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The New Zealand Medical Journal

 Journal of the New Zealand Medical Association, 13-February-2009, Vol 122 No 1289

Lymph node infarction and its association with lymphoma: a short series and literature review
Rajpal Singh Punia, Neerja Dhingra, Rajan Chopra, Harsh Mohan, Sandeep Chauhan
Abstract
Aims Lymph node infarction is an extremely rare phenomenon. An infarcted lymph node can proceed, or occur simultaneously with, lymphoma. In the present study we review the literature on lymph node infarction and describe our experience of such cases.
Methods Six cases of lymph nodes with a diagnosis of lymph node infarction were archived from the records of the Pathology Department. Clinical information of the patients was obtained from the case records. Haematoxylin andeosin stained sections were reviewed.
Results A diagnosis of non-Hodgkin lymphoma was made in 5 of the 6 patients. The diagnosis was made concurrent to the lymph node infarction in 2 cases while in 3 cases the diagnosis was made on subsequent follow up biopsies. The aetiology of lymph node infarction could not be established in one case.
Conclusion The pathologist should be cautious when examining an infarcted lymph node. Though all patients might not develop lymphoma, they require a close follow-up and repeat biopsies to detect the subsequent development of lymphoma.

Lymph node infarction, a syndrome of spontaneous coagulative necrosis of lymph nodes is a rare phenomenon because of its abundant vascularity. The condition was first described in man by Davies and Stansfeld way back in 1972.1 It can be due to various non-neoplastic and neoplastic conditions. An infarcted lymph node can proceed, or occur simultaneously with, lymphoma. The incidence of lymphoma in patients with lymph node infarction varies from as high as 89% to as low as 32% in various studies.2–4 In the present short series, we review the literature on lymph node infarction and describe our experience of such cases.

Methods

From the archives of the Pathology Department (Government Medical College and Hospital, Chandigarh, India), cases of lymph nodes with a diagnosis of lymph node infarction were retrieved. Cases studied dated from1998 to 2007. All the cases showed areas of coagulation necrosis with loss of cell nuclei but with well preserved cell outlines, occupying a substantial part or whole of the lymph node. Clinical and follow-up information of the patients were obtained from the case records.
Hematoxylin and eosin (H&E) stained sections were studied. In addition, results of ancillary histochemical and immunohistochemical stains were noted wherever available.
Cases with well recognised infectious aetiologies of lymph necrosis (such as tuberculosis, syphilis, lymphogranuloma venereum, leishmaniasis, or cat-scratch disease) were excluded from the study, as were the cases showing only focal necrosis, which is known to be associated with drug associated intranodal microvasculitis, systemic lupus erythematosus, and other idiopathic vasculitic conditions.

