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Year : 2013  |  Volume : 14  |  Issue : 3  |  Page : 47-53

Neonatal erythroderma (red baby)

1 Department of Dermatology and Venereology, Maulana Azad Medical College, New Delhi, India
2 Department of Dermatology, Army College of Medical Sciences, Delhi Cantonment, New Delhi, India

Date of Web Publication26-Nov-2013

Correspondence Address:
Rashmi Sarkar
Department of Dermatology and Venereology, Maulana Azad Medical College, New Delhi -110 002
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2319-7250.122160

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Erythroderma in neonates is a rare but a well established life threatening entity. Though it has been studied extensively in adults, the literature is lacking in the paediatric age group. The underlying etiological causes of neonatal erythroderma are pre-existing cutaneous diseases, infections, immunodeficiency disorders, metabolic and nutritional disorders and drugs. It is a challenge to diagnose the underlying etiology of neonatal erythroderma due to the rare specific presentation of the characteristic clinical signs and histopathological changes. In this review we discuss the incidence, etiology, specific points in history and examination which can be useful at arriving at the diagnosis and outline of management.

Keywords: Immunodeficiency disorders, neonatal erythroderma, treatment of neonatal erythroderma

How to cite this article:
Sarkar R, Garg S, Garg VK. Neonatal erythroderma (red baby). Indian J Paediatr Dermatol 2013;14:47-53

How to cite this URL:
Sarkar R, Garg S, Garg VK. Neonatal erythroderma (red baby). Indian J Paediatr Dermatol [serial online] 2013 [cited 2022 Jan 16];14:47-53. Available from: https://www.ijpd.in/text.asp?2013/14/3/47/122160

  Introduction Top

Erythroderma, also called as exfoliative dermatitis is defined as the inflammation of the skin causing erythema and scaling, involve >90% of body surface area. Erythroderma has been studied extensively in adults, but the literature is lacking in pediatric age group. In contrast to adults in which erythroderma is usually drug induced or a secondary manifestation [1] of an underlying disease, neonatal erythroderma is usually a primary manifestation of various conditions.

  Etiology Top

Due to non-specific clinical and histopathological features, the underlying cause of erythroderma is difficult to establish and is often delayed. The various disorders reported to cause neonatal erythroderma is shown in [Table 1]. [2]
Table 1: Causes of neonatal erythroderma

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Due to the rare presentation of erythroderma in the neonatal period, there is limited data available on this disorder

In a retrospective Indian study by Sarkar, [3] out of 19,999 patients of pediatric age group, 20 (0.11%) neonates and infants were diagnosed with erythroderma. The various etiological causes of erythroderma in this study were: [4]

  • Infections-40%

    1. Staphylococcal scalded skin syndrome (SSSS)-30%
    2. Candidiasis-10%

  • Ichthyosiform erythroderma-25%

    1. Non-bullous ichthyosiform erythroderma (NBIE)-15%
    2. Collodion babies-10%

  • Atopic dermatitis-15%
  • Infantile seborrheic dermatitis-10%
  • Erythroderma of unknown etiology-10%

In another study by Sarkar et al., [5] the incidence of childhood erythroderma was found to be 17 (0.11%) out of 16,000 pediatric patients seen, with a male: female 0.89:1 and the mean age of onset being 3.3 years. Out of these 17 patients, 8 (47%) were infants and 9 (53%) were between 1 and 12 years. The underlying etiology was drugs (29%), ichthyosis (18%), psoriasis (18%), SSSS (18%), atopic dermatitis (11%) and infantile seborrheic dermatitis with dermatophytosis (6%). The various drugs causing erythroderma were phenytoin, phenobarbitone, amoxicillin and indigenous medicine.

In another Indian study, [6] out of 80 patients of all age group diagnosed with erythroderma, the incidence of erythroderma in children was 7 (8.5%). Out of these seven cases, only three cases were in the age group between 0 and 3 years with almost equal male to female ratio.

In a retrospective study by Pruszkowski et al. [7] on 51 cases of erythroderma in neonates and infants, excluding those with blister formation, the various underlying diseases were:

  • Immunodeficiency-30%
  • Ichthyosis (simple and complex)-24%
  • Netherton syndrome-18%
  • Eczematous and paulosquamous dermatitis-20%
  • Erythroderma of unknown etiology-10%

Ichthyosis was the underlying cause in 15 out of 16 (32%) patients had congenital erythroderma, barring one who had Omenn's syndrome. A total of 6 patients presented with collodion membrane at birth.


