Thursday, December 9, 2021

Arthropod Bites

December 09, 2021 0

 

Arthropod Bites

Primary Care Visit Report   

A 26-year-old male with no past medical history presented with a rash on bilateral arms and wrists. The patient had woken up with the skin lesions 1 day prior. They were very itchy. They had gotten progressively worse since they appeared and seemed to become more symptomatic after he showered. The patient applied topical Benadryl cream which did not help. 
 Vitals were normal. On exam, there were multiple scattered  erythematous pap-ules      with some excoriations on bilateral arms. There were no lesions in the web spaces of his fi ngers and no burrows. His right arm had an area of linear lesions, otherwise the lesions were diffusely scattered. 
 The lesions seemed to be bites; however, Primary Care was unsure of the source. The patient was treated for scabies with permethrin cream, and referred to dermatol-ogy in case the lesions did not clear up.  

Discussion from Dermatology Clinic 


Differential Dx   


  Arthropod bites  
  Scabies  
  Urticaria  
  Folliculitis     

Favored Dx   
On physical examination, the lesions appear to be arthropod bites. The phylum arthropods includes centipedes, millipedes,  spiders  , scorpions, and insects. The offending biter is diffi cult to identify without more details from the history, such as whether the individual has any pets (could suggest  fl ea   bites), if anyone else in the house has bites (scabies, fl eas, or bed bugs), or whether he spent time outdoors with his arms exposed ( mosquitoes     , outdoor bugs). The distribution of the bites would not be typical of scabies, which tend to appear around the wrists and interdigital spaces. Furthermore, scabies lesions typically feature more extensive excoriation.  

Overview   


 Arthropod bites are a signifi cant cause of morbidity worldwide [ 1 ]. Arthropod bites and  stings   cause a range of symptoms in humans, ranging from mildly uncomfortable to life threatening. The majority of arthropod bites cause local reactions; however, some bites can cause toxic and anaphylactic reactions [ 2 ]. Many arthropods serve as vectors for diseases such as malaria, dengue, West Nile virus, Rocky Mountain spotted fever, Southern tick-associated rash illness (STARI), and Lyme disease. 
 The species of concern in the USA include the black widow and brown recluse  spiders  , the lone star, black-legged ( Ixodes scapularis ) and dog ticks, bed bugs,  fl eas  , biting  flies, and  mosquitoes  . Their signifi cance is due to prevalence, severity of bite symptoms, or potential to transmit disease [ 1 ,  2 ]. Specifi cally, black widow spider bites cause severe muscle spasms and brown recluse spider bites can cause skin necrosis.  Tick   and mosquito bites are common, and the species are vectors for a number of diseases named above. 
 It is diffi cult to estimate the overall prevalence of bug  bites  , as many of them do not require any treatment. Systemic reactions from  hymenoptera   (insects such as  bees  ,  wasps  , and hornets)  stings   have a lifetime prevalence ranging from 0.3 % in children to 7.5 % in adults [ 3 ,  4 ]. Fatalities associated with insect bites are very rare; however, some bites may require emergency management.  
     Presentation   
 Arthropod bites present in a variety of ways. Multiple bites will present as dis-tinct pruritic lesions, often with a central  punctum   and surrounding erythema.  Hymenoptera   (e.g.,  wasps  ,  bees  ) bites may be accompanied by pain, burning or stinging sensations, as well as local edema.  Bed bug bites   typically manifest in groups of three lesions (referred to as breakfast, lunch, and dinner lesions); however, such a pattern is not specifi c to bed bugs and cannot preclude other insects, as  fl eas   are also known to cause a similar bite pattern (see Chap.   40     for more on bed bugs). 
  Scabies   lesions usually involve papules with burrows containing a serpiginous line with a tiny black speck at the end, and present on the wrists, elbows, interdigital web spaces, and lower abdomen (see Chap.   41    ).  Spider   bites are more likely to pres-ent with extreme pain, although this again is not a symptom specifi c to spider bites. Any insect bite can cause vesicle formation. Although it is not necessarily the case, patients with bites from infesting, indoor bugs may report family members also experiencing bites. Bites from outdoor bugs are more likely to occur on parts of the body that are exposed to the environment, such as the neck and extremities.  
     Workup   
 Patient history is helpful in diagnosing bug  bites  , as they may recall a biting incident. Additionally, patients should be asked about outdoor activities, clothes worn and areas exposed during time outdoors, pets, and whether family members or room-mates have also experienced bites. 
 If scabies are suspected, a scraping can be done and viewed under a microscope. Mineral oil is applied to a burrow or lesion, which is then scraped laterally with a number 15 blade. The scrapings are placed on a glass slide and viewed under a microscope. Microscopy may reveal eggs, mites, or fecal matter. Applying  KOH   to the slide may help visualize mite debris by dissolving keratin. Suspected cases of lice should include inspection of the hair shaft for any nits.  
     Treatment   
 Treatment of bites depends on the insulting arthropod and the accompanying symp-toms. All bite wounds should be cleaned and remaining stingers, if any, should be removed using the edge of a bank card or butter knife to push them out. Tweezers are not recommended as squeezing the stinger may cause further venom release, although the amount of venom might be very small. Symptomatic relief should be provided either in the way of  antihistamines   to control itch,  topical steroids   to con-trol infl ammation, and ice packs or analgesics for pain [ 1 ,  2 ]. 
 Bites such as the ones in this case are usually best treated with topical  steroids     . A medium potency steroid can be used on the limbs and trunk (excluding intertriginous areas), such as betamethasone valerate ointment 0.1% (Class III) applied to individ-ual lesions twice daily for up to 2 weeks. Sedating antihistamines such as hydroxy-zine may be taken by patients experiencing pruritus that interrupts their sleep. 
 Bites causing  anaphylaxis   should be treated with epinephrine or other vasoactive medications.  Tick   bites in geographical areas with high incidence of Lyme may be treated with a prophylactic 200 mg single dose of doxycycline if the tick species has been identifi ed and was attached for more than 36 h [ 2 ]. Severe  spider   bites may require treatment with an antivenom. Secondary infection on bite sites should be treated with an appropriate antibiotic, as determined by a wound culture. Treatment for  bed bug bites   (which are also treated with  topical steroids  ) and scabies are dis-cussed in more detail in their respective chapters.  
     Follow-Up   
 Patient follow up is somewhat dependent on the offending insect. Although many  mosquito  -born diseases are concentrated in tropical and subtropical areas, they still occur in North  America  . Patients with recent travel history and  mosquito   bites should be aware of common symptoms of malaria and dengue. Uncomplicated bug  bites   should resolve within 1–2 weeks of treatment with corticosteroid, although post infl ammatory hyperpigmentation may persist for several months.   
reactions; however, some bites can cause toxic and anaphylactic reactions [ 2 ]. Many arthropods serve as vectors for diseases such as malaria, dengue, West Nile virus, Rocky Mountain spotted fever, Southern tick-associated rash illness (STARI), and Lyme disease. 
 The species of concern in the USA include the black widow and brown recluse  spiders  , the lone star, black-legged ( Ixodes scapularis ) and dog ticks, bed bugs,  fl eas  , biting  flies, and  mosquitoes  . Their signifi cance is due to prevalence, severity of bite symptoms, or potential to transmit disease [ 1 ,  2 ]. Specifi cally, black widow spider bites cause severe muscle spasms and brown recluse spider bites can cause skin necrosis.  Tick   and mosquito bites are common, and the species are vectors for a number of diseases named above. 
 It is diffi cult to estimate the overall prevalence of bug  bites  , as many of them do not require any treatment. Systemic reactions from  hymenoptera   (insects such as  bees  ,  wasps  , and hornets)  stings   have a lifetime prevalence ranging from 0.3 % in children to 7.5 % in adults [ 3 ,  4 ]. Fatalities associated with insect bites are very rare; however, some bites may require emergency management.  
     Presentation   
 Arthropod bites present in a variety of ways. Multiple bites will present as dis-tinct pruritic lesions, often with a central  punctum   and surrounding erythema.  Hymenoptera   (e.g.,  wasps  ,  bees  ) bites may be accompanied by pain, burning or stinging sensations, as well as local edema.  Bed bug bites   typically manifest in groups of three lesions (referred to as breakfast, lunch, and dinner lesions); however, such a pattern is not specifi c to bed bugs and cannot preclude other insects, as  fl eas   are also known to cause a similar bite pattern (see Chap.   40     for more on bed bugs). 
  Scabies   lesions usually involve papules with burrows containing a serpiginous line with a tiny black speck at the end, and present on the wrists, elbows, interdigital web spaces, and lower abdomen (see Chap.   41    ).  Spider   bites are more likely to pres-ent with extreme pain, although this again is not a symptom specifi c to spider bites. Any insect bite can cause vesicle formation. Although it is not necessarily the case, patients with bites from infesting, indoor bugs may report family members also experiencing bites. Bites from outdoor bugs are more likely to occur on parts of the body that are exposed to the environment, such as the neck and extremities.  
     Workup   
 Patient history is helpful in diagnosing bug  bites  , as they may recall a biting incident. Additionally, patients should be asked about outdoor activities, clothes worn and areas exposed during time outdoors, pets, and whether family members or room-mates have also experienced bites. 
 If scabies are suspected, a scraping can be done and viewed under a microscope. Mineral oil is applied to a burrow or lesion, which is then scraped laterally with a number 15 blade. The scrapings are placed on a glass slide and viewed under a microscope. Microscopy may reveal eggs, mites, or fecal matter. Applying  KOH   to the slide may help visualize mite debris by dissolving keratin. Suspected cases of lice should include inspection of the hair shaft for any nits.  
     Treatment   
 Treatment of bites depends on the insulting arthropod and the accompanying symp-toms. All bite wounds should be cleaned and remaining stingers, if any, should be removed using the edge of a bank card or butter knife to push them out. Tweezers are not recommended as squeezing the stinger may cause further venom release, although the amount of venom might be very small. Symptomatic relief should be provided either in the way of  antihistamines   to control itch,  topical steroids   to con-trol infl ammation, and ice packs or analgesics for pain [ 1 ,  2 ]. 
 Bites such as the ones in this case are usually best treated with topical  steroids     . A medium potency steroid can be used on the limbs and trunk (excluding intertriginous areas), such as betamethasone valerate ointment 0.1% (Class III) applied to individ-ual lesions twice daily for up to 2 weeks. Sedating antihistamines such as hydroxy-zine may be taken by patients experiencing pruritus that interrupts their sleep. 
 Bites causing  anaphylaxis   should be treated with epinephrine or other vasoactive medications.  Tick   bites in geographical areas with high incidence of Lyme may be treated with a prophylactic 200 mg single dose of doxycycline if the tick species has been identifi ed and was attached for more than 36 h [ 2 ]. Severe  spider   bites may require treatment with an antivenom. Secondary infection on bite sites should be treated with an appropriate antibiotic, as determined by a wound culture. Treatment for  bed bug bites   (which are also treated with  topical steroids  ) and scabies are dis-cussed in more detail in their respective chapters.  
     Follow-Up   
 Patient follow up is somewhat dependent on the offending insect. Although many  mosquito  -born diseases are concentrated in tropical and subtropical areas, they still occur in North  America  . Patients with recent travel history and  mosquito   bites should be aware of common symptoms of malaria and dengue. Uncomplicated bug  bites   should resolve within 1–2 weeks of treatment with corticosteroid, although post infl ammatory hyperpigmentation may persist for several months.   
    Questions for the Dermatologist 
–  Is there a way to tell which insect is doing the biting?  
 No, unfortunately there is not. All bites are infl ammatory reactions to saliva or an antigen present in the bite. There are some diagnostic clues.  Flea   bites tend to be smaller than  bed bug bites  , but this is not always true. History is most helpful in determining which bug is doing the biting. If bites are found following an out-door activity like a picnic, they are probably outdoor bugs. Presence of blood on the sheets and new bites when the patient wakes up are suggestive of bed bugs. Bites in the dead of winter are more likely to be bed bugs. In that case patients should look for engorged bugs between 4 and 5 am, along the seams of their mattress. 
–  How can insect bites be distinguished from other rashes?  
  Rashes   tend to spread out and extend to different parts of the body. Eczematous rashes may have indiscreet edges. They do not appear as discrete lesions the way bites do. Bites have clear demarcations and appear as individual lesions in groups. 
–  Is there a way to tell whether the bites are caused by bed bugs? Scabies? Is therea lab test for any of the above?  
 There is no lab test for different types of bug  bites  . Suspected scabies lesions can be scraped and viewed under a microscope to look for eggs and droppings. Scrapings are placed in mineral oil on a glass slide and viewed under a microscope on low power. Otherwise defer to history. 
–  What is the best treatment for insect bites that are not scabies?  
 The best treatment is topical  steroids     . Medium potency steroids can be used on the arms and legs twice daily for a short period of time, i.e., 2 weeks.     
   References 
1.   Schwartz RA, Steen CJ. Chapter 210. Arthropod bites and stings [Internet]. In: Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, Wolff K, editors. Fitzpatrick’s dermatology in general medicine. 8th ed. New York: McGraw-Hill; 2012. [cited 2015 Jan 21]. Available from:   http://accessmedicine.mhmedical.com.ezproxy.cul.columbia.edu/content.aspx?bookid=392& Sectionid=41138941    .  
2.    Juckett G. Arthropod bites. Am Fam Physician. 2013;88(12):841–7.  
 3.    Baker TW, Forester JP, Johnson ML, Stolfi  A, Stahl MC. The HIT study: Hymenoptera identi-fi cation test—how accurate are people at identifying stinging insects? Ann Allergy Asthma Immunol. 2014;113(3):267–70.
4.    Ruëff F, Przybilla B, Biló MB, Müller U, Scheipl F, Aberer W, Birnbaum J, Bodzenta-Lukaszyk 
A, Bonifazi F, Bucher C, Campi P, Darsow U, Egger C, Haeberli G, Hawranek T, Körner M, Kucharewicz I, Küchenhoff H, Lang R, Quercia O, Reider N, Severino M, Sticherling M, Sturm GJ, Wüthrich B. Predictors of severe systemic anaphylactic reactions in patients with Hymenoptera venom allergy: importance of baseline serum tryptase-a study of the European Academy of Allergology and Clinical Immunology Interest Group on Insect Venom Hypersensitivity. J Allergy Clin Immunol. 2009;124(5):1047–54.   

