Dermatitis Artefacta

Dermatitis artefacta is defined as the deliberate and conscious production of self-inflicted skin lesions to satisfy an unconscious psychological or emotional need.[2, 1] These skin lesions serve as powerful, self-expressive, nonverbal messages. Patients often deny responsibility for their creation.

Excoriation disorder is differentiated from dermatitis artefacta by its compulsive nature. Dermatitis artefacta is also referred to as "factitious dermatitis."[2, 3] Psychiatric conditions, in particular depression,[4, 5] anxiety,[5] personality disorders,[5] delusional disorders, anddissociative disorders,[6] may be coexistent in as many as 25–33% of all dermatologic conditions.[7]

Dermatitis artefacta may occur in persons of any age and commonly manifests within the context of chronic medical or dermatologic conditions. These self-induced skin lesions may be present continuously, or they may be episodic, occurring during periods of heightened psychosocial stress or uncontrolled psychoses. Patients with dermatitis artefacta require both dermatologic assessment and psychosocial support.[8]

The pathophysiology of dermatitis artefacta is poorly understood. Genetics, psychosocial factors, and personal or family history of psychiatric illness may all play a role. Commonly, a family member is involved in the medical field, and patients tend to be well versed in medical terminology.

Acute episodes of dermatitis artefacta often represent a maladaptive response to a psychosocial stressor. Long-standing cases may be secondary to underlying anxiety or depression, emotional deprivation, an unstable body image, or a personality disorder with borderline features. Many dermatitis artefacta patients also have an associated chronic medical or dermatologic condition.

The cause of dermatitis artefacta is multifactorial. One should be sure to rule out hypochondriasis, substance abuse disorder, and psychotic disorders.

A genetic predisposition is likely. Many psychiatric disorders tend to be familial.

Psychiatric illnesses that may be associated with dermatitis artefacta include anxiety disorders, major depressive disorder, dysthymia, body dysmorphic disorder, factitious disorders, and somatoform disorders. The following must be taken into account:

• Neuropsychological trauma - Child abuse or neglect, sexual abuse, and posttraumatic stress disorder

• Personality disorders - Attention-seeking traits (eg, borderline or dependent), obsessions, and compulsions

• Psychosocial factors - Poor coping mechanisms, family dysfunction, and inadequate social support structure[9]

Chronic illnesses commonly associated with dermatitis artefacta include the following:

• Dermatologic disorders – Acne, alopecia (eg, alopecia areata or androgenic alopecia), atopic dermatitis, chronic idiopathic urticaria, psoriasis, rosacea, and vitiligo

• Chronic pain syndromes

• Any other long-standing medical illness

The prevalence of dermatitis artefacta in the pediatric population is 1 case in 23,000 persons. The condition is poorly recognized and underreported,[10] and many patients are lost to follow-up. Consequently, dermatitis artefacta probably is considerably more common than is typically thought.

The highest incidence of dermatitis artefacta occurs between late adolescence (11–14 years) and early adulthood. Most patients with dermatitis artefacta are female.[11] In persons younger than 16 years, the female-to-male ratio is 4.7–7:1, whereas in the general population, it is 3–20:1. No racial or ethnic predisposition has been noted for dermatitis artefacta.

Mild cases of dermatitis artefacta secondary to identifiable psychosocial stressors usually have a good outcome; cure is possible. However, chronic cases of dermatitis artefacta that are associated with chronic dermatologic or medical issues usually have a poor outcome, and cure generally is not possible.

Continuous or repeated episodes of self-mutilation may result in disfiguring scars on exposed areas of the body. Approximately 30% of all dermatologic conditions are associated with a psychiatric disorder. Suicide is an important consideration in patients with a comorbid psychiatric illness.

The unique presentation and appearance of skin lesions may be a cause of significant concern both for patients and for parents or caregivers.

During initial patient visits, confrontational issues regarding the etiology of lesions should be avoided. During subsequent visits, one may gradually begin to address the role of psychosocial factors or psychiatric issues that may contribute to the self-inflicted skin lesions.[12] Regular assessment of the risk of self-harm (suicide) or harm towards others is essential.

