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Abscess of axilla. Primary Tubercular Abscess of the Axilla: A Rare Case Study and Comprehensive Analysis

What are the characteristics of primary tubercular abscess in the axilla. How is it diagnosed and treated. What are the implications for clinical practice and future research.

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Understanding Tubercular Abscesses: An Overview

Tubercular abscesses are a manifestation of extrapulmonary tuberculosis, a condition that affects organs and tissues outside the lungs. While pulmonary tuberculosis remains the most common form of the disease, extrapulmonary cases account for a significant portion of tuberculosis infections worldwide. Tubercular abscesses typically develop as a result of Mycobacterium tuberculosis infection spreading to soft tissues, often secondary to bone involvement or lymph node suppuration.

However, primary tubercular abscesses, especially in unusual locations like the axilla, are exceedingly rare. These cases present unique diagnostic and treatment challenges for healthcare professionals. Understanding the characteristics, pathogenesis, and management of such rare presentations is crucial for improving patient outcomes and advancing our knowledge of tuberculosis manifestations.

The Rarity of Primary Axillary Tubercular Abscesses

Primary tubercular abscesses of the axilla are extremely uncommon in medical literature. This case study presents what is believed to be the first reported instance of a primary tubercular abscess manifesting in the axillary region. The rarity of this condition raises several questions:

  • Why are primary tubercular abscesses in the axilla so uncommon?
  • What factors contribute to the development of such localized infections?
  • How does the axillary location affect diagnosis and treatment approaches?

The uniqueness of this case underscores the importance of considering tuberculosis in the differential diagnosis of axillary swellings, even in the absence of pulmonary symptoms or a history of tuberculosis exposure.

Clinical Presentation and Diagnostic Challenges

The case study describes a 24-year-old woman presenting with a left axillary swelling persisting for one month, accompanied by mild pain in the last week. Notably, the patient exhibited no constitutional symptoms typically associated with tuberculosis, such as fever, weight loss, or night sweats. The absence of these classic symptoms presents a significant diagnostic challenge, potentially leading to delayed or missed diagnoses in similar cases.

Key aspects of the clinical presentation include:

  • A diffuse, non-tender swelling in the left axilla
  • Lack of inflammatory signs
  • Normal breast and spine examinations
  • No history of tuberculosis or known exposure

The initial differential diagnosis considered a hypertrophied axillary tail of Spence, highlighting the importance of maintaining a broad differential when evaluating axillary masses.

Diagnostic Workup and Findings

The diagnostic process for this case involved a comprehensive workup, including:

  1. Ultrasound imaging revealing a biloculated collection in the axilla
  2. Laboratory tests showing a normal leucocyte count and elevated ESR
  3. Positive Mantoux test
  4. Normal chest X-ray
  5. Needle aspiration yielding sterile pus on culture
  6. PCR test detecting Mycobacterium tuberculosis

This systematic approach to diagnosis demonstrates the importance of combining imaging studies, laboratory tests, and molecular diagnostic techniques in cases of suspected extrapulmonary tuberculosis. The detection of M. tuberculosis through PCR testing proved crucial in establishing the definitive diagnosis, especially given the sterile culture results.

Pathogenesis of Primary Tubercular Abscesses

The development of a primary tubercular abscess in the axilla raises questions about the pathogenesis of such localized infections. While the exact mechanism remains unclear in this case, several hypotheses can be considered:

  • Hematogenous spread of M. tuberculosis to soft tissues
  • Direct inoculation through minor skin breaches
  • Lymphatic spread from an undetected primary focus

Understanding the pathogenesis of primary tubercular abscesses is crucial for developing targeted prevention and treatment strategies. Further research is needed to elucidate the specific mechanisms by which M. tuberculosis establishes isolated soft tissue infections in the absence of apparent pulmonary or lymph node involvement.

Treatment Approach and Patient Outcome

The management of this rare case of primary axillary tubercular abscess involved a combination of medical and surgical interventions. The treatment approach included:

  1. Initiation of anti-tubercular therapy (ATT)
  2. Surgical drainage of the abscess
  3. Completion of a 6-month ATT regimen

This multifaceted approach highlights the importance of combining pharmacological treatment with surgical intervention in managing tubercular abscesses. The patient’s positive response to treatment, evidenced by wound healing and successful completion of the ATT course, underscores the effectiveness of this management strategy.

Long-term Follow-up and Recurrence Prevention

While the case report does not provide information on long-term follow-up, it raises important questions about the risk of recurrence and the need for ongoing monitoring in patients with primary tubercular abscesses. Future studies should address:

  • Optimal duration of follow-up for patients with extrapulmonary tuberculosis
  • Strategies for early detection of recurrence
  • The role of preventive measures in high-risk populations

Implications for Clinical Practice

The presentation of a primary tubercular abscess in the axilla has several important implications for clinical practice:

  1. Heightened awareness of atypical tuberculosis presentations
  2. Inclusion of tuberculosis in the differential diagnosis of axillary swellings
  3. Importance of thorough diagnostic workup, including molecular testing
  4. Need for a multidisciplinary approach involving surgeons, infectious disease specialists, and radiologists

Clinicians should maintain a high index of suspicion for tuberculosis, even in cases presenting with isolated soft tissue swellings and without typical constitutional symptoms. This approach can lead to earlier diagnosis and improved patient outcomes.

Epidemiological Considerations and Global Health Impact

The case study highlights the ongoing challenges posed by tuberculosis, particularly in regions with high disease prevalence. In India, where this case was reported, tuberculosis remains a significant public health concern. The epidemiological landscape of tuberculosis in the Indian subcontinent reveals:

  • 54% of cases present as pulmonary tuberculosis
  • 34% manifest as extrapulmonary tuberculosis
  • 12% exhibit both pulmonary and extrapulmonary involvement

These statistics underscore the importance of comprehensive tuberculosis control programs that address both pulmonary and extrapulmonary manifestations of the disease. The recognition and proper management of rare presentations, such as primary axillary tubercular abscesses, contribute to overall tuberculosis control efforts and help reduce disease burden.

Global Tuberculosis Prevalence and Control Strategies

The global prevalence of tuberculosis, estimated at around 30 million cases, with a significant proportion found in India, highlights the need for continued research, improved diagnostic techniques, and effective treatment strategies. Addressing rare and atypical presentations of tuberculosis is crucial for comprehensive disease control.

Key aspects of global tuberculosis control include:

  • Enhanced surveillance and reporting systems
  • Development of rapid and accurate diagnostic tools
  • Implementation of effective treatment regimens
  • Public health interventions targeting high-risk populations
  • Research into novel therapeutics and vaccine development

Differential Diagnosis of Axillary Swellings

The initial misdiagnosis of the axillary swelling as a hypertrophied axillary tail of Spence emphasizes the importance of considering a broad differential diagnosis for axillary masses. Clinicians should be aware of various potential etiologies, including:

  1. Benign breast conditions (e.g., fibroadenomas, cysts)
  2. Malignancies (e.g., breast cancer, lymphoma)
  3. Infectious processes (bacterial, fungal, or mycobacterial)
  4. Inflammatory conditions (e.g., hidradenitis suppurativa)
  5. Vascular anomalies
  6. Neurogenic tumors

A systematic approach to evaluating axillary swellings, incorporating clinical examination, imaging studies, and when necessary, tissue sampling, can help ensure accurate diagnosis and appropriate management.

Role of Imaging in Diagnosis

The case study highlights the valuable role of imaging in the diagnostic process. Ultrasound examination revealed a biloculated collection in the axilla, providing crucial information for further management. The use of imaging modalities in evaluating axillary swellings offers several advantages:

  • Non-invasive assessment of soft tissue structures
  • Characterization of fluid collections or solid masses
  • Guidance for needle aspiration or biopsy procedures
  • Evaluation of adjacent anatomical structures

While ultrasound was the primary imaging modality used in this case, other techniques such as CT or MRI may be valuable in complex cases or when further characterization is needed.

Advances in Tuberculosis Diagnostics

The successful diagnosis of the primary tubercular abscess in this case relied heavily on molecular diagnostic techniques, specifically PCR testing for Mycobacterium tuberculosis. This highlights the importance of advanced diagnostic tools in detecting extrapulmonary tuberculosis, especially in cases where conventional methods may yield inconclusive results.

Recent advances in tuberculosis diagnostics include:

  1. Gene Xpert MTB/RIF assay for rapid detection of M. tuberculosis and rifampicin resistance
  2. Line probe assays for detecting drug resistance
  3. Next-generation sequencing for comprehensive drug susceptibility testing
  4. Interferon-gamma release assays for latent tuberculosis detection
  5. Lipoarabinomannan (LAM) urine tests for tuberculosis diagnosis in HIV-positive individuals

These innovative diagnostic approaches contribute to more accurate and timely diagnosis of tuberculosis, particularly in challenging cases such as extrapulmonary or paucibacillary infections.

Importance of Molecular Testing in Extrapulmonary Tuberculosis

The case study underscores the critical role of molecular testing in diagnosing extrapulmonary tuberculosis. PCR detection of M. tuberculosis provided the definitive diagnosis when conventional culture methods failed to yield results. This highlights several key points:

  • Increased sensitivity of molecular techniques compared to traditional culture methods
  • Rapid turnaround time for results, allowing for earlier treatment initiation
  • Ability to detect M. tuberculosis in paucibacillary specimens
  • Potential for simultaneous detection of drug resistance markers

The integration of molecular diagnostic techniques into the standard workup for suspected extrapulmonary tuberculosis can significantly improve diagnostic accuracy and timeliness.

Future Research Directions

This rare case of primary tubercular abscess in the axilla opens up several avenues for future research:

  1. Epidemiological studies to determine the true incidence of primary soft tissue tuberculosis
  2. Investigation of risk factors predisposing individuals to localized extrapulmonary tuberculosis
  3. Evaluation of optimal treatment durations for primary tubercular abscesses
  4. Development of targeted diagnostic algorithms for atypical tuberculosis presentations
  5. Exploration of host-pathogen interactions in the context of localized tubercular infections

Additionally, further research is needed to elucidate the pathogenesis of primary tubercular abscesses and to develop more effective strategies for prevention and early detection of extrapulmonary tuberculosis.

