Cutaneous abscess: Difference between revisions

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'''For patient information click [[{{PAGENAME}} (patient information)|here]]'''
'''For patient information click [[Abscess (patient information)|here]]'''


{{CMG}};{{AE}}{{MehdiP}}
{{CMG}};{{AE}}{{MehdiP}}<br>
 
{{SK}}Skin abscess<br>
'''To return to abscess main page, click [[Abscess|here]].'''
==Overview==
==Overview==
Cutaneous abscess is defined as a collection of pus in skin layers and may occur in any body surface. Although, there is a rare type of sterile skin abscess that is secondary to injection mostly in diabetic patients who use insulin. diagnosis is clinical and consist of a painful, tender, indurated, and usually erythematous nodule or mass that is varying in size. Systemic sign and symptoms are rare except in sever and multiple abscess especially in immunocompromised patients. Treatment is based on incision and drainage associated with antibiotics.
Cutaneous abscess is defined as a collection of [[pus]] in the [[dermis]] or [[subcutaneous tissue]] and appears as a [[Swelling|swollen]], [[Erythema|red]], [[Tenderness (medicine)|tender]], and fluctuant [[mass]], often with surrounding [[cellulitis]] and may occur in any part of the body. Although, there is a rare type of [[sterile]] skin abscess that is secondary to injection mostly in [[diabetic]] patients who use [[insulin]]. diagnosis is clinical and consist of a painful, tender, indurated, and usually [[erythematous]] [[nodule]] or mass that is varying in size. Systemic sign and symptoms are rare except for sever and multiple abscess especially in [[immunocompromised]] patients. Treatment is, [[incision and drainage]] associated with [[Antibiotic|antibiotics]].
==Historical perspective==
==Historical perspective==
Alexander Ogston, a scottish surgeon first described the pyogenic abscess in the late 19th century.<ref name="pmid6369479">{{cite journal |vauthors= |title=Classics in infectious diseases. "On abscesses". Alexander Ogston (1844-1929) |journal=Rev. Infect. Dis. |volume=6 |issue=1 |pages=122–8 |year=1984 |pmid=6369479 |doi= |url=}}</ref>
Alexander Ogston, a scottish surgeon first described the [[pyogenic abscess]] in the late 19th century.<ref name="pmid6369479">{{cite journal |vauthors= |title=Classics in infectious diseases. "On abscesses". Alexander Ogston (1844-1929) |journal=Rev. Infect. Dis. |volume=6 |issue=1 |pages=122–8 |year=1984 |pmid=6369479 |doi= |url=}}</ref>
==Classification==
==Classification==
Cutaneous abscess may be classified as sterile abscess and infectious abscess.
Cutaneous abscess may be classified as sterile abscess and infectious abscess.
*Sterile abscesses are mainly seen in diabetic patients secondary to insulin injection.
*Sterile abscesses are mainly seen in [[diabetic]] patients secondary to [[insulin]] injection.
*Infectious abscesses are mostly secondary to staphylococcus aureus infection.
*Infectious abscesses which are mostly due to [[staphylococcus aureus]] infection.
==Pathophysiology==
==Pathophysiology==
[[abscess]] is usually caused by [[staphylococcus aureus]] [[bacterial]] [[infection]] to an injured [[breast]] [[skin]]. [[Staphylococcus aureus]] could form [[abscess]] by secretion of several killing agents like [[enzymes]] and [[toxins]]. In a reaction to these [[bacterial]] substances, assembled [[white blood cells]] in this tissue produces anti-bacterial [[Antibodies|anti-bodies]] that help in killing the [[bacteria]]. However, these cells cause damage to the [[soft tissue]] contributing in the [[abscess]] formation.<ref name="pmid25749135">{{cite journal| author=Kobayashi SD, Malachowa N, DeLeo FR| title=Pathogenesis of Staphylococcus aureus abscesses. | journal=Am J Pathol | year= 2015 | volume= 185 | issue= 6 | pages= 1518-27 | pmid=25749135 | doi=10.1016/j.ajpath.2014.11.030 | pmc=4450319 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25749135  }} </ref>  
[[Abscess]] is usually caused by [[staphylococcus aureus]] [[bacterial]] [[infection]] in an injured [[skin]]. [[Staphylococcus aureus]] could form [[abscess]] by secretion of several [[enzymes]] and [[toxins]]. In a reaction to these [[bacterial]] substances, assembled [[white blood cells]] in this tissue produces anti-bacterial [[Antibodies|anti-bodies]] that help in [[bacteria]]<nowiki/>l elimination. However, these cells cause damage to the [[soft tissue]] contributing in the [[abscess]] formation.<ref name="pmid25749135">{{cite journal| author=Kobayashi SD, Malachowa N, DeLeo FR| title=Pathogenesis of Staphylococcus aureus abscesses. | journal=Am J Pathol | year= 2015 | volume= 185 | issue= 6 | pages= 1518-27 | pmid=25749135 | doi=10.1016/j.ajpath.2014.11.030 | pmc=4450319 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25749135  }} </ref>  
===Pathogenesis===  
===Pathogenesis===  
Skin serves as a barrier from pathogen entry. Breech in the skin surface allow the pathogen entry to cause local inflammation. PMNs are the first and the most important responding cells in abscess formation.<ref name="pmid23435331">{{cite journal |vauthors=Kolaczkowska E, Kubes P |title=Neutrophil recruitment and function in health and inflammation |journal=Nat. Rev. Immunol. |volume=13 |issue=3 |pages=159–75 |year=2013 |pmid=23435331 |doi=10.1038/nri3399 |url=}}</ref> Neutrophils, are responsible for phagocytosis. Once the pathogen is opsonized by complement system, it will be recognized by neutrophils and the phagocytosis process will begin. After phagocytosis the bactricidal process will begin by producing superoxide radicals and other reactive oxygen species (ROS).<ref name="pmid15240752">{{cite journal |vauthors=Quinn MT, Gauss KA |title=Structure and regulation of the neutrophil respiratory burst oxidase: comparison with nonphagocyte oxidases |journal=J. Leukoc. Biol. |volume=76 |issue=4 |pages=760–81 |year=2004 |pmid=15240752 |doi=10.1189/jlb.0404216 |url=}}</ref>