Blistering Dactylitis

December 09, 2021 0

Blistering Dactylitis


Primary Care Visit Report   

A 37-year-old female with no past medical history presented with redness and peeling skin on bilateral hands and fingers after sustaining a dog bite 2 weeks prior. The patient was bitten on both hands when she jumped in to separate a dog fight. The patient initially went to an emergency room and was given  tetanus   and  rabies vaccines. Three days later, her fingers were swelling so she went back to the ER and was admitted for 3 days of IV  antibiotics   (vancomycin and ampicillin/sulbactam) and was discharged on amoxicillin/clavulanate and doxycycline, which she was taking at the time of this visit. 

 While the pain and stiffness in her fingers had improved somewhat, the patient remained concerned because she noticed the night prior that certain areas had become “red and bumpy” and about 4 h later, the skin on her fingers began to peel. The patient had no fever or chills, and felt fine otherwise. 

 At the time of this visit, the patient was status post three rabies vaccinations on Day 0, Day 3 and Day 7 and was due for the fourth vaccine, though she found out from its owner that the dog who bit her was up to date on its rabies  vaccinations. 

 Vitals were normal. On exam, on bilateral hands, there were multiple erythematous lesions with erythematous bases at the sites of the  dog bites  . There was peeling on the periphery of many of the lesions, and many were indurated and tender to palpation. 

Specifi cally, the right hand pinky finger had erythema and tenderness to palpation spanning the full circumference of her fi nger (dorsal and ventral aspect) at the distalinterphalangeal joint and extending proximally with limited active range of motion (but full passive range of motion) at the distalinterphalangeal joint. At the periphery of the erythema, the skin was peeling. The left thumb had a 1.5 cm × 1.0 cm erythematous lesion with peeling skin at the periphery, with some induration and tenderness to palpation. The left fourth finger had a 3.0 cm × 1.5 cm erythematous, tender and indurated  lesion   with peeling at the periphery at the  proximal interphalangeal joint. She had limited active range of motion at this joint (normal passive range of motion). No warmth on any of the lesions. Peripheral pulses were normal. 

