ACUTE MEDICINE II

Acute dermatological Key points

emergencies C Dermatological emergencies can present with a wide range of
cutaneous and systemic clinical features
George Coltart
Adam Fityan
C Clues that a skin rash is concerning include associated pyrexia,
systemic symptoms, pain, purpura, blisters and mucosal
involvement
Abstract
C Some severe drug rashes can occur up to 6 weeks after
Acute dermatological emergencies cover a wide range of severe skin
starting a medication. A thorough review of all medication
eruptions. Several of these rashes are potentially life-threatening and
started within this period is important to ensure that the
carry significant morbidity and mortality. Dermatological emergencies
causative drug is identified and stopped
occur across all spectrums of age, race and gender. Rapid diagnosis
is vital to instigating appropriate treatment and reversing the underlying
C When managing dermatological emergencies, support the skin
precipitant. High-quality multidisciplinary management with specialist
with the regular application of a greasy emollient and monitor
nurses, general physicians and dermatologists is essential to ensure
for and manage the pathological effects of skin failure
patients can be kept systemically stable while appropriate treatments
are instigated. In this article we aim to cover some of the most signifi-
cant emergency dermatological presentations and their management.
Keywords Dermatology; DRESS; emergency; erythroderma; MRCP; Specific dermatological emergencies
pemphigus; StevenseJohnson syndrome; toxic epidermal necrolysis; Erythroderma
vasculitis Erythroderma is the term given to a condition presenting with
widespread erythema and scale affecting >90% of a patient’s
body surface area (BSA).1 Erythroderma can be idiopathic or
Definition and aetiology occur as a result of a drug reaction or primary dermatological
disease such as eczema or psoriasis. More rarely, conditions such
Dermatological emergencies can result from the flaring of a pri-
as pityriasis rubra pilaris or cutaneous lymphoma (Sezary syn-
mary dermatological disease, or occur in response to underlying
drome) can present as erythroderma. Clinicians should enquire
systemic disease or as a reaction to exogenous stimuli such as
about preceding rashes or the recent introduction of a new
drugs or infections. Severe rashes can cause failure of normal
medication that might guide the diagnosis.
skin function and/or herald significant systemic conditions that
Additional features include shivering, peripheral oedema,
require urgent treatment.
lymphadenopathy (dermatopathic), tachycardia, hypothermia or

General principles of management

Any widespread skin eruption can impair the normal physio-
logical skin functions summarized in Table 1. In managing any Physiological functions of the skin
dermatological emergency, meticulous nursing care is essential
Physiological role of skin Pathological effect of
to ensure skin integrity is maintained. Bland emollient ointments
skin dysfunction
with a high lipid content (e.g. 50:50 liquid:white soft paraffin)
helps to maintain the skin barrier function, preventing loss of Homeostasis Thermoregulation Hypo/hyperthermia
heat and water, and provides symptomatic relief to patients. Loss Prevention of fluid and Electrolyte abnormalities
of the skin barrier impairs thermoregulation and can cause sig- electrolyte loss Dehydration
nificant transepidermal water loss (up to 2.5 litres/day in High-output cardiac
erythrodermic patients); therefore patient temperature, fluid failure
status and electrolytes must be carefully monitored. Patients with Environmental Barrier against trauma Infection
an impaired skin barrier function can be vulnerable to secondary protection and pathogens
bacterial and viral infections, and therefore require close moni- Immunosurveillance Infection/allergies
toring and prompt treatment if identified.1 Protection against Photosensitivity
ultraviolet light Cutaneous malignancy
Endocrine Vitamin D synthesis Hypocalcaemia/
George Coltart BA BMBCh is a Academic Clinical Fellow at University osteopenia
Hospital Southampton/University of Southampton, UK. Competing Neurological Sensation of external Numbness/pain
interests: none declared. stimuli
Adam Fityan BM BSc (Hons) FRCP (UK) (Dermatology) is a Consultant Cosmetic Visual appearance to Psychosocial impact
Dermatologist at University Hospital Southampton and Honorary others
Consultant Dermatologist at St John’s Institute of Dermatology,
Guy’s Hospital, London, UK. Competing interests: none declared. Table 1

MEDICINE xxx:xxx 1 Ó 2020 Published by Elsevier Ltd.

