When examining the umbilical cord immediately after birth which blood vessels are present in a normal umbilical cord select all that apply?

Fetal placental circulation system

Fetal blood flows via umbilical arteries, in order to reach the villous capillaries through finer vessels of chorionic plate. The fetal surface is connected to blood circulation by two umbilical arteries (UA), which bring deoxygenated blood to the terminal villi. These terminal villi of placenta that are in direct contact with oxygen-rich maternal blood in the intervillous space, where the gas exchange takes place. The umbilical arteries are the strong muscular vessels, having a mean diameter of about 1.1–4.2 mm between 15 and 40 weeks' of pregnancy (ultra-sonographically measured) [22] and their size increases up to approximately 2.5 mm at term [23]. Umbilical arteries are the longest blood vessels in the human usually do not divide along the length of the umbilical cord, but they only branch over the fetal surface of placenta to form chorionic plate arteries, to provide blood supply to the terminal villi. The oxygenated nutrient-rich blood returns to the fetus via a single umbilical vein.

Pathogenesis

At parturition the umbilical arteries retract into the abdomen and close by smooth muscle contraction in response to the increased partial pressure of oxygen in the blood, and the umbilical vein and urachus remain outside the abdomen. The vein closes rapidly by smooth muscle contraction, and the urachus shrinks and dries within a few days.

Of the umbilical structures, the urachus is the most commonly infected in calves, with Actinomyces pyogenes being the most frequently identified organism involved. Escherichia coli, Proteus, Enterococcus, Streptococcus, and Staphylococcus species have also been identified as causative agents; therefore antimicrobial therapy should be based on culture results.

5.514.9.2 Derivation of Chondrocytes from Umbilical Cord Cells and Umbilical Cord Blood Cells

The umbilical cord consists of umbilical veins and arteries and the supporting mesenchyme called Wharton's jelly (Figure 6) where MSC-like cells can be isolated. These cells are denoted WJCs and are derived from the surrounding matrix between the umbilical blood vessels.91 The cells meet the criteria for stem cells as they have inherent self-renewal capacity and can be induced to differentiate into various cell types. The advantage of cells derived from the umbilical cord matrix is (i) the isolation of large numbers of cells without subsequent expansion in culture and (ii) that the cells are derived from fetal structures and could, like umbilical cord blood cells, thus have a better immunotolerance in the recipient patient.

The question whether the different compartments of the umbilical cord have different MSCs has been addressed in experiments with cells isolated from umbilical cord blood, umbilical vein subendothelium, and the Wharton's jelly. Within Wharton's jelly, MSCs can been isolated from three indistinct regions: the perivascular zone, the intervascular zone, and the subamnion. It is not clear whether cells isolated from these different compartments of the umbilical cord represent distinctly different populations of MSCs. The WJCs express MSC surface markers, thus suggesting that they are of the MSC family; however, in experimental settings, WJCs differ from BMSCs because WJCs are slower in differentiating into adipocytes.92 Since many features are shared with MSCs such as poor ability to differentiate to adipocytes, shorter doubling times than BMSCs, and greater numbers of passages to senescence, it not clear whether the MSCs derived from umbilical cord blood are different from those found in Wharton's jelly. For an extensive review, see Troyer and Weiss.93

However, the potential use of MSCs derived from umbilical cord or cord blood in the treatment of cartilage defects in humans remains to be established. Although the availability and immunogenicity could be of advantage, no scientific data today exist that support the notion that the cells are of lineage other than the bone default pathway.

Circulation

Deoxygenated blood leaves the fetