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Determining Etiology:Contents 6.1 Overview 71 6.2 A Cutaneous Ulcer in Which the Clinical Diagnosis Is Not Established 72 6.2.1 Possibilities of Histologic Picture 72 6.2.2 Intravascula

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41 Maessen-Visch MB, Koedam MI, Hamulyak K, et al:

Atrophie blanche Int J Dermatol 1999; 38 : 161–172

42 Schwaegerle SM, Bergfeld WF, Senitzer D, et al

Pyo-derma gangrenosum: a review J Am Acad Dermatol

1988; 18 : 559–568

43 Phillips TJ, Salman SM, Rogers GS: Nonhealing leg

ulcers: A manifestation of basal cell carcinoma J Am

Acad Dermatol 1991; 25 : 47–49

44 Harris B, Eaglstein WH, Falanga V: Basal cell

carci-noma arising in venous ulcers and mimicking

gran-ulation tissue J Dermatol Surg Oncol 1993; 19 :

150–152

45 Brodell RT, Wagamon K: The persistent nonhealing

ulcer Could it be basal cell carcinoma? Postgrad

Med 2001; 109 : 29–32

46 Blank AA, Schnyder UW: Squamous cell carcinoma

and basal cell carcinoma within the clinical picture

of a chronic venous insufficiency in the third stage.

Dermatologica 1990; 181 : 248–250

47 Ackroyd S, Young AE: Leg ulcers that do not heal Br

Med J 1983; 286 : 207–208

48 Pierard G, Fumal I, Pierard-Franchimont C: Cold

in-juries In: Freedberg IM, EisenAZ, Wolff K, Austen

KF, Goldsmith LA, Katz SI (eds) Fitzpatrick’s

Der-matology in General Medicine, 6th edn New York:

McGraw-Hill 2003; pp 1211–1220

49 Karmody AM, Powers SR, Monaco VJ, et al: ‘Blue toe’

syndrome: An indication for limb salvage surgery.

Arch Surg 1976; 111 : 1263–1268

50 Freund NS: Cholesterol emboli syndrome following

cardiac catheterization Postgrad Med 1990; 87 :

55–60

51 Morton RS: The treponematoses In: Champion RH,

Burton JL, Burns DA, Breathnach SM (eds)

Rook/Wilkinson/Ebling Textbook of Dermatology,

6th edn Oxford: Blackwell Scientific Publications.

1998; pp 1237– 1275

52 Ohtsuka T, Yamakage A, Yamazaki S: Digital ulcers

and necroses: novel manifestations of angiocentric

lymphoma Br J Dermatol 2000; 142 : 1013–1016

53 Russwurm R, Hagedorn M: Lichen ruber ulcerosus.

Hautarzt 1989; 40 : 233–235

54 Parodi A, Ciulla P, Rebora A: An old lady with

scar-ring alopecia and an ulcerated sole Ulcerative

li-chen planus Arch Dermatol 1991; 127 : 407–410

55 Micalizzi C, Tagliapietra G, Farris A: Ulcerative

li-chen planus of the sole with rheumatoid arthritis.

Int J Dermatol 1998; 37 : 862–863

56 Barbarulo AM, Metha N, Bucalo B, et al: Recurrent

disseminated herpes zoster and cytomegalic

peri-anal ulcer: a case report and review of the literature.

Cutis 2001; 67 : 43–46

57 Pariser RJ: Histologically specific skin lesions in

dis-seminated cytomegalovirus infection J Am Acad

Dermatol 1983; 9 : 937–946

58 Rodot S, Lacour JP, Elslande L, et al: Ecthyma

gan-grenosum caused by Klebsiella pneumoniae Int J

in-62 Brandt O,Abeck D, Breitbart E, Ring J: Perianal tismus gangraenosus Hautarzt 1997; 48 : 199–202

ergo-63 Baptista AP, Mariano A, Machado A: Peranal ulcers caused by ergotamine-containing suppositories Ac-

