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18 Overview ofManagement inLower Limb Edema
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281
1. Age
2. Onset - Acute or Chronic
3. Increase in size - Sudden or Gradual
4. If it is exacerbated/relieved in any specifi position
5. Association with pain
6. History of trauma
7. History of systemic illness
1. Inspection - Skin changes, Scars, Ulcers,
Engorged Veins, etc.
2. Palpation - Local rise of temperature, Tenderness,
Pitting or Non Pitting
3. Special Tests
Yes
1. Treat the underlying
cause
2. Symptomatic relief
for the edema
HISTORY
Clinical Examination
Systemic Disease
Blood
Investigations
1. Routine hematology
2. PT/INR
3. D-dimer
Deep Vein Thrombosis
No
Duplex
Ultrasound
Venous Insufficiency
Yes No No Yes
Medical Management Other Investigations
1. Anticoagulant3 like
warfarin, LMWH
2. Physical therapy
3. Compression Stocking
4. Lifestyle modifications
FAILS
Venous Thrombectomy
1. CT
2. MRI
3. ICG-LG
4. Lymphoscintigraphy
Lymphedema Confirmed
Physical Modalities and
Compression Therapy
Medical Management
FAILS
Bypass and Debulking
Procedures
MEDICAL
MANAGEMENT
FAILS
1. Radio frequency ablation
sclerotherapy
2. Vein I igation/Stripping
Fig. 18.3 Algorithm for evaluation and management of limb edema
282
S. K. Tiwary and V. K. Katiyar
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S. K. Tiwary and V. K. Katiyar
Pregnancy andLower Limb Swelling
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19
MarceloBelliniDalio, LeandroAugustoGardenghi,
andNeiRodriguesAlvesDezotti
19.1 Introduction
Lower limb swelling is present in about 80% of all pregnancies [1, 2]. Healthy
women without any evidence of venous disease often present oedema during late
pregnancy [3]. The so-called physiologic gestational oedema is not in itself dangerous, but it can cause signicant anxiety. Pregnant women frequently seek consultations with obstetricians, clinicians, and also vascular specialists [4].
In some common situations, lower limb swelling can be a manifestation of a
pathological condition. Leg oedema is one of the core features of preeclampsia,
together with raised blood pressure and proteinuria [5]. Painful leg oedema is a
manifestation of deep venous thrombosis [6]. Chronic venous disease is also a cause
of severe leg swelling in pregnant women, associated with varicose veins and skin
changes [7].
This chapter aims to discuss the physiology, causes, and management of lower
limb swelling in pregnancy.
19.2 Physiologic Gestational Oedema
Most pregnant women present pitting oedema of the ankles and legs, especially at
the end of the day (Figs.19.1 and 19.2). Commonly, they require increased shoe
sizes. Symptoms such as pain, feeling of heaviness, night cramps, and paraesthesiae
are also reported. Usually, the symptoms are mild, and there is neither redness nor
severe pain on physical examination. These latter ndings may raise the suspicion
M. B. Dalio (*) · L. A. Gardenghi · N. R. A. Dezotti
University of São Paulo, Ribeirão Preto Medical School, Department of Surgery and
Anatomy, Division of Vascular and Endovascular Surgery, São Paulo, Brazil
e-mail: mbdalio@usp.br
© 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_19
285
286
Fig. 19.1 Digital image of
a young primigravida in
her third trimester with
physiologic gestational
oedema. There are mild
foot and ankle oedema in
both limbs. The oedema is
pitting, cold, symmetrical,
and there is neither redness
nor severe pain
M. B. Dalio et al.
of a pathological cause. Typically, the oedema is more pronounced in the last trimester [8]. Gestational oedema can be monitored in the prenatal care through
maternal weight gain. The average weight gain during pregnancy approximates
12.5 kg or 27.5 Ib [9]. Physiologic gestational oedema generally resolves in the
postpartum [10].
Two key factors cause gestational oedema: the hormonal and the mechanical:
• The hormonal factor consists of the effects of pregnancy hormones. Oestrogen
and progesterone trigger many systemic changes, leading to alterations in the
venous system [11, 12]. The volume and the pressure are increased, causing
venous distension and stasis. The venous wall also has an increased distensibility
[7]. Furthermore, a surge of corticotrophin and oestrogen produces vasodilata-
tion [13]. To prevent maternal immunoreactivity to the foetus, hypertrophic adre-
nal glands create a transient, physiologic hypercortisolism [14]. A nitric
oxide-mediated vessel engorgement also increases the oedematous effect [13].
