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Byung-Boong LEE

Professor of Surgery and Director, Center for Lymphedema and Vascular Malformations, George Washington University School of Medicine, Washington DC, USA

Venous embryology can explain many of the defects resulting in venous anomalies in later life, yet is often overlooked. Venous malformations are vascular malformations that only affect the venous system. They are classified into two different types depending on the embryological stage when the defective development occurs. Venous malformations originating during the early stage of embryogenesis are termed extratruncular, while those originating during the late stage of embryogenesis are classified as truncular. A defect at any point in the complex development stages of the evolution and involution of multiple paired embryonic veins can result in various conditions of defective venous trunkTherefore, truncular lesions in general are associated with more serious hemodynamic consequences than extratruncular lesions due to their direct involvement with the truncal venous system.

This review provides a detailed overview of venous embryology and a number of truncular venous malformations to illustrate how a thorough knowledge of this subject can aid in their diagnosis and treatment.

A thorough understanding of vascular system anatomy is a prerequisite for all vascular specialists. However, a knowledge of venous embryology is seldom acquired even though all mature and named vessels originate from their precursor, embryonic vessels, and vascular anomalies are closely linked to them.

Vascular anomalies are relatively rare and difficult to understand and interpret. Yet, venous embryology is one of the most neglected areas of basic science in medicine despite its critical ability to explain the many obscure conditions related to anomalous anatomy (eg, membranous occlusion of suprahepatic inferior vena cava as a cause of primary Budd-Chiari Syndrome).1,2

Such venous anomalies are a result of the defective development of embryonic veins during the vascular trunk formation period in the later stage of embryonic development.3,4 A benign narrowing (stenosis) of the jugular-azygos vein system is a good example of how defective development can cause a unique condition, in this case chronic cerebrospinal venous insufficiency (CCSVI).5,6

A basic knowledge of vascular embryology and in particular, the evolutional and involutional development of the venous system involved in the maturation of the truncal vein, is essential for the recognition and interpretation of a number of venous anomalies.7,8

When the embryo starts to grow at an exponential rate in the early stage of embryogenesis, rapid growth and expansion of the embryonic vessels must follow suit to fulfill their critical role as the channels to supply essential nutrient requirements. A defect at any point in the complex development stages of evolution and involution of multiple paired embryonic veins can result in congenital vascular malformations (CVM).9,10 The prevalence of defective development in the vascular structure of the newborn is in the range of 1% to 3%.

As CVMs are birth defects that arise during the various stages of development of the vascular system,11,12 they can involve one or more components: artery, vein, lymphatics, and/or capillary vessels. Venous malformations are vascular malformations that only affect the venous system.13,14 They may exist alone as an independent lesion or combined with other CVMs as lymphatic malformations,15,16 arteriovenous malformations,17,18 and/or capillary malformations.19,20 The clinical behavior of the malformation is solely dependent on the embryonic stage at which the developmental arrest/defect occurs.

When defective development occurs in the early stage of embryogenesis, the embryonic vessels remain in the form of reticular networks and do not evolve into the vascular trunk formation. After birth these networks can remain as independent clusters of primitive venous tissue without direct involvement of the main venous trunk itself (eg, extratruncular venous malformation) (Figure 1). These primitive vascular structures maintain the mesenchymal cell properties and its evolutional ability to proliferate when stimulated by exogenous (eg, surgery, trauma) or endogenous factors (menarche, pregnancy, female hormones).7,8,10,21,22

When defective development occurs in the vascular trunk formation period in the later stage of embryonic development, the defects involve named vessels (eg, iliac, femoral, and popliteal vessels) and are limited to the vessel trunk itself. Examples of such truncular venous malformations include popliteal vein aneurysm, absence/aplasia of the femoral vein, jugular vein stenosis/webs, and hypoplastic iliac vein (Figure 2). These are embryologically mature lesions, which no longer possess the evolutionary capacity to proliferate. However, truncular lesions present with more serious hemodynamic consequences in general compared with extratruncular lesions due to their direct involvement with the truncal venous system (eg, avalvulosis, marginal veins, popliteal vein aneurysm, inferior vena cava stenosis/occlusion).23,24

Figure 1 (A D). Extratruncular venous malformation (VM) 1A depicts a clinical condition of extratruncular venous malformation (VM) lesions affecting the entire left lower leg, but mostly limited superficially to the soft tissue level. 1B (whole body blood pool scintigraphy) displays compatible findings to show the extent of the lesion on the same extremity. On the contrary, 1C shows a benign looking VM lesion in the right lateral upper thigh mimicking varicose veins. However, it is the tip of the iceberg of extensive lesions infiltrating into the surrounding soft tissue as well as the muscles, shown in MRI (1D).

Figure 2 (A and B). Truncular venous malformation (VM) 2A demonstrates angiographic findings of a truncular VM lesion consisting of an aneurysmal dilatation of the right popliteal vein; this truncular lesion is the outcome of developmental arrest during the vascular trunk formation period in the later stage of embryonic development. 2B also presents angiographic findings of another type of truncular VM lesion this time a stenotic condition involving the right internal jugular vein trunk along its junction with the superior vena cava (Courtesy of Professors P Zamboni and R.Galeotti for 2B).

Based on the above definitions, the modified Hamburg Classification separates venous malformations into two different types: extratruncular and truncular, depending on the embryological stage when the defective development occurred (Table I).25,26 Venous malformations originating from the early stage of embryogenesis are classified as extratruncular together with all other types of vascular malformation from the same early stage (eg, lymphangioma). Venous malformations originating from the late stage of embryogenesis are classified as truncular.

As all truncular lesions involve the already formed, established venous trunk to varying degrees, they present as either hypoplastic or hyperplastic vessels/lesions causing obstruction or dilatation (eg, internal jugular vein aneurysm, iliac vein stenosis), depending on the defect.27,28 It should be noted that intraluminal defects within the vein (eg, vein webs or membrane) can result in similar conditions of stenosis or obstruction (Figure 3).29,30

Table I. The modified Hamburg classification of congenital vascular malformations. * Based on the predominant vascular structure in the malformation. ** Based on anatomy and developmental arrest at the different stages of embryonic life: extratruncular form from earlier stages; truncular form from late stages.

Figure 3 (A and B). Truncular venous malformation (VM) 3A shows angiographic findings for a truncular VM lesion involving a segmental stenosis of the left iliac vein. This benign looking condition precipitated a severe chronic venous insufficiency to the affected lower extremity. 3B shows another form of truncular VM involving an aneurysmal dilatation of the right internal jugular vein (Courtesy of Professors P. Zamboni and R. Galeotti for 3B).

Less frequently, truncular venous malformations may present as a persistent fetal remnant vein that has failed to involute or regress normally. This unique condition, which involves the lower extremity venous system, is known as marginal/sciatic/lateral embryonic veins31,32 and represents the venous malformation component of Klippel-Trenaunay Syndrome (Figure 4).3,4,21,22

As a consequence of their direct involvement with the venous system, the chronic venous congestion and hypertension due to venous reflux or occlusion caused by truncular venous malformations result in more tissue and organ damage than extratruncal lesions. Membranous, focal, or segmental lesions can cause suprahepatic stenosis of the inferior vena cava along the proximal terminal segment, a condition known as primary Budd-Chiari syndrome. This has a profound hemodynamic impact, not only on the lower extremities where it causes chronic venous hypertension, but also on the liver where it results in severe portal hypertension due to hepatic venous outlet obstruction. This congenital/developmental anomaly most frequently involves Asian and African races (Figure 5).33,34

The cerebrospinal venous circulation is not exempt from truncular venous malformations. Cerebrospinal venous malformations carry the potential risk of long-term chronic venous hypertension to the brain resulting in various clinical conditions/illnesses such as CCSVI.35,36

An example of CCSVI, internal jugular vein valve incompetence (IJVVI), has been postulated to be the cause of transient global amnesia.37,38 IJVVI is diagnosed when retrograde jugular vein flow is detected by extracranial duplex ultrasound during Valsalva maneuver. It is believed that IJVVI may produce transient mesiotemporal ischemia by venous congestion. This mechanism requires a patent venous pathway from the affected internal jugular vein through the transverse sinus, confluence, straight sinus, and vein of Galen into the basal vein of Rosenthal and into the internal cerebral veins.

