Uterine Tube (Fallopian Tube) Anatomy

Uterine tubes (also known as oviducts or fallopian tubes) are structures found in females that connect bilaterally to the uterus. They lie in close proximity to the ovaries and function to transport the oocyte from the ovary to the uterus each month. In the presence of sperm and after fertilization, the fallopian tube transports the zygote to the narrow intrauterine segment of the tube from where it descends into the uterus for implantation. Secondary to their primary role as a conduit for the ova, sperm, and zygote, the uterine tubes are responsible for ~1/3 of infertility cases and are often targeted in surgical sterilization procedures. Additionally, they provide anatomical and immunological barriers, preventing colonization of the abdominal cavity by pathogens. An ascending infection through the vagina can cause inflammation of the tubal lumen (salpingitis), ultimately leading to internal scarring and potential occlusion of the fimbriated, lateral end (near ovary). This can result in hydrosalpinx, increased risk for ectopic pregnancy, and infertility due to tubal factors. ^{[1, 2]}

Embryology

The paramesonephric (Müllerian) ducts develop in both male and female embryos but become prominent during the formation of the female reproductive system. Each duct begins as a linear invagination of the coelomic epithelium. The cranial portion of the ducts develop into the uterine tubes, with the initial coelomic invagination remaining as the abdominal opening of the tube. The fimbriae become defined as the cranial end as the mesonephros degenerates. As development continues, the caudal vertical parts of the two ducts fuse to form the uterovaginal primordium, which gives rise to the lower part of the uterus. In females, the mesonephric duct becomes vestigial. This vestigial region is a remnant of the degenerated male system known as the Wolffian duct and is clinically important because secondary (paratubal) cysts can form and are at times confused as an ovarian cyst. The cranial portion transforms into the longitudinal duct of the epoophoron, while the caudal portion is known as Gartner's duct. ^[3]

Gross anatomy

The uterine tubes are attached to the upper part of the body of the uterus and their ostia open into the uterine cavity. The medial opening (uterine ostium) of the uterine tube is located at the superior angle of the uterine cavity. ^[3]  These tubes exit the uterus through an area referred to as the cornua, forming a connection between the endometrial and peritoneal cavities. Each uterine tube is approximately 10 cm in length and 1 cm in diameter and is situated within the mesosalpinx, which is a fold in the broad ligament.

Each uterine tube consists of four anatomical regions from caudal to cranial: the uterine part, isthmus, ampulla, and infundibulum (see Table 1). ^[3]

Table 1. Anatomical Regions of the Uterine Tube (Open Table in a new window)

Fimbriae are mucosal finger-like folds — each 1 mm wide — attached to the infundibulum and extend beyond the fallopian tube's muscular wall. During ovulation, the fimbriae swell and extend due to engorgement of the vessels in the lamina propria, aiding in the capture of the oocyte. These fimbriae create currents and eddies that help sweep the oocyte into the infundibulum.  All fimbriae, similar to the mucosal lining of the tube, are covered by a ciliated epithelium with cilia that beat toward the ampulla of the fallopian tube. ^[3] The lateral portion of the uterine tube with its fimbriae, ends in an orientation encircling the ovary.

Vascular supply

Arteries

Arterial supply to the uterine tube is from branches of the uterine and ovarian arteries. The ovarian artery originates from the abdominal aorta just below the renal arteries, while the uterine artery arises from the anterior division of the internal iliac artery. The ovarian artery supplies the lateral portion of the tube. This artery continues in the mesosalpinx to anastomose with branches from the uterine artery. The medial portion (closest to the uterus) of the uterine tube is supplied by the uterine artery. ^[3]

Veins

The lateral two thirds of the uterine tube are drained by the pampiniform plexus, which leads to the ovarian veins; these veins empty into the inferior vena cava on the right side and the renal vein on the left. The medial one third of the uterine tubes are drained via the uterine plexus into the internal iliac veins. ^[3]

Lymphatics

Lymphatic drainage of the uterine tubes is through uterine vessels to the internal iliac nodes and through ovarian vessels to the lateral aortic nodes. ^{[4, 5]} Additionally, lymph can potentially reach the inguinal nodes via the round ligament of the uterus. ^[3]

Nerve supply

Nerve supply to the uterine tube is via both the ovarian plexus (innervates lateral tube) and the uterine (pelvic) plexus (innervates medial tube). Both plexuses are mixed containing sympathetic and parasympathetic fibers. The ovarian plexus receives sympathetic fibers from T11-L1 and parasympathetic fibers from the vagus nerve. The pelvic plexus receives sympathetic fibers from sacral splanchnic nerves and parasympathetic fibers from pelvic splanchnic nerves (S2-4). Visceral afferent pain fibers retrace sympathetic pathways from the uterine tubes back to thoracic segments 11-12 (T11-T12) and lumbar segment 1 (L1).

