History

Fact Explanation
Common wart- Initially a single smooth skin colored plaque or multiple plaques appear.As time progresses, the lesion enlarges and surface becomes irregular.The common sites are hands, face and genitals. [1] Warts are defined as small growths (1 mm -1 cm or more in diameter) with rough surfaces. Human Papilloma Virus(HPV)[2] types 1,2 and 4 are the pathogens.Infection occurs, when the virus enters breaches in skin,in immunosuppression, or when virus migrates to other sites.There is hyperkeratosis in the affected areas.[1]
Planter warts- There is a solitary or few areas of rough skin with mild protrusion from the soles.There might be mild pain at the sites. This is caused by HPV 1–4, 27, 29, 57[3].Infection occurs when the virus enters breaches in skin, in immunosuppression, or when virus migrates to other sites.There is hyperkeratosis in the affected areas.[1]
Mosaic warts- Multiple,small rough areas of skin on soles,palms, can be the presentation. They are not painful. Caused by HPV 2.[3] Infection occurs, when the virus enters breaches in skin, in immunosuppression, or when virus migrates to other sites.There is hyperkeratosis in the affected areas.[1]
Plane warts- There are multiple, smooth papules, commonly found on face, back of the hands, legs.There is mild erythema or brownish discoloration.They are usually painless. The causative virus is HPV-3,10, 28, 29,[3]. The erythema is due to mild inflammation following immunological reaction. The pathogenesis is similar to other viral warts.[1]
Anogenital warts- Papillomatous lesions resembling cauliflower is present.The lesions can be painful. The pathogen is HPV -6,11,16,18.[1] Commonly seen on the mucous membranes of the vagina, urethra, anus, and mouth. Intra-anal warts occur in receptive anal intercourse.Pain, bleeding, or difficulty with intercourse can occur in these patients. Urethral lesions obstruct passage of urine.[4]
Facial warts- The lesions have a digitate appearance.They are painless and found on the beard area. This is common in adult males and it spreads with shaving.[1]
Risk factors History of contact with a patient- The mode of transmission is direct skin to skin contact.[2] Indirect transmission is possible with the contact of contaminated surfaces( e.g-communal washing areas)[2] Walking barefoot has a increased risk of plantar warts.[3] Meat handlers are at risk of hand warts[3]
The presence of other diseases as risk factors The patient may have sexual promiscuity and may have other sexually transmitted diseases. Immunodeficiency can lead to widespread growth of warts.(HIV, Epidermodysplasia verruciformis)[1]
The presence of complications such as malignant transformation (Ex- Cervical carcinoma) Cervical cancer has been the main disease,where a pathogen responsible for warts(HPV 16,18) gives rise to malignant transformation.[1] Others include Epidermodysplasia verruciformis has increased risk of malignent transformation,but the disease is rare.[1] Immunocompromised patient (Renal allograft recipients) can have malignant transformation following HPV infections.[1]
References
  1. WELLER, Richard P.J.B. et al ed.Clinical Dermatology.4th ed.Oxford:Blackwell Publishing Ltd.2008.pp.235-239
  2. Warts and verrucae.Clinical Knowledge Summaries.NICE [online].2009 [viewed 12 May 2014].Available form:http://cks.nice.org.uk/warts-and-verrucae
  3. MULHEM E, PINELIS S. Treatment of nongenital cutaneous warts. Am Fam Physician [online] 2011 Aug 1, 84(3):288-93 [viewed 12 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/21842775
  4. KODNER CM, NASRATY S. Management of genital warts. Am Fam Physician [online] 2004 Dec 15, 70(12):2335-42 [viewed 12 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/15617297