Figure 4 (A and B). Truncular venous malformation: marginal/lateral embryonic vein 4A depicts a clinical condition of the marginal/lateral embryonic vein along the lateral aspect of the left lower extremity. This unique vein structure is a persistent fetal remnant vessel following the failure of normal involution/regression and its avalvulosis causes severe venous reflux. Marginal vein remains are a hallmark of Klippel-Trenaunay syndrome, representing its venous malformation component. 4B presents angiographic findings of this marginal vein, which is the only remaining major venous drainage route with a lack of normal development of the deep venous system. Surgical excision to control venous hypertension is therefore contraindicated.

Figure 5 (A D). Suprahepatic inferior vena cava (IVC) occlusive lesion: primary Budd-Chiari syndrome A common cause of suprahepatic IVC occlusion is focal stenosis (shown in 5A and 5B) and segmental stenosis (5C), although membranous bstruction by the web is the most common cause among Asians (5D). These are relatively simple congenital VM, which develop during the late vessel trunk formation stage. However, they have a profound hemodynamic impact on the liver with portal hypertension due to hepatic venous outlet obstruction in addition to chronic venous insufficiency affecting the lower extremities.

There are now also data supporting a role for CCVI in the development of multiple sclerosis as reported in the International Union of Phlebology Consensus on Venous Malformations 2009.39 It is hypothesized that truncular venous malformations causing stenosis along the internal jugular, innominate, superior vena cava, and azygos vein system, may contribute to the development or exacerbation of multiple sclerosis.40,41

The heart and blood vessels develop from the mesoderm as isolated masses and cords of mesenchymal cells as early as 15 to 16 days in order to rapidly deliver sufficient nutrients to the exponentially proliferating cells and dispose of waste products via connection with maternal blood vessels in the placenta.42-44 By the beginning of the fourth week of gestation, an extensive network of blood vessels has formed from the mesenchyme as clusters of angiogenetic cells throughout the embryonic body to establish a communication with extra-embryonic vessels and to create a primitive vascular system: the Vitelline- Umbilical-Cardinal Vein System (Figures 6 and 7).42-44

The primitive vascular structure in complex capillary and reticular plexuses in the early embryonic stage is soon replaced by the newly developed paired cardinal veins as an axial, truncal venous system. In addition, the paired vitelline vessels from the yolk sac develop into the hepatic portal system, while the paired umbilical vessels from the chorion and body stalk form the ductus venosus. The anterior and posterior cardinal veins merge to become the common cardinal veins, draining centrally into the sinus venosus (sinus horns) and also receiving the vitelline and umbilical veins (Figure 6). At 4 weeks, the paired umbilical veins return blood from the placenta to capillary networks in the liver. During the fifth week of development, the right umbilical vein degenerates, involutes together with the proximal portion of the left umbilical veins, leaving only the distal part of the left umbilical vein as a single vein to return blood from the placenta to the embryo.

Figure 6. Embryonic veins at the fifth week of gestation: anterior/posterior/common cardinal vein and vitelline/umbilical vein developmental process The embryo demonstrates the development of paired sets of vitelline and umbilical veins in its fifth week, which initially drain the yolk sac and allantois, but later drain the intestines and the placenta, respectively. Paired sets of anterior and posterior cardinal veins join to form the common cardinal veins, draining centrally into the sinus venosus. The common cardinal veins also receive vitelline and umbilical veins, as depicted.

Figure 7. Embryonic veins at the seventh week of gestation: vitelline/umbilical vein developmental process At the seventh week of embryonic development, the entire right umbilical vein and proximal left umbilical vein regress. The distal left umbilical vein subsequently anastomoses with the hepatic sinuses to form the ductus venosus. The ductus venosus allows venous blood from the umbilical vein and the portal vein direct access to the inferior vena cava (IVC). The distal/upper-most segment of the right vitelline vein remains as the most proximal segment of the IVC reaching the heart via paired sinus venosus, while all other parts of the vitelline veins regress/involute completely.

At 8 weeks, the distal left umbilical vein anastomoses with the hepatic sinuses to form the ductus venosus. This newly formed structure allows venous blood from the umbilical vein and portal vein to bypass the liver and flow into the inferior vena cava and finally to reach the heart via the paired sinus venosus (Figure 7).

The part of the body distal to the developing heart (head, neck, upper torso, and upper limbs) drains through the bilateral anterior cardinal veins also known as the precardinal veins, whereas, the caudal portion of the body (body and lower limbs) drains through the bilateral posterior cardinal veins also known as the postcardinal veins.45,46

Numerous large tributary vessels develop from the anterior cardinal veins and converge as cerebral plexuses. Blood passes from the plexuses to the heart through the anterior cardinal and common cardinal veins. The anterior cardinal (precardinal) veins, common cardinal, and terminal/proximal posterior cardinal (postcardinal) veins go through a major evolutionary process to become the veins of the heart, the superior vena cava (SVC), and its tributaries.

Paired anterior cardinal veins anastomose to allow blood to drain from the left anterior cardinal vein into the right anterior cardinal vein. This anastomosis grows from the left anterior cardinal vein to the right anterior cardinal vein to form the left brachiocephalic (innominate) vein.

The portion of the left anterior cardinal vein distal to the anastomosis, becomes the left internal jugular vein and joins the left subclavian vein from the developing upper limb. The left anterior cardinal vein proximal to the brachiocephalic anastomosis regresses/atrophies with the terminal segment of the left posterior cardinal vein, ultimately becoming the Great Cardiac Vein. The oblique vein of the left atrium (Vein of Marshall) at the back of the left atrium and the coronary sinus of the heart comprise the Great Cardiac Vein. The distal portions of the bilateral anterior cardinal veins therefore become the bilateral internal jugular veins and the blood from the left internal jugular vein passes through the left brachiocephalic vein, draining directly into the SVC (Figure 8).47,48

On the right-hand side, the proximal part of the right anterior cardinal vein forms the SVC with the right common cardinal vein in conjunction with the right horn of the sinus venosus (Figure 8). The SVC therefore consists of three different segments: 1. Right anterior cardinal vein proximal to the brachiocephalic anastomosis 2. Right common cardinal vein 3. Right horn of the sinus venosus

These veins are further involved in the formation of the arch of azygos vein together with the proximal segment of the right posterior cardinal vein. The termination of the left posterior cardinal vein transforms into the Great Cardiac Vein, which drains into the left atrium. The azygos venous system is initially derived from the paired supracardinal venous systems, one of three cardinal veins that drain the caudal portion of the body together with the postcardinal (posterior cardinal) veins.49,50

Figures 8 (top) and 9 (bottom). Precardinal/anterior cardinal vein developmental process Paired anterior cardinal veins form common cardinal veins with paired posterior cardinal veins, draining centrally into the sinus venosus (sinus horns) as depicted. Paired anterior cardinals soon form an anastomosis between them; the connection grows from the left to the right anterior cardinal vein to form the left brachiocephalic (innominate) vein. The left anterior cardinal vein distal (cranial) to the anastomosis becomes the left internal jugular vein, while the left anterior cardinal vein proximal to the brachiocephalic anastomosis regresses/atrophies to become the base of the coronary sinus of the heart as displayed. The right anterior cardinal (precardinal) vein proximal to the right brachiocephalic vein forms the superior vena cava (SVC) with the common cardinal, and terminal/proximal segment of the posterior cardinal (postcardinal) vein.

Three sets/pairs of cardinal veins: precardinal, postcardinal, and supracardinal, evolve to form the azygos venous system. The azygos venous system is initially derived from the paired supracardinal vein. The proximal segment of the right supracardinal vein forms the arch of azygos vein together with the cranial part of the right posterior cardinal vein, while the cranial part of the left supracardinal vein becomes the hemiazygos and also accessory azygos veins as displayed in 9. The hemiazygos vein on the left side drains into the azygos vein located in the right side before draining into the SVC. The accessory hemiazygos vein runs along the course of the involuted left common cardinal vein and drains into the hemiazygos vein before it crosses over the midline to the azygos vein.