Eczematous dermatitis

Infantile seborrheic dermatitis

It usually presents during the neonatal period with greasy yellow scales on the scalp and skin folds involving the retroauricular area, neck and axilla and diaper area. It may also present as psoriasiform lesions and rarely as erythroderma. There is considerable overlap in the clinical presentation of infantile seborrheic dermatitis and atopic dermatitis and in a study it was found that around 15% of patients diagnosed with infantile seborrheic dermatitis eventually developed atopic dermatitis. [8]

Atopic dermatitis

It is a rare cause of erythroderma in neonatal period. The lesions are mostly vesicular and exudative in nature and are usually present on the face especially on the cheeks and flexures with sparing of the nappy area. The appreciation of itch sensation develops only after the neonatal period in the 2 nd or 3 rd month of life. [8],[9] In only 18% of children who have atopic dermatitis, the rash begins in the neonatal period. [10]

Disorders of keratinization


The various types of ichthyosis reported to cause erythroderma include non-bullous congenital ichthyosiform erythroderma, epidermolytic hyperkeratosis or bullous ichthyosis, Harlequin ichthyosis, Netherton syndrome, Keratitis-ichthyosis-deafness syndrome, Sjogren-Larson syndrome, Chanarin-Dorfman syndrome, Tay syndrome, Conradi-Hunerman syndrome (CHS), Erythrokeratodermas, CHILD syndrome, Gottron's syndrome and non-classifiable neuroichthyosis.


The child presents with a collodion membrane at birth which exfoliates to reveal underlying erythroderma covered by fine white gray scales. The child may develop deep fissures in the skin along with flexion contractures. [11]

Bullous ichthyosiform erythroderma/epidermolytic hyperkeratosis

It is an autosomal dominant disorder. The child presents with mild erythroderma along with flaccid blisters leading to erosions at the site of trauma and later goes on to develop progressive hyperkeratosis with grey waxy scales. The initial presentation can be differentiated from SSSS and epidermolysis bullosa as the child is apyrexic, stable and there is presence of focal hyperkeratosis. The course of the disease may be complicated by presence of recurrent infections, dehydration and malnutrition leading to mortality. There may be presence of linear epidermal nevus with histology of epidermolytic hyperkeratosis in parents of such children. [11]

Netherton's syndrome

It is the most common multisystem ichthyosiform syndrome which is characterized by triad of ichthyosis linearis circumflexa with variable erythroderma, trichorrhexis nodosa and atopy. It is an autosomal recessive disorder with mutation in SPINK5 gene. It presents with erythroderma, which is usually present at birth. Complications include development of cutaneous and systemic infections, hypernatremia dehydration, diarrhea and failure to thrive. Repeated eyebrow and eyelash examination by dermatoscope, light or scanning microscope can help in clinching the diagnosis at an early stage.


In this syndrome erythroderma in a swirled pattern is present since birth. Other abnormalities include presence of skeletal defects like chondrodysplasia punctata with epiphyseal stippling and cataract. [12]


Psoriasis, with its bimodal age of onset at 16-22 years and 57-60 years is a very rare cause of congenital and neonatal erythroderma. [11],[13] Only 2% cases of psoriasis start before the age of 2 years. [13] Psoriasis which is present at birth or during the neonatal period is called as congenital psoriasis and the erythrodermic variant is most rare and severe. [13] A family history of psoriasis and human leukocyte antigens-B17 antigen is positive in more than 50% patients with congenital psoriasis. [13] It usually begins as a recalcitrant diaper dermatitis, which eventually progresses to a generalized pustular form of psoriasis associated with early onset of arthropathy, [14] Staphylococcal infection and growth retardation. The child is toxic with episodes of high fever. It closely resembles NBIE and can be differentiated from it by a positive family history, presence of uninvolved skin and psoriasiform histology in psoriasis and presence of ectropion in NBIE.

Pityriasis rubra pilaris

Congenital erythrodermic PRP has been reported [15] and is inherited as an autosomal dominant trait. Unlike the acquired form, it runs a long course and may persist throughout life.