In most cases, patients with dermatitis artefacta are otherwise healthy and do not provide a substantial indicative history; on occasion, they may relate vague accounts of antecedent events. These patients report a personal history of chronic dermatoses, including acne, alopecia (ie, alopecia areata, androgenic alopecia), atopic dermatitis, chronic idiopathic urticaria, psoriasis, rosacea, or vitiligo.

Dermatitis artefacta patients may also have a personal or family history of psychiatric illness, including anxiety, depression, personality disorder (borderline, dependent, or obsessive-compulsive), dissociative disorder, body dysmorphic disorder, or posttraumatic stress disorder. Typically, they are reluctant to seek a consultation with a psychiatrist.

Patients may have a personal history of chronic medical conditions, chronic pain syndromes, or both. They may report a history of childhood neglect or abuse, sexual abuse, or psychological trauma.

Münchausen syndrome by proxy (a form of dermatitis artefacta) manifests as skin lesions caused by a parent or caregiver (often the mother). It usually occurs with children younger than 5 years.

Pertinent information from the history includes the following:

• Patient’s quality of life with regard to health-related issues

• Patient’s perception of the skin condition

• Role of a psychosocial stressor

• Presence of a lengthy medical file with numerous consultations

• Extensive list of previously used medications

• History of substance abuse

Inquiries should also be made about family members or significant others and their reaction to the skin lesions. Anger, frustration, and impatience are commonly reported reactions.

Dermatitis artefacta is a challenging clinical diagnosis. Factors suggesting this diagnosis include the following:

• Absence of other dermatoses to explain the lesions

• Histologic findings that are inconsistent with the clinical presentation

The morphology of the dermatitis artefacta skin lesions is variable and bizarre and typically depends on the mechanism of injury. Features may include sharp margins adjacent to normal skin, geometric shapes, and linear tracks (such as occur secondary to exposure to corrosive liquids). Most often, the dermatitis artefacta lesions are found at sites accessible to the patient, usually within reach of the dominant hand. Typical locations are as follows:

• Face (45%)

• Distal upper extremity (ie, hand and forearm; 24%)

• Lower extremities (31%)

• Trunk (24%)

• Upper arm (7%)

• Scalp (7%)

The appearance of the dermatitis artefacta lesions may vary as follows:

• Superficial erosion (50%)

• Hyperpigmented macule or purpura (30-42%)

• Excoriation (17%)

• Deep necrosis or ulceration (17%)

• Irritant dermatoses (17%)

• Papules (17%)

• Crusts (8%)

• Scars - Pinpoint, star-shaped, or atypically shaped (8%)

• Onychodystrophy

• Other – Keratosis or tattoolike appearance

Overall, 72% of patients have 1 type of lesion morphology, 41% have 2 types, and 31% have 3 types. In 66% of patients, involvement is limited to 1 body segment; in 34%, 2 body segments are involved.

Dermatitis artefacta must be distinguished from dermatitis neglecta, excoriation disorder, trichotillomania, and painful bruise syndrome. Other conditions that may be associated with or may mimic dermatitis artefacta include the following:

• Pyoderma gangrenosum[13, 14]

• Acquired hemophilia[15]

• T-cell lymphoma[16]

• Hepatitis C virus–associated porphyria cutanea tarda[17]

No specific laboratory blood tests are required to establish a diagnosis of dermatitis artefacta, nor are any diagnostic imaging studies indicated. In addition, no other general tests are required. The only test that is particularly useful in this setting is a s kin biopsy.

A skin biopsy of a representative dermatitis artefacta lesion may be performed to rule out any underlying pathology and, in some cases, to establish a definite diagnosis. The histologic findings in dermatitis artefacta are usually nonspecific and are often dependent on the mechanism of injury (eg, foreign body reaction with giant cells and noninfectious material for self-injection).

