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Ulcerations oftheLower Extremity

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Ulcers of the lower extremity may be caused by a number of factors. Shape, location, size, appearance, and underlying systemic and/or skin disease aid in diagnosis. Chronic lower extremity wounds may be of diabetic, neuropathic, pressure, or vascular origin [1, 2]. Less common causes are those that arise from inammation, infection, trauma, physical agents such as radiation or chemicals, tumors, vasculitides, poor nutrition, underlying internal disease, and connective tissue diseases such as rheumatoid arthritis [3].

13.1 Diagnosis

Proper diagnosis requires a thorough patient history including the wound’s onset, progression, pain level and other symptoms, underling illnesses, duration, and previous or ongoing treatments. Examination entails evaluation of a number of factors including shape of the ulcer, size, base, coloration, appearance of surrounding tissue, location, and associated skin lesions if present.

13.1.1 Shape

Ulcer shape and border should be noted. Ulcers may be sloping, scooped out, or punched out and round, oval, stellate, or polyangular in conguration.

Yellow wounds are covered with a collection of necrotic cellular debris. A yellowish membrane is common in arterial ulcers and in the presence of some infections [4]. These wounds require cleansing, surgical, or autolytic debridement.

A reddened base is indicative of granulation. Protection and occlusion will hasten the healing process. Granulation tissue is composed of thousands of capillary loops that resemble small granules in the wound bed. Pink wounds are a sign of early epithelization and require protection so that the epithelium can thicken, mature, and allow collagen to re-organize.

13.1.3 Peri-wound Skin

Peri-wound skin may be characterized as scaling, oozing, keratotic, erythematous, inamed, purpuric, hyper- or hypopigmented, edematous, or indurated.

13.1.4 Location

The location of an ulcer often helps to dene causation. Venous ulcers usually occur on the lower legs on the area just above the medial malleoli [4]. Arterial ulcers have a predilection for the toes and distal forefoot [4]. Diabetic ulcers are commonly found on the plantar surface of the foot [5].

13.1.2 Base

The ulcer base may be dry, soft, moist, granular, or brotic. The appearance of the ulcer base not only aids in diagnosing the type of wound but also helps monitor the state of healing. Some wound care clinics have adopted a simple visual classication system based on color; black, yellow, red, or pink.

Black wounds are necrotic or ischemic and usually

warrant debridement and at times revascularization.

13.2 Arterial Ulcers

Atherosclerosis is the main cause of arterial or ischemic ulcers [4]. Risk factors include smoking and diabetes. Patients may experience intermittent claudication in their calves and/or rest pain. Distal pedal pulses are diminished and/or absent, and capillary rell is delayed. Arterial ulcers are often found on the toes and bony prominences sur-

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Fig. 13.1 Arterial ulcer on second toe

13 Ulcerations oftheLower Extremity

Fig. 13.2 Diabetic foot ulcer

rounded by shiny, taut skin. The ulcers are “punched out” in appearance with a round circumference and smooth edges (Fig.13.1).

13.3 Diabetic Ulcers

Diabetics have a 20% lifetime risk of developing a foot ulcer [5]. Contributing factors include diabetes-associated peripheral neuropathy and vascular disease. The ulcers are characteristically painless even when infected. The most common location is on the plantar foot. The borders are punched out, with a hyperkeratotic rim. Over 80% of lower extremity amputations are attributed to complications from diabetic ulcerations. Treatment includes debridement of devitalized tissue, off-loading to reduce pressure, and appropriate wound dressings to maintain a moist healing environment (Fig.13.2).

13.4 Venous Ulcers

Venous or stasis ulcers are the most common type of leg ulceration [4]. They develop secondary to sustained venous hypertension. Lesions are usually shallow with a ruddycolored base and irregular wound margin. Edema, varicosities, and altered pigmentation with thickened skin termed lipodermatosclerosis are often present. Discomfort is variable. Venous ulcers are most frequently encountered above the ankle and below the proximal calf (Figs.13.3 and 13.4).

Fig. 13.3 Venous stasis ulcer

13.7 Calciphylaxis

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Fig. 13.5 Pyoderma gangrenosum

Fig. 13.4 Lipodermatosclerosis on the leg

13.5 Pyoderma Gangrenosum

Pyoderma gangrenosum presents as an ulceration with violaceous peri-wound skin [6]. The disorder occurs most commonly on the lower extremity. The condition can be precipitated or worsened by minor trauma, referred to as “pathergy.” Ulcers expand rapidly and are very painful. Most cases are idiopathic but lesions can be associated with chronic inammatory bowel disease, arthritis, and autoimmune disorders. Diagnosis is one of the exclusions as there are no conrmatory laboratory tests and biopsy is nonspecic, performed primarily to rule out other pathologies. Lesions are often misdiagnosed as venous stasis ulcers when they occur on the medial aspect of the leg. No single specic therapy has proven universally successful and treatment options include intralesional steroids, oral corticosteroids, cyclosporine, infusion of iniximab, and surgical intervention (skin grafts) (Fig.13.5).

13.6 Sickle Cell Ulcer

The most common cutaneous presentation of sickle cell disease is a leg ulcer which is more frequent in sickle cell anemia than in the trait [7]. These ulcers are extremely painful,

Fig. 13.6 Sickle cell ulcer on the lateral malleolus

may have a punched-out appearance, and occur most commonly over the medial and lateral malleoli. Networks of sickled red cells obstructing the microcirculation to the skin, anemia, and in situ thrombosis factor into pathogenesis. Local trauma to the area may also precipitate ulcer formation. Ulcers tend to be chronic and recurrent and treatment is challenging. Standard local wound care and pain management are mainstays of therapy (Fig.13.6).

13.7 Calciphylaxis

Calciphylaxis is a rare, life-threatening disorder of intra- and extravascular calcication that most commonly arises in individuals aficted with end-stage renal disease. Narrowing and occlusion of subcutaneous microvessels result in necrotic skin lesions that are exquisitely painful. Early lesions are often found on the legs and begin as reticulated, indurated,

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Fig. 13.7 Calciphylaxis

13 Ulcerations oftheLower Extremity

Fig. 13.8 Pressure ulcer on the posterior heel

ulcerated plaques, and nodules which progress to ulcerations [8]. The prognosis is poor with most patients dying within 1year of diagnosis [9].

Management involves a multi-disciplinary approach ideally including nephrology, dermatology, wound care, and pain management. Sodium thiosulfate, a chelator of calcium, has been used intravenously and intralesionally to induce remission (Fig.13.7).

13.8 Pressure Ulcers

Pressure ulcers, also known as decubitus ulcers and bedsores, are a result of constant and prolonged pressure on a bony prominence [10]. The heel and lateral/medial malleoli are commonly affected sites in patients who are bedridden and are not able to make postural changes regularly. Treatment involves reducing pressure exerted on the area, minimizing the ulcer’s contact with a hard surface, decreasing moisture, and decreasing bioburden to prevent sepsis [10]. The most widely used classication system for pressure ulcers is the NPUAP (national pressure ulcer advisory panel) system [10] (Fig.13.8).

References

1. Eaglstein WH, Falanga V. Chronic wounds. Surg Clin North Am. 1997;77:689–700.

2. Gist S, Tio-Matos I, Falzgraf S, Cameron S, Beebe M.Wound care in the geriatric client. Clin Interv Aging. 2009;4:269–87.

3. Labropoulos N, Manalo D, Patel NP, Tiongson J, Pryor L, Giannoukas AD.Uncommon leg ulcers in the lower extremity. J Vasc Surg. 2007;45(3):568–73.

4. Grey JE, Harding KG, Enoch S. Venous and arterial leg ulcers. BMJ. 2006;332(7537):347–50.

5. Edmonds ME, Foster AV. Diabetic foot ulcers. BMJ. 2006;332(7538):407–10.

6. Barbe M, Batra A, Golding S, Hammond O, Higgins JC, O'Connor A, Vlahovic TC.Pyoderma gangrenosum: a literature review. Clin Podiatr Med Surg. 2021;38(4):577–88. https://doi.org/10.1016/j.

cpm.2021.06.002.

7. Sahu T, Verma HK, Ganguly S, Sinha M, Sinha R.Common, but neglected: a comprehensive review of leg ulcers in sickle cell disease. Adv Skin Wound Care. 2021;34(8):423–31. https://doi.

org/10.1097/01.ASW.0000755924.12513.40.

8. Ghosh T, Winchester DS, Davis MDP, El-Azhary R, Comfere NI.Early clinical presentations and progression of calciphylaxis. Int J Dermatol. 2017;56(8):856–61. https://doi.org/10.1111/ijd.13622.

