pelvic congestion syndrome physiology and pathophysiology s. lakhanpal md, facs president & ceo...

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Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

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Page 1: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Pelvic Congestion SyndromePhysiology and Pathophysiology

S. Lakhanpal MD, FACSPresident & CEO

Center for Vein Restoration

Page 2: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Center for Vein Restoration has forty centers mostly in the Mid-Atlantic and the

NE, providing state of the art vascular care in a compassionate and cost efficient

manner in the outpatient setting.

Page 3: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Center for Vein RestorationMaryland/Virginia/DC Offices

CVR

CVM

VIENNA

TYSONS CORNER

DC 2- VARNUM ST

FREDRICK

CATONSVILLE

FAIRFAX/FAIROAKS

FREDRICKSBURG

HERNDON

OWINGS MILLS

MANASSAS

Page 4: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Center for Vein RestorationNY, NJ, CT and PA Offices

CVR

CVM

STAMFORDWHITE PLAINS

SCARSDALE

HACKENSACK

NORWALK

NORTH BERGENMONTCLAIR

BRISTOL

PA

NY CT

NJ

WOODLAND PARK

Page 5: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Center for Vein RestorationMichigan Offices

CVR

CVM

GRAND RAPIDS

Page 6: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

To understand the physiology of Pelvic venous congestion it is imperative we consider the infra-

diaphragmatic venous system in its entirety.

Page 7: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Physiology: Hemodynamics of the infra-diaphragmatic

venous system

Page 8: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Pathophysiology of PCS

Page 9: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Pathogenesis of PCSPelvic Venous Hypertension

Primary Pelvic Congestion Syndrome:

• Increase in vein capacity due to – Multiple pregnancies or – Effect of estrogens

Secondary Pelvic Congestion Syndrome:

Obstructing anatomic anomalies may lead to secondary PCS.

– May–Thurner syndrome– Retroaortic left renal

vein– Nutcracker

phenomenon

Page 10: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Primary PCS

Page 11: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Pregnancy – (Mechanical obstruction) Endocrine Factors

Increased vascularity

60 X Increased Flow

Estrogen

Ovarian / Internal Iliac Vein Dilation

Ovarian & Internal Iliac Vein Reflux (valve dysfunction)

Increased NO

SM RelaxationLoss of responsiveness

Primary PCS - Pathogenesis

Pelvic Varicosities

Page 12: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Secondary PCS

Page 13: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Pathogenesis of Secondary PCS.

Obstructing anatomic anomalies may lead to secondary PCS.

– Compression from the right common iliac artery on the left common iliac vein against the spine and pelvic brim is known to cause iliofemoral deep venous thrombosis (May–Thurner syndrome) as well as the pelvic varices of PCS.

– Retroaortic left renal vein, there may be obstruction of the left ovarian vein leading to symptomatic pelvic varices.

– Left ovarian vein and the left renal vein may by compressed by the superior mesenteric artery (Nutcracker phenomenon) as well.

Page 14: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Pathogenesis of Pain in PCS.

• Blood pooling in the pelvic and ovarian veins may cause further engorgement, thrombosis, and mass effect on nearby nerves, collectively contributing to pelvic pain.

• Exacerbation of symptoms with menstruation, sexual activity and ovulation suggests increased arterial flow to the pelvis at these times. This results in pooling of venous blood in the pelvis varicosities.

• The characteristic severe dull aching pain of PCS is thought to be a direct result of the presence of ovarian and pelvic varicosities, much like the leg pain resulting from lower extremity varicose veins.

• Presence of cross-over veins can cause confusion, leading to increased symptoms on the right side despite a more prominent left ovarian vein

Page 15: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Pathophysiology: From Primary & Secondary

PCS

To pelvic pain or atypical(pelvic escape) varicosities with leg symptoms or both.

Page 16: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

SECONDARY PCS

FORMATION OF PELVIC VARICES

PRIMARY PCS

PELVIC FLOOR INCOMPETENCE

PELVIC LEAKS TO LOWER LIMBS (Pelvic Escape)

PELVICVENOUS

HYPERTENSION

COMPRESSIVESYMPTOMS

PELVIC CONGESTIONSYNDROME

+ PELVIC VARICES

PELVIC FLOOR COMPETENCE

FORMATION OFVULVAL, ATYPICAL VARICES,

ETC…

Pathophysiology of PCS

Page 17: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Hemodynamic Monitoring of Venous StenosisJ Vasc Surg 1986; 4:42-54

• Arm foot venous pressure differential– Venous pressures in the dorsum of the hand and foot were

measured simultaneously– A positive foot venous pressure of up to 4mm is considered

normal• Foot venous pressure elevation with reactive hyperemia

– Required to test adequacy of collateralization during periods of increased flow.