Potential for Biomarker Discovery

The unique presentation of this case suggests the potential for identifying novel biomarkers specific to extrapulmonary tuberculosis. Future research directions in this area may include:

  • Proteomic analysis of tubercular abscess fluid
  • Investigation of host immune responses in localized tubercular infections
  • Identification of genetic factors influencing susceptibility to extrapulmonary tuberculosis
  • Development of point-of-care diagnostic tests for extrapulmonary tuberculosis

Such research could lead to improved diagnostic tools and personalized treatment approaches for patients with atypical tuberculosis presentations.

Conclusion

The case of primary tubercular abscess in the axilla presents a rare and intriguing manifestation of extrapulmonary tuberculosis. This unique presentation challenges our understanding of tuberculosis pathogenesis and highlights the importance of maintaining a high index of suspicion for atypical presentations of the disease. The successful diagnosis and management of this case underscore the value of comprehensive diagnostic approaches, including advanced molecular techniques, and the effectiveness of combined medical and surgical interventions.

As we continue to face the global challenge of tuberculosis control, recognizing and properly managing rare presentations such as this contributes to our overall understanding of the disease and helps refine diagnostic and treatment strategies. Future research focusing on the epidemiology, pathogenesis, and optimal management of primary tubercular abscesses will be crucial in advancing our ability to combat this persistent public health threat.

The lessons learned from this case emphasize the need for continued vigilance, interdisciplinary collaboration, and ongoing research in the field of tuberculosis. By sharing knowledge of rare presentations and leveraging advanced diagnostic and treatment modalities, we can work towards more effective tuberculosis control and improved patient outcomes worldwide.

Primary Tubercular Abscess of the Axilla—a Rare Case

Indian J Surg. 2017 Dec; 79(6): 563–565.

,, and

Ameet Kumar

No 7 Air Force Hospital, Nathu Singh Road, Kanpur Cantt, Kanpur, UP 208004 India

T. S. Ramakrishnan

No 7 Air Force Hospital, Nathu Singh Road, Kanpur Cantt, Kanpur, UP 208004 India

Samaresh Sahu

No 7 Air Force Hospital, Nathu Singh Road, Kanpur Cantt, Kanpur, UP 208004 India

No 7 Air Force Hospital, Nathu Singh Road, Kanpur Cantt, Kanpur, UP 208004 India

Corresponding author.

Received 2010 Mar 29; Accepted 2010 Mar 29.

Copyright © Association of Surgeons of India 2017

Abstract

Tuberculosis can be broadly classified as pulmonary and extrapulmonary. Though pulmonary tuberculosis is the most common presentation, extrapulmonary tuberculosis is also an important entity. A tubercular cold abscess secondary to involvement of an adjacent bone or suppuration of lymph nodes is a well-known entity; however, a primary cold abscess is rare. We report a case of a young girl who presented with an axillary swelling which turned out to be a primary tubercular abscess of the axilla. To the best of our knowledge, this is the first reported case of a primary tubercular abscess presenting in the axilla. A primary tubercular abscess, though rare, should be considered as a possible diagnosis in appropriate clinical settings backed by evidence of Mycobacterium tuberculosis in form of AFB microscopy, L-J culture, BACTEC culture, or PCR test.

Keywords: Primary cold abscess, Tuberculosis, Axilla

Introduction

Tuberculosis can be broadly classified as pulmonary and extrapulmonary. Though pulmonary tuberculosis is the most common presentation, extrapulmonary tuberculosis is also an important entity. The sites involved in extrapulmonary tuberculosis are lymph nodes, abdomen, bones and joints including spine, genitourinary system, and central nervous system. Others may present with abscess, fistula, and cutaneous lesion [1]. A tubercular cold abscess secondary to involvement of an adjacent bone or suppuration of lymph nodes is a well-known entity; however, a primary cold abscess is rare [2]. We report one such case which was diagnosed as primary tubercular abscess of the axilla. To the best of our knowledge, this is the first reported case of a primary tubercular axillary abscess.

Case Report

A 24-year-old lady presented with a swelling in her left axilla of 1 month duration with mild pain for 1 week. She had no constitutional symptoms and denied past history of tuberculosis or any contact with a patient of tuberculosis. On examination, she was afebrile and had a diffuse swelling in her left axilla which was non-tender and had no features of inflammation (Fig. ). Her breast and spine examination was normal. A tentative diagnosis of hypertrophied axillary tail of Spence was made.

Diffuse swelling in the left axilla of the patient without signs of inflammation

An ultrasound of the axilla revealed a biloculated collection, measuring 37 × 23 and 41 × 38 mm (Fig. ). The axillary tail of Spence was superficial to these two loculi and there were no sizeable lymph nodes (Fig. ). Her leucocyte count was 6400 cells/cm, ESR was 40 mm/h, Mantoux test was positive (18 × 12 mm), and chest X-ray was normal. A guided needle aspiration of this collection revealed frank pus which was sterile on culture and no acid fast bacilli was seen on ZN staining. The pus was sent for PCR test which detected Mycobacterium tuberculosis. Her X-ray of the dorsal spine was normal.

Ultrasound image of the axilla showing an intercommunicating (arrows) biloculated collection (marked as 1 and 2)

Color Doppler of left axilla showing the axillary vessels with no significant lymph nodes

She was started on anti-tubercular therapy (ATT) and underwent drainage of the abscess. The wound healed well and she completed 6 months of ATT which she tolerated well.

Discussion

Globally, the prevalence of tuberculosis is around 30 million and approximately one third of the cases are found in India. In the Indian subcontinent, pulmonary tuberculosis constitutes 54% of all cases, 34% present with extrapulmonary tuberculosis and 12% with both pulmonary and extrapulmonary manifestations [3]. Tuberculosis of the soft tissues is not uncommon and cases like tubercular bursitis, tuberculous synovitis, and tuberculous spondylitis secondary to adjacent bone involvement have been reported [4]. Soft tissue tuberculosis can also present as an abscess either due to adjacent bone involvement or following suppuration of lymph nodes. However, isolated soft tissue involvement is rare.

The mode of spread of infection to the soft tissues is presumed to be hematogenous in such cases [5]. There are sporadic reports of primary soft tissue tuberculosis presenting as gluteal abscess that have been presumed to be syringe transmitted either through used needles or due to coughing by the infected nursing staff over the site of injection [6]. Agrawal et al. have reported a case of primary cold abscess where they thought that the spread was hematogenous [2]. There are a few other reports of isolated tubercular involvement of muscles in the literature [7].

Our case presented with an axillary swelling and in the absence of constitutional symptoms was initially thought to be due to hypertrophied axillary tail of Spence. People with extrapulmonary tuberculosis often do not have the classical symptoms and physical findings associated with pulmonary disease and tuberculosis may not be even considered in the initial differential diagnoses [1]. The incidence of active pulmonary tuberculosis in soft tissue tuberculosis is only 29%. The chest X-ray of our case showed no evidence of pulmonary tuberculosis.

The diagnosis in our case was based on the clinical presentation of axillary swelling without constitutional symptoms, raised ESR, positive Mantoux test, finding of a diffuse swelling in the axilla without signs of inflammation, features of abscess on ultrasound, and was clinched by the detection of M. tuberculosis by PCR. Although AFB microscopy and conventional Lowenstein Jensen (L-J) culture remain the cornerstone of the diagnosis of TB, these methods are either slow or their sensitivity is quite low. PCR is a rapid and sensitive method for the early diagnosis of pulmonary and extrapulmonary tuberculosis when compared with AFB microscopy, L-J culture, or BACTEC culture. In one of the studies, the sensitivity, specificity, and positive and negative predictive values for PCR test were 93.1, 97.7, 90.0, and 98.5%, respectively, for non-respiratory specimens [8].

The other differential diagnosis that could have been considered was that of a pyogenic axillary abscess but the absence of features of inflammation and a sterile culture precluded this diagnosis. This case was labeled primary tubercular abscess as there was no evidence of involvement of the dorsal spine, breast, or axillary lymph nodes.

Conclusion

A primary tubercular abscess, though rare, should be considered as a possible diagnosis in appropriate clinical settings backed by evidence of M. tuberculosis in form of AFB microscopy, L-J culture, BACTEC culture, or PCR test. Our case assumes significance in view of the fact that, to the best of our knowledge, it is the first reported case of a primary tubercular axillary abscess.

Compliance with Ethical Standards

References

1. Karim MM, Chowdhury SA, Hussain MM, Faiz MA. A clinical study on extrapulmonary tuberculosis. J Bangladesh Coll Phys Surg. 2006;24:19–28. [Google Scholar]2. Agrawal A, Jain A. Tuberculous cold abscess. Indian J Pediatr. 2007;74:771–773. doi: 10.1007/s12098-007-0137-4. [PubMed] [CrossRef] [Google Scholar]3. Medical Research Council National survey of tuberculosis notifications in England and Wales in 1983: characteristics of disease. Tubercle. 1987;68:19–32. [PubMed] [Google Scholar]4. Abdelwahab IF, Kenan S, Hermann G, Klein MJ, Lewis MM. Tuberculous peroneal tenosynovitis. A case report. J Bone Joint Surgery. 1993;75(11):1687–1690. doi: 10.2106/00004623-199311000-00014. [PubMed] [CrossRef] [Google Scholar]

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6. Abdelwahab IF, Kenan S, Hermann G, Klein MJ. Tuberculous gluteal abscess without bone involvement. Skelet Radiol. 1998;27:36–39. doi: 10.1007/s002560050333. [PubMed] [CrossRef] [Google Scholar]7. Nuwal P, Dixit R. Tuberculosis of rectus abdominis muscle. Indian J Chest Dis Allied Sci. 2007;49:239–240. [Google Scholar]8. Pfyffer GE, Kissling P, Jahn EM, Welscher HM, Salfinger M, Weber R. Diagnostic performance of amplified Mycobacterium tuberculosis direct test with cerebrospinal fluid, other nonrespiratory, and respiratory specimens. J Clin Microbiol. 1996;34:834–841. [PMC free article] [PubMed] [Google Scholar]

Causes, Symptoms, Tests, and Treatment

Abscess Overview

A skin abscess is a tender mass generally surrounded by a colored area from pink to deep red. Abscesses are often easy to feel by touching. The vast majority of them are caused by infections. Inside, they are full of pus, bacteria and debris.