Generalized mastocytosis

It usually presents at birth or in the neonatal period. [16],[17] Diffuse infiltration of mast cells in the skin causes diffuse thickening, lichenification and erythema. The skin feels doughy and there can be appearance of orange papules. A positive Darier's sign (wheal formation on stroking of skin) is often present and trivial trauma to the skin causes urticaria and bulla formation. Systemic symptoms with flushing, gastrointestinal and respiratory involvement are often present. Children who have congenital diffuse or erythrodermic mastocytosis may have systemic involvement of gastrointestinal tract, liver, spleen, bone and lymph nodes. They should therefore be investigated with complete blood count, liver function test, bone scan and gastrointestinal studies. [11] Severe complication include anaphylaxis and diarrhea.

Toxic epidermal necrolysis

Cases of TEN though rare in neonates have been reported to be caused by Staphylococcus aureus sepsis and toxicity by polysorbate in neonatal period.

Ectodermal dysplasia

There is a report of erythroderma in a family with ectrodactyly, ectodermal dysplasia and cleft lip. [18]



Also known as Ritter's disease or pemphigus neonatorum, is a "super antigen" mediated disease caused by exfoliative toxins A and B produced by Staphylococcus. These toxins cause lymphokine release (interleukin 2 and tumor necrosis factor) by T cells. Congenital and neonatal SSSS has been described following chorioamnionitis. [19],[20] The child is febrile, toxic and irritable. Over the next 2 days, the child develops macular rash which progresses to erythroderma accompanied by skin tenderness. This is followed by development of subcorneal blisters and generalized exfoliation of skin. Nikolsky's sign is positive.

Toxic shock syndrome

The neonate gets infected with S. aureus either during the intrauterine period or during labor. It is caused by exotoxin toxic shock syndrome toxin 1 and 2 and rarely by streptococcal exotoxin. It presents with scarlet fever like rash, which progresses to erythroderma and is accompanied by fever, hypotension and shock.

Congenital cutaneous candidiasis

The ascending infection from the vaginal candidiasis in mother causes infection of the amnion and it is acquired at the time of delivery. [18],[21] It begins as a maculopapular rash, which turns into pustules and spreads in a centrifugal pattern. The lesions coalesce and lead to erythroderma. Nail changes include paronychia and dystrophic nails. [22] There is no involvement of the diaper region and the oral cavity [23] as unlike neonatal candidiasis the infection is not acquired during passage through the birth canal. The cutaneous lesions resolve spontaneously. Systemic involvement can lead to pneumonia and septicemia especially in a preterm baby, therefore culture of urine, blood and cerebrospinal fluid (CSF) should be done.

Immunodeficiency disorders

They usually do not present at birth due to the protective immunity offered by maternal antibodies. Various immunodeficiencies like Omenn's syndrome, severe combined immunodeficiency, Wiskott-Aldrich syndrome, secretory IgA deficiency, maternal-fetal graft-versus-host reaction (GVHR) and other types of GVHR have been reported to cause erythroderma.

Immunodeficiency should be suspected as a cause for erythroderma when the neonate presents with severe erythroderma associated with marked skin infiltration, severe alopecia without hair and eyebrow dysplasia, failure to thrive, serious recurrent infections, chronic diarrhea and resistance to topical steroids. Histological finding of significant epidermal and dermal lymphocytic infiltration along with satellite cell necrosis of keratinocytes help in establishing the diagnosis of Omenn syndrome or immunodeficiency. [7]

Omenn's syndrome

It is an autosomal recessive form of severe combined deficiency of familial reticuloendotheliosis with eosinophilia. There is defect in both humoral and cellular immunity. [24] It presents clinically with erythroderma, which is present at birth or during the neonatal period along with diffuse alopecia, recurrent infections, chronic diarrhea, lymphadenopathy, hepatospenomegaly and failure to thrive. Biochemical abnormalities include eosinophillia, marked leukocytosis, increased clonal T cells, decreased B cells, anemia, raised IgE and hypogammaglobulinemia.

Digeorge syndrome and severe combined immunodeficiency

They begin as dermatitis and evolve into erythroderma.


It may be caused by T cell immunodeficiency or exchange transfusion resulting in transplacental transfer of immunocompetent maternal lymphocytes to an immunodeficient infant during intrauterine or postnatal exchange transfusion. It presents as an erythematous morbilliform eruption, which progresses to erythroderma and sloughing. The rash differs from that seen in Omenn syndrome is being more morbilliform and less eczematous. Other manifestation includes fever, hepatosplenomegaly, lymphadenopathy, eosinophilia and lymphocytosis. The rash usually presents as erythroderma at birth or within 2-3 weeks of birth in patients with T cell immunodeficiency. In contrast the rash may be minimal and transient in an immunocompetent neonate as the number of cells transferred is less.