9. Nigwekar SU, Thadhani R, Brandenburg VM. Calciphylaxis. N Engl J Med. 2018;378(18):1704–14. https://doi.org/10.1056/

NEJMra1505292.

10. Zaidi SRH, Sharma S.Pressure ulcer. [2022 Feb 9]. In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2022.

Drug Eruptions oftheLower Extremity

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A drug eruption is an adverse cutaneous reaction to a medication. Such untoward events are usually mild and promptly resolve upon discontinuation of the inciting drug. Other adverse events such as toxic epidermal necrolysis are associated with systemic involvement and may be life-threatening. Often the offending drug is readily ascertained by history of recent exposure. Sometimes the cause is not as obvious, especially when a patient is on multiple medications or when the reaction resembles other skin disorders. Note as well that drug eruptions can be triggered by over-the-counter, nonprescription medications often overlooked when history is obtained. Several types of drug reactions have been described and include the following:

14.1 Morbilliform Drug Eruptions

The majority of drug eruptions present as morbilliform rashes. Antibiotics account for over 30% of these reactions with amoxicillin-clavulanic acid, cephalexin, and ciprooxacin common offenders [1]. Other drug classes include antihypertensives, nonsteroidal anti-inammatory drugs, and anticonvulsants. Morbilliform eruptions result from a delayed T-cell mediated immune response. The initial rash may occur within 1–2days following prior exposure or may be delayed up to 8weeks after rst time dosing. Morbilliform drug eruptions commence as erythematous papules and patches that coalesce a few days after onset. Sites of involvement are usually the trunk and extremities; involvement of the face is uncommon. Differentiation from a viral exanthem may be difcult clinically. Discontinuation of the causative drug along with antihistamines and topical steroids usually results in prompt clearance (Fig.14.1).

Fig. 14.1 Morbilliform eruption is the most common manifestation of a drug hypersensitivity reaction

14.2 Fixed Drug Eruption

Fixed drug eruption is an adverse event to a drug that is marked by the development of well-demarcated macules on the skin or mucosal surfaces. Classic is the appearance of the rash at the same location following ingestion of the causative drug [2]. Lesions are often dusky red in hue and circular to ovoid in appearance. Lesions may increase in severity with

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Fig. 14.2 Fixed drug eruption manifests as a well-dened patch that recurs at the same site following re-exposure to a drug

subsequent exposures leaving residual hyperpigmentation. The most commonly involved agents include nonsteroidal anti-inammatory drugs, antibiotics, anticonvulsants, and antimalarials. The underlying pathogenesis involves activation of intraepidermal CD8+ T-cells (Fig.14.2) [3].

14.3 Acute Generalized Exanthematous Pustulosis

Acute generalized exanthematous pustulosis (AGEP) is an uncommon skin rash induced by medication. The rash presents as sterile pustules and papules arising on an erythematous background [4]. Patients may present with fever, pruritus, and elevated white count. Agents that have been implicated include aminopenicillins, quinolones, terbinane, ketoconazole, and uconazole. The rash usually arises within 48h after exposure to the medication. The dermatitis presents on the trunk and intertriginous areas and infrequently involves the mucous membranes. Differential diagnosis includes pustular psoriasis and folliculitis. Symptoms improve within days following discontinuation of the causative drug (Fig.14.3).

14 Drug Eruptions oftheLower Extremity

Fig. 14.3 Acute generalized exanthematous pustulosis is a drug reaction characterized by the onset of papules and pustules on an erythematous base

References

1. Krispinsky AJ, Shedlofsky LB, Kaffenberger BH.The frequency of low-risk morbilliform drug eruptions observed in patients treated with different classes of antibiotics. Int J Dermatol. 2020;59(6):647–

55. https://doi.org/10.1111/ijd.14703.

2. Flowers H, Brodell R, Brents M, etal. Fixed drug eruptions: presentation, diagnosis, and management. South Med J. 2014;107:724–7.

3. Shiohara T.Fixed drug eruption: pathogenesis and diagnostic tests. Curr Opin Allergy Clin Immunol. 2009;9(4):316–21.

4. Szatkowski J, Schwartz RA. Acute generalized exanthematous pustulosis (AGEP): a review and update. J Am Acad Dermatol. 2015;73(5):843–8. https://doi.org/10.1016/j.jaad.2015.07.017.