66 Senti G, Schleiffenbaumb B, Dummera R: Vaginal cers as initial presentation of subacute myelomono- cytic leukemia Dermatology 1999; 199 : 346–348

ul-67 Magro CM, Crowson AN: Cutaneous manifestations

of Behçet’s disease Int J Dermatol 1995; 34 : 159–165

68 Slutzki S, Bogokowsky H,Gilboa Y, et al: induced skin necrosis Int J Dermatol 1984; 23 : 117–119

Coumadin-69 Defranzo AJ, Marasco P, Argenta LC: duced skin necrosis of the skin Ann Plast Surg 1995;

leish-73 Hay RJ, Adriaans B: Bacterial infections In: pion RH, Burton JL, Burns DA, Breathnach SM (eds) Rook/Wilkinson/Ebling Textbook of Dermatology, 6th edn Oxford: Blackwell Scientific Publications 1998; pp 1097–1179

Cham-74 Odom BO, James WD, Berger TG (eds) Bacterial fections In: Andrews’ Diseases of the Skin: Clinical Dermatology, 9th edn Philadelphia: WB Saunders 2000; pp 307–357

in-75 Tsao H, Swartz MN, Weinberg AN, Johnson RA: Soft tissue infections; erysipelas, cellulitis and gangre- nous cellulitis In: Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI, Fitzpatrick TB (eds) Fitzpatrick’s Dermatology in General Medi- cine, 5th edn New York: McGraw-Hill 1999; pp 2213– 2231

76 Irvine AD, Bruce IN, Walsh M,et al: Dermatological presentation of disease associated with antineu- trophil cytoplasmic antibodies: a report of two con- trasting cases and a review of the literature Br J Der- matol 1996; 134 : 924–928

77 Weninger W, Kain R, Tschachler E, et al:

Microscop-ic polyangiitis with eosinophilia- an overlap drome or separate disease entity? A case report and review of the literature Hautarzt 1997; 48 : 332–338

syn-78 Peterson LL: Hydralazine-induced systemic lupus erythematosus presenting as pyoderma gangreno-

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sum-like ulcers J Am Acad Dermatol 1984; 10 :

379–384

79 Skaria AM, Ruffieux P, Piletta P, et al: Takayasu

arter-itis and cutaneous necrotizing vascularter-itis

Dermatol-ogy 2000; 200 : 139–143

80 Frances C: Dermato-mucosal manifestations of

Beh-çet’s disease Ann Med Interne (Paris) 1999; 150 :

535–541

81 Schlesinger IH, Farber GA: Cutaneous ulceration

re-sembling pyoderma gangrenosum in the primary

antiphospholid syndrome: a report of two

addition-al cases and review of the literature J La State Med

Soc 1995; 147 : 357–361

82 Helm KF, Peters MS, Tefferi A, et al: Pyoderma

gan-grenosum-like ulcer in a patient with large granular

lymphocytic leukemia J Am Acad Dermatol 1992;

27 : 868–871

83 Massa MC, Doyle JA: Cutaneous cryptococcosis

simulating pyoderma gangrenosum J Am Acad

Dermatol 1981; 5 : 32–36

84 Ryan TJ, Burnand KG: Diseases of the veins and

ar-teries – leg ulcers In: Champion RH, Burton JL,

Ebling FJG (eds) Rook/Wilkinson/Ebling Textbook

of Dermatology, 5th edn Oxford: Blackwell

Scientif-ic PublScientif-ications 1992; pp 1963–2013

85 Weinberg AN, Swartz MN: Miscellaneous bacterial infections with cutaneous manifestations In: Freed- berg IM, EisenAZ, Wolff K, Austen KF, Goldsmith

LA, Katz SI and Fitzpatrick TB (eds) Fitzpatrick’s Dermatology in General Medicine, 5th edn New York: McGraw-Hill 1999; pp 2257–2273

86 Gwakrodger DJ: Mycobacterial infections In: Champion RH, Burton JL, Burns DA, Breathnach SM (eds) Rook/Wilkinson/Ebling Textbook of Derma- tology, 6th edn Oxford: Blackwell Scientific Publica- tions 1998; pp 1181–1214

