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93. Cushing CA, Phillips LG. Evidence-based medicine: pressure sores. Plast Reconstr Surg. 2013;132(6):1720–32. https://doi.org/10.1097/
PRS.0b013e3182a808ba.
94. Kuo PJ, Chew KY, Kuo YR, Lin PY.Comparison of outcomes of pressure sore reconstructions among perforator aps, perforator-based rotation fas­ciocutaneous aps, and musculocutaneous aps. Microsurgery. 2014;34(7):547–53. https://doi.
org/10.1002/micr.22257.
95. Chen YC, Huang EY, Lin PY.Comparison of gluteal perforator aps and gluteal fasciocutaneous rotation aps for reconstruction of sacral pressure sores. J Plast Reconstr Aesthet Surg. 2014;67(3):377–82.
https://doi.org/10.1016/j.bjps.2013.12.029.
96. Garg M, Rubayi S, Montgomerie JZ.Postoperative wound infections following myocutaneous ap surgery in spinal injury patients. Paraplegia. 1992;30(10):734–9. https://doi.org/10.1038/
sc.1992.141.
97. Thornhill-Joynes M, Gonzales F, Stewart CA, etal. Osteomyelitis associated with pressure ulcers. Arch Phys Med Rehabil. 1986;67(5):314–8.
98. Tavakoli K, Rutkowski S, Cope C, etal. Recurrence rates of ischial sores in para- and tetraplegics treated with hamstring aps: an 8-year study. Br J Plast Surg. 1999;52(6):476–9. https://doi.org/10.1054/
bjps.1999.3126.
99. Evans GR, Dufresne CR, Manson PN.Surgical cor­rection of pressure ulcers in an urban center: is it efcacious? Adv Wound Care. 1994;7(1):40–6.
100. Chen HC, Weng CJ, Noordhoff MS. Coverage of multiple extensive pressure sores with a single lleted lower leg myocutaneous free ap. Plast Reconstr Surg. 1986;78(3):396–8. https://doi.
org/10.1097/00006534- 198609000- 00021.
101. Hung SJ, Chen HC, Wei FC. Free aps for recon­struction of the lower back and sacral area. Microsurgery. 2000;20(2):72–6. https://doi.
org/10.1002/(sici)1098- 2752(2000)20:2<72::aid­micr5>3.0.co;2- 1.
102. Yamamoto Y, Nohira K, Shintomi Y, Igawa H, Ohura T.Reconstruction of recurrent pressure sores using free aps. J Reconstr Microsurg. 1992;8(6):433–6.
https://doi.org/10.1055/s- 2007- 1006727.
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104. Kim JH, Kwon HJ, Moon SH, Oh DY, Jun YJ, Rhie JW.Trochanteric area reconstruction with free ap using perforators as recipients: an alternative and effective option. Microsurgery. 2020;40(1):32–7.
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Lower Limb Ulcers: Clinical
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andDiagnostic Workout
VittorioRamella, MartinIurilli, AlessiaDe Grazia, andLauraGrezar
43
43.1 Introduction andGeneral Framework
43.1.1 Introduction
Successful treatment of leg ulcers depends on an accurate diagnosis based on clinical, laboratory, and instrumental data.
Most of these lesions found in this anatomical
region have an ischemic or venous etiology.
Infectious ulcers are more common in tropical countries; neoplastic ones are less frequent, but it is very important to be aware of this possibility at lastly there are a number of etiologies less com­mon and with a more complex classication.
Ulcers associated with rheumatoid disease and diabetes are also frequent.
Physical examination should be directed at the site of the ulcer, its fundus, and edges, before analyzing the potential venous or arterial components.
The rst approach in the management of leg ulcers is represented by an in-depth diagnostic and clinical picture of the patients and their lesions.
Early recognition of the ulcer and knowledge of its various possible etiologies can be a com­plex path: it is fundamental to identify the poten­tial high-risk patients in order to increase early
prevention features that are the key to lead to the healing of these wounds in the shortest possible time, improving outcomes and quality of life, and reducing complications.