Sympathetic Supply:

1. Preganglionic: Neuron cell bodies originate in the intermediolateral nuclei of T11-L1 heading for the ovarian plexus.  Additionally, sacral splanchnic nerves supply sympathetic fibers to the pelvic plexus.
2. Postganglionic: Superior hypogastric plexus feeds the ovarian plexus (supplies lateral uterine tube) and hypogastric and sacral splanchnic nerves contribute to the pelvic plexus, which supplies the medial (attached to uterus) uterine tube.
3. Visceral afferent (pain) fibers: Retrace sympathetic nerve pathways, entering the spinal cord through corresponding dorsal roots T11-L1. ^[3]

Parasympathetic Supply:

1. Preganglionic: Derived from pelvic splanchnic nerves (S2, S3, S4). These flow into the inferior hypogastric plexus and then out to the uterus and uterine tubes. Additionally, the vagus nerve contributes parasympathetic fibers to the ovarian plexus.
2. Visceral afferent fibers: Retrace the parasympathetic nerves and carry visceral afferent sensory fibers for reflex activity ^[3]

Microscopic anatomy

Histologically, the uterine tubes are composed of three layers — the visceral mucosa, muscularis, and serosa. 

The mucosa has many folds, called plicae, which are most evident in the ampulla. It is lined by a single-layered, tall, columnar epithelium primarily composed of ciliated cells and secretory (peg) cells, along with occasional intraepithelial lymphocytes. Ciliated cells (see image below) are more common in the lateral part of the uterine tube, while secretory cells predominate medially.  Their activities vary across the menstrual cycle and with age; the same has been summarized in Table 2. ^[3]

Electron micrograph of normal uterine tube mucosa. (Courtesy of Brian Bear, MD)

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Table 2. Uterine Tube Microscopy (Open Table in a new window)

The lamina propria provides vascular connective tissue support and abundant lymphatic drainage vessels and binds the mucosa to the muscularis layer. ^[3] The muscularis layer is a layer of smooth muscle that surrounds the mucosa. It has an inner circular or spiral layer and an outer, thinner longitudinal layer. Its contractile activity produces peristaltic movements assisting in the propulsion of gametes and the fertilized ovum. ^[3]

The outermost layer is the serosa; it is highly vascular and primarily composed visceral peritoneum. ^[6]  

A study by Weigert et al has shown that during menopause, the uterine tubes undergo atrophic changes characterized by age-related loss of ciliated and secretory function. ^[1]  Growing morphologic and molecular evidence suggests that a significant number of high-grade serous ovarian cancers can originate from the uterine tube epithelium, particularly from the fimbriae rather than the ovaries. ^[2]  Recent studies have detected dysplastic regions with high proliferation rates, activation of the PI3 kinase pathway, and overexpression of p53 in the uterine tube mucosa of females with invasive high-grade serous cancer (HGSC), thereby implicating the uterine tube epithelium as a potential origin site for developing HGSC. It is the standard of care to remove the tubes during hysterectomy when possible because it lowers the risk of high-grade serous fallopian tube cancers that originate from the uterine epithelium. ^[7]

Tubo-ovarian abscess and salpingitis

Tubo-ovarian abscess (TOA) and salpingitis are infectious in nature and are typically associated with an ascending infection from the lower female pelvic organs (also known as pelvic inflammatory disease). TOA primarily affects sexually active females of reproductive age but can occur without other pelvic inflammatory disease (PID) sequelae. Chlamydia (Chlamydia trachomatis) and gonorrhea (Neisseria gonorrhoeae) are responsible for 50% of PID ^[8]  and therefore the majority of TOA cases. Furthermore, PID can be a polymicrobial infection, involving enteric (Escherichia coli, Bacteroides fragilis, group B Streptococci), respiratory (Haemophilus influenzae, Streptococcus pneumoniae, Staphylococcus aureus), anaerobic pathogens, linked to bacterial vaginosis (Peptostreptococcus, Bacteroides species), and/or emerging pathogens such as Mycoplasma genitalium. ^[9]

