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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3825_Библиотеки_им_академика_М_И_Перельмана
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Fig. 7.6 Filariasis
(elephantiasis)-secondary
lymphedema
S. R. Pandey and M. M. R. Rai
Even after radical lymph node excision for malignancy, lymphedema does not
always ensue. When it does occur, it is often a late complication. The reasons for
this late development are uncertain, but gradual failure of distal lymphatics, which
have to “pump” lymph at a greater pressure through damaged proximal ducts, has
been postulated. The transected lymphatics will regenerate after node clearance procedures. If combined with radiotherapy, however, the risk of lymphedema is higher,
as brous scarring reduces regrowth of ducts [19].
7.2.4 Lipedema
Lipedema is also known as lipomatosis of the leg (Fig.7.7). The clinical features of
lipedema include early age of onset, female exclusivity, and positive family history
in some patients [20, 21]. The clinical signs include elastic symmetrical enlargement of both legs with sparing of the feet. so-called riding breech thighs and stove
pipe legs, [22] hypothermia of the skin, a negative Stemmer sign, and plantar positioning alterations. Weight loss does not affect leg appearance [21].
7 Dierential Diagnosis ofLower Extremity Oedema
Fig. 7.7 Lipedema
85
7.2.5 Postoperative Swelling
Postoperative edema occurs predominantly after arterial reconstruction. The incidence of peripheral edema following arterial reconstruction is high, especially if the
procedure is a femoropopliteal bypass [23]. If the swelling is signicant (>4.5-cm
increase in diameter), it is more likely to be due to thrombosis of the tibial or popliteal veins [24]. Following arterial reconstruction, there may be impairment of lymphatic drainage or lymphatic disruption secondary to the surgical dissection in the
thigh and popliteal region. The swelling may persist for up to 3 months
7.2.6 Compartment Syndrome
Compartment syndrome occurs when excessive pressure builds up inside an
enclosed muscle space in the body. Compartment syndrome usually results from
bleeding or swelling after an injury.
Acute compartment syndrome usually develops over a few hours after a serious
injury to an arm or leg. Some symptoms of acute compartment syndrome include:
• New and persistent deep ache in an arm or leg
• Pain that seems greater than expected for the severity of the injury
• Numbness, pins-and-needles, or electricity-like pain in the limb
• Swelling, tightness, and bruising
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Fig. 7.8 Compartment
syndrome
S. R. Pandey and M. M. R. Rai
Emergency fasciotomy is needed to release edema.
Symptoms of chronic compartment syndrome (Fig. 7.8) (exertional compartment syndrome) include worsening of aching or cramping in the affected muscle
(buttock, thigh, or lower leg) within a half-hour of starting exercise. Symptoms usually go away with rest, and muscle function remains normal. Exertional compartment syndrome can feel like shin splints and be confused with that condition.
7.2.7 Systemic Diseases
Lower extremity edema mainly seen in systemic diseases can be cardiac cause
(Fig.7.9) hepatic cause (Fig.7.10), or renal cause. Cardiac also presents JVD and
crackles. Hepatic presents ascites, scleral icterus, and spider angiomas. Renal
presents oliguria or anuria.
7.2.8 Venous Malformation
Lower extremity edema also noted in congenital venous malformation such as
KTS. (Fig.7.11)
7 Dierential Diagnosis ofLower Extremity Oedema
Fig. 7.9 Cardiac edema
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Fig. 7.10 Hepatic edema
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Fig. 7.11 Venous
malformation in KTS
S. R. Pandey and M. M. R. Rai
7.3 Summary
In approaching lower limb edema, a variety of etiologies and differential diagnoses
must be considered to facilitate a systematic approach to patients presenting with
either acute or chronic lower extremity edema in a unilateral or bilateral fashion.
Milestone-scientic literatures published globally during the last 10 years on
differential diagnosis of lower extremity edema:
1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7536506/
2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5948740/
3. https://ddxof.com/lower- extremity- edema/
4. https://www.researchgate.net/publication/303916366_Management_of_
Patients_With_Venous_Leg_Ulcers_Challenges_and_Current_Best_Practice
5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6657795/
6. https://www.hindawi.com/journals/ulcers/2013/413604/
7. https://journals.sagepub.com/doi/10.1177/0268355519870690
8. https://www.msdmanuals.com/professional/gynecology- and- obstetrics/
symptoms- during- pregnancy/lower- extremity- edema- during- late- pregnancy
9. https://pubmed.ncbi.nlm.nih.gov/7695655/
7 Dierential Diagnosis ofLower Extremity Oedema
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References
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Phys. 2013;88(2):102–10.
