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A. Savlania and S. Pitchai
18.11 Summary
Renal nutcracker syndrome is very rare entity to
diagnose, which can afict patients from childhood to late adulthood. Diagnosis of NCS can
be made in patients who present with micro- to
macroscopic haematuria and left side ank pain,
and radiological evaluation conrms the haemodynamically signicant LRV compression.
It is unclear why LRV compression results in
symptoms in some patients and many remain
asymptomatic in spite of imaging showing classical compression of LRV.Continued disabling
symptoms require intervention after period of
conservative management has failed. Over the
time multiple surgical procedures have been
described for its management, but most commonly used procedure is left renal vein transposition which has shown durable and consistent
results. Recent data favours the endovascular
stenting as acceptable and preferred line of
management over the surgery, although more
data on long-term result is awaited considering
durability of procedure.
References
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2. Shin JI, Lee JS.Nutcracker phenomenon or nutcracker
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10. Wilson-Storey D, MacKinlay GA. The superior
mesenteric artery syndrome. J R Coll Surg Edinb.
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Anterior and posterior nutcracker syndrome: a report
on 11 cases. Transplant Proc. 2003;35(2):851–3.
12. Radisic MV, Feldman D, Diaz C, etal. Unexplained
hematuria during pregnancy: right-sided nutcracker
phenomenon. Int Urol Nephrol. 2007;39(3):709–11.
13. Sharper KRL, Jackson JE, Williams G. The nutcracker syndrome: an uncommon cause of haematuria. Br J Urol. 1994;74:144–6.
14. Satyapal KS. The renal veins: a review. Eur J Anat.
2003;7(Suppl 1):43–52.
15. Savlania A, Sashidhar K, Sidharth V, etal. Collateral
venous drainage of solitary functioning left kidney
with occluded renal vein following juxtarenal aortic
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16. Urban BA, Ratner LE, Fishman EK. Threedimensional volume-rendered CT angiography of
the renal arteries and veins: normal anatomy, variants, and clinical applications. Radiographics.
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17. Hohenfellner M, Steinbach F, Schultz-Lampel D, etal.
Nutcracker syndrome: new aspects of pathophysiology, diagnosis and treatment. J Urol. 1991;146:685–8.
18. Lau JLT, Lo R, Chan FL, et al. The posterior nutcracker. Haematuria secondary to retroaortic left renal
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19. Wei SM, Chen ZD, Zhou M.Intravenous stent placement for treatment of nutcracker syndrome. J Urol.
2003;170:1934–5.
20. Zhang HK, Shen LG, Li M, etal. Diagnosis and treatment of left renal venal entrapment syndrome. Chin J
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renal vein hypertension: a cause of occult hematuria.
Radiology. 1982;145(3):647–50.
25. Stewart BH, Reiman G.Left renal venous hypertension “nutcracker” syndrome: managed by direct renocaval reimplantation. Urology. 1982;20(4):365–9.
26. Scultetus AH, Villavicencio JL, Gillespie DL. The
nutcracker syndrome: its role in the pelvic venous disorders. J Vasc Surg. 2001;34(5):812–9.
27. Maleux G, Stockx L, Wilms G, etal. Ovarian vein
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28. Zerhouni EA, Siegelman SS, Walsh PC, et al.
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29. Unlu M, Orguc S, Serter S, etal. Anatomic and hemodynamic evaluation of renal venous ow in varicocele formation using color Doppler sonography with
emphasis on renal vein entrapment syndrome. Scand
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30. Park SJ, Lim JW, Ko YT, et al. Diagnosis of pelvic
congestion syndrome using transabdominal and
transvaginal sonography. AJR Am J Roentgenol.
2004;182(3):683–8.
31. Rogers A, Beech A, Braithwaite B.Transperitoneal laparoscopic left gonadal vein ligation can be the right treatment option for pelvic congestion symptoms secondary
to nutcracker syndrome. Vascular. 2007;15(4):238–40.
32. Wendel RG, Crawford ED, Hehman KN. The “nutcracker” phenomenon: an unusual cause for renal varicosities with haematuria. J Urol. 1980;123(5):761–3.
33. Takebayashi S, Ueki T, Ikeda N, etal. Diagnosis of the
nutcracker syndrome with color Doppler sonography:
correlation with ow patterns on retrograde left renal
venography. AJR Am J Roentgenol. 1999;172:39–43.
