Spontaneous infarction of superficial nodes

J. clin. Path., 1972, 25, 689-696

Spontaneous infarction of superficial lymph nodesJ. DOUGLAS DAVIES AND A. G. STANSFELD'

From the Department of Histopathology, St Bartholomew's Hospital, London

SYNOPSIS Five cases of extensive infarction of lymph nodes were traced in just over 16 years'surgical material. All presented with painful swelling in a superficial lymph node chain. None wasdiagnosed clinically; two were interpreted as fibroadenoma of the axillary tail of the breast, and twoas a femoral hernia. Microscopically the lymph nodes in the first three weeks after infarction werecharacterized by extensive necrosis of medullary and cortical lymphoid cells, but the central reticulinarchitecture and a narrow, incomplete rim of viable subcapsular lymphoid tissue were preserved.Reactive perinodal inflammation and the formation of granulation tissue resembled the reaction tomyocardial infarction. The late stage of the lesion was characterized by incomplete regeneration oflymphoid tissue in the lymph nodes. The lesions appeared attributable to thrombosis of veins withinthe substance and the hila of the nodes.

Though experimental infarction of lymph nodes hasbeen produced in dogs (Holman and Self, 1938;Tilak and Howard, 1964; Kister, Conklin, andHabif, 1965) and rabbits (Osogoe and Courtice,1968), spontaneous infarction of previously normallymph nodes in man has rarely been recorded(Holman and Self, 1938). However, such infarction oflymph nodes may be commoner than is generallyappreciated as four cases were found on review ofsurgical material received in one department in thelast 16 years, and the fifth was received during thepreparation of the manuscript of this paper. Theclinical features and microscopic findings of thefive cases are described, and the pathogenesis of thelesions and their morphological evolution areconsidered.

Material and Methods

Sections of lymph nodes classified as showing necro-sis, calcification, circulatory disturbances, andnecrotizing inflammation, received between January1956 and January 1972 in the Department of Histo-pathology, St Bartholomew's Hospital, were re-viewed. Excluded from further consideration werenecroses associated with specific infections, drug-induced hypersensitivity reactions, lymphomata, andmetastatic tumours. From the paraffin blocks ofthose cases selected for further study additionalsections were cut at a nominal depth of 5 ,um. These'Present address: Department of Pathology, University of Bristol,Bristol BS8 1TD. Requests for reprints should be addressed there.Received for publication 4 May 1972.

were stained by Harris' haematoxylin and eosin, andGordon and Sweet's method for reticulin. Whenappropriate PAS, Gram, or Ziehl-Neelsen prepara-tions were examined.

Case Reports

The cases are presented in ascending order of histo-logical maturity. In none of the cases were causativemicroorganisms detected.

CASE 1A 43-year-old woman with a six-month history of alump in the left breast was submitted to mastectomyand axillary clearance for an infiltrating ductaladenocarcinoma of the breast. All 10 lymph nodesfrom the left axilla were free of necrosis and meta-stasis. Postoperative irradiation was not given, but 11days after the mastectomy she complained of apainful lump in the right anterior triangle of theneck. Clinically the pain was attributed to tightbandaging. Three days later, at the time of bilateralo6phorectomy, the swollen nodes in the right anteriortriangle were excised. Subsequently there were nofurther similar symptoms, but a second primarycarcinoma in the right breast was detected 30 monthslater. Six months afterwards tumour recurred in theright chest wall.

HISTOPATHOLOGYSeven lymph nodes (St. B.H. S.H. 3694/67), up to0-8 cm long, were received from the right anteriortriangle of the neck. Microscopically two of the

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nodes were almost entirely necrotic, and a third waspartially necrosed. The remaining four nodesexhibited non-specific reactive enlargement of thefollicular germinal centres and paracortical areas. Intwo instances there was fresh extravation of ery-throcytes into the cortical and medullary lymphsinuses. None of the nodes contained secondarycarcinoma.The two extensively necrotic lymph nodes showed

eosinophilic ghosts of lymphoid cells amidst afibrinous exudate in cortex and medulla (Fig. 1).Only a few peripherally situated lymphoid follicles inthese nodes retained stainable lymphoid cells. In thenecroses the original reticulin architectural patternwas preserved (Fig. 2). The necrosis in the third nodewas similar but it was limited to one pole of thenode.A striking feature of the necrotic nodes was a

corona comprising an exudate of polymorpho-nuclears and fibrin in the perinodal connective tissue.