Dermatitis artefacta is a challenging condition whose management requires dermatologic and, often, psychiatric expertise.[8, 18, 19] A detailed assessment of the patient history for chronic dermatoses, chronic medical conditions, psychiatric illnesses, and psychosocial problems is necessary. General dermatologic care measures include baths, debridement, emollients, and topical antimicrobials. Any underlying psychiatric disorder that may be present should be addressed.

No surgical care is required for dermatitis artefacta. Hospitalization may be required for some patients, depending on the severity of the skin lesions and the risk of suicide. Consultation with a psychiatrist is recommended.

An effective therapeutic relationship in dermatitis artefacta patients requires a nonjudgmental, empathetic, and supportive environment. Every effort should be made to avoid discussing the etiology of the condition or confronting the patient regarding the behavior. Developing a good rapport with the patient and encouraging the patient to return for follow-up appointments are important.

A psychiatric evaluation is warranted in dermatitis artefacta patients if severe self-mutilation is noted or if there is any evidence of psychiatric illness, psychosis, suicide risk, or need for hospitalization.

Complementary adjuvant therapies in dermatitis artefacta patients may include acupuncture, cognitive-behavioral therapy (eg, aversion therapy, systemic desensitization, or operant conditioning), biofeedback and relaxation therapy (eg, for anxiety-related dermatitis artefacta), and hypnosis.[20]

Topical antimicrobials are the medications most commonly prescribed for dermatitis artefacta; however, these agents are of limited efficacy when used alone. Oral antibiotics may be given for impetiginized lesions.

In many instances, treating the underlying psychiatric disorder with antidepressants, antianxiety drugs, and antipsychotic agents is necessary.[21, 22] Analgesics should be avoided because of the high probability for dependence and addiction.

Selective serotonin reuptake inhibitors (SSRIs; eg, paroxetine, sertraline, citalopram, and fluoxetine) are first-line therapy for depression. A tricyclic antidepressant (TCA) with antihistamine, antipruritic, and antidepressant properties (eg, doxepin) is recommended for depression with or without agitation and with pruritus as the primary symptom. A TCA with analgesic properties (eg, amitriptyline) is appropriate for depression with pain sensations (eg, burning, chafing, or stinging) as the primary symptom.

Typical (eg, pimozide) and atypical antipsychotics (eg, risperidone, olanzapine,[23] quetiapine) may be considered for short-term use, particularly if skin lesions are associated with psychotic or delusional symptoms.

Frequent follow-up visits with a dermatologist, a psychiatrist, or both are recommended for dermatitis artefacta patients. It should be kept in mind that such patients are often lost to follow-up.

In cases of Münchausen syndrome by proxy, removal of the child to a safe environment is mandatory.

Medications used in the treatment of dermatitis artefacta and associated conditions include the following:

• and oral antimicrobials

• Antidepressants (selective serotonin reuptake inhibitors [SSRIs] and tricyclic antidepressants [TCAs])

• Antipsychotic agents (typical and atypical)

Class Summary

Topical antimicrobials are used to treat the localized skin infections that often accompany self-inflicted lesions.

Neomycin/polymyxin B/bacitracin topical (Neo-Polycin, Neosporin)

Neomycin is used for treatment of minor infections; it inhibits bacterial protein synthesis and growth. Polymyxin B disrupts the bacterial cytoplasmic membrane, permitting leakage of intracellular constituents and causing inhibition of bacterial growth. Bacitracin prevents transfer of mucopeptides into the growing cell wall, thereby inhibiting bacterial growth.

Fusidic acid

Fusidic acid is a topical antibacterial that inhibits bacterial protein synthesis, causing bacterial death.

Class Summary

Oral antibiotics are given to treat impetiginized skin lesions.

Cephalexin (Keflex)

Cephalexin is a first-generation cephalosporin that inhibits bacterial replication by inhibiting bacterial cell-wall synthesis. It is bactericidal and effective against rapidly growing organisms forming cell walls. Resistance occurs through alteration of penicillin-binding proteins.