– Through the foot venipuncture resting venous pressure was recorded.

– Inflow occlusion with a thigh cuff pumped up to 300mm Hg. For three minutes, thigh cuff was released and foot venous pressure changes due to hyperemia were recorded.

• After an initial increase the curve stabilized at a higher level of initial resting pressure

• Venous pressure increment of up to 6mm Hg is achieved in normal subjects

Page 18: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Hemodynamic Monitoring of Venous StenosisJ Vasc Surg 1986; 4:42-54

1 R a ju

- - • -

- •

+

-

• •

VENOGRAPHIC "NORMAL" OBSTRUCTION VENOGRAM

30

25 +

+

2 0 • +

- +

a , 1 5 +

:c +

E ++ E 10 • +

++

• ++ • 5 • 't+ 4 mmHg r+++----;

++ .. - & m m Hg

++ ++ 1-------j I :

+ - '+++ : • t

• .. • ++ - • 0 • ..

+.............

Fig. 2. Patient with previous inferior vena cava ligation Fig. 1. Differential of arm/foot venous pressure and in crement of foot venous pressure induced by reactive hy peremia in group of patients whose phlebograms were nor mal or showed venous obstruction. Note higher arm ve nous pressure in a few patients with negative arm/foot venous pressure differential. Closed circle = = arm/foot dif ferential; plus sign = = reactive hyperemia increment.

Page 19: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Hemodynamic Monitoring of Venous StenosisJ Vasc Surg 1986; 4:42-54

Table I. Varying degrees of severity of venous obstruction

Arm/foot

R eac tive hyp erem ia-in d uce d

G ra de o f v e no u s o bstruc tio n N o . o f p a tien ts v e n o u s p re ssu re d iffe re n tia l* ven o u s p re ssu re e lev atio n f

Grade 1 2 F u lly c o m p e n sa te d

Grade II 8 + P a rt ia l ly c o m p e n sa te d

Grade III 8 + + P a rt ia l ly d e c o m p e n sa te d

Grade IV 3 + Total decompcnsation

* P lu s s ig n = g re a te r th a n 4 m m H g . tP lu s s ig n = g re a te r th a n 6 m m H g . F o r d e ta ils s e e te x t.

Table II. Diagnostic accuracy of techniques used to detect venous obstruction

Arm/foot ven o u s pre ssu re d iffe ren tia l*

Reactive hyperemia ven o u s pre ssu re e lev a tion t

B oth tec h n iq ues com b in ed

D o p pler ex am ina tiom +

(% ) (%) (%) (%)

Sensitivitv 6 5 80 90 84 Specificity 9 1 96 9 3 79 Positive predictive value 89 94 95 76 Negative predictive value 9 1 85 94 86

NOTE: Twenty limbs had phlebographically demonstrated obstruction and 24 limbs had normal phlebograms. * O b s tru c t io n = g re a te r th a n 4 m m H g . tO b s tru c t io n = g re a te r th a n 6 m m H g . :j:Data available for only 19 limbs with phkbographically demonstrated obstruction and 24 normal limbs.

Page 20: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

The Logic (or Lack of) of 50% Stenosis by IVUSNeglen & Raju: J Vasc Surg 2002;35:694-700

• The determination of the hemodynamic significance of a venous stenosis is difficult.• In most papers that describe venous stenting, venous hemodynamic assessment is

lacking. • The significance of the stenosis is commonly determined with the presence of

stenosis and the corresponding clinical signs and symptoms.• Although positive hemodynamic test results (eg, decreased plethysmographic ouflow

fraction, increased hand/foot pressure differential, increased hyperemia pressure differential, pull-through gradient of > 2 to 3 mm Hg, and increased pressure after intraarterial papaverine hydrochloride injection) may indicate hemodynamic significance, healthy test results do not exclude it.

• Despite the lack of positive hemodynamic results with available methods, balloon dilation and stenting of stenotic iliac veins guided with morphologic area stenosis of more than 50% on IVUS results appear to have apparent clinical benefits for the patients. High rates of healing of ulcers, resolution of edema, and relief of pain have been objectively shown.

• No available preoperative or intraoperative pressure tests appeared to adequately measure the hemodynamic significance of a venous stenosis. No correlation was found between the morphologic degree of stenosis and the preoperative and intraoperative tests, whether or not collaterals were present.

• It is apparent that our methods for the assessment of hemodynamic stenosis in the venous system are not optimal

Page 21: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

The Logic (or Lack of) of 50% Stenosis by IVUSNeglen & Raju: J Vasc Surg 2002;35:694-700

• The concept of a significant obstruction being a stenosis of >70% to 80% is derived from observations on the arterial system.

