How does an axillary abscess caused by Streptococcus pyogenes lead to venous thrombosis. What are the diagnostic challenges in identifying the bacterial etiology. How can 16S PCR and gene sequencing aid in accurate diagnosis and treatment.

Clinical Presentation and Initial Diagnosis

A 62-year-old woman presented with a complex case of axillary abscess complicated by venous thrombosis. The patient, previously healthy except for atopic eczema, worked as a technician in a microbiology department. She initially reported a 7-day history of fever, chills, and nausea, accompanied by pain in her left axilla.

Upon admission, the patient’s temperature was 39.5°C, and physical examination revealed tenderness in the left axilla. However, there were no visible signs of erysipelas, lymphangitis, or enlarged lymph nodes. Initial laboratory tests showed:

• White blood cell count: 18 × 10^9/liter (neutrophil count: 17 × 10^9/liter)
• C-reactive protein (CRP) level: 53 mg/liter
• Normal renal and liver function tests
• Normal coagulation test results

How did the initial presentation challenge the diagnostic process? The absence of visible signs of infection and normal coagulation test results initially masked the severity of the condition, leading to a delay in appropriate treatment.

Disease Progression and Complications

Seven days after the initial presentation, the patient was hospitalized due to persistent axillary pain and intermittent chills. The disease progression was marked by:

• Fluctuating body temperature between 38.0°C and 39.9°C
• Increased white blood cell count: 21 × 10^9/liter (neutrophil count: 19 × 10^9/liter)
• Significantly elevated CRP level: 393 mg/liter

Despite the initiation of antibiotic treatment with cefuroxime and clindamycin, the patient’s condition worsened. On the 6th day after admission, a swelling of the left arm developed, and venous flebography confirmed the presence of venous thrombosis in the axillary vein.

Why did venous thrombosis develop as a complication? The proximity of the abscess to the axillary vein, coupled with the inflammatory response and potential procoagulant factors expressed by the Streptococcus pyogenes, likely contributed to the formation of the venous thrombosis.

Advanced Imaging and Diagnostic Techniques

As the patient’s condition evolved, more advanced diagnostic techniques were employed:

1. Plain X-ray of the shoulder: Revealed degenerative changes in the acromio-clavicular joint
2. Initial ultrasonographic examination: Showed no signs of edema or abscess
3. Magnetic Resonance Imaging (MRI) scan: Revealed a multilobulated lesion of 7 by 4 by 7 cm in the left axilla
4. Renewed ultrasonographic examination: Visualized the abscess, which was subsequently punctured under CT guidance

What role did advanced imaging play in the diagnosis? The MRI scan was crucial in identifying the abscess, which was not visible on initial ultrasound, highlighting the importance of employing multiple imaging modalities in complex cases.

Microbiological Identification and 16S PCR

Despite the clinical presentation suggesting a bacterial infection, conventional microbiological methods failed to identify the causative agent:

• Blood cultures: Negative
• Direct cultures of abscess material: Negative
• Anaerobic blood culture bottle inoculated with abscess material: No growth detected

Given the limitations of traditional culture methods, molecular techniques were employed:

1. PCR amplification of the 16S rRNA gene from abscess material
2. Subsequent PCR amplification of the emm gene

How did 16S PCR contribute to the diagnosis? The use of 16S PCR allowed for the identification of Streptococcus pyogenes when conventional culture methods failed, demonstrating the value of molecular techniques in challenging cases.

Streptococcus pyogenes: Serotype and Virulence Factors

Through molecular analysis, the following characteristics of the Streptococcus pyogenes isolate were determined:

• Serotype: M41
• Evidence of expressed procoagulant factors (based on serology)

Why is the identification of the specific serotype and virulence factors important? Understanding the serotype and virulence factors can provide insights into the pathogen’s behavior, potential complications, and guide targeted treatment strategies.

Procoagulant Factors and Thrombosis

The expression of procoagulant factors by the S. pyogenes isolate may have played a significant role in the development of venous thrombosis. These factors can interact with the host’s coagulation system, promoting thrombus formation.

How do bacterial procoagulant factors contribute to thrombosis? Bacterial procoagulant factors can activate the coagulation cascade, inhibit fibrinolysis, and promote platelet aggregation, all of which increase the risk of thrombus formation.