Cephalexin is effective for treatment of infections caused by streptococci or staphylococci, including penicillinase-producing staphylococci; it may be used to initiate therapy when such infections are suspected. It is given orally when outpatient management is indicated. Cephalexin is recommended for impetigo caused by Staphylococcus aureus resistant to erythromycin. Its primary activity is against skin flora. It is used for treatment of skin infections or for prophylaxis in minor procedures.

Erythromycin (E.E.C. 400, PCE, Ery-Tab)

Erythromycin is used to treat staphylococcal and streptococcal infections in patients with hypersensitivity or with a contraindication to penicillin or cephalexin. It may result in gastrointestinal (GI) upset, in which case prescription of an alternative macrolide or a change to 3-times-daily dosing is advisable. Erythromycin covers most potential etiologic agents, including Mycoplasma spp; it is less active against Haemophilus influenzae.

Erythromycin inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. It has the added advantage of being a good anti-inflammatory agent by virtue of its ability to inhibit migration of polymorphonuclear leukocytes.

Although a 10-day treatment course seems to be standard, treating until the patient has been afebrile for 3-5 days seems to be more rational. In children, age, weight, and severity of infection determine the proper dosage. When twice-daily dosing is desired, half of the total daily dose may be taken every 12 hours. For more severe infections, the dose should be doubled.

Class Summary

SSRIs (including paroxetine, citalopram, and sertraline as well as fluoxetine) are first-line therapy for depression. For dermatitis artefacta associated with obsessive-compulsive disorder, use of an SSRI for at least 6 months to 1 year, in conjunction with psychotherapy, is recommended. Choice of an agent depends on adverse effects and drug interactions. Adverse effects of SSRIs seem to be idiosyncratic; thus, if dosing is started at a conservative level and advanced as tolerated, relatively few reasons exist to recommend one SSRI over another.

Fluoxetine (Prozac)

Fluoxetine selectively inhibits presynaptic serotonin reuptake, with minimal or no effect on reuptake of norepinephrine or dopamine. Because it may cause more adverse GI effects than other SSRIs currently available, it is not recommended as a first choice. It may be given as a liquid or as a capsule, in a single dose or divided doses. The presence of food does not appreciably alter medication levels.

Because of the long half-life (72 hours), it may take as long as 4-6 weeks to achieve steady-state levels. The long half-life is both an advantage and a drawback. If the drug works well, an occasional missed dose is not a problem; if problems occur, eliminating all active metabolites takes a long time.

Sertraline (Zoloft)

Sertraline selectively inhibits presynaptic serotonin reuptake, with minimal or no effect on reuptake of norepinephrine or dopamine.

Paroxetine (Paxil, Pexeva)

Paroxetine is a potent selective inhibitor of neuronal serotonin reuptake. It also has a weak effect on norepinephrine and dopamine neuronal reuptake. For maintenance, the dosing should be adjusted so as to maintain the patient on the lowest effective dosage, and the patient should be periodically reassessed to determine the need for continued treatment.

Fluvoxamine (Luvox CR)

Fluvoxamine enhances serotonin activity through selective reuptake inhibition at the neuronal membrane. It does not significantly bind to alpha-adrenergic, histamine, or cholinergic receptors and thus has fewer adverse effects than TCAs. Fluvoxamine has been shown to reduce repetitive thoughts, maladaptive behaviors, and aggression and to increase social relatedness and language use.

Citalopram (Celexa)

Citalopram enhances serotonin activity through selective reuptake inhibition at the neuronal membrane. No head-to-head comparisons of SSRIs have been done; however, on the basis of metabolism and adverse effects, citalopram is considered the SSRI of choice for patients with head injury.

Escitalopram (Lexapro)

Escitalopram is an SSRI and an S-enantiomer of citalopram. It is used for the treatment of depression. Its mechanism of action is thought to be potentiation of serotonergic activity in the CNS, resulting from inhibition of CNS neuronal reuptake of serotonin. The onset of depression relief may be obtained after 1-2 weeks—sooner than is possible with other antidepressants.