 Since the patient was already on  antibiotics   yet continued to have further worsening of pain and developed new areas of erythema and peeling, I was concerned about an abscess and referred her immediately to a hand surgeon for further evaluation. The hand surgeon examined her and was not concerned for an abscess but did recom-mend her for physical therapy.  

    Discussion from Dermatology Clinic 

     Differential Dx   

  Blistering dactylitis  

  Epidermolysis bullosa simplex, localized type

  Bullous impetigo       

Favored Dx   

The open lesions following  dog bites   most likely contracted a  bacterial infection ,  resulting in blistering dactylitis.  

Overview   

Blistering dactylitis is a condition indicative of a superfi cial infection caused by  β-hemolytic streptococcal bacteria  , or by   Staphylococcus aureus   , both of which are commonly found in  dog   saliva.  Animal bites      are common, with over one million animal bites occurring annually [ 1 ]. It is estimated that half of all Americans will experience a mammalian bite dur-ing their lifetime, and  dog bites   account for the majority of reported bites (80–90 %) although the infection rates are low (2–20 % of bites) [ 2 ]. Children are more likely to be bitten than adults, and are more likely to experience injuries to the neck and face versus adults who are more commonly bitten on the upper extremities. Bites on the hand are the most likely to develop infections [ 3 ].  

Presentation   

Patients in the acute blistering phase of blistering dactylitis present with superfi cial, tender blisters over the fat pads of the palmar aspects of the fi ngertips. Fingers may be erythematous and swollen, and blisters can ooze. The acute blistering phase may be very short-lived, and patients may not notice  bullae  , especially if they are small or burst soon after onset. Lesions tend to be asymptomatic; however, some patients may complain of pain and tenderness in the area, and they may be febrile.  

Workup   

Obtain a bacterial culture of the blister fl uid. Cultures should rule out  MRSA  infections, which are unlikely but can occur after  dog bites  .  

Treatment   

Blisters can be incised and drained [ 4 ], and the wounds should be irrigated.  Rabies   and  tetanus   vaccines should be administered, if indicated. The patient should start a course of prophylactic  antibiotics  , the type of which should be determined by bacteri-ology [ 1 ]. Penicillin or ampicillin are effective against many components of dogs’ oral fl ora and doxycycline provides a good alternative in children older than 8 years [ 1 ]. The combination of amoxicillin and clavulanic acid has demonstrated effi cacy in treating  dog bites      as well [ 1 ]. If cultures reveal  MRSA  , an appropriate substitute anti-biotic such as trimethoprim/ sulfamethoxazole or doxycycline should be initiated.  

     Follow-Up   

 Patients should follow up at the end of their antibiotic course to ensure the infection has cleared. Further treatment may not be necessary, unless patients complain their symptoms have not resolved.   

    Questions for the Dermatologist 

–  What do I need to be concerned about when it comes to dog (or other animal)

bites?  

 The three factors contributing to potential infection are the biting animal’s oral fl ora, the bite recipient’s skin fl ora, and environmental organisms.  Rabies   would be high on the list of concerns.  Dog bites   themselves would not cause  tetanus  , but breaks in skin following the bite increase the risk of exposure to  C. tetani . Dogs’ saliva can contain  Pasteurella ,   Staphylococcus   , and   Streptococcus  species  , and, rarely, poten-tially fatal   Capnocytophaga canimorsus    [ 5 ]. Bacterial culturing should be part of the general workup. This is particularly important in  animal bites   with open wounds because bacteria can easily enter the wound. If no culture is taken and the prescribed antibiotic is not working, it will be less obvious which antibiotic to prescribe. 

–  Does the peeling skin signify normal healing? Or is it something to be concerned about?  

 The toxins produced by bacteria cause exfoliative dermatitis. The most reassuring sign is that normal skin is repopulating underneath the peeling skin. That is a sign of recovery. 

Two weeks after a dog bite is there anything else I should be worried about beyond the actual bite?

Ensure any tetanus concerns have been addressed, and find out if the biting dog’s rabies vaccinations are current. Otherwise, the patient should be managed supportively.

– In this case, the peeling did not occur until 2 weeks after the dog bites and after she has already been on 2 weeks of antibiotics . Is this common? Does this signify a super-infection from the initial dog bite, or just a new phase of the initial infection?

 Blisters that are seen in infectious blistering conditions are very superficial and rupture quite easily. It is possible that following  bacterial infection  , the patient briefl y formed superfi cial blisters that collapsed and later began to peel. The patient may not have experienced a specifi c bullous phase; however, at some point the  blisters were probably unroofed, and as the skin dried out it began to fall off and peel. Rather than signifying a super-infection, the peeling skin is more likely part of the initial infection.     

   References 

       1.   Brook I. Management of human and animal bite wound infection: an overview. Curr Infect Dis Rep. 2009;11(5):389–95.

    2.   Griego RD, Rosen T, Orengo IF, Wolf JE. Dog, cat, and human bites: a review. J Am Acad Dermatol. 1995;33(6):1019–29.

    3.   Oehler RL, Velez AP, Mizrachi M, Lamarche J, Gompf S. Bite-related and septic syndromes caused by cats and dogs. Lancet Infect Dis. 2009;9(7):439–47.

    4.   McCray MK, Esterly NB. Blistering distal dactylitis. J Am Acad Dermatol. 1981;5(5):592–4.

    5.   Thomas N, Brook I. Animal bite-associated infections. Expert Rev Anti Infect Ther. 2011;9(2):215–26.   

Paronychia

December 09, 2021 1

 

Paronychia

Primary Care Visit Report   

A 32-year-old male with no past medical history presented with swelling of his right hand fourth finger, near his fingernail. It started the day prior to this visit, and he said he felt a lot of pressure in the fingertip. He tried icing it overnight with no improvement. 

Vitals were normal. On exam, the skin lateral to the fingernail on his right hand fourth finger was  erythematous, edematous, warm, and very tender to palpation. There was minimal fluctuance. 

This was treated as paronychia. His finger was first soaked in warm water for 30 min, then an incision and  drainage  procedure was performed with a digital nerve block. However, no pus was expressed. The patient was sent home with instructions to soak his finger in warm water twice daily and to apply bacitracin to the area. He was asked to return to the office if the redness and swelling persisted or worsened.  

Discussion from Dermatology Clinic 

Differential Dx   

  Bacterial paronychia  

  Candidal paronychia  

  Drug-induced paronychia  

  Nail fold dermatitis  

  Herpetic whitlow  

  Ingrown nail     

Favored Dx   

Clinical examination and history are consistent with acute bacterial paronychia. It is apparent from physical examination that the patient is a nail biter, which is one of the predisposing factors for paronychia.  

Overview   

Paronychia is a common infl ammation of the proximal nail fold and  periungual soft tissues  , which is classifi ed as acute when it lasts fewer than 6 weeks, and chronic when it lasts greater than 6 weeks. The majority of cases are acute paronychia, which is most commonly associated with bacterial infection following mild local trauma, while chronic paronychia is associated with candidiasis. Predisposing factors for paronychia are exposure to chemical irritants, mechanical factors such as nail biting, picking, or fi nger sucking, and systemic conditions, such as diabetes and HIV [ 1 ,  2 ]. Less frequently, paronychia has been associated with use of certain medications, such as protease inhibitors, antiretrovirals, and chemotherapeutic agents. 

The most common bacterial pathogen involved in acute paronychia is  Staphylococcus aureus   .   Streptococcus pyogenes   ,   Pseudomonas aeruginosa   , and   Proteus  species   are involved with less frequency [ 1 – 3 ]. Most cases of bacterial paro-nychia are caused by mixed fl ora, and paronychia that comes in contact with oral fl ora, as in nail biting and fi nger sucking, typically involves anaerobic bacteria [ 2 ,  4 ].   Candida albicans    is often found in chronic paronychia. The pathogenesis of chronic paronychia is usually complex and multifactorial, and is currently thought to be an infl ammatory process which may feature an overlying acute (i.e., bacterial) paro-nychia.  Chronic    paronychia   is associated with excessive moisture, which may be the result of frequent immersion of the hands in water, as happens with occupational wet work. Paronychial herpes simplex virus lesions are referred to as herpetic whitlow.  