Examination

Fact Explanation
Common wart- Initially a single smooth skin colored plaque or multiple plaques are appears.As time progresses, the lesion enlarges and surface becomes irregular.Common sites are hands and face Human Papilloma Virus(HPV) types 1,2 and 4 are the pathogens.Infection occurs when the virus enters breaches in skin, in immunosuppression, or when virus migrates to other sites.There is hyperkeratosis in the affected areas.[1]
Planter warts- There is a solitary or few areas of rough skin with mild protrusion from the soles.There is a roughened margin.Paring produces bleeding capillaries. Infection occurs when the virus enters breaches in skin, in immunosuppression, or when virus migrates to other sites.There is hyperkeratosis in the affected areas.[1]
Mosaic warts- Multiple,small rough areas of skin on soles,palms, can be the presentation. Infection occurs when the virus enters breaches in skin, in immunosuppression, or when virus migrates to other sites.There is hyperkeratosis in the affected areas.[1]
Plane warts- There are multiple, smooth papules, commonly found on face, back of the hand and legs.There is mild erythema or brownish discoloration. The causative virus is HPV-3. The erythema is due to mild inflammation following immunological reaction. The pathogenesis is similar to other viral warts.[1]
Anogenital warts- Papillomatous lesions resembling cauliflower is present.The surface is moist and there is maceration.The lesions are vascular.These can coalesce and form fungating plaques. The pathogen is HPV -6,11,16,18.[1]
Facial warts- The lesions have a Digitate appearance.They are painless and found on the beard area. This is common in adult males and it spreads with shaving.[1]
Signs of other diseases Such as a vaginal discharge and ulcers may indicate a STI or cervical carcinoma. Signs of other infections(skin,respiratory) in immunocompromised patients.
References
  1. WELLER, Richard P.J.B. et al ed.Clinical Dermatology.4th ed.Oxford:Blackwell Publishing Ltd.2008.pp.235-239

Differential Diagnoses

Fact Explanation
Molluscum contagiosum The lesions are dome-shaped and have smooth surfaces.Typically there is central umbilication and a keratin plug.[1],[2].[3].[4] Commonly found on head and neck areas.[2]
Plantar corns The lesions are typically observed on pressure areas.There is no bleeding on paring.[1][4]
Granuloma annulare The lesions are commonly found around knuckles.They are purple colored macules with nodules fused in to a annular lesion.[1][2]
Condylomata lata This is observed in syphilis.The lesions are flat and less demarcated[1]
Epthelial malignancy A Squamous cell carcinoma can present initially as a small scaling nodule. Actinic keratoses will be present and this will progress in to an ulcer with a indurated edge.The base consists with granulation tissue.Common in sun exposed areas.[1]
Lichen planus The lesions are itchy, violaceous in color and have the typical Wickham's striae[4]
References
  1. WELLER, Richard P.J.B. et al ed.Clinical Dermatology.4th ed.Oxford:Blackwell Publishing Ltd.2008.pp.235-239
  2. BROWN,Robin Graham.BURNS,Tony.Lecture notes:Dermatology.10th ed.Sussex:WILEY-BLACKWELL.2011.PP.26,163,
  3. STULBERG DL, HUTCHINSON AG. Molluscum contagiosum and warts. Am Fam Physician [online] 2003 Mar 15, 67(6):1233-40 [viewed 13 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/12674451
  4. STERLING JC, HANDFIELD-JONES S, HUDSON PM, BRITISH ASSOCIATION OF DERMATOLOGISTS. Guidelines for the management of cutaneous warts. Br J Dermatol [online] 2001 Jan, 144(1):4-11 [viewed 13 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/11167676

Investigations - for Diagnosis

Fact Explanation
Biopsy Usually the diagnosis is by clinical appearance.[1] but shave biopsy can be used in diagnosing filliform warts.[2] Indications for biopsy include: an uncertain diagnosis, an immunocompromised patient, poor response to treatment, pigmented warts, suspected malignant change(induration, fixity,ulceration) or a high risk for HPV-related malignancy (e.g. abnormal Papanicolaou smears). [4] Histological appearance shows papilomatosis,hyperkeratosis and parakeratosis. Capillaries appear prominent and thrombosed. HPV infected keratinocytes are larger and contain pyknotic neuclei and perinucler halo.[3]
HPV typing Performed occasionally in special circumstances. (E.g- genital warts in suspected child abuse)[3]
References
  1. Warts and verrucae.Clinical Knowledge Summaries.NIEC[online].2009[viewed 12 May 2014].Available form:http://cks.nice.org.uk/warts-and-verrucae
  2. Surgical procedures.DermNet NZ[online].DermNet New Zealand Trust.2014[viewed 13 May 2014].Available form:http://www.dermnetnz.org/doctors/lesions/procedures.html
  3. STERLING JC, HANDFIELD-JONES S, HUDSON PM, BRITISH ASSOCIATION OF DERMATOLOGISTS. Guidelines for the management of cutaneous warts. Br J Dermatol [online] 2001 Jan, 144(1):4-11 [viewed 13 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/11167676
  4. KODNER CM, NASRATY S. Management of genital warts. Am Fam Physician [online] 2004 Dec 15, 70(12):2335-42 [viewed 13 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/15617297