Skin serves as a barrier from [[pathogen]] entry. Breech in the skin surface allow the pathogen entry to cause local [[inflammation]]. Polymorphonuclear cells ([[PMNs|PMNs)]] are the first and the most important responding cells in abscess formation.<ref name="pmid23435331">{{cite journal |vauthors=Kolaczkowska E, Kubes P |title=Neutrophil recruitment and function in health and inflammation |journal=Nat. Rev. Immunol. |volume=13 |issue=3 |pages=159–75 |year=2013 |pmid=23435331 |doi=10.1038/nri3399 |url=}}</ref> [[Neutrophil|Neutrophils]], are responsible for [[phagocytosis]]. Once the pathogen is [[opsonized]] by [[complement system]], it will be recognized by [[neutrophils]] and the [[phagocytosis]] process will begin. After [[phagocytosis]] the bactricidal process will begin by producing [[superoxide]] radicals and other [[reactive oxygen species]] (ROS).<ref name="pmid15240752">{{cite journal |vauthors=Quinn MT, Gauss KA |title=Structure and regulation of the neutrophil respiratory burst oxidase: comparison with nonphagocyte oxidases |journal=J. Leukoc. Biol. |volume=76 |issue=4 |pages=760–81 |year=2004 |pmid=15240752 |doi=10.1189/jlb.0404216 |url=}}</ref>
===Genetic factors===
===Genetic factors===
PMNs are the most important cellular defense. Genetic disorders that negatively affect PMN function may predispose persons to recurrent cutaneous abscess formation. For example, chronic granulomatous disease, which is a genetic disorder characterized by the inability of PMNs and other phagocytes to produce superoxide, often presents with severe and recurrent S. aureus infections.<ref name="pmid6872404">{{cite journal |vauthors=Bieluch VM, Tally FP |title=Pathophysiology of abscess formation |journal=Clin Obstet Gynaecol |volume=10 |issue=1 |pages=93–103 |year=1983 |pmid=6872404 |doi= |url=}}</ref>
[[Neutrophil|PMNs]] are the most important cellular defense. Genetic disorders that negatively affect [[PMN]] function may predispose persons to recurrent cutaneous abscess formation. For example, [[chronic granulomatous disease]], which is a genetic disorder characterized by the inability of [[Neutrophil|PMNs]] and other [[Phagocyte|phagocytes]] to produce [[superoxide]], often presents with severe and recurrent [[Staphylococcus aureus|S. aureus]] infections.<ref name="pmid6872404">{{cite journal |vauthors=Bieluch VM, Tally FP |title=Pathophysiology of abscess formation |journal=Clin Obstet Gynaecol |volume=10 |issue=1 |pages=93–103 |year=1983 |pmid=6872404 |doi= |url=}}</ref>
==Causes==
==Causes==
[[Category:Infectious disease]]
===Common causes===
*[[Staphylococcus aureus|S. aureus]] (either [[S. aureus|methicillin-susceptible]] or [[Methicillin-resistant staphylococcus aureus|methicillin-resistant S. aureus]]) is counting for 75% of cases.<ref name="pmid24947530">{{cite journal |vauthors=Stevens DL, Bisno AL, Chambers HF, Dellinger EP, Goldstein EJ, Gorbach SL, Hirschmann JV, Kaplan SL, Montoya JG, Wade JC |title=Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America |journal=Clin. Infect. Dis. |volume=59 |issue=2 |pages=147–59 |year=2014 |pmid=24947530 |doi=10.1093/cid/ciu296 |url=}}</ref>
*Mixed flora (including [[Staphylococcus aureus|S. aureus]] together with [[Streptococcus pyogenes|S. pyogenes]] and [[gram-negative bacilli]] with [[anaerobes]])<ref name="pmid7548575">{{cite journal |vauthors=Summanen PH, Talan DA, Strong C, McTeague M, Bennion R, Thompson JE, Väisänen ML, Moran G, Winer M, Finegold SM |title=Bacteriology of skin and soft-tissue infections: comparison of infections in intravenous drug users and individuals with no history of intravenous drug use |journal=Clin. Infect. Dis. |volume=20 Suppl 2 |issue= |pages=S279–82 |year=1995 |pmid=7548575 |doi= |url=}}</ref><ref name="pmid16914702">{{cite journal |vauthors=Moran GJ, Krishnadasan A, Gorwitz RJ, Fosheim GE, McDougal LK, Carey RB, Talan DA |title=Methicillin-resistant S. aureus infections among patients in the emergency department |journal=N. Engl. J. Med. |volume=355 |issue=7 |pages=666–74 |year=2006 |pmid=16914702 |doi=10.1056/NEJMoa055356 |url=}}</ref>
*[[Anaerobes]], mostly seen in [[injecting drug users]].<ref name="pmid7548575">{{cite journal |vauthors=Summanen PH, Talan DA, Strong C, McTeague M, Bennion R, Thompson JE, Väisänen ML, Moran G, Winer M, Finegold SM |title=Bacteriology of skin and soft-tissue infections: comparison of infections in intravenous drug users and individuals with no history of intravenous drug use |journal=Clin. Infect. Dis. |volume=20 Suppl 2 |issue= |pages=S279–82 |year=1995 |pmid=7548575 |doi= |url=}}</ref>
===Less common causes===
[[Nontuberculous mycobacteria]], [[blastomycosis]], [[nocardiosis]], and [[cryptococcosis]].<ref name="pmid7548575">{{cite journal |vauthors=Summanen PH, Talan DA, Strong C, McTeague M, Bennion R, Thompson JE, Väisänen ML, Moran G, Winer M, Finegold SM |title=Bacteriology of skin and soft-tissue infections: comparison of infections in intravenous drug users and individuals with no history of intravenous drug use |journal=Clin. Infect. Dis. |volume=20 Suppl 2 |issue= |pages=S279–82 |year=1995 |pmid=7548575 |doi= |url=}}</ref>
==Differentiating cutaneous abscess from other Diseases==
*Cutaneous abscess must be differentiated from other causes of [[lower limb]] [[edema]] like [[chronic venous insufficiency]], acute [[Deep vein thrombosis|deep venous thrombosis]], [[lipedema]], [[myxedema]], [[lymphatic filariasis]] and causes of [[generalized edema]].
 