• The mechanical factor involves the compression generated by the enlarged
uterus, which is more present during late pregnancy [15]. The compression is
exerted over the inferior vena cava and the pelvic veins, causing an elevation in
hydrostatic pressure, venous dilatation, stasis, and oedema [12, 15]. When the
19 Pregnancy andLower Limb Swelling
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Fig. 19.2 Digital image of
a 22-week primigravida
exhibiting typical
physiologic gestational
oedema: pitting foot and
ankle oedema in both
limbs
287
pregnant woman lies on her left side, the uterus moves left, and the compressive
effect is suppressed [16]. The mechanical factor also predisposes to deep venous
thrombosis [6].
All these factors contribute to cause dilatation of lower limb veins and oedema.
Venous dilatation, rather than reux, is the most common vascular alteration during
pregnancy [17, 18]. However, pregnancy-induced venous dilatation also causes valvular incompetence and reux in healthy gravidae [7]. As occurs with gestational
oedema, this novel venous reux often resolves in the postpartum [17, 19, 20]. It is
not well established if venous reux that appears during pregnancy causes worsening of lower limb oedema [8].
A clinical investigation conducted by our group employed duplex scan to analyse
the association of lower limb oedema with venous reux in healthy primigravidae
288
Edema No Edema
Puerperium
No reflux
M. B. Dalio et al.
1st trimester
nd
2
trimester
rd
trimester
3
Fig. 19.3 Occurrence of lower limb oedema and reux during the three trimesters of pregnancy
and the postpartum. (Data from Gardenghi LA, Dezotti NR, Dalio MB, Joviliano EE, Piccinato CE
(2017) Gestational lower limb edema and venous reux in healthy primigravidae. Int Angiol
36:569–573)
40%15% 45%
75%20%
100%
100%
5%
Reflux
during pregnancy and in the postpartum [21]. We found that no woman presented
with oedema or reux in the rst trimester. In the second trimester, reux was found
in 5% of patients and oedema was found in 20%. In the third trimester, 15% developed reux and 55% developed oedema. Both in the second and in the third trimester, reux and oedema were not associated. In the postpartum, neither reux nor
oedema was found (Fig.19.3). Almost all reux was in the supercial venous system. Only one patient developed reux in the deep venous system. The supercial
system is more subjected to develop reux than the deep system [22]. Curiously, all
new reux developed only on the left side. This could be explained by the anatomic
relationships between the left common iliac vein and the right common iliac artery.
The iliac bifurcation is usually a site of physiologic compression, and the presence
of a gravid uterus may exacerbate it [15]. We concluded that lower limb oedema was
not associated with venous reux. Both were present in the second and in the third
trimesters and resolved spontaneously in the postpartum. Both are products of the
same physiological changes that occur in pregnancy, which are discussed above.
19.3 Management ofPhysiologic Gestational Oedema
The basis of management of lower limb swelling in pregnancy is adequate prenatal
care. During prenatal visits, clinical history, physical examination, and maternal
weight gain should be assessed to exclude any pathological condition. Routine and
specic laboratory exams help to monitor normal conditions. Imaging investigations are usually not necessary in physiologic oedema. The pathological causes of
oedema during pregnancy and their management are discussed below. Gravidae
with physiologic gestational oedema should be informed that the swelling is
expected and may worsen as the pregnancy progresses. They should be reassured
that oedema will improve within a few months after giving birth [23].
19 Pregnancy andLower Limb Swelling
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289
Some simple measures help to control oedema. These interventions are low-cost
and are unlikely to be harmful [24]:
• Avoid standing or sitting for a prolonged time;
• Periodic calf exion-extension movements;
• Daytime and night rest, with legs, elevated 15–20cm;
• In the third trimester, rest lying on the left side;
• Physical activity;
• If it is a planned pregnancy, organize to have the last trimesters during the
cold season.
Treatments used for lower limb oedema during pregnancy include compression
therapy, venoactive drugs, water immersion, and reexology [25].
Compression therapy continues to be the standard therapy in the treatment of
gestational oedema [10]. It works by exerting a contact pressure on the tissue, leading to supercial venous system compression. Consequently, the deep venous system ow accelerates, the venous return improves, the insufcient venous valves
regenerate, and venous hypertension decreases. When used during pregnancy, compression therapy leads to a lesser increase in lower leg volume. It is well tolerated
by pregnant women and there is an improvement in their subjectively perceived
symptoms [26]. There is no consensus regarding the type of compression. Both
class I (15–20mmHg) and class II (20–30mmHg) compression materials can be
used. Women may use maternity pantyhose, above-knee or below-knee compression stockings. The choice must be made on an individual basis. Compression therapy should be initiated at the start of oedema and continued until four weeks after
the childbirth [24].