Biopsy Techniques oftheLower

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Extremity

A skin biopsy is the gold-standard in the histopathologic diagnosis of dermatological conditions. Often, skin biopsies are performed on suspicious pigmented lesions to rule out skin cancer. However, skin neoplasms and inammatory skin conditions may appear similar and are difcult to distinguish from one another clinically [1]. In these cases, a biopsy not only facilitates a histopathologic diagnosis but may direct the treatment plan. In addition, a biopsy can be curative or possibly lifesaving when one excises the lesion in toto or when the biopsy identies a treatable malignant diagnosis. Ultimately, a biopsy both can complement and conrm the diagnosis [2].

On the lower extremity, skin biopsies are generally performed on the following: suspicious neoplasms, inammatory skin conditions, and blistering rashes [2]. Providers should obtain informed consent and forewarn the patient about the possible need for further surgery post-biopsy. For example, after the initial biopsy, another surgical procedure may be necessary for a malignant lesion to be excised in toto. One should also counsel the patient about the possibility of a painful or thickened scar, especially when involving the plantar foot.

The techniques covered in this chapter are shave, punch, excisional/incisional, curettage, and nail. Choosing which type of biopsy to use in various clinical scenarios is paramount to facilitate the diagnosis (Table15.1).

15.1 Shave Biopsy

The shave biopsy is the most supercial of all the skin biopsies as the specimen encompasses only epidermis and supercial dermis. It is useful for pedunculated or exophytic lesions and is not recommended for the identication of inammatory skin conditions. Lightly shaving scale from a supercial fungal infection edge for mycological testing is not considered a shave biopsy. Two methods for the shave are the classically described technique with the device cut-

Table 15.1 Type of biopsy to use in various clinical scenarios

Biopsy method Clinical scenario Shave Skin tags, exophytic lesions, nevi Punch Skin rashes, non-melanoma skin cancer (BCC,

Incisional/ excisional ellipse Curettage Verruca, supercial non-melanoma skin cancer

Nail Longitudinal melanonychia, longitudinal

BCC basal cell carcinoma, SCC squamous cell carcinoma, HE hematoxylin and eosin, DIF direct immunouorescence

ting parallel to the skin or saucerization which creates a slightly deeper specimen. Either of these versions may be performed with one of the following: #10 or #15 surgical blades, an autoclaved razor blade that is bent slightly in a half circle, or a BioBlade (Miltex®) which has a exible blade.

After the surgical site has been prepared, the provider performs either an intradermal injection or a local block of choice, such as a digital block or a “V” block. To perform an intradermal injection, the authors use a 1cc syringe of lidocaine with a 30-gauge or 27-gauge, ½ inch needle and slowly inltrate the uid under the lesion. When using lidocaine with epinephrine, there is a blanching effect which may make visualization of the lesion difcult. No matter which local anesthetic is used, the intradermal injection technique offers immediate anesthesia allowing one to perform the biopsy without delay.

Applying the preferred instrument to the skin, a “shaving” motion is used to remove the lesion either parallel to the skin lesion or “saucerized” with a slightly deeper central section. Hemostasis is then obtained by either using a Hyfrecator or applying a topical agent like aluminum chloride. Drawbacks

SCC), vasculitis, blistering rash (edge of blister for HE stain, perilesional for DIF), ulcers Melanoma, panniculitis

(BCC, SCC) that has been diagnosed

erythronychia, glomus tumor, diagnosis of inammatory nail disorders (psoriasis, lichen planus, etc.)

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of this technique include a pigmented or cosmetically displeasing scar due to secondary wound closure and a lacking histological picture due to the absence of a full thickness specimen (Figs.15.1, 15.2, 15.3, 15.4, 15.5, and 15.6).

15.2 Punch Biopsy

In contrast to the shave, the punch biopsy offers a full thickness specimen. A punch biopsy encompasses the epidermis, dermis, and supercial subcutaneous tissue. Therefore, physicians should reserve the punch biopsy for neoplasms, blistering disorders, and inammatory skin conditions. A punch biopsy may be considered excisional if the lesion is completely encompassed in the diameter of the tool. It may be

15 Biopsy Techniques oftheLower Extremity

Fig. 15.3 Using a #10 blade, the shave biopsy is performed

Fig. 15.1 Pigmented lesion on the lateral aspect of the ankle

Fig. 15.2 Injection of local anesthesia utilizing the intradermal

technique

Fig. 15.4 A Hyfrecator is used to achieve hemostasis

also used as an incisional biopsy if sampling a small area from a larger lesion.