Please cite this article as: Coltart G, Fityan A, Acute dermatological emergencies, Medicine, https://doi.org/10.1016/j.mpmed.2020.12.011
Descargado para Ronald Eduardo Lozano Acosta (loacro@yahoo.com) en Cayetano Heredia Pervuvian University de ClinicalKey.es por Elsevier en febrero 24, 2021.
Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2021. Elsevier Inc. Todos los derechos reservados.
 ACUTE MEDICINE II
features of high-output cardiac failure. Fluid balance and elec-
trolytes should be monitored closely, and skin biopsy considered
if the underlying cause is unclear.
Ointment emollients should be applied 2-hourly to support the
skin. Moderate potency topical corticosteroids can be beneficial.
A proportion of patients require the introduction of systemic
therapy to control the disease; this should be tailored to the
underlying cause.
Drug reactions
Severe cutaneous adverse reactions (SCARs) to drugs represent a
significant proportion of dermatological emergencies. Almost all
drugs can cause skin rashes, but some drugs, particularly anti-
epileptics, antibiotics, non-steroidal anti-inflammatory drugs
(NSAIDs) and diuretics, are more commonly associated with
severe eruptions. The onset of the rash often post-dates the start
of the offending drug by several weeks, so a careful drug history
of all medications taken in the preceding 3 months is vital to
identify and promptly remove the causative drug. The most
common SCARs and their time of onset are summarized in Table
2.
The vast majority of drug rashes do not meet the criteria for
SCARs and present with a maculopapular exanthem without
systemic features. These typically occur 1e3 weeks after starting
a new medication. Although it can look alarming, it is not an
emergency and generally settles spontaneously within 1e2
weeks of discontinuing the causative drug. The features in Table
3 can help differentiate a simple maculopapular exanthem from
SCARs.
StevenseJohnson syndrome (SJS)/toxic epidermal necrolysis
(TEN): SJS/TEN is a severe, life-threatening mucocutaneous
blistering drug eruption. Less commonly, it occurs secondary to
Mycoplasma pneumoniae (Mycoplasma-induced rash with
mucositis). SJS and TEN are a continuation of the same condi-
tion, differentiated by the extent of BSA blistering (SJS <10%
BSA epidermal detachment, SJS/TEN 10e30%, TEN >30%).
SJS/TEN presents with a generalized dusky erythematous
macular rash after 1e3 days of a flu-like prodrome. Patients are
systemically unwell, with fever and dehydration. Atypical targets
(a rash with a darker or sometimes purpuric centre and lighter
rim) are followed by the development of flaccid blisters and su-
perficial skin loss (Figure 1). Eliciting tenderness and a positive
Nikolsky’s sign (the epidermis sloughs off with mild finger-tip
pressure) helps in differentiating SJS/TEN from other SCARs.
Extensive mucositis is typical, presenting with red and painful
eyes progressing to conjunctival erosions, genital erosions and
ulceration of mouth and lips with overlying haemorrhagic crust.
Involvement of other membranes can present as difficulty
swallowing, urinary retention, diarrhoea, cough and respiratory
distress sometimes requiring intubation.
A skin biopsy with direct immunofluorescence is essential to
differentiate SJS/TEN from other blistering or mucocutaneous
conditions, such as pemphigus.
SJS/TEN is a multisystem disease often requiring manage-
ment in a specialist burns unit or an intensive care unit with
access to specialist dermatology input. Early removal of the
causative drug is key to halting disease progression. Ointment
MEDICINE xxx:xxx
Please cite this article as: Coltart G, Fityan A, Acute dermatological emergencies, Medicine, https://doi.org/10.1016/j.mpmed.2020.12.011
Descargado para Ronald Eduardo Lozano Acosta (loacro@yahoo.com) en Cayetano Heredia Pervuvian University de ClinicalKey.es por Elsevier en febrero 24, 2021.
Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2021. Elsevier Inc. Todos los derechos reservados.
emollients must be liberally applied to the skin to maintain
barrier function, while early ophthalmology input is vital to
prevent long-term scarring.2 Systemic therapy with corticoste-
roids, ciclosporin, intravenous immunoglobulins and anti-
tumour necrosis factor biological agents is often used despite
limited evidence.
SJS/TEN carries a high mortality that increases with the per-
centage of BSA involvement. Significant long-term sequelae
include cutaneous scarring, blindness, pulmonary fibrosis,
chronic kidney disease and autoimmune conditions (Sjo €gren’s
disease).
Drug reaction with eosinophilia and systemic symptoms
(DRESS): DRESS is a type 4, T-cell-mediated hypersensitivity
reaction to a drug that affects the skin and other organ systems,
particularly the liver, but also the kidneys, lungs, heart and
nerves. It can occur up to 6 weeks after starting a new drug. It
often presents with a maculopapular rash (although pustules and
target lesions can occur), sometimes in association with facial
oedema. High fever and lymphadenopathy are common, and
mucosal involvement is present in 25% of patients. Other
symptoms and signs depend on the organ systems affected and
can include hepatomegaly, shortness of breath, diarrhoea and
headache.
A full blood count (FBC) shows eosinophilia (>2.0  109/litre
in 30% of cases). Blood films may show atypical lymphocytes.
Biochemistry reveals hepatic or renal impairment, but this can
occur after the onset of the rash. Viruses including EpsteineBarr
virus, cytomegalovirus and human herpesvirus 6/7 can reac-
tivate late in the disease, which can account for a relapse in the
skin symptoms and liver impairment.
DRESS often settles spontaneously after withdrawing the
inducing medication. If there is evidence of significant systemic
involvement, immunosuppression with systemic corticosteroids
or ciclosporin is indicated. DRESS carries a 5e10% mortality,
and long-term sequelae include autoimmune endocrine abnor-
malities, particularly thyroid disease, which should be monitored
in the year after recovery.3
Acute generalized exanthematous pustulosis (AGEP): AGEP
manifests as a rapid progression of an erythematous rash,
particularly affecting the proximal flexures, which develops tens
to hundreds of pinhead-sized, superficial, sterile, non-follicular
pustules that can coalesce. Fever is usually present, but other-
wise systemic involvement is not usually a feature. Blood tests
demonstrate neutrophilia (>7.0  109/litre) and bacterial culture
of pustule fluid is negative.
Generally, symptoms spontaneously resolve after withdrawal
of the medication without requiring specific treatment. AGEP
carries a good prognosis with a low mortality, and usually re-
solves within a week of discontinuing the offending agent. The
main differential diagnosis to consider is that of pustular psori-
asis, which can be distinguished with skin biopsy.
Infections
Viral infections: viruses frequently induce florid rashes, partic-
ularly maculopapular exanthems, which are indistinguishable
from maculopapular drug reactions. Most are not dangerous,
2 Ó 2020 Published by Elsevier Ltd.
 ACUTE MEDICINE II