Painful and warm to touch, abscesses can show up any place on your body. The most common sites on the skin in your armpits (axillae), areas around your anus and vagina (Bartholin gland abscess), the base of your spine (pilonidal abscess), around a tooth (dental abscess), and in your groin. Inflammation around a hair follicle can also lead to the formation of an abscess, which is called a boil (furuncle).

Unlike other infections, antibiotics alone will not usually cure an abscess. In general an abscess must open and drain in order for it to improve. Sometimes draining occurs on its own, but generally it must be opened with the help of a warm compress or by a doctor in a procedure called incision and drainage (I&D).

Abscess Causes

When our normal skin barrier is broken, even from minor trauma, or small tears, or inflammation, bacteria can enter the skin. An abscess can form as your body’s defenses try to kill these germs with your inflammatory response (white blood cells = pus). Obstruction in a sweat or oil (sebaceous) gland, or a hair follicle or a pre-existing cyst can also trigger an abscess. 

The middle of the abscess liquefies and contains dead cells, bacteria, and other debris. This area begins to grow, creating tension under the skin and further inflammation of the surrounding tissues. Pressure and inflammation cause the pain.

People with weakened immune systems get certain abscesses more often. Those with any of the following are all at risk for having more severe abscesses. This is because the body has a decreased ability to ward off infections.

Other risk factors for abscess include exposure to dirty environments, exposure to persons with certain types of skin infections, poor hygiene, and poor circulation.

Abscess Symptoms

Most often, an abscess becomes a painful, compressible mass that is red, warm to touch, and tender.

  • As some abscesses progress, they may “point” and come to a head so you can see the material inside and then spontaneously open (rupture).
  • Most will continue to get worse without care. The infection can spread to the tissues under the skin and even into the bloodstream.
  • If the infection spreads into deeper tissue, you may develop a fever and begin to feel ill.

Abscess Treatment: Self-Care at Home

  • If the abscess is small (less than 1 cm or less than a half-inch across), applying warm compresses to the area for about 30 minutes 4 times daily may help.
  • Do not attempt to drain the abscess by squeezing or pressing on it. This can push the infected material into the deeper tissues.
  • Do not stick a needle or other sharp instrument into the abscess center, because you may injure an underlying blood vessel or cause the infection to spread.

 

When to Seek Medical Care

Call your doctor if any of the following occur with an abscess:

  • You have a sore larger than 1 cm or a half-inch across.
  • The sore continues to enlarge or becomes more painful.
  • The sore is on or near your rectal or groin area.
  • You develop a fever.
  • You notice red streaks, which can mean the infection is spreading.
  • You have any of the medical conditions listed above.

Go to a hospital’s Emergency Department if any of these conditions occur with an abscess:

  • Fever of 102°F or higher, especially if you have a chronic disease or are on steroids, chemotherapy, or dialysis
  • A red streak leading away from the sore or with tender lymph nodes (lumps) in an area anywhere between the abscess and your chest area (for example, an abscess on your leg can cause swollen lymph nodes in your groin area)
  • Any facial abscess larger than 1 cm or a half-inch across

Exams and Tests

The doctor will take a medical history and may ask you:

  • How long the abscess has been present
  • If you recall any injury to that area
  • What medicines you may be taking
  • If you have any allergies
  • If you have had a fever at home

The doctor will examine the abscess and surrounding areas. If it is near your anus, the doctor will perform a rectal exam. If an arm or leg is involved, the doctor will feel for a lymph gland either in your groin or under your arm.

Medical Treatment

The doctor may open and drain the abscess.

  • The area around the abscess will be numbed with medication. It is often difficult to completely numb the area, but local anesthesia can make the procedure almost painless.

  • The area will be covered with an antiseptic solution and sterile towels placed around it.
  • The doctor will cut open the abscess and totally drain it of pus and debris.
  • Once the sore has drained, the doctor may insert some packing into the remaining cavity to allow the infection to continue to drain. It may be kept open for a day or two.
    • A bandage will then be placed over the packing, and you will be given instructions about home care.
    • Most people feel better immediately after the abscess is drained.
    • If you are still experiencing pain, the doctor may prescribe pain pills for home use over the next 1-2 days.
    • You are usually sent home with oral antibiotics.

 

Next Steps: Follow-up

Follow carefully any instructions your doctor gives you.

  • The doctor may have you remove the packing yourself with instructions on the best way to do this. This may include soaking or flushing.
  • Be sure to keep all follow-up appointments.
  • Report any fever, redness, swelling, or increased pain to your doctor immediately.

Prevention

Maintain good personal hygiene by washing your skin with soap and water regularly.

  • Take care to avoid nicking yourself when shaving your underarms or pubic area.
  • Seek immediate medical attention for any puncture wounds, especially if:
    • You think there may be some debris in the wound.
    • The puncture wound was caused by a bite – human, insect or animal.
    • You have one of the listed medical conditions.
    • You are on steroids or chemotherapy.

Outlook

Once treated, the abscess should heal.

  • Many people require antibiotics, but you may not.
  • The pain often improves immediately and subsides more each day.
  • Wound care instructions from your doctor may include wound repacking, soaking, washing, or bandaging for about 7 to 10 days. This usually depends on the size and severity of the abscess.
  • After the first 2 days, drainage from the abscess should be minimal to none. All sores should heal in 10-14 days.

Bilateral Scrofuloderma of the Axilla Masquerading as Hidradenitis Suppurativa | HTML

Hansgeorg Müller, Klaus Eisendle, Bernhard Zelger and Robert Zangerle

Department of Dermatology and Venereology, Medical University Innsbruck, Anichstrasse 35, AT-6020 Innsbruck, Austria. E-mail: [email protected]

Accepted May 26, 2008.

Sir,

Scrofuloderma is a cutaneous manifestation of tuberculosis that results from direct extension of an underlying tuberculous focus, such as lymph node to the overlying skin. It occurs mainly on the skin over the cervical lymph nodes or above the bony areas. The clinical appearance is characterized by subcutaneous nodules that enlarge gradually and suppurate to form sinus tracts, which can become draining fistulas. When strictly confined to the apocrine gland body areas, these clinical features are also the hallmark of hidradenitis suppurativa. We report here a rare case of scrofuloderma of the axillary areas that clinically mimicked chronic hidradenitis suppurativa and that was misdiagnosed for several years.

CASE REPORT

A 97-year-old man was admitted to our department with a several year history of depressed scars in both axillae. Initially, the lesions had appeared as firm, subcutaneous nodules that had been gradually enlarging and had lead to chronic suppuration and ulcer formation. All of the ulcers had completely healed but with disfiguring scarring. With the diagnosis of hidradenitis suppurativa the patient had underwent wide surgical excision of the affected skin, afterwards some of the lesions had recurred locally. On admission, the patient showed no symptoms of focal or systemic infection, and had no history of acute illness or trauma. His past medical history was unremarkable, he was taking no medications. Physical examination revealed a scar tethered to a subcutaneous mass in the right axilla and multiple puckered, hypertrophic scars overlying palpable nodules in the left axilla (Fig. 1). Mild purulent drainage was present. He also had bilateral axillary lymphadenopathy with lymph node calcification and cutaneous fistulas detected by ultrasound. A biopsy showed massive necrosis and abscess formation, and poorly formed caseous tubercles composed of lymphocytes, plasma cells, macrophages, epitheloid cells and multinucleated giant cells (Fig. 2a). Immunohistochemical staining for Mycobacteria revealed the presence of multiple acid-fast bacilli (Fig. 2b). On polymerase chain reaction (PCR) testing, the biopsy specimen was negative. A purified protein derivate (PPD RT 23 SSI 2 T.U.) test showed a strongly positive reaction (20 mm infiltration), systemic examination was unremarkable. The diagnosis of scrofuloderma (Tuberculosis cutis colliquativa) was made and the patient was started on rifampicin, isoniazid and pyrazinamide. Within a month of therapy, the scrofuloderma had resolved. After 8 weeks, the culture from the biopsy became positive for M. bovis. Antibiotic susceptibility testing confirmed an innate resistance against pyrazinamide and therapy was continued with rifampicin and isoniazid for a total of 9 months.

Fig. 1. Bilateral scrofuloderma of the axillary regions caused by Mycobacterium bovis infection. Clinical picture showing depressed hypertrophic scars in the (a) right and (b) left axilla.

Fig. 2. (a) Photomicrograph from a biopsy specimen showing necrosis, abscess formation and caseous tubercles (H&E, original magnification × 100). (b) Mycobacteria staining showing multiple acid-fast bacilli (original magnification × 300).

DISCUSSION

Scrofuloderma is a cutaneous manifestation of tuberculosis that results from breakdown of skin overlying a tuberculosis focus, usually at a lymph node (1). This leads to the formation of “cold abscesses” in the skin that gradually enlarge, result in formation of ulcers and multiple skin fistulas with drainage of purulent discharge (2). Healing occurs very slowly, resulting in irregular, hypertrophic scars. It is often associated with systemic tuberculosis (3). Cervical gland infection (parotidal, submandibular, and supraclavicular regions) seems to be the commonest underlying focus, with the face and neck being the most frequently affected skin sites (4). Not uncommonly, scrofuloderma secondary to bone and joint involvement sometimes presents to the orthopaedic surgeon (5). Tuberculin sensitivity is usually marked.