Treatment Approach and Challenges

The treatment of this complex case involved a multifaceted approach:

1. Initial antibiotic therapy: Cefuroxime and clindamycin
2. Anticoagulation therapy: Low-molecular-weight heparin and warfarin
3. Abscess drainage: Guided by CT scan

What challenges did the treatment approach face? The initial antibiotic therapy was empirical and may not have been optimal for the specific strain of S. pyogenes. The delayed identification of the abscess also postponed drainage, a crucial step in managing the infection.

Antibiotic Considerations

The choice of antibiotics in this case is critical. While cefuroxime and clindamycin provide broad-spectrum coverage, targeted therapy based on the identified pathogen and its antibiotic susceptibility profile would be ideal.

Why is targeted antibiotic therapy important in such cases? Targeted therapy can improve efficacy, reduce the risk of antibiotic resistance, and minimize potential side effects associated with broad-spectrum antibiotics.

Implications for Clinical Practice and Future Research

This case study highlights several important points for clinical practice:

• The value of molecular diagnostic techniques in culture-negative infections
• The importance of considering deep-seated infections in patients with persistent symptoms
• The need for a high index of suspicion for complications such as venous thrombosis in axillary infections
• The potential role of bacterial virulence factors in disease progression and complications

How can this case inform future research and clinical practice? It underscores the need for further investigation into the relationship between specific S. pyogenes serotypes and their propensity to cause severe complications. Additionally, it highlights the potential for developing rapid molecular diagnostic tools for use in clinical settings.

Advancements in Rapid Diagnostics

The case demonstrates the need for more rapid and accurate diagnostic methods in clinical microbiology. While 16S PCR proved valuable in this instance, the development of point-of-care molecular tests could further improve patient outcomes.

What potential benefits could rapid molecular diagnostics offer in such cases? Faster identification of pathogens and their virulence factors could lead to earlier initiation of targeted therapy, potentially reducing the risk of complications and improving overall patient outcomes.

Occupational Health Considerations

Given the patient’s occupation as a technician in a microbiology department, this case raises important occupational health considerations:

• Potential exposure to pathogenic bacteria in the workplace
• The importance of proper personal protective equipment (PPE) and safety protocols
• The need for regular health monitoring for individuals working with infectious agents

How can occupational health practices be improved to prevent similar cases? Implementing rigorous safety protocols, providing comprehensive training on handling infectious materials, and ensuring proper PPE usage can help mitigate the risk of occupational exposure to pathogens.

Zoonotic Potential and Public Health Implications

While Streptococcus pyogenes is primarily a human pathogen, its presence in a microbiology laboratory setting raises questions about potential zoonotic transmission or laboratory-acquired infections.

What measures can be taken to prevent laboratory-acquired infections? Strict adherence to biosafety protocols, regular safety audits, and ongoing education on emerging pathogens and their handling can help reduce the risk of laboratory-acquired infections.

Emerging Trends in Streptococcus pyogenes Infections

This case contributes to the growing body of knowledge on invasive Streptococcus pyogenes infections. Recent studies have reported an increase in the incidence of severe S. pyogenes infections, including those associated with uncommon complications like venous thrombosis.

Are certain strains of S. pyogenes more likely to cause severe complications? Research suggests that specific M protein types and the presence of certain virulence factors may be associated with an increased risk of invasive disease and complications. Further epidemiological studies are needed to elucidate these relationships.

Global Surveillance and Antibiotic Resistance

The identification of specific S. pyogenes serotypes through molecular methods contributes to global surveillance efforts. This information is crucial for tracking the spread of virulent strains and monitoring antibiotic resistance patterns.

How can global surveillance data inform clinical practice? By understanding the prevalence and characteristics of circulating S. pyogenes strains, clinicians can make more informed decisions about empiric antibiotic therapy and be more alert to potential complications associated with specific serotypes.

Interdisciplinary Approach to Complex Infections

This case underscores the importance of an interdisciplinary approach in managing complex infections. The involvement of multiple specialties, including infectious diseases, radiology, and hematology, was crucial in diagnosing and treating this patient.

• Infectious Diseases: Guiding antibiotic therapy and infection management
• Radiology: Providing crucial imaging for diagnosis and intervention
• Hematology: Managing the venous thrombosis complication
• Clinical Microbiology: Employing advanced diagnostic techniques

How can healthcare systems promote effective interdisciplinary collaboration? Implementing regular case conferences, developing clear communication channels between specialties, and fostering a culture of collaborative decision-making can enhance patient care in complex cases.