Metabolic and nutritional disorders

Dermatitis beginning in the perioral region along with failure to thrive in a neonate with erythroderma should prompt the physician to think of metabolic and nutritional factors as a possible etiological cause.

Zinc deficiency (Acrodermatitis enteropathica)

It begins with psoriasiform lesions in the periorificial region. Other symptoms include diarrhea, failure to thrive and photophobia.

Essential fatty acid deficiency

It results from either malabsorption or maldigestion due to severe gastroenteritis, malnutrition and cystic fibosis. [25] It presents with dermatitis involving the intertriginous regions along with lichenification and desquamation.

Cystic fibrosis

It manifests with recalcitrant psoriasiform rash in the diaper area along with irritability and growth failure.

Holocarboxylase synthetase deficiency

Skin lesions manifest as erythroderma, alopecia and candidiasis. Cutaneous lesions may begin as sharply defined dermatitis involving the scalp, eyebrows, eyelashes, perioral, perianal and other flexural creases. [26] Child is acutely ill, dehydrated and can have ketoacidosis. Diagnosis is confirmed by holocarboxylase synthestase deficiency in skin fibroblast.

Biotinase deficiency

Child presents usually around 3 months of age with acrodermatitis enteropathica like skin lesions along with patchy alopecia. It may be accompanied by presence of hypotonia, lethargy and seizures. Children with this deficiency who are breast fed are likely to develop the features of the disease earlier when compared to bottle fed infants due to low biotin content in the human milk.

Other nutritional deficiency disorders

Neonates with diet deficient in amino acid isoleucine (maple syrup urine disease), arginine, citrulline (citrullinemia) and carbamoyl phosphate synthetase present with acrodermatitis enteropathica like lesions. [11],[18],[27]


Though there are reports of penicillin, ampicillin, aminoglycosides and cephalosporins causing a maculo-papular rash, erythroderma has only been reported with ceftriaxone [28] and vancomycin. [29]

Leiner's disease

In this disorder dysfunction of the complement pathway involving the C5 complement causes yeast opsonization defect. [30] It presents with erythroderma, susceptibility to infection, diarrhea and failure to thrive.

  Management Top

Due to the non-specific clinical signs and histological presentation, the diagnosis of underlying etiology of erythroderma is often delayed. In a study by Pruszkowski et al., [7] it took 11 months for the diagnosis of the underlying disorder to be made. Neonates presenting with erythroderma are mostly misdiagnosed and treated for eczemas with topical steroids leading to Cushing's syndrome. [31] Essential points in clinical history which can help in pointing to the underlying etiology are:

  Clinical History Top

  • Family history-BIE, psoriasis, PRP, Omenn's syndrome, Netherton's syndrome, atopy
  • History of (H/O) consanguinity-Ichthyosis, Netherton syndrome, primary immunodeficiency disorder
  • Congenital onset-ichthyosis, infections, immunodeficiency disorders
  • Recurrent infection-immunodeficiency disorders.
  • Neurological complaints
  • Blood transfusion-GVHR
  • Preceding purulent infection-SSSS
  • Concomitant infection in mother-TSS, CCC
  • Failure to thrive-Netherton syndrome, immunodeficiency diseases, metabolic disorders
  • Diarrhoea-GVHR, Netherton syndrome, Omenn syndrome
  • Periorificial dermatitis-metabolic and nutritional disorders
  • Blisters-SSSS, mastocytosis, BIE
  • Collodion baby-NBIE and other ichthyosis
  • Fever-SSSS, GVHR, TSS
  • Atopy-Netherton's syndrome, atopic dermatitis
  • Presence of linear epidermal nevus in family members-BIE
  • H/O unexplained death in previous children-Omenn's syndrome. [32]

  Examination Top

The examination should focus on the following points:

  • Type of scales (ichthyosiform or fine scales)
  • Spared areas
  • Presence of specific lesion (keratotic follicular papules, well defined erythematous scaly plaques, bulla, erosions)
  • Skin induration-immunodeficiency, atopic dermatitis, neuroichthyosis
  • Dariers sign-matocytosis
  • Positive Nikolsky's sign-SSSS
  • Skin tenderness-SSSS, TEN, TSS
  • Distribution (flexor or extensor)
  • Nail changes-paronychia and dystrophy in CCC
  • Alopecia-Omenn's syndrome, GVHR, Netherton's syndrome, Biotin metabolism disorders, citrullinemia [33],[34]
  • Hair dysplasia-Netherton syndrome
  • Mucosal examination
  • Palmoplanter thickening-PRP
  • Swirled pattern of erythroderma-CHS
  • Lymphadenopathy - Omenn's syndrome, GVHR, atopic dermatitis
  • Shock-TSS. [32]

  Investigations Top

The following investigations can be done depending on the clinical suspicion.

  • Skin biopsy

    It is essential and as in adults, it is advisable to take 2-3 specimens simultaneously from different sites. [35] In the three studies of childhood erythroderma, histopathology showed histology of dermatitis or psoriasiform changes. In these studies histopathology contributed to detect the underlying etiology in 50%, [5] 45%, [4] and 35% [5] of cases. Special stains which can be used are periodic acid-Schiff for Candida and immunohistochemical staining
  • Swabs from skin, eyes, nose and umbilicus - SSSS, TSS, CCC
  • Culture of urine, blood and CSF-candidiasis
  • KOH mount - candidiasis
  • Dermatoscopy-Netherton syndrome
  • Hair microscopy-Netherton syndrome
  • High vaginal swab from mother-S. aureus or CCC.
  • Hair and skin scraping for potassium hydroxide mount-CCC
  • Complete blood count
  • Eosinophil count - It is markedly increased in Omenn syndrome and Netherton syndrome. It is mildly increased in atopic dermatitis
  • Serum IgE and other immunoglobulins-Omenn syndrome, Netherton syndrome, atopic dermatitis
  • Zinc and alkaline phosphate levels-acrodermatitis enteropathica
  • Assays of essential fatty acids, amino acids, holocarboxylase and biotinase-to rule out metabolic disorders
  • Sweat chloride levels-cystic fibrosis
  • Holocarboxylase syntethase activity in leukocytes and fibroblasts-hydroxysteroid dehydrogenase
  • Blood for fatty acid levels-essential fatty acid deficiency
  • Genetic analysis for SPINK5-Netherton syndrome.
  • X-ray-CHN
  • Histamine and its metabolite levels in serum or urine-mastocytosis
  • Serum electrolytes-hypernatremic dehydration
  • Serum albumin.

  Treatment Top

Child should be monitored for vital signs, electrolyte levels and oral or parenteral fluid intake.

Treatment Should Focus On

  • Correction of hematological, biochemical and metabolic imbalance
  • Prevention and treatment of infections
  • Correction of caloric and protein intake
  • Maintenance of fluid and electrolyte balance
  • Prevention of hyperpyrexia
  • Maintenance of skin barrier by topical application of bland emollients, antifungals, topical antibiotics, wet dressings, topical steroids in localised areas and use of systemic antibiotics
  • Treatment of specific disease. [2],[32]
  • Short course of systemic steroids may be required for the treatment of atopic dermatitis and drug induced erythroderma. Systemic methotrexate or acitretin may be used for treating psoriasis. Long term retinoids may be required to treat ichthyosis. [36]

  Complications Top

The following complications can occur in neonatal erythroderma:

  • Septicemia
  • Infection
  • Hypoalbunimea
  • Hyperpyrexia
  • Hypernatremic dehydration
  • Failure to thrive.

  Prognosis Top

Neonatal erythroderma is a life threatening condition and the mortality of neonatal and infantile erythroderma in a study was found to be 16% [7] with severe dermatosis persisting in 67% of survivors. In this study the most severe types of erythroderma which were unresponsive to treatment with topical steroids were due to psoriasis, Netherton syndrome and immunodeficiency. Prognosis is dependent on the underlying cause of erythroderma. Drugs, seborrheic dermatitis, nutritional causes and SSSS causing erythrodermas respond favorably to treatment.

  Conclusion Top

Erythroderma in neonates is a rare but a well-established life-threatening entity. It is a challenge to diagnose the underlying etiology due to the rare specific presentation of the characteristic clinical signs and histopathological changes. Management is mainly supportive with correction of the hematological, biochemical and metabolic imbalance and treatment of the underlying cause.

  References Top

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