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Fig. 6.8 Pitting test by US probe: (a) A positive squeezing test by US.(b) The thickness of the subcutaneous layer reduces signicantly with disappearing of dermal edema

A. Caggiati and L. Caggiati

DE consists of an increase of water content of the dermis, with dermal thickening and hypoechogenicity. In most cases, edema is limited to the papillary dermis.

Tissue echogenicity is evaluated by the visual comparison of US ndings from the swollen limb areas and the adjacent or contralateral homologous areas.

Finally, US allows us to better evaluate the pitting phenomena by compressing the skin with the probe instead of the nger. This maneuver allows us to quantify the compression-related reduction of skin thickness, the time of recovery of the initial conditions, and structural changes provoked by the pressure exerted on the skin. (Fig.6.8). Skin squeezing by the US probe is negative in the presence of inammatory processes and lipedema.

A positive squeezing test (Fig.6.8) easily reveals those legs in which a mechanical treatment (manual or pneumatic lymphatic drainage, massotherapy, etc.) may effectively reduce the SCL or CL edema.

However, US does not allow for a differential diagnosis of the cause of leg edema. In fact, current knowledge is limited to the differential diagnosis between edema of the subcutaneous layer and increase in volume of the muscular compartment. With regard to subcutaneous edema, US allows us to discriminate between inammatory and non-inammatory causes.

Funding The author was kindly supported by Bauerfeind AG, Germany.

References

1. Vasquez MA, Rabe E, McLafferty CK, Shortell RB, Marston WA, Gillespie D, et al. Revision

of the venous clinical severity score: venous outcomes consensus statement: special communication of the American venous forum ad hoc outcomes working group. J Vasc Surg. 2010;52:1387–96.

6 Investigations ofLower Limb Edema

2. Wittens C, Davies AH, Baekgaerd N, Broholm R, Cavezzi A, Chastanet S, et al. Editor’s

choice. Management of chronic venous disease: clinical practice guidelines of the European Society for Vascular Surgery (ESVS). Eur J Vasc Endovasc Surg. 2015;49:678–737.

3. Rabe E, Carpentier P, Maggioli A. Understanding lower leg volume measurements used in

clinical studies focused on venous leg edema. Int Angiol. 2018;37(6):437–43.

4. Berard A, Kurz X, Zuccarelli F, et al. And the VEINES group: reliability study of the leg-O-

meter, an improved tape measure device, in patients with chronic venous insufciency of the leg. Angiology. 1998;49:169–73.

5. Mosti G, Caggiati A.The effects of water immersion and walking on leg volume, ankle cir-

cumference and epifascial thickness in healthy subjects with occupational edema. Phlebology. 2021;36(6):473–80. https://doi.org/10.1177/0268355520984065. Epub 2021 Jan 6. PMID: 33407051

6. Rabe E, Stucker M, Ottilinger B.Water displacement leg volumetry in clinical studies. A

discussion of error sources. BMC Med Res Methodol. 2010 Jan;13(10):5. https://doi.

org/10.1186/1471-2288-10-5.

7. Wall R, Lips O, Seibt R, Rieger MA, Steinhilber B.Intra- and inter-rater reliability of lower

leg water plethysmography, bioelectrical impedance and muscle twitch force for the use in standing work evaluation. Physiol Meas. 2017;38(5):701–14.

8. Devoogdt L, Van Nuland G, Christiaens C, Van Kampen M.A new device to measure upper

limb circumferences: validity and reliability. Int Angiol. 2010;29(5):401–7.

9. Perrin M, Guex JJ.Edema and leg volume: methods of assessment. Angiology. 2000;51:9.12.

10. Blume J, Langenbahn H, Champvallins M.Quantication of edema using the volumeter tech-

nique: therapeutic application of Daon 500 mg in chronic venous insufciency. Phlebology. 1992;2(Suppl):37–40.

11. Tierney S, Aslam M, Rennie K, et al. Infrared optoelectronic volumetry, the ideal way to mea-

sure limb volume. Eur J Vasc Endovasc Surg. 1996;12:412–7.

12. Northeld JW, Holroyd B, et al. Validation of an optoelectronic limb volumeter (Perometer).

Lymphology. 1997;30:77–97.

13. Veraart JCJM, Neumann HAM. Leg volume measurements with a modied optoelectronic

measurement system. Phlebology. 1995;10:62–4.

14. Tischer T, Oye S, Wolf A, Feldhege F, Jacksteit R, Mittelmeier W, Bader R, Mau-Moeller

A.Measuring lower limb circumference and volume - introduction of a novel optical 3D volumetric measurement system. Biomed Tech (Berl). 2020;65(2):237.