Results

A total of 3938 lymph node biopsies were received during the study period (1998–2007). These included isolated lymph node biopsies as well as nodes removed as part of resection specimens for other pathologies. Out of these only 6 cases were associated with lymph node infarction. The clinical features and pathologic findings of these cases are as follows (Table 1):
Table 1.Clinical profile of cases
Case no.
Age (years)/sex
Site
Interval between first biopsy and final diagnosis
Final diagnosis
1
26/M
Cervical, axillary
1 month
NHL—Diffuse mixed small and large B cell type
2
36/M
Axilllary
6 months
NHL—Diffuse large B cell type
3
51/M
Cervical
Concurrent
NHL—Diffuse large B cell type
4
30/M
Posterior triangle neck
4 months
NHL—Diffuse mixed small and large B cell type
5
35/M
Mesenteric
Concurrent
NHL—Diffuse large B cell type
6
42/F
Cervical
24 months
Reactive lymphoid hyperplasia
NHL=non-Hodgkin lymphoma.
Clinical profile—Cases were distributed over an age range of 26 to 51 years, the mean age being 38.75 years. There were five male patients and one female patient. In five of the six patients, the affected lymph nodes were of the head and neck region while in one patient, mesenteric nodes were involved. Two patients (cases 1 and 2), underwent fine needle aspiration prior to the biopsy. However, the smears showed only necrotic material and a definitive diagnosis could not be established.
Pathologic findings—Nine lymph node biopsies were received from the six patients. The excised lymph nodes were enlarged in size. Cut sections showed widespread necrosis visible to the naked eye in four biopsies. Microscopic examination of the H&E stained sections revealed poorly stained ghost-like cells (Figure 1). There was no evidence of nuclear karyorrhexis or histiocytic infiltration of the necrotic areas. However, histiocytic infiltrates and vascular granulation tissue were seen surrounding the areas of infarction necrosis.
Reticulin stain demonstrated the residual reticulin framework within the necrotic areas. Stains for fungi and acid fast bacilli were negative. The necrotic areas were thus typical coagulative lesions of ischemic type. In five of the six patients a diagnosis of non-Hodgkin lymphoma was made (Figure 2). The diagnosis was made at the same time as the lymph node infarction in two cases (cases 3 and 5), while in two cases (cases 1 and 4) lymphoma was diagnosed on the second biopsy and in one case (case 2) on the third biopsy.
In the latter three cases, the initial biopsies exhibited extensive necrosis without any viable areas sufficient to render a diagnosis. All the five cases were diagnosed as B-cell lymphomas, three were of diffuse large cell type, while the other two were of diffuse mixed small and large cell type. The lymphoma cells were positive for the immunohistochemical stain CD 20 but were negative for CD 3. The aetiology of lymph node infarction could not be established in one case. Subsequent lymph node biopsy of this case showed reactive follicular hyperplasia; this patient was alive with no evidence of lymphoma 2 years after initial presentation.
Figure 1. Photomicrograph showing complete infarction of the lymph node showing eosinophilic cell ghosts (H&E stain, ×100)
Figure 2. Photomicrograph showing a focus of infarction associated with
non-Hodgkin lymphoma (H&E stain, ×200)