O-Beta-hydroxyethyl rutoside is a semi-synthetic compound that relieves leg
symptoms of varicose veins. The mode of action is probably based on a direct effect
on the capillary wall and capillary functions [27]. In a recent study, rutosides
reduced oedema and also feeling of heaviness, night cramps, and paraesthesiae in
late pregnancy, without causing neonatal mortality or congenital malformation.
However, there is not enough data to assess its safety in pregnancy. The study had
less than 100 patients [25].
Water immersion has been proposed to control gestational oedema. During
immersion, water pressure is exerted uniformly from all sides and drives the extravascular uid into the intravascular space, decreasing oedema. A single, safe, and
well-tolerated 45-min water exercise session signicantly decreased severe bilateral
lower leg oedema in uncomplicated pregnancies [28].
Reexology and other types of leg massage have also been used to control leg
swelling in pregnant women. In a recent review, reexology showed a trend in
improving leg oedema and could be recommended in women with troublesome leg
symptoms. However, the sample size was too small to be able to draw conclusions
[4]. It is important to consider that professional massage requires specialist training,
and it is likely to be a costly treatment [23].
290
M. B. Dalio et al.
19.4 Pathological Causes ofLower Limb Swelling
During Pregnancy
Although present in 80% of normal pregnancies, lower limb oedema can indicate a
pathological condition in some situations. Adequate prenatal care is crucial to detect
these pathological conditions. When evaluating pregnant women with severe bilateral oedema, physicians should consider systemic diseases such as preeclampsia,
malnutrition, diabetes, renal and hepatic disease, or congestive heart failure [29].
Severe unilateral or asymmetric oedema should raise the suspicion of deep venous
thrombosis or infection. Chronic venous disease is a common cause of leg swelling
during pregnancy and can cause unilateral and bilateral oedema.
Preeclampsia is one of the most dangerous obstetric condition, and cannot be
ignored in pregnant women who complain of leg swelling [25]. A placental dysfunction triggers a cascade of events that lead to systemic inammation and hypoxia.
Preeclampsia can progress rapidly to severe complications, including the death of
both mother and foetus [5]. It is diagnosed during the third trimester by the presence
of lower limb oedema, new-onset hypertension, and either proteinuria or signs and
symptoms of end-organ dysfunction [30]. Early diagnosis is essential. The current
management of preeclampsia includes perinatal blood pressure control and monitoring, prenatal aspirin therapy in high-risk women, betamethasone for patients <34
weeks, parenteral magnesium sulphate, and careful follow-up of postpartum blood
pressures. Timely delivery of the foetus and the placenta remains the only denitive
treatment [5].
Deep venous thrombosis and its most severe complication, pulmonary embolism, cause signicant maternal mortality [31]. The hormonal factor creates a natural prothrombotic state. The mechanical factor causes decreased venous ow
velocity, venous dilatation, and stasis. Both factors promote the formation of blood
clots in the deep venous system. Vascular trauma during delivery, especially with
assistive devices and caesarean section, further increases postpartum thrombotic
risk. The most important risk factors for deep venous thrombosis in pregnancy are
previous thrombosis, thrombophilia, and age >35 years [6].
Pregnancy-associated deep venous thrombosis manifests as painful unilateral leg
oedema. Sometimes it is difcult to establish a diagnosis since oedema is widespread during pregnancy. D-dimers levels are largely unreliable because they continuously increase during normal pregnancy. Duplex scan is the standard of care for
diagnosing pregnancy-associated deep venous thrombosis [32].
All pregnant women diagnosed with deep venous thrombosis should be treated
with systemic anticoagulation. For those with contraindication to anticoagulation,
an inferior vena cava lter may be an option. Low-molecular-weight heparin is the
preferred choice in patients with a normal kidney function. It can be administered
subcutaneously once or twice a day. In patients with a glomerular ltration rate
<30ml/min, unfractionated heparin can be used. It is typically started with a continuous intravenous infusion and transitioned to dose-adjusted twice-a-day subcutaneous doses. The therapeutic ranges can be monitored by partial thromboplastin
time or anti-Xa levels [6]. Following delivery, therapeutic anticoagulation can be
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