Mastitis pathophysiology: Difference between revisions

Jump to navigation Jump to search
m (Bot: Removing from Primary care)
 
(23 intermediate revisions by 5 users not shown)
Line 4: Line 4:


==Overview==
==Overview==
Most clinically significant cases of non-puerperal mastitis start as [[inflammation]] of the ductal and lobular system (galactophoritis) and possibly the immediate surrounding tissue (refer to the image below). Development of non-puerperal mastitis is the result of secretory stasis whereas puerperal mastitis occurs when bacteria, often from patients skin or the baby's mouth/nostrils,<ref>{{cite journal | title=A case-control study of mastitis: nasal carriage of ''Staphylococcus aureus'' | author=Amir LH, Garland SM, Lumley J. | journal=BMC Family Practice. | year=2006 | volume=7 | pages=57 | doi=10.1186/1471-2296-7-57}}</ref> enters a milk duct through a crack in the nipple.
Most clinically significant cases of non-puerperal mastitis start as [[inflammation]] of the ductal and [[lobular]] system and possibly the immediate surrounding [[tissue]]. Development of non-puerperal mastitis is the result of secretory [[stasis]] whereas puerperal mastitis occurs when [[bacteria]], often from the patient's [[skin]] or the baby's [[mouth]]/[[nostrils]],<ref>{{cite journal | title=A case-control study of mastitis: nasal carriage of ''Staphylococcus aureus'' | author=Amir LH, Garland SM, Lumley J. | journal=BMC Family Practice. | year=2006 | volume=7 | pages=57 | doi=10.1186/1471-2296-7-57}}</ref> enters a [[milk]] [[duct]] through a crack in the [[nipple]].
 
<gallery>
Image:Breast.png|Cross-section of the breast: 1) Chest wall, 2) Pectoralis muscles, 3) Lobules, 4) Nipple, 5) Areola, 6) Milk duct, 7) Fatty tissue and 8) Skin
Image:Breast1.jpg|Surface anatomy of the breast
</gallery>


==Pathophysiology==
==Pathophysiology==


===Non-puerperal Mastitis: Pathogenesis===


Most clinically significant cases of non-puerperal mastitis start as [[inflammation]] of the ductal and lobular system (galactophoritis) and possibly the immediate surrounding tissue.  Development of puerperal mastitis occurs when bacteria, often from patients skin or the baby's mouth/nostrils,<ref>{{cite journal | title=A case-control study of mastitis: nasal carriage of ''Staphylococcus aureus'' | author=Amir LH, Garland SM, Lumley J. | journal=BMC Family Practice. | year=2006 | volume=7 | pages=57 | doi=10.1186/1471-2296-7-57 }}</ref> enters a milk duct through a crack in the nipple.
===Anatomy of the breast===
The images below show a general overview of [[breast]] [[anatomy]].


Development of non-puerperal mastitis is the result of secretory stasis in about 80% of cases. The retained secretions can get infected or lead to [[inflammation]] by causing mechanical injury leading to leakage of the [[lactiferous duct|lactiferous ducts]]. [[Autoimmune]] reaction to the [[secretion|secretions]] may also be a factor.
[[Image:Breast.png|thumb|center|Cross-section of the breast - By Original author: Patrick J. Lynch. Reworked by Morgoth666 to add numbered legend arrows. - Patrick J. Lynch, medical illustrator, CC BY 3.0, https://commons.wikimedia.org/w/index.php?curid=2676813]]


===Peurperal Mastitis: Pathogenesis===
1) Chest wall <br>2) Pectoralis muscles <br>3) Lobules <br>4) Nipple <br>5) Areola <br>6) Milk duct <br>7) Fatty tissue <br>8) Skin


Development of Peurperal mastitis occurs when bacteria, often from patients skin or the baby's mouth/nostrils <ref>{{cite journal | title=A case-control study of mastitis: nasal carriage of ''Staphylococcus aureus'' | author=Amir LH, Garland SM, Lumley J. | journal=BMC Family Practice. | year=2006 | volume=7 | pages=57 |    doi=10.1186/1471-2296-7-57 }}</ref> enters a milk duct through a crack in the nipple.