87 Dowd PM: Reactions to cold In: Champion RH, ton JL, Burns DA, Breathnach SM (eds) Rook/Wil- kinson/Ebling Textbook of Dermatology, 6th edn Oxford: Blackwell Scientific Publications 1998;

Bur-pp 957– 972

88 Kalter DC, Rudolph A, McGavran M: Livedo laris due to multiple cholesterol emboli J Am Acad Dermatol 1985; 13 : 235–242

reticu-89 Ramos-e-Silva M, Rebello PF: Leprosy Recognition and treatment Am J Clin Dermatol 2001; 2 : 203–211

Chapter 5 Determining Etiology

70

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Determining Etiology:

Contents

6.1 Overview 71

6.2 A Cutaneous Ulcer in Which

the Clinical Diagnosis Is Not Established 72

6.2.1 Possibilities of Histologic Picture 72

6.2.2 Intravascular Occlusion 72

6.2.3 Vasculitis 76

6.2.4 Other Histologic Patterns 79

6.2.5 Insufficient Histologic Data 80

6.3.4 ‘Unexpected’ Histologic Findings

in Certain Types of Cutaneous Ulcers 82

6.4 Suspected Malignancy 82

6.4.1 When Should Malignancy Be Suspected? 82

6.4.2 Epithelioma as a Primary Lesion 83

6.4.3 Epithelioma Developing

in a Long-Standing Cutaneous Ulcer 83

6.5 An Ulcerated Nodule or Plaque 84

6.5.1 Ulcers Developing Within a Nodule

or a Plaque 84

6.5.2 Granulomatous Histologic Pattern 84

6.5.3 Seeking an Infectious Cause 84

In most cases, routine blood tests should beperformed for every patient presenting with acutaneous ulcer where the diagnosis is not es-tablished These routine workups, which gener-ally include tests such as erythrocyte sedimen-tation rate, complete blood count, and bloodchemistry, may direct the physician towards theetiology in certain cases In many other situa-tions with cutaneous ulcers, the anamnesis andphysical examination may suggest the need for

a more specific and focused investigation.For example, an ulcer suspected of being re-lated to hemolytic anemia requires the perfor-mance of a blood smear, which may reveal sick-led cells, spherocytes, etc

Similarly, when a connective-tissue disease

is suspected, the workup should include tory parameters such as anti-nuclear factor,rheumatoid factor, cryoglobulin level, or anti-neutrophil cytoplasmic antibody (ANCA)

labora-In cases of cutaneous ulcers, histologic imens may provide valuable information re-garding their etiology The histologic hallmark

spec-of a cutaneous ulcer is dictated by its medical

definition, namely, the absence of epidermis and

the partial or complete absence of dermis Yet

the question is not whether there is an ulcer butwhat the underlying pathology is Therefore,the biopsy should not be taken from the ulceritself, but rather from an area adjacent to the ul-cer margin, covered by dermis and epidermis;where specific histologic features may be iden-tified

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In order to cover all the clinical possibilities

that may derive from the histology of a

cutane-ous ulcer, a broad knowledge of

dermatopa-thology is required Nevertheless, our purpose

here is not to review the entire gamut of

cur-rently available dermatopathological

knowl-edge, but to relate only the most practical

clini-cal implications arising from histologic

fea-tures of cutaneous ulcers

A biopsy should be considered from an

ulcer’s margin under the following

condi-tions:

5An ulcer in which the clinical

diag-nosis is not established:when

histo-ry, physical examination and theulcer’s appearance do not provide aconcrete diagnosis i.e., when there is

no clinical clue, or when one wants

to confirm a suspected/doubtful agnosis

di-5A non-healing ulcer:Biopsy should

be considered when dealing with anulcer that does not heal within three

to four months of optimal treatment

This is subject to the clinical set-up(see below)

5Suspected malignancy:when the

ulcer is suspected of being nant/cancerous Under these cir-cumstances, a biopsy should be per-formed as early as possible

malig-Each of the above possibilities is discussed

below

6.2 A Cutaneous Ulcer in Which

the Clinical Diagnosis

Is Not Established

6.2.1 Possibilities of Histologic Picture

Sometimes, neither the history nor the physical

examination provides any clues to assist in

arriving at a diagnosis A biopsy from an areaadjacent to the ulcer margin should be done, inorder to obtain diagnostic clues