{| class="wikitable"
 
|-
 
! rowspan="2" | Diseases
 
! colspan="7" |Symptoms
 
! rowspan="2" | Signs
 
! rowspan="2" | Gold standard Investigation to diagnose
|-
!History
!Onset
!Pain
!Fever
!Laterality
!Scrotal swelling
!Symptoms of primary disease
|-
|([[Cellulitis]]-erysipelas-[[skin abscess]])
|
* Acute painful [[swelling]]
* [[Fever]]
|Acute
| +
| +
|Unilateral
| -
| -
|
* [[Tenderness]], hotness, and may be fluctuation if [[abscess]] formed.
* [[Lymphangitis]] in nearby [[Lymph node|lymph nodes]].
* [[Toxemia]] and [[fever]] in severe cases.
* [[Cellulitis]] involves the deeper [[dermis]] and [[erysipelas]] involves the upper dermis.<ref name="pmid24947530">{{cite journal| author=Stevens DL, Bisno AL, Chambers HF, Dellinger EP, Goldstein EJ, Gorbach SL et al.| title=Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America. | journal=Clin Infect Dis | year= 2014 | volume= 59 | issue= 2 | pages= 147-59 | pmid=24947530 | doi=10.1093/cid/ciu296 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24947530  }}</ref>
|
* Usually it doesn't need any laboratory tests to diagnose.<ref name="pmid27434444">{{cite journal| author=Raff AB, Kroshinsky D| title=Cellulitis: A Review. | journal=JAMA | year= 2016 | volume= 316 | issue= 3 | pages= 325-37 | pmid=27434444 | doi=10.1001/jama.2016.8825 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27434444  }}</ref>
* [[Blood cultures]] are warranted for patients in the following circumstances:<ref name="pmid10834819">{{cite journal| author=Woo PC, Lum PN, Wong SS, Cheng VC, Yuen KY| title=Cellulitis complicating lymphoedema. | journal=Eur J Clin Microbiol Infect Dis | year= 2000 | volume= 19 | issue= 4 | pages= 294-7 | pmid=10834819 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10834819  }}</ref>
# [[Toxicity|Systemic toxicity]]
# Extensive [[skin]] or [[soft tissue]] involvement
# Underlying [[comorbidities]]
# persistent [[cellulitis]]
* In patients with recurrent [[cellulitis]], serologic ''testing for [[beta-hemolytic streptococci]]'' is a good diagnostic tool''.''<ref name="pmid4005155">{{cite journal| author=Leppard BJ, Seal DV, Colman G, Hallas G| title=The value of bacteriology and serology in the diagnosis of cellulitis and erysipelas. | journal=Br J Dermatol | year= 1985 | volume= 112 | issue= 5 | pages= 559-67 | pmid=4005155 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4005155  }}</ref>
|-
 
| [[Lymphatic filariasis]]
 
|
* History of living in endemic area or travelling to it
|Chronic
|<nowiki>+</nowiki>
| +
|Bilateral
| +
|<nowiki>-</nowiki>
|
* [[Hepatomegaly]]
* [[Lymphedema]]
* [[Elephantiasis]]
* [[Lymphangitis]]
* [[Hydrocele]]
* Scrotal [[elephantiasis]]
* [[Lymphadenopathy|Lymphadenopathies]]
* [[Rhonchi]] may be present in patients with Pulmonary tropical eosinophilia syndrome.
|
'''Preparing blood smears'''
* Thick smears
# Thick smears consist of a thick layer of dehemoglobinized (lysed) [[Red blood cell|red blood cells]] (RBCs). 
# Thick smears allow a more efficient detection of parasites (increased sensitivity).
* Thin smears consist of [[blood]] spread in a layer such that the thickness decrease.
'''By the ultrasound''', the following findings can be observed:
* Dilated lymphatic channels
* Living worms tend to be in motion which called "filarial dance" sign.
 
|-
 
| [[Chronic venous insufficiency]]
 
|
* History of untreated [[varicose veins]]
* Painful bilateral [[lower limb]] [[swelling]] that increases with standing and decreases by rest and [[leg]] elevation.
|Chronic
|<nowiki>+</nowiki>
| -
|Bilateral
| +
 
(If congenial)
| -
|
* Typical varicose veins
* [[Skin]] change distribution correlate with varicose veins sites in the medial side of [[ankle]] and [[leg]]
* Reduction of [[swelling]] with limb elevation.
|
* [[Duplex ultrasound]] will demonstrate typical findings of [[Venous insufficiency|venous valvular insufficiency]]
|-
|[[Deep venous thrombosis|Acute deep venous thrombosis]]
|
* History of prolonged recumbency
* Classic symptoms of [[DVT]] include acute unilateral [[swelling]], [[pain]], and [[erythema]] 
|Acute
| +
| -
|Unilateral
| -
|May be associated with primary disease mandates recumbency for long duration
|
* Dilated [[superficial veins]]
* Difference in [[Calf muscle|calf]] diameter is twice as likely to have [[DVT]](most impotant sign )<ref name="pmid16027455">{{cite journal| author=Goodacre S, Sutton AJ, Sampson FC| title=Meta-analysis: The value of clinical assessment in the diagnosis of deep venous thrombosis. | journal=Ann Intern Med | year= 2005 | volume= 143 | issue= 2 | pages= 129-39 | pmid=16027455 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16027455  }}  [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16539361 Review in: ACP J Club. 2006 Mar-Apr;144(2):46-7]  [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17213086 Review in: Evid Based Med. 2006 Apr;11(2):56]</ref>
* Calf pain on passive [[dorsiflexion]] of the [[foot]] ([[Homan's sign]]) isn't realiable sign.
 
|
* [[Compression ultrasonography]] (CUS) with [[Doppler ultrasound|doppler]] is the diagnostic test of choice
* [[D-dimer]] level is used for unprobable cases
|-
|[[Lipedema]]
|
* Family history especially in women; [[X-linked dominant]] or [[autosomal dominant]] condition.<ref name="pmid20358611">{{cite journal| author=Child AH, Gordon KD, Sharpe P, Brice G, Ostergaard P, Jeffery S et al.| title=Lipedema: an inherited condition. | journal=Am J Med Genet A | year= 2010 | volume= 152A | issue= 4 | pages= 970-6 | pmid=20358611 | doi=10.1002/ajmg.a.33313 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20358611  }}</ref>
* Abnormal deposition of fat and [[edema]] and [[easy bruising]].
|Chronic
| +
| -
|Bilateral
| -
|<nowiki>-</nowiki>
|
* Tender with palpation
 
* Negative '''Semmer sign''' to differentiate from lymphedema.<ref name="pmid23939641">{{cite journal| author=Trayes KP, Studdiford JS, Pickle S, Tully AS| title=Edema: diagnosis and management. | journal=Am Fam Physician | year= 2013 | volume= 88 | issue= 2 | pages= 102-10 | pmid=23939641 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23939641  }}</ref>
* Pinching the [[skin]] on the upper surface of the [[toes]]. If it is possible to grasp a thin fold of [[tissue]] then it is negative result.
* In a positive result, it is only possible to grasp a [[lump]] of [[tissue]].
 
|
* MRI offers strong qualitative and quantitative parameters in the diagnosis of [[lipedema]] <ref name="pmid9412843">{{cite journal| author=Dimakakos PB, Stefanopoulos T, Antoniades P, Antoniou A, Gouliamos A, Rizos D| title=MRI and ultrasonographic findings in the investigation of lymphedema and lipedema. | journal=Int Surg | year= 1997 | volume= 82 | issue= 4 | pages= 411-6 | pmid=9412843 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9412843  }}</ref>
|-
|[[Myxedema]]
|
* History of untreated [[hypothyroidism]].
* Infiltration of the skin with [[Glycosaminoglycan|glycosaminoglycans]] with associated water retention.
|Chronic
| +
| -
|Bilateral
| -
| +
([[hypothyroidism]] )
|
* [[Pretibial myxedema]]
|
* [[Thyroid function tests|Thyroid function tests.]]
|-
|Other causes of [[generalized edema]]
|
* History of chronic general condition (cardiac-liver-renal)
|Chronic
| -
| -
|Bilateral
| -
|<nowiki>+</nowiki>
|
|
* According to the primary cause ( Echo- [[LFTs]]- RFT)
|}
 