Adverse drug reactions

Adverse drug reaction Clinical features Common causative agents Time from exposure
to onset of symptoms

Angioedema Cutaneous: facial swelling, urticaria
Other: wheeze/stridor
AGEP Cutaneous: macular erythematous rash
(especially of the proximal flexures), plethora
of small pustules (can coalesce)
Other: fever, neutrophilia
SJS/TEN Cutaneous: mucositis of 2 mucous
membranes, dusky erythema with epidermal
detachment, Nikolsky positive
Other: fever, diarrhoea, dyspnoea,
cardiovascular instability
Vasculitis Cutaneous: palpable purpuric papules
(especially on the lower legs)
Other: systemic involvement (kidneys, joints,
nerves)
DRESS Cutaneous: polymorphic rash (often
maculopapular), facial oedema
Other: fever, lymphadenopathy, systemic
involvement (liver, kidneys)
Maculopapular Cutaneous: erythematous maculopapular
exanthem eruption, usually starting on upper trunk
before becoming widespread
Other: not usually associated with systemic
symptoms
Antibiotics (especially penicillins), NSAIDs, Minutes to hours
immunomodulators, contrast agents,
neuromuscular agents, nuts, venom
Antibiotics (especially b-lactams), 2e5 days
sulfonamides, antifungals, calcium channel
blockers, hydroxychloroquine, carbamazepine,
paracetamol
Antibiotics, sulfonamides, anticonvulsants 5e28 days
(lamotrigine, carbamazepine, phenytoin),
allopurinol, paracetamol, NSAIDs
Antibiotics, anti-TNF-a agents, allopurinol, 7e21 days
phenytoin, sulfasalazine
Antiepileptics (carbamazepine, lamotrigine, 15e40 days
phenytoin, phenobarbital), allopurinol,
antibiotics
Anything, especially antibiotics (b-lactams), 7e21 days
sulfonamides, allopurinol, antiepileptics,
NSAIDs

TNF, tumour necrosis factor.