The Role of Clinical Decision Support Systems

As medical knowledge expands and cases become more complex, the integration of clinical decision support systems (CDSS) into practice becomes increasingly valuable. These systems can help clinicians navigate complex diagnostic and treatment algorithms.

How might a CDSS have impacted this case? A well-designed CDSS could have flagged the persistent symptoms and laboratory abnormalities, prompting earlier consideration of deep-seated infection and potentially expediting the diagnostic process.

Patient Education and Follow-up

The management of complex infections like this one extends beyond the acute phase of illness. Patient education and appropriate follow-up are crucial components of care:

1. Educating the patient about the nature of the infection and its potential complications
2. Providing clear instructions for antibiotic and anticoagulation therapy
3. Scheduling regular follow-up appointments to monitor recovery and address any lingering symptoms
4. Offering psychological support, as needed, to address any anxiety related to the illness experience

Why is comprehensive patient education important in cases like this? Proper education can improve treatment adherence, help patients recognize potential complications early, and contribute to better overall outcomes.

Long-term Monitoring and Rehabilitation

Given the severity of the infection and the development of venous thrombosis, long-term monitoring and rehabilitation may be necessary:

• Regular vascular assessments to monitor for post-thrombotic syndrome
• Physical therapy to address any residual functional impairment of the affected arm
• Ongoing surveillance for recurrent streptococcal infections

How can healthcare providers ensure comprehensive long-term care for patients with complex infections? Developing personalized care plans, coordinating with multiple specialties for follow-up, and utilizing patient-centered approaches can help address the diverse needs of these patients over time.

Axillary Abscess Complicated by Venous Thrombosis: Identification of Streptococcus pyogenes by 16S PCR

J Clin Microbiol. 2010 Sep; 48(9): 3435–3437.

Published online 2010 Jun 30. doi: 10.1128/JCM.00373-10

,^1,*,¹,²,¹ and ¹

Author information Article notes Copyright and License information Disclaimer

We report a case of an axillary abscess with Streptococcus pyogenes complicated by venous thrombosis. Bacterial etiology and typing were obtained by PCR and sequencing of the 16S rRNA and M-protein genes from abscess material. The bacterium was of serotype M41, and serology indicated that it had expressed procoagulant factors.

A 62-year-old woman presented at our department with a 7-day history of fever, chills, and nausea. She was previously healthy, apart from having atopic eczema, and she worked as a technician in a microbiology department handling bacterial specimens. For some months, she had experienced pain in the left part of her thoracic wall, which she related to repetitive movements. Two days prior to admission, she started to feel pain in her left axilla. On the day of admission, she had vomited and suffered from diarrhea. At admission, she had a temperature of 39.5°C. The routine physical examination was normal, except for a slight tenderness upon palpation of the left axilla. There were no signs of erysipelas, lymphangitis, or enlarged lymph nodes in the axilla. Laboratory investigation revealed a white blood cell count of 18 × 10⁹/liter (the neutrophil count was 17 × 10⁹/liter), a C-reactive protein (CRP) level of 53 mg/liter, and normal renal and liver function test results. Coagulation test results were within normal limits, with a PT(INR) [prothrombin time (international normalized ratio)] of 1.1, an aPTT (activated partial thromboplastin time) of 36 s, and a platelet count of 329 × 10⁹/liter. After two aerobic and two anaerobic blood cultures (BacT/Alert; bioMérieux, Durham, NC) and a urinary culture were obtained, the patient was sent home and told to return if she got worse. No antibiotics were prescribed. Blood cultures turned out negative.