34. Braedel HU, Schindler E, Polsky MS.Selective renal
phlebography in the diagnosis of renal pelvic and ureteric varices. Br J Urol. 1977;49(5):365–70.
35. Fitoz S, Ekim M, Ozcakar ZB, et al. Nutcracker
syndrome in children: the role of upright position
examination and superior mesenteric artery angle
measurement in the diagnosis. J Ultrasound Med.
2007;26(5):573–80.
36. Stavros AT, Sickler KJ, Menter RR. Color duplex
sonography of the nutcracker syndrome (aortomesenteric left renal vein compression). J Ultrasound Med.
1994;13(7):569–74.
37. Zhang H, Li M, Jin W, etal. The left renal entrapment
syndrome: diagnosis and treatment. Ann Vasc Surg.
2007;21(2):198–203.
38. Sayfan J, Halevy A, Oland J, etal. Varicocele and left
renal vein compression. Fertil Steril. 1984;41(3):411–7.
39. Takahashi Y, Sano A, Matsuo M. An ultrasonographic classication for diverse clinical symptoms
of pediatric nutcracker phenomenon. Clin Nephrol.
2005;64(1):47–54.
40. Takahashi Y, Sano A, Matsuo M.An effective “transluminal balloon angioplasty” therapy for pediatric
chronic fatigue syndrome with nutcracker phenomenon. Clin Nephrol. 2000;53(1):77–8.
41. Kim SH, Cho SW, Kim HD, et al. Nutcracker syndrome: diagnosis with Doppler US. Radiology.
1996;198:93–7.
42. Fu W, etal. Diagnosis of the nutcracker phenomenon
by multislice helical computed tomography angiography. Chin Med J. 2004;117:1873–5.
43. Kim KW, Cho JY, Kim SH, et al. Diagnostic value
of computed tomographic ndings of nutcracker syndrome: correlation with renal venography and renocaval
pressure gradients. Eur J Radiol. 2011;80(3):648–54.
44. Andrianne R, Limet R, Waltregny D, etal. Hematuria
caused by nutcracker syndrome: preoperative conrmation of its presence. Prog Urol. 2002;12:1323–6.
45. He Y, Wu Z, Chen S, etal. Nutcracker syndrome—
how well do we know it? Urology. 2014;83(1):12–7.
46. Shokeir AA, el-Diasty TA, Ghoneim MA.The nutcracker syndrome: new methods of diagnosis and
treatment. Br J Urol. 1994;74(2):139–43.
47. Tanaka H, Waga S. Spontaneous remission of persistent severe haematuria in an adolescent with nutcracker syndrome: seven years’ observation. Clin Exp
Nephrol. 2004;8(1):68–70.
48. Reed NR, Kalra M, Bower TC, etal. Left renal vein
transposition for nutcracker syndrome. J Vasc Surg.
2009;49:386–93; discussion: 393-4.
49. Ha T-S, Lee E-J.ACE inhibition can improve orthostatic proteinuria associated with nutcracker syndrome. Pediatr Nephrol. 2006;21(11):1765–8.
50. Neste MG, Narasimham DL, Belcher
KK. Endovascular stent placement as a treatment
for renal venous hypertension. J Vasc Interv Radiol.
1996;7:859.
51. d’Archambeau O, Maes M, De Schepper AM. The
pelvic congestion syndrome: role of the “nutcracker
phenomenon” and results of endovascular treatment.
JBR-BTR. 2004;87:1–8.
52. Erben Y, Gloviczki P, Kalra M, etal. Treatment of
nutcracker syndrome with open and endovascular
interventions. J Vasc Surg Venous Lymphat Disord.
2015;3(4):389–96.
53. Hartung O, Azghari A, Barthelemy P, et al.
Laparoscopic transposition of the left renal vein into
the inferior vena cava for nutcracker syndrome. J Vasc
Surg. 2010;52:738–41.
54. Chuang CK, etal. The nutcracker syndrome managed
by autotransplantation. J Urol. 1997;157:1833–4.
55. Salehipour M, etal. The role of renal autotransplantation in treatment of nutcracker syndrome. Saudi J
Kidney Dis Transpl. 2010;21:237–41.