Note: SCARs listed in italics

Table 2

especially in the absence of the features listed in Table 3. It is vesicular, urticarial and maculopapular exanthema.4 Purpura
beyond the scope of this article to cover all the potential emer- and livedoid skin changes are associated with a more severe
gency presentations of viral infections in the skin; instead we disease phenotype. A chilblain-like rash (known in the media as
discuss two infections that readers should be aware of. ‘covid toe’) may be seen on the hands and feet several weeks
Although it is early in our understanding, it is recognized that after COVID-19 has resolved; it is thought to be caused by
COVID-19 has several cutaneous manifestations, including disease-associated vasculopathy.
Eczema herpeticum (Figure 2) is a potentially severe super-
added herpes simplex virus (HSV) infection in patients with
atopic eczema. Patients are often febrile, presenting with a
Warning signs that might suggest a severe rash painful, diffuse eruption of monomorphic (similar shape and
size) vesicles and erosions on eczematous skin. Treatment con-
C Fever sists of aciclovir and, if required, topical corticosteroids for
C Purpura eczema. Involvement of or around the eyes requires urgent
C Lymphadenopathy ophthalmology review to prevent long-term complications of
C Angioedema HSV infection.
C Mucosal involvement (conjunctiva, nasopharynx, mouth, urethra,
anus) Bacterial infections: Necrotizing fasciitis is a life-threatening
C Blistering or epidermal detachment bacterial infection of the subcutaneous fat and fascia most
C Rash is painful commonly caused by haemolytic group A Streptococcus or
C Dysfunction of other organ systems (liver, kidneys, lungs, heart, Staphylococcus aureus. In the early stages the appearance can be
etc) hard to differentiate from simple cellulitis. Pain out of proportion
to the skin changes, the development of purpura, blistering,
Table 3

MEDICINE xxx:xxx 3 Ó 2020 Published by Elsevier Ltd.

Please cite this article as: Coltart G, Fityan A, Acute dermatological emergencies, Medicine, https://doi.org/10.1016/j.mpmed.2020.12.011
Descargado para Ronald Eduardo Lozano Acosta (loacro@yahoo.com) en Cayetano Heredia Pervuvian University de ClinicalKey.es por Elsevier en febrero 24, 2021.
Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2021. Elsevier Inc. Todos los derechos reservados.
 ACUTE MEDICINE II

aetiology, for example new asthma in eosinophilic granuloma-

Figure 1 Toxic epidermal necrolysis e large areas of epidermal loss
with adjacent erythema and blistering.
tous polyangiitis or sinusitis in granulomatous polyangiitis.
Physicians should assess for systemic involvement and check
inflammatory markers (erythrocyte sedimentation rate, C-reac-
tive protein), FBC, renal function, urinalysis (identifying hae-
maturia or proteinuria) and liver function. Imaging should be
considered depending on the presentation. A vasculitic screen
should be undertaken and should include hepatitis B/C serology,
HIV antibody, complement concentrations, antinuclear anti-
bodies, ANCA, rheumatoid factor, cryoglobulins, immunoglob-
ulins and serum electrophoresis. Skin biopsy can be helpful to
confirm the diagnosis. Management focuses on treating the un-
derlying cause.
Purpura fulminans is an acute life-threatening intravascular
thrombosis often occurring in response to infection (most
commonly Neisseria meningitidis). Patients present with irreg-
ular, well-defined purpura, which later become necrotic from the
micro-occlusion of vessels and subsequent haemorrhage.

Figure 2 Eczema herpeticum e multiple monomorphic erosions and

vesicles on the face.

anaesthesia and palpable crepitus caused by the formation of gas

within the tissue are clues to the diagnosis. Immediate surgical
debridement and intravenous antibiotics are essential.
Staphylococcal scalded skin syndrome is a toxin-mediated
blistering condition caused by Staph. aureus. It predominantly
affects children. Patients present with painful superficial blisters
or erosions on an erythematous base that predominantly affects
the flexures. Treatment consists of antibiotics to eliminate the
toxin-producing Staph. aureus, analgesia and supportive skin
care. Mortality is low (0.3%) in children, but higher (up to 4%)
in adults.5