Seven days later, the patient returned with persistent axillary pain and intermittent chills and was hospitalized. Her body temperature fluctuated between 38.0°C and 39.9°C in the following days. Her white blood cell count was 21 × 10⁹/liter (her neutrophil count was 19 × 10⁹/liter), and her CRP level was 393 mg/liter. Upon examination of the axillary region, pain was provoked by palpation but no enlarged lymph nodes or suspected abscesses were felt and no signs of arthritis were noted. Treatment with cefuroxime and clindamycin was instituted due to suspicion of a soft-tissue infection in the axillary region. A plain X-ray of the shoulder showed degenerative changes in the acromio-clavicular joint, and ultrasonographic examination of the axilla was normal, with no signs of edema in the musculature or in the subcutaneous layer and no signs of abscess. A slight improvement occurred over the following days. Renewed blood cultures taken at the time of admission turned out negative. On the 6th day after admission, a swelling of the left arm developed and venous flebography confirmed the presence of a venous thrombosis in the axillary vein. Coagulation tests were done and showed a PT(INR) of 1.1, an aPTT of 40 s, and a platelet count of 430 × 10⁹/liter. Low-molecular-weight heparin and warfarin treatment was initiated. A magnetic resonance imaging (MRI) scan revealed a multilobulated lesion of 7 by 4 by 7 cm in the left axilla approximately 1.5 cm from the skin enclosing the axillary vein with a contrast signal in the periphery and surrounding edema (Fig. ). A renewed ultrasonographic examination could visualize the abscess, which was punctured led by a computed tomography scan. Abscess material was added to an anaerobic blood culture bottle (BacT/Alert). Direct cultures were negative, and no growth in the bottle was detected.

Open in a separate window

S. pyogenes causing an axillary abscess. (A) MRI picture, T2 weighted with short inversion time inversion recovery sequencing, showing the abscess in the left axilla. The arrow indicates the abscess, and the arrowhead indicates the caput humeri. (B) Time course of titers of antibodies against various streptococcal surface antigens, where day 1 is the first day of illness.

Abscess material was also subjected to PCR amplification of the 16S rRNA gene and subsequently of the emm gene. DNA was extracted from 200 μl of abscess material using Bio Robot EZ-1 with a DNA Tissue kit (Qiagen, Hilden, Germany) after treatment with proteinase K according to the instructions of the manufacturer. Amplification was carried out in a 50-μl reaction mixture containing 1× PCR buffer (Qiagen), 3 mM MgCl₂, 200 μM each deoxynucleoside triphosphate, 1.0 U of HotStarTaq DNA polymerase (Qiagen), 10 pmol of each primer, and 5 μl of template. P515f (5′-TGCCAGCMGCCGCGGTWAT-3′ [12]) and P1067r (5′-AACATYTCACRACACGAGCT-3′[this study]) were used as PCR and sequencing primers. A pre-PCR step of 15 min at 95°C was followed by 40 cycles of 93°C for 50 s, 52°C for 50 s, and 72°C for 50 s. A final step of 5 min at 72°C terminated the amplification. Tubes with no target DNA and Escherichia coli DNA were included as negative and positive controls, respectively. Both strands of the approximately 520-bp PCR product were sequenced using the BigDye Terminator Cycle Sequencing kit (Applied Biosystems Inc., Foster City, CA) and analyzed on an ABI PRISM 3100 Genetic Analyzer (Applied Biosystems Inc.) by BMLabbet (Furulund, Sweden). The sequence was identical (523/523 bp) to the 16S rRNA gene of Streptococcus pyogenes available at the National Center for Biotechnology Information (www.ncbi.nlm.nih.gov).

The emm gene encoding the S. pyogenes M protein was amplified from abscess material, as described above, using primers derived from conserved parts of the emm1 gene (5′-GCTTAGAAAATTAAAAACAGG-3′ [emm for] and 5′-GCGTTTTACAACTGCTGC-3′[emm rev]). A 1.2-kbp fragment was generated, and sequencing, as described above, with emmfor yielded a sequence which was highly similar (596/598 bp) to the hypervariable part of the emm41 gene. These results are strongly suggestive of S. pyogenes serotype M41 as the causative agent, and treatment with clindamycin was continued for a total of 3 weeks. The patient had an uncomplicated recovery.

Antibodies directed toward the variable part of the cell wall-attached M protein of S. pyogenes are believed to confer serotype-specific protection. Stored serum samples obtained from the patient several years before the present episode were available, and levels of immunoglobulin G (IgG) antibody against S. pyogenes PAM (plasminogen-binding group A streptococcal M-like protein), an M-like protein expressed by serotype M41 (19), and other virulence determinants in these samples were compared to IgG antibody levels in convalescence-phase sera. ELISA (enzyme-linked immunosorbent assay) was performed essentially as described previously (2). The following S. pyogenes antigens were used for coating: PAM at 0.5 μg/ml, GRAB (protein G-related α₂M-binding protein) at 0.8 μg/ml, IdeS (IgG-degrading enzyme of S. pyogenes) at 1.1 μg/ml, SpeB (the secreted streptococcal cysteine proteinase) at 0.5 μg/ml, and SclA and SclB (streptococcal collagen-like proteins A and B, respectively, both from serotype M41) at 4 μg/ml. Antigens were purified as described previously (2, 13, 19). Serum samples were diluted 1:500 (PAM, GRAB, IdeS, and SpeB) or 1:50 (SclA and SclB). All antigens gave an absorbance of at least 0.5 when tested with Octagam (human IgG at 50 mg/ml; Octapharma) or a positive-control serum at the same dilutions as the patient serum samples. There was a marked increase in the levels of IgG antibodies against PAM, a collagen-like surface protein (SclB), and SpeB, whereas levels of IgG antibodies against other streptococcal surface proteins remained unchanged (Fig. ). Anti-streptolysin O and anti-DNase B antibody levels on day 21 of illness were elevated.