56. Thompson PN, Darling RC 3rd, Chang BB, et al. A
case of nutcracker syndrome: treatment by mesoaortic
transposition. J Vasc Surg. 1992;16:663–5.
57. Chung BI, Gill IS. Laparoscopic splenorenal venous
bypass for nutcracker syndrome. J Vasc Surg.
2009;49(5):1319–23.
58. Barnes RW, Fleisher HL 3rd, Redman JF, et al.
Mesoaortic compression of the left renal vein (the socalled nutcracker syndrome): repair by a new stenting
procedure. J Vasc Surg. 1988;8:415–21.
59. Hohenfellner M, D’Elia G, Hampel C, et al.
Transposition of the left renal vein for treatment of
the nutcracker phenomenon: long-term follow-up.
Urology. 2002;59:354–7.
60. Chen S, Zhang H, Shi H, etal. Endovascular stenting for treatment of nutcracker syndrome: report
of 61 cases with long-term follow up. J Urol.
2011;186:570–5.
61. Wang X, Zhang Y, Li C, etal. Results of endovascular treatment for patients with nutcracker syndrome. J
Vasc Surg. 2012;56:142–8.
62. Cohen F, Amabile P, Varoquaux A, etal. Endovascular
treatment of circumaortic nutcracker syndrome. J
Vasc Interv Radiol. 2009;20:1255–6.
Venous Trauma
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ArvindKohli andGurjitSingh
19
19.1 Introduction
There has been an ever-increasing incidence of
vascular trauma all over the world. Extremity
injuries contribute for 80% of all cases of vascular injuries, and out of them, lower extremities
are involved in two thirds of these patients. Males
are affected in 90% and females in 10% cases.
The true incidence of isolated venous trauma is
underreported. Quan etal. [1] reported that only
25% of extremity vascular trauma had isolated
venous injury. Despite the variability in magnitude of trauma, most of venous injuries (75%)
occur concomitantly with arterial injury.
19.2 Challenges ofVascular
Injuries
These injuries are the most dramatic challenges
facing trauma surgeons because the repair is often
urgent. Gaining control of and reconstructing a
major vascular injury can be technically demanding. The fundamental difference between elective
vascular surgery and vascular trauma is the physiology of the wounded patient. A lacerated major
vessel is typically only one component of the
multi-trauma complex that includes injuries to
other organs and systems. These patients are often
critically ill and rapidly approaching a point of
physiologic irreversibility. In these dramatic clinical circumstances, the key to a favorable outcome
is maintaining correct priorities [2].
19.3 Etiology
The leading cause of vascular injury in general
and venous injuries in particular continues to be
penetrating wounds, out of which gunshot wounds
contribute to 70–80% of all cases requiring intervention, whereas stab wounds are the next
common cause (5–10%) of cases requiring intervention. Blunt trauma occurs in (5-10%)of cases
subsequent to road trafc accidents along with
presence of fracture of long bones of dislocation
of joints therebyincresing the risk of venous injury.
Iatrogenic injury accounts for 5% of cases, that
includes Endovascular procedures like central
lineplacement and endovascular and venous cardiac interventions [3].
19.4 Distribution ofVenous
Trauma
A. Kohli
Department of CTVS, GMC, Jammu, India
G. Singh (*)
Division of CTVS, JK Medicity Hospital, Jammu, India
© Springer Nature Singapore Pte Ltd. 2018
A. K. Khanna, R. Jindal (eds.), Venous Disorders, https://doi.org/10.1007/978-981-13-1108-6_19
Majority of vein injuries (90%) affect the extremities with almost similar distribution in upper and
lower extremitiy. Clouse etal. [4] have described
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the incidence of venous injuries as femoral
(17%), IVC (15%), jugular (15%), brachial
(14%), and popliteal vein (8%).
19.5 Diagnosis
Diagnosis of venous injuries may not be obvious
on clinical examination as they in most of cases
form part of the polytrauma. Patients present
with a growing hematoma, or blood discharge
from a penetrating wound. In most of the cases,
the venous injuries are detected during exploration of a major arterial injury.
Color Doppler ultrasound scan detects intimal tears, thrombosis, contusion, pseudoaneurysms, and arteriovenous stulae. Although the
color doppler scan is operator dependent, it has
sensitivity of 95% and specicity of 99% with
overall accuracy of 98%.