J. Douglas Davies and A. G. Stansfeld

This inflammatory reaction hugged the edge of thenecrotic nodes and few polymorphonuclears hadcrossed the largely intact marginal sinuses to enterthe necroses. Many extranodal veins and lymphaticvessels were cuffed by a mixed inflammatory infiltratecomprising neutrophil and eosinophil granulocytes,lymphocytes, histiocytes, and a few plasma cells.Numerous small intranodal veins and several extra-nodal veins (Fig. 3) and lymphatic vessels containedfresh occlusive thrombi.

CASE 2A 52-year-old woman presented with a three-dayhistory of a painful lump in the axillary tail of theright breast. Other axillary lymph nodes were notpalpable. Her general health had previously beengood and she was not receiving any drugs. Sixteendays after the onset of symptoms the presumptivefibroadenoma in the axillary tail was excised and onrapid frozen section shown to be a necrotic lymph

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FIG. 1 FIG. 2

Fig. I Case 1: early infarction of lymph node showing small thrombosed veins in node, and perinodal corona of poly-morphonuclears (H & E x 60).Fig. 2 Section adjacent to Figure 1. Retention of reticulin in necrotic lymph node (silver reticulin x 60).


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Spontaneous infarction of superficial lymph nodes

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Fig. 3 Case 1: recent thrombosis of vein close to lymphnode (H & E x 60).

WAiVt.Fig. 4 Case 2: lymph node infarct at 16 days. Foci oflymphocytes survive beneath marginal sinus. Perinodalmononuclear infiltrate (H & E x 60).

Fig. 5 Section adjacent toFigure 4. Focal reticulincondensation close to marginalsinus. Dilatation of deep lymphsinuses (silver reticulin x 60).

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Fig. 6 Case 2: organizing thrombus in hilar vein(H & E x 150).

node. No further similar symptoms have recurred inthe two months since operation.

HistopathologyThe lymph node from the axillary tail of breast(St. B.H. S.H. 513/72), 0 8 cm long, exhibitedwhitish yellow discoloration of its cut surface.Miscroscopy showed extensive necrosis of the node.Only sparse foci of lymphoid cells remained peri-pherally beneath the marginal sinus (Fig. 4) anddeeply around small intranodal arteries and veins.The marginal sinus itself was intact but containednumerous degenerate sinus-lining histiocytes and a

patchy lymph coagulum. Within the necrotic areas ofthe node there was extensive fibrin exudation,thrombosis of the intranodal veins, and necrosis oftheir walls. Despite the widespread nature of thenecroses the reticulin architecture of the central partof the node was retained (Fig. 5). However, theGordon and Sweet's preparations did show dila-tation of the deep lymphatic sinuses and an accen-

tuated reticulin network in the lymphoid tissueimmediately beneath the marginal sinus. Thisperipheral reticulin change was accompanied by


increased vascularity of the superficial cortex of thelymph node.The capsule of the node was thickened, fibrous,

and possessed prominent blood vessels. The peri-nodal connective tissue, particularly in the hilarregion, contained a moderate inflammatory exudate,comprising lymphocytes, plasma cells, histiocytes, afew eosinophils, and fibroblasts and newly formedcapillaries. A mononuclear exudate surroundedmany extranodal veins, and a vein in the hilum wasoccluded by an organizing thrombus (Fig. 6).

CASE 3A 33-year-old woman presented with an eight-dayhistory of a painful lump in the axillary tail of theleft breast. Six years earlier diabetes mellitus hadbeen diagnosed at the time of delivery of a stillborninfant. The lesion in the axillary tail was diagnosedclinically as a fibroadenoma, and 17 days after itsdiscovery was excised under local anaesthesia. Whenlast seen 13 years afterwards diabetes mellitus wassatisfactorilly controlled by insulin and there hadbeen no recurrence of the axillary lesion.

HistopathologyThe lymph node from the axillary tail of the breast(St. B.H. S.H. 3261/56) was 0-6 cm long. Its cutsurface was grey with reddish-brown mottling.Miscroscopically its appearances closely resembledthose seen in case 2. The extensive necrosis of thenode, sparing only an incomplete narrow rim ofperipheral cortical tissue, the preservation of thereticulin architecture in the necroses, and the exten-sive thrombosis of intranodal veins were all asdescribed in the preceding case. Dilatation of thecentral lymph sinuses was, however, much lesspronounced.