Investigations - Fitness for Management

Fact Explanation
Gynecological procedures such as PAP smear, colposcopy guided biopsy. HPV 16,18 is a risk factor in cervical carcinoma.[1][2] The tests mentioned are useful in detecting cervical cancer. [2]
Complete blood count (CBC) with differential leukocyte count. This is done as a part of immunological investigations in suspected immunodeficiency.[3]
Leukocyte function tests, and lymphocyte subsets. Performed in the further investigation of immunosupression, if the patient's CBC is suggestive in addition to clinical findings. [3]
References
  1. WELLER, Richard P.J.B. et al ed.Clinical Dermatology.4th ed.Oxford:Blackwell Publishing Ltd.2008.pp.235-239
  2. HPV and Cancer.National cancer institute fact sheet.National cancer institute[online].National Institutes of Health.2012[viewed 13 May 2014].available form:http://www.cancer.gov/cancertopics/factsheet/Risk/HPV
  3. WEILER CR, BANKERS-FULBRIGHT JL. Common variable immunodeficiency: test indications and interpretations. Mayo Clin Proc [online] 2005 Sep, 80(9):1187-200 [viewed 13 May 2014] Available from: doi:10.4065/80.9.1187

Management - General Measures

Fact Explanation
Patient education Following should be highlighted : warts are not harmful, they are usually asymptomatic and resolve without treatment, though they are contagious, the risk of transmission is low.[1]
Steps to minimize transmission Advise patient on the following: a waterproof plaster should cover the wart when the patient is swimming, avoid sharing personal belongings such as footwear and clothing. [1]
Steps to limit auto-inoculation Should avoid scratching, avoid biting nails or sucking fingers that have warts, keep feet dry and change socks daily.[1]
References
  1. Warts and verrucae.Clinical Knowledge Summaries.NIEC[online].2009[viewed 12 May 2014].Available form:http://cks.nice.org.uk/warts-and-verrucae

Management - Specific Treatments

Fact Explanation
Topical treatment for palmoplantar warts. Topical salicylic acid (applied daily for up to 12 weeks) can be used.[1][2] Salicylic acid solubilize the cell surface proteins and act as a keratolytic agent. [4] Following salicylic acid treatment, viricidals such as formaldehyde or glutaraldehyde paint should be applied.[1][2]
Non pharmacological treatments for non-genital warts. Cryotherapy causes tissue necrosis by freezing. This is done once every 3 or 4 weeks for up to four cycles. Liquid nitrogen, carbon dioxide snow, dimethyl ether and propane are the agents used in cryotherapy.[1][3] Other treatment options include photodynamic therapy with aminolevulinic acid , ablation therapy, laser therapy and surgical removal of the wart. [2][6] Facial warts are best treated with electrocautery, a Hyfrecator or by cryotherapy.[1]
Podophyllotoxin or Imiquimod cream Used commonly for genital warts. Imiquimod acts as a immune response modifier that induces Keratinocytes to produce cytokines and cause wart regression.[1][5]
Non-pharmacological treatment for genital warts Cryotherapy, electrosurgery and laser treatment are effective treatment options.[1][5]
Specialist referral Consider referring to a dermatologist or a plastic surgeon in the following situations: facial warts, uncertain diagnosis, multiple recalcitrant warts in a immunocompromised patient, extensive growth, unresponsive to topical treatment or cryotherapy.[2]
References
  1. WELLER, Richard P.J.B. et al ed.Clinical Dermatology.4th ed.Oxford:Blackwell Publishing Ltd.2008.pp.235-239
  2. Warts and verrucae.Clinical Knowledge Summaries.NIEC[online].2009[viewed 13 May 2014].Available form:http://cks.nice.org.uk/warts-and-verrucae
  3. Cryotherapy.DermNet NZ[online].DermNet New Zealand Trust.2014[viewed 13 May 2014].Available form:http://dermnetnz.org/procedures/cryotherapy.html
  4. KATZUNG,Bertram .MASTERS,Susan B.TREVOR,Anthony J.Basic & Clinical Pharmacology.12th ed.New York:McGraw-Hill.2012.pp.1074
  5. KODNER CM, NASRATY S. Management of genital warts. Am Fam Physician [online] 2004 Dec 15, 70(12):2335-42 [viewed 13 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/15617297
  6. MULHEM E, PINELIS S. Treatment of nongenital cutaneous warts. Am Fam Physician [online] 2011 Aug 1, 84(3):288-93 [viewed 13 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/21842775