15. Mosti G, Bergamo G, Oberto S, Bissacco D, Chiodi L, Kontothanassis D, Caggiati A. The

feasibility of underwater computerized strain gauge plethysmography and the effects of hydrostatic pressure on the leg venous Haemodynamics. EJVES Vasc Forum. 2020;47:60–2.

16. Rosfors S, Persson LM, Blomgren L.Computerized venous strain-gauge plethysmography is a

reliable method for measuring venous function. Eur J Vasc Endovasc Surg. 2014;47(1):81–6.

17. Kogo H, Murata J, Murata S, Higashi T.Validity of a new quantitative evaluation method

that uses the depth of the surface imprint as an indicator for pitting edema. PLoS One. 2017;12(1):e0170810.

18. Nishibe T, Nishibe M, Akiyama S, et al. Bioelectrical impedance analysis of leg edema and

its association with venous functions in patients with saphenous varicose veins. Int Angiol. 2020;39:284–9.

19. Barnes MD, Mani R, Barrett DF, et al. How to measure changes in edema in patients with

chronic venous ulcers? Phlebology. 1992;7:31–5.

20. Jaffrin MY, Morel H.Body uid volumes measurements by impedance: a review of bioimped-

ance spectroscopy (BIS) and bioimpedance analysis (BIA) methods. Med Eng Phys. 2008 Dec;30(10):1257–69.

21. Marotel M, Cluzan RV, Pascot M, et al. Tomodensitomtrie de 150 cas de lymphoedemes des

membres inferieurs. J Radiol. 1998;79:1373–8.

22. Ling H, et al. Volumetric differences in the suprafascial and subfascial compartments of patients

with secondary unilateral lower limb lymphedema. Plastic Reconstr Surg. 2020;145:1528–37.

Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/

A. Caggiati and L. Caggiati

23. Cluzan RV, Pereti IDDI, Alliot AF, et al. Cutaneous and subcutaneous changes in lymphedema

analysed with high resolution MR imaging, indirect lymphography and lymphoscintigraphy. In: Whitte M, Whitte C, editors. Progress in lymphology XIV.Lymphology; 1994. p. 305–8.

24. Arrivé L, Derhy S, Dahan B, El Mouhadi S, Monnier-Cholley L, Menu Y, Becker C.Primary

lower limb lymphoedema: classication with non-contrast MR lymphography. Eur Radiol. 2018 Jan;28(1):291–300.

25. Czerniec SA, Ward LC, Meerkin JD, Kilbreath SL. Assessment of segmental arm soft tis-

sue composition in breast cancer-related lymphedema: a pilot study using dual energy X-ray absorptiometry and bioimpedance spectroscopy. Lymphat Res Biol. 2015 Mar;13(1):33–9.

26. Dietzel R, Reisshauer A, Jahr S, Calaore D, Armbrecht G.Body composition in lipoedema

of the legs using dual-energy X-ray absorptiometry: a case-control study. Br J Dermatol. 2015;173(2):594–6. https://doi.org/10.1111/bjd.13697. Epub 2015 Jul 2. PMID: 25641018

27. Hidding JT, Viehoff PB, Beurskens CH, van Laarhoven HW, Nijhuis-van der Sanden MW, van

der Wees PJ.Measurement properties of instruments for measuring of lymphedema: systematic review. Phys Ther. 2016;96(12):1965–81.

28. Caggiati A.Utrasonography of skin changes in legs with chronic venous disease. Eur J Vasc

Endovasc Surg. 2016 Oct;52(4):534–42.

29. Caggiati A, Caggiati L.Sonography of leg venous edema. Acta Phlebologica. 2018;19:59–62.

30. Caggiati A.Ultrasound of verrucous hyperplasia of the skin related to venous stasis and effects

of compression treatment. J Vasc Surg Cases Innov Technol. 2019;5(3):225–7.

Differential Diagnosis ofLower Extremity Oedema

SandeepRajPandey andMoorooteeaMehtaRaakaRai

7.1 Introduction

Lower extremity edema with a wide range of possible etiologies is a common problem in older patients. The diagnosis can be narrowed by categorizing the edema according to its duration, distribution, and accompanying symptoms. The differential diagnosis includes systemic illnesses such as heart failure, liver disease, malnutrition, and thyroid disorder; local conditions such as pelvic tumors, infection, trauma, venous thrombosis, chronic venous diseases, cellulitis, lymphoedema, and lipoedema; and various medications (antihypertensives, hormones, chemotherapy, NSAIDs, etc.) known to increase the risk of edema of the lower extremities. Patients with lower limb edema are frequently referred to vascular specialists for differential diagnosis evaluation and further management. Appropriate therapy is based on the presentation of edema and its identied etiology and differential diagnoses.