Class Summary

TCAs are used to treat the underlying psychiatric disorder in patients with dermatitis artefacta.

Doxepin

Doxepin has antihistamine, antipruritic, and antidepressant properties. It may be effective in patients with depression (with agitation) and a primary symptom of pruritus. Doxepin increases concentrations of serotonin and norepinephrine in the central nervous system (CNS) by inhibiting their reuptake by the presynaptic neuronal membrane; such inhibition is associated with a decrease in symptoms of depression.

Amitriptyline

Amitriptyline may be effective for depression with primary symptoms of pain sensations (eg, burning, chafing, or stinging). Analgesia can usually be achieved with doses lower than 50 mg given at bedtime. Amitriptyline inhibits reuptake of serotonin or norepinephrine at the presynaptic neuronal membrane, thereby increasing CNS concentrations. It may increase or prolong neuronal activity; reuptake of these biogenic amines is important physiologically in terminating transmitting activity.

Clomipramine (Anafranil)

Clomipramine is a dibenzazepine compound belonging to the TCA family. It affects serotonin uptake, and its metabolite, desmethylclomipramine, affects norepinephrine uptake.

Nortriptyline (Pamelor)

Nortriptyline has demonstrated effectiveness in the treatment of chronic pain. It may inhibit the reuptake of serotonin and/or norepinephrine by the presynaptic neuronal membrane, which, in turn, increases their synaptic concentration in the CNS.

Desipramine (Norpramin)

This is the original TCA used for depression. These agents have been suggested to act by inhibiting reuptake of noradrenaline at synapses in central descending pain modulating pathways located in the brainstem and spinal cord.

Class Summary

Typical antipsychotics are used to treat the underlying psychiatric disorder in patients with dermatitis artefacta.

Pimozide (Orap)

Pimozide is a centrally acting dopamine-receptor antagonist that has been shown to be effective for delusions of parasitosis. It is available in a 2-mg scored tablet in the United States; 2-, 4-, and 10-mg tablets are available in Canada. Clinical response usually occurs within 10-14 days.

Class Summary

Atypical antipsychotics carry a lower risk of extrapyramidal adverse effects than typical antipsychotics.

Risperidone (Risperdal)

Risperidone has been shown to be effective for delusions of parasitosis. It binds to dopamine D2 receptors with 20-times lower affinity than that for serotonin 5-HT2 receptors. Risperidone alleviates negative symptoms of psychoses and reduces the prevalence of extrapyramidal adverse effects. It is indicated for treatment of psychotic disorders, including schizophrenia and bipolar disorder. Clinical response usually occurs within 10-14 days.

Iloperidone (Fanapt)

Iloperidone is an atypical antipsychotic agent indicated for acute treatment of schizophrenia. Its precise mechanism of action is unknown. It antagonizes D2 and 5-HT2 receptors. However, it shows high affinity for 5-HT2A, D2, and D3 receptors and low-to-moderate affinity for D1, D4, H1, 5-HT1A, 5HT6, 5-HT7, and NE alpha1 receptors.

Paliperidone (Invega)

Paliperidone is the active metabolite of risperidone. Its therapeutic effects consist of mixed central serotonergic and dopaminergic antagonism. Unlike risperidone, paliperidone exhibits 10-fold lower affinity for alpha-2 and 5-HT2A receptors and almost 3- to 5-fold lower affinity for 5-HT1A and 5HT1D, respectively.

Olanzapine (Zyprexa)

Olanzapine may inhibit serotonin, muscarinic, and dopamine effects. Its efficacy is comparable to that of risperidone; it has fewer dose-dependent adverse effects but is associated with more concern about weight gain.

Quetiapine (Seroquel)

Quetiapine may act by antagonizing dopamine and serotonin effects. Its efficacy is comparable to those of risperidone and olanzapine; it has fewer dose-dependent adverse effects and is associated with less concern about weight gain.