 
{| style="border: 0px; font-size: 90%; margin: 3px;" align=center
!align="center" style="background:#DCDCDC;"|Disease
!align="center" style="background:#DCDCDC;"|Clinical features
|-
|align="left" style="background:#DCDCDC;"|[[Folliculitis]]
|style="padding: 5px 5px; background: #F5F5F5;" align="left" |Hair follicle [[inflammation]], presents as pruritic [[rash]] or [[Pustules|pustule]].<ref name="pmid15554731">{{cite journal |vauthors=Luelmo-Aguilar J, Santandreu MS |title=Folliculitis: recognition and management |journal=Am J Clin Dermatol |volume=5 |issue=5 |pages=301–10 |year=2004 |pmid=15554731 |doi= |url=}}</ref><ref name="pmid25441463">{{cite journal |vauthors=Laureano AC, Schwartz RA, Cohen PJ |title=Facial bacterial infections: folliculitis |journal=Clin. Dermatol. |volume=32 |issue=6 |pages=711–4 |year=2014 |pmid=25441463 |doi=10.1016/j.clindermatol.2014.02.009 |url=}}</ref>
|-
|align="left" style="background:#DCDCDC;"|[[Hidradenitis suppurativa|Suppurative hydradenitis]]
|style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Inflammation]] in intertriginous areas ([[axillae]], [[Inguinal region|inguinal area]], inner [[thighs]], [[Perianal abscess|perianal]] and [[perineal]] areas, [[mammary]],..)
Presents as painful inflamed [[nodule]], sinus tract and commedons. Associated with systemic symptoms. Needs surgical debridement and  systemic antibiotic.<ref name="pmid19682181">{{cite journal |vauthors=Revuz J |title=Hidradenitis suppurativa |journal=J Eur Acad Dermatol Venereol |volume=23 |issue=9 |pages=985–98 |year=2009 |pmid=19682181 |doi=10.1111/j.1468-3083.2009.03356.x |url=}}</ref>
|-
|align="left" style="background:#DCDCDC;"|[[Epidermoid cyst]]
|style="padding: 5px 5px; background: #F5F5F5;" align="left" |Cyst or nodule presents with central punctum. May be secondarily infected.<ref name="pmid11996426">{{cite journal |vauthors=Zuber TJ |title=Minimal excision technique for epidermoid (sebaceous) cysts |journal=Am Fam Physician |volume=65 |issue=7 |pages=1409–12, 1417–8, 1420 |year=2002 |pmid=11996426 |doi= |url=}}</ref>
|-
|align="left" style="background:#DCDCDC;"|Nodular [[lymphangitis]]
|style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Subcutaneous]] swelling along with [[lymphatics]]. mostly due to [[Sporothrix schenckii]].<ref name="pmid8480962">{{cite journal |vauthors=Kostman JR, DiNubile MJ |title=Nodular lymphangitis: a distinctive but often unrecognized syndrome |journal=Ann. Intern. Med. |volume=118 |issue=11 |pages=883–8 |year=1993 |pmid=8480962 |doi= |url=}}</ref>
|-
|align="left" style="background:#DCDCDC;"|[[Myiasis]]
|style="padding: 5px 5px; background: #F5F5F5;" align="left" |Enlarging nodule secondary to [[insect bite]] and due to penetration of fly larvae into subdermal tissue. caused by [[Dermatobia hominis]], the [[botfly]] and [[Cordylobia anthropophaga]], the tumbu fly.<ref name="pmid8432924">{{cite journal |vauthors=Arosemena R, Booth SA, Su WP |title=Cutaneous myiasis |journal=J. Am. Acad. Dermatol. |volume=28 |issue=2 Pt 1 |pages=254–6 |year=1993 |pmid=8432924 |doi= |url=}}</ref>
|}
 
==Epidemiology and Demographics==
*It is estimated that 4% of children experience the cutaneous abscess.<ref name="pmid22743746">{{cite journal |vauthors=Holsenback H, Smith L, Stevenson MD |title=Cutaneous abscesses in children: epidemiology in the era of methicillin-resistant Staphylococcus aureus in a pediatric emergency department |journal=Pediatr Emerg Care |volume=28 |issue=7 |pages=684–6 |year=2012 |pmid=22743746 |doi=10.1097/PEC.0b013e31825d20e1 |url=}}</ref><br>
A national emergency department visit survey from 1996 to 2005 showed:
*Emergency department visits for abscesses more than doubled over the 10-year study period (1.2 million in 1996 to 3.28 million in 2005).
===Gender===
Men and women are affected equally.
===Age===
It is more common among adults age 19 to 45 years.
==Risk Factors==
Risk factors for developing cutaneous abscess include:<ref name="pmid17420430">{{cite journal |vauthors=McNamara DR, Tleyjeh IM, Berbari EF, Lahr BD, Martinez J, Mirzoyev SA, Baddour LM |title=A predictive model of recurrent lower extremity cellulitis in a population-based cohort |journal=Arch. Intern. Med. |volume=167 |issue=7 |pages=709–15 |year=2007 |pmid=17420430 |doi=10.1001/archinte.167.7.709 |url=}}</ref><ref name="pmid16267325">{{cite journal |vauthors=Gordon RJ, Lowy FD |title=Bacterial infections in drug users |journal=N. Engl. J. Med. |volume=353 |issue=18 |pages=1945–54 |year=2005 |pmid=16267325 |doi=10.1056/NEJMra042823 |url=}}</ref>
*Skin barrier disruption due to [[trauma]] (such as [[abrasion]], [[penetrating wound]], [[Pressure ulcers|pressure ulcer]], [[Venous ulcer|venous leg ulcer]], [[insect bite]], [[Intravenous drug use (recreational)|injection drug use]])
*Skin inflammation (such as [[eczema]], [[radiation therapy]])
*[[Edema]] due to impaired [[lymphatic drainage]]
*[[Edema]] due to [[venous insufficiency]]
*[[Obesity]]
*[[Immunosuppression]] (such as [[diabetes]] or [[HIV AIDS|HIV infection]])
*Breaks in the skin between the toes (toe web intertrigo); these may be clinically inapparent
*Preexisting skin infection (such as [[tinea pedis]], [[impetigo]], [[varicella]])
*[[Hemodialysis]]
==Natural History, Complications and Prognosis==
===Natural History===
If cutaneous abscess left untreated it may drain spontaneously. However, in severe cases it may cause systemic spread and result in [[sepsis]].<ref name="pmid6444142">{{cite journal |vauthors=Llera JL, Levy RC, Staneck JL |title=Cutaneous abscesses: natural history and management in an outpatient facility |journal=J Emerg Med |volume=1 |issue=6 |pages=489–93 |year=1984 |pmid=6444142 |doi= |url=}}</ref>
 
Recurrence may occur in 20% of patients<ref name="pmid33197926">{{cite journal| author=Vella V, Galgani I, Polito L, Arora AK, Creech CB, David MZ | display-authors=etal| title=Staphylococcus aureus skin and soft tissue infection recurrence rates in outpatients: a retrospective database study at three US medical centers. | journal=Clin Infect Dis | year= 2020 | volume=  | issue=  | pages=  | pmid=33197926 | doi=10.1093/cid/ciaa1717 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33197926  }} </ref>.
 