Several mechanisms are thought to lead to the pathogenesis of mastitis as shown below:
* Secretory disease or [[galactorrhea]].
* Changes in [[permeability]] of lactiferous ducts (retention syndrome).
* Blockage of lactiferous ducts, for example duct plugging caused by squamous [[metaplasia]] of lactiferous ducts.
* Trauma, injury.
* Mechanical irritation caused by [[retention syndrome]] or [[Fibrocystic]] Condition.
* [[Infection]].
* Autoimmune reaction to luminal fluid.


Approximately a quarter of patients may be [[hyperprolactinemia|hyperprolactinemic]]. There have been strong association with [[fibrocystic breast disease|fibrocystic condition]] and [[thyroid]] conditions. Up to half of patients may experience transient [[hyperprolactinemia]] possibly caused by [[inflammation]] or treatment and significant number may have abnormally high [[Prolactin]] reserve.<ref name="pmid2918655">{{cite journal| author=Peters F, Schuth W| title=Hyperprolactinemia and nonpuerperal mastitis (duct ectasia). | journal=JAMA | year= 1989 | volume= 261 | issue= 11 | pages= 1618-20 | pmid=2918655 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2918655  }} </ref> <ref name="pmid26179543">{{cite journal| author=Kutsuna S, Mezaki K, Nagamatsu M, Kunimatsu J, Yamamoto K, Fujiya Y et al.| title=Two Cases of Granulomatous Mastitis Caused by Corynebacterium kroppenstedtii Infection in Nulliparous Young Women with Hyperprolactinemia. | journal=Intern Med | year= 2015 | volume= 54 | issue= 14 | pages= 1815-8 | pmid=26179543 | doi=10.2169/internalmedicine.54.4254 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26179543  }} </ref>
'''Surface anatomy of the breast'''


[[TSH]], [[Prolactin]], and [[IGF-1]] are important sytemic factors in galactopoiesis. The significance of these factors in secretory disease is not well documented but it has been asserted that the mechanisms of secretory disease and galactopoiesis are closely related.


Alveolar and ductal [[epithelia]] permeability is mostly controlled by tight junction regulation and is closely linked to galactopoiesis and secretory disease. The tight junctions are regulated by a multitude of systemic (prolactin, [[progesterone]], [[glucocorticoid]]s) and local (intramammary pressure, [[TGF-beta]], [[osmotic]] balance) factors.
[[Image:Breast1.jpg|thumb|center|Surface anatomy of the breast - By Original: Ralf RoletschekDerivative: علاء نجار - Derivative from this file, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=46044299]]


Current smokers have the worst [[prognosis]] and highest rate of recurrent [[abscess]]es.<ref name="pmid20727287">{{cite journal| author=Risager R, Bentzon N| title=[Smoking and increased risk of mastitis]. | journal=Ugeskr Laeger | year= 2010 | volume= 172 | issue= 33 | pages= 2218-21 | pmid=20727287 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20727287  }} </ref>
===Pathogenesis===
====Non-puerperal Mastitis====


[[Acromegaly]] may present with symptoms of non-puerperal mastitis.
Most clinically significant cases of non-puerperal mastitis start as [[inflammation]] of the ductal and [[lobular]] system and possibly the immediate surrounding [[tissue]].


===Microscopic pathology===
Development of non-puerperal mastitis is the result of secretory [[stasis]] in about 80% of cases.  The retained [[secretions]] can get infected or lead to [[inflammation]] by causing mechanical [[injury]] leading to leakage of the [[lactiferous duct|lactiferous ducts]].  [[Autoimmune]] reaction to the [[secretion|secretions]] may also be a factor.


Histopathology of granulomatous mastitis shows characteristic distribution of granulomatous inflammation which remains the gold standard for diagnosis.<ref name="pmid20030652">{{cite journal| author=Ocal K, Dag A, Turkmenoglu O, Kara T, Seyit H, Konca K| title=Granulomatous mastitis: clinical, pathological features, and management. | journal=Breast J | year= 2010 | volume= 16 | issue= 2 | pages= 176-82 | pmid=20030652 | doi=10.1111/j.1524-4741.2009.00879.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20030652  }} </ref>