Nonetheless, it is crucial to have an effect on predisposing factors in order to reduce costs and hospitalization, most patients are already debili­tated considering that many have illnesses such as diabetes or venous insufciency, and the aim of the process is to heal them in the fastest time possible in order to restore their quality of life.
Indeed, the rst approach consists of having a complete framework of the patient, which includes vital parameters, the remote pathologi­cal anamnesis, even considering their psychoso­cial status and quality of life, independence in everyday life, and last but not least the evaluation of the lesions.
43.1.2 Medical History andClinical
Examination
In the medical history, we proceed with: identication of any
initial trauma onset of lesion assessment of comorbidity progression of signs
and symptoms
previous treatments
identication of previous loco-regional and vascular surgery
V. Ramella (*) · M. Iurilli · A. De Grazia · L. Grezar Plastic Surgery Unit, University of Trieste, Cattinara Hospital, Trieste, Italy
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 M. Maruccia et al. (eds.), Pearls and Pitfalls in Skin Ulcer Management,
https://doi.org/10.1007/978-3-031-45453-0_43
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On clinical examination, the following are assessed: the depth the smell the surface assessment of drainage, if any the appearance the temperature of the skin assessment of infection by observation of the presence
of cellulitis or inammation, edema, and markers of inammation
The “probing to bone” test maneuver should always be included in the initial assessment of all ulcers with suspected infection. This test has a specicity of 85% and a sensitivity of 66% [1].
Other diagnostic tests to determine infection are deep tissue and/or bone sampling; hemato­chemical tests such as C-reactive protein and white blood cell count; and imaging with radiog­raphy, CT scan, and MRI.
For the diagnosis of osteomyelitis, the gold standard is MRI, as radiography is positive 7–15days after onset.
Properly classifying ulcers is essential to make a correct prognosis, establish proper treat-
ment, plan intervention trials, and facilitate com­munication and education of healthcare providers.
The mode of collection of the microbiological sample is considerably important. The sample should come from deep tissue or stula drainage without contact with adjacent skin.
Biopsy of the deep tissue gives more assur­ance, while syringe aspiration is preferred in case of vesicles, bullae, or abscesses, and if a swab is used, it is recommended to “curetect” the lesion rst. The amount of collection should be suf­cient for culture.
The time between collection of the material and inoculation into the culture medium should be minimized.
Collections should be made before the admin­istration of antibiotics.
43.1.3 Clinical Diagnostic Criteria
Perilesional skin Ulcer site Margins
Intact Single or
multiple
Phlegmasic Near foci
of infection
Macerated Semi-
concealed sites
Dry Near joints Rounded: capacity to
Near pressure points
Sloping: tendency to heal (e.g., venous and posttraumatic ulcers)
Stepped: loss of substance (e.g., trophic ulcers, venereal ulcers, residual of skin necrosis)
Undermined: greater involvement of the subcutis than the skin (e.g., ulcers on osteomyelitic focus)
invasion (e.g., ulcerations caused by basal cell cancer)
Everted: strong invasiveness of the causative disease (e.g., ulcerations caused by squamous cell cancer)
WBP SCORE Fund (V.FALANGA)
% granulation 0: dry lesion, dressing
% brin 1: totally controlled,
% necrosis 2: partially controlled,
Essudate WBP SCORE (V.FALANGA) MODIFIED Depth
remains adhered to the fundus
little to no amount, requires no absorbent dressing or dressing can stay in place a week
moderate amount, dressing can be changed every 2–3days
3: uncontrolled, hyper-absorbent wound, required absorbent dressing change once or more per day
Epidermal
Supercial dermal: papillary dermis
Deep dermal: reticular dermis
Subdermal
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43.1.4 Instrumental Diagnostic Criteria
• ABI (ankle-brachial index) or Winsor Index
– <0.4, severe vasculopathy – 0.4 < ABI < 0.9, mild moderate
vasculopathy – 0.91<ABI<0.99, uncertain value – 1<ABI<1.29, normal value – >1.3, uncompressible arteries with possible
calcications
• TcPO2 (Transcutaneous Oximetry), assess­ment of tissue oxygenation
– TcPO2>60mmHg, normal – 30< TcPO2<60 mmHg, functional isch-
emia (associated with stage 2a according to Leriche Fontain)
– 10 < TcPO2 < 30 mmHg, moderate isch-
emia (associated with stage 2b or 3 accord­ing to Leriche Fontain)
– <10 mmHg, severe ischemia (associated
with stage 4 according to Leriche Fontain)
• Eco-Color-Doppler
– In arterial ulcers, it conrms peripheral
obliterative arteriopathy and characterizes it in terms of stenosis/obstruction, plaque type, hemodynamics, and lesion pattern.