S. pyogenes, or group A Streptococcus, is an important human pathogen causing a variety of diseases ranging from mild skin infections like impetigo to life-threatening necrotizing fasciitis and toxic shock-like syndrome. Soft-tissue infections caused by S. pyogenes, such as erysipelas and cellulitis, are characterized by diffuse spreading of inflammation in the tissue. The bacterium also causes tonsillitis, and following this infection, abscess formation in the peritonsillar and pharyngeal tissues is relatively common. Abscess formation at other sites occurs rarely. Cases of abscesses with S. pyogenes in the brain (6, 7, 9, 17), in the epidural space (10, 16), in the mediastinum (5), in the lung (8), in the spleen (4), in the retroperitoneum (11), in the pericolic tissue (15), in muscular tissue (1, 3, 18), and in periprosthetic breast tissue (14) have been reported. Considering how common S. pyogenes infections are, abscess formation at sites other than those around the tonsils is distinctly uncommon. To our knowledge, this is the first reported case with an axillary abscess due to S. pyogenes. Though no signs of erysipelas or lymphangitis were present, we believe that the bacteria entered through the skin and spread to the axillary lymph nodes.

The complicating venous thrombosis, which drew attention to the abscess, was probably due to compression of the axillary vein by the abscess. A previous report (3) of an abscess with S. pyogenes causing venous thrombosis also indicated vein compression as the pathogenetic mechanism behind thrombosis formation. However, S. pyogenes binds many components of the coagulation system and the M41 serotype expresses the SclA and SclB proteins, which recruit thrombin-activatable fibrinolysis inhibitor to the bacterial surface (13). By serology, we could show that SclB was expressed during the infection, which could mediate a more procoagulatory state at the site of infection. This molecular mechanism may also have contributed to the thrombosis seen.

The use of 16S PCR and sequencing was invaluable for correct diagnosis in this case, as all cultures were negative. This diagnostic procedure should always be considered in cases where antibiotic treatment has already been commenced. Moreover, DNA extraction from the abscess material made molecular typing of the isolate possible, demonstrating that also the presence of, for example, resistance genes can be detected without culturable bacteria.

Ulrika Ringdahl and Lisa Påhlman generously provided the E. coli PAM-expressing clone and SclA and SclB, respectively. Anna Kahn helped with the MRI picture.

This work was supported in part by Swedish Government Funds for Clinical Research (ALF).

We have no conflicts of interest to report.

^▿Published ahead of print on 30 June 2010.

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Cutaneous abscess of left axilla

1. 
   ICD-10-CM Codes
   


›

2. 
   L00-L99
   


›

3. 
   L00-L08
   


›

4. 
   L02-
   


›

5. 
   2023 ICD-10-CM Diagnosis Code L02.412

Cutaneous abscess of left axilla

2016 2017 2018 2019 2020 2021 2022 2023 Billable/Specific Code

• L02. 412 is a billable/specific ICD-10-CM code that can be used to indicate a diagnosis for reimbursement purposes.
• The 2023 edition of ICD-10-CM L02.412 became effective on October 1, 2022.
• This is the American ICD-10-CM version of L02.412 – other international versions of ICD-10 L02.412 may differ.