In this case the condensation of the reticulinnetwork and vascularity of the peripheral lymphoidtissue were accompanied in many areas by vasculartrabecular anastomoses across the marginal sinus.The appearances suggested well developed communi-cations between the vessels in the periphery of thelymph node and those in the vascular fibrous capsuleand the perinodal connective tissue. In the perinodalareolar tissue were numerous lymphocytes, plasmacells, eosinophils, and histiocytes. Much of thisleucocytic infiltrate cuffed small veins, but throm-bosis was not found in the few large extranodalvessels that were included in the biopsy.

CASE 4A 53-year-old man was admitted as an emergencywith a presumptive diagnosis of a strangulated leftfemoral and an uncomplicated direct left inguinalhernia. An increasingly tender lump in the left groin


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had been noted forabout oneweek. Diabetes mellitus, q56%}jC4> o

necessitating diet and tolbutamide therapy had been 2diagnosed six years earlier. He was also hypertensive g(BP 190/105 mim Hg). Examination showed a directinguinal hernia and enlarged tender inguinal lymph inodes. A focus of infection in the drainage area of theleft inguinal lymph nodes was not detected. Atherniorrhaphy, at least two weeks after the onset ofpain, the most enlarged inguinal lymph node wasexcised. Aerobic and anaerobic cultures of the nodewere sterile, and organisms were not seen in Gramand Ziehl-Neelsen stains of smears from the node. No!,Ufurther episodes attributable to infarction of lymphnodes occurred, but five years later he died after r@ j lErepeated episodes of congestive cardiac failure 3associated with left bundle branch block. Postmortem h1examination was not performed.

Histopathology X D r, < ;J 7A single enlaiged inguinal lymph node (St. B.H.S.H. 2838/61), 2-0 cm long, showed central yellowdiscoloration and softening. Microscopically, as inthe preceding three cases, there was extensive central ,necrosis of the node with ghost-like remnants oflymphoid cells, numerous thrombosed and necroticvenous channels, and a preserved reticulin archi- , *,j§'t 2tecture. Only a small cap of peripheral lymphoidtissue (Fig. 7), including in this instance an intactlymphoid follicle with a germinal centre and a Fig. 8 Case 4: dense reticulin ofgranulation tissuenarrow rim of fibroblasts and lymphoid cells around extending across distorted marginal sinus (top) toa cortical artery, remained viable. necrosis (bottom) (Silver reticulin x 60).

wFig.7 Case 4: infarct(bottom right) bounded bygranulation tissue, and cap

, ~~~ofsurviving lymphoid tissue(upper left) (H & E x 35).

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Closely enveloping the necrotic area, and crossingthe marginal sinus was a band of maturing granu-lation tissue (Fig. 8) comprising numerous fibro-blasts, capillaries, and a mixed infiammatoryinfiltrateof polymorphonuclears, lymphocytes, and histio-cytes. Neither giant cells nor epithelioid granulomatawere, however, present. Venous thrombosis was notfound in the perinodal tissue but several of theextranodal lymphatic vessels were occluded by afibroblastic thickening of the intima. An adjacentmuscular artery, though not thrombosed, exhibitedluminal reduction associated with foamy histiocytesin the intima.

CASE 5A 54-year-old woman with a 25-year history ofvaricose veins complained of a swelling in the leftgroin. The swelling had appeared one year before,accompanied by a tight feeling in the groin, about amonth after both saphenous veins had been tied closeto the sapheno-femoral junctions. Years previouslybilateral stripping of the long saphenous veins,ligations and injection of sclerosing agents had beenperformed. On this occasion a provisional clinicaldiagnosis of a femoral hernia was made, but onexploration a 5 cm-long fibrous-walled cyst wasfound among the inguinal lymph nodes. There wasno sign of a femoral hernia.