– In venous ulcers, it allows the assessment
of whether there is obstruction, whether it is acute or chronic, whether it is supercial or deep; whether there is thrombotic resid­ual; whether there is supercial or deep venous insufciency; it can document whether there is lymphedema and study regional lymph node stations [2, 3].
• X-ray
• Ultrasound
• MRI
• Lymphoscintigraphy in the investigation of lymphatic and infectious system diseases
• Angiography: essential when there is intent for revascularization, but an invasive method, not without risks such as hematomas, pseu­doaneurysms, and arterial lesions.
Winsor Index, which records the ratio of tibial artery systolic pressure to humeral artery sys­tolic pressure, and TcPO2, which highlights tis­sue oxygenation of peripheral districts. We consider critical peripheral ischemia to be that situation that has indices below the threshold values of 0.9 for ABI and 30mmHg for TcPO2. In elderly or diabetic patients, it is not uncom­mon to nd false negatives, due to the incom­pressibility of vessels caused by glycosylation or the presence of calcications, so additional tests, such as TcPCO2 or the toe-brachial index, where the abnormal value is considered <6, may be necessary [4].
If peripheral ischemia is detected by the ABI index measurement and TcPO2 is present, an echocolordoppler of the femoro-popliteal-tibial axis and the arteries proper to the foot (common plantar, dorsal foot) can be performed. This examination allows for dening the patency sta­tus and any hemodynamic changes of the femoral- distal arterial axis.
The diagnostic pathway of obstructive arteri­opathy can be completed by arteriography. This examination should be conducted with appropri­ate timing and exposures in order to visualize the arteries of the leg and the arteries proper to the feet.
AngioRMN is an important examination espe­cially when vascular involvement involves other sites besides the lower limbs, which is indicated in some special cases for a better denition of the extent of arteriopathy especially for the purpose of surgical revascularization.
43.1.5 Laboratory Diagnostic Criteria
– Cell blood count, indices of inammation,
hemogenic tests, electrolytes, blood glucose,
and immunological.
– Deep swab and tissue sampling for microbio-
logical examination.
– Tissue biopsy.
The objective examination is completed by an evaluation of the pulses and peripheral pressures with a portable Doppler, measurement of the
When, in addition to ischemia, we are faced with infection, the indication for surgery and the likelihood of amputation increase exponentially.
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To check the level of bacterial load, in the presence of clinical signs of infection such as perilesional inammation, pain, or increased exudate, deep tissue collection should be taken and sent for microbiological examination.
The culture test result, when positive, is accompanied by an antibiogram in which the individual antibiotics tested are indicated accord­ing to the degree of sensitivity or resistance.
The bacterial load and minimum inhibitory concentration (MIC) of the drug should also be given.
As ulcer infection often leads to osteomyelitis, evaluation of the underlying bone is critical, since this pathology does not involve any particu­lar symptomatology that clinically highlights it.