The following code(s) above L02.412 contain annotation back-references

Annotation Back-References

In this context, annotation back-references refer to codes that contain:

• Applicable To annotations, or
• Code Also annotations, or
• Code First annotations, or
• Excludes1 annotations, or
• Excludes2 annotations, or
• Includes annotations, or
• Note annotations, or
• Use Additional annotations

that may be applicable to L02.412:

• L00-L99

  2023 ICD-10-CM Range L00-L99

  Diseases of the skin and subcutaneous tissueType 2 Excludes

  • certain conditions originating in the perinatal period (P04-P96)
  • certain infectious and parasitic diseases (A00-B99)
  • complications of pregnancy, childbirth and the puerperium (O00-O9A)
  • congenital malformations, deformations, and chromosomal abnormalities (Q00-Q99)
  • endocrine, nutritional and metabolic diseases (E00-E88)
  • lipomelanotic reticulosis (I89. 8)
  • neoplasms (C00-D49)
  • symptoms, signs and abnormal clinical and laboratory findings, not elsewhere classified (R00-R94)
  • systemic connective tissue disorders (M30-M36)
  • viral warts (B07.-)

  Diseases of the skin and subcutaneous tissue

• L00-L08

  2023 ICD-10-CM Range L00-L08

  Infections of the skin and subcutaneous tissueType 2 Excludes

  • hordeolum (H00.0)
  • infective dermatitis (L30.3)
  • local infections of skin classified in Chapter 1
  • lupus panniculitis (L93.2)
  • panniculitis NOS (M79.3)
  • panniculitis of neck and back (M54.0-)
  • Perlèche NOS (K13.0)
  • Perlèche due to candidiasis (B37.0)
  • Perlèche due to riboflavin deficiency (E53.0)
  • pyogenic granuloma (L98.0)
  • relapsing panniculitis [Weber-Christian] (M35.6)
  • viral warts (B07.-)
  • zoster (B02.-)

  Use Additional

  • code (B95-B97) to identify infectious agent.

  Infections of the skin and subcutaneous tissue

• L02

  ICD-10-CM Diagnosis Code L02

  Cutaneous abscess, furuncle and carbuncle

  2016 2017 2018 2019 2020 2021 2022 2023 Non-Billable/Non-Specific Code

  Type 2 Excludes

  • abscess of anus and rectal regions (K61. -)
  • abscess of female genital organs (external) (N76.4)
  • abscess of male genital organs (external) (N48.2, N49.-)

  Use Additional

  • code to identify organism (B95-B96)

  Cutaneous abscess, furuncle and carbuncle

• L02.4

  ICD-10-CM Diagnosis Code L02.4

  Cutaneous abscess, furuncle and carbuncle of limb

  2016 2017 2018 2019 2020 2021 2022 2023 Non-Billable/Non-Specific Code

  Type 2 Excludes

  • Cutaneous abscess, furuncle and carbuncle of groin (L02.214, L02.224, L02.234)
  • Cutaneous abscess, furuncle and carbuncle of hand (L02.5-)
  • Cutaneous abscess, furuncle and carbuncle of foot (L02.6-)

  Cutaneous abscess, furuncle and carbuncle of limb

Approximate Synonyms

• Abscess of left axilla
• Left abscess of axilla
• Left axillary abscess

ICD-10-CM L02.412 is grouped within Diagnostic Related Group(s) (MS-DRG v40. 0):

• 573 Skin graft for skin ulcer or cellulitis with mcc
• 574 Skin graft for skin ulcer or cellulitis with cc
• 575 Skin graft for skin ulcer or cellulitis without cc/mcc
• 602 Cellulitis with mcc
• 603 Cellulitis without mcc
• 791 Prematurity with major problems
• 793 Full term neonate with major problems

Convert L02.412 to ICD-9-CM

Code History

• 2016 (effective 10/1/2015): New code (first year of non-draft ICD-10-CM)
• 2017 (effective 10/1/2016): No change
• 2018 (effective 10/1/2017): No change
• 2019 (effective 10/1/2018): No change
• 2020 (effective 10/1/2019): No change
• 2021 (effective 10/1/2020): No change
• 2022 (effective 10/1/2021): No change
• 2023 (effective 10/1/2022): No change

ICD-10-CM Codes Adjacent To L02. 412

L02.235 Carbuncle of perineum

L02.236 Carbuncle of umbilicus

L02.239 …… unspecified

L02.3 Cutaneous abscess, furuncle and carbuncle of buttock

L02. 31 Cutaneous abscess of buttock

L02.32 Furuncle of buttock

L02.33 Carbuncle of buttock

L02.4 Cutaneous abscess, furuncle and carbuncle of limb

L02.41 Cutaneous abscess of limb

L02. 411 Cutaneous abscess of right axilla

L02.412
Cutaneous abscess of left axilla

L02.413 Cutaneous abscess of right upper limb

L02.414 Cutaneous abscess of left upper limb

L02. 415 Cutaneous abscess of right lower limb

L02.416 Cutaneous abscess of left lower limb

L02.419 …… unspecified

L02.42 Furuncle of limb

L02.421 Furuncle of right axilla

L02. 422 Furuncle of left axilla

L02.423 Furuncle of right upper limb

L02.424 Furuncle of left upper limb

Reimbursement claims with a date of service on or after October 1, 2015 require the use of ICD-10-CM codes.