Presentation   

Acute  paronychia   presents as rapid-onset periungual erythema, swelling, and ten-derness.  Acute paronychia   may develop within hours, and there may be ulceration and purulence. It usually presents on a solitary digit [ 2 ]. 

Chronic  paronychia      can lead to changes in the nails, such as thickening, ridging, and discoloration [ 1 ]. Chronic paronychia is not usually purulent, and it may be long-standing. More than one fi ngernail is often involved.  

Workup   

 Physical examination and history are usually suffi cient to make a diagnosis. A bac-terial or fungal culture of contents expressed from the wound may be performed to confi rm the offending pathogen; however, it is often not necessary.  

Treatment   

 Treatment approach depends on whether the paronychia is acute or chronic, and the severity of infl ammation. Acute bacterial  paronychia      may be treated with  warm water compresses  , and topical or oral antibiotics. Warm water compresses for 20 min up to three times a day may be suffi cient treatment for mild cases of acute paronychia with minimal infl ammation and no abscess. Their main role in treatment of severe cases is as adjunct therapy [ 1 ,  2 ]. Topical antibiotics such as  mupirocin   can be added to cases with more severe erythema, applied after each warm compress or soak. Oral antibiotics are appropriate for severe cases with severe infl ammation [ 1 ]. For patients not exposed to oral fl ora (no nail biting and/or a paronychia of a toe), coverage of skin fl ora alone is appropriate—such as cephalexin 500 mg three or four times daily or dicloxacillin 250 mg four times daily. If oral fl ora exposure is present, amoxicillin/clavulanate 875/125 twice a day is appropriate. MRSA should be  covered by the chosen antibiotic where there is a signifi cant community  MRSA   presence [ 3 ,  4 ]. Clindamycin is a good option for MRSA coverage. 

Alternately, although there is no evidence to the authors’ knowledge of I&D having better or worse outcomes than oral antibiotics alone [ 2 ,  5 ], clinically it is com-mon practice to perform an  incision and drainage (I&D)   on acute paronychia with an abscess. After appropriate local anesthesia (i.e., a digital block), a scalpel inci-sion in the affected cuticle margin can relieve pressure and allow the patient some immediate symptomatic relief. Often incision and  drainage   can be suffi cient to treat paronychia with abscess or oral antibiotics can be added after the I&D along with warm soaks which would help ensure the abscess would continue to drain. Oral antibiotics are typically prescribed for a 5 day course if an I&D is performed, or a 7–10 day course without I&D. Cases with nail irregularities can be referred to a dermatologist or hand surgeon. 

 Chronic  paronychia     , thought to be caused by prolonged exposure (often occupa-tional) to water, features   Candida albicans    in up to 95 % of cases [ 1 ]. The role of  C. albicans  in prolonging paronychia is unknown, and chronic paronychia is con-sidered an infl ammatory disorder. This variant may be treated with topical or oral (in severe cases)  antifungals   such as itraconazole and fl uconazole; however, there is greater improvement when potent topical corticosteroids are used instead [ 6 ,  7 ]. A 2-week course of a potent topical  steroid   (Class I or II) is recommended for chronic paronychia. Additionally protective measures, such as wearing gloves, should be used in order to keep hands dry and away from irritants or allergens. If these treatments do not resolve the chronic paronychia, a course of antifungal ther-apy can then be added. Since chronic paronychia is now considered to be an eczem-atous process, it is equally important to address any underlying factors contributing to pathogenesis, including keeping hands dry in cases where excessive moisture is a causative factor, or treating systemic illness such as diabetes or HIV.

     Follow-Up   

 Patients should be reevaluated after 1–2 weeks of treatment. Clinical improvement rather than cure may be the outcome for chronic paronychia. Avoiding environmen-tal irritants, picking and biting habits, or other known triggers are essential in achieving a long-term cure. Recalcitrant cases should be referred to dermatology or hand surgery.   

while chronic paronychia is associated with candidiasis. Predisposing factors for paronychia are exposure to chemical irritants, mechanical factors such as nail biting, picking, or fi nger sucking, and systemic conditions, such as diabetes and HIV [ 1 ,  2 ]. Less frequently, paronychia has been associated with use of certain medications, such as protease inhibitors, antiretrovirals, and chemotherapeutic agents. 

 The most common bacterial pathogen involved in acute paronychia is   Staphylococcus aureus   .   Streptococcus pyogenes   ,   Pseudomonas aeruginosa   , and   Proteus  species   are involved with less frequency [ 1 – 3 ]. Most cases of bacterial paro-nychia are caused by mixed fl ora, and paronychia that comes in contact with oral fl ora, as in nail biting and fi nger sucking, typically involves anaerobic bacteria [ 2 ,  4 ].   Candida albicans    is often found in chronic paronychia. The pathogenesis of chronic paronychia is usually complex and multifactorial, and is currently thought to be an infl ammatory process which may feature an overlying acute (i.e., bacterial) paro-nychia.  Chronic    paronychia   is associated with excessive moisture, which may be the result of frequent immersion of the hands in water, as happens with occupational wet work. Paronychial herpes simplex virus lesions are referred to as herpetic whitlow.  

     Presentation   

 Acute  paronychia   presents as rapid-onset periungual erythema, swelling, and ten-derness.  Acute paronychia   may develop within hours, and there may be ulceration and purulence. It usually presents on a solitary digit [ 2 ]. 

 Chronic  paronychia      can lead to changes in the nails, such as thickening, ridging, and discoloration [ 1 ]. Chronic paronychia is not usually purulent, and it may be long-standing. More than one fi ngernail is often involved.  

     Workup   

 Physical examination and history are usually suffi cient to make a diagnosis. A bac-terial or fungal culture of contents expressed from the wound may be performed to confi rm the offending pathogen; however, it is often not necessary.  

     Treatment   

 Treatment approach depends on whether the paronychia is acute or chronic, and the severity of infl ammation. Acute bacterial  paronychia      may be treated with  warm water compresses  , and topical or oral antibiotics. Warm water compresses for 20 min up to three times a day may be suffi cient treatment for mild cases of acute paronychia with minimal infl ammation and no abscess. Their main role in treatment 

of severe cases is as adjunct therapy [ 1 ,  2 ]. Topical antibiotics such as  mupirocin   can be added to cases with more severe erythema, applied after each warm compress or soak. Oral antibiotics are appropriate for severe cases with severe infl ammation [ 1 ]. For patients not exposed to oral fl ora (no nail biting and/or a paronychia of a toe), coverage of skin fl ora alone is appropriate—such as cephalexin 500 mg three or four times daily or dicloxacillin 250 mg four times daily. If oral fl ora exposure is present, amoxicillin/clavulanate 875/125 twice a day is appropriate. MRSA should be  covered by the chosen antibiotic where there is a signifi cant community  MRSA   presence [ 3 ,  4 ]. Clindamycin is a good option for MRSA coverage. 

 Alternately, although there is no evidence to the authors’ knowledge of I&D hav-ing better or worse outcomes than oral antibiotics alone [ 2 ,  5 ], clinically it is com-mon practice to perform an  incision and drainage (I&D)   on acute paronychia with an abscess. After appropriate local anesthesia (i.e., a digital block), a scalpel inci-sion in the affected cuticle margin can relieve pressure and allow the patient some immediate symptomatic relief. Often incision and  drainage   can be suffi cient to treat paronychia with abscess or oral antibiotics can be added after the I&D along with warm soaks which would help ensure the abscess would continue to drain. Oral antibiotics are typically prescribed for a 5 day course if an I&D is performed, or a 7–10 day course without I&D. Cases with nail irregularities can be referred to a dermatologist or hand surgeon. 

