissue will reduce the risk of sepsis from
bacterial overgrowth
• Dressings will provide an analgesic eect over the tender
exposed dermis
• In order to reduce bacterial overgrowth topical agents containing silver
nitrate which may be present in dressings
• As these conditions are immunogenic, immunomodulating drugs such as
corticosteroids, cyclosporine A, and intravenous immunoglobulin have
been considered. Their use is controversial and these should not be
commenced until discussion with the transferring or admitting burns unit
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CHAPTER39 Desquamating skin disorders
Prognosis
The SCORTEN system was introduced to predict mortality in patients with
TENS and seven signicant factors were identied:
• Age >40years
• Evidence of cancer or haematological malignancy
• Tachycardia >120 beats/ minute
• TBSA involvement at day 1>10%
• Serum urea level >10mmol/ L
• Serum glucose level >14mmol/ L
• Serum bicarbonate level >20mmol/ L
The probability of death is given by the formula:
P(death)=e
where logit =– 4.448+1.237(SCORTEN)
Generally mortality rates are estimated (Table 39.2).
Table39.2 Mortality rates
No of risk factors Mortality rate
0– 1 3.2%
2 12.1%
3 35.3%
4 58.3%
>5 >90%
Adapted from Bastuji- Garin S, et al. SCORTEN: a severity- of- illness score for toxic epidermal
necrolysis. Journal of In vestigative Dermatology 2000;155(2):149– 53, Copyright © 2000.
The Society for Investigative Dermatology, Inc., with permission from Elsevier, http:// www.
jidonline.org/ article/ S0022- 202X(15)40939- X/ abstract.
logit
/ 1+e
logit
Further reading
Bastuji- Garin S, Fouchard N, Bertocchi M, etal. SCORTEN:a severity- of- illness score for toxic epi-
dermal necrolysis. Journal of Investigative Dermatology 2000;115:149– 53.
Creamer D, Walsh SA, Dziewulski P, et al. U.K. guidelines for the management of Stevens–
Johnson syndrome/ toxic epidermal necrolysis in adults 2016. British Journal of Dermatology
2016;174:1194– 227.
Guillaume JC, Roujeau JC, Revuz J, etal. The culprit drugs in 87 cases of toxic epidermal necrolysis
(Lyell syndrome). Archives of Dermatology 1987;123:1166– 70.
Yetiv J, Bianchini JR, Owens JA. Etiological factors in Stevens- Johnson syndrome. Southern Medical
Journal 1980;73:599– 602.
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Chapter40
339
Military burns
History 340
Epidemiology 340
Causes 340
General management 340
Burn infections 341
Outcomes 341
Prevention 341
Specic causes 1.Explosive weapons 342
Specic causes 2.Incendiary weapons 344
Specic causes 3.Chemical weapons 344
Specic causes 4.Cold burns 345
References 346
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CHAPTER40 Military burns
History
The concept of a dedicated burn team and unit was established in 1940 by
McIndoe at East Grinstead during the Battle of Britain.
Epidemiology
• 5% of all war casualties (troops and civilians) are burns,1 60% are
accidental and 40% combat.2 Combat burns are associated with greater
Injury Severity Scores, full thickness burns, and inhalation injury
• Mainly aects young males and exposed areas, eg. face and hands
• The majority are 75% TBSA,4 Up to 25% are >20% total body surface
area (TBSA)
5
Causes
• Explosive weapons (main5). Ordnance devices produce fragments from
the casing, Improvised explosive devices (IEDs) produce fragments from
and within the casing and cause more burns
2
• Incendiary weapons, eg. white phosphorous or napalm
• Chemical weapons. Can be lethal (eg. blistering) or incapacitating.
Blistering agents cause burns, eg. mustard gas.
• Radiation or nuclear weapons
• Environment, eg. contact, scald, electrical, cold (frostbite)
General management
During triage >70% TBSA have expectant care, 20– 70% TBSA +/ –
inhalation injury receive early evacuation, and <20% TBSA have delayed
hospital care.
• Levels of care include Level IMedical Support within the eld, Level
II Aid Station +/ - surgical capability, Level III Field Hospital oering
subspecialty care and Level IV Tertiary Burns Centre in home country.
Most soldiers arrive back within 2– 4days
• Resuscitation follows ATLS and EMSB/ ABA guidelines including
warming, IV crystalloid via the Parkland or modied Brooke formula,7
IV antibiotics, and tetanus prophylaxis if associated contaminated
battleeld wounds, and analgesia. Blisters are left intact until arrival in a
clean environment and wounds are dressed8 During evacuation chemical
thromboprophylaxis is given and nasogastric tubes are placed for enteral
feeding
• Early escharotomy is considered if deep circumferential burns prior to
transport8 but denitive surgery is performed early (<5days post injury)
in the burns centre
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2
3
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Burn infections
• Major organisms include Acinetobacter baumannii >Pseudomonas
aeruginosa >Klebsiella pneumoniae >Staphylococcus aureus. For the
rst 15days Acinetobacter and Staphylococcus predominate. After
15days Pseudomonas and Klebsiella predominate
3
• Topical antimicrobials dressings used include Mafenide acetate
(Sulfamylon), Silver sulfadiazine (eg. Flamazine), silver nitrate solution,
and silver- impregnated dressings (eg. Acticoat). Systemic antibiotics are
given in infected wounds
• Infection associated mortality occurs at higher rates in combat burns.
The main infections causing death include fungus (eg. Aspergillus),
Pseudomonas, and Klebsiella
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Outcomes
• Gross functional outcomes are good and similar to civilians3 but face and
hand burns can lead to long- term physical and psychological morbidity
• Mortality in military burns at the burn centre is 74%, which is similar
to civilians with same age range.3 The main cause is infection (760%).9
TBSA burn, presence of inhalation injury, ventilator days, and age >
40years are predictors of mortality
Prevention
• Pre- deployment education reduces preventable non- combat burns
• Fire- protective clothing reduces the severity of burn injuries
• Personal protective equipment may reduce penetrating injury
PREVENTION
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