Hydradenitis. What is dangerous? Causes, symptoms, treatments

If you feel itching and pain in the armpits and a lump is felt, then you probably have hidradenitis . These are the first signs that the patient usually feels. Hidradenitis is easily distinguished from boils and other abscesses by its characteristic purple-bluish tint. The next sign, which will immediately appear if left untreated, is an increase in body temperature to 38.5 ° C. A temperature of 39 ° C and above, combined with weakness and headache, means that hydradenitis has led to a more dangerous disease – phlegmon (purulent hydradenitis), which, in turn, can lead to rotting of the lymph nodes. But often, if the disease is not treated, hydradenitis breaks out on its own on about the fifth day. In this case, fistulous passages and comedones (blackheads) can form.

However, in no case should you squeeze out an abscess on your own ! If an abscess is found, treat the lesion with antiseptic agents (miramistin, chlorhexidine, hydrogen peroxide, 5% iodine solution, 2% salicylic acid alcohol solution), apply a bandage with Vishnevsky ointment or antibacterial ointments (levomekol, neomycin, baneocin). Then be sure to see a doctor! If you have a simplified form of hidradenitis, then treatment will be limited to taking antibiotics and anti-inflammatory drugs. If you have a complicated form of hidradenitis, then the treatment will be carried out by surgery. After the operation, dressing with Levomekol is performed, which subsequently changes every two days. The procedures are carried out until the incisions are completely healed. If hydradenitis has caused a general infection, then treatment is carried out with the help of vaccines and immunoglobulins (gamma globulin or staphylococcal vaccine).

There are traditional methods of treating this disease , but they can only be used at an early stage and only after an interview with a doctor. The most effective are plantain, aloe and celery. To apply to inflammation, the plantain is crushed until the juice is released; aloe is cut lengthwise; celery is crushed to the state of gruel.

The causes of the disease are most often staphylococci, penetrating into the tissue through injuries, cuts resulting from shaving the armpits. It can also be reduced immunity, increased sweating. Therefore, as the main preventive measures, it is necessary to maintain normal body weight, limit (or rather exclude) the use of perfumes and observe the rules of personal hygiene, as often as possible, eat foods high in iodine and vitamins C and D.

The material is informational. Medicinal products, biologically active supplements and other products are indicated as an example of their possible use and / or application, which in no way constitutes a recommendation for their use. Before using drugs, dietary supplements and medical equipment and other products, be sure to consult a specialist.

Breast abscess – Into-Sana

Breast abscess is an inflammatory process that develops against the background of infectious diseases of the breast, which is characterized by the presence of a limited cavity with purulent accumulations inside. It occurs predominantly in women with mastitis, cysts, or breast cancer. An abscess always acts as a secondary pathology and is more common in women who have recently given birth.

Contents:

• Causes of breast abscess
• Types of breast abscess
• Symptoms of breast abscess
• Diagnosis of breast abscess
• Methods of treatment of breast abscess
• Sequelae of breast abscess

Causes of breast abscess

This pathology is not considered an independent disease, but acts as a complication of existing ones. The occurrence of an abscess is due to the penetration of pathogenic bacteria into the breast tissue, such as streptococcus, proteus, staphylococcus, E. coli. They enter the body through microcracks in the nipple, which are observed primarily during lactation. Also, one of the predisposing factors for the development of an abscess is the stagnation of milk in the chest, which occurs due to the refusal of breastfeeding or neglect of the procedure for decanting the remaining milk. It is also worth noting the insufficient level of hygiene, as one of the possible causes of an abscess. In cases where there is any damage to the nipple or irritation, contaminated injuries can become the basis for the development of infection.

In addition to the above, there are such causes of this pathology:

• mastitis and other inflammatory processes in the mammary gland;
• various mechanical injuries of the chest: bruises, blows, and resulting hematomas.