===Complications===
A wide range of complications are possible in the course of skin abscess including: [[Bacteremia]], [[endocarditis]], [[osteomyelitis]], metastatic infection, [[sepsis]], and [[toxic shock syndrome]].<ref name="pmid27434444">{{cite journal |vauthors=Raff AB, Kroshinsky D |title=Cellulitis: A Review |journal=JAMA |volume=316 |issue=3 |pages=325–37 |year=2016 |pmid=27434444 |doi=10.1001/jama.2016.8825 |url=}}</ref>
===Prognosis===
Depending on the extent of the disease, the prognosis may vary. However, the prognosis is generally regarded as good.
 
Patients who require hospitalization for ICU admission, operating room surgical intervention, or death have one of the following six risk factors upon presentation<ref name="pmid30420232">{{cite journal| author=Mower WR, Kadera SP, Rodriguez AD, Vanderkraan V, Krishna PK, Chiu E et al.| title=Identification of Clinical Characteristics Associated With High-Level Care Among Patients With Skin and Soft Tissue Infections. | journal=Ann Emerg Med | year= 2018 | volume=  | issue=  | pages=  | pmid=30420232 | doi=10.1016/j.annemergmed.2018.09.020 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30420232  }} </ref>:
* abnormal cross-sectional imaging result ("air or gas, abscess or fluid collection, osteomyelitis, or suspicion of osteomyelitis")
* systemic inflammatory response syndrome
* previous infection at the same location
* infection involving the hand * diabetes* age >65 years
 
==Diagnosis==
===History and symptoms===
====History====
A detailed history must be taken from all patients. Specific area of focus when obtaining a history from the patient include:
*Recent [[trauma]]
*Recent [[weight change]]
*Recent immunosuppresive drugs
*Underlying comorbidities ([[lymphedema]], [[malignancy]], [[neutropenia]], [[immunodeficiency]], [[splenectomy]], [[diabetes]])
====Symptoms====
The hallmark of the cutaneous abscess is painful, tender, indurated, and usually [[erythematous]] [[nodule]].
==Physical examination==
===Appearance of the Patient===
Patients are usually well appearing.
===Vital signs===
Vital signs are within normal limits unless there is complication.
===Skin===
Indurated, tender and [[erythematous]] [[nodule]] with signs of local inflammation is the presenting feature.
<br style="clear:both" />
[[image:thigh abscess.jpg|left]]
<br style="clear:both" />
==Laboratory findings==
[[Leukocytosis]] and increased level of [[Acute phase reactant|acute phase reactants]] ([[ESR]], [[CRP]]) are the most common laboratory findings.
==Treatment==
Treatment is based on [[incision and drainage]] and sometimes antibiotic therapy is required. Cure rates with drainage alone are about 85% or higher.<ref name="pmid17846141">{{cite journal |vauthors=Rajendran PM, Young D, Maurer T, Chambers H, Perdreau-Remington F, Ro P, Harris H |title=Randomized, double-blind, placebo-controlled trial of cephalexin for treatment of uncomplicated skin abscesses in a population at risk for community-acquired methicillin-resistant Staphylococcus aureus infection |journal=Antimicrob. Agents Chemother. |volume=51 |issue=11 |pages=4044–8 |year=2007 |pmid=17846141 |pmc=2151464 |doi=10.1128/AAC.00377-07 |url=}}</ref><ref name="pmid20346539">{{cite journal |vauthors=Schmitz GR, Bruner D, Pitotti R, Olderog C, Livengood T, Williams J, Huebner K, Lightfoot J, Ritz B, Bates C, Schmitz M, Mete M, Deye G |title=Randomized controlled trial of trimethoprim-sulfamethoxazole for uncomplicated skin abscesses in patients at risk for community-associated methicillin-resistant Staphylococcus aureus infection |journal=Ann Emerg Med |volume=56 |issue=3 |pages=283–7 |year=2010 |pmid=20346539 |doi=10.1016/j.annemergmed.2010.03.002 |url=}}</ref>
 
Patients who require hospitalization for ICU admission, operating room surgical intervention, or death have one of the following six risk factors upon presentation<ref name="pmid30420232">{{cite journal| author=Mower WR, Kadera SP, Rodriguez AD, Vanderkraan V, Krishna PK, Chiu E et al.| title=Identification of Clinical Characteristics Associated With High-Level Care Among Patients With Skin and Soft Tissue Infections. | journal=Ann Emerg Med | year= 2018 | volume=  | issue=  | pages=  | pmid=30420232 | doi=10.1016/j.annemergmed.2018.09.020 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30420232  }} </ref>:* abnormal cross-sectional imaging result* systemic inflammatory response syndrome* previous infection at the same location* infection involving the hand * diabetes* age >65 years
 