The onset of hidradenitis suppurativa is usually after puberty, when the apocrine sweat glands start developing, but it can also affect elderly patients. The early lesions are solitary, painful nodules that may persist for weeks or months without any change. If subcutaneous extension occurs, it may appear as indurated plaques. The nodules develop into abscesses and eventually rupture externally, draining purulent material. Healing occurs with dense fibrosis and marked scarring, and recurrences crop up in and around the original site. This leads to chronic sinus formation. In contrast to scrofuloderma, regional lymphadenopathy is characteristically absent.

In the 1930s, 40% of cows in the UK were infected with M. bovis and there were 50,000 new cases of human M. bovis infection every year (6). Transmission to humans occurs usually via infected milk, although it can also occur via aerosol droplets. Actual infections in humans are rare due to pasteurization killing any bacteria in infected milk. However, in areas of the developing world where pasteurization is not routine, M. bovis is a relatively common cause of human tuberculosis (7). It can be transmitted from human to human – there was an outbreak in Birmingham, UK, in 2004 – and from human to cattle (8, 9), but such occurrences are rare. Historically, a high prevalence of scrofuloderma was seen in children infected with M. bovis from contaminated milk.

Our patient was not living in a high-risk population for tuberculosis infection and was therefore considered low-risk. Apart from high age, he had no risk factors for tuberculosis reactivation. Notably, the clinical manifestation was strictly confined to the axillary areas. A detailed medical history revealed that he was raised on a farm in an area with a high prevalence of childhood tuberculosis transmitted via contaminated unpasteurized milk.

In conclusion, clinicians should consider axillary scrofuloderma as a rare differential diagnosis in elderly patients with suspected chronic hidradenitis suppurativa showing an atypical clinical course. In clinically unclear cases, an ultrasound examination and/or a biopsy should be made.

ACKNOWLEDGEMENT

The authors have no funding source for this work to declare or conflict of interest to disclose.

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7. O’Reilly LM, Daborn CJ. The epidemiology of Mycobacterium bovis infections in animals and man: a review. Tuber Lung Dis 1995; 76: 1–46.

8. Griffith AS, Munro WT. Human pulmonary tuberculosis of bovine origin in Great Britain. J Hyg 1944; 43: 229–240.

9. Tice FJ. Man, a source of bovine tuberculosis in cattle. Cornell Vet 1944; 34: 363–365.

Specific Organisms and Therapeutic Regimens

Author

Bao Anh Patrick Dinh Tran, MD Resident Physician, Department of Dermatology, Howard University College of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Mary Piazza Maiberger, MD Assistant Professor of Dermatology, Howard University College of Medicine; Assistant Clinical Professor of Dermatology, George Washington University School of Medicine and Health Sciences; Chief of Dermatology and Residency Program Site Director, Washington DC VA Medical Center

Mary Piazza Maiberger, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, Washington DC Dermatological Society, Women’s Dermatologic Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Jasmeet Anand, PharmD, RPh Adjunct Instructor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief Editor

Thomas E Herchline, MD Professor of Medicine, Wright State University, Boonshoft School of Medicine; Medical Consultant, Public Health, Dayton and Montgomery County (Ohio) Tuberculosis Clinic

Thomas E Herchline, MD is a member of the following medical societies: Alpha Omega Alpha, Infectious Diseases Society of America, Infectious Diseases Society of Ohio

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Med Learning Group<br/>Received research grant from: Regeneron.

Additional Contributors

Joseph U Becker, MD Fellow, Global Health and International Emergency Medicine, Stanford University School of Medicine

Joseph U Becker, MD is a member of the following medical societies: American College of Emergency Physicians, Phi Beta Kappa, Society for Academic Emergency Medicine, Emergency Medicine Residents’ Association

Disclosure: Nothing to disclose.