This chapter deals with those topics that arespecifically relevant to the histopathology ofskin ulcers, such as intravascular occlusion orvasculitis In addition, we shall discuss the steps

to be taken if the histologic specimen does notprovide sufficient diagnostic information

6.2.2 Intravascular Occlusion

Intravascular occlusion may manifest in

sever-al forms, depending on the pathologic processleading to occlusion Conditions characterized

by intravascular occlusion are listed inTable 6.1

Coagulopathies are common forms of vascular occlusion [1, 2] In these cases, intra-vascular occlusion is reflected histologically bythe presence of fibrin thrombi within the lumen

intra-of blood vessels (Fig 6.1) Fibrin thrombi pear as amorphous eosinophilic material inhematoxylin and eosin (H&E) stain; they may

ap-be more obvious in a periodic acid-Schiff (PAS)stain In severe forms of coagulopathy, areas ofcutaneous necrosis may be observed [2].Fibrin thrombi may be accompanied byunique features such as cholesterol clefts incholesterol emboli (Fig 6.2) or calcium deposi-tion in calciphylaxis (Fig 6.3) Other histologicfeatures may also be involved in intravascularocclusion For example, in sickle cell anemia,blood vessels are occluded by the sludging ofsickled erythrocytes [3, 4] (Fig 6.4)

Note that intravascular occlusion and thepresence of fibrin thrombi within the lumen ofblood vessels may variably appear in vasculiticprocesses as well Yet, vasculitis also has uniquecharacteristics, such as the infiltration of whiteblood cells within the wall of blood vessels oractual signs of damage to the vessel wall (seeSect 6.2.3) In this section, we present condi-

tions of intravascular occlusion which are not

accompanied by vasculitis

In some cases, the clinical diagnosis isstraightforward and the histology simply com-plements the history and physical examination

Chapter 6 Biopsy and Laboratory Investigation

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Fig 6.1.

A fibrin thrombus within

the lumen of a blood vessel

Table 6.1.Intravascular occlusion

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For instance, the diagnosis of coumarin

necro-sis may be reached when anamnenecro-sis confirms

intake of the drug a few days before ulceration

Similarly, cutaneous ulcers and splenomegaly

in a young patient raise the possibility of

hemo-lytic anemia

6.2.2.1 Histologic Features

In conditions such as coagulopathies, nemias, or anti-phospholipid syndrome, thehistopathologic features may be similar, and anaccurate diagnosis cannot be established bybiopsy alone On the other hand, in other condi-tions, specific histologic features may assist indetermining the ulcer’s etiology

dysprotei-Chapter 6 Biopsy and Laboratory Investigation

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Histologic clues such as those mentioned

be-low should be sought (presented in Schema

6.1):

5Microcalcifications in small to

me-dium sized vessels:This histologicfinding appears in calciphylaxis It

is well demonstrated by a Von Kossastain [17–19]

5Bizarre forms of red blood cells:

Bi-zarre forms of red blood cells such

as sickled erythrocytes or tes may be found within capillaries

spherocy-in ulcers caused by hemolytic mia; extravasation of red blood cellsmay be seen [3, 4, 11]

ane-5Cholesterol clefts:Cholesterol

em-boli are characterized by the ence of cholesterol clefts within thefibrinous material [20–22] Note thatthe absence of typical cholesterolclefts does not necessarily rule outthe diagnosis of cholesterol emboli[25, 26] It may be difficult to locateand identify cholesterol emboli, and

pres-a deep biopsy mpres-ay be needed [2]

6.2.2.2 Other Histologic Clues

Atrophie Blanche In the initial stages ofatrophie blanche, the entity might still not beidentified by histology; i.e., fibrin thrombiwithin blood vessels may be the sole finding.However, more severe cases may present fea-tures such as infarction with hemorrhage or aninflammatory infiltrate In late atrophic lesions,

a thin epidermis is usually seen, and the dermisbecomes sclerotic [2, 13]