===Medical therapy===
Antibiotic therapy is indicated in some circumstances that include and the duration based on severity and clinical response varies between 3 to 7 days:<ref name="pmid21208910">{{cite journal |vauthors=Liu C, Bayer A, Cosgrove SE, Daum RS, Fridkin SK, Gorwitz RJ, Kaplan SL, Karchmer AW, Levine DP, Murray BE, J Rybak M, Talan DA, Chambers HF |title=Clinical practice guidelines by the infectious diseases society of america for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children |journal=Clin. Infect. Dis. |volume=52 |issue=3 |pages=e18–55 |year=2011 |pmid=21208910 |doi=10.1093/cid/ciq146 |url=}}</ref><ref name="pmid24973422">{{cite journal |vauthors=Stevens DL, Bisno AL, Chambers HF, Dellinger EP, Goldstein EJ, Gorbach SL, Hirschmann JV, Kaplan SL, Montoya JG, Wade JC |title=Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America |journal=Clin. Infect. Dis. |volume=59 |issue=2 |pages=e10–52 |year=2014 |pmid=24973422 |doi=10.1093/cid/ciu444 |url=}}</ref><ref name="pmid26962903">{{cite journal |vauthors=Talan DA, Mower WR, Krishnadasan A, Abrahamian FM, Lovecchio F, Karras DJ, Steele MT, Rothman RE, Hoagland R, Moran GJ |title=Trimethoprim-Sulfamethoxazole versus Placebo for Uncomplicated Skin Abscess |journal=N. Engl. J. Med. |volume=374 |issue=9 |pages=823–32 |year=2016 |pmid=26962903 |pmc=4851110 |doi=10.1056/NEJMoa1507476 |url=}}</ref>
*Single abscess ≥2 cm
*Multiple lesions
*Extensive surrounding [[cellulitis]]
*Associated [[immunosuppression]] or other comorbidities
*Systemic signs of toxicity ([[fever]] >100.5°F/38°C, [[hypotension]], or sustained [[tachycardia]])
*Inadequate clinical response to [[incision and drainage]] alone
*Presence of an indwelling medical device (such as prosthetic joint, vascular [[graft]], or [[pacemaker]])
*High risk for transmission of [[S. aureus]] to others (such as in athletes, military personnel)
====Antibiotic therapy<ref name="pmid28657870">{{cite journal| author=Daum RS, Miller LG, Immergluck L, Fritz S, Creech CB, Young D et al.| title=A Placebo-Controlled Trial of Antibiotics for Smaller Skin Abscesses. | journal=N Engl J Med | year= 2017 | volume= 376 | issue= 26 | pages= 2545-2555 | pmid=28657870 | doi=10.1056/NEJMoa1607033 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28657870  }} </ref><ref name="pmid21690621">{{cite journal |vauthors=Talan DA, Krishnadasan A, Gorwitz RJ, Fosheim GE, Limbago B, Albrecht V, Moran GJ |title=Comparison of Staphylococcus aureus from skin and soft-tissue infections in US emergency department patients, 2004 and 2008 |journal=Clin. Infect. Dis. |volume=53 |issue=2 |pages=144–9 |year=2011 |pmid=21690621 |doi=10.1093/cid/cir308 |url=}}</ref><ref name="pmid20346539">{{cite journal |vauthors=Schmitz GR, Bruner D, Pitotti R, Olderog C, Livengood T, Williams J, Huebner K, Lightfoot J, Ritz B, Bates C, Schmitz M, Mete M, Deye G |title=Randomized controlled trial of trimethoprim-sulfamethoxazole for uncomplicated skin abscesses in patients at risk for community-associated methicillin-resistant Staphylococcus aureus infection |journal=Ann Emerg Med |volume=56 |issue=3 |pages=283–7 |year=2010 |pmid=20346539 |doi=10.1016/j.annemergmed.2010.03.002 |url=}}</ref>====
:*Preferred regimen: [[Trimethoprim-sulfamethoxazole]] one or two double strength doses (160 mg of trimethoprim and 800 mg of sulfamethoxazole) PO twice daily
:*Alternative regimen (1): [[Clindamycin]] 300-450 mg PO three to four times daily
:*Alternative regimen (2): [[Doxycycline]] 100 mg PO twice daily
:*Alternative regimen (3): [[Minocycline]] 200 mg PO once, then 100 mg PO twice daily
:*Alternative regimen (4): [[Linezolid]] 600 mg PO twice daily
:*Alternative regimen (5): [[Tedizolid]] 200 mg PO once daily
 
===Surgery===
Incision and drainage is the preferred method of treatment for cutaneous abscesses.<ref name="pmid24620867">{{cite journal |vauthors=Singer AJ, Talan DA |title=Management of skin abscesses in the era of methicillin-resistant Staphylococcus aureus |journal=N. Engl. J. Med. |volume=370 |issue=11 |pages=1039–47 |year=2014 |pmid=24620867 |doi=10.1056/NEJMra1212788 |url=}}</ref>
The following video, shows this procedure.{{#ev:youtube|MwgNdrA18fM}}
 
==Prevention==
===Primary prevention===
Avoid sharing personal hygiene items (razors, towels and brushes).<ref name="pmid21208910">{{cite journal |vauthors=Liu C, Bayer A, Cosgrove SE, Daum RS, Fridkin SK, Gorwitz RJ, Kaplan SL, Karchmer AW, Levine DP, Murray BE, J Rybak M, Talan DA, Chambers HF |title=Clinical practice guidelines by the infectious diseases society of america for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children |journal=Clin. Infect. Dis. |volume=52 |issue=3 |pages=e18–55 |year=2011 |pmid=21208910 |doi=10.1093/cid/ciq146 |url=}}</ref>
===Secondary prevention===
Decolonization of the index patient and of household contacts may be considered for patients with recurrent infections by using:<ref name="pmid21208910">{{cite journal |vauthors=Liu C, Bayer A, Cosgrove SE, Daum RS, Fridkin SK, Gorwitz RJ, Kaplan SL, Karchmer AW, Levine DP, Murray BE, J Rybak M, Talan DA, Chambers HF |title=Clinical practice guidelines by the infectious diseases society of America for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children |journal=Clin. Infect. Dis. |volume=52 |issue=3 |pages=e18–55 |year=2011 |pmid=21208910 |doi=10.1093/cid/ciq146 |url=}}</ref>
* Mupirocin
**Apply 2% [[mupirocin]] ointment in nasal flares by using sterile applicators twice a day for 5 days.
**Topical [[mupirocin]] applied to the nares.<ref name="pmid18843708">{{cite journal |author=van Rijen M, Bonten M, Wenzel R, Kluytmans J |title=Mupirocin ointment for preventing Staphylococcus aureus infections in nasal carriers |journal=Cochrane Database Syst Rev |volume= |issue=4 |pages=CD006216 |year=2008 |pmid=18843708 |doi=10.1002/14651858.CD006216.pub2 |url=}}</ref> In this [[randomized controlled trial]], patients used nasal mupirocin twice daily 5 days a month for 1 year.<ref name=Raz1996>{{cite journal | author = Raz R, Miron D, Colodner R, Staler Z, Samara Z, Keness Y | title = A 1-year trial of nasal mupirocin in the prevention of recurrent staphylococcal nasal colonization and skin infection. | journal = Arch Intern Med | volume = 156 | issue = 10 | pages = 1109-12 | year = 1996 | id = PMID 8638999}}</ref> The does is about 1 centimeter of ointment on a swab applied to each nares.<ref name="pmid10348762">{{cite journal |author=Harbarth S, Dharan S, Liassine N, Herrault P, Auckenthaler R, Pittet D |title=Randomized, placebo-controlled, double-blind trial to evaluate the efficacy of mupirocin for eradicating carriage of methicillin-resistant Staphylococcus aureus |journal=Antimicrob. Agents Chemother. |volume=43 |issue=6 |pages=1412–6 |year=1999 |month=June |pmid=10348762 |pmc=89288 |doi= |url=http://aac.asm.org/cgi/pmidlookup?view=long&pmid=10348762 |issn=}}</ref>
* Chlorhexidine
**Apply 4% [[Chlorhexidine gluconate]] solution for all body parts except for face, mucus membranes and open wounds followed by rinsing daily for 5 days.
A more intensive regimen, although not used in this setting, has been described<ref name="pmid30763195">{{cite journal| author=Huang SS, Singh R, McKinnell JA, Park S, Gombosev A, Eells SJ et al.| title=Decolonization to Reduce Postdischarge Infection Risk among MRSA Carriers. | journal=N Engl J Med | year= 2019 | volume= 380 | issue= 7 | pages= 638-650 | pmid=30763195 | doi=10.1056/NEJMoa1716771 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30763195  }} </ref>.
To prevent recurrent infections due to ''[[Staphylococcus aureus]]'', consider the following measures:
**[[Chlorhexidine]] baths,<ref name=Watanakunakorn>{{cite journal | author = Watanakunakorn C, Axelson C, Bota B, Stahl C | title = Mupirocin ointment with and without chlorhexidine baths in the eradication of Staphylococcus aureus nasal carriage in nursing home residents. | journal = Am J Infect Control | volume = 23 | issue = 5 | pages = 306-9 | year = 1995 | id = PMID 8585642}}</ref> in a [[randomized controlled trial]], nasal recolonization with S. aureus occurred at 12 weeks in 24% of nursing home residents receiving mupirocin ointment alone (6/25) and in 15% of residents receiving mupirocin ointment plus chlorhexidine baths daily for the first three days of mupirocin treatment (4/27). Although these results did not reach [[statistical significance]], the baths are easy to do.
 