Discussion

Lymph nodes constitute a substantial component of the immune system strategically located in various areas of the body. They serve as areas of antigen retention and a site of immunologic education and expansion of lymphocyte populations. As part of this normal function, they react to both endogenous and exogenous substances with a variety of specific morphological and functional responses.5
Spontaneous infarction of lymph nodes, first described by Davies and Stansfeld is a rare occurrence.1 It is characterised by diffuse coagulation necrosis with loss of cell nuclei but, early on, with well preserved cell outlines. It has been estimated that one case of lymph node infarction will be encountered in every 450 lymph node biopsies.3 The reason for the apparent rarity of lymph node infarction may lie in the abundance of the vascular supply and in the well- developed anastomoses. The phenomenon has been reported in association with various neoplastic and non-neoplastic conditions.
The non-neoplastic conditions associated with infarction are polyarteritis nodosa, viral infections, cholesterol atheromatous embolism, thrombosis, gold injections, intestinal volvulus, postmediastinoscopy, and mononeuritis multiplex. Hemorrhagic infarction of hilar lymph nodes has also been reported recently in association with heart lung transplantation. Some cases of lymph node infarction may occur due to vascular compromise or other undetermined causes.6–8 Lymph node infarction may also follow fine-needle aspiration biopsy.4
The neoplastic lesions most commonly associated with infarction are lymphoma and metastatic tumors.2,4 The most frequent association is with lymphoma, even when not apparent at the time of initial presentation; subsequent biopsy will reveal lymphoma in a large number of patients.2,3,4,9–12
The anatomical distribution of these lesions in our study is similar to the other reports showing that majority of the affected nodes were in the head and neck region.3,9 In cases where lymphoma manifests itself subsequent to infarction, it invariably does so within 2 years.2,3 In our patients the diagnosis of lymphoma was made concurrent to nodal infarction in two cases and within a span of 6 months in the other three cases.
Some authors have suggested a pre-lymphomatous potential of lymph node infarction but it is still a matter of debate.2,3,11 The incidence of lymphoma in patients with infarcted lymph nodes ranges from as high as 89% to as low as 32% in various studies.2-4 Cleary et al2 reported the occurrence of lymphoma in 16 (89%) of 18 patients with lymph node infarction while Maurer et al3 found the occurrence of lymphoma in 20 (39%) of 51cases. Two of the patients in the latter report developed Hodgkin’s disease. These authors found a high incidence of large cell lymphomas in such patients as was also seen in three of our five cases.
The incidence of lymphoma in patients of nodal infarction in our series was 83.33% (five of the six cases). All these patients developed non-Hodgkin lymphoma; there was no case of Hodgkin’s disease.
The present short series highlights the diagnostic approach in a case of lymph node infarction. The pathologist should be cautious when examining an infarcted lymph node so as not to miss the correct diagnosis. If the cause of infarction is not apparent in the initial biopsy, the clinician should be alerted. Though all patients might not develop lymphoma, they require close follow-up and repeat biopsies to detect the subsequent development of lymphoma.
Further larger studies are needed to clarify the relationship between infarction and lymphoma.
Competing interests: None known.
Author information: Rajpal Singh Punia, Neerja Dhingra, Rajan Chopra, Harsh Mohan, Sandeep Chauhan*
Departments of Pathology & Internal Medicine*, Government Medical College and Hospital,Chandigarh, India
Correspondence: Neerja Dhingra, Department of Pathology, Government Medical College and Hospital, Sector 32- A, Chandigarh, 160 030. India. Fax: +91 172 2665375; email address: drneerjadhingra@yahoo.co.in
References:
  1. Davies JD, Stansfeld AG. Spontaneous infarction of superficial lymph nodes. J Clin Pathol. 1972;25(8):689–96.
  2. Cleary KR, Osborne BM, Butler JJ. Lymph node infarction foreshadowing malignant lymphoma. Am J Surg Pathol. 1982;6:435–42.
  3. Maurer R, Schmid U, Davies JD, et al. Lymph-node infarction and malignant lymphoma: a multicentre survey of European, English and American cases. Histopathology. 1986;10(6): 571–88.
  4. Strauchen JA, Miller LK. Lymph node infarction. An immunohistochemical study of 11 cases. Arch Pathol Lab Med. 2003;127:60–3.
  5. Elmore SA. Histopathology of the lymph nodes. Toxicol Pathol. 2006;34(5):425–54.
  6. Rao IS, Loya AC, Ratnakar KS, Srinivasan VR. Lymph node infarction-a rare complication associated with disseminated intra vascular coagulation in a case of dengue fever. BMC Clin Pathol. 2005;12(5):11.
  7. Kojima M, Nakamura S, Sugihara S, et al. Lymph node infarction associated with infectious mononucleosis: report of a case resembling lymph node infarction associated with malignant lymphoma. Int J Surg Pathol. 2002;10(3):223–6.
  8. Roberts C, Batstone PJ, Goodlad JR. Lymphadenopathy and lymph node infarction as a result of gold injections. J Clin Pathol. 2001;54(7):562–64.
  9. Toriumi DM, Goldschmidt RA, Wolff AP. Lymph node infarction and malignant lymphoma: a case report. J Otolaryngol. 1988;17(2):128–30.
  10. Angelucci D, Artese L, De Lutiis M, et al. Primary lymph node infarct and malignant non-Hodgkin's lymphoma. Description of a case. Pathologica. 1989;81(1071):83–9.
  11. Bhargava S, Tewari CP, Arun A. Lymph node infarction and lymphoma. Indian J Cancer. 1989;26(4):233–9.
  12. Pietrafitta JJ, Grasberger RC, Deckers PJ, et al. Superficial lymph node infarction. J Surg Oncol. 1983;24(3):212–4.
     
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