Purpura
Cutaneous vasculitis is rarely an emergency in itself, but can
signify a systemic vasculitis that requires urgent treatment to
prevent damage to other organs such as kidneys, lungs and
nerves. The most common cause of a cutaneous vasculitis is
leucocytoclastic vasculitis, which is usually induced by infection
or medication, resolving spontaneously with removal of the un-
derlying cause. However, the differential diagnosis is broad, and
includes antineutrophil cytoplasmic antibody (ANCA)-associated
vasculitides, immunoglobulin (Ig) A vasculitis, Kawasaki disease
and polyarteritis nodosum, among many others.
Vasculitis presents with the ‘4Ps’: Palpable, Painful, Purpuric
(i.e. non-blanching) Papules. These are most often best seen on
the lower legs in a gaiter distribution, but can be widespread Figure 3 Cutaneous vasculitis e palpable purpura over the lower
(Figure 3). The history and examination can reveal clues to the limbs.

MEDICINE xxx:xxx 4 Ó 2020 Published by Elsevier Ltd.

Please cite this article as: Coltart G, Fityan A, Acute dermatological emergencies, Medicine, https://doi.org/10.1016/j.mpmed.2020.12.011
Descargado para Ronald Eduardo Lozano Acosta (loacro@yahoo.com) en Cayetano Heredia Pervuvian University de ClinicalKey.es por Elsevier en febrero 24, 2021.
Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2021. Elsevier Inc. Todos los derechos reservados.
 ACUTE MEDICINE II

Patients are typically very unwell, are hypotensive and develop
disseminated intravascular coagulation.
Blistering e pemphigus vulgaris
Pemphigus vulgaris is an acquired autoimmune condition that
presents with widespread flaccid and easily ruptured blisters and
erosions of the skin and mucous membranes.
Skin biopsy demonstrates intraepithelial separation (acan-
tholysis) and blistering. The diagnosis is confirmed by the pres-
ence of intercellular IgG deposition (targeting desmoglein 1 and
3) within the epidermis on direct immunofluorescence biopsy.
Systemic corticosteroids (0.5e1 mg/kg prednisolone) are
required to initially control the disease while introducing steroid-
sparing immunosuppressants such as azathioprine, mycophe-
nolate mofetil or rituximab. A scalded skin syndrome in U.S. children. Br J Dermatol 2018; 178:
KEY REFERENCES
1 Sterry Wolfram, Erythroderma M Steinholf, Bolognia JL, Jorizzo JL,
Schaffer JV. Dermatology. 3rdh edn. Erythroderma: Elsevier, 2012;
171e81 [chapter 10].
2 Creamer D, Walsh SA, Dziewulski P, et al. UK guidelines for the
management of Stevens-Johnson syndrome/toxic epidermal nec-
rolysis in adults 2016. Br J Dermatol 2016; 174: 1194e227.
3 Husain Z, Reddy BY, Schwartz RA. DRESS Syndrome. Part II.
Management and therapeutics. J Am Acad Dermatol 2013; 68: 709.
e1e9; quiz 718e20.
4 Galvan Casas C, Catala  A, Carretero Herna
ndez G, et al. Classifi-
cation of the cutaneous manifestations of COVID-19: a rapid pro-
spective nationwide consensus study in Spain with 375 cases. Br J
Dermatol 2020; 183: 71e7.
5 Staiman A, Hsu DY, Silverberg JI. Epidemiology of staphylococcal
704e8.

TEST YOURSELF
To test your knowledge based on the article you have just read, please complete the questions below. The answers can be found at the
end of the issue or online here.

Question 1 What is the most likely diagnosis?