Taking an X-ray is therefore the rst assess­ment to detect changes in the bone segments. Usually, the radiograph is positive a few weeks after the onset of the infectious phase. Cortical irregularity of the bone underlying an ulcer is already a suspicious sign. Bone rarefaction or destruction can reveal signs of osteomyelitis. They appear when 30–50% of the bone is destroyed [5].
Since irregularity, rarefaction, and destruction of the bone may be present in various clinical pic­tures such as in diabetes, trauma, Charcot pathol­ogy, and dysgenesis, and an accurate differential diagnosis may be necessary.
The only predictive and diagnostic test for osteomyelitis is bone biopsy.
The most sensitive examination is MRI, which provides diagnostic accuracy in 80–90% of cases, as well as precise anatomic denition, useful for osteomyelitis surgery.
43.2 Dierential Diagnosis
43.2.1 Vascular Ulcers
43.2.1.1 Venous-Based Ulcers
Venous ulceration is dened as an ulceration related to perforating, saphenous, or deep venous incompetence, or a combination of these. In these patients, deep venous reux is usually associated with calf perforating vein incompetence.
Saphenous vein reux usually accompanies this condition.
Up to half of the patients presenting with venous ulcers in the lower extremities have lesions resulting completely from saphenous vein incompetence.
Clinical cases with varicose veins and con­comitant ankle ulcers often highlight perforating vein incompetence on clinical examination.
It is common for patients to report a recent or past local trauma; a previous episode of deep venous thrombosis is also common but not so recurring.
Last but not least, the possibility of a congeni­tal thrombophilic disease has to be reported if present [6].
The patient needs to be asked if they have ever had calf swelling (as opposed to ankle swelling which is typical in varicose veins and incompe­tence of perforating vessels) and, above all, if there are symptoms suggestive of venous claudi­cation: intense calf pain that starts when the patient walks for 100 or 200m.
It is fundamental to distinguish this kind of pain from the dull, deaf, ache that some patients feel standing for a prolonged period of time which is common when having venous incompetence.
Venous ulcers can be found more commonly on the medial malleolus region, to a lesser extent on the lateral. They are usually associated with a less serious saphenous ineffectiveness.
Sometimes these lesions can be found posteri­orly or even be circumferential; their depth varies from 1 to 2mm to an extent till the deep fascia.
It can be helpful to know that usually, they are much deeper than the varicose and vasculitic ones.
An inammatory context always goes with this type of lesion, especially around the ankle, also with visible narrow supercial veins, pig­mentation, and lipodermatosclerosis.
To be noted that patients with venous ulcers could not have varicose veins.
When the patient comes to the hospital rst, it is common that these lesions are infected, the wound could also present little foreign bodies, wigglers, and slough.
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Once these things are removed and the wound correctly washed and debrided, the bottom could be lled with the granulation tissue of pink/red color.
If the edges are undermined, you should think about infectious diseases such as tuberculosis or other chronic infections.
The purpose of the clinical examination is to not only identify all sites of venous reux or obstruction but also to exclude the possibility of arterial inadequacy as a contributing factor.
Patients need to be examined both in laying and standing positions, signs of obstruction have to be accessed proximally (iliac and femo­ral veins) and distally (saphenous and ankle veins), lipodermatosclerosis needs to be reported just as signs of pigmentation, skin texture and thickness, and signs of inammation (rubor, tumor, calor, dolor). Even abdominal examina­tion and rectal examination are important and they are mandatory for every patient with a swollen limb.
Toes and forefoot require attention in order to detect any sign of ischemia (cianosis and capil­lary rell).
The arterial pulse of the ankle and feet needs to be palpated with bare hands or better by a Doppler ultrasound, such as the ABI index.
As mentioned earlier, a Doppler ultrasound is useful to detect both the insufciency of the saphenous veins and the perforator veins.
However, the most effective method to study the venous system of the lower limb is the Duplex ultrasound, which should be performed in every case of detected venous lesions in order to dene the extent of the problem.
This technique allows the identication of the incompetent veins and the potential obstruction of some segments.