Stain Type.The type of stain used may giveand clues for diagnosis: Precipitated cryoglob-ulins appear bright red with PAS stain, whileother fibrinoid depositions, caused by otherprocesses, tend to stain lighter [2] As men-tioned above, deposition of calcium withinblood vessels, as appears in calciphylaxis, may

be identified by using the Von Kossa stain [19]

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5Anti-thrombin III level

5Resistance to activated protein C

5Analysis of DNA to factor V Leiden

Although the scheme for histological

identifi-cation shown in Fig 6.5 is quite comprehensive,

we have encountered isolated cases of

cutane-ous ulcers with fibrin thrombi in which,

follow-ing thorough investigation, a definite etiology

could not be identified

6.2.3 Vasculitis

Fully developed vasculitis is characterized

by the following histologic features [1] (seeFig 6.6):

5Infiltration of white blood cellswithin the wall of blood vessels

5Deposits of fibrin within the walland lumen of blood vessels

5Extravasation of red blood cells –secondary to injury of the bloodvessels

Other signs of damage to the wall may bepresent, such as the degeneration of collagenfibers, and the necrosis of endothelial cells andsmooth muscle cells

A special type of vasculitis that manifests

unique features is leukocytoclastic vasculitis,

the hallmark of which is the presence of morphonuclear cells and fragmented nuclei,usually termed ‘nuclear dust’

poly-Note that when vasculitis results in the mation of cutaneous ulcers, we expect to identi-

for-fy a form of necrotizing vasculitis in the

histo-logic specimen, showing necrotic areas with

Chapter 6 Biopsy and Laboratory Investigation

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significant damage to blood vessels and

sur-rounding tissues

The literature is replete with a wide range of

different classifications of vasculitic lesions,

and there is no one accepted classification

Most authors present differing specific

classifi-cations

Tables 6.2, 6.3, and 6.4 present a reasonable

and convenient classification of types of

vascu-litis that tend to be associated with ulceration

These tables are based, in part, on the following:

1 Classification of vasculitis, as presented by

A.B Ackerman [1]

2 Classification of the vasculitis syndromes, as

presented by A.S Fauci [27] in Harrison’s

Principles of Internal Medicine

3 The definitions of vasculitis as delineated by

the Chapel Hill Consensus Conference in 1992

[28, 29]

Accurate identification of the subtype of

vas-culitis is determined by the following data:

5Type of vessel involved (arterial

system versus venous system)

5Size of vessel involved (e.g.,

postca-pillary venule)

5Type of infiltrate: neutrophilic?

lym-phocytic?

5Presence or absence of

leukocytoc-lasis (fragmented neutrophilic clei)

nu-Table 6.3 presents conditions associated withsmall-vessel leukocytoclastic vasculitis

In some cases of vasculitis, the pathologywill not be obvious in a given histologic speci-men The lesion may be in its early stages, whenthe vasculitic process may not yet be evident Inother cases, the specific site from which the bi-opsy was taken will not reflect the pathologyaccurately Therefore, if a histologic specimen isnot diagnostic, the biopsy should be repeated.Grunwald et al [33] have shown that directimmunofluorescence is a very sensitive test,which may confirm the presence of vasculitis inconditions where routine histologic specimenssometimes fail to do so (e.g., in the early and re-solving stages of the vasculitic process)

Where there is histologic evidence of litis, the following laboratory workup should

vascu-be considered, depending on the clinical up:

set-5Erythrocyte sedimentation rate

5Complete blood count

Vasculitis: note the damaged vessel

wall, infiltrated by inflammatory

cells

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5p-antineutrophil cytoplasmic

anti-body (pANCA)

5Serum markers for malignancy

5Chest X-ray

5Abdominal ultrasound

5Fecal occult blood testing

In some cases, even after extensive tion, no definite explanation for the vasculitiscan be found Such cases remain defined asidiopathic vasculitis, in which a specific diseasemay become apparent at a later date

investiga-Chapter 6 Biopsy and Laboratory Investigation

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Table 6.2.Cutaneous ulcers characterized by vasculitis

Vasculitis induced by an exogenous stimulus:

Other vasculitic processes

쐌 Vasculitis associated with malignancy

쐌 Nodular vasculitis (erythema induratum)

쐌 Erythema elevatum diutinum

is not necessarily associated with vasculitis Lesions in Behcet’s disease may appear without histologic evidence

of vasculitis [32].

d Mixed cryoglobulinemia may be associated with several systemic or infectious diseases such as rheumatoid thritis, Sjögren's disease, chronic lymphocytic leukemia and hepatitis C.