 Chronic  paronychia     , thought to be caused by prolonged exposure (often occupa-tional) to water, features   Candida albicans    in up to 95 % of cases [ 1 ]. The role of  C. albicans  in prolonging paronychia is unknown, and chronic paronychia is con-sidered an infl ammatory disorder. This variant may be treated with topical or oral (in severe cases)  antifungals   such as itraconazole and fl uconazole; however, there is greater improvement when potent topical corticosteroids are used instead [ 6 ,  7 ]. A 2-week course of a potent topical  steroid   (Class I or II) is recommended for chronic paronychia. Additionally protective measures, such as wearing gloves, should be used in order to keep hands dry and away from irritants or allergens. If these treatments do not resolve the chronic paronychia, a course of antifungal ther-apy can then be added. Since chronic paronychia is now considered to be an eczem-atous process, it is equally important to address any underlying factors contributing to pathogenesis, including keeping hands dry in cases where excessive moisture is a causative factor, or treating systemic illness such as diabetes or HIV.

     Follow-Up   

 Patients should be reevaluated after 1–2 weeks of treatment. Clinical improvement rather than cure may be the outcome for chronic paronychia. Avoiding environmental irritants, picking and biting habits, or other known triggers are essential in achieving a long-term cure. Recalcitrant cases should be referred to dermatology or hand surgery.   

    Questions for the Dermatologist 

–  What conditions lead to paronychia? Is nailbiting a factor?  

 There are two forms of paronychia:  acute      and  chronic     .  Nail biting   can predispose someone to either form by exposing the nail fold to pathogens. Pathogens in the acute form are typically strep and staph, while in the chronic form it’s   Candida.  The acute form presents acutely tender and swollen with purulence. The chronic form is characterized by a boggy, ragged cuticle. Wet work (e.g., restaurant food prep, new moms) can predispose people to the chronic form. 

–  Is different treatment required for nail biters (i.e., different antibiotics)?  

 The type of paronychia tends to determine the treatment. Acute paronychia would get treated with antibiotics, and chronic paronychia would get treated with topical steroids and/or  antifungals  . Nail biting could predispose someone to either form. However, acute paronychia in nail biters would warrant treatment with antibiotics that specifi cally cover oral fl ora. 

–  When are oral antibiotics indicated?  

 Oral  antibiotics   are indicated for acute paronychia, and in practice I almost always treat with oral antibiotics. Treatment purely with topical antibiotics is generally not successful because it is diffi cult for them to penetrate the nail fold. I use cephalosporins and penicil-lins to treat staph and strep paronychia. Some paronychias are caused by   pseudomonas   , most commonly following manicures. They can be identifi ed by a blue-green hue to the purulence and lateral nail fold. Those cases can be treated with ciprofl oxacin. 

–  How do you know when to I&D? If it doesn’t seem ready to I&D, what is the best

treatment?  

 The decision to I&D comes down to the extent of the abscess and edema. Acute paronychia is generally a tiny abscess. If it’s very tender and very swollen, I will try to drain it. If it is only a little bit pink and tender, and it is not ready to I&D, I try oral antibiotics fi rst. I also consider whether the patient can tolerate the potential pain of the procedure. 

–  Are there common mistakes made when doing an I &  D     for paronychia?  

 The strong part of the nail is proximal to the proximal nail fold. That is where the matrix is located, which would need to be avoided in such a procedure in order to avoid causing damage. Any procedure done on the side of the nail is well away from the matrix, so the risk of causing permanent dystrophy is low. I often need to try a couple of punctures before finding the pus pocket. 

–  Can paronychia resolve with warm water soaks and topical antibiotics alone?

Should anything be put in the water?  

 Usually it cannot, but warm water soaks and hot compresses can be added as adjunctive therapy. It is helpful to massage the area after a 20-min soak or hot compress. 

Massaging can get the abscess to open up on its own and drain. Treatment exclusively with hot compresses and warm water soaks is not recommended except in very mild cases, and should only be used if a patient is very resistant to using antibiotics. The next step if paronychia advances is dactylitis, where infection extends to the fi nger pad, and that is a much bigger problem. The compresses can be done with warm water, Burow’s solution, or vinegar dissolved in a 1:1 ratio with warm water.     

   References 

1.    Shafritz AB, Coppage JM. Acute and chronic paronychia of the hand. J Am Acad Orthop Surg. 2014;22(3):165–74.

2.    Rigopoulos D, Larios G, Gregoriou S, Alevizos A. Acute and chronic paronychia. Am Fam Physician. 2008;77(3):339–46.

3.   Ritting AW, O’Malley MP, Rodner CM. Acute paronychia. J Hand Surg Am. 2012;37(5): 1068–70.

4.   Tully AS, Trayes KP, Studdiford JS. Evaluation of nail abnormalities. Am Fam Physician. 2012;85(8):779–87.

5.    Shaw J, Body R. Best evidence topic report. Incision and drainage preferable to oral antibiotics in acute paronychial infection? Emerg Med J. 2005;22(11):813–4.

6.   Tosti A, Piraccini BM, Ghetti E, Colombo MD. Topical steroids versus systemic antifungals in the treatment of chronic paronychia: an open, randomized double-blind and double dummy study. J Am Acad Dermatol. 2002;47(1):73–6.

7.    Hay RJ. The management of superfi cial candidiasis. J Am Acad Dermatol. 1999;40(6 Pt 2): S35–42.   


Periungual Warts

December 09, 2021 0

 

Periungual Warts

Primary Care Visit Report   

A 32-year-old male with no past medical history presented with redness, scaling, and induration around his fingernails for 1 year. He had previously been prescribed terbinafi ne cream, which improved the redness but the periungual rash persisted. 

Vitals were normal. On exam, verrucous, well-demarcated, skin-colored to lightly pigmented papules and erythema were present on the periungual areas of all digits. Some induration and scaling was noted. 

 The differential considered was warts (or  verrucae  ) alone versus verrucae accom-panied by fungal involvement as the patient reported improvement with terbinafi ne. The patient was referred to dermatology for further evaluation.  

    Discussion from Dermatology Clinic 

     Differential Dx   

    Periungual warts  

  Acquired periungual fi brokeratoma

  Lichen planus  

  Angiokeratoma  

  Onychomatricoma  

  Periungual  callus    

  Squamous cell carcinoma     

     Favored Dx   

 Some of the patient’s lesions feature the dark, central puncta typical of common warts. The appearance and history is consistent with verrucous lesions.  

     Overview   

 Cutaneous warts are more prevalent in men than women. The median affected age in both genders is during the third decade, but prevalence peaks in school-age years. Palms and feet are the most commonly affected sites although they can occur any-where on the body [ 1 ]. Warts may appear more frequently in immunosuppressed populations, such as organ transplant recipients, or those with HIV infections, and demonstrate more extensive involvement and recalcitrance in those cases. 

  Cutaneous warts   are caused by  human papillomavirus  . Over 150 different strains have been identifi ed, but HPV 1, 2, 4, 7, 27, 57, and 65 appear to be frequently linked with cutaneous warts [ 2 ,  3 ]. Rarely, types 16 and 18 can cause periungual warts and are considered high risk for transforming into squamous cell carcinoma.  

     Presentation   

  Periungual warts   are warts that appear adjacent to nails of the hands and feet. Warts typically present as small, rough, caulifl ower-like papules. Black puncta, tiny dots representing blood vessels, often appear at the center of the hyperkeratotic, dome- shaped lesions. These may also cause pinpoint bleeding if the growth is shaved down. Warts in children may resolve spontaneously over a period of several months to a year, while they may persist for several years in adults.  

     Workup   

 Clinical examination is usually sufficient for diagnosis.  Biopsy   should be performed in immunocompromised patients, or in recalcitrant, long-standing warts to rule out high risk strains of HPV, Bowen’s disease, and squamous cell carcinoma [ 4 ].  

     Treatment   

 The approaches to wart treatment include topical, intralesional, and laser therapies. Surgical options include electrodesiccation, a tissue destruction technique using electrical current, and excision but are not fi rst-line due to risk of scarring and the likelihood of recurrence [ 5 ]. The elected therapy should take into account patient age and immunity, tolerance for discomfort, lesion size and number, and desired speed to resolution. 

  Cryotherapy   with liquid nitrogen is a very common and successful approach to therapy. It can be directly sprayed or applied with a cotton tipped applicator, depending on patient age, as younger children may have diffi culty tolerating extensive spraying, and location of lesion. Clearance rates can be as high as 85 % and perhaps higher when warts are pared down to get rid of thickened, dead skin prior to freezing [ 6 ,  7 ]. Spray should be applied at a 90° angle, 1–2 cm away from the skin. Frost can be achieved by spraying continuously for about 4–5 s then allowing the skin to thaw for about 10 s. This freeze thaw cycle should be repeated 2–3 times per visit. Treatment may require several sessions before the wart resolves. In our practice, we average three treatment sessions. 