HistopathologyAdjacent to the cyst were several pinkish inguinallymph nodes (St. B.H. S.H. 1291/72), up to 2-2 cmlong. Microscopically the cyst proved to be necroticlymphoid tissue surrounded by collagenous, acellularfibrous tissue. It seems likely that this structurerepresented a former lymph node but its internalarchitecture was almost totally lost. The appearancesof the remaining nodes, however, were illuminating(Fig. 9). The lymphoid tissue ofthe surviving inguinallymph nodes was restricted to peripheral islands oflymphoid nodules lacking germinal centres, andscattered perivascular lymphoid aggregates encircledby prominent lymph sinuses. The marginal sinuseswere incomplete. They were particularly discon-tinuous and distorted between the lymphoid nodules,at which point fibrous and vascular trabeculae passedfrom the fibrosed perinodal tissue to the medullaryand hilar region of the nodes. Both medullae andhila of the nodes were bare of lymphoid and plasmacells. They were occupied by anastomosing lymphaticvessels and veins, many of which were occluded bypartially recanalized thrombi. Further vascularabnormalities within the nodes were plexiform areasof recanalization of the marginal and central lymphsinuses and haemosiderin encrustation of the fibroticwalls of small arteries in the cortical lymphoid tissue.Many veins in the perinodal areolar tissue containedold, partially recanalized, occlusive thrombi.

.*., .4- '........, X 1:1- "', 141'.,. . ", '..".----U-.-iL.:.

Fig. 9 Case 5:peripheral islands oflymphoid tissuearound centralanastomosing lymphsinuses andrecanalizingthrombosed hilarvein (H & E x 10).


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Discussion

Despite the challenge implicit in Holman and Self's(1938) provocative statement that infarction oflymph nodes in man 'is a rarity, if it ever occurs', wehave been unable to trace any morphologicaldescription of changes that have been ascribed toinfarction in previously normal lymph nodes.However, infarction of lymphomatous or metastaticneoplasms in lymph nodes is well known. Suchnecrosis of neoplasms may be sufficiently extensiveas to mask the primary pathology. Several cases inour material apart from the five reported here,though not recognized with confidence when firstseen, were found on review to be examples ofinfarcted neoplasms. Reticulin stains of the necrotictissue proved particularly useful in the distinction ofsuch cases.The absence of granulomatous inflammation

readily distinguishes the necrosis in the five casesfrom that seen in tuberculosis, and various fungal andviral infections. Both inguinal lesions lacked thebrisk cellular infiltration of the necrosis, and thedense plasma cell accumulation and endarteritis thatwe have seen in a case of recently acquired syphiliticlymphadenitis. Furthermore the lesions describedhere do not resemble the generally focal necrosesseen in the lymphadenopathies of hypersensitivitydiseases involving small vessels, drug-inducedhypersensitivity reactions (Schwartz, 1966; Krasznaiand Szegedi, 1969), the Shwartzman phenomenon inlymph nodes (Koplik, 1937), or the larger haemor-rhagic lesions resembling infarcts in acute suppura-tive lymphadenitis (Lennert, 1961).The human lymph nodes considered here show

striking resemblances to lymph nodes subjected toexperimental infarction. After ligation of the entirearterial and venous vasculature of the popliteal lymphnode of rabbits Osogoe and Courtice (1968) found atsix hours a loss of cortical lymphocytes, and by 24hours more widespread necrosis of the lymphoidtissue, with only a narrow rind of surviving lymphoidtissue close to the marginal and medullary sinuses.Occlusion of both blood vascular and lymphaticvessels led to a more rapid and extensive necrosis ofthe lymphoid cells, leaving an incomplete andnarrow rim of surviving lymphoid tissue im-mediately deep to the marginal sinus. Devas-cularized autografts of lymph nodes in dogsrapidly necrosed, and in the first few days afteroperation showed such a brisk inflammatoryinfiltrate that infection was suspected (Holman andSelf, 1938). Months later such nodes in dogs werereduced to fibrous nubbins (Tilak and Howard,1965; Kister et al, 1965). Preservation of the lym-phatic vessels appears to mitigate the effect upon the

lymph nodes of blood vascular occlusion (Holmanand Self, 1938) and to facilitate nodal regenerationafter infarction (Osogoe and Courtice, 1968). It isinteresting, in view of the preservation of thereticulin architecture of the freshly infarcted humanlymph nodes, that regeneration of the lymphoidtissue occurred in the lymph nodes after arterial andvenous occlusion in rabbits within 14 days (Osogoeand Courtice, 1968), and to a lesser extent at sixmonths in dogs (Tilak and Howard, 1964).We feel that the microscopic findings in the five

