The skin and nervous system develop adjacent to each other as the ectoderm and neuroectoderm, respectively, in the embryo and remain interconnected throughout life. Dermatitis artefacta is defined as the deliberate and conscious production of self-inflicted skin lesions to satisfy an unconscious psychological or emotional need. These skin lesions serve as powerful, self-expressive, nonverbal messages. Patients often deny responsibility for their creation. Neurotic excoriation is differentiated from dermatitis artefacta by its conscious compulsive nature. Dermatitis artefacta falls under the general category of factitious disorders, which excludes neurotic excoriations, delusional disorders, malingering, and Münchhausen syndrome (except Münchhausen syndrome by proxy).1
Psychiatric conditions, in particular depression,2,3 anxiety,3 personality disorders,3 delusional disorders, and dissociative disorders,4 are often coexistent in 25-33% of all dermatological conditions.5 Dermatitis artefacta may occur in persons of any age and commonly manifests within the context of chronic medical and/or dermatological conditions. These self-induced skin lesions may be present continuously, or they may be episodic, occurring during periods of heightened psychosocial stress and/or uncontrolled psychoses. Patients with dermatitis artefacta require both dermatological assessment and psychosocial support.
The pathophysiology of dermatitis artefacta is poorly understood. Multifactorial causes include genetics, psychosocial factors, and personal or family history of psychiatric illness. 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 dermatological condition.
Dermatitis artefacta is a challenging clinical diagnosis. It is suggested based on findings that include an absence of other dermatoses to explain the lesions and histological findings that are inconsistent with the clinical presentation.
The cause of dermatitis artefacta is multifactorial. One should be sure to rule out hypochondriasis, substance abuse disorder, and psychotic disorders.
Dermatitis artefacta is a challenging condition that requires dermatologic and, often, psychiatric expertise.
Topical antimicrobials are the most commonly prescribed medication; however, topical agents alone have shown limited efficacy. In many instances, treating the underlying psychiatric disorder with antidepressants, antianxiety drugs, and antipsychotic agents is necessary.14,15 Analgesics should be avoided because of the high probability for dependence and addiction.
Self-inflicted lesions are often accompanied by a localized skin infection.
Bacitracin prevents transfer of mucopeptides into growing cell wall, inhibiting bacterial growth.
Neomycin is used for treatment of minor infections; inhibits bacterial protein synthesis and growth. Polymyxin B disrupts bacterial cytoplasmic membrane, permitting leakage of intracellular constituents and causing inhibition of bacterial growth.
Apply 1-4 times/d to affected areas and cover with sterile bandages prn
Administer as in adults
None reported
Documented hypersensitivity; epithelial herpes simplex keratitis; mycobacterial and fungal infections
C – Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution when treating extensive burns (>20% BSA) because absorption of neomycin is possible and may cause nephrotoxicity and ototoxicity; prolonged use may result in overgrowth of nonsusceptible organisms
Topical antibacterial that inhibits bacterial protein synthesis, causing bacterial death.
Apply to affected area bid for 2 wk
Administer as in adults
None reported
Documented hypersensitivity
C – Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Discontinue if irritation or sensitivity occurs
For impetiginized skin lesions.
First-generation cephalosporin that inhibits bacterial replication by inhibiting bacterial cell wall synthesis. Bactericidal and effective against rapidly growing organisms forming cell walls. Resistance occurs by alteration of penicillin-binding proteins. Effective for treatment of infections caused by streptococci or staphylococci, including penicillinase-producing staphylococci. May use to initiate therapy when streptococcal or staphylococcal infection is suspected. Used orally when outpatient management is indicated. Recommended for impetigo caused by Staphylococcus aureus resistant to erythromycin. Primary activity against skin florae. Used for skin infections or prophylaxis in minor procedures.
500 mg PO q6h for 10 d
25-50 mg/kg/d PO q6h for 10 d; not to exceed 3 g/d
Coadministration with aminoglycosides increases nephrotoxic potential
Documented hypersensitivity
B – Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy
Use with hypersensitivity or contraindication to penicillin or cephalexin. May result in GI upset, prompting prescription of an alternative macrolide or a change to tid dosing. Covers most potential etiologic agents, including Mycoplasma species.
Less active against Haemophilus influenzae. Although 10 d seems to be a standard course of treatment, treating until patient has been afebrile for 3-5 d seems more rational. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections.