The right supracardinal vein remains as the azygos vein together with the distal portion of the right posterior cardinal vein to form the arch of azygos vein. The left supracardinal vein becomes the hemiazygos vein and accessory azygos vein. The hemiazygos vein on the left drains into the azygos vein located on the right side and subsequently into the SVC. The accessory hemiazygos vein, which runs along the course of the involuted left common cardinal vein, drains into the hemiazygos vein before it crosses the midline to flow into the azygos vein (Figure 9).

Due to the complex nature of the various stages of evolution and involution of multiple paired embryonic veins, several anomalous conditions associated with the SVC can develop. These may affect the common cardinals, anterior and posterior cardinals, and primitive jugular veins. The likelihood of development anomalies associated with the SVC is relatively high due to the involvement of three different embryonic vein segments.

For example, a left-sided SVC may develop from persistent left anterior and left common cardinal veins,51,52 and is often associated with the absence of the right SVC.53,54 In this condition, the right brachiocephalic vein crosses the midline to join a vertical left brachiocephalic vein, thus forming a left SVC. As a consequence of this developmental defect of the common cardinal vein, the persistent left SVC can be associated with the presence of two azygos veins. When a left SVC is present, the anatomy of the azygos veins may be reversed; the hemiazygos vein (the remnant of the proximal part of the left posterior cardinal vein) located on the left, will drain directly into the left-sided SVC, in the way that a normal azygos vein (the remnant of the proximal part of the right posterior cardinal vein) would drain into the SVC on the right side. This anomalous condition is the result of a developmental arrest/defect during the late stage of embryogenesis. The left SVC is grouped with other similar truncular venous malformations (eg, double SVC, internal jugular vein stenosis/aneurysm).

A double SVC is another well-known vein anomaly that occurs as a result of failure of degeneration/involution of the left anterior cardinal vein proximal to the brachiocephalic anastomosis.55,56 The double SVC is further subgrouped based on combined anomalous veins.

The posterior cardinal (postcardinal) veins are the first pair of embryonic veins to arise that drain the caudal body. They soon become integrated and taken over by the newly developing subcardinal and supracardinal veins.57-59 The shift of the systemic venous return to the right atrium in early embryonic life initiates the radical remodeling of these cardinal (embryonic) venous systems. The postcardinal, subcardinal, and supracardinal veins go through extensive evolution as well as involution for complex remodeling to form the inferior vena cava (IVC), which drains the trunk and lower extremities (Figure 10).60,61

Figure 10 (A-C). Developmental process for the inferior vena cava involving postcardinal, supracardinal, and subcardinal veins Three pairs of the post-/sub-/supracardinal veins go through extensive evolution and involution to form the inferior vena cava (IVC) as well as hepatic veins, together with the bilateral vitelline and umbilical veins. The role of postcardinal (posterior cardinal) veins, the first pair of embryological veins for venous drainage of the caudal body, is soon taken over by developing pairs of subcardinal and supracardinal veins, to form the IVC as shown.

The IVC is formed in a complicated series of developmental stages from the following embryonic structures (Figure 11): 1. Suprahepatic the most proximal segment of the IVC develops from the persistent proximal portion of the right vitelline vein, which is the precursor of the common hepatic vein. 2. A new hepatic segment develops from an anastomosis between the right vitelline vein and the right subcardinal vein distal/dorsal to the developing liver to connect this proximal-most (suprahepatic) segment to the distally located right subcardinal vein, while allowing drainage of the hepatic veins/liver. 3. The renal/mesenteric segment of the IVC is represented by a preserved segment of the right subcardinal vein. 4. The new junctional segment of the IVC is formed through an anastomosis between the right subcardinal vein and the more distally located right supracardinal vein. 5. The infrarenal segment is represented by the preserved segment of the right supracardinal vein. 6. The last segment of the IVC is formed as a new segment to connect the right supracardinal and most distal part of the bilateral posterior cardinal veins.

The IVC therefore undergoes a complicated fusion of multiple segments of different embryonic veins: vitelline, supracardinal, subcardinal, and posterior cardinal, anastomoses between these veins, as well as between sub- and supracardinal veins. As a result there is a high likelihood of developmental anomalies occurring during this complicated embryogenic process.

The complex embryological development is such that variations and anomalies are common where embryological connections persist, either alone or in conjunction with aplasia or hypoplasia of normally developing channels.62,63 There are therefore many different congenital anomalies of the IVC involving its length, location, duplication, abnormal connection and draining, and residual remnants of the embryonic tissue such as webs, membranes, etc.

Double/duplicated IVC occurs as a result of the bilateral persistence of the supracardinal veins,64,65 while a leftsided IVC is the result of caudal regression of the right supracardinal vein instead of the left supracardinal vein, which fails to involute/regress and persists (Figure 11).66,67

The absence of the suprarenal IVC arises from cava/iliac vein agenesis.68,69 When the right subcardinal vein fails to anastomose with the liver, the IVC drains into the arch of the azygos vein and the hepatic veins drain independently through the diaphragm into the right atrium (Figure 12). A posterior/retroaortic left renal vein is another example of defective regression of the anterior portion of the renal ring (1%-2%).70,71

Figure 11 (A-C). Left-sided IVC (11A) is one of the IVC anomalies that occurs as a result of failure of normal evolution and involution of the three pairs of cardinal veins. Other related anomalies are Double/ duplicated IVC (11B) and absence of IVC development (11C).

Figure 12. Failure of subcardinal vein to anastomose with the liver When normal anastomosis of the right subcardinal vein with the liver fails due to abnormal development of the hepatic segment of the IVS, the distal part of the IVC drains directly into the arch of the azygos vein and the hepatic veins drain independently through the diaphragm into the right atrium.

Membranous, focal, segmental, and obstructive lesions in the suprahepatic IVC belong to a group of intraluminal defects of the vein wall that cause varying degrees of stenosis and obstruction, and together with venectasia and aneurysm cause venous dilatation.72,73

Truncal venous development of the lower extremities occurs in three phases to form matured veins in the later stage of embryogenesis (Figure 13).74,75

First phase: primitive fibular (peroneal) vein Early venous outflow from the primitive lower limb occurs through a lateral/posterior fibular (peroneal) vein into the posterior cardinal vein; this is the first embryonic vein of the limb.

Figure 13 (A and B). Truncal venous development of the lower extremities occurs in three phases. 13A (left) depicts the first phase of truncal vein development involving evolution of the primitive fibular (peroneal) vein, which becomes the first embryonic vein of the lower limb. In the second phase (right), the primitive fibular vein develops two branches: the anterior tibial vein and connecting branch. The anterior tibial vein and primitive fibular veins together now constitute the sciatic vein, which is the second embryonic vein. 13B (left) illustrates the third phase in which the femoral vein is formed by a connecting branch from the middle of the sciatic vein, to establish a new definitive deep venous system. The sciatic vein (right) regresses and the femoral vein is further evoluted, following anastomoses with sciatic veins, and passes down the leg as the posterior tibial vein to complete the evolution of the veins along the lower limb.

Second phase: sciatic vein The primitive fibular vein develops two branches: the anterior tibial vein and the connecting branch. The anterior (medial) tibial vein becomes the main deep draining vein of the calf. The anterior tibial vein and primitive fibular veins together now constitute the sciatic vein, which is the second embryonic vein. A part of the primitive fibular vein distal to the anterior tibial vein/branch evolutes to become the short/lesser saphenous vein.