Types of breast abscess

Today in mammology there is a well-defined classification of abscesses. According to the location of suppuration, there are:

• Subcutaneous abscess . Such a formation is easy to diagnose, since it is located superficially.
• Subareolar – placed under the nipple or its areola.
• Intramammary – occurs with a deep form of congestive mastitis and is localized in the parenchyma of the mammary gland. If this type of abscess lies deep, it is almost impossible to visually identify it, and the presence of pathology can only be judged by indirect signs.
• Retromammary is the most dangerous form of pathology. With this type of disease, the abscess is located in the back of the mammary gland, there is a threat of a breakthrough of a purulent formation into the chest cavity.

In addition, single and multiple abscesses are distinguished, as well as unilateral (those that are localized in one mammary gland) and bilateral (when both glands are involved in the pathological process).

Breast abscess symptoms

The disease begins acutely – the body temperature rises sharply (up to 39°C). The following symptoms observed in patients are:

• Throbbing pain in the chest, aggravated by various movements – walking, running, riding in transport. Breastfeeding becomes almost impossible due to severe pain. With palpation of the chest, it is possible to accurately determine the epicenter of pain.
• Over the site of the abscess, the skin becomes hot, red.
• Enlargement of the mammary gland in volume due to the occurrence of edema.
• Often there is purulent discharge from the nipple.
• An increase in the size of the axillary lymph nodes on the side of the lesion and pain on palpation.
• Intoxication phenomena are observed, characterized by the following symptoms: general weakness, dizziness, loss of appetite, nausea, vomiting is possible.

The severity of symptoms may vary depending on the type of abscess, as well as the severity of the process.

Diagnosis of breast abscess

To diagnose an inflammatory process, the doctor performs a visual examination and palpation of the breast. If the purulent formation is not deep under the skin, these procedures may be enough. However, a number of additional laboratory and instrumental studies are often used to make an accurate diagnosis.

The most common instrumental diagnostic method is X-ray of the breast (mammography) . With its help, it is possible to establish the location of the abscess, its shape and size. The advantage of the method is that due to the high resolution of the resulting image, even the smallest abscesses can be distinguished.

Blood test is carried out in order to identify the inflammatory process occurring in the body. It is indicated by an increased level of leukocytes, an accelerated ESR (erythrocyte sedimentation rate).

Bacteriological culture , taken from the nipple, is carried out in order to detect the pathogenic microflora that served as the causative agent of a breast abscess.

Ultrasound (sonography) of the breast allows you to determine the exact location of purulent formations, their number, shape, size, depth, communication with the milk ducts and with each other. When using this method, the doctor can also determine the stage of development of the disease.

Another effective diagnostic method is computed tomography (CT) . It is used for unsatisfactory data from ultrasound and mammography. With its help, a series of layered images is obtained, from which it is possible to compose a three-dimensional image of the area under study. CT is indispensable in diagnosing a retromammary abscess, since it is impossible to obtain a reliable result in other ways.

Methods of treatment of breast abscess

Treatment of this pathology involves surgery. The doctor performs an autopsy of the formed abscess and its subsequent drainage . All these manipulations are carried out after hospitalization in a surgical hospital.

The operation takes place in several stages. The surgeon makes a small radial incision from the nipple to the base of the breast. Such incisions are the least traumatic, and the scars remaining after them are practically invisible. The wound is examined, all available abscesses are opened, the pus is removed. After that, drainage is established, the wound is sutured only partially. The patient remains under observation all the time while the drainage is installed (from 3 to 4 days). During this period, the surgeon examines the gland, washing the cavity cleared of pus with antiseptics. As soon as any discharge through the drainage stops, the wound is sutured tightly.

For a small single abscess, needle aspiration can be performed. Such an intervention is the least traumatic and does not leave a scar, however, with multiple abscesses, it is ineffective.

In addition to surgery, the patient is prescribed medication. Antibiotics are prescribed to fight the causative agent of infection, as well as drugs aimed at treating the pathology that caused the abscess (mastitis, cysts, etc.). Analgesics are prescribed to reduce pain.

Consequences of breast abscess

The prognosis for recovery with adequate treatment and compliance with all the rules is favorable, the mammary gland retains all its functions. In case of incorrect or late treatment, various complications are observed:

• fistula, which is an artificially formed channel connecting the organ with the environment;
• development of phlegmon;
• purulent breakthrough into the milk ducts;
• removal of the mammary gland;
• death.