ICD-10-CM/PCS MS-DRG v34.0 Definitions Manual

L02411Cutaneous abscess of right axilla
L02412Cutaneous abscess of left axilla
L02413Cutaneous abscess of right upper limb
L02414Cutaneous abscess of left upper limb
L02415Cutaneous abscess of right lower limb
L02416Cutaneous abscess of left lower limb
L02419Cutaneous abscess of limb, unspecified
L02421Furuncle of right axilla
L02422Furuncle of left axilla
L02423Furuncle of right upper limb
L02424Furuncle of left upper limb
L02425Furuncle of right lower limb
L02426Furuncle of left lower limb
L02429Furuncle of limb, unspecified
L02431Carbuncle of right axilla
L02432Carbuncle of left axilla
L02433Carbuncle of right upper limb
L02434Carbuncle of left upper limb
L02435Carbuncle of right lower limb
L02436Carbuncle of left lower limb
L02439Carbuncle of limb, unspecified
L02511Cutaneous abscess of right hand
L02512Cutaneous abscess of left hand
L02519Cutaneous abscess of unspecified hand
L02521Furuncle right hand
L02522Furuncle left hand
L02529Furuncle unspecified hand
L02531Carbuncle of right hand
L02532Carbuncle of left hand
L02539Carbuncle of unspecified hand
L02611Cutaneous abscess of right foot
L02612Cutaneous abscess of left foot
L02619Cutaneous abscess of unspecified foot
L02621Furuncle of right foot
L02622Furuncle of left foot
L02629Furuncle of unspecified foot
L02631Carbuncle of right foot
L02632Carbuncle of left foot
L02639Carbuncle of unspecified foot
L02811Cutaneous abscess of head [any part, except face]
L02818Cutaneous abscess of other sites
L02821Furuncle of head [any part, except face]
L02828Furuncle of other sites
L02831Carbuncle of head [any part, except face]
L02838Carbuncle of other sites
L0291Cutaneous abscess, unspecified
L0292Furuncle, unspecified
L0293Carbuncle, unspecified
L03011Cellulitis of right finger
L03012Cellulitis of left finger
L03019Cellulitis of unspecified finger
L03021Acute lymphangitis of right finger
L03022Acute lymphangitis of left finger
L03029Acute lymphangitis of unspecified finger
L03031Cellulitis of right toe
L03032Cellulitis of left toe
L03039Cellulitis of unspecified toe
L03041Acute lymphangitis of right toe
L03042Acute lymphangitis of left toe
L03049Acute lymphangitis of unspecified toe
L03111Cellulitis of right axilla
L03112Cellulitis of left axilla
L03113Cellulitis of right upper limb
L03114Cellulitis of left upper limb
L03115Cellulitis of right lower limb
L03116Cellulitis of left lower limb
L03119Cellulitis of unspecified part of limb
L03121Acute lymphangitis of right axilla
L03122Acute lymphangitis of left axilla
L03123Acute lymphangitis of right upper limb
L03124Acute lymphangitis of left upper limb
L03125Acute lymphangitis of right lower limb
L03126Acute lymphangitis of left lower limb
L03129Acute lymphangitis of unspecified part of limb
L03211Cellulitis of face
L03212Acute lymphangitis of face
L03213Periorbital cellulitis
L03221Cellulitis of neck
L03222Acute lymphangitis of neck
L03311Cellulitis of abdominal wall
L03312Cellulitis of back [any part except buttock]
L03313Cellulitis of chest wall
L03314Cellulitis of groin
L03315Cellulitis of perineum
L03316Cellulitis of umbilicus
L03317Cellulitis of buttock
L03319Cellulitis of trunk, unspecified
L03321Acute lymphangitis of abdominal wall
L03322Acute lymphangitis of back [any part except buttock]
L03323Acute lymphangitis of chest wall
L03324Acute lymphangitis of groin
L03325Acute lymphangitis of perineum
L03326Acute lymphangitis of umbilicus
L03327Acute lymphangitis of buttock
L03329Acute lymphangitis of trunk, unspecified
L03811Cellulitis of head [any part, except face]
L03818Cellulitis of other sites
L03891Acute lymphangitis of head [any part, except face]
L03898Acute lymphangitis of other sites
L0390Cellulitis, unspecified
L0391Acute lymphangitis, unspecified
L0501Pilonidal cyst with abscess
L0502Pilonidal sinus with abscess
L0591Pilonidal cyst without abscess
L0592Pilonidal sinus without abscess
L080Pyoderma
L081Erythrasma
L0881Pyoderma vegetans
L0882Omphalitis not of newborn
L0889Other specified local infections of the skin and subcutaneous tissue
L089Local infection of the skin and subcutaneous tissue, unspecified
L100Pemphigus vulgaris
L101Pemphigus vegetans
L102Pemphigus foliaceous
L103Brazilian pemphigus [fogo selvagem]
L104Pemphigus erythematosus
L105Drug-induced pemphigus
L1081Paraneoplastic pemphigus
L1089Other pemphigus
L109Pemphigus, unspecified
L110Acquired keratosis follicularis
L111Transient acantholytic dermatosis [Grover]
L118Other specified acantholytic disorders
L119Acantholytic disorder, unspecified
L120Bullous pemphigoid
L121Cicatricial pemphigoid
L122Chronic bullous disease of childhood
L1230Acquired epidermolysis bullosa, unspecified
L1231Epidermolysis bullosa due to drug
L1235Other acquired epidermolysis bullosa
L128Other pemphigoid
L129Pemphigoid, unspecified
L130Dermatitis herpetiformis
L131Subcorneal pustular dermatitis
L138Other specified bullous disorders
L139Bullous disorder, unspecified
L14Bullous disorders in diseases classified elsewhere
L200Besnier’s prurigo
L2081Atopic neurodermatitis
L2082Flexural eczema
L2083Infantile (acute) (chronic) eczema
L2084Intrinsic (allergic) eczema
L2089Other atopic dermatitis
L209Atopic dermatitis, unspecified
L210Seborrhea capitis
L211Seborrheic infantile dermatitis
L218Other seborrheic dermatitis
L219Seborrheic dermatitis, unspecified
L22Diaper dermatitis
L230Allergic contact dermatitis due to metals
L231Allergic contact dermatitis due to adhesives
L232Allergic contact dermatitis due to cosmetics
L233Allergic contact dermatitis due to drugs in contact with skin
L234Allergic contact dermatitis due to dyes
L235Allergic contact dermatitis due to other chemical products
L236Allergic contact dermatitis due to food in contact with the skin
L237Allergic contact dermatitis due to plants, except food
L2381Allergic contact dermatitis due to animal (cat) (dog) dander
L2389Allergic contact dermatitis due to other agents
L239Allergic contact dermatitis, unspecified cause
L240Irritant contact dermatitis due to detergents
L241Irritant contact dermatitis due to oils and greases
L242Irritant contact dermatitis due to solvents
L243Irritant contact dermatitis due to cosmetics
L244Irritant contact dermatitis due to drugs in contact with skin
L245Irritant contact dermatitis due to other chemical products
L246Irritant contact dermatitis due to food in contact with skin
L247Irritant contact dermatitis due to plants, except food
L2481Irritant contact dermatitis due to metals
L2489Irritant contact dermatitis due to other agents
L249Irritant contact dermatitis, unspecified cause
L250Unspecified contact dermatitis due to cosmetics
L251Unspecified contact dermatitis due to drugs in contact with skin
L252Unspecified contact dermatitis due to dyes
L253Unspecified contact dermatitis due to other chemical products
L254Unspecified contact dermatitis due to food in contact with skin
L255Unspecified contact dermatitis due to plants, except food
L258Unspecified contact dermatitis due to other agents
L259Unspecified contact dermatitis, unspecified cause
L26Exfoliative dermatitis
L270Generalized skin eruption due to drugs and medicaments taken internally
L271Localized skin eruption due to drugs and medicaments taken internally
L272Dermatitis due to ingested food
L278Dermatitis due to other substances taken internally
L279Dermatitis due to unspecified substance taken internally
L280Lichen simplex chronicus
L281Prurigo nodularis
L282Other prurigo
L290Pruritus ani
L298Other pruritus
L299Pruritus, unspecified
L300Nummular dermatitis
L301Dyshidrosis [pompholyx]
L302Cutaneous autosensitization
L303Infective dermatitis
L304Erythema intertrigo
L305Pityriasis alba
L308Other specified dermatitis
L309Dermatitis, unspecified
L400Psoriasis vulgaris
L401Generalized pustular psoriasis
L402Acrodermatitis continua
L403Pustulosis palmaris et plantaris
L404Guttate psoriasis
L408Other psoriasis
L409Psoriasis, unspecified
L410Pityriasis lichenoides et varioliformis acuta
L411Pityriasis lichenoides chronica
L413Small plaque parapsoriasis
L414Large plaque parapsoriasis
L415Retiform parapsoriasis
L418Other parapsoriasis
L419Parapsoriasis, unspecified
L42Pityriasis rosea
L430Hypertrophic lichen planus
L431Bullous lichen planus
L432Lichenoid drug reaction
L433Subacute (active) lichen planus
L438Other lichen planus
L439Lichen planus, unspecified
L440Pityriasis rubra pilaris
L441Lichen nitidus
L442Lichen striatus
L443Lichen ruber moniliformis
L448Other specified papulosquamous disorders
L449Papulosquamous disorder, unspecified
L45Papulosquamous disorders in diseases classified elsewhere
L490Exfoliation due to erythematous condition involving less than 10 percent of body surface
L491Exfoliation due to erythematous condition involving 10-19 percent of body surface
L492Exfoliation due to erythematous condition involving 20-29 percent of body surface
L493Exfoliation due to erythematous condition involving 30-39 percent of body surface
L494Exfoliation due to erythematous condition involving 40-49 percent of body surface
L495Exfoliation due to erythematous condition involving 50-59 percent of body surface
L496Exfoliation due to erythematous condition involving 60-69 percent of body surface
L497Exfoliation due to erythematous condition involving 70-79 percent of body surface
L498Exfoliation due to erythematous condition involving 80-89 percent of body surface
L499Exfoliation due to erythematous condition involving 90 or more percent of body surface
L500Allergic urticaria
L501Idiopathic urticaria
L502Urticaria due to cold and heat
L503Dermatographic urticaria
L504Vibratory urticaria
L505Cholinergic urticaria
L506Contact urticaria
L508Other urticaria
L509Urticaria, unspecified
L510Nonbullous erythema multiforme
L511Stevens-Johnson syndrome
L512Toxic epidermal necrolysis [Lyell]
L513Stevens-Johnson syndrome-toxic epidermal necrolysis overlap syndrome
L518Other erythema multiforme
L519Erythema multiforme, unspecified
L52Erythema nodosum
L530Toxic erythema
L531Erythema annulare centrifugum
L532Erythema marginatum
L533Other chronic figurate erythema
L538Other specified erythematous conditions
L539Erythematous condition, unspecified
L54Erythema in diseases classified elsewhere
L550Sunburn of first degree
L551Sunburn of second degree
L552Sunburn of third degree
L559Sunburn, unspecified
L560Drug phototoxic response
L561Drug photoallergic response
L562Photocontact dermatitis [berloque dermatitis]
L563Solar urticaria
L564Polymorphous light eruption
L565Disseminated superficial actinic porokeratosis (DSAP)
L568Other specified acute skin changes due to ultraviolet radiation
L569Acute skin change due to ultraviolet radiation, unspecified
L570Actinic keratosis
L571Actinic reticuloid
L572Cutis rhomboidalis nuchae
L573Poikiloderma of Civatte
L574Cutis laxa senilis
L575Actinic granuloma
L578Other skin changes due to chronic exposure to nonionizing radiation
L579Skin changes due to chronic exposure to nonionizing radiation, unspecified
L580Acute radiodermatitis
L581Chronic radiodermatitis
L589Radiodermatitis, unspecified
L590Erythema ab igne [dermatitis ab igne]
L598Other specified disorders of the skin and subcutaneous tissue related to radiation
L599Disorder of the skin and subcutaneous tissue related to radiation, unspecified
L600Ingrowing nail
L601Onycholysis
L602Onychogryphosis
L603Nail dystrophy
L604Beau’s lines
L605Yellow nail syndrome
L608Other nail disorders
L609Nail disorder, unspecified
L62Nail disorders in diseases classified elsewhere
L630Alopecia (capitis) totalis
L631Alopecia universalis
L632Ophiasis
L638Other alopecia areata
L639Alopecia areata, unspecified
L640Drug-induced androgenic alopecia
L648Other androgenic alopecia
L649Androgenic alopecia, unspecified
L650Telogen effluvium
L651Anagen effluvium
L652Alopecia mucinosa
L658Other specified nonscarring hair loss
L659Nonscarring hair loss, unspecified
L660Pseudopelade
L661Lichen planopilaris
L662Folliculitis decalvans
L663Perifolliculitis capitis abscedens
L664Folliculitis ulerythematosa reticulata
L668Other cicatricial alopecia
L669Cicatricial alopecia, unspecified
L670Trichorrhexis nodosa
L671Variations in hair color
L678Other hair color and hair shaft abnormalities
L679Hair color and hair shaft abnormality, unspecified
L680Hirsutism
L681Acquired hypertrichosis lanuginosa
L682Localized hypertrichosis
L683Polytrichia
L688Other hypertrichosis
L689Hypertrichosis, unspecified
L700Acne vulgaris
L701Acne conglobata
L702Acne varioliformis
L703Acne tropica
L704Infantile acne
L705Acne excoriee
L708Other acne
L709Acne, unspecified
L710Perioral dermatitis
L711Rhinophyma
L718Other rosacea
L719Rosacea, unspecified
L720Epidermal cyst
L7211Pilar cyst
L7212Trichodermal cyst
L722Steatocystoma multiplex
L723Sebaceous cyst
L728Other follicular cysts of the skin and subcutaneous tissue
L729Follicular cyst of the skin and subcutaneous tissue, unspecified
L730Acne keloid
L731Pseudofolliculitis barbae
L732Hidradenitis suppurativa
L738Other specified follicular disorders
L739Follicular disorder, unspecified
L740Miliaria rubra
L741Miliaria crystallina
L742Miliaria profunda
L743Miliaria, unspecified
L744Anhidrosis
L74510Primary focal hyperhidrosis, axilla
L74511Primary focal hyperhidrosis, face
L74512Primary focal hyperhidrosis, palms
L74513Primary focal hyperhidrosis, soles
L74519Primary focal hyperhidrosis, unspecified
L7452Secondary focal hyperhidrosis
L748Other eccrine sweat disorders
L749Eccrine sweat disorder, unspecified
L750Bromhidrosis
L751Chromhidrosis
L752Apocrine miliaria
L758Other apocrine sweat disorders
L759Apocrine sweat disorder, unspecified
L80Vitiligo
L810Postinflammatory hyperpigmentation
L811Chloasma
L812Freckles
L813Cafe au lait spots
L814Other melanin hyperpigmentation
L815Leukoderma, not elsewhere classified
L816Other disorders of diminished melanin formation
L817Pigmented purpuric dermatosis
L818Other specified disorders of pigmentation
L819Disorder of pigmentation, unspecified
L820Inflamed seborrheic keratosis
L821Other seborrheic keratosis
L83Acanthosis nigricans
L84Corns and callosities
L850Acquired ichthyosis
L851Acquired keratosis [keratoderma] palmaris et plantaris
L852Keratosis punctata (palmaris et plantaris)
L853Xerosis cutis
L858Other specified epidermal thickening
L859Epidermal thickening, unspecified
L86Keratoderma in diseases classified elsewhere
L870Keratosis follicularis et parafollicularis in cutem penetrans
L871Reactive perforating collagenosis
L872Elastosis perforans serpiginosa
L878Other transepidermal elimination disorders
L879Transepidermal elimination disorder, unspecified
L88Pyoderma gangrenosum
L89000Pressure ulcer of unspecified elbow, unstageable
L89001Pressure ulcer of unspecified elbow, stage 1
L89002Pressure ulcer of unspecified elbow, stage 2
L89003Pressure ulcer of unspecified elbow, stage 3
L89004Pressure ulcer of unspecified elbow, stage 4

Hand and Arm Guidelines After Your Axillary Lymph Node Dissection

This information describes how to prevent infection and reduce swelling in your hand and arm after your axillary lymph node dissection surgery. Following these guidelines may help prevent lymphedema.