Histologically, Lupus matitis is seen as lymphocytic lobular panniculitis and hyaline sclerosis of the adipose tissue. Treatment is primarily medical due to exacerbation of disease by surgical intervention. This histologic finding is required to make an accurate diagnosis.<ref name="pmid19098467">{{cite journal| author=Summers TA, Lehman MB, Barner R, Royer MC| title=Lupus mastitis: a clinicopathologic review and addition of a case. | journal=Adv Anat Pathol | year= 2009 | volume= 16 | issue= 1 | pages= 56-61 | pmid=19098467 | doi=10.1097/PAP.0b013e3181915ff7 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19098467  }} </ref>
====Puerperal Mastitis====


===Terminology===
Development of puerperal mastitis occurs when [[bacteria]], often from patients [[skin]] or the baby's [[mouth]]/[[nostrils]],<ref>{{cite journal | title=A case-control study of mastitis: nasal carriage of ''Staphylococcus aureus'' | author=Amir LH, Garland SM, Lumley J. | journal=BMC Family Practice. | year=2006 | volume=7 | pages=57 | doi=10.1186/1471-2296-7-57 }}</ref> enters a [[milk]] [[duct]] through a crack in the [[nipple]].


Depending on appearance, symptoms, aetiological assumptions and histopathological findings a variety of terms has been used to describe mastitis and various related aspects.
Several mechanisms, listed below, are thought to lead to the pathogenesis of mastitis:
* Secretory disease or [[galactorrhea]]
* Changes in [[permeability]] of [[lactiferous duct]]s (retention syndrome)
* Blockage of [[lactiferous duct]]s, for example duct plugging caused by [[squamous metaplasia]] of [[lactiferous duct]]s
* [[Trauma]] or [[injury]]
* Mechanical irritation caused by [[retention syndrome]] or [[Fibrocystic Disease|fibrocystic]] condition
* [[Infection]]
* [[Autoimmune]] reaction to [[luminal]] [[fluid]]


* '''Galactopoiesis:''' means milk production
Approximately a quarter of patients may be [[hyperprolactinemia|hyperprolactinemic]].  There has been a strong association with [[fibrocystic breast disease|fibrocystic condition]] and [[thyroid]] conditions.  Up to 50% of patients may experience transient [[hyperprolactinemia]] possibly caused by [[inflammation]] or treatment and a significant number of patients may have abnormally high [[prolactin]] reserve.<ref name="pmid2918655">{{cite journal| author=Peters F, Schuth W| title=Hyperprolactinemia and nonpuerperal mastitis (duct ectasia). | journal=JAMA | year= 1989 | volume= 261 | issue= 11 | pages= 1618-20 | pmid=2918655 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2918655}}</ref><ref name="pmid26179543">{{cite journal| author=Kutsuna S, Mezaki K, Nagamatsu M, Kunimatsu J, Yamamoto K, Fujiya Y et al.| title=Two Cases of Granulomatous Mastitis Caused by Corynebacterium kroppenstedtii Infection in Nulliparous Young Women with Hyperprolactinemia. | journal=Intern Med | year= 2015 | volume= 54 | issue= 14 | pages= 1815-8 | pmid=26179543 | doi=10.2169/internalmedicine.54.4254 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26179543}}</ref>


* '''Secretory disease:''' this refers to inappropriate secretory activity in the lobular and lactiferous duct system. This frequently leads to galactophoritis.
[[TSH]], [[prolactin]], and [[IGF-1]] are important systemic factors in [[galactopoiesis]].  The significance of these factors in secretory [[disease]] is not well documented but it has been asserted that the mechanisms of secretory disease and [[galactopoiesis]] are closely related.


* '''Retention syndrome (retention mastitis):''' accumulation of secretions in the ducts with mainly intraductal inflammation.  
[[Alveolar]] and ductal [[epithelia]] [[permeability]] is mostly controlled by [[tight junction]] regulation and is closely linked to [[galactopoiesis]] and secretory disease.  The [[tight junctions]] are regulated by a multitude of systemic ([[prolactin]], [[progesterone]], [[glucocorticoid]]s) and local (intramammary pressure, [[TGF-beta]], [[osmotic]] balance) factors.


* '''Galactostasis:''' like retention syndrome where the secret is known to be milk.
[[Acromegaly]] may present with symptoms of non-puerperal mastitis.