Third phase: femoral vein with persisting sciatic vein A connecting branch growing medially from the middle of the sciatic vein connects with a new proximal medial vessel that will become the femoral vein and the definitive deep venous system, while the sciatic vein regresses. A third embryonic vein of the leg develops to become the femoral vein, which terminates in the posterior cardinal vein, anterior to the sciatic vein. This advances toward the connecting branch of the lateral fibular/sciatic vein. The femoral vein is further evoluted with anastomoses to sciatic veins and passes down the leg as the posterior tibial vein, to finish the evolution of the veins along the lower extremity. This third embryonic vein is also known as the precursor of the long/greater saphenous vein.

With a defect in the second stage, the lateral fibular vein will persist and become the marginal vein. However, if a defect occurs in the passage to the third stage, a sciatic vein will remain as the main draining vein of the limb. As an embryonic vein, a persisting marginal vein is always valveless and can cause a severe reflux resulting in chronic venous hypertension/stasis as well as a high risk of venous thrombosis and subsequent pulmonary embolism among Klippel-Trenaunay syndrome patients.76,77

The venous development of the upper extremities is almost identical to that of the lower extremities.74,75 The ulnar portion of the border/marginal vein persists, forming the subclavian, axillary, and basilic veins at different levels. The subclavian vein eventually drains into the anterior cardinal vein, which subsequently evolutes to the internal jugular vein. The cephalic vein develops secondarily in relationship to the radial border vein, and it later anastomoses with the external jugular vein and finally opens into the axillary vein.

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Chronic Budd-Chiari syndrome due to congenital membranous obstruction of the inferior vena cava: clinical experience. Aust N Z J Surg. 1989;59:335-338. 31. Kim YW, Lee BB, Cho JH, Do YS, Kim DI, Kim ES. Haemodynamic and clinical assessment of lateral marginal vein excision in patients with a predominantly venous malformation of the lower extremity. Eur J Vasc Endovasc Surg. 2007;33:122-127. 32. Mattassi R. Approach to marginal vein: current issue. Phlebology. 2007;22:283- 286. 33. Lee BB, Laredo J, Deaton D, et al. Endovascular management of Budd- Chiari Syndrome suprahepatic inferior vena cava occlusive disease. In: Heuser RR, Henry M, eds. Textbook of Peripheral Vascular Interventions. Second edition. Section XII. Chapter 83. London, UK: Informa Healthcare, Informa UK Ltd;2008:725-731 34. Zamboni P, Pisano L, Mari C, Galeotti R, Feo C, Liboni A. Membranous obstruction of the inferior vena cava and Budd-Chiari syndrome. Report of a case. J Cardiovasc Surg. 1996 (Torino); 37:583-587. 35. Abe T, Singer RJ, Marks MP, Norbash AM, Crowley RS, Steinberg GK. Coexistence of occult vascular malformations and developmental venous anomalies in the central nervous system: MR evaluation. Am J Neuroradiol. 1998;19:51-57. 36. Schaller B. Physiology of cerebral venous blood flow: from experimental data in animals to normal function in humans. Brain Res Rev. 2004;46:243- 260. 37. Schreiber SJ, Doepp F, Klingebiel R, Valdueza JM. Internal jugular vein valve incompetence and intracranial venous anatomy in transient global amnesia. J Neurol Neurosurg Psychiatry. 2005;76:509-513. 38. Akkawi NM, Agosti C, Rozzini L, Anzola GP, Padovani A. Transient global amnesia and disturbance of venous flow patterns. Lancet. 2001;357:957. 39. Lee BB, Bergan J. Gloviczki P, et al; International Union of Phlebology (IUP). Diagnosis and treatment of venous malformations Consensus Document of the International Union of Phlebology (IUP)-2009. Int Angiol. 2009;28:434-451. 40. Nedelmann M, Kaps M, Mueller-Forell W. Venous obstruction and jugular valve insufficiency in idiopathic intracranial hypertension. J Neurol. 2009;256:964-969. 41. Leriche H, Aubin ML, Aboulker J. Cavo-spinal phlebography in myelopathies. Stenoses of internal jugular and azygos veins, venous compressions and thrombosis. Acta Radiol Suppl. 1976;347:415-417. 42. Langman J. Medical Embryology. 5th ed. Baltimore, MD: Williams and Wilkins;1985:212217. 43. Warwick R, Williams P. Grays Anatomy. 37th ed. Edinburgh, London, Melbourne, New York: Churchill Livingstone;1989:326-327. 44. Hamilton WJ, Mossman HW. Hamilton, Boyd & Mossmans Human Embryology. 4th ed. Cambridge: Heffer;1972:261. 45. Collins P. Embryology and development. In: Williams PL, Bannister LH, Berry MM, et al (eds). Grays Anatomy: The Anatomical Basis of Medicine and Surgery. 38th ed. Edinburgh: Churchill Livingston;1995:327. 46. Padget DH. The development of the cranial venous system in man, from the viewpoint of comparative anatomy. Contrib Embryol Carneg Inst Washington. 1957;36:79-140. 47. Beattie J. The importance of anomalies of the superior vena cava in man. Canad Med Assoc J. 1931;25:281-284. 48. FitzGerald DP. The study of developmental abnormalities as an aid to that of human embryology, based on observations on a persistent left superior vena cava. Dublin J Med Sci. 1909;14-18. 49. Keyes DC, Keyes HC. A case of persistent left superior vena cava with reversed azygos system. Anat Rec. 1925;31:23-26. 50. Nandy K, Blair CB, Jr. Double superior vena cavae with completely paired azygos veins. Anat Rec. 1965;15:1-9. 51. Huffmire AP, Bower GC. A case of persistence of the left superior vena cava in an aged adult. Anat Rec. 1919- 20;17:127-129. 52. Basu BN. Persistent left superior vena cava, left duct of Cuvier and left horn of the sinus venosus. J Anat. 1932;66:628-270. 53. Greenfield WS. Persistence of the left vena cava superior, with absence of right. Trans Pathol Soc Lond. 1876;27:120-124. 54. Atwell WJ, Zoltowski P. A case of a left superior vena cava without a corresponding vessel on the right side. Anat Rec. 1938;70:525-532. 55. Howden R. Case of double superior vena cava with left -sided arrangement of the azygos vein. J Anat Physiol. 1887;21:72-75. 56. Gruber W. Duplicitt der vena cava superior, mit vorkommen zweir nenae azygae und einer sufficienten valvula an der mndung der vena azygos sinistra. Arch Pathol Anat Physiol Klin Med. 1880;81:462-465. 57. Krizan Z, Herman O, Dzidrov V. Teilweiser fortbestand des supracardinalsystems neben der normalen vena cava inferior beim menschen. Acta Anat. 1958;34:312- 325. 58. Lewis FT. The development of vena cava inferior. Am J Anat. 1902;1. 59. Bailey FR, Miller AM. Development of the vascular system. In: Textbook of Embryology. 2nd edition. New York: William Woon and Company;1911:222-291. 60. Nemec J, Heifetz S. Persistence of left supracardinal vein in an adult patient with heart-hand syndrome and cardiac pacemaker. Congenit Heart Dis. 2008;3:219-222. 61. McClure CFW, Butler EG. The development of the vena cava inferior in man. Am J Anat. 1925:35:331-383. 62. Cornillie P, Van Den Broeck W, Simoens P. Origin of the infrarenal part of the caudal vena cava in the pig. Anat Histol Embryol. 2008;37:387-393. 63. Nemec J, Heifetz S. Persistence of left supracardinal vein in an adult patient with heart-hand syndrome and cardiac pacemaker. Congenit Heart Dis. 2008;3:219-222. 64. Hashmi ZA, Smaroff GG. Dual inferior vena cava: two inferior vena cava filters. Ann Thorac Surg. 2007;84:661- 663. 65. Esposito S, Mansueto G, Amodio F, et al. Duplication of the vena cava inferior with a continuation into the vena azygos. A report of a rare case. Minerva Chir. 1999;54:261-265. 66. Munechika H, Cohan RH, Baker ME, Cooper CJ, Dunnick NR. Hemiazygos continuation of a left inferior vena cava: CT appearance. J Comput Assist Tomogr. 1988;12:328-330. 67. Honma S, Tokiyoshi A, Kawai K, Koizumi M, Kodama K. Left inferior vena cava with regressed right inferior vena cava. Anat Sci Int. 2008;83:173- 178. 68. Gil RJ, Prez AM, Arias JB, Pascual FB, Romero ES. Agenesis of the inferior vena cava associated with lower extremities and pelvic venous thrombosis. J Vasc Surg. 2006;44:1114- 1116. 69. Romagnoli R, Bertolani M, Saviano M, Pantusa M, Modena MG, Benassi A. Developmental interruption of the intra-hepatic segment of the inferior vena cava with azygos-hemiazygos continuation. Eur J Radiol. 1984;4:244- 247. 70. Trigaux JP, Vandroogenbroek S, De Wispelaere JF, Lacrosse M, Jamart J. Congenital anomalies of the inferior vena cava and left renal vein: evaluation with spiral CT. J Vasc Interv Radiol. 1998;9:339-345. 71. Royal SA, Callen PW. CT evaluation of anomalies of the inferior vena cava and left renal vein. AJR Am J Roentgenol. 1979;132:759-763. 72. Walden R, Hiss J, Morag B, Adar R. Congenital membranous obstruction of the inferior vena cava. Isr J Med Sci. 1978;14:342-346. 73. Wang ZG, Zhu Y, Wang SH, et al. Recognition and management of Budd-Chiari syndrome: report of one hundred cases. J Vasc Surg. 1989;10:149-156. 74. Lewis FT. The development of the veins in the limbs of rabbit embryo. Am J Anat. 1905;5:1-120. 75. Wyman J. On symmetry and homology in. limbs. Proc Boston Soc Nat Hist. 1867;11:246-278. 76. Gloviczki P, Stanson AW, Stickler GB, et al. Trenaunay syndrome: the risks and benefits of vascular interventions. Surgery. 1991;110:469-479. 77. Noel AA, Gloviczki P, Cherry KJ Jr, Rooke TW, Stanson AW, Driscoll DJ et al. Surgical treatment of venous malformations in Klippel-Trenaunay syndrome. J Vasc Surg. 2000;32:840- 847.