Prior to inltration of local anesthetic, the provider may pinch the skin to nd the relaxed skin tension lines [2]. By making the incision parallel to these skin lines, one can use these as a guide to give the best scar outcome. Postpreparation of the site, an intradermal injection of local anesthetic of the surgeon’s choice is inltrated under the lesion. After a small wheal has been raised, the area is ready to be biopsied.

Once local anesthesia has been obtained, the provider applies an appropriately sized disposable punch instrument

15.3 Excisional andIncisional Biopsies

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Fig. 15.5 Utilizing an autoclaved razor blade to perform the shave

Fig. 15.7 Injection of local anesthesia prior to punch procedure

The depth of applying a punch biopsy into the tissue must be considered carefully due to the unique anatomical surfaces and varying skin thicknesses of the lower extremity. For example, when applying a punch tool to the dorsum of the foot, the provider should be careful in controlling the depth of the biopsy to avoid important structures deep to the lesion such as vascular structures, tendons/ligaments, and bone. In contrast, the entire blade of the punch may be applied on the plantar foot skin. Once the punch has been performed, gently lift the circular button of skin and subcutaneous tissue upwards. Using an iris scissor, cut the fatty attachment as deeply as possible to give the full thickness specimen to pathology. For most skin lesions, the specimen can be sent in formalin. However, if you are sending the specimen for direct immunouorescence (DIF) staining, you should consult the pathology lab for the best medium for transport (i.e., Michel’s Fixative) since formalin can negatively affect proteins needed for the study [2]. Proceed to suture the defect or use steri-strips to cover the wound. The patient may return in 10 to 14 days for both suture removal and histopathologic diagnosis review (Figs. 15.7,

15.8, and 15.9).

Fig. 15.6 The specimen after the shave procedure

to the skin. This may range from 2 to 6mm (diameter), but most providers utilize a 3 or 4 mm punch tool for lower extremity lesions [1]. Use the dominant hand to hold the punch instrument, while the other hand places a gentle perpendicular force to the relaxed skin tension lines away from the lesion. This enables the provider to avoid “dog ears” when closing the defect with suture.

15.3 Excisional andIncisional Biopsies

Excisional and incisional biopsies both provide a full thickness specimen. When a lesion can be extirpated with a small margin of unaffected skin, an excisional elliptical biopsy is warranted [1]. In circumstances where a small area of a large lesion is sampled, an incisional elliptical biopsy is the procedure of choice.

Like the punch biopsy, it is important to consider relaxed skin tension lines. The elliptical incision axis ideally should be parallel to the relaxed skin tension lines for optimal scar outcome. Once you have obtained consent and prepared the

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15 Biopsy Techniques oftheLower Extremity

Fig. 15.8 Application of the punch tool

Fig. 15.9 Excision of the punch specimen

surgical site, use the local anesthetic technique of your choice. With this biopsy technique, the clinician draws an ellipse or fusiform shape with a 3:1 length to width ratio, a 30-degree angle at both corners of the incision, and a 2mm border around the lesion [3].

After the rst pass of the #15 blade to outline the incision, deepen the incision to include the subcutaneous tissue. Proceed to dissect the ellipse of skin carefully in one plane and send the specimen in formalin (or another media if sending for DIF). One may employ simple interrupted or running nylon sutures to close the defect.

The technique for incisional biopsy is the same as the excisional biopsy. The only difference is an incisional biopsy does not remove the lesion completely (Figs. 15.10 and

15.11).

Fig. 15.10 Elliptical incision being performed

Fig. 15.11 Removal of lesion

15.4 Curettage andElectrodesiccation

Clinicians use curettage and electrodesiccation when treating verruca or a previously biopsied non-melanoma skin cancer such as supercial basal cell carcinoma. Curettage has limited utilization and provides a fragmented specimen to the pathologist. It does not aid in diagnosing inammatory skin disorders, neoplasms, and other diseases [2].

Post skin preparation and inltration of local anesthesia, the provider should apply the curette with rm strokes over the lesion. Only the tissue sample from the rst pass with the curette is sent to pathology and in formalin. The curetted material following electrodesiccation will not aid in the diagnosis. Following curettage, topical hemostasis is applied

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