19.6 Angiography
Angiography is the premium procedure for diagnosis of vascular injuries both arterial and venous.
Where hybrid operating suits are available, angiography can be performed in the operating room
enabling the surgeon to identify the injury and
manage expeditiously. Angiography has sensitivity of 92–96%, specicity of above 96%, and
accuracy of 98%.
19.7 CT VenoGram (CTV)
With the advent of improved CT scan, detection
of venous injuries has greatly improved. In fact
CTV is becoming a viable alternative to angiography. Occasionally CTV can be nondiagnostic
due to signicant artifact from bullet fragments
or other foreign bodies. It has to be complemented with DSA which gives sensitivity of
90–100% and specicity of 98–100%.
19.8 Magnetic Resonance
Venography (MRV)
MRV is used less frequently in acute settings.
Metal implants such as cerebral aneurysm clips
and cardiac pacemakers preclude the use of MRI,
or it is difcult to ascertain whether the patient
have such devices in emergency situation [2, 3, 5].
19.9 Treatment ofVenous Injuries
19.9.1 Immediate Treatment
Although the controversy continues in polytrauma with profound hemorrhage and severe
venous injuries, ligation of the injured vein is a
life-saving procedure. Nevertheless, ligation
may not be an appropriate solution in all patients,
and it appears that there is merit in repair of
many injured lower extremity veins, particularly
the popliteal vein when it is a single return conduit, assuming that the patient’s general condition will permit, in an attempt to prevent acute
venous hypertension initially and chronic venous
hypertension and phlegmasia of the leg
subsequently.
Various modalities for operative management
of venous trauma have been advocated keeping in
view the nature of injury. The aim is to save the
limb and prevent long-term venous dysfunction.
Operative procedures include ligation of the
injured vein, lateral venorrhaphy, end-to-end
anastomosis, venous patch angioplasty, and
venous interposition graft. Many reports suggest
that lateral venorrhaphy produces good patency
rates; however, more complex repairs are also
known to give optimal long-term results. Venous
ligation is indicated in polytrauma with profuse
hemorrhage and associated injuries which necessitates priority and in cases where there are complex venous lacerations. Time consumed for
performing these repairs is worrying factor for
outcome.
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Venous repair using interposition prosthetic or
vein graft is debatable keeping in view the postoperative patency; however, if interposed, reverse
saphenous vein graft is considered to have better
outcome than prosthetic graft. The use of temporary shunts both in repair of venous and arterial
injuries is recommended, and use of shunts maintains patency without the use of systemic anticoagulation in the short term [6].
Endovascular management of venous injuries
has been described like the use of endovascular
balloon inserted through the femoral vein for
control of unrelenting venous hemorrhage from
injured iliac vein thereby enabling the surgeons
to repair that segment in good time. In addition in
selected patients, use of venous stents for managing venous injuries of the iliac, IVC, and axillary
vein has been described.
Conclusion
Aggressive management after vein ligation can
minimize complications by implementation of
limb elevation, compression, and early fasciot-
omy when indicated. Repair of venous injuries
is not mandatory for limb salvage or prevention
of long-term morbidity. However, aggressive
approach to venous repair specically with
injury to popliteal vein should be followed.
References
1. Quan RW, Adams ED, Cox MW, etal. The management of trauma venous injury: civilian and wartime
experiences. Perspect Vasc Surg Endovasc Ther.
2006;18(2):149–56.
2. Gillespie D, Quan RW.The management of extremity
venous trauma. In: Gloviczki P, editor. Handbook of
venous disorders: guidelines of the American venous
forum. 3rd ed. Chap. 51. London: Hodder Arnold;
2009. p.569–72.
3. Rich NM. Management of venous trauma. Surg Clin
North Am. 1988;68:809–21.
4. Clouse WD, etal. In-theater management of vascular
injury: 2 years of the Balad Vascular Registry. J Am
Coll Surg. 2007;204:625–32.
5. Qi Y, Gillespie DL. Venous trauma: new lessons
and old debates. Perspect Vasc Surg Endovasc Ther.
2011;23(2):74–792.