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Venous embryology: the key to understanding anomalous ...

The Italian Journal of Anatomy and Embryology was founded in 1901 by Giulio Chiarugi, Anatomist at Florence University, and hence ever devoted to the progress and diffusion of science in the fields of Anatomy, Histology and Embryology. The Journal will continue to be devoted to publish original, research or review papers dealing with the entire field of anatomy and embryology of vertebrates, from clinical anatomy to cell and developmental biology, with special regard to human and veterinary medicine and including medical education in those fields.

Assistant Editors Maria Simonetta Pellegrini Faussone Gabriella B. Vannelli

Past-Editors I. Fazzari E. Allara G.C. Balboni E. Brizzi G. Gheri

Editorial Board

Giuseppe Anastasi (Professor of Anatomy, University of Messina, Italy) Pepa Atanassova (Professor of Histology, Plovdiv, Bulgaria) Daniele Bani (Professor of Histology, University of Florence, Italy) Raffaele De Caro (Professor of Anatomy, University of Padua, Italy) Mirella Falconi Mazzotti (Professor of Anatomy, University of Bologna, Italy) Antonio Filippini (Professor of Histology, University of Rome "La Sapienza", Italy) Eugenio Gaudio (Professor of Anatomy, University of Rome "La Sapienza", Italy) Krzysztof Gil (Associate Professor of Pathophysiology, Jagiellonian University of Krakow, Poland) Menachem Hanani (Emeritus of Physiology, Hebrew University of Jerusalem) Nadir M. Maraldi (Emeritus of Histology, University of Bologna, Italy) Hanne B. Mikkelsen (Professor of Anatomy and Cell Biology, University of Copenhagen) Giovanni Orlandini (Emeritus of Anatomy, University of Florence, Italy) Maria Simonetta Pellegrini Faussone (Emeritus of Histology, University of Florence, Italy) Laurentiu M. Popescu (Bucharest, Romania) Alessandro Riva (Emeritus of Anatomy, University of Cagliari, Italy) Ajai K. Srivastav (Professor of Zoology, Gorakhpur, India) Gabriella B. Vannelli (Professor of Anatomy, University of Florence, Italy)

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Italian Journal of Anatomy and Embryology