* '''Galactophoritis:''' inflammation of the lobular and lactiferous duct system, mainly resulting from secretory disease and retention syndrome.
===Microscopic pathology===
 
* '''Plasma cell mastitis:''' plasma cells from the intraductal inflammation infiltrate surrounding tissue.
 
* '''Duct ectasia:''' this refers to widening of lactiferous ducts. It is relatively common finding in breast examinations and it increases with age. Strongly correlated with cyclic and very strongly with noncyclic breast pain.
 
* '''Duct ectasia syndrome:''' this was formerly used as synonym for nonpuerperal mastitis with recurring breast abscess, nipple discharge and possibly associated fibrocystic condition with blue dome cysts. Recent research shows that duct ectasia is only very weakly correlated with mastitis symptomes (inflammation, breast abscess).
 
* '''Squamous metaplasia of lactiferous ducts:''' This refers to cuboid cells in the epithelial lining of lactiferous ducts that transform ([[squamous metaplasia]]) to squamous epithelial cells. Can be seen in many cases of subareolar abscesses.
 
* '''Subareolar abscess:''' [[abscess]] bellow or in close vicinity of the [[areola]]. Mostly resulting from galactophoritis.
 
* '''Retroareolar abscess:''' deeper (closer to chest) than the lobular ductal  system and thus deeper than a subareolar abscess.


* '''Periductal inflammation (periductal mastitis):''' infiltrative inflammation of the tissue surrounding lactiferous ducts. Almost synonym for subaerolar abscess.
[[Histopathology]] of [[granulomatous]] mastitis shows characteristic distribution of [[granulomatous]] [[inflammation]] which remains the gold standard for diagnosis.<ref name="pmid20030652">{{cite journal| author=Ocal K, Dag A, Turkmenoglu O, Kara T, Seyit H, Konca K| title=Granulomatous mastitis: clinical, pathological features, and management. | journal=Breast J | year= 2010 | volume= 16 | issue= 2 | pages= 176-82 | pmid=20030652 | doi=10.1111/j.1524-4741.2009.00879.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20030652}}</ref>


* '''Fistula:''' is a tract draining an abscess cavity
Histologically, [[lupus]] mastitis is seen as [[lymphocytic]] [[lobular]] [[panniculitis]] and [[hyaline]] [[sclerosis]] of the [[adipose tissue]]. This histologic finding is required to make an accurate diagnosis.<ref name="pmid19098467">{{cite journal| author=Summers TA, Lehman MB, Barner R, Royer MC| title=Lupus mastitis: a clinicopathologic review and addition of a case. | journal=Adv Anat Pathol | year= 2009 | volume= 16 | issue= 1 | pages= 56-61 | pmid=19098467 | doi=10.1097/PAP.0b013e3181915ff7 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19098467}}</ref>
 
* '''Zuska's disease:''' periareolar abscess associated with squamous metaplasia of lactiferous ducts. This may also have associated nipple discharge.


==References==
==References==
{{reflist|2}}
{{reflist|2}}
{{WS}}
{{WH}}


[[Category:Dermatology]]
[[Category:Dermatology]]
[[Category:Needs overview]]
[[Category:Emergency mdicine]]
[[Category:Disease]]
[[Category:Up-To-Date]]
[[Category:Infectious disease]]
[[Category:Infectious disease]]
[[Category:Needs overview]]
[[Category:Gynecology]]
[[Category:Primary care]]
[[Category:Surgery]]
 
{{WS}}
{{WH}}

Latest revision as of 22:39, 29 July 2020

Mastitis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Mastitis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications, and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X Ray

CT

MRI

Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Case Studies

Case #1

Mastitis pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Mastitis pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Mastitis pathophysiology

CDC on Mastitis pathophysiology

Mastitis pathophysiology in the news

Blogs on Mastitis pathophysiology

Directions to Hospitals Treating Mastitis

Risk calculators and risk factors for Mastitis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

Overview

Most clinically significant cases of non-puerperal mastitis start as inflammation of the ductal and lobular system and possibly the immediate surrounding tissue. Development of non-puerperal mastitis is the result of secretory stasis whereas puerperal mastitis occurs when bacteria, often from the patient's skin or the baby's mouth/nostrils,[1] enters a milk duct through a crack in the nipple.