If this procedure is not available, venography can be used as long as you have an expert radiolo­gist in vascular procedures.
43.2.1.2 Arterial-Based Ulcers
Ischemic ulcers may be located on the toes or forefoot in an area of cyanotic and obviously pre­gangrenous skin. Another common site is the heel, especially in bedridden patients. These
ulcers are usually accompanied by severe pain at rest and are not difcult to diagnose.
Ischemic ulcers may also occur on the dorsum of the foot or anterior surface of the leg or may mimic venous ulcers by being located above the medial or lateral malleolus [7].
The fundus of a typical ischemic ulcer is usu­ally lled with pale yellow purulent exudate and necrotic debris, often with islands of gangrenous tissue. The removal of necrotic debris will likely reveal a deep fascia or tendon, with little or no granulation tissue. The edges are poorly epitheli­alized and may be pierced.
A history of ischemic pain at rest is common in severe cases, while lesser degrees of ischemia are usually associated with claudication intermit­tens. Patients are often heavy smokers. Many patients are elderly and bedridden. This is espe­cially true for heel ulcers, which are usually described as pressure lesions.
Ischemic ulceration usually occurs in an area of clear ischemic skin, which may be cyanotic or pale and shiny [8].
It is necessary to evaluate the pulses: femoral, popliteal, and ankle. Edema may make the last one more difcult to perceive, in which case Doppler ultrasonography should be used. It is not sufcient to palpate only one ankle pulse, such as the dorsalis pedis, and then consider if there is adequate arterial perfusion; it is necessary to pal­pate both.
The ankle pulse pressure of diabetic patients with ischemic ulcers may appear normal. This is due to increased arterial wall stiffness in patients with diabetes, attributable to calcication, which makes the measurement of arterial pulse pressure unreliable. Ischemic ulcers can also result from small vessel insufciency, particularly in throm­boangiitis obliterans (Buerger’s disease) and vas­culitis. Ankle pulse pressure may be normal. Diagnosis depends on the clinical examination of the capillary rell time of the toe, which is mark­edly increased with ischemia. Measurement of the toe pulse pressure by photoplethysmography (PPG) and a miniature sphygmomanometric cuff may also be useful. The pressure gradient between the ankle and toes should not normally exceed 30mmHg.
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Duplex examination (ECD) of the arteries of the lower extremities is the most effective method for determining the presence and distribution of arterial stenosis and occlusions. This technique can be used to evaluate vessels of various cali­bers. The severity of a stenosis can be accurately assessed by measuring the peak ow velocity at the stenosis versus the peak ow velocity in the adjacent non-stenotic vessel. The ratio of these measurements is called the systolic peak velocity ratio. The length of the stenosis can also be assessed. This information is essential in deter­mining whether an arterial lesion has an indica­tion for treatment with an endovascular technique.
Angiography is usually reserved for the con­rmation of ultrasound results before angioplasty or surgery.
43.2.1.3 Mixed Vascular-Based Ulcers
Ankle ulceration due to a combination of arterial and venous insufciency is not uncommon, espe­cially in the elderly. Much of the workload in the management of leg ulcers falls on community nurses, and modern training courses teach the skills needed to measure the Winsor index to detect this problem [9]. This prevents misman­agement of the patient by avoiding the adverse effects of applying a high-compression bandage to a severely ischemic limb.
These patients are more likely to provide a history of varicose veins or previous deep vein thrombosis than a history suggestive of arterial insufciency. Objective examination also likely suggests that the ulcer is purely venous in origin. There is often no obvious cyanosis or other phys­ical signs indicative of decreased arterial supply. Accurate examination of the arterial pulses of the foot is therefore very important in all patients with a venous ulcer.
Doppler ultrasound measurement of ankle pulse pressure is essential. Doppler ultrasonogra­phy can be used to identify sites of venous incom­petence. Comprehensive patient assessment includes duplex ultrasound evaluation of the arte­rial and venous systems of the lower extremity to plan effective treatment in these patients.