In children, age, weight, and severity of infection determine proper dosage. When bid dosing is desired, half the total daily dose may be taken q12h. For more severe infections, double the dose. Has added advantage of being a good anti-inflammatory agent by inhibiting migration of polymorphonuclear leukocytes.
250 mg erythromycin stearate/base (or 400 mg ethylsuccinate) PO q6h, or 500 mg q12h (1 h ac or 2 h pc)
Alternatively, 333 mg PO q8h; increase to 4 g/d depending on severity of infection
30-50 mg/kg/d (base or ethylsuccinate) PO divided q6-8h; not to exceed 2 g/d (base) or 3.2 g/d (ethylsuccinate)
Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis; decreases metabolism of repaglinide, thus increasing serum levels and effects
Documented hypersensitivity; hepatic impairment
B – Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in liver disease; estolate formulation may cause cholestatic jaundice; adverse GI effects are common (give doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occurs
First-line therapy for depression. Other medications in this category include paroxetine, citalopram, and sertraline. For dermatitis artefacta associated with obsessive-compulsive disorder, the use of an SSRI for at least 6 months to 1 year accompanied by psychotherapy is recommended.
Selectively inhibits presynaptic serotonin reuptake with minimal or no effect in reuptake of norepinephrine or dopamine.
May cause more adverse GI effects than other SSRIs currently available, which is the reason it is not recommended as a first choice. May be given as a liquid and a cap.
May give as single dose or in divided doses. Presence of food does not appreciably alter medication levels. May take up to 4-6 wk to achieve steady-state levels because of long half-life (72 h).
Long half-life is both an advantage and a drawback. If it works well, an occasional missed dose is not a problem; if problems occur, eliminating all active metabolites takes a long time. Choice depends on adverse effects and drug interactions. Adverse effects of SSRIs seem to be quite idiosyncratic; thus, if dosing is started at a conservative level and advanced as tolerated, relatively few reasons exist to recommend one over another.
20 mg/d PO in morning and increase after several wk by 20 mg/d; not to exceed 80 mg/d
Note: If patient is taking 20 mg/d, may initiate once-weekly dosing with 90-mg delayed-release product 7 d after last daily dose of 20 mg
<8 years: Not established
>8 years: 10-20 mg PO qd
Increases toxicity of diazepam and trazodone by decreasing clearance; also increases toxicity of MAOIs and highly protein-bound drugs; serotonin syndrome (ie, myoclonus, rigidity, confusion, nausea, hyperthermia, autonomic instability, coma, eventual death) occurs with simultaneous use of other serotonergic agents (eg, anorectic agents, tramadol, buspirone, trazodone, clomipramine, nefazodone, tryptophan); discontinue other serotonergic agents at least 2 wk prior to SSRI initiation
Documented hypersensitivity; concurrently taking MAOIs or took them in last 2 wk; coadministration with thioridazine
B – Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in hepatic impairment and history of seizures; discontinue MAOIs at least 14 d before initiating therapy
These agents are used to treat the underlying psychiatric disorder.
Has antihistamine, antipruritic, and antidepressant properties. May be effective for depression (with agitation) and a primary symptom of pruritus.
Increases concentration of serotonin and norepinephrine in CNS by inhibiting their reuptake by presynaptic neuronal membrane, which is associated with a decrease in symptoms of depression.
30-150 mg/d PO hs or 2-3 divided doses; gradually increase dose to 300 mg/d prn; maintain effective dose for at least 6-8 wk
<12 years: Not recommended
>12 years: 25-50 mg/d PO hs or bid/tid and increase gradually to 100 mg/d
Decreases antihypertensive effects of clonidine but increases effects of sympathomimetics and benzodiazepines; effects of desipramine increase with phenytoin, carbamazepine, and barbiturates
Documented hypersensitivity; urinary retention; acute recovery phase following myocardial infarction; glaucoma
C – Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in cardiovascular disease, conduction disturbances, seizure disorders, urinary retention, hyperthyroidism, and thyroid replacement therapy
May be effective for depression with primary symptoms of pain sensations (eg, burning, chafing, stinging). Analgesia usually requires doses <50 mg qhs.
Inhibits reuptake of serotonin and/or norepinephrine at presynaptic neuronal membrane, which increases concentration in CNS. May increase or prolong neuronal activity because reuptake of these biogenic amines is important physiologically in terminating transmitting activity.