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6.2.4 Other Histologic Patterns

In some cases, a unique histologic pattern may

be seen (e.g., a specific type of tumor, or a cific inflammatory process), which provides anaccurate diagnosis Yet, there is a huge range ofpossible causes of skin ulcers Hence, manydiagnoses may be revealed in a histologic spec-imen obtained from a cutaneous ulcer A broadknowledge of dermatopathology is needed toidentify all the histologic possibilities

spe-The classic textbooks of dermatopathologydeal with this issue very well

5Histologic Diagnosis of Inflammatory Skin Diseases: An Algorithmic Method Based on Pattern Analysis (A B Ackerman)

5Lever’s Histopathology of the Skin (Elder, Elenitsas, Jaworsky and Johnson)

6.2

t

Table 6.3.Small vessel leukocytoclastic vasculitis a, b

Vasculitis induced by an exogenous stimulus:

Vasculitis associated with malignancy

a More detailed discussions regarding vasculitis and its classification can be found in dermatopathology texts We

do wish to make the point, however, that although in most of the conditions listed in the above table the trate is largely neutrophilic, in certain types of vasculitis there is typically a lymphocytic vasculitis (e.g., in col- lagen diseases such as SLE and some cases of drug-induced vasculitis or arthropod bites [1, 2].

infil-b Erythema elevatum diutinum also manifests small vessel leukocytoclastic vasculitis [28].

Table 6.4.Cutaneous ulcers in which medium-sized

vas-culitis or large cell vasvas-culitis may be identified a, b

a Wegener’s granulomatosis presents as

leukocytocla-stic vasculitis of small vessels together with vasculitis

of large venous vessels [1].

b Polyarteritis nodosa may present as leukocytoclastic

vasculitis of small vessels and as large vessel arterial

vasculitis [1].

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Note that in most cases, the presence of