43.2.1.4 Vasculitic-Based Ulcers
If there is a clear history of rheumatoid arthritis, scleroderma, polyarteritis nodosa, or other condi­tions with a known tendency for vasculitis, the diagnosis should be straightforward. Difculties emerge when the patient presents with an appar­ent venous ulcer and no other obvious manifesta­tions of vasculitis.
Rheumatoid ulcers are usually serpiginous and shallow. Often multiple, they may involve the lateral or posterior surfaces of the leg, but they do not seldom appear in the malleolar regions and mimic venous ulceration, although usually without surrounding lipodermatosclero­sis. Diligent examination of the hands and other joints will usually show evidence of rheumatoid arthritis.
The diagnosis can be conrmed by serologic testing for the rheumatoid factor. Other systemic inammatory markers (e.g., erythrocyte sedi­mentation rate, ESR) may also be used.
Vasculitic ulcers are in general usually present as small, multiple, and painful. They may be present in the lower leg or foot.
Specic investigations for vasculitis include the Rose–Waaler test and latex test for rheuma­toid antibodies and tests for autoantibodies.
Anti-DNA double-stranded antibodies are elevated in SLE (normal: 6–8mg/L).
Anti-neutrophil cytoplasmic antibodies (ANCA) are elevated in polyarteritis nodosa and Wegener’s granulomatosis. In many cases of vas­culitis, a specic cause cannot be identied.
In these cases, a biopsy of the ulcer edge including healthy skin and diseased skin may be useful.
43.2.2 Diabetic Ulcers
Diabetic ulcers can be the result of peripheral neuropathy, ischemia, or infection, factors that are common in this disease or could be a combi­nation of all [10].
Speaking of ischemia as a prevalent part, these lesions could be found on the toes, forefoot, or heel, especially in bedridden patients.
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Regarding neuropathy which is typical in dia­betes, these ulcers are the result of the pressure on the sole of a Charcot’s foot.
Charcot foot is a condition that causes the weakening of the bones in the foot that can occur in people with signicant nerve damage (neurop­athy). The bones are weakened enough to frac­ture, and with continuous pressure and walking the foot eventually changes shapes.
It is typically associated with diabetes and is a serious condition that can lead to severe defor­mity, disability, and even amputation [11, 12].
Charcot foot develops as a result of neuropa­thy which decreases sensation and the ability to feel temperature, pain, or trauma. Because of the diminished sensation, the patient may continue to walk even with some injuries that makes it worse.
Symptoms of peripheral neuropathy include hyperesthesia, burning pain, paresthesia, and sen­sation of cold and heat, which worsen overnight.
Signs consist of reduced pain perception, tem­perature, and vibration.
Some patients come to the hospital with wounds but sometimes they are not aware of dia­betes; it is fundamental to have blood glucose and urine examination and if the result is abnor­mal they should be addressed to the specialist.
After evaluating the location and appearance of the ulcers, a neurologic examination may not show any signs of peripheral neuropathy.
Also, venous diseases should be considered and excluded by examination and ultrasound, as mentioned before, and even arterial examination should be done.
The absence or reduction of ankle pulse should be investigated by arteriography; periph­eral ischemia in diabetic patients is often attrib­uted to microangiopathy and it is mandatory to remember that this kind of patients have a major incidence of atherosclerosis that could lead to occlusion of the main limb vessels [13].
others. Many patients with venous or ischemic ulcers provide a history of precipitating trauma. It is good medical practice that all patients pre­senting to the emergency department with abra­sions or lacerations of the lower leg be examined carefully for signs of venous reux or arterial insufciency. If healing is slow, diabetes should be ruled out. Simple but necessary investigations are often omitted, and the initial laceration may develop into a chronic ulceration. It should be remembered that abrasions and lacerations of the lower leg and ankle are always slow to heal, espe­cially in the elderly, even in the presence of nor­mal arteries and veins. A tight bandage or cast can cause skin necrosis and ulceration, particu­larly in the elderly and those with minor ischemia.