Detailed evaluation of lower extremity edema differential diagnoses mainly depends on:

History [1, 2]

1. Duration in acute is (<72h) vs. chronic.

2. Pain is common in deep vein thrombosis, CRPS, less severe in venous

insufciency.

S. R. Pandey (*) Annapurna Hospital, Kathmandu, Nepal

M. M. R. Rai Victoria Hospital, Quatre Bornes, Mauritius

https://doi.org/10.1007/978-981-16-6206-5_7

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S. R. Pandey and M. M. R. Rai

3. If systemic disease:

Cardiac disease presents orthopnea and paroxysmal nocturnal dyspnea.

Renal disease has proteinuria.

Hepatic disease presents jaundice and ascites.

4. Malignancy condition presents lymphedema.

5. Ther’s improvement with elevation/recumbency in venous insufciency.

6. In OSA there is snoring and daytime somnolence.

7. Medications: B-blocker, calcium channel blockers, hormones, nonsteroidal

anti-inammatory drugs.

Physical Exam [1, 2]

1. Distribution: can be unilateral, bilateral, or generalized

2. Quality: can be pitting or non-pitting

3. TTP: DVT, cellulitis

4. Varicose veins: venous insufciency

5. Kaposi–Stemmer: inability to pinch dorsum of foot at base of 2nd toe

(lymphedema)

Lower extremity edema either unilateral or bilateral is acute or chronic:

Unilateral acute lower limb edema mainly occurs due to deep vein thrombosis, cellulitis, ruptured Baker’s cyst, ruptured medial head of gastrocnemius, and compartment syndrome.

Unilateral chronic lower limb edema may occur due to venous insufciency, lymphedema as a result of radiation, surgery, abdominal or pelvic malignancy, bacterial infection and complex regional pain syndrome, pelvic tumor or lymphoma causing external pressure on veins, congenital venous malformations, and May– Thurner syndrome (iliac-vein compression syndrome).

Bilateral acute lower limb edema mainly occurs due to drugs or bilateral deep vein thrombosis or acute worsening of systemic diseases (heart failure, renal disease).

Bilateral chronic lower limb edema occurs due to systemic disease mainly cardiac, renal (nephritic syndrome, glomerulonephritis), hepatic or pulmonary hypertension, venous insufciency bilaterally, OSA, Lymphedema (secondary to tumor, radiation, bacterial infection, lariasis), lipedema, premenstrual edema, pelvic tumor or lymphoma causing external pressure, dependent edema, diuretic-indued edema, preeclampsia, anemia, protein losing enteropathy, malnutrition, malabsorption, restrictive pericarditis, restrictive cardiomyopathy, late pregnancy, and idiopathic edema.

7 Dierential Diagnosis ofLower Extremity Oedema

7.2 Brief Details ofCommon Causes

7.2.1 DVT andChronic Venous Disease

Deep vein thrombosis occurring mainly in the soleal plexus results in obstruction to venous ow. One of a swollen, warm, tender calf is the clinical picture of DVT.The resulting edema is pitting (Fig.7.1) in nature and is usually much softer than in established lymphedema. Often, there are underlying risk factors, such as recent surgery or immobility, malignancy, a preceding long duration ight >6h., or thrombophilia. The diagnosis is conrmed with duplex scanning or venography. Treatment is with anticoagulation [3].

One of the long-term sequelae of DVT is post-thrombotic syndrome (PTS). Here, there is reux in the deep venous system, or deep venous insufciency, resulting in chronic swelling of the limb, lipodermatosclerosis, and varicose veins, and in severe cases, venous ulceration (Figs.7.2 and 7.3). On clinical grounds alone, this may be more difcult to differentiate from lymphedema, and further investigation, as outlined later in lymphedema details below in Sect. 2.3, may be required [3].

Fig. 7.1 DVT pitting edema

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Fig. 7.2 Varicose veins

S. R. Pandey and M. M. R. Rai

7.2.2 Cellulitis

Recurrent cellulitis can complicate venous disease (Fig. 7.4) of the lower limb, exacerbating swelling and venous hypertension and making venous ulcers harder to treat because lymph exudes through ulcers.

Key features which distinguish cellulitis are it is typically unilateral and acute and often presents with systemic symptoms (fever, leukocytosis).

Risk factors of cellulitis are immunosuppression, previous episodes, DM, PVD, etc.

7.2.3 Lymphedema

Lymphedema is found in both sexes, although women are investigated for this disease more often than men. It can be seen at any age as already noted, and two-thirds of cases are unilateral. The distal part of the leg is affected initially, with proximal extension occurring later. The feet are not spared. Patients with complete absence of lymphatics have a history of long-term swelling, while those with impaired lymphatics have a shorter history.