• These conclusions may, however, not be applicable in the venous system because there are many fundamental differences. – An arterial stenosis has high peripheral resistance downstream,

and the iliac vein stenosis has low resistance. The effects of the venous obstruction are upstream (lack of emptying) rather than downstream (lack of perfusion), which results in a different set of signs and symptoms.

– The contralateral veins converge beyond the iliac stenosis, which may mitigate any pressure gradient at rest.

– Finally, the venous velocity is lower at rest and the geometry of the narrowing may be more important in the venous system.

– When a venous stenosis should be considered “critical” is not known.

• Collaterals may look impressive on venographic results, but they may be of little functional value.

Page 22: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

The Hemodynamic Significance of CollateralsNeglen & Raju: J Vasc Surg 2002;35:694-700

• In this study, the collateral flow did not appear to adequately compensate for the outflow obstruction in many instances.

• Despite the presence of collaterals, the rate of a significant obstruction as per preoperative pressure measurements were the same as in limbs without collaterals. – One third of the limbs with collateral formation still had

increased pressure gradient on papaverine hydrochloride injection during surgery

– on average, these limbs had a tighter area stenosis than did the limbs without collaterals.

• The presence of collaterals should perhaps be looked on as an indicator of a more severe stenosis, although significant obstruction may exist with no collateral formation.

Page 23: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Hemodynamics of the Infra-diaphragmatic Venous System

The Concept of Ambulatory Venous Hypertension

Page 24: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Hemodynamic Monitoring of Venous StenosisJ Vasc Surg 1986; 4:42-54

• The diagnosis and treatment of venous disease did not progress for a long time because of lack of suitable investigative techniques.

• Goal of the investigations for lower extremity disease;– Establish the presence or absence of post ambulatory venous

hypertension(AVH)– Identify the hemodynamic cause of this (P)AVH.

• Goal for infra-diaphragmatic pelvic disease– Identify the hemodynamic significance of a lesion.

• Phlebography(venography) is purely an anatomic not hemodynamic.

Page 25: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

How does the calf muscle pump function?

Page 26: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Normal Venous Pressures in the Lower Extremity

• Hydrostatic pressure in the saphenous vein(at the ankle) at rest in a patient: 90-100mmHg.

• The pressure in the saphenous vein at the end of exercise is called Ambulatory venous pressure(AVP).

– Normally Post exercise Hydrostatic pressure is reduced to <30 mmHg.– When active contractions cease Volume filling begins within 5-7 seconds, about

30-40 seconds are required to restore hydrostatic pressure in the normal limb.

Page 27: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Normal Pressure Relationships in the Lower Extremity

• Pressure is reduced from the resting hydrostatic pressure to a mean of 22mmHg within 7-12 steps.

• When resuming a static standing position hydrostatic pressure is restored to in a mean of 31 seconds.

• When resuming a static standing position the volume is restored to baseline a mean of 40 seconds.

• The pressures at the skin and superficial veins correlate best to the dermal pathophysiological changes

• During the contractions the intravenous pressures in the deep veins is higher than that of the superficial veins, however it is in the post contraction, relaxation phase that the pressure gradient favors superficial to deep flow.

Fig 8 The pressure and volume changes with activation of the calf muscle pump are demonstrated. Beginning in the standing posture, the hydrostatic pressure baseline is demonstrated in a dependent, but non-weight bearing limb. The subject then performs 10 t...

Mark H. Meissner , Gregory Moneta , Kevin Burnand , Peter Gloviczki , Joann M. Lohr , Fedor Lurie , Mark A. Matto...The hemodynamics and diagnosis of venous diseaseJournal of Vascular Surgery, Volume 46, Issue 6, Supplement, 2007, S4 - S24http://dx.doi.org/10.1016/j.jvs.2007.09.043

Page 28: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Fig 7 Relative venous hydrostatic ( HP ) and dynamic ( DP ) pressures at various heights ( Ht ) and distances from the right atrium ( RA ) in the upright individual...

Mark H. Meissner , Gregory Moneta , Kevin Burnand , Peter Gloviczki , Joann M. Lohr , Fedor Lurie , Mark A. Matto...The hemodynamics and diagnosis of venous diseaseJournal of Vascular Surgery, Volume 46, Issue 6, Supplement, 2007, S4 - S24http://dx.doi.org/10.1016/j.jvs.2007.09.043

Relative Venous Hydrostatic and Dynamic Pressures at Various Heights

Page 29: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Post Exercise Pressures of > 30 mmHg

=Ambulatory Venous

Hypertension

Page 30: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Please refer back to the complete presentation on ‘Pelvic Congestion Syndrome’.

Page 31: Pelvic Congestion Syndrome Physiology and Pathophysiology S. Lakhanpal MD, FACS President & CEO Center for Vein Restoration

Thank You