25-150 mg/d mg PO hs; use minimum effective dose
Children: 0.1 mg/kg PO hs; increase as tolerated over 2-3 wk to 0.5-2 mg/d hs
Adolescents: 25-50 mg/d PO initially; increase gradually to 100 mg/d in divided doses
Phenobarbital may decrease effects; coadministration with CYP2D6 enzyme system inhibitors (eg, cimetidine, quinidine) may increase levels; inhibits hypotensive effects of guanethidine; may interact with thyroid medications, alcohol, CNS depressants, barbiturates, and disulfiram
Documented hypersensitivity; use of MAOIs within 14 d of initiating therapy; history of seizures, cardiac arrhythmias, glaucoma, or urinary retention
C – Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in cardiac conduction disturbances and history of hyperthyroidism, renal, impairment, or hepatic impairment; avoid use in elderly persons
These agents are used to treat the underlying psychiatric disorder.
Previously shown to be effective for delusions of parasitosis. Centrally acting dopamine-receptor antagonist. Available in 2-mg scored tab in United States; 2-, 4-, and 10-mg tab available in Canada. Clinical response usually occurs within 10-14 d.
1-2 mg PO qd initially; increase by 2-4 mg at weekly intervals; not to exceed 10 mg/d or 200 mcg/kg/d (0.2 mg/kg/d); maintain effective therapeutic dose for at least 1 mo and then titrate down in 1-mg decrements over 1-2 wk until minimum effective dose is achieved
Not established
Increases toxicity of MAOIs, alfentanil, CNS depressants, and guanabenz
Documented hypersensitivity; history of cardiac arrhythmias or long QT syndrome; concurrently with macrolide antibiotics
C – Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
ECG recommended at initiation of therapy and regular intervals thereafter; careful observation for appearance of extrapyramidal symptoms (eg, akathisia, rigidity, dystonia, irreversible tardive kinesia) necessary in geriatric patients; adverse effect of restlessness (akathisia) may be treated with diphenhydramine or benztropine
Lower risk of extrapyramidal adverse effects than with typical antipsychotics.
Previously shown to be effective for delusions of parasitosis. Binds to dopamine D2 receptor with 20-times lower affinity than for 5-HT2 receptor. Improves negative symptoms of psychoses and reduces prevalence of extrapyramidal adverse effects. Indicated for treatment of psychotic disorders, including schizophrenia and bipolar disorder. Clinical response usually occurs within 10-14 d.
2-6 mg PO qhs; start at 0.5 or 1 qhs; may divide into bid dosing
<16 years: Not recommended
>16 years: 0.5-1 mg PO bid; not to exceed 6 mg/d
Coadministration with carbamazepine may decrease effects; may inhibit effects of levodopa; clozapine may increase levels; oral solution not compatible with cola or tea
Documented hypersensitivity.
C – Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May cause extrapyramidal reactions, hypotension, tachycardia, and arrhythmias; hyperglycemia may occur and, in some cases, be extreme, resulting in ketoacidosis, hyperosmolar coma, or death; do not split or chew oral disintegrating tab
May inhibit serotonin, muscarinic, and dopamine effects. Efficacy similar to risperidone; has fewer dose-dependent adverse effects but is associated with more concern about weight gain.
Adult
5-20 mg/d PO in divided doses; lower doses recommended for dermatology-related psychoses
Children: Not established
Adolescents: Administer as in adults
Fluvoxamine may increase effects; antihypertensives may increase risk of hypotension and orthostatic hypotension; levodopa, pergolide, bromocriptine, charcoal, carbamazepine, omeprazole, rifampin, and cigarette smoking may decrease effects
Documented hypersensitivity
C – Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in narrow-angle glaucoma, cardiovascular disease, cerebrovascular disease, prostatic hypertrophy, seizure disorders, hypovolemia, and dehydration; hyperglycemia may occur and in some cases be extreme, resulting in ketoacidosis, hyperosmolar coma, or death; administration of more than 1 IM injection is associated with substantial orthostatic hypotension (33%), thus, maintain patient in recumbent position and monitor blood pressure before repeating IM doses
May act by antagonizing dopamine and serotonin effects. Efficacy similar to risperidone and olanzapine. Fewer dose-dependent adverse effects and less concern for weight gain.
25 mg PO bid; titrate to 150-750 mg/d PO; not to exceed 800 mg/d; lower doses recommended for dermatology-related psychoses
Children: Not established
Adolescents: Administer as in adults