7 Dierential Diagnosis ofLower Extremity Oedema

Fig. 7.3 PTS

Fig. 7.4 Cellulitis edema

The initial symptom is usually painless swelling. The patient may also complain of a feeling of heaviness in the limb, especially at the end of the day and in hot weather. Symptoms may vary throughout the menstrual cycle [4].

On initial examination, the swelling is seen as pitting edema, but with time, brosis in the subcutaneous tissues causes the classical non-pitting signs [4]. The

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S. R. Pandey and M. M. R. Rai

distribution is asymmetrical, and patients have a positive Stemmer sign (the inability to pinch the skin of the dorsum of the second toe between the thumb and forenger) [5]. Early in the disease process, the edema can spread proximally (or distally), but this is uncommon after the rst year. Radial enlargement, however, is usually progressive if treatment is not instituted. With time, skin changes are seen over the affected area; the skin becomes thicker (hyperkeratosis) and rougher (papillomatosis) and skin turgor is increased [4, 6]. In severe cases, the skin can break down, with lymph exuding through any skin breaks. This compromises healing and leads to an increased risk of infection. Recurrent infections, cellulitis, and lymphangitis are common. This unfortunately can lead to further deterioration in lymphatic drainage, ending in a vicious cycle of infection and worsening edema.

Lymphangiosarcoma is a rare late complication of lymphedema [4]. This was originally described in the lymphedematous arms of patients following radical mastectomy (Stewart Treves syndrome [7]) but has also been described in patients with Milroy disease [8]. It appears to be an earlier complication following radical mastectomy than in those with congenital lymphedema (average, 10 vs 38 years postdiagnosis) [9]. Treatment is primary radiotherapy, with surgery reserved for patients with discrete, nonmetastatic disease.

7.2.3.1 Primary Lymphedema

This is caused by a congenital abnormality or dysfunction in the lymphatic system and can be further classied according to age at initial examination (Fig.7.5). The congenital form is detected at birth or in the rst year of life and may either be sporadic or familial. The familial form is known as Milroy disease and is rare [10]. It is thought to result from an autosomal inheritance of a single gene [11]. The onset of lymphedema praecox is between the ages of 1 and 35 years [4]. The onset of lymphedema tarda occurs after 35 years of age [4].

The most common of these is the praecox variety. Primary lymphedema is more common in females, especially lymphedema praecox, where the onset is particularly common around menarche [5]. Symptoms may be linked to a minor trauma [12], suggesting that the abnormal lymphatics have coped under normal circumstances but are unable to cope with an increase in tissue uid.

Alternatively, primary lymphedema can be classied according to the abnormality found in the lymphatics. Thus, it may be aplastic, hypoplastic, or hyperplastic. These terms suggest an abnormality in the development of the lymphatic system. While this is true for congenital lymphedema, cases of later-onset primary lymphedema might be due to an acquired abnormality. It is difcult to prove whether the abnormal lymphatics seen when these patients were investigated had existed in the same state since birth. Browse and Stewart have made a case for a new classication system that disposes of these terms [13].

Primary hypoplastic lymphedema can be further subdivided into proximal and distal hypoplasia. The most common form of primary lymphedema is distal hypoplasia. It is milder, often bilateral, and symptoms are conned to below the knee. Not surprisingly, proximal disease causes more severe symptoms, with whole-limb swelling. Patients with primary hyperplastic lymphedema have an increased

7 Dierential Diagnosis ofLower Extremity Oedema

Fig. 7.5 Primary lymphedema

number and size of lymphatics. It is unusual in that it has a male preponderance and is more often familial [14]. An association with other congenital abnormalities is sometimes seen. The thoracic duct may be absent or abnormal in such patients.

7.2.3.2 Secondary Lymphedema

Secondary lymphedema is edema due to a reduction in lymph ow by an acquired cause. The causes of secondary lymphedema include trauma [15, 16], recurrent infection [17], and malignancy, including metastatic disease. In the developed world, the most common cause of secondary lymphedema is malignancy (including that resulting from cancer treatment). Lymphedema is common in the developing world secondary to infection with the parasitic nematode Wuchereria bancrofti (otherwise known as lariasis and in complicated stage elephantiasis), making this the most common cause of lymphedema worldwide (Fig.7.6).

It is unusual for surgery alone to cause lymphedema, as lymphatics have excellent regenerative capabilities. Some series have shown signicant lymphatic damage in more than 60% of patients undergoing varicose vein surgery [18]. Lymphedema is unusual after varicose vein surgery, but patients should be examined preoperatively, as vein stripping can signicantly exacerbate mild lymphedema. Patients with venous disease have been shown to have impaired lymphatic drainage [18].

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