 Topical 50 % salicylic acid has a lower clearance rate at approximately 24 % and thus does not appear to be more effective than  cryotherapy      [ 7 ,  8 ]. It may be used for patients desiring a more conservative treatment approach. Imiquimod 5 % cream is an immune response modifi er than may be successful when used as a  combination therapy   with salicylic acid or other destruction methods (e.g., paring, cryotherapy), but unlikely to produce complete clinical clearance on its own [ 9 ]. 

 Intralesional candida antigen causes upregulation of immune responses which are thought to then target warts.  Candida   injections have been found to achieve clearance in 74 % of patients, and are particularly useful in recalcitrant warts [ 3 ]. Candida injections can cause local erythema and pruritus. Intralesional bleomycin injections at a concentration of 1 mg/ml demonstrated complete resolution without recurrence after a year in one study [ 10 ].  Bleomycin   works as a chemotherapeutic agent that interferes with the reproduction of viral cells. Injections should not be administered more than two times per site over the course of treatment in order to avoid risk of local necrosis and Raynaud’s disease. 

 Patients may be referred to a dermatologist for treatment with  pulsed dye laser (PDL)  . PDL targets the microvasculature that supplies verrucous growths. When the blood supply is eliminated, the warts become necrotic and eventually fall off. PDL treatment is advantageous because patients do not experience much pain and there is low risk of scarring; however, clearance rates are lower, at 34 %, after an average of 2–4 treatments [ 3 ,  5 ].  

     Follow-Up   

 The specifi cs of patient follow-up will depend on the course of treatment elected; however, all patients should return for reevaluation 2 weeks after initial therapy to monitor progress.  Cryotherapy   and PDL should be repeated every 2 weeks until warts have resolved. Candida and bleomycin injections may clear warts after one treatment, but warts should be monitored under a dermatoscope to confi rm no resid-ual puncta are visible. Some patients may opt to take conservative approaches like salicylic acid treatment, or occlusion under duct tape, in which case they may be instructed to return for treatment if the  warts   grow too bothersome.   

    Questions for the Dermatologist 

–  Do warts often have a superimposed fungal infection?  

 No. However, if the position of a wart is lifting the nail plate, that would predispose the area to a secondary fungal infection by improving the access of that pathogen. 

–  Do warts spread? Could this patient somehow be auto-infecting himself?  

 Yes,  warts   can spread. Viral particles can be transmitted by scratching and picking. It is common to see children who are biting or sucking warts to later develop them on their lips. 

–  What are the contact precautions, if any, for someone with warts?  

It is not necessary to isolate patients with warts. They are transmittable by prolonged skin-to-skin contact. Family members should be advised to wear sandals in the shower if the patient has plantar warts, and they should not share bath scrub brushes.

Are there any special considerations when doing cryotherapy on someone with warts on every finger? Is there a clinical indication for treating one hand at a time?

The considerations should be discussed with the patient. There is no medical reason for treating one hand at a time, but patients have varying tolerance. Some patients may want the warts gone as soon as possible. Others may not be able to tolerate extensive treatment, and would prefer to take their time treating potentially blistering lesions. 

– Are there any specifi c precautions when using cryotherapy around the nail area so as not to cause any permanent nail disfi guring? i.e., do you do cryotherapy for shorter amount of time or a lesser number of freeze thaw cycles? 

  Nail growth   comes from the nail matrix underneath the proximal nail fold. Freezing periungual warts, unless very aggressively with a wide area of tissue damage, is unlikely to impact that anatomic nail unit. With cryotherapy treatment on any region of the body, cycles with 4–5 s of continuous spraying followed by about 10 s of thawing aim to minimize tissue damage, which in turn avoids destruction of any underlying structures.     

   References 

 1.   Kyriakis K, Pagana G, Michalides C, Emmanuelides S, Palamaras I, Terzoudi S. Lifetime prevalence fluctuations of common and plane viral warts. J Eur Acad Dermatol Venereol. 2007;21(2):260–2.

 2.   De Koning MN, Quint KD, Bruggink SC, Gussekloo J, Bouwes Bavinck JN, Feltkamp MC, Quint WG, Eekhof JA. High prevalence of cutaneous warts in elementary school children and ubiquitous presence of wart-associated HPV on clinically normal skin. Br J Dermatol. 2015. doi:  10.1111/bjd.13216    . Accessed 24 Oct 2014.

 3.   Herschthal J, McLeod MP, Zaiac M. Management of ungual warts. Dermatol Ther. 2012; 25(6):545–50.

 4.   Riddel C, Rashid R, Thomas V. Ungual and periungual human papillomavirus-associated squamous cell carcinoma: a review. J Am Acad Dermatol. 2011;64(6):1147–53.

 5.   Tosti A, Piraccini BM. Warts of the nail unit: surgical and nonsurgical approaches. Dermatol Surg. 2001;27(3):235–9.

 6.   Zimmerman EE, Crawford P. Cutaneous cryosurgery. Am Fam Physician. 2012;86(12): 1118–24.

 7.   Ko J, Bigby M. Randomized controlled trial of cryotherapy with liquid nitrogen vs topical salicylic acid vs wait-and-see for cutaneous warts. Arch Dermatol. 2012;148(7):840–2.

 8.   Kwok CS, Gibbs S, Bennett C, Holland R, Abbott R. Topical treatments for cutaneous warts. Cochrane Database Syst Rev. 2012;9, CD001781.

 9.   Ahn CS, Huang WW. Imiquimod in the treatment of cutaneous warts: an evidence-based review. Am J Clin Dermatol. 2014;15(5):387–99.

    10.   Soni P, Khandelwal K, Aara N, Ghiya BC, Mehta RD, Bumb RA. Effi cacy of intralesional bleomycin in palmoplantar and periungual warts. J Cutan Aesthet Surg. 2011;4(3):188–91.   

Digital Mucous Cyst

December 09, 2021 0

 Digital Mucous Cyst Treatment 

Digital Mucous Cyst


Primary Care Visit Report   

A 59-year-old female with no past medical history presented with a lesion on the pinky finger of her right hand. She first noticed the sore about 2–3 months prior. It was not painful, but it had started to distort her fingernail. 

Vitals were normal. On exam, on the right hand fifth digit, just proximal to the nail bed, there was a 2 mm soft, non-tender, fluctuant mass with nail deformation. 

This was treated as a digital mucous  cyst  , and the patient was referred to dermatology for surgical excision.  

Discussion from Dermatology Clinic      

Differential Dx   

     Favored Dx   

Digital mucous cyst (DMC) is the favored diagnosis. The mass’s presentation as nontender and fluctuant, its persistence without change over 2 months, and its location on the  proximal nail fold   are all features consistent with DMC.  

Overview   

Digital mucous cysts, sometimes referred to as mucoid or myxoid cysts , are  benign  cysts of the fingers and toes. They lack epithelial lining, making them  pseudocysts .  They typically appear between the fourth and seventh decade, and are twice as likely to occur in women than men [ 1 ]. They are thought to arise from mucoid degeneration of connective tissue [ 2 ]. 

Two distinct forms have been described:  myxomatous   and  ganglion   type DMCs [ 1 ,  3 – 6 ]. The myxomatous type occurs due to metabolic changes in fi broblasts that lead to overproduction of hyaluronic acid, which then gets trapped, creates a cystic space and leads to a DMC. These are not connected directly to the adjacent joint. Ganglion type DMCs are associated with degenerative joint disease and occur more frequently in people with osteoarthritis. Ganglion type cysts are anchored directly to the affected joint (usually the  distal interphalangeal joint  ) via a pedicle, and are fi lled with synovial fluid [ 3 – 5 ]. 

 The two types are clinically indistinguishable, and a definitive diagnosis can only be made during surgery if a pedicle is observed, or by histopathology.  