human cases detailed above present distinctiveappearances and an orderly chronological sequence.In the early stages there is a selective necrosis of thelymphoid cells furthest from their blood supply. Atthis time the reticulin framework of the node ispreserved in most instances. The inflammatoryevents in the perinodal connective tissue are re-markably similar, both in morphology and timecouise, to those seen around human myocardialinfarcts (Malloiy, White, and Salcedo-Salgar, 1939).The heavy polymorphonuclear leucocytic infiltrateat three days was largely confined to the perinodalconnective tissue, in which respect it differs funda-mentally from the polymorphonuclear exudate ofsuppurative lymphadenitis. By the third week thepolymorphonuclear leucocytes are increasingly re-placed by mononuclear cells, and a zone of vascularand maturing granulation tissue appears in closeapposition to the periphery of the necrosis. Finally,months after infarction in those nodes that are notirrevocably damaged, there is evidence of regenera-tion of lymphoid tissue. This regeneration, pre-sumably effected by means of the lymphoid cellcirculation, is not complete for the stigmata ofgranulation tissue, fibrosed necrotic blood vessels,recanalization of occluded lymph and blood vessels,and the disturbed architectural arrangement of thelymphoid tissue remain. The initial event leading toall five nodal infarcts appeared to be thrombosis ofintranodal and hilar veins. In most instances thecause of the thrombosis was not apparent but it mayhave arisen in a superficial thrombophlebitis.

Aside from frank infarction, there have been fewaccounts of the effects of blood vascular lesions uponlymph nodes in man. A notable exception is therecent account by Haferkamp, Rosenau, and Lennert(1971) of the vascular transformation of lymph nodesthat were drained by thrombosed veins. Possiblytheir cases differed from ours in that large veins werethrombosed, but it seems likely that the atrophy oflymphoid tissue they noted in two of their three caseswas of ischaemic origin; irradiation of coexistingtumour was not responsible for this atrophy (Hafer-kamp, 1972, personal communication). Somewhatsimilar, but far less advanced, changes comprising

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vascular congestion and cortical depletion oflympho-cytes were described by Mohiuddin (1965) in themesenteric lymph nodes of rats shortly after experi-mental occlusion of the portal vein.The reason for the apparent rarity of lymph node

infarction may lie in the abundance of the vascularsupply and in the well developed anastomoses.Nevertheless the classical studies of Calvert (1897)and Dabelow (1938-39) show that the major arterialsupply and venous drainage of lymph nodes passthrough the nodal hilum and extend radially tosupply the medullary and cortical structures.Anastomoses through the capsule of lymph nodeswere, however, found by Calvert and Dabelow andby Herman, Ohba. and Mellins (1969) to link theinternal blood vessels of the nodes with those in theperinodal connective tissue. Additionally, it is likelythat hilar anastomoses accompany the expansion ofhilar connective tissue that develops in agingsuperficial lymph nodes (Denz, 1947). Furtheranastomoses, between the lymphatic and venouschannels, have been postulated to explain the trans-fer from lymphatic to venous vessels of bacteria(Lancet, 1961), air (Pressman and Simon, 1961), andlymphangiography oil (Bron, Baum, and Abrams,1963); more recently they have been shown inelectron microscopic studies (Pressman, Dunn, andBurtz, 1967). Finally, the arterial supply, at least tothe submandibular lymph nodes in many species,including man, is often not limited to a single namedartety (Miyata, 1966). Thus the very abundance ofthe vasculature of lymph nodes may protect themagainst infarction. Possibly anastomoses may accountfor the sparing of the subcapsular tissues in thosenodes which are infarcted. It is also possible that theregenerative capacity of infarcted nodes is related totheir vascular architecture and the mobile nature oftheir lymphoid population.

We are grateful to Mr J. W. Miller and colleagues forthe histological preparations and to Mr P. Crockerfor the photomicrography. Our thanks are also dueto surgical colleagues for access to the clinicalrecords of the patients under their care.

J. Douglas Davies and A. G. StansfeldReferences

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Dabelow, A. (1938-39). Die Blutgefassversorgung der lymphatischenOrgane. Anat. Anz., 87, Erg.-Heft., 179-224.

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