A 42-year-old man presented with 3 days of fever, a rash and
worsening pain in his mouth and eyes. He had been started on
carbamazepine 2 weeks previously for the treatment of newly
diagnosed epilepsy. He had no other past medical history of note
and was taking no other medications.
On clinical examination, his temperature was 38.4 C, heart rate
125 beats/minute, blood pressure 105/65 mmHg, respiratory rate
22/minute, and oxygen saturation 99% on room air. He had a
dusky red macular rash affecting 15% of his body surface area;
this was Nikolsky positive. He had florid, painful conjunctivitis.
Examination of his mouth showed diffuse inflammation and ul-
ceration of the lips and oral mucosa.
Investigations
 Haemoglobin 14.3 g/litre (13.5e17.5)
 White cell count 12.4  109/litre (4.0e11.0)
 Neutrophil count 8.5  109/litre (2.0e7.0)
 Lymphocyte count 0.7  109/litre (1.0e3.5)
 Eosinophil count 0.3  109/litre (0.0e0.5)
 Sodium 143 mmol/litre (135e145)
 Potassium 4.2 mmol/litre (3.5e5.0)
 Urea 11.2 mmol/litre (3.2e7.4)
 Creatinine 105 micromol/litre (49e90)
 pH 7.32 (7.35e7.45)
 Lactate 2.6 mmol/litre (0.5e2.0)
 Bicarbonate 18 mmol/litre (22e29)
 Glucose 8 mmol/litre (4.0e5.4)
A. Erythema multiforme
B. Mycoplasma-induced rash with mucositis
C. Pemphigus vulgaris
D. Staphylococcal scalded skin syndrome
E. StevenseJohnson syndrome/toxic epidermal necrolysis
Question 2
A 42-year-old man presented with 3 days of fever and 2 days of a
worsening rash. His GP had started him on amoxicillin 3 days
previously to treat a presumed lower respiratory tract infection.
He had been taking paracetamol and ibuprofen for the last week
for a general malaise. He had a past medical history of hyper-
tension for which he had been taking ramipril for the previous 9
months, and had been started on lamotrigine 5 weeks previously
for treatment of newly diagnosed epilepsy.
On clinical examination, he had an urticated erythematous rash
over his trunk, upper limbs and face. There was a macular ery-
thema associated with oedema of the face. Widespread lymph-
adenopathy was noted. His temperature was 38.4 C, heart rate
95 beats/minute, blood pressure 135/78 mmHg, respiratory 16/
minute, and oxygen saturation 99% on room air.

MEDICINE xxx:xxx 5 Ó 2020 Published by Elsevier Ltd.

Please cite this article as: Coltart G, Fityan A, Acute dermatological emergencies, Medicine, https://doi.org/10.1016/j.mpmed.2020.12.011
Descargado para Ronald Eduardo Lozano Acosta (loacro@yahoo.com) en Cayetano Heredia Pervuvian University de ClinicalKey.es por Elsevier en febrero 24, 2021.
Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2021. Elsevier Inc. Todos los derechos reservados.
 ACUTE MEDICINE II

Investigations Question 3
 Haemoglobin 14.3 g/litre (13.5e17.5) A 22-year old woman presented with a 2-day history of fever and
 White cell count 10.1  109/litre (4.0e11.0) deterioration in her skin condition. She had severe atopic
 Neutrophil count 6.5  109/litre (2.0e7.0) eczema.
 Lymphocyte count 2.6  109/litre (1.0e3.5) On clinical examination, she had symmetrically distributed
 Eosinophil count 2.1  109/litre (0.0e0.5) monomorphic vesicles over her face, trunk and limb flexures.
 Sodium 143 mmol/litre (135e145) She had bilateral cervical and axillary lymphadenopathy. Her
 Potassium 4.2 mmol/litre (3.5e5.0) temperature was 38.3 C, heart rate 88 beats/minute, and blood
 Urea 7.2 mmol/litre (3.2e7.4) pressure 116/68 mmHg.
 Creatinine 86 micromol/litre (49e90)
 Bilirubin 19 micromol/litre (0e21) What is the most appropriate initial treatment?
 Alanine aminotransferase 80 IU/litre (10e45) A. Co-amoxiclav intravenously
 Alkaline phosphatase 140 IU/litre (30e130) B. Aciclovir orally
 Albumin 34 g/litre (32e50) C. Ciclosporin orally
D. Prednisolone orally
E. Clobetasone butyrate ointment 0.05% w/w topically
What is the likely causative agent?
A. Amoxicillin
B. Ibuprofen
C. Lamotrigine
D. Paracetamol
E. Ramipril

MEDICINE xxx:xxx 6 Ó 2020 Published by Elsevier Ltd.

Please cite this article as: Coltart G, Fityan A, Acute dermatological emergencies, Medicine, https://doi.org/10.1016/j.mpmed.2020.12.011
Descargado para Ronald Eduardo Lozano Acosta (loacro@yahoo.com) en Cayetano Heredia Pervuvian University de ClinicalKey.es por Elsevier en febrero 24, 2021.
Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2021. Elsevier Inc. Todos los derechos reservados.