Specific chronic lymphangitis includes tuberculous, syphilis, leprosy, fungal, and parasitic forms filaria type. In particular for the tuberculous forms, the lymphatic vessels play an important role. The vessel walls are thickened and disseminated with tubercles and the lumen may also contain caseous material. Large numbers of bacilli can be disseminated in the lumen of the thoracic duct, leading to generalized miliary tuberculosis.
Heartworm disease infestation is found in tropical climates India, Brazil, China and is most commonly caused by Wuchereria Bancrofti and Brugia Malayi. Lymphatic and lymph node damage occurs when the parasite dies and gets stuck in the lymphatic collectors, causing destruction of the valves and lesions to the vessel wall.
Lymphadenitis can also be divided into acute and chronic forms and, in most cases, represents a satellite manifestation of the inflammatory-infectious process of the native site. Acute lymphadenitis includes the hyperemic-edematous or hyperplastic form and the purulent form. In hyperplastic lymphadenitis, the lymph nodes are swollen and have a soft consistency due to edema and hyperaemia, with the presence of enlarged macrophages in phagocytic activity and serous fluid containing lymphocytes, blood cells and granulocytes.
Other frequent features in inflammatory states of the lymph nodes are histiocytosis of the sinuses and hyperplasia of the lymphatic follicles follicular lymphadenitis.
Purulent lymphadenitis is characterized by suppurative or suppurative-necrotic foci. Suppurative outbreaks, at first punctiform, can then flow together giving rise to abscesses that can involve the whole lymph node and also the capsule periadenitis and the surrounding tissues phlegmonic, peri-glandular or adeno-phlegmonic. It can also form cutaneous fistulas or fistulas towards internal organs bronchi, esophagus, peritoneum.
Nonspecific chronic lymphadenitis is characterized by proliferative and sclerotic phenomena. The lymph nodes are increased in volume and consistency and, in addition to histiocytosis of the sinuses, hypertrophy of the germinal centers of the follicles and proliferation of the reticular cells of the pulp, there is a thickening of the capsule, trabeculae and reticular mesh, with consequent reduction in the lymphocyte number.
The lymphoglandular structure in advanced stages is subverted by a process of progressive sclerohyalinosis. Among the specific forms of chronic lymphadenitis, the tuberculosis form is further distinguished into a nodular epithelioid form the lymph node appears sprinkled with grayish nodules, the typical tubercles, consisting mainly of giant epithelioid cells like Langhan cells and in a caseous form when the caseosis is massive, the lymph nodes, increased in volume and consistency, often appear grouped in large packs and have a white-yellowish and friable surface, seeming like cooked potato.
The evolution of the lesions is represented mainly by the total or partial calcification of the caseous masses, which remain encapsulated by a capsular and pericapsular connective reaction. On the contrary, if the caseous substance undergoes a softening phenomena, associated with a process of caseous peri-adenitis, it is possible for it to be emptied outwards, or in a serous cavity in a bronchus, in the esophagus, etc. Other forms of specific chronic lymphadenitis include sarcoidosis, syphilis, toxoplasmosis, mononucleosis and lymphadenopathy associated to HIV.
Sarcoidosis is characterized histologically by the presence of characteristic epithelioid granulomas sarcoid nodules in several locations.
The most frequently affected organs are the lymph nodes benign lymphogranuloma or Besnier-Boeck-Schaumann disease , lung, skin, eyes and bones. In syphilitic lymphadenitis, the lymph nodes may be affected by syphilitic infection in all three stages of the disease: conspicuous hyperplasia of lymphatic follicles, inflammatory changes of the parenchymal, hilar and capsular vessels, periadenitis and an increase in reticular fibers pulp and collagen trabeculae and capsule.
In toxoplasmosis, the lymph nodes mostly cervico-nuchal have increased volume and consistency, with conservation of the lymph node architecture and the presence of numerous micronodules of epithelioid histiocytes in the pulp and secondary follicles, hyperplasia of lymphatic follicles, immature histiocytosis of the sinuses, and plasmocytic hyperplasia. Mononucleosic lymphadenitis is characterized by moderately increased lymph node volume, with pulp hyperplasia, which is characteristized by heterogeneity of the cell population lymphocytes, reticular cells, plasma cells, immunoblasts, etc.
In HIV, there are 4 evolutionary degrees of lymphadenopathy:. We recognize two forms of acute lymphangitis: the reticular or diffused erysipeloid and the truncular, depending on whether the vessels of the dermal network are involved or the lymphatic collectors are directly involved.