Traumatic ulcers can be self-induced. Dummy ulcers can be quite bizarre in site and appearance because they are inicted by agents such as elas­tic bands tied tightly around the calf. The possi­bility of self-iniction should always be kept in mind in patients whose ulcers are excessively slow in healing or repeatedly reoccur.
43.2.4 Pressure Ulcers
Martorell described painful leg ulcers in severely hypertensive patients. Most of them were located on the posterior surface of the leg, unlike the typ­ical ischemic ulcers usually found on the dorsum of the foot or the anterior surface of the leg. It has been suggested that most, if not all, of these ulcers, are caused by the embolization of athero­sclerotic debris into small dermal vessels. However, Martorell described a “hyalinosis” of the tunica intima with stenosis of the arteriolar lumen.
43.2.5 Edema Ulcers
43.2.3 Post-traumatic Ulcers
Traumatic ulcers can result from any type of trauma: accidental, self-induced, iatrogenic, and
Ulceration is extremely rare in lymphedema, whether primary or secondary to lariasis or malignant lymph node involvement or iatrogenic. When they occur, these ulcers are usually small,
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indolent, and painless and appear on the anterior aspect of the ankle or leg.
Patients usually recount a long history of swelling of the back of the foot and ankle. The condition is often hereditary, and primary famil­ial lymphedema is known as Milroy’s disease.
Lymphedema is swelling of the limb in the presence of a normal venous system. This can be easily established by performing duplex ultraso­nography. Failure to demonstrate a venous cause in a patient with lower extremity edema does not prove that the patient has lymphedema, but it greatly limits the range of possible diagnoses. Doppler ultrasound examination of the ankle pulses is important in any case of doubt, as isch­emic ulceration and lymphedema may coexist.
The most appropriate method to study lym­phatic function in order to conrm the diagnosis is quantitative isotope scintigraphy.
In patients with congestive heart or renal fail­ure, ulceration may occur in the grossly distended skin of severely edematous legs. Examination usually shows no evidence of venous insuf­ciency, although some impairment of arterial supply is likely in these elderly patients. The ulcers are usually distributed over all surfaces of the leg; they are shallow and may have a serpiginous outline. Treatment should be directed primarily at correcting congestive failure and reducing edema of the leg. Liver cirrhosis is also among the edemigenous syndromes, and declivous edema can also be caused by blockage of the portal system of another nature.
43.2.6 Infectious-Based Ulcers
43.2.6.1 Tropical Ulcers
These are chronic ulcers of the lower leg or back of the foot that occur among poor people in tropi­cal countries and are of mixed bacteriology [14].
The most common pathogens are
Pseudomonas aeruginosa, Proteus mirabilis, and Proteus vulgaris, and also Treponema vincenti
and Bacillus fusiformis. The diagnosis of tropical ulcer should exclude an ulcer with a specic
underlying cause, such as ischemia, diabetes, or hemoglobinopathies.
43.2.6.2 Infective Ulcers ofOther Nature
Leg ulcers due to specic infections are also more common in tropical countries. Tuberculous skin ulcers (scrofula) may occur on the legs, but are more common elsewhere and are character­ized by an undermined, irregular, bluish, and crumbly edge. The ulcers are often multiple, and the patient usually has signs of pulmonary or skeletal tuberculosis.
Secondary syphilis is nowadays very rare after the introduction of antibiotics, but occasionally a syphilitic gingiva may ulcerate, forming a pain­less, circular, perforated ulcer with a crust of skin at the base.
Other specic infections include leprosy, Guinea worm, caused by the nematode Dracunculus medinensis, and anthrax (Woolsorter’s disease), which rarely occur on the lower limb. Buruli pustule, or Baghdad pustule, is caused by tropical Leishmania and transmitted by sand y. Actinomycosis, epidermophytosis, blastomycosis, moniliasis, and mycetoma (Madura’s foot) are other infections that can cause leg ulceration.