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About Your Lymphatic System

Figure 1. Normal lymph drainage

Your lymphatic system has 2 jobs:

  • It helps fight infection.
  • It helps drain fluid from areas of your body.

Your lymphatic system is made up of lymph nodes, lymphatic vessels, and lymphatic fluid (see Figure 1).

  • Lymph nodes are small bean-shaped glands located along your lymphatic vessels. Your lymph nodes filter your lymphatic fluid, taking out bacteria, viruses, cancer cells, and other waste products.
  • Lymphatic vessels are tiny tubes, like your blood vessels, that carry fluid to and from your lymph nodes.
  • Lymphatic fluid is the clear fluid that travels through your lymphatic system. It carries cells that help fight infections and other diseases.

Axillary lymph nodes are a group of lymph nodes in your armpit (axilla) that drain the lymph fluid from your breast and arm. Everyone has a different number of axillary lymph nodes. An axillary lymph node dissection is a surgery to remove a group of axillary lymph nodes.

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About Lymphedema

Sometimes, removing lymph nodes can make it hard for your lymphatic system to drain properly. If this happens, lymphatic fluid can build up in the area where the lymph nodes were removed. This extra fluid causes swelling called lymphedema.

Lymphedema can develop in the arm, hand, breast, or torso on your affected side (the side where your lymph nodes were removed).

Signs of lymphedema

Lymphedema can develop suddenly or gradually. It can happen months or years after your surgery.

Watch for these signs of lymphedema in your affected arm, hand, breast, and torso:

  • A feeling of heaviness, aching, or pain
  • A tight feeling in your skin
  • Less flexibility
  • Swelling
  • Skin changes, such as tightness or pitting (skin that stays indented after pressing on it)

If you have swelling, you may notice that:

  • The veins in your affected hand are less noticeable than on your other hand.
  • The rings on your affected finger(s) are tighter or don’t fit.
  • The shirt sleeve on your affected side feels tighter than usual.

If you have any signs of lymphedema or aren’t sure, contact your healthcare provider.

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Lowering Your Risk of Developing Lymphedema

It’s important to prevent infection and swelling to lower your risk of developing lymphedema.

Preventing infection

You’re more likely to get lymphedema if you get an infection in your affected arm. This is because your body will make extra white blood cells and lymphatic fluid to fight the infection, and this extra fluid may not drain properly.

Follow these guidelines to lower your risk of getting an infection.

  • Be careful not to get sunburned. Use a sunblock with an SPF of at least 30. Reapply it often.
  • Use insect repellent to avoid stings and bug bites.
  • Use a lotion or cream daily to help protect the skin on your affected arm and hand.
  • Don’t cut your cuticles on your affected hand. Instead, push them back gently with a cuticle stick.
  • Wear protective gloves when doing yard work or gardening, washing dishes, or cleaning with harsh detergent or steel wool.
  • Wear a thimble when you’re sewing.
  • Be careful if you shave under your affected arm. Think about using an electric razor. If you get a cut while shaving, take care of it following the instructions below.

If you notice any signs of infection (such as redness, swelling, skin that’s warmer than usual, or tenderness), call your healthcare provider.

 

Caring for cuts and scratches
  1. Clean the area with soap and water.
  2. Apply antibiotic ointment, such as Bacitracin® or Neosporin®.
  3. Cover the area with a bandage, such as a Band-Aid®.
Caring for burns
  1. Apply a cold pack to the area or run the area under cool tap water for about 10 minutes.
  2. Clean the area with soap and water.
  3. Cover the area with a bandage, such as a Band-Aid.
  4. Preventing swelling

Right after your surgery

Some mild swelling after surgery is normal. This swelling may last for up to 6 weeks. It’s often temporary and will gradually go away. You may also feel pain or other sensations such as twinges and tingling after your surgery. Follow these guidelines to help relieve the swelling after your surgery.

  • Do your exercises 5 times per day. If your healthcare provider told you to do them more or less often, follow their instructions.
  • Keep doing your exercises until you get back your normal range of shoulder and arm movement. This can take 4 to 6 weeks after surgery.
    • If you feel a stretch in your chest or under your arm, it may be helpful to keep doing the stretching exercises for even longer.
    • If you don’t get your normal range of motion back after 4 to 6 weeks, call your healthcare provider.

 

Over the long term

Doing the following things may help lower your risk of developing lymphedema.

  • Ask your healthcare providers to use your unaffected arm for blood draws, injections (shots), intravenous (IV) lines, and blood pressure measurements.
    • In some situations, if blood can’t be drawn from your unaffected arm, it’s OK to use your affected arm. Your healthcare provider can discuss this with you.
    • If an injection can’t be given in your unaffected arm, buttocks, thigh, or abdomen (belly), it’s OK to get it in your affected arm.
    • If your blood pressure can’t be measured using your unaffected arm, it’s OK to use your affected arm.
    • If lymph nodes were removed on both sides of your body, talk with your healthcare provider about which arm is be safest to use.
  • Stay at or safely work towards a healthy body weight.
  • Use your unaffected arm or both arms to carry heavy packages until you get your strength back on your affected side.
  • Exercise and stretch your muscles regularly. Talk with your doctor or nurse about which exercises are right for you.
    • When you start doing exercise and activity again, build up slowly and gradually. If you feel discomfort, stop and take a break. Exercise shouldn’t cause pain.
    • Check with your healthcare provider before you start doing any strenuous exercise, such as lifting weights or playing tennis.
  • Don’t wear tight or heavy jewelry or clothing that has tight elastic and leaves a mark. These things can lead to swelling.
  • Don’t use heating pads or hot packs on your affected arm, shoulder, or torso.
  • If you develop swelling in your arm or hand, make a note of when it started. If it doesn’t go away after 1 week, call your healthcare provider.

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When to Call Your Healthcare Provider

Call your healthcare provider if:

  • Any part of your arm, hand, breast, or torso on your affected side:
    • Feels hot
    • Is red
    • Is more painful
    • Is more swollen
  • You have a fever of 101 °F (38. 3 °C) or higher
  • You’re doing your exercises as instructed by your healthcare provider but don’t get your normal range of motion back after 4 to 6 weeks.
  • You have swelling that doesn’t go away after 1 week.

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90,000 Gostishchev. General Surgery – Page 37

Certain forms of erysipelas, diagnosed on the basis of clinical signs, are essentially phases of the development of the process, the course of which can be suspended at one stage or another.

Clinical manifestations and diagnostics

The disease proceeds with severe clinical manifestations. Violation of the general condition is preceded by the development of local symptoms. A small group of patients has a prodromal period, which is characterized by malaise, weakness, and headache. The disease often begins acutely, with tremendous chills, severe headache. There is a sharp tachycardia, increased respiration, body temperature in a short period reaches 40-41 C. Of the general manifestations of intoxication, insomnia is noted, the amount of urine decreases, protein, erythrocytes, leukocytes, hyaline and granular cylinders are determined in it.

In the blood – pronounced leukocytosis and neutrophilia, moderate anemia, a decrease in the number of eosinophils, however, with the onset of recovery, neutrophilia decreases, eosinopenia disappears, and lymphocytosis appears.Sometimes an enlargement of the liver and spleen can be noted. In some cases, severe intoxication leads to changes in the central nervous system with the appearance of excitement, severe headache, and sometimes delirium.

Local symptoms of erythematous erysipelas are burning pain, a feeling of heat in the affected area, the appearance of bright redness with clear, as if jagged, borders. More often, erysipelas is localized on the face, head, and lower extremities. In outline, the entire affected area is similar to a geographical map, areas of hyperemia resemble flames.The skin in the area of ​​inflammation is edematous, its temperature is increased, pain is more intense along the periphery, there is also a more pronounced redness, the intensity of which gradually decreases in the center of the lesion. In areas where the skin is inactive, tightly connected to the underlying tissues, the redness usually breaks off.

For the bullous form of erysipelas, in addition to the signs of the erythematous form, the appearance of bubbles of various sizes, filled with serous, purulent or hemorrhagic exudate, in which streptococci are detected, is characteristic.The exudate is highly contagious and can become a source of contact transmission of erysipelas. The duration of this form of the disease is usually 1-2 weeks. By the end of the disease, the body temperature drops critically with profuse sweating. After the local inflammation subsides, strong peeling of the epidermis remains, and significant hair loss is noted on the hairy parts of the skin.

In the phlegmonous form of erysipelas, changes on the skin surface (hyperemia, itching, pain) may be less pronounced, but the general symptoms are more pronounced than in the erythematous and bullous forms.The general condition of the patient is severe: tachycardia, high body temperature, chills.

In emaciated, weakened and elderly patients, the disease from a phlegmonous form can turn into a necrotic one, which is characterized by the appearance of skin necrosis – black limited painless dense areas in places of pronounced hyperemia, edema, blisters.

Localization of erysipelas determines some features of the course of the disease. On the face, the process is characterized by facial edema, especially the eyelids. Phlegmonous form of erysipelas

90,000 Publications in the media

Hydradenitis – acute purulent inflammation of the apocrine sweat glands; more often women 30-40 years old are ill.

Etiology • Blockage of the apocrine gland •• Violation of the formation of the apocrine duct in the embryonic period •• Compression of the duct by the dilated secretory part of the gland •• Hyperhidrosis, abrasions, diaper rash •• Bacterial infection: staphylococcus, streptococcus • Hormonal reorganization system • Hormonal reorganization triads of follicle blockage •• Spherical acne •• Exfoliating panniculitis of the head •• Purulent hydradenitis.

Risk factors • Obesity • Diabetes mellitus • Hypercholesterolemia • Slow metabolism • Hypersensitivity to perfumes (eg deodorants).

Pathomorphology • Acute inflammation (in the initial stages of infiltration, then – purulent fusion of the gland) • In the chronic phase – fibrous cords of fistulous tracts, periodically opening; relapses of acute abscesses.