Appendicitis may lead to TOAs through bacterial translocation or direct spread. A ruptured appendix can seed the peritoneal cavity with a significant quantity of bacteria. These bacteria, of intestinal origin, can cause significant peritonitis and salpingitis leading to long term tubal disease, intra-abdominal adhesions, and infertility. ^{[10, 11]}

Females with salpingitis or TOA usually present with fever and acute onset of abdominal pain and foul-smelling mucopurulent vaginal discharge. The uterine tube in a patient with TOA is commonly filled with pus (pyosalpinx). The diagnosis is usually a clinical one, and it is confirmed via ultrasonography, laboratory study findings such as elevated white blood cell count, a positive culture of the cervix confirming etiology of chlamydia or gonorrhea, and/or surgical identification if removal is necessary. Transabdominal and transvaginal ultrasonography are the preferred initial imaging techniques for evaluating pelvic pain in women of reproductive age. MRI based techniques provide clearer visualization of tubal changes linked to TOA. ^[12]

Patients with salpingitis and TOA are treated with intravenous antibiotics to cover common organisms that may have caused the ascending infection, usually chlamydia and/or gonorrhea. Treatment is started before culture results are finalized. The goal of treatment is to resolve the symptoms and to maintain tubal function (see also Pelvic Inflammatory Disease Empiric Therapy and Pelvic Inflammatory Disease Organism-Specific Therapy). Depending on the severity of infection, surgery to remove the uterine tube is warranted in some cases.

Sequelae of these infections include infertility, chronic pain, and increased risk for ectopic pregnancy. Loss of ciliated projections increases the risk of ectopic pregnancy secondary to loss of motility within the tube (see image below).

(A) EM normal uterine tube mucosa. (B) EM uterine tube mucosa devastated from PID.

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Hydrosalpinx

Hydrosalpinx occurs when fluid accumulates within the ampullar lumen due to obstruction of the infundibulum. The most common cause of hydrosalpinx is PID. Hydrosalpinx is associated with diminished IVF outcomes as evidenced by decreased live birth rates and increased pregnancy loss. Studies have shown that pre-IVF (in vitro fertilization) salpingectomy can improve pregnancy rates and overall reproductive outcomes. ^[7]

Ectopic pregnancy

Ectopic pregnancy (EP) is caused by the implantation of a fertilized ovum either within the uterine tube or anywhere other than the endometrial cavity (see image below). In tubal ectopic pregnancy, the lamina propria reacts like the endometrium and forms many decidual cells. ^{[11, 13]} The risk factors include a history of EP, uterine tube damage, prior pelvic or uterine tube surgery, complications from pelvic infections, infertility, smoking, age over 35 years, PID, endometriosis, anatomical variants, pregnancy with an intrauterine device, and the use of assisted reproductive technology. Conversely, no significant association with EP risk has been found for oral contraceptive use, prior pregnancy termination, emergency contraception failure, cesarean delivery, or pregnancy loss. ^[14]

Sites and frequencies of ectopic pregnancy. By Donna M. Peretin, RN. (A) Ampullary, 80%; (B) Isthmic, 12%; (C) Fimbrial, 5%; (D) Cornual/Interstitial, 2%; (E) Abdominal, 1.4%; (F) Ovarian, 0.2%; (G) Cervical, 0.2%.

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Tubal ectopic pregnancy is the most common type and has high maternal morbidity and mortality when ruptured (see image below). ^[14]  Because the lumen of the uterine tube is small, it cannot contain a growing pregnancy. Once the embryo or fetus becomes large enough, it can invariably rupture through the wall of the uterine tube, becoming a medical emergency. Infrequently it can be expelled through the lateral tubal opening into the abdomen. Immediate surgical intervention is needed in this situation. If only one of the uterine tubes is removed, it is still possible for pregnancy to occur on the opposite side.

Ectopic pregnancy within uterine tube. (Courtesy of Brian Bear, MD)

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The current diagnostic standard for EP is a combination of ultrasound imaging and serial quantitative β-hCG levels. Experimental markers such as activin-AB and PAPP-A have shown promising potential for earlier diagnosis and detection of ectopic pregnancy. ^[14]  If the ectopic pregnancy is detected on ultrasonography before it becomes too advanced, medical treatment with methotrexate may be used in some cases. When medical management is contraindicated or ineffective, surgical interventions such as salpingostomy or salpingectomy may be performed. ^[14]