==References==
{{reflist|2}}
 
[[Category:Dermatology]]
[[Category:Dermatology]]
[[Category:General surgery]]
[[Category:General surgery]]
[[Category:Emergency medicine]]
[[Category:Disease]]
[[Category:Up-To-Date]]
[[Category:Surgery]]

Latest revision as of 08:20, 14 December 2020

Cutaneous abscess
Abscess

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

Synonyms and keywords:Skin abscess
To return to abscess main page, click here.

Overview

Cutaneous abscess is defined as a collection of pus in the dermis or subcutaneous tissue and appears as a swollen, red, tender, and fluctuant mass, often with surrounding cellulitis and may occur in any part of the body. Although, there is a rare type of sterile skin abscess that is secondary to injection mostly in diabetic patients who use insulin. diagnosis is clinical and consist of a painful, tender, indurated, and usually erythematous nodule or mass that is varying in size. Systemic sign and symptoms are rare except for sever and multiple abscess especially in immunocompromised patients. Treatment is, incision and drainage associated with antibiotics.

Historical perspective

Alexander Ogston, a scottish surgeon first described the pyogenic abscess in the late 19th century.[1]

Classification

Cutaneous abscess may be classified as sterile abscess and infectious abscess.

Pathophysiology

Abscess is usually caused by staphylococcus aureus bacterial infection in an injured skin. Staphylococcus aureus could form abscess by secretion of several enzymes and toxins. In a reaction to these bacterial substances, assembled white blood cells in this tissue produces anti-bacterial anti-bodies that help in bacterial elimination. However, these cells cause damage to the soft tissue contributing in the abscess formation.[2]

Pathogenesis

Skin serves as a barrier from pathogen entry. Breech in the skin surface allow the pathogen entry to cause local inflammation. Polymorphonuclear cells (PMNs) are the first and the most important responding cells in abscess formation.[3] Neutrophils, are responsible for phagocytosis. Once the pathogen is opsonized by complement system, it will be recognized by neutrophils and the phagocytosis process will begin. After phagocytosis the bactricidal process will begin by producing superoxide radicals and other reactive oxygen species (ROS).[4]

Genetic factors

PMNs are the most important cellular defense. Genetic disorders that negatively affect PMN function may predispose persons to recurrent cutaneous abscess formation. For example, chronic granulomatous disease, which is a genetic disorder characterized by the inability of PMNs and other phagocytes to produce superoxide, often presents with severe and recurrent S. aureus infections.[5]

Causes

Common causes

Less common causes

Nontuberculous mycobacteria, blastomycosis, nocardiosis, and cryptococcosis.[7]

Differentiating cutaneous abscess from other Diseases

Diseases Symptoms Signs Gold standard Investigation to diagnose
History Onset Pain Fever Laterality Scrotal swelling Symptoms of primary disease
(Cellulitis-erysipelas-skin abscess) Acute + + Unilateral - -
  • Usually it doesn't need any laboratory tests to diagnose.[9]
  • Blood cultures are warranted for patients in the following circumstances:[10]
  1. Systemic toxicity
  2. Extensive skin or soft tissue involvement
  3. Underlying comorbidities
  4. persistent cellulitis
Lymphatic filariasis
  • History of living in endemic area or travelling to it
Chronic + + Bilateral + -

Preparing blood smears

  • Thick smears
  1. Thick smears consist of a thick layer of dehemoglobinized (lysed) red blood cells (RBCs).
  2. Thick smears allow a more efficient detection of parasites (increased sensitivity).
  • Thin smears consist of blood spread in a layer such that the thickness decrease.

By the ultrasound, the following findings can be observed:

  • Dilated lymphatic channels
  • Living worms tend to be in motion which called "filarial dance" sign.
Chronic venous insufficiency Chronic + - Bilateral +

(If congenial)

-
  • Typical varicose veins
  • Skin change distribution correlate with varicose veins sites in the medial side of ankle and leg
  • Reduction of swelling with limb elevation.
Acute deep venous thrombosis Acute + - Unilateral - May be associated with primary disease mandates recumbency for long duration
Lipedema Chronic + - Bilateral - -
  • Tender with palpation
  • Negative Semmer sign to differentiate from lymphedema.[14]
  • Pinching the skin on the upper surface of the toes. If it is possible to grasp a thin fold of tissue then it is negative result.
  • In a positive result, it is only possible to grasp a lump of tissue.
  • MRI offers strong qualitative and quantitative parameters in the diagnosis of lipedema [15]
Myxedema Chronic + - Bilateral - +

(hypothyroidism )

Other causes of generalized edema
  • History of chronic general condition (cardiac-liver-renal)
Chronic - - Bilateral - +
  • According to the primary cause ( Echo- LFTs- RFT)


Disease Clinical features
Folliculitis Hair follicle inflammation, presents as pruritic rash or pustule.[16][17]
Suppurative hydradenitis Inflammation in intertriginous areas (axillae, inguinal area, inner thighs, perianal and perineal areas, mammary,..)