Select Search World Factbook Roget's Int'l Thesaurus Bartlett's Quotations Respectfully Quoted Fowler's King's English Strunk's Style Mencken's Language Cambridge History The King James Bible Oxford Shakespeare Gray's Anatomy Farmer's Cookbook Post's Etiquette Brewer's Phrase & Fable Bulfinch's Mythology Frazer's Golden Bough All Verse Anthologies Dickinson, E. Eliot, T.S. Frost, R. Hopkins, G.M. Keats, J. Lawrence, D.H. Masters, E.L. Sandburg, C. Sassoon, S. Whitman, W. Wordsworth, W. Yeats, W.B. All Nonfiction Harvard Classics American Essays Einstein's Relativity Grant, U.S. Roosevelt, T. Wells's History Presidential Inaugurals All Fiction Shelf of Fiction Ghost Stories Short Stories Shaw, G.B. Stein, G. Stevenson, R.L. Wells, H.G. Reference > Anatomy of the Human Body > I. Embryology > 12. The Branchial Region CONTENTSBIBLIOGRAPHIC RECORDILLUSTRATIONSSUBJECT INDEX Henry Gray(18211865).Anatomy of the Human Body.1918. 12. The Branchial Region The Branchial or Visceral Arches and Pharyngeal Pouches.In the lateral walls of the anterior part of the fore-gut five pharyngeal pouches appear (Fig. 42); each of the upper four pouches is prolonged into a dorsal and a ventral diverticulum. Over these pouches corresponding indentations of the ectoderm occur, forming what are known as the branchial or outer pharyngeal grooves. The intervening mesoderm is pressed aside and the ectoderm comes for a time into contact with the entodermal lining of the fore-gut, and the two layers unite along the floors of the grooves to form thin closing membranes between the fore-gut and the exterior. Later the mesoderm again penetrates between the entoderm and the ectoderm. In gill-bearing animals the closing membranes disappear, and the grooves become complete clefts, the gill-clefts, opening from the pharynx on to the exterior; perforation, however, does not occur in birds or mammals. The grooves separate a series of rounded bars or arches, the branchial or visceral arches, in which thickening of the mesoderm takes place (Figs. 40 and 41). The dorsal ends of these arches are attached to the sides of the head, while the ventral extremities ultimately meet in the middle line of the neck. In all, six arches make their appearance, but of these only the first four are visible externally. The first arch is named the mandibular, and the second the hyoid; the others have no distinctive names. In each arch a cartilaginous bar, consisting of right and left halves, is developed, and with each of these there is one of the primitive aortic arches. 1 FIG. 42 Floor of pharynx of embryo shown in Fig. 40. (See enlarged image) The mandibular arch lies between the first branchial groove and the stomodeum; from it are developed the lower lip, the mandible, the muscles of mastication, and the anterior part of the tongue. Its cartilaginous bar is formed by what are known as Meckels cartilages (right and left) (Fig. 43); above this the incus is developed. The dorsal end of each cartilage is connected with the ear-capsule and is ossified to form the malleus; the ventral ends meet each other in the region of the symphysis menti, and are usually regarded as undergoing ossification to form that portion of the mandible which contains the incisor teeth. The intervening part of the cartilage disappears; the portion immediately adjacent to the malleus is replaced by fibrous membrane, which constitutes the spheno-mandibular ligament, while from the connective tissue covering the remainder of the cartilage the greater part of the mandible is ossified. From the dorsal ends of the mandibular arch a triangular process, the maxillary process, grows forward on either side and forms the cheek and lateral part of the upper lip. The second or hyoid arch assists in forming the side and front of the neck. From its cartilage are developed the styloid process, stylohyoid ligament, and lesser cornu of the hyoid bone. The stages probably arises in the upper part of this arch. The cartilage of the third arch gives origin to the greater cornu of the hyoid bone. The ventral ends of the second and third arches unite with those of the opposite side, and form a transverse band, from which the body of the hyoid bone and the posterior part of the tongue are developed. The ventral portions of the cartilages of the fourth and fifth arches unite to form the thyroid cartilage; from the cartilages of the sixth arch the cricoid and arytenoid cartilages and the cartilages of the trachea are developed. The mandibular and hyoid arches grow more rapidly than those behind them, with the result that the latter become, to a certain extent, telescoped within the former, and a deep depression, the sinus cervicalis, is formed on either side of the neck. This sinus is bounded in front by the hyoid arch, and behind by the thoracic wall; it is ultimately obliterated by the fusion of its walls. 2 FIG. 43 Head and neck of a human embryo eighteen weeks old, with Meckels cartilage and hyoid bar exposed. (After Klliker.) (See enlarged image) FIG. 44 Under surface of the head of a human embryo about twenty-nine days old. (After His.) (See enlarged image) From the first branchial groove the concha auricul and external acoustic meatus are developed, while around the groove there appear, on the mandibular and hyoid arches, a number of swellings from which the auricula or pinna is formed. The first pharyngeal pouch is prolonged dorsally to form the auditory tube and the tympanic cavity; the closing membrane between the mandibular and hyoid arches is invaded by mesoderm, and forms the tympanic membrane. No traces of the second, third, and fourth branchial grooves persist. The inner part of the second pharyngeal pouch is named the sinus tonsillaris; in it the tonsil is developed, above which a trace of the sinus persists as the supratonsillar fossa. The fossa of Rosenmller or lateral recess of the pharynx is by some regarded as a persistent part of the second pharyngeal pouch, but it is probably developed as a secondary formation. From the third pharyngeal pouch the thymus arises as an entodermal diverticulum on either side, and from the fourth pouches small diverticula project and become incorporated with the thymus, but in man these diverticula probably never form true thymus tissue. The parathyroids also arise as diverticula from the third and fourth pouches. From the fifth pouches the ultimobranchial bodies originate and are enveloped by the lateral prolongations of the median thyroid rudiment; they do not, however, form true thyroid tissue, nor are any traces of them found in the human adult. 3 The Nose and Face.During the third week two areas of thickened ectoderm, the olfactory areas, appear immediately under the fore-brain in the anterior wall of the stomodeum, one on either side of a region termed the fronto-nasal process (Fig. 44). By the upgrowth of the surrounding parts these areas are converted into pits, the olfactory pits, which indent the fronto-nasal process and divide it into a medial and two lateral nasal processes (Fig. 45). The rounded lateral angles of the medial process constitute the globular processes of His. The olfactory pits form the rudiments of the nasal cavities, and from their ectodermal lining the epithelium of the nasal cavities, with the exception of that of the inferior meatuses, is derived. The globular processes are prolonged backward as plates, termed the nasal lamin: these lamin are at first some distance apart, but, gradually approaching, they ultimately fuse and form the nasal septum; the processes themselves meet in the middle line, and form the premaxill and the philtrum or central part of the upper lip (Fig. 48). The depressed part of the medial nasal process between the globular processes forms the lower part of the nasal septum or columella; while above this is seen a prominent angle, which becomes the future apex (Figs. 45, 46), and still higher a flat area, the future bridge, of the nose. The lateral nasal processes form the al of the nose. 4 FIG. 45 Head end of human embryo of about thirty to thirty-one days. (From model by Peters.) (See enlarged image) FIG. 46 Same embryo as shown in Fig. 45, with front wall of pharynx removed. (See enlarged image) FIG. 47 Head of a human embryo of about eight weeks, in which the nose and mouth are formed. (His.) (See enlarged image) FIG. 48 Diagram showing the regions of the adult face and neck related to the fronto-nasal process and the branchial arches. (See enlarged image) FIG. 49 Primitive palate of a human embryo of thirty-seven to thirty-eight days. (From model by Peters.) On the left side the lateral wall of the nasal cavity has been removed. (See enlarged image) FIG. 50 The roof of the mouth of a human embryo, aged about two and a half months, showing the mode of formation of the palate. (His.) (See enlarged image) Continuous with the dorsal end of the mandibular arch, and growing forward from its cephalic border, is a triangular process, the maxillary process, the ventral extremity of which is separated from the mandibular arch by a > shaped notch (Fig. 44). The maxillary process forms the lateral wall and floor of the orbit, and in it are ossified the zygomatic bone and the greater part of the maxilla; it meets with the lateral nasal process, from which, however, it is separated for a time by a groove, the naso-optic furrow, that extends from the furrow encircling the eyeball to the olfactory pit. The maxillary processes ultimately fuse with the lateral nasal and globular processes, and form the lateral parts of the upper lip and the posterior boundaries of the nares (Figs. 47, 48). From the third to the fifth month the nares are filled by masses of epithelium, on the breaking down and disappearance of which the permanent openings are produced. The maxillary process also gives rise to the lower portion of the lateral wall of the nasal cavity. The roof of the nose and the remaining parts of the lateral wall, viz., the ethmoidal labyrinth, the inferior nasal concha, the lateral cartilage, and the lateral crus of the alar cartilage, are developed in the lateral nasal process. By the fusion of the maxillary and nasal processes in the roof of the stomodeum the primitive palate (Fig. 49) is formed, and the olfactory pits extend backward above it. The posterior end of each pit is closed by an epithelial membrane, the bucco-nasal membrane, formed by the apposition of the nasal and stomodeal epithelium. By the rupture of these membranes the primitive choan or openings between the olfactory pits and the stomodeum are established. The floor of the nasal cavity is completed by the development of a pair of shelf-like palatine processes which extend medial-ward from the maxillary processes (Figs. 50 and 51); these coalesce with each other in the middle line, and constitute the entire palate, except a small part in front which is formed by the premaxillary bones. Two apertures persist for a time between the palatine processes and the premaxill and represent the permanent channels which in the lower animals connect the nose and mouth. The union of the parts which form the palate commences in front, the premaxillary and palatine processes joining in the eighth week, while the region of the future hard palate is completed by the ninth, and that of the soft palate by the eleventh week. By the completion of the palate the permanent choan are formed and are situated a considerable distance behind the primitive choan. The deformity known as cleft palate results from a non-union of the palatine processes, and that of harelip through a non-union of the maxillary and globular processes (see page 199). The nasal cavity becomes divided by a vertical septum, which extends downward and backward from the medial nasal process and nasal lamin, and unites below with the palatine processes. Into this septum a plate of cartilage extends from the under aspect of the ethmoid plate of the chodrocranium. The anterior part of this cartilaginous plate persists as the septal cartilage of the nose and the medial crus of the alar cartilage, but the posterior and upper parts are replaced by the vomer and perpendicular plate of the ethmoid. On either side of the nasal septum, at its lower and anterior part, the ectoderm is invaginated to form a blind pouch or diverticulum, which extends backward and upward into the nasal septum and is supported by a curved plate of cartilage. These pouches form the rudiments of the vomero-nasal organs of Jacobson, which open below, close to the junction of the premaxillary and maxillary bones. 5 FIG. 51 Frontal section of nasal cavities of a human embryo 28 mm. long. (Kollmann.) (See enlarged image) The Limbs.The limbs begin to make their appearance in the third week as small elevations or buds at the side of the trunk (Fig. 52). Prolongations from the muscle- and cutis-plates of several primitive segments extend into each bud, and carry with them the anterior divisions of the corresponding spinal nerves. The nerves supplying the limbs indicate the number of primitive segments which contribute to their formationthe upper limb being derived from seven, viz., fourth cervical to second thoracic inclusive, and the lower limb from ten, viz., twelfth thoracic to fourth sacral inclusive. The axial part of the mesoderm of the limb-bud becomes condensed and converted into its cartilaginous skeleton, and by the ossification of this the bones of the limbs are formed. By the sixth week the three chief divisions of the limbs are marked off by furrowsthe upper into arm, forearm, and hand; the lower into thigh, leg, and foot (Fig. 53). The limbs are at first directed backward nearly parallel to the long axis of the trunk, and each presents two surfaces and two borders. Of the surfaces, onethe future flexor surface of the limbis directed ventrally; the other, the extensor surface, dorsally; one border, the preaxial, looks forward toward the cephalic end of the embryo, and the other, the postaxial, backward toward the caudal end. The lateral epicondyle of the humerus, the radius, and the thumb lie along the preaxial border of the upper limb; and the medial epicondyle of the femur, the tibia, and the great toe along the corresponding border of the lower limb. The preaxial part is derived from the anterior segments, the postaxial from the posterior segments of the limb-bud; and this explains, to a large extent, the innervation of the adult limb, the nerves of the more anterior segments being distributed along the preaxial (radial or tibial), and those of the more posterior along the postaxial (ulnar or fibular) border of the limb. The limbs next undergo a rotation or torsion through an angle of 90 around their long axes the rotation being effected almost entirely at the limb girdles. In the upper limb the rotation is outward and forward; in the lower limb, inward and backward. As a consequence of this rotation the preaxial (radial) border of the fore-limb is directed lateralward, and the preaxial (tibial) border of the hind-limb is directed medialward; thus the flexor surface of the fore-limb is turned forward, and that of the hind-limb backward. 6 FIG. 52 Human embryo from thirty-one to thirty-four days. (His.) (See enlarged image) FIG. 53 Embryo of about six weeks. (His.) (See enlarged image)