Clinical picture • Dense node (nodes) with a diameter of 0.5-3 cm, located under the skin, then the infiltrate begins to protrude above the skin and acquires a characteristic purple-cyanotic hue • Inflammation can capture several sweat glands or pass from one gland to another • Localization: axillary, anogenital, pubic, peri-umbilical areas, scalp, neck, face • Itching of the skin • Local pain • With the development of an abscess – fluctuation, possibly the formation of a fistulous course • Restriction of movement in the shoulder joint • Body temperature increased • Recovery is accompanied by scarring , the formation of fistulous passages, comedones (blackheads).

Laboratory tests • Normocytic anemia • Leukocytosis • Increased ESR.

Special studies – sowing of culture from the outbreak: staphylococci, streptococci, E. coli , Proteus, in case of chronic course – anaerobic saprophytic flora.

Differential diagnosis • Furunculosis • Axillary lymphadenitis • Specific infections • Lymphogranulomatosis • Lymphosarcoma • Adverse reactions to antibiotics • Inflammatory bowel disease with anogenital fistulas.

TREATMENT

Management tactics • Local treatment with disinfectants (bactericidal soap), antiseptic preparations • Elimination of local factors causing blockage of the follicle (hygiene procedures) • Symptomatic treatment of acute manifestations.

Indications for hospitalization • The severity of the inflammatory syndrome, the stage of abscess formation and the need for surgery under general anesthesia, age over 60 years, the presence of severe concomitant pathology • With small inflammatory foci and their superficial location, local anesthesia is possible for surgical treatment and subsequent outpatient observation • After surgery, patients are hospitalized in the department of purulent surgery.

Surgical treatment • Opening and drainage of the lesion • Excision of the affected tissues, fistulous passages • Curettage (cleansing), electrocoagulation, carbon dioxide laser • With prolonged course and ineffectiveness of therapy, excision and transplantation of skin from healthy areas are indicated.

Drug therapy

• Antibiotics: •• Tetracycline 250 mg 4 r / day or 500 mg 3 r / day, or •• doxycycline on the first day, 100 mg 2 r / day, then 100 mg 1 r / day, or •• erythromycin 0.25 g 4 r / day orally for 7-14 days •• Clindamycin 2% solution in the form of lotions •• Neomycin in the form of an ointment •• Other antibiotics, depending on the sensitivity of the microflora.

• NSAIDs, for example diclofenac 25 mg 2 r / day.

• Local application of 2% boric alcohol or 10% camphor alcohol, dimethyl sulfoxide solution (1: 5). Physiotherapy treatment: dry heat, UFO.

• Specific immunotherapy – staphylococcal vaccine, toxoid, g -globulin.

Complications • Phlegmon • Lymphedema • Contractures • Squamous cell carcinoma in the fistulous passages • Dissemination of infection • Arthritis.

Course and prognosis • Most often the course is long-term recurrent • Spontaneous resolution is rare • Separate foci resolve slowly (10-30 days) • Progression of scarring • Formation of fistulous tracts.
Prevention • Hygiene measures: appropriate clothing for environmental conditions (temperature, humidity), wearing tight clothing should be avoided • Normalization of body weight in obesity • Thorough toilet of the armpits • Elimination of irritating perfumery and cosmetic substances.

Synonyms • Tuberous abscess • Bitch udder

MKD-10 • L73.2 Purulent hydradenitis

Purulent hydradenitis – Symptoms, diagnosis and treatment

Chronic inflammatory skin disease, predominantly affecting the contiguous areas of the body (ie, axillary region, groin, perineum and area under the mammary gland).

Treatment often requires an interdisciplinary approach. Consideration should be given to contacting an appropriate specialist early to discuss therapeutic and surgical options.

Drug treatment is divided into 4 main categories: antibiotics, anti-inflammatory drugs, hormonal agents, and systemic retinoids. Longer use of antibiotics is necessary for effective treatment.

Using only incision and drainage will lead to relapse of the disease.

May cause significant morbidity with scarring, chronic pain, lymphedema and social stigma. With an uncontrolled course, the disease can be complicated by sepsis and transform into cutaneous squamous cell carcinoma.

Purulent hydradenitis (HH) is a chronic inflammatory dermatosis that primarily affects the contiguous areas of the body (armpit, groin, perineum and sub-mammary glands). [1] Jemec GB.Clinical practice. Hidradenitis suppurativa. N Engl J Med. 2012; 366: 158-164.
http://www.ncbi.nlm.nih.gov/pubmed/22236226?tool=bestpractice. com
[2] Lee RA, Yoon A, Kist J. Hidradenitis suppurativa: an update. Adv Dermatol. 2007; 23: 289-306.
http://www.ncbi.nlm.nih.gov/pubmed/18159906?tool=bestpractice.com
Although the name and definition imply that the disease originates in the sweat glands, the pathogenesis is likely to be built around hair follicles, with the involvement of the sweat glands as a minor constituent.It is a constituent of the “follicular occlusive tetrad”, which includes nodular-cystic acne, exfoliating cellulite of the scalp, pilonidal cysts and HH. Clinically, the disease presents with inflammatory papules, nodules and abscesses that can lead to scarring. [3] Jemec GB. Hidradenitis suppurativa. J Cutan Med Surg. 2003; 7: 47-56.
http://www.ncbi.nlm.nih.gov/pubmed/12457209?tool=bestpractice.com
Drainage of pus and the presence of fistulous tracts are typical for more advanced variants of the disease

Articles and recommendations

In this section, visitors can familiarize themselves with the recommendations of the clinic’s doctors on care procedures, learn about new products in cosmetology, get other useful information from the articles published by our specialists

Atheroma or epidermal cyst

Atheroma (epidermal cyst) is a benign neoplasm, a subcutaneous cyst filled with a pasty substance, containing sebum and desquamated epithelium (Fig. one). On the skin above the neoplasm, a hole is often noticeable, from which, when pressed, a discharge with an unpleasant odor is released. Sometimes atheromas are multiple.

Fig. 1.http: //www.mgido.ru/hirurgiya/ateroma.php

The peak of the appearance of atheroma falls on 20-30 years. In men, atheromas are twice as common. Typically, epidermal cysts are found on the scalp, face, ears, neck, shoulders, back, and chest.

Atheroma is terrible not so much for its presence as for the risk of complications. When an infection enters the atheroma, the contents increase in volume, soft tissues swell, and pain joins. Purulent inflammation leads to an abscess or phlegmon, which can lead to sepsis. Sometimes atheroma becomes a chronic focus of infection. It is extremely rare for epidermal cysts to become malignant.

For the diagnosis of atheroma (epidermal cyst), a survey and examination of the surgeon is enough. In some cases, it is required to additionally conduct an ultrasound examination, consultation of an oncologist and a dermatologist.

During the period of inflammation, radical removal of atheroma is sharply difficult, therefore, surgical treatment is limited only to the opening and drainage of the cyst. Therefore, it is recommended to remove epidermal cysts only by surgery in a planned manner until signs of inflammation appear.

Before the operation, the doctor will definitely ask about the tolerance of drugs, the presence of allergies, concomitant diseases, for example, diabetes mellitus, about taking drugs that affect the blood coagulation system.The latter may be a contraindication to surgery. In accordance with generally accepted treatment protocols, he will prescribe a preoperative laboratory examination.

The operation to remove atheroma is performed, as a rule, on an outpatient basis, under local anesthesia. The duration of the actual surgical intervention is 15-25 minutes, but the total time taken together with the preparation, followed by the application of a bandage, and the paperwork is 45-70 minutes.

Fig. 2.https://slingers.ru/ateroma-ili-kista-salnoi-zhelezy-chto-eto-i-kak-s-etim.html

Planned surgery allows you to completely relieve the patient of atheroma and usually follows the following algorithm:

  1. Preparation and treatment of the operating field with disinfectants.
  2. Anesthesia of the area around the atheroma with local anesthetics.
  3. An incision is made over the atheroma.
  4. Further, the atheroma is isolated and exfoliated.Atheroma can be removed in two different ways: without breaking the entire membranes, or with the extraction of the contents of the atheroma in the first place and the membranes in the second. The latter method is used if a small skin incision is made or the atheroma is fragmented.
  5. Next, hemostasis is carried out – that is, they stop bleeding from damaged vessels, if any.
  6. Treat the wound with disinfectants.
  7. Apply sutures to the wound if required. Depending on where the atheroma was located, absorbable, cosmetic, ordinary or reinforced sutures are applied (especially on parts of the body that are actively involved in the movement of the body, for example, in the armpits and on the lower back).
  8. Apply an aseptic dressing to the wound or a sticker, depending on the location of the former atheroma. Do not bandage for small incisions or on the scalp.

A small scar remains in the area of ​​the incision, which is finally formed within a year.

Be sure to consult a qualified surgeon or dermatologist at the Medical and Cosmetology Clinic at the address: Omsk, st. Irtysh embankment 39, tel.8 (3812) 31-47-00.

Information prepared by a surgeon, candidate of medical sciences Kolesnikova Irina Vladimirovna.

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90,000 Make an ultrasound of the mammary glands in Bryansk: prices, preparation

Ultrasound of the mammary glands is a method for detecting benign and malignant formations, other pathological processes (inflammation, abscess) in the mammary gland. The method is absolutely harmless, it is widely used both as an independent method and in combination with mammography (X-ray examination of the mammary glands).It is especially relevant for preventive examinations of women with the aim of early detection of breast cancer.

Indications for ultrasound

To prevent the development and avoid complications of the above diseases, an ultrasound of the mammary glands is prescribed for the following symptoms and complaints of the patient:

  • enlarged lymph nodes in the armpit;
  • swelling and seals in the mammary glands, in the armpits, in the area of ​​the shoulders from the side of the chest;
  • puckered, inverted, swollen, or hardened nipples;
  • peeling of the skin in the area of ​​the mammary glands;
  • bloody or purulent discharge;
  • changes in the volume, shape, or structure of the breast;
  • pain and discomfort in the area of ​​the glands;
  • the formation of cavities in the mammary glands, when raising the arms up.

In addition to the listed symptoms, breast ultrasound diagnostics is mandatory for women before or after breast augmentation, reduction and removal (full or partial) operations. Ultrasound diagnostics can be used to monitor the position of the needle during biopsy.

Preparation for ultrasound examination

Breast ultrasound does not require any special preliminary preparation. But for a more objective assessment of the condition of the breast, it is recommended to conduct a study 8-12 days from the onset of menstruation.If a woman is taking hormonal contraceptives or is already in menopause, the time of the procedure does not matter.

Prices
Breast ultrasound 650

Hydradenitis – Medical portal “Healthy Chuvashia”

Hydradenitis

Hydradenitis (popularly called “bough udder”) is a purulent inflammation of the sweat glands.

Most often, hydradenitis occurs in the armpit, where there are not only many sweat glands, but they are very large and have a tortuous course.

Hydradenitis differs from a boil in the absence of a rod – a central necrotic focus characteristic of a boil. However, despite the ease of diagnosis and the simplicity of the structure of the abscess, the treatment of hydradenitis is no less complicated, and in some cases, much more difficult and longer than other abscesses.

Causes of hydradenitis

Predisposed to hydradenitis:

people with excessive sweating suffering from certain endocrine diseases (diabetes mellitus, diseases of the thyroid gland, pancreas, adrenal glands, pituitary gland) suffering from skin diseases (dermatitis, eczema, diaper rash) who do not sufficiently monitor the cleanliness of the body or abuse deodorants working in dirty conditions

Small skin lesions (abrasions, scratches, for example, when shaving the armpits), which, if personal hygiene rules are not followed, create conditions for the penetration of infectious agents (mainly staphylococci and streptococci) into the ducts of the sweat glands, also predispose to the disease with hydradenitis.

Signs of hydradenitis

Usually, the disease begins with the appearance of one or more painful spherical seals in the thickness of the skin of the armpit. Then they gradually increase, rising above the surrounding skin. The skin in this place becomes purple-red or bluish-purple. The pain gets worse.

Increase in body temperature is often absent, although malaise is sometimes observed.

As the inflammatory process develops in the center, softening appears and one or more narrow holes are formed, through which pus is abundantly secreted.

Hand movements are painful in this case.

Often, inflammation affects several sweat glands or passes from one gland to another, and a large number of inflammatory foci are formed in the armpit, which merge into a dense infiltrate that occupies the entire armpit.

As a result of this, the armpit acquires a characteristic appearance, which is popularly called “bough udder”.

With the involvement of the surrounding subcutaneous fatty tissue in the process, phlegmon may develop, with the involvement of lymph nodes – lymphadenitis.

In this case, the purulent process is accompanied by severe soreness, fever, headache, weakness.

With inadequate treatment, reduced immunity, hypovitaminosis, the process can take on a chronic relapsing course, forming whole conglomerates of inflammatory nodes at different stages of development, which lead to very serious consequences, including sepsis and death.

Diagnosis of hydradenitis

The clinical picture of hydradenitis is so typical that it is not difficult for a doctor to establish a diagnosis.The obligatory moment of diagnostics is the tank. sowing secretions on flora and sensitivity.

Treatment of hydradenitis

It is necessary to start the treatment of hydradenitis before the disease is started, and therefore, to consult a doctor in a timely manner, without bringing the matter to an abscess, which already requires surgical intervention.

In case of improper or late treatment, exacerbation of hydradenitis can be repeated dozens of times.

With a timely and competent approach to treatment, recovery occurs within 7-14 days on an outpatient basis, although in some cases the terms are lengthened and inpatient treatment is required.

With the formation of an abscess, there is only one way of treatment – immediate surgical intervention:

Adequate opening of the abscess, evacuation and drainage of pus Antibiotic therapy taking into account the sensitivity of the microflora Daily ointment dressings with
antiseptics and physiotherapy When the process spreads to adjacent tissues, radical excision of the focus of infection in a hospital under anesthesia with subsequent forced limitation of limb mobility is necessary. shows specific immunotherapy, restorative and vitamin therapy.

Warming compresses are prohibited, as they contribute to the spread of infection.

In any case, treatment should be carried out under the supervision of a qualified physician.

Do not open or squeeze out hydradenitis yourself! This always leads to serious consequences in the form of the spread of infection up to sepsis (pus in the blood), the appearance of abscesses not only in the subcutaneous tissue, but also in the lungs, liver, spleen, brain, kidneys. This is often the cause of death, especially in childhood and old age.

Source: subscribe.ru

Mastitis | SHiFA Medical Center

Content

Inflammation of breast tissue is not always associated with pregnancy and breastfeeding. What is this disease, why does it occur and what methods of prevention are there?

What is mastitis

Mastitis is an inflammation of the mammary glands. The process can be limited to the milk ducts or also spread to the glands located in the areola area.As a rule, the disease begins with a phase of serous inflammation, and then turns into a purulent form. With the accumulation of pus in the tissues of the mammary gland, abscesses are found. The most severe form of mastitis is accompanied by thrombosis (clogging) of vessels with foci of necrotic changes.

A distinctive feature of mastitis – the disease usually develops in one mammary gland. Bilateral mastitis practically does not occur.

In the etiology of non-lactational mastitis: low immunity, frequent colds, hypothermia, infection.

Disease statistics

According to data published in WHO, the incidence of mastitis among women during lactation does not exceed 10%, but can go up to 30%. The most dangerous is considered to be 2 and 3 weeks after childbirth. Moreover, 95% of all cases of lactational mastitis occur in the first 12 weeks.

Mastitis not associated with the lactation period is much less common (10-15% of all cases). Approximately 75% of non-lactational mastitis occurs between the ages of 14 and 45.The study authors note that 50% of women with non-lactational mastitis had a history of multiple abortions or short lactation.

Despite the fact that non-lactation mastitis is rare, every woman should remember that there is always a risk of breast inflammation. Therefore, at the first signs of the disease, it is imperative to consult with a mammologist and start treatment.

Types of mastitis

Depending on the increase in symptoms, the course and duration of the disease, 2 forms of mastitis are distinguished:

  • sharp
  • chronic

The disease always begins to develop in an acute form and is successfully treated in the early stages.But if it is not diagnosed and not treated, then it becomes chronic.

According to the period in which the disease develops, mastitis happens:

  • lactation
  • non-lactation

The cause of lactational mastitis in most cases is an infectious agent (mainly staphylococcus aureus). The infection can come from the outside, for example, through cracks in the nipples due to inappropriate breastfeeding. Another way is hematogenous, associated with the presence of the pathogen in the body of the mother herself.Also, lactational mastitis can be caused by lactostasis – stagnation of milk in the milk ducts.

Non-lactational mastitis is associated with infections, reduced immunity and hypothermia. Also, one of the causes of mastitis is a violation of hormonal imbalance in endocrine disorders and diseases of the female genitourinary system.

The following types of mastitis are distinguished by morphological characteristics:

  • serous
  • infiltrative
  • purulent
  • phlegmonous
  • abscess
  • infiltrative-purulent: diffuse, nodular

This division of the disease is conditional, because one form of mastitis quickly turns into another, some patients have a mixed form, that is, areas of inflammation with different morphological signs are found.

Clinical picture

If acute mastitis begins with stagnation of milk in the postpartum period, then the woman first feels a slight heaviness, chest pain. On palpation in any of the lobules, a large induration is clearly felt. After expressing, there is a short-term relief, but then the symptoms begin to increase again. The body temperature may also rise slightly.

With mastitis caused by staphylococcus, the disease manifests itself sharply and more clearly. The body temperature rises, weakness, chills are felt.The pain in the chest is sharp, sometimes unbearable. The mammary gland swells and grows in size. Omission of early treatment of serous mastitis leads to an infiltrative form, and after a couple of days – to a purulent form. With a purulent form with phlegmons, the body temperature can rise to 40-41 °. This condition is a threat to a woman’s life, so the patient must be hospitalized immediately.

In chronic mastitis, the clinical picture is usually mild. During the period of exacerbation, the body temperature rises, hyperemia of the skin appears (pink or red spots), under which painful seals are felt.The nipple may also retract. Usually the lymph nodes from the armpit are inflamed.

Diagnosis of the disease

In case of discomfort, pain, skin flushing, breast lumps, it is urgent to see a mammologist. To clarify the diagnosis and differential diagnosis with breast cancer, an examination is performed. The doctor prescribes a general clinical blood test, bacteriological culture of secretions from the nipple, ultrasound of the mammary glands, mammography, MRI and other studies.

Tactics and methods of treatment

Non-suppurative forms of mastopathy are treated with conservative methods. It can be antibacterial therapy, anti-inflammatory drugs, physiotherapy. During lactation, feeding is not stopped, but only from a healthy breast. All milk is carefully expressed from the inflamed breast so that it does not stagnate.

For purulent mastitis, antibiotics, immunostimulants, and physiotherapy are prescribed. Feeding is sometimes continued with a healthy breast, and all milk is expressed from the inflamed breast without a trace.

In any form of mastitis, it is absolutely impossible to stop treatment without the permission of a doctor, even if the symptoms have almost completely disappeared. The mammary gland is prone to recurrence of inflammation. Therefore, if an infection remains in the tissues, then there is a great risk that the body will not cope with it on its own and acute mastitis will turn into a chronic form.

If foci with purulent contents are found in the mammary gland, then they are opened. During the operation, pus and necrotic tissue areas are removed.In surgical treatment, samples of the removed tissue are sent for histological examination to rule out a malignant neoplasm (breast cancer).

Methods of prevention of mastopathy

  • breastfeeding at the request of the baby, no regimen
  • observance of hygiene (first of all, it is a thorough treatment of cracks and abrasions on the nipples)
  • increasing immunity

Would you like to learn about the prevention of mastitis and consult a mammologist? Are you worried about chest pains, nipple discharge? Do you have a fever, chills, and chest fullness and pain? Call us right now and come urgently to the appointment! Remember that inflammatory diseases of the breast are rapid and very dangerous.