Presents as painful inflamed nodule, sinus tract and commedons. Associated with systemic symptoms. Needs surgical debridement and systemic antibiotic.[18]

Epidermoid cyst Cyst or nodule presents with central punctum. May be secondarily infected.[19]
Nodular lymphangitis Subcutaneous swelling along with lymphatics. mostly due to Sporothrix schenckii.[20]
Myiasis Enlarging nodule secondary to insect bite and due to penetration of fly larvae into subdermal tissue. caused by Dermatobia hominis, the botfly and Cordylobia anthropophaga, the tumbu fly.[21]

Epidemiology and Demographics

  • It is estimated that 4% of children experience the cutaneous abscess.[22]

A national emergency department visit survey from 1996 to 2005 showed:

  • Emergency department visits for abscesses more than doubled over the 10-year study period (1.2 million in 1996 to 3.28 million in 2005).

Gender

Men and women are affected equally.

Age

It is more common among adults age 19 to 45 years.

Risk Factors

Risk factors for developing cutaneous abscess include:[23][24]

Natural History, Complications and Prognosis

Natural History

If cutaneous abscess left untreated it may drain spontaneously. However, in severe cases it may cause systemic spread and result in sepsis.[25]

Recurrence may occur in 20% of patients[26].

Complications

A wide range of complications are possible in the course of skin abscess including: Bacteremia, endocarditis, osteomyelitis, metastatic infection, sepsis, and toxic shock syndrome.[9]

Prognosis

Depending on the extent of the disease, the prognosis may vary. However, the prognosis is generally regarded as good.

Patients who require hospitalization for ICU admission, operating room surgical intervention, or death have one of the following six risk factors upon presentation[27]:

  • abnormal cross-sectional imaging result ("air or gas, abscess or fluid collection, osteomyelitis, or suspicion of osteomyelitis")
  • systemic inflammatory response syndrome
  • previous infection at the same location
  • infection involving the hand * diabetes* age >65 years

Diagnosis

History and symptoms

History

A detailed history must be taken from all patients. Specific area of focus when obtaining a history from the patient include:

Symptoms

The hallmark of the cutaneous abscess is painful, tender, indurated, and usually erythematous nodule.

Physical examination

Appearance of the Patient

Patients are usually well appearing.

Vital signs

Vital signs are within normal limits unless there is complication.

Skin

Indurated, tender and erythematous nodule with signs of local inflammation is the presenting feature.


Laboratory findings

Leukocytosis and increased level of acute phase reactants (ESR, CRP) are the most common laboratory findings.

Treatment

Treatment is based on incision and drainage and sometimes antibiotic therapy is required. Cure rates with drainage alone are about 85% or higher.[28][29]

Patients who require hospitalization for ICU admission, operating room surgical intervention, or death have one of the following six risk factors upon presentation[27]:* abnormal cross-sectional imaging result* systemic inflammatory response syndrome* previous infection at the same location* infection involving the hand * diabetes* age >65 years

Medical therapy

Antibiotic therapy is indicated in some circumstances that include and the duration based on severity and clinical response varies between 3 to 7 days:[30][31][32]

Antibiotic therapy[33][34][29]

  • Preferred regimen: Trimethoprim-sulfamethoxazole one or two double strength doses (160 mg of trimethoprim and 800 mg of sulfamethoxazole) PO twice daily
  • Alternative regimen (1): Clindamycin 300-450 mg PO three to four times daily
  • Alternative regimen (2): Doxycycline 100 mg PO twice daily
  • Alternative regimen (3): Minocycline 200 mg PO once, then 100 mg PO twice daily
  • Alternative regimen (4): Linezolid 600 mg PO twice daily
  • Alternative regimen (5): Tedizolid 200 mg PO once daily

Surgery

Incision and drainage is the preferred method of treatment for cutaneous abscesses.[35] The following video, shows this procedure.{{#ev:youtube|MwgNdrA18fM}}

Prevention

Primary prevention

Avoid sharing personal hygiene items (razors, towels and brushes).[30]

Secondary prevention

Decolonization of the index patient and of household contacts may be considered for patients with recurrent infections by using:[30]

  • Mupirocin
    • Apply 2% mupirocin ointment in nasal flares by using sterile applicators twice a day for 5 days.
    • Topical mupirocin applied to the nares.[36] In this randomized controlled trial, patients used nasal mupirocin twice daily 5 days a month for 1 year.[37] The does is about 1 centimeter of ointment on a swab applied to each nares.[38]
  • Chlorhexidine
    • Apply 4% Chlorhexidine gluconate solution for all body parts except for face, mucus membranes and open wounds followed by rinsing daily for 5 days.

A more intensive regimen, although not used in this setting, has been described[39]. To prevent recurrent infections due to Staphylococcus aureus, consider the following measures:

    • Chlorhexidine baths,[40] in a randomized controlled trial, nasal recolonization with S. aureus occurred at 12 weeks in 24% of nursing home residents receiving mupirocin ointment alone (6/25) and in 15% of residents receiving mupirocin ointment plus chlorhexidine baths daily for the first three days of mupirocin treatment (4/27). Although these results did not reach statistical significance, the baths are easy to do.

References

  1. "Classics in infectious diseases. "On abscesses". Alexander Ogston (1844-1929)". Rev. Infect. Dis. 6 (1): 122–8. 1984. PMID 6369479.
  2. Kobayashi SD, Malachowa N, DeLeo FR (2015). "Pathogenesis of Staphylococcus aureus abscesses". Am J Pathol. 185 (6): 1518–27. doi:10.1016/j.ajpath.2014.11.030. PMC 4450319. PMID 25749135.
  3. Kolaczkowska E, Kubes P (2013). "Neutrophil recruitment and function in health and inflammation". Nat. Rev. Immunol. 13 (3): 159–75. doi:10.1038/nri3399. PMID 23435331.
  4. Quinn MT, Gauss KA (2004). "Structure and regulation of the neutrophil respiratory burst oxidase: comparison with nonphagocyte oxidases". J. Leukoc. Biol. 76 (4): 760–81. doi:10.1189/jlb.0404216. PMID 15240752.
  5. Bieluch VM, Tally FP (1983). "Pathophysiology of abscess formation". Clin Obstet Gynaecol. 10 (1): 93–103. PMID 6872404.
  6. 6.0 6.1 Stevens DL, Bisno AL, Chambers HF, Dellinger EP, Goldstein EJ, Gorbach SL, Hirschmann JV, Kaplan SL, Montoya JG, Wade JC (2014). "Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America". Clin. Infect. Dis. 59 (2): 147–59. doi:10.1093/cid/ciu296. PMID 24947530.
  7. 7.0 7.1 7.2 Summanen PH, Talan DA, Strong C, McTeague M, Bennion R, Thompson JE, Väisänen ML, Moran G, Winer M, Finegold SM (1995). "Bacteriology of skin and soft-tissue infections: comparison of infections in intravenous drug users and individuals with no history of intravenous drug use". Clin. Infect. Dis. 20 Suppl 2: S279–82. PMID 7548575.
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