Pathophysiology

Anatomy of the breast

The images below show a general overview of breast anatomy.

Cross-section of the breast - By Original author: Patrick J. Lynch. Reworked by Morgoth666 to add numbered legend arrows. - Patrick J. Lynch, medical illustrator, CC BY 3.0, https://commons.wikimedia.org/w/index.php?curid=2676813

1) Chest wall
2) Pectoralis muscles
3) Lobules
4) Nipple
5) Areola
6) Milk duct
7) Fatty tissue
8) Skin


Surface anatomy of the breast


Surface anatomy of the breast - By Original: Ralf RoletschekDerivative: علاء نجار - Derivative from this file, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=46044299

Pathogenesis

Non-puerperal Mastitis

Most clinically significant cases of non-puerperal mastitis start as inflammation of the ductal and lobular system and possibly the immediate surrounding tissue.

Development of non-puerperal mastitis is the result of secretory stasis in about 80% of cases. The retained secretions can get infected or lead to inflammation by causing mechanical injury leading to leakage of the lactiferous ducts. Autoimmune reaction to the secretions may also be a factor.


Puerperal Mastitis

Development of puerperal mastitis occurs when bacteria, often from patients skin or the baby's mouth/nostrils,[2] enters a milk duct through a crack in the nipple.

Several mechanisms, listed below, are thought to lead to the pathogenesis of mastitis:

Approximately a quarter of patients may be hyperprolactinemic. There has been a strong association with fibrocystic condition and thyroid conditions. Up to 50% of patients may experience transient hyperprolactinemia possibly caused by inflammation or treatment and a significant number of patients may have abnormally high prolactin reserve.[3][4]

TSH, prolactin, and IGF-1 are important systemic factors in galactopoiesis. The significance of these factors in secretory disease is not well documented but it has been asserted that the mechanisms of secretory disease and galactopoiesis are closely related.

Alveolar and ductal epithelia permeability is mostly controlled by tight junction regulation and is closely linked to galactopoiesis and secretory disease. The tight junctions are regulated by a multitude of systemic (prolactin, progesterone, glucocorticoids) and local (intramammary pressure, TGF-beta, osmotic balance) factors.

Acromegaly may present with symptoms of non-puerperal mastitis.

Microscopic pathology

Histopathology of granulomatous mastitis shows characteristic distribution of granulomatous inflammation which remains the gold standard for diagnosis.[5]

Histologically, lupus mastitis is seen as lymphocytic lobular panniculitis and hyaline sclerosis of the adipose tissue. This histologic finding is required to make an accurate diagnosis.[6]

References

  1. Amir LH, Garland SM, Lumley J. (2006). "A case-control study of mastitis: nasal carriage of Staphylococcus aureus". BMC Family Practice. 7: 57. doi:10.1186/1471-2296-7-57.
  2. Amir LH, Garland SM, Lumley J. (2006). "A case-control study of mastitis: nasal carriage of Staphylococcus aureus". BMC Family Practice. 7: 57. doi:10.1186/1471-2296-7-57.
  3. Peters F, Schuth W (1989). "Hyperprolactinemia and nonpuerperal mastitis (duct ectasia)". JAMA. 261 (11): 1618–20. PMID 2918655.
  4. Kutsuna S, Mezaki K, Nagamatsu M, Kunimatsu J, Yamamoto K, Fujiya Y; et al. (2015). "Two Cases of Granulomatous Mastitis Caused by Corynebacterium kroppenstedtii Infection in Nulliparous Young Women with Hyperprolactinemia". Intern Med. 54 (14): 1815–8. doi:10.2169/internalmedicine.54.4254. PMID 26179543.
  5. Ocal K, Dag A, Turkmenoglu O, Kara T, Seyit H, Konca K (2010). "Granulomatous mastitis: clinical, pathological features, and management". Breast J. 16 (2): 176–82. doi:10.1111/j.1524-4741.2009.00879.x. PMID 20030652.
  6. Summers TA, Lehman MB, Barner R, Royer MC (2009). "Lupus mastitis: a clinicopathologic review and addition of a case". Adv Anat Pathol. 16 (1): 56–61. doi:10.1097/PAP.0b013e3181915ff7. PMID 19098467.

Template:WS Template:WH