inflam-matory cells within the histologic section

can-not be used as a diagnostic clue, except where a

unique pattern of distribution is identified Any

cutaneous ulcer is subject to inflammatory

pro-cesses, independent of its primary basic

pathol-ogy These inflammatory responses may

mani-fest (but not necessarily) as infiltrations of

var-iable numbers of inflammatory cells within the

superficial dermis, usually around blood

ves-sels Sometimes, the inflammatory infiltrate

re-sults from superficial secondary infection and

has no etiologic significance Nevertheless, in

some cases, a unique pattern of distribution of

inflammatory cells (e.g., numerous plasma cells

in syphilis, or a granulomatous pattern) may

provide important diagnostic clues A detailed

discussion of inflammatory patterns would

en-tail covering the entire field of

dermatopathol-ogy, and is beyond the scope of this chapter

6.2.5 Insufficient Histologic Data

Sometimes the histologic data do not seem to

provide even the slightest diagnostic clue In

such a case, it is advisable to thoroughly scan the

entire slide and biopsy specimen to see if it

sho-ws certain specific histologic characteristics

such as fibrin thrombi, vasculitis, a

granuloma-tous pattern (detailed below), or some other

specific pattern If this step does not provide

further clues, another biopsy from a different

area of the same ulcer should be considered,

sin-ce there may be considerable variation among

different specimens taken from the same ulcer

When certain conditions are suspected, a

bi-opsy containing deep dermis and subcutaneous

tissue should be considered For example, in

polyarteritis nodosa and nodular vasculitis, a

superficial biopsy may not reveal the presence

of vasculitis Similarly, as suggested in the

sec-tion on vasculitis, direct immunofluorescence

of a tissue specimen from the ulcer margin may

confirm the diagnosis of vasculitis

Figure 6.7 summarizes the approach to the

diagnosis of ulcers when the history and

physi-cal examination do not lead to a diagnosis It

includes the main histologic findings and their

clinical implications

6.3 A Non-Healing Ulcer

6.3.1 The Various Histologic Patterns

Biopsy should be considered when dealing with

an ulcer that does not heal within 3–4 months

of optimal treatment (depending on the clinicalset-up) In these cases, additional parametersmay influence the decision as to whether the ul-cer should be sampled For example, when theaffected area is too close to a bone (i.e., an ulcerlocated over the anterior tibia), it may beappropriate to postpone the biopsy for a while,giving the ulcer a longer period of time to heal.Classical examples of non-healing ulcers arethose where the clinical features suggest the di-agnosis of a ‘venous ulcer’ or an ‘ischemic ulcer’

in a patient with peripheral arterial disease Inthese cases, it is not the role of the histologicspecimen to establish a diagnosis Diagnoses ofsuch cases are based on physical examinationand specific tests such as Doppler flowmetry ofleg arteries or Doppler ultrasonography of thelower limb venous system

In such cases, the main purpose of the biopsy

is to confirm that the ulcer, which appears to bebenign, is not, in fact, caused by some otherunderlying process such as malignancy Occa-sionally, histologic data may direct the physiciantowards other conditions such as infectious pro-cesses or pyoderma gangrenosum The histolog-

ic possibilities of non-healing ulcers are

(fi-5A variable degree of inflammation

5Presence of hemosiderin

5Extravasation of red blood cells

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Fig 6.7.Algorithm for laboratory workup when clinical diagnosis has not been established

Fig 6.8.The possible histologic patterns, in the case of a non-healing ulcer

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The presence of fibrin cuffs is considered to be

a typical histologic finding in venous ulcers

These are organized structures composed of

fi-brin, laminin, fibronectin, tenascin, collagen,

and trapped leukocytes [35] It is suggested that

high venous pressure results in dermal leakage

of fibrinogen with subsequent formation of

pericapillary fibrin layers [35] Pericapillary

fi-brin is positively stained by Martius scarlet

blue Its presence may be also confirmed by

di-rect immunofluorescence [36]

Falanga et al [36] documented the presence

of pericapillary fibrin in 14 (93%) of 15 patients

with venous ulceration but in only one of 14

pa-tients (7%) who had cutaneous ulcers of other

etiologies Burnard et al found that

pericapil-lary fibrin can be found in the skin of patients

with venous insufficiency, whether the skin is

ulcerated or not [37] However, cuffing can be

seen if appropriate staining has been carried

out, provided that its structure has not been

de-stroyed by an inflammatory response, which

frequently accompanies ulceration

Note that fibrin cuffs may be seen in

diabet-ic ulcers, including ischemdiabet-ic diabetdiabet-ic ulcers

[38] and in pressure ulcers [39] However, while

in venous insufficiency the fibrin is organized

in concentric lamellae, in diabetic ulcers the

fi-brin tends to appear as fragmented and diffuse

deposits [38]

6.3.3 The Histologic Characteristics

of Ischemic Ulcers

The narrowing or occlusion of blood vessels

can be seen in diabetic ulcers and ischemic

ulcers as a result of thickening of the blood

ves-sel wall [38] This process is caused by an

abnor-mal proliferation of endothelial cells or smooth

muscle cells [38] Narrowing or occlusion of

blood vessels may also be seen as a result of

ath-erosclerotic disease

These processes involve only blood vessels of

the deep plexus, and these histologic

character-istics are not seen within the superficial plexus;

therefore, most punch biopsies, which are

rela-tively superficial, will not reveal the above

Malignancy may be suspected under the lowing circumstances:

fol-5When an ulcer arises within aprominent, heavily infiltrated nod-ule or tumor (e.g., ulceration ofmelanoma or a cutaneous lesion oflymphoma)

5When granulation tissue extendsbeyond the ulcer margin: this mayoccur in basal cell carcinoma (BCC)

or squamous cell carcinoma (SCC)[40]

5When specific characteristic tures are observed, such as the typi-cal pearly border of a BCC

fea-Chapter 6 Biopsy and Laboratory Investigation

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