2. Ely JW, Osheroff JA, Chambliss ML, Ebell MH.Approach to leg edema of unclear etiology. J
Am Board Family Med: JABFM. 2006;19(2):148–60.
3. Myint F, Platts A, Hamilton G.Thrombophilia. Peds. Vascular and Endovascular Surgery. WB
Saunders Co Ltd 2001;415–50.
4. Schirger A.Lymphedema. Cardiovasc Clin. 1983;13:293–305.
5. Harwood CA, Bull RH, Evans J, Mortimer PS.Lymphatic and venous function in lipoedema.
Br J Dermatol. 1996;13:41–6.
6. Lewis JM, Wald ER.Lymphedema praecox. J Pediatr. 1984;104:641–8.
7. Mortimer PS.Swollen lower limb-2: lymphoedema. BMJ. 2000;32:1527–9.
8. Stewart FW, Treves N.Lymphangiosarcoma in postmastectomy lymphedema: a report of six
cases in elephantiasis chirurgica. Cancer. 1948;1:64–81.
9. Brostrom LA, Nilsonne U, Kronberg M, Soderberg G.Lymphangiosarcoma in chronic heredi-
tary oedema (Milroy’s disease). Ann Chir Gynaecol. 1989;78:320–3.
10. Chen KT, Gilbert EF.Angiosarcoma complicating generalized lymphangiectasia. Arch Pathol
Lab Med. 1979;103:86–8.
11. Milroy WF.Chronic hereditary edema: Milroy’s disease. JAMA. 1928;91:1172–5.
12. Salem AH, Mulhim AM, Grant C, Khwaja MS.Milroy’s disease in a Saudi family. J R Coll
Surg (Edin). 1986;31:143–6.
13. Allen EV.Lymphedema of the extremities: classication, etiology and differential diagnosis.
Arch Int Med 1934;54606-624.
14. Wolfe JH, Kinmonth JB.The prognosis of primary lymphedema of the lower limbs. Arch Surg.
1981;116:1157–60.
15. Ter SE, Alavi A, Kim CK, Merli G.Lymphoscintigraphy: reliable test for the diagnosis of
lymphedema. Clin Nucl Med. 1993;18:646–54.
16. Cambria RA, Gloviczki P, Naessens JM, Wahner HW.Noninvasive evaluation of the lymphatic
system with lymphoscintigraphy: a prospective, semiquantitative analysis in 386 extremities. J
Vasc Surg. 1993;18:773–82.
17. Richards TB, McBiles M, Collins PS.An easy method for diagnosis of lymphedema. Ann Vasc
Surg. 1990;4:255–9.
18. Browse NL, Stewart G. Lymphoedema: pathophysiology and classication [review]. J
Cardiovasc Surg. 1985;26:91–106.
19. Wright NB, Carty HM. The swollen leg and primary lymphoedema. Arch Dis Child.
1994;71:44–9.
20. Rudkin GH, Miller TA.Lipedema: a clinical entity distinct from lymphedema. Plast Reconstr
Surg. 1994;94:841–7.
21. Harwood CA, Bull RH, Evans J, Mortimer PS.Lymphatic and venous function in lipoedema.
Br J Dermatol. 1996;13:41–6.
22. Vrouenraets BC, Klaase JM, Bbvan K, Geel BN, Eggermont AM, Franklin HR.Long-term
morbidity after regional isolated perfusion with melphalan for melanoma of the limbs: the
inuence of acute regional toxic reactions. Arch Surg. 1995;130:43–7.
23. Karakousis CP, Driscoll DL. Groin dissection in malignant melanoma. Br J Surg.
1994;81:1771–4.
24. Heyn R, Raney RB Jr, Hays DM, etal. Late effects of therapy in patients with paratesticu-
lar rhabdomyosarcoma: Intergroup Rhabdomyosarcoma Study Committee. J Clin Oncol.
1992;10:614–23.
Complications ofLower Limb Edema
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SatendraKumar
8.1 Introduction
Accumulation of excess uid in interstitium which occurs as the capillary ltration
exceeds the limits of lymphatic drainage, producing noticeable clinical signs and
symptoms, is dened as edema. There are two uid compartments in the human
body, namely intracellular and extracellular spaces. Extracellular space contains
one-third of total body water, which is further divided into intravascular plasma
volume (25%) and the extravascular interstitial space (75%). Hydrostatic pressures
and oncotic pressures maintain the uid balance between these compartments.