The superficial lymphangitis dermato-lymphangitis is also distinguished from the deep form by the involvement of the subfascial lymphatic structures. Protein-rich lymphatic fluid serves an excellent medium for the growth of many bacterial strains. Furthermore, stagnation of lymphatic fluid due to impaired lymph drainage accompanied by reduced lymphatic clearance can cause a decrease in local immunity, increasing the cellulitis risk [ 25 , 26 ].
In patients without lymphedema, cellular material produced by bacteria is eliminated by phagocytosis and then it is effectively cleared through lymphatic drainage. However, in lymphedema patients, bacterial toxins in lymphatic tissue that cannot be drained sufficiently cause systemic symptoms due to cytokine release in response to the presence of excessive lymph fluid [ 25 ].
Once bacteria invade the edematous tissue, eradication can be difficult, and there is always a risk of cellulitis recurrence if the local immune system is impaired.
Another study reported that positive blood cultures were more common when cellulitis occurred after lower-extremity lymphedema [ 25 ]. Besides, in the laboratory findings to confirm differential inflammatory changes between the two extremity groups, there were no significant differences in most of the average values and cellulitis with lymphangitis episodes between the patients with upper and lower extremity lymphedema.
Generally, it is difficult to identify inflammatory changes based on WBC count, ESR, or CRP in cases of cellulitis with lymphangitis, with the exception of severe cases that are accompanied by ulceration, blistering, or systemic symptoms, such as bacteremia or fever.
Thus, most laboratory methods, including blood culture, have a relatively low diagnostic yield in cellulitis. Once bacteria invade the edematous tissue, complete eradication is difficult, and there is always a risk of cellulitis reoccurrence if the local immune system is impaired. To inhibit these pathogenic processes, antibiotics with broad anti-streptococcal activity and immunomodulatory action are used.
In our study, the evaluation of antibiotic treatments was limited to two hospital sites; hence, future studies should assess antibiotic treatment regimes in a larger, more diverse population at a broader scale because there is still no established treatment protocol, and the types of antibiotics used for treating cellulitis with lymphangitis are highly variable. Some additional study limitations should be noted.
First, we did not consider the underlying diseases that can interact with cellulitis, such as allergic dermatitis, diabetes mellitus, or tinea pedis. Second, our study did not include patients with severe symptoms, such as bacteremia with abnormality found in the laboratory findings. Third, we did not account for skin diseases, such as necrotizing fasciitis or erysipelas, other than lymphangitis. Fourth, we did not consider the relative risk for cellulitis according to the grade and stage of lymphedema, nor did we conduct an imaging analysis using methods like lymphoscintigraphy.
Finally, this study was conducted retrospectively in only two regional hospitals and no comparison was made between patients diagnosed with and without cellulitis in lymphedema groups; thus, the results may not be generalizable to all rehabilitation centers. In this study, there was high risk of cellulitis with lymphangitis in patients after occurrence of lower-extremity lymphedema.
Cellulitis in lymphedema patients can worsen the ongoing edema despite continuous treatment; continued worsening increases the possibility of systemic infection, which further increases the need for immediately effective antibiotics to prevent exacerbation of the inflammatory response.
An understanding of the risk for cellulitis will enable physicians to better counsel patients about the prognosis, and it will also facilitate further research on treatment. National Center for Biotechnology Information , U. Journal List Ann Rehabil Med v. Ann Rehabil Med. Published online Apr Find articles by Sae In Park.
Find articles by Eun Joo Yang. Find articles by Dong Kyu Kim. Find articles by Ho Joong Jeong. Find articles by Ghi Chan Kim. Find articles by Young-Joo Sim. Author information Article notes Copyright and License information Disclaimer. Corresponding author. Corresponding author: Young-Joo Sim. Received May 20; Accepted Sep 8. This article has been cited by other articles in PMC. Abstract Objective To evaluate the prevalence and associated factors involved in cellulitis with lymphangitis among a group of Korean patients who were being treated for lymphedema.
Methods This was a retrospective medical record study among 1, patients diagnosed with lymphedema. Results Ninety-nine lymphedema patients experienced complications such as cellulitis with accompanying lymphangitis.
Conclusion The prevalence rate of cellulitis with lymphangitis in patients with lymphedema was 7. Keywords: Cellulitis, Lymphangitis, Lymphedema. Data collection Patient data were extracted and recorded in a case report form CRF.
Table 1 Number of age- and sex-specific cases and total cellulitis a with lymphangitis b cases among patients with lymphedema c. Open in a separate window. M, male; F, female. Table 2 Clinical presentation and characteristics of cellulitis a with lymphangitis b episodes in patients with lymphedema c. Table 3 Prevalence and recurrence rates of cellulitis a with lymphangitis b in patients with lymphedema c. If your institution subscribes to this resource, and you don't have a MyAccess Profile, please contact your library's reference desk for information on how to gain access to this resource from off-campus.
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