6. Quan RW, Gillespie DL, Stuart RP, Chang AS,
Whittaker DR.The effect of vein repair on the risk of
venous thromboembolic events: a review of more than
100 traumatic military venous injuries. J Vasc Surg.
2008;47(3):571–7.
Therapeutic Options
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inLymphedema
WaldemerLechOlszewski
andMarzannaTeresaZaleska
20
20.1 Introduction
Lymphedema of limbs characteristically means
increase in the volume of extremity caused by
accumulation of tissue uid, proliferation of
broblasts and adipocytes, and excessive production of collagen. There is also increase in inltrating immune cell mass. Bacterial colonization
ensues as the result of lack of lymphatic transport
away of microbes penetrating the foot and palm
skin. Under physiological conditions capillary
ltrate-tissue uid ows into the lymphatics and
is transported via the collecting lymphatic trunks
to the blood circulation. The transported calculated volume for one lower limb ranges from 20
to over 200 ml in some cases during 24 h [1].
Obliteration of the transport lymphatic channels
and sinuses of regional lymph nodes causes stasis
of intercellular water, proteins, and migrating
immune cells. Contractility of the lymphatics
disappears. Tissue changes are hyperkeratosis,
brosis, and accumulation of tissue uid/lymph
under the epidermis with occasional lymphorrhea
[2]. The most common complication of tissue
uid stasis is bacterial dermato-lymphangio-ade-
W. L. Olszewski (*)
Central Clinical Hospital, Ministry of Internal Affairs,
Warsaw, Poland
M. T. Zaleska
Deptartment of Applied Physiology,
Mossakowski Medical Research Center, Polish
Academy of Sciences, Warsaw, Poland
nitis (DLA) [3]. For a long time, there was no
awareness of the progressive tissue changes leading to the development of elephantiasis, and
accumulation of mobile uid was considered as
the main event in increased volume of the limb.
20.2 How Important Is
Restoration ofTissue Fluid
Outow fromLimb Tissues?
For centuries lymphedema was considered as an
accumulation of excess water with proteins that
should be treated by total excision of the diseased
tissue or drainage procedures as various types of
bridging tissue aps between the lymphedematous and healthy regions. Operations designed by
Charles [4], Sistrunk [5], Thompson [6], or
Goldsmith [7] were widely applied with rather
unsatisfactory results. Delayed wound healing,
leakage of tissue uid from the denuded surfaces,
and chronic inammation of foot tissues, continuously penetrated by environmental microbes,
were the common events.
The actual understanding of the pathomechanism of development of lymphedema and tissue
changes, based on the contemporary human studies, drastically changed the surgical approach to
therapy of lymphedema. Modern techniques of
imaging of the lymphatic vascular system (X-ray
contrast lymphography, lymphoscintigraphy,
near-infrared lymphography, angiography, CT,
© Springer Nature Singapore Pte Ltd. 2018
A. K. Khanna, R. Jindal (eds.), Venous Disorders, https://doi.org/10.1007/978-981-13-1108-6_20
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W. L. Olszewski and M. T. Zaleska
and MRI), discovery of spontaneous lymphatic
contractility, visualization of sites of accumulation of stagnant tissue uid, and evidence for the
presence of bacterial ora in stagnant tissue uid/
lymph allowed not only to redesign old types of
surgery but also to propose procedures restoring
lymph ow by microsurgical anastomoses [8–
11]. This has been further possible by the
improvement of optics of operating microscopes
and production of ultrathin traumatic sutures.
Additional impact on the development of microsurgical procedures had also the long-term lymphangiographic observations of gradual
obliteration of peripheral segments of collecting
trunks after skin infections (erysipelas) and/or
their proximal obliteration after lymphadenectomy, the so-called die-back phenomenon [12].
They prompted surgeons to early surgical intervention by performing anastomoses of the still
patent collectors with the neighboring veins.
Furthermore, debulking surgery, still indicated
for millions of patients, has become more satisfactory due to pretreatment with antibiotics controlling colonizing microbes resulting in fast
healing of surgical wounds. Moreover, antibiotic
prophylaxis saved foot tissues, deprived of lymphatic drainage, from chronic inammation [3].