Apart from these, other two factors that play an important role in uid balance are
vessel wall permeability and lymphatic system. Any disturbance in this homeostasis
leads to the accumulation of uid in the interstitial space that is called edema [1].
There is renal retention of sodium and water to maintain intravascular volume
and hemodynamic stability by diffusion of water and electrolytes into interstitial
compartment. Mechanism of this cascade is via renal vasoconstriction reducing glomerular ltration, increases sodium reabsorption proximally mediated by angiotensin II and norepinephrine, and increases sodium and water reabsorption in the
collecting tubules which is mediated by aldosterone and antidiuretic hormone.
Endothelium-derived factors like nitric oxide and prostaglandins also limit sodium
and water excretion, therefore promoting edema [2].
Albumin, one of the impermeable proteins, is a major contributor to maintaining
intravascular oncotic pressure. A level below 2g/dl of plasma often results in edema.
Hypoproteinemia is seen in many conditions like nephrotic syndrome, severe nutritional deciency, and severe liver disease in which hepatic synthetic function is
impaired. Some drugs, like calcium channel blockers, especially dihydropyridines
cause more selective arteriolar vasodilatation leading to peripheral edema. Apart
8
S. Kumar (*)
Institute of Medical Sciences, Banaras Hindu University, Varanasi, India
© The Author(s), under exclusive license to Springer Nature Singapore Pte
Ltd. 2022
S. K. Tiwary (ed.), Approach to Lower Limb Oedema,
https://doi.org/10.1007/978-981-16-6206-5_8
91
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from these, other uncommon conditions are myxedema, lymphedema, and idiopathic edema. Impaired lymphatic transport leads to lymphedema causing accumulation of lymphatic uid in the interstitium mostly in extremities [3].
S. Kumar
8.2 Complications ofLower Limb Edema
8.2.1 Pain
Pain can present as a spectrum of discomfort ranging from fullness or heaviness,
dragging, throbbing, and itching or aching to frank pain. It gets exacerbated by
standing, progressive throughout the day. It is typically felt in the muscles in the calf
or thigh which is relieved by rest and limb elevation.
Venous claudication leading to bursting pain is experienced during exercise,
although rare. This is associated only with severe outow obstruction. Night cramps
may be occurring frequently, often after a long day of standing without exercise.
8.2.2 Superficial Thrombophlebitis
It is a common complication of varicose veins, probably due to over prominence of
veins, which makes them more susceptible to local trauma. Spontaneous thrombophlebitis is rare and often associated with deep venous thrombosis. It may be caused
by occult malignancy (Trousseau phenomenon). It is characterized by a tender, hot,
thickened area along the course of a varicose vein, often extremely painful, which
may be associated with fever and malaise. Long saphenous vein (60% to 80%) is
most commonly affected followed by the small/short saphenous vein (10% to 20%)
[4, 5]. If thrombophlebitis occurs in long saphenous vein, it has the potential to
propagate beyond the sapheno-femoral junction into the common femoral vein,
resulting in iliofemoral thrombosis which can result in pulmonary embolism (PE).
8.2.2.1 Investigations
Supercial thrombophlebitis used to be a clinical diagnosis traditionally. However,
lately it has been realized that there is association of concomitant DVT or
PE.Physical examination underestimates the severity of disease in up to 77% cases.
Compressive ultrasonography can identify concomitant DVT, evaluate the extent of
the thrombus, and conrm the diagnosis [6–8].
D-dimer testing has limited utility in diagnosing SVT.It is variably elevated in
SVT and therefore cannot be used to distinguish isolated SVT from DVT [6].
8.2.2.2 Management
• In low-risk supercial thrombophlebitis management strategies are aimed to
control symptoms and decrease the extension of thrombosis and risk for PE [6].
Low risk cases are dened as those not associated with the presence of or predis-
position to other thromboembolic diseases. In these patients, nonsteroidal anti-
inammatory agents, heat, and anticoagulants can be used [9].
8 Complications ofLower Limb Edema
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• High-risk cases are dened as those patients with an SVT of at least 5cm in
length in the lower extremity, SVT proximal to the knee, especially within 10cm
of the sapheno-femoral junction, the presence of severe symptoms, greater
saphenous vein involvement, previous SVT/venous thromboembolic disease,
active malignancy, or recent surgery [6]. These patients are a candidate to receive
fondaparinux 2.5mg/day subcutaneously for 45days [10].
• Topical and surgical treatments were also evaluated in this Cochrane review.