43.2.6.3 Osteomyelitis Ulcers
Chronic osteomyelitis of the tibia can be identi­ed by forming a sinus that can mimic a venous ulceration.
Osteomyelitis can occur anywhere in the leg, but it is more likely to be mistaken for venous ulceration when it occurs, as is commonly the case, in the lower third of the medial surface of the leg. It is very difcult to distinguish the appearance of necrotic plaque from venous ulcer­ation. Osteomyelitis of the toes may occur in association with ischemic ulceration.
Rarely, there may be a history of pulmonary or abdominal tuberculosis or a history of local trauma. The radiographic examination normally shows bone destruction and sequestration forma­tion typical of osteomyelitis.
43 Lower Limb Ulcers: Clinical andDiagnostic Workout
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43.2.7 Neoplastic Ulcers [15]
43.2.7.1 Squamous Cell Carcinoma Ulcer
Squamous cell carcinoma can develop in an inveterate venous ulcer and is known as Marjolin’s ulcer.
Squamous cell carcinoma should be suspected in the presence of excessive tissue growth at the base or edge of the ulcer. Biopsy and histological examination should be performed urgently.
Squamous cell carcinoma may also develop per primum on the leg and mimic a venous ulceration.
43.2.7.2 Basal Cell Carcinoma Ulcer
Basal cell carcinoma may occasionally present on the leg. The appearance is less likely to mimic that of venous ulceration than squamous cell car­cinoma, and the diagnosis is established by biopsy.
43.2.7.3 Ulcerated Melanoma
Malignant melanoma is common in the foot and lower leg, but it is very unlikely to be confused with venous ulceration.
43.2.7.4 Sarcoma Ulceration
Kaposi’s sarcoma may present with skin ulcer­ations. The ulcers are usually small and multiple, similar to vasculitic ulcers. Currently rare, ulcer­ated Kaposi’s sarcoma is likely to become an increasing differential diagnosis with the spread of acquired immunodeciency syndrome (AIDS). Bone tumors, sarcoma, and osteoclastoma may also present with ulceration of the leg.
43.2.7.5 Ulcerated Lymphoma
Cutaneous B- and T-cell lymphomas associated with pyoderma gangrenosum and skin ulcers have been described. Pyoderma gangrenosum is also a rare complication of ulcerative colitis or Crohn’s disease.
43.2.8 Other Ulcers [16]
43.2.8.1 Steroid Ulcers
Patients on long-term steroid treatment may develop skin ulcers, particularly in the lower extremities, especially in the elderly. These are usually broad, shallow, serpiginous ulcers with poorly epithelialized edges, and the surrounding skin is thin and fragile. They are often similar to rheumatoid ulcers and are known to be slow to heal.
43.2.8.2 Neuropathic Ulcers
Patients with paraplegia or peripheral neuropathy may develop ulcers. Generally, ulcerations are misrecognized pressure injuries. Treatment is the prevention of pressure lesions, and once the pathogenic noxa is removed ulcer healing occurs easily by cleaning and standard dressings. Pressure injuries of various kinds can occur, including from decubitus medical devices such as catheters.
43.2.8.3 Dermatitis Ulcers
Dermatitis by contact with stinging substances can cause existing ulcers not to heal or new ulcers to develop. This condition is due to sensitivity to medicated bandages or local antibacterials. The skin is red and scaly, and the ulcers are usually shallow with a yellow base, and can appear on any surface of the body.
The skin around ulcers is more sensitive than normal skin, and contact dermatitis is a common complication of ulcer dressings. For this reason, local steroids, antibiotics, medicated dressings and bandages (particularly zinc) should be scru­pulously avoided and replaced by simpler alternatives.
Today, cotton bandages and compression stockings are available and should be prescribed for patients who are allergic to nylon. Lycra is commonly used in the manufacture of elastic stockings, and its use avoids allergies to rubber.