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I. Embryology. 12. The Branchial Region. Gray, Henry. 1918 ...

Professor Guido Pennings' provocatively entitled BioNews commentary'Donor children do not benefit from being told about their conception' (see BioNews 900)purports to highlight the shortcomings of existing research supporting a pro-disclosure agenda, and castigates counsellors and researchers who advocate parental disclosure. Pennings' commentary follows up and repeats much of the contents of his longer paper published in Human Reproductionto which we and 35 other researchers, professionals and members of the donor conception community from around the world have since responded.

Professor Pennings' own views on non-disclosure of donor conception and the associated topic of donor anonymity are well known, so it is not surprising that he is out of step with the views with which we have been associated over the years. However, as an experienced academic and researcher himself, and as someone asserting the need for evidence-based policy and practice, we are extremely disappointed that Professor Pennings' recent comments fall short of the academic rigour readers might have reasonably expected.

First, Professor Pennings seems happy to condemn counsellors for their alleged failings:'Beliefs are expressed and pushed upon during counselling; this is an outright violation of the non-directiveness rule that stipulates that the moral values and views of the patients (parents and would-be-parents) must be respected.' But he does not cite any supporting evidence whatsoever (we know of none). Discussing contemporary research findings, including their limitations, with potential recipients of donated gametes/embryos neither equates with 'pushing' beliefs upon a patient nor violates the principles of non-directive counselling. On the contrary, it provides a valued opportunity for prospective parents to arrive at well-informed decisions through seeking clarification where needed, talking through any fears and uncertainty - particularly in relation to future parent-child relationships - and exploring possible disclosure strategies.

Second, Professor Pennings ignores the legal and policy mandates in several jurisdictions, multi-disciplinary professional bodies' guidelines and international human rights conventions which encourage parental disclosure through acknowledging donor-conceived individuals' right to knowledge of their origins [1]. For example, the UK's Human Fertilisation and Embryology Act 1990 Section 13 6C (as revised in 2008) requires clinics offering donor conception to inform prospective recipients of donated gametes and embryos of:

Third, the research Professor Pennings selected for critique forms only part of the available research evidence (for example, see Blyth and colleagues [2] for a more comprehensive review of relevant literature). The quality of Professor Pennings' review and analysis fails to meet normal expectations of a scholarly literature review. Professor Pennings also ignores relevant transferable research evidence on the impact of disclosure issues on the psychological and social well-being of adopted children and adults and that of secrecy in families.

Fourth, the available research, including the research he says he has analysed, provides a far more nuanced analysis of disclosure of donor conception than he asserts, with authors appropriately and thoughtfully taking account of such matters as child development perspectives and social context in their discussions [2-6]. Contrary to his conclusions, there is reliable evidence that the earlier donor-conceived children learn about the nature of their conception, the more favourable the outcomes both for the individual's identity formation and for family relationships. Evidence also reports that discovering one's donor conception later in life and/or in unplanned ways can result, for some, in long-term psychological distress and impair inter-familial and inter-personal relationships.

Fifth, in proposing that disclosure provides no benefits, Professor Pennings negates both the methodology of qualitative research and its recruitment methods, even though it has enabled the reporting of the lived experiences of those for whom disclosure has mattered most: donor-conceived individuals. In a research field severely hampered by the promotion of secrecy since the outset of donor conception as a medical procedure, qualitative findings significantly add to our understanding and are crucial to the development of well-informed evidenced-based practice.

Those with genuine intent to know about the needs of individuals born from donor conception do not need to search too hard.[2-6] With the advent of biotechnology and DNA registries, the question no longer remains whether there should be disclosure to children born following donor conception.[6] Rather, the focus should be on the what, how and when to disclose, and how these can best be achieved by parents within the intricacies of their sociocultural worlds.

Link:
Donor-conceived people do benefit from being told about their conception - BioNews

Women are freezing their eggs because men are refusing to commit to starting a family, a leading professor has warned.

Joyce Harper, professor of embryology at University College London, says it is wrong to think women freeze their eggs because they are obsessed by climbing the career ladder when, in reality, many are deserted by their partners when the issue of starting a family is raised.

As soon as the women mention Should we start having a family, should we think about it? the men have said, Bye, Harper said.

Unlike female fertility, which declines rapidly after the age of 35, men are able to father children into their fifties and older.

She said: It is easier for the men. They can just delay it

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Women freeze their eggs as partners get cold feet - The Times (subscription)

COUNCIL ROCK SCHOOLS The Council Rock Education Foundation will use a recent $12,000 donation from Customers Bank to fund a district-wide embryology project, CREF officials said.

The project is part of Council Rock's science, technology, engineering, art and mathematics emphasis, school district officials said. It will give more than 800 fourth-graders across the district the opportunity to learn about the stages of embryonic development as they incubate, observe, record data and hatch avian eggs, they added.

This interactive learning project enhances the fourth-grade curriculum, school district officials said.

"Contributions from Customers Bank and others are key sources of funding for student initiatives not covered by the annual school budget," said Council Rock Superintendent Robert Fraser. "We are most fortunate to have a very vibrant and robust education foundation and dedicated local businesses that support innovative programs to enhance our students' learning experiences."

Since 2007, the foundation has awarded more than $200,000 in grants to fund educational initiatives across the school district not possible under the regular budget, CREF officials said.

"Customers Bank is dedicated to supporting local partners like CREF that are working to grow innovative programs that ignite our children's passion for learning," said Customers Bank Vice President Kevin Beaupariant.

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Donation to Council Rock Education Foundation to be used for embryology project - The Intelligencer

A SIMPLE treatment appears to offer a cheap alternative to IVF for women who are struggling with infertility, say scientists.

They have found that women whose fallopian tubes are flushed with poppy seed oil are more likely to become pregnant.

For 100 years, doctors have used poppy seed oil to check for blockages in womens reproductive systems. The oil is used because it contains iodine, which glows white in scans to show whether the tubes are clear.

Poppy seed can boost female fertility, says expects. Image: Pixabay

But doctors noticed that when they swapped it for water mixed with iodine, fewer became pregnant - indicating that the poppy oil boosted patients fertility.

Scientists at the University of Adelaide found that 40% of women whose fallopian tubes were flushed with poppy seed oil became pregnant within six months.

This compares with 29 per cent whose tubes were flushed with the water and iodine solution.

Figures from the Human Fertility and Embryology Authority show that 32% of women up to 35 become pregnant after IVF, although this falls to just 14% once they hit 40.

Professor Ben Mol, who led the study, believes he may have been conceived following the procedure. He said yesterday: "The rates of successful pregnancy were significantly higher in the oil-based group - and after only one treatment.