Rivaroxaban 10mg daily for 45days was found to be non-inferior to fondaparinux
in the prevention of venous thromboembolic complications with a comparable
safety prole in the SURPRISE trial [11]. Additionally, it recommended further
study on the use of nonsteroidal anti-inammatory agents and low-molecular-
weight heparins [9].
• In case of Trousseau syndrome, the main objective is to eliminate the underlying
malignancy. Heparin is the recommended treatment because multiple pathways
contribute to the development of the thrombus. Fondaparinux has also been eval-
uated but found to be less efcacious than heparin [12].
8.2.2.3 Complications
Two signicant complications of SVT are DVT and PE.It has been found in multiple studies that 6–36% of patients have concomitant DVT with SVT.These same
studies clinically suspected concomitant PE in 2–13%, and regular performance of
lung scans revealed that the rate of asymptomatic PE approached 33% [4]. Other
retrospective studies from both primary and secondary/tertiary centers have reported
coexisting DVT or symptomatic PE on initial presentation to be 25–30%.
Symptomatic PE is present in about 5–7% of these patients [4, 5]. However, with the
use of a more rigorous screening process in asymptomatic patients, the incidence of
coexisting PE increased to 17%. 14–70% of patients with thrombus up to 3cm from
the sapheno-femoral junction progress to DVT, and they require prior treatment [8].
8.2.3 Dermatitis
The earliest cutaneous sequela of chronic venous insufciency with venous hypertension is dermatitis which can lead to venous leg ulceration and lipodermatosclerosis. Chronic inammatory changes lead to deposition of brin and hemosiderin
with local edema, which can result in venous dermatitis or varicose eczema over
time. It is seen in middle-aged and elderly patients. It can also occur in young
patients with acquired venous insufciency due to surgery, trauma, or thrombosis.
Retrograde ow related to incompetent venous valves, valve destruction, or obstruction of the venous system leads to venous hypertension causing dermatitis. It results
in an inammatory process that is mediated by metalloproteinases. Red blood cells
extravasate in the interstitium and release ferric ions which upregulate these metalloproteinases [13].
There is a progressive loss of epithelium, which can result in spontaneous venous
ulceration.
94
S. Kumar
8.2.3.1 Investigations
Radiological examination—Venous Doppler studies may reveal deep venous thrombosis or severe valve damage due to past thrombosis.
8.2.3.2 Treatment
• Compression therapy—Compression therapy is done by specialized stockings
that deliver a controlled pressure gradient (measured in mm Hg) to the affected
leg. These are suitable for long-term management of edema but not for the heal-
ing of stasis ulcers. Compression stockings should be applied early in the morn-
ing before the patient rises from bed.
• High-level compression can be done by using elastic wraps compression (Unna)
boots. Some more sophisticated devices such as end-diastolic compression boots
can be used.
• Nonsteroidal calcineurin inhibitors like tacrolimus and pimecrolimus may be
used in the management of stasis dermatitis [14].
• In patients with chronic quiescent stasis dermatitis can be managed with bland
topical emollients to maximize epidermal moisture. Petroleum jelly is very effec-
tive and does not contain any contact sensitizers.
8.2.4 Lipodermatosclerosis
It forms a part of the pathological progression of venous disease that ultimately
results in skin ulceration followed by progressive brosis. It is also known as sclerosing panniculitis as it is more encompassing nomenclature and more accurately
reecting the true nature of the process [15]. It is sometimes also called fat necrosis,
folliculitis, or chronic cellulitis.
Acute lipodermatosclerosis was rst described by Kirsner etal. in 1993 [16]. The
area is red to violaceous, scaling, tender, and warm. The sharp demarcation of the
induration noted in chronic LDS may be absent in acute stage. Well-demarcated,
indurated, exquisitely tender “cellulitis” that involves the lower legs in patients
should prompt the clinician to consider a diagnosis of LDS [17]. The chronic phase
most often develops following the acute phase or may occur independently [18]. It
is characterized by hyperpigmented thick, hard, tight, and contracted skin in the
lower third of the patient’s leg associated with pain mostly conned to the medial
aspect. Skin tightening may eventually lead to constriction of the ankle region giving the leg the characteristic “inverted champagne bottle” appearance. Patients with
classic chronic LDS may develop acute onset of pain and represent an “acute on
chronic” form of LDS.The ulceration rate associated with LDS has been estimated
to be around 13% in a recent retrospective analysis [15].
Risk factors for development of LDS [15, 17, 19]:
(1) Female gender
(2) High BMI
(3) Systemic hypertension
(4) History of venous abnormalities like chronic venous insufciency
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