High-efciency diathermy scalpels facilitated tissue resection without using ligatures frequently
being expulsed from the debulking wounds for
months. Various types of external compression as
bandages, stockings, and intermittent pneumatic
compression devices have improved the longterm results of surgery, forcing tissue uid ow
through newly formed pathways either to the
veins or the non-swollen parts of the body.
accumulated lymph and directing its ow to the
venous system distally to the site of lymphatic
obstruction. The operation mimicked the natural
anastomosis of the thoracic duct with the subclavian vein, by with the creation of microsurgical
shunts between the lymphatics and veins. The
physiological principles of the operation were
based on the observations of natural anatomical
lymphovenous communications in the retroperitoneal space in animals and in humans in cases
of obstruction of the thoracic duct. In our project, the lymph node was cut transversely, and
lymph oozing started from the cortical sinuses
(Fig.
20.1). Then, the node was implanted end-
to-side into an excised wall window of the neighboring vein. First experimental operations were
performed on dogs, and the mesenteric lymph
node after transection and its distal part with
afferent lymphatics were implanted into the inferior vena cava. Lymph owed freely into the vein
because pressure in the vena cava was slightly
negative at inspiration. These shunts created in
dogs remained patent throughout their life.
In 1966, we carried out the rst ve operations
of microsurgical lymphovenous shunts in
humans, directing the stream of stagnant lymph
of the lymphedematous lower limbs to the femoral vein [8–11]. Over the course of time, various
modications of the lymphovenous shunt operations have been introduced and tried by us and
other authors. The number of operations around
the world cannot at present be accurately estimated; however, more than 100 thousand should
have been performed. The worldwide experience
in indications, technique, and results was
described in abundant literature [
(Fig.20.2).
13–43]
20.3 Physiological Operations
20.3.1 Lymphonodo- and/or
Lymphatico-Venous
Microsurgical Shunts
With the developing technique of microsurgery
in the 1960, we thought of using microsurgical methods for the creation of articial lymphovenous shunts [8–11]. The operation of
microsurgical lymphovenous was designed for
decompressing the lymphedematous limb of the
20.3.2 Microsurgical Inguinal
Lymphovenous Shunts
Two types of shunts are performed, the lymph
node-saphenous vein (LNSV) and afferent lymphatics-saphenous vein (LVSV) or other supercial veins.
Detailed Indications
Lymphedema at an early stage (I and II) of postinammatory, postsurgical, and hyperplastic type
20 Therapeutic Options inLymphedema
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207
Fig. 20.1 Pictures illustrating the rst lymphovenous
microsurgical shunts performed in dogs in 1966. Upper
left – lymph node with afferent lymphatics and node
sinuses. Lower left – transverse section of the node and
implantation to the vein and contrast medium injected into
the node owed to the vein. Upper right– contrast medium
Fig. 20.2 Typical picture of obstructive lymphedema of
the lower limb for surgical treatment. Conservative therapy unsuccessful
FV FV
ILN
LVS
ILNILN
SV/FV
LVS
VEIN
LVS
FV
SV SV
ILN
CAPS
FV
LVS
FV
injected into the vein implanted mesenteric node ows to
the IVC.Lower right– various modications of microsurgical lymph node and lymphatic–vein anastomoses. FV
femoral vein, ILN inguinal lymph node, SV saphenous vein,
LVS lymphatic vessels, ILN caps inguinal lymph node cap-
sule (no parenchyma)
with at least one calf or thigh lymphatic and a
single inguinal or iliac lymph node is visible on
the functional lymphoscintigraphy (performed
during limb pneumatic massage or after standard
time walking). Surgical lymphovenous shunts
should be performed as soon as obstructive
lymphedema is diagnosed. Also preventive shunts
at the time of inguinal or axillary lymphadenectomy are highly recommended. The long-term
follow-up would show the efcacy of the early
intervention.
Lack of indications: (a) stages III and IV with
no lymphatics or nodes on lymphoscintigraphy,
(b) idiopathic lymphedema with soft skin, pitting
edema, but no lymphatic structures on
lymphoscintigraphy
Contraindications: (a) recent attacks of dermato-lymphangio-adenitis (DLA) and (b) skin
ulcer
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W. L. Olszewski and M. T. Zaleska
Postoperative Clinical Evaluation
Criteria
They include (a) decrease in leg circumference,
(b) improved exion in the ankle (to 80°) and
knee joints (minimum 90°), (c) increase in the
softness (compliance) of tissues, and (d) subsidence of limb pain during long-lasting upright
position. The volume of the limb will never be
the same as it was before the lymphatic injury.