Presentation   

Digital mucous cysts are translucent, round, dome-shaped lesions that appear on lateral or dorsal aspects of  distal interphalangeal joints  , or on the  proximal nail folds   of digits. They most frequently appear as solitary lesions; however, there have been a few reports of multiple DMCs [ 3 ]. They typically appear on fingers, although they also sometimes appear on toes [ 2 ]. DMCs tend to be under 1 cm in size. They are usually asymptomatic. They may sometimes discharge spontaneously, or cause reduced range of motion, pressure to the nail bed, nail deformities, and pain, espe-cially as the cysts enlarge [ 1 ,  3 ].  

Workup   

Some of the differential diagnoses can be ruled out based on history.  Acral fi bro-keratomas   are usually preceded by local trauma; tumors (GCTTS, histiocytoma) would exhibit rapid growth. 

Digital mucous cysts tend to be compressible, can be  transilluminated  , and express clear or yellow viscous, jelly-like contents when incised. White structures appear on compression, consistent with increased collagen [ 2 ,  7 ]. If diagnosis is unclear, imaging studies (plain X-ray, MRI, CT, ultrasound) may be done to determine the nature of the growth. 

If a  biopsy is performed to rule out malignancy, histopathology of mucous cyst would reveal a cystic space with mucinous content, increased fi broblasts in the  dermis, and no apparent lining of the cyst wall [ 3 ].  

Treatment   

DMCs are  benign   and may not require treatment. Asymptomatic cysts can be monitored. Some digital mucous cysts may spontaneously resolve. If patients are bothered by cosmetic appearance, they experience discomfort, or the DMC is causing nail deformity or functional impairment cysts may be treated. Treatment options include incision and drainage, intralesional steroids (e.g., triamcinolone acetonide 5–10 mg/ml), sclerotherapy (e.g., 1 % sodium tetradecyl sulfate),  cryosurgery  ,  elec-trodesiccation  , CO 2  laser, and surgical excision. Of these the most effective is surgical excision, with cure rates up to 100 % [ 1 ,  4 – 6 ,  8 ,  9 ]. 

 A conservative approach of incision and drainage followed by steroid injection is favored. This may be done in a primary care setting [ 6 ].  I&D   usually requires several treatments as fluid tends to re-accumulate, and leads to cure rates of up to 72 % [ 5 ,  6 ].  Steroid   injection alone is associated with high recurrence rates [ 6 ].  Cryosurgery   has a 56–86 % cure rate [ 5 ]. It requires unroofi ng and draining the cyst, and freezing down to the cyst base. Frost should be maintained for about 10 s, which can be achieved by spraying continuously for about 4–5 s, then allowing it to thaw. This freeze-thaw cycle should be repeated 2–3 times per visit. Patients desiring treatment by sclerotherapy, electrodesiccation, CO 2  laser, or surgery should be referred to dermatology or hand surgery.  

Follow-Up   

The literature on DMCs suggests a possible risk of infection, although the link is controversial [ 5 ,  8 ,  9 ]. Patients should be instructed to report back to the office if they notice any tenderness, redness, or swelling consistent with infl ammation. 

 If patients are dissatisfi ed with the treatment modality or progress, they may be referred to one of the above specialists for more aggressive therapy. Patients choosing conservative treatment should be made aware of the likelihood they may need to return for multiple treatments. In most cases, any nail abnormalities return to normal after the DMC has resolved, or when the nail grows out [ 8 ].   

    Questions for the Dermatologist 

– Is the I&D done on digital mucous cysts different than the I&D done for abscesses

or paronychia? Could the I&D have been done in a primary care office?

Digital mucous cysts are incised and drained in the same way, and this procedure can

be performed in primary care. However, they have a higher recurrence rate when they

are treated in this manner, which is one of reasons to excise them rather than I&D.

– Will the nail bed become normal again after the cyst has been drained and

removed?

The nail itself will grow out normally as long as the nail matrix was not traumatized.

There may be dystrophy if the DMC caused trauma to the nail matrix.

– Can digital mucous cysts become infected? Do they ever require antibiotics?

DMCs do not tend to become infected. Antibiotics would only be warranted if a

secondary infection occurred after manipulation of the DMC.

– If the cyst starts draining on its own, does it require further I&D , or is it considered

to be resolving?

If the cyst starts draining on its own, it may not require further treatment. Monitoring

the area of recurrence would be an acceptable approach.

References

1.   Park SE, Park EJ, Kim SS, KIM CW. Treatment of digital mucous cysts with intralesional sodium tetradecyl sulfate injection. Dermatol Surg. 2014;40(11):1249–54.

2.   Salerni G, Alonso C. Images in clinical medicine. Digital mucous cyst. N Engl J Med. 2012;366(14):1335.

3.   Hur J, Kim YS, Yeo KY, Kim JS, Yu HJ. A case of herpetiform appearance of digital mucous cysts. Ann Dermatol. 2010;22(2):194–5.

4.   Hernández-Lugo AM, Domínguez-Cherit J, Vega-Memije ME. Digital mucous cyst: the ganglion type. Int J Dermatol. 1999;38(7):533–5.

5.   de Berker D, Lawrence C. Ganglion of the distal interphalangeal joint (myxoid cyst): therapy by identifi cation and repair of the leak of joint fl uid. Arch Dermatol. 2001;137(5):607–10.

6.    Zuber TJ. Offi ce management of digital mucous cysts. Am Fam Physician. 2001;64(12): 1987–90.

7.   Loder RT, Robinson JH, Jackson WT, Allen DJ. A surface ultrastructure study of ganglia and digital mucous cysts. J Hand Surg Am. 1988;13(5):758–62.

8.   Johnson SM, Treon K, Thomas S, Cox QG. A reliable surgical treatment for digital mucous cysts. J Hand Surg Eur Vol. 2014;39(8):856–60.

9.   Arenas-Prat J. Digital mucous cyst excision using a proximally based skin fl ap. J Plast Surg Hand Surg. 2014;11:1–2.   

Basal Cell Carcinoma diagnosis and Treatment

December 09, 2021 0

 Basal Cell Carcinoma Diagnosis and Treatment 

Basal Cell Carcinoma

Primary Care Visit Report   

A 50-year-old female with no past medical history presented with a rash on her left upper arm that had been there, per the patient, “for at least 10 years.” She said it changed in appearance sometimes but was always dry, scaly, and often itchy. The patient said she tried her best not to scratch it. She also reported that the lesion occasionally bled spontaneously. In the past, she had applied hydrogen peroxide and apple cider vinegar with no effect. She had also tried over-the-counter hydrocortisone cream and moisturizer, both of which made the scab and scale go away, revealing a red base. 

 Vitals were normal. On exam, on her left upper arm, there was a 2.5 cm × 2.5 cm erythematous, scaly plaque with irregular borders and peripheral scab. 

 The lesion was suspected to be  psoriasis   as the patient previously had a rash in her intergluteal cleft, which was diagnosed and treated as inverse psoriasis. However, she was referred to dermatology for further evaluation. At the dermatology clinic, the arm lesion was biopsied and found to be basal cell carcinoma. She subsequently underwent Mohs surgery to remove it.  

    Discussion from Dermatology Clinic 

     Differential Dx   

    Basal cell carcinoma  

  Amelanotic melanoma  

  Bowen’s disease  

  Extramammary Paget’s disease  

  Squamous cell carcinoma  

  Lichenoid keratosis     

     Favored Dx   

 In this case,  biopsy   was diagnostic of basal cell carcinoma (BCC).  Psoriatic lesions   would typically be more thickened. Long-standing pruritic, scaly lesions located in sunexposed areas and accompanied by spontaneous bleeding, as well as the patient’s  fair skin   and age, are aspects of the history and physical examination that would raise clinical suspicion of BCC in the absence of biopsy results. This patient’s  BCC   appears to belong to the superficial subtype (discussed in more detail below), as the lesions are fl at and scaly.  

     Overview   

  Skin cancers   are the most commonly occurring type of cancer, with over one million diagnoses per year in the USA [ 1 ,  2 ]. BCC is a  neoplasm   of  keratinocytes   (an epi-dermal cell that produces keratin) of the lowest, or basal, layer of the epidermis, and accounts for 75–80 % of  non-melanoma skin cancers   [ 1 ,  2 ]. It affects men more commonly than women, and is considered a cancer of the elderly, although inci-dence is increasing overall particularly among younger women [ 1 – 4 ]. BCC pre-dominantly affects fair-skinned people [ 2 ]. The actual incidence of BCC is diffi cult to estimate as non-melanoma skin cancers may not be included in cancer registry statistics [ 1 ,  5 ]. Additionally, in some countries only the fi rst instance of BCC is reported, and recurrence as well as multiple lesions are common [ 3 ]. 