"This is an important outcome for women who would have had no other course of action other than to seek IVF treatment. It offers new hope to infertile couples.

"Over the past century, pregnancy rates among infertile women reportedly increased after their tubes had been flushed with either water or oil during this X-ray procedure. Until now, it has been unclear whether the type of solution used in the procedure was influencing the change in fertility.

"Our results have been more exciting than we could have predicted. My mother went from being infertile for years to becoming pregnant. I was born in 1965. I have a younger brother, so its entirely possible - in fact, based on our research, its highly likely - that my brother and I are both the result of this technique."

The study of 1119 women was also carried out by experts at VU University Medical Centre in Amsterdam.

The authors, whose results are published in the New England Journal of Medicine, say their findings could spare some women the huge cost and emotional strain associated with IVF treatment.

They believe the high natural iodine content of the oil could be behind the phenomenon.

Research on mice suggests it creates a better environment for a woman's egg in the womb and is thought to make the womb more receptive to being implanted by an embryo.

The act of flushing out the tubes could help couples conceive by clearing debris that could prevent sperm from reaching the egg. - Daily Mail

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Poppy seed oil can boost female fertility | IOL - Independent Online

COUNCIL ROCK SCHOOLS The Council Rock Education Foundation will use a recent $12,000 donation from Customers Bank to fund a district-wide embryology project, CREF officials said.

The project is part of Council Rock's science, technology, engineering, art and mathematics emphasis, school district officials said. It will give more than 800 fourth-graders across the district the opportunity to learn about the stages of embryonic development as they incubate, observe, record data and hatch avian eggs, they added.

This interactive learning project enhances the fourth-grade curriculum, school district officials said.

"Contributions from Customers Bank and others are key sources of funding for student initiatives not covered by the annual school budget," said Council Rock Superintendent Robert Fraser. "We are most fortunate to have a very vibrant and robust education foundation and dedicated local businesses that support innovative programs to enhance our students' learning experiences."

Since 2007, the foundation has awarded more than $200,000 in grants to fund educational initiatives across the school district not possible under the regular budget, CREF officials said.

"Customers Bank is dedicated to supporting local partners like CREF that are working to grow innovative programs that ignite our children's passion for learning," said Customers Bank Vice President Kevin Beaupariant.

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Donation to Council Rock Education Foundation to be used for embryology project - Bucks County Courier Times

MEDWAY The following events will take place at Medway Public Library, 26 High St. For information and to register for events and programs, visit medwaylib.org. Contact childrens librarian Lucy Anderson with any questions at landerson@minlib.net or 508-533-3217.

Toddler Jam: 11 a.m. Tuesdays and Wednesdays. For newborns to age 3. This drop-in program will include stories, fingerplay and songs accompanied by mountain dulcimer. Children must be accompanied by a parent/caregiver.

Its Story Time!: 11 a.m. Thursdays and Fridays. For ages 10 months to 5 years. A drop-in story time with songs, stories and craft. All children must be accompanied by a caregiver. These ages are flexible.

PAWS to Read: 6 to 7:15 p.m. June 7. Each child will get a 15-minute one-on-one reading session with a visiting therapy dog. Children must be able to read independently, as this is not a tutoring session but rather an opportunity to practice reading skills with a good listener. For grades two to six.

Junior Lego Duplo Club: 11 a.m. June 10. Participants can enjoy an hour of free play with Duplos, easier than Legos for little hands. For ages 3-6.

Parachute Playgroups: 11 a.m. June 6 and 13. Participants will listen to a story, play parachute games, learn new songs, strengthen muscles, sharpen listening skills and make a craft. For ages 2 and older.

Embryology Club: 4 p.m. Thursdays, June 8 through July 13. Participants can learn all about the development and hatching of chicks. Participants can join for a six-week 4-H Impact Club on Embryology. Each child will be assigned an egg to watch over while the group learna about what is happening inside, how to candle the eggs to see them growing and the basics of caring for the baby chicks after they hatch. Registration is required.

BFG Breakout Box: 3:30 p.m. June 12. For ages 8-11. Advanced registration is required.

Summer Reading Kickoff with Davis Bates and Roger Tincknell: 3 p.m. June 27 This is a program for families celebrating reading and the cultural heritage of the United States. Award winning performers Roger Tincknell and Davis Bates share participatory stories and songs designed to amuse, inspire and create a feeling of community, while encouraging reading and awareness of the natural world. The program includes trickster stories, international folktales and folk songs and contemporary childrens songs. Instruments played will include banjo, guitar, mandolin and spoons.

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Medway Public Library announces events - Wicked Local Medway

May 19, 2017 Credit: University of Huddersfield

Experts at the University of Huddersfield are researching the emergence of a new style of family creation that sees couples "adopt" embryos and, after the child is born, remain in contact with the donors and in many cases develop a special relationship with them.

Some of the couples who have experienced the system so far available only in the USA and New Zealand have given highly positive responses to the UK-based research team.

One comment from a recipient who had made contact with an embryo donor was: "Not only were we given our daughter, but a whole family too two families actually, or one big family."

The researchers are Dr Lucy Frith, who is Reader in Bioethics at the University of Liverpool; University of Huddersfield Professor Emeritus Eric Blyth, an authority on social work who has a long track record of research into infertility treatments; and University of Huddersfield senior lecturer Dr Steve Lui, who has a background working and researching in the field of embryology.

The team has been examining the policies of the Snowflakes Embryo Adoption Program, operated in the USA by the organisation Nightlight Christian Adoptions. In 1997, when it discovered that thousands of human embryos were being stored in fertility clinics, this group began to connect couples who had stored embryos that they did not plan to use themselves with couples who could not conceive and it encourages them to remain in contact.

The pairings have resulted in the birth of over 500 babies, and a number of the children have met the women and men whose genetic material they carry, and their full genetic siblings living in donor families. This summer, many of them will attend an event celebrating the 20th anniversary of the scheme.

In the UK, children who are born as the result of egg, sperm and embryo donation have the right, once they reach 18, to ask the Human Fertilisation and Embryology Authority to disclose the identity of their biological parents.

Therefore, the Snowflakes Embryo Adoption Program in the USA proved to be a valuable research opportunity for the UK researchers. They hope to continue the project monitoring developments as the children who resulted from adopted embryos become older. Their current findings have been reported in a new article.

Titled Family building using embryo adoption: relationships and contact arrangements between provider and recipient families, it appears in the leading journal Human Reproduction.

The Snowflakes organisation offered its clients the opportunity to participate in the research, conducted by email. The article describes study participants' responses and the statistical data that it yielded. Phase Two of the project provided participants in the embryo adoption programme with the opportunity to give their appraisal of the scheme and several comments from both recipient and donor couples are relayed in the article. They include:

In their conclusion, the article's authors acknowledge that: "The use of embryos provided by a third party for family building is a contested form of reproductive technology. A conditional programme of embryo donation, such as that which operates in New Zealand and of which Snowflakes is an example, is even more contentious and couching embryo donation as adoption has caused controversy".

But they add that "conditional or embryo adoption programmes could provide an alternative to an anonymous, clinic-based model and give those who have unused embryos the opportunity to choose who they wish to donate to and if they wish to have and maintain contact in the longer term".

Dr Steve Lui, one of the researchers, said that an open adoption system could prove to be better. It enables children to learn about genetic factors that could be important for medical reason.

"Also, the issue of 'where do I come from?' is very important for the child in the long term. If you are open about it, then it won't come as a shock at a later point in their life."

Professor Blyth added: "Our study sheds light on how different families that become connected to each other following open embryo donation/adoption relate to each other. This is likely to become a more common pattern of family relations as policies and practices regarding gamete and embryo donation embrace increased transparency."

Explore further: Children can benefit when adoptive and biological parents share adoption stories

More information: Lucy Frith et al. Family building using embryo adoption: relationships and contact arrangements between provider and recipient familiesa mixed-methods study, Human Reproduction (2017). DOI: 10.1093/humrep/dex048

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'Adopted' embryo programme produces new style extended families - Medical Xpress