Lymphedema is a condition characterized by an
increase in extravascular uid and protein
volume, proliferation of broblasts and keratinocytes, and deposition of a large mass of extracellular matrix. The water content increases by 50%,
and the dry mass increases by 20%. All these factors should be taken into consideration in the
evaluation of results of the microsurgical shunts.
Moreover, the adjuvant therapy as manual and
pneumatic massage and wearing of elastic garments further obscure objective evaluation of
response to therapy.
Most authors report good early results, but
subsequent deterioration may occur as early as
6months after the operation [11–34]. There are,
however, exceptions with cases observed with
permanent improvement after 10–40years.
20.3.3 Microsurgical Lymphatico-
Venous Shunts at Dierent
Levels oftheLower andUpper
Limb
A number of modications of surgical lymphatico-venous shunts have been developed since
the publication of our technique in 1967 and
1968 [13–38]. They included end-to-end and
end-to-side anastomoses and interposition of
vein fragments bridging the ends of severed
lymphatics.
20.3.4 Super-Microsurgical
Lymphatico-Venous Shunts
Development of high-dissolving power optics
and superne atraumatic sutures as well as
infrared lymphography opened the way for per-
forming multiple anastomoses between the
small supercial lymphatics and the neighboring veins. Various technical modications of
anastomoses have been proposed [39–43]. The
early results seem to be satisfactory; however,
only the long-term follow-up will prove their
effectiveness.
The microsurgical lymph node or lymphatic
vessel to vein shunts have their established position among the therapy modalities for lymphedema of lower limbs. Our and others’
long-lasting experience indicates that (a) only
patients with lymphedema with local segmental
obstruction but still partly patent and contracting
distal lymphatics and without an active inammatory process in the skin, subcutaneous tissue,
and lymph vessels present satisfactory results;
(b) classied according to the etiology of lymphedema, the best results are obtained in cases of
hyperplastic, followed by postsurgical and
postinammatory types; and (c) primary idiopathic lymphedema of non-genetic type should
be treated with conservative means.
20.4 Creation ofArticial Lymph
(Edema Fluid) Flow Pathways
by Implantation
ofHydrophobic Silicone
Tubings
None of the so far applied conservative and surgical methods proved to restore the shape and
function of the limbs to normal conditions. In
advanced cases of lymphedema, all main lymphatics are obstructed, and tissue uid accumulates in the interstitial spaces, spontaneously
forming “blind channels” or “lakes” (Figs.20.3,
20.4, 20.5, and 20.6). The only solution would
be to drain these spaces by creating articial
pathways for edema uid to ow away to the
non-obstructed regions where absorption of
uid can take place. This can be achieved by the
formation of articial pathways for edema uid
to ow by subcutaneous implantation of silicone tubings “lymphatics” placed along the
limb from the most distal parts to its root and
continue to more proximal regions with uid
Pa
tissue fluid
OUND
AND BYPASSING INGUINAL CREASE
20 Therapeutic Options inLymphedema
https://t.me/med1917
Fig. 20.3 Schematic
presentation of tissue
changes in a
lymphedematous limb.
Collecting trunks are
obstructed. Tissue uid
forms spontaneous
tissue lakes and
channels. It nds its way
to the femoral canal and
to the buttock and
lumbar region. To
facilitate ow away,
articial channels
bypassing the inguinal
obstruction site should
be constructed
thway of
Tissue
spontaneous
channels
209
flow
Obliterated lymphatics
IMPLANTED TUBINGS FACILITATE FLUID ACCUMULATION AR
Fig. 20.4 The tissue uid channels and subepidermal
dilated microlymphatics are shown on a lymphoscintigram (yellow and light blue shadows)
absorption capacity (Fig. 20.7). In the lower
limbs, this is an implant from the foot to the
hypogastrium or lumbar region and in the upper
limbs from the hand dorsum to the scapular area
Fig. 20.5 Histological picture of tissue uid channels in
lymphedema
[44, 45]. This is a three-modality procedure: (1)
silicone tubing implantation, (2) intermittent
pneumatic compression and elastic support, and
(3) prophylactic antibiotics to prevent bacterial
colonization.
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