 The pathogenesis of BCC is complex, and represents an interaction between genetic, phenotypic and environmental factors [ 5 ]. The main genetic abnormality in BCC is thought to be upregulation of the Hedgehog (HH) signaling pathway found on the   PTCH1    gene, which is responsible for normal tissue maintenance in adult life. UV radiation appears to induce mutations that inactivate  PTCH1 ,  p53  and other tumor sup-pressor genes [ 2 ].  PTCH1  mutations are present in 68–90 % of sporadic BCCs [ 2 ,  5 ]. 

 Unlike squamous cell carcinoma which is related to cumulative  sun exposure ,  BCC is believed to be associated with intermittent, intense sun exposure, and expo-sure early in life [ 1 ,  2 ,  4 ]. Although BCC most often presents on sun-exposed areas, UV exposure is not entirely predictive of lesion location, as BCC can also arise on areas of the body that are not typically sun-exposed [ 4 ]. The tendency to develop mul-tiple lesions has a genetic link and may be suggestive of basal nevus  syndrome   [ 2 ]. Other risk factors for developing BCC include age, male sex, fair complexion, light-colored eyes, red hair, immunosuppressed status, and exposure to ionizing radiation [ 1 ,  2 ].  

     Presentation   

 Basal cell carcinomas typically present as dry, crusting, non-healing plaques that are pink to red in color. They can be pearly and translucent. They often feature small dilated blood vessels called  telangiectasias   and raised edges. Patients may complain of pruritus. Pain is associated with ulceration, depth of invasion, and the morphea-form variant of BCC—a variant with innocuous surface characteristics but deep, wide extension [ 6 ]. BCCs typically appear on sun-exposed areas of the head, neck, trunk, and extremities; however, they can occur anywhere. Patients may describe healing followed by recurrence of lesion, and bleeding spontaneously or after slight trauma. Larger  lesions   may feature partial necrosis. BCC tends to be destructive of local tissue and is usually not metastatic; however, long-standing, untreated BCC can invade subcutaneous layers, muscle, and bone. 

 There are fi ve clinical subtypes of BCC, each presenting slightly differently. The most common subtype is  nodular BCC  , which typically occurs on the head and neck [ 2 ].  Pigmented BCC   presents as a hyperpigmented, translucent nodule.  Superfi cial BCCs   are fl at plaques that tend to occur on the trunk and resemble eczema. They are the second most common variant.  Morpheaform    BCC   (also called infi ltrating or sclerosing BCC) is a more aggressive variant that appears as a shiny, hypopigmented fi rm plaque most often located on the head and neck. This variant tends to be more painful [ 6 ]. Patients presenting with a scar without history of trauma should be evaluated for morpheaform BCC. Fibroepithelioma of Pinkus is a variant that looks similar to a skin tag, and usually presents on the lower back [ 2 ].  

     Workup   

 BCCs are diagnosed by shave or punch  biopsy  . Histopathology varies between sub-types and reveals basal cells with large nuclei, little cytoplasm, and stromal retraction.  

     Treatment   

 The goal of treatment is ensuring full removal of malignant tissue.  Cryosurgery,   topical chemotherapy such as imiquimod 5 %, electrodessication and curettage, sur-gical  excision  , and  Mohs micrographic surgery   are the main treatment modalities. Surgical treatment has the lowest failure rate and Mohs surgery specifi cally has the lowest recurrence rate [ 1 ,  2 ]. Treatment approach usually depends on the size, loca-tion, and depth of lesion. 

 Any  lesions   that generate suspicion of BCC should be biopsied, and if the lesion is small enough full removal should be attempted. Initial  biopsy   of the lesion may be performed in a primary care setting if the treating physician has experience performing biopsies. Patients can be referred to dermatology to discuss biopsy results that are confi rmed BCC, or to perform the initial biopsy if needed. Any sub-sequent treatment should be undertaken by a dermatologist.  

     Follow-Up   

 Histologically confi rmed complete  excision   of BCC is associated with <2 % local recurrence after 5 years [ 5 ]. Factors that are associated with recurrence, metastasis, and poor prognosis are lesions greater than 5 cm in size, location on ears or centro-facially, morpheaform subtype, poor delineation, incomplete  excision  , and histo-logical features of infi ltration, micronodular appearance, and perivascular or perineural involvement. 

 Patients with BCCs on the trunk are more likely to develop future lesions  anywhere on the body, but especially on the trunk [ 7 ]. Other factors associated with poor prognosis are immunocompromised status, presence of multiple lesions, and involvement of lymph nodes, or metastasis [ 1 ,  2 ,  5 ]. Metastasis is very unlikely, occurring in fewer than 0.55 % of cases [ 2 ]. When it does occur, it usually affects sentinel nodes, or the lungs. 

 Patients with a history of  BCC   should be screened for new lesions twice yearly. Some precautions may be taken to help prevent new lesions, including wearing SPF daily, avoiding prolonged exposure to the sun or tanning beds, and wearing protec-tive clothing.   

    Questions for the Dermatologist 

–  What is the natural course of basal cell carcinoma if left untreated?  

 The lesion persists and there is slow local tissue destruction. 

The patient reported having the lesion for 10 years. Is it common for BCC to go

undiagnosed for that long?

It is fairly uncommon. Progression of lesions in this case are slower than average.

Typically lesions are more painful and bleed spontaneously 6 months after they appear.

– Does the process (i.e., inactivation of tumor suppressor genes) that gave rise to

the BCC on her arm make it more likely for BCC to occur in other parts of her

skin, like her leg?

Patients with one BCC are more likely to develop others. Genetic changes to

tumor suppressor genes are probably happening locally, and the lesions develop

independently. However, they may be refl ective of an environmental exposure such

as UV radiation , which would affect multiple sites on the body. If those changes are

happening in one area, they are more likely to happen in another.

– If the patient gets more lesions in the future, would they be more likely to be

BCC?

Correct. A patient with primary BCC is at increased risk for developing subsequent

BCC lesions.

– Is there anything in the patient’s history that is indicative of BCC, e.g. the lesions

spontaneously bleeding?

Irritation, bleeding, and the persistence of lesions would raise suspicion of BCC

Reference 

           1.    Rubin AI, Chen EH, Ratner D. Basal-cell carcinoma. N Engl J Med. 2005;353(21):2262–9.  

                2.    Carucci JA, Leffell DJ, Pettersen JS. Chapter 115. Basal cell carcinoma. In: Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, Wolff K, editors. Fitzpatrick’s dermatology in general medicine. 8th ed. New York: McGraw-Hill; 2012. p. 1294–303.

    3.   de Vries E, Micallef R, Brewster DH, Gibbs JH, Flohil SC, Saksela O, Sankila R, Forrest AD, Trakatelli M, Coebergh JW, Proby CM, EPIDERM Group. Population-based estimates of the occurrence of multiple vs fi rst primary basal cell carcinomas in 4 European regions. Arch Dermatol. 2012;148(3):347–54.

      4.    Xiang F, Lucas R, Hales S, Neale R. Incidence of nonmelanoma skin cancer in relation to ambi-ent UV radiation in white populations, 1978–2012. JAMA Dermatol. 2014;150(10):1063–71.

        5.    Madan V, Lear JT, Szeimies RM. Non-melanoma skin cancer. Lancet. 2010;375(9715): 673–85.

     6.   Yosipovitch G, Mills KC, Nattkemper LA, Feneran A, Tey HL, Lowenthal BM, Pearce DJ, Williford PM, Sangueza OP, D’Agostino Jr RB. Association of pain and itch with depth of invasion and infl ammatory cell constitution in skin cancer: results of a large clinicopathologic study. JAMA Dermatol. 2014;150(11):1160–6.

    7.   Ramachandran S, Fryer AA, Smith A, Lear J, Bowers B, Jones PW, Strange RC. Cutaneous basal cell carcinomas: distinct host factors are associated with the development of tumors on the trunk and on the head and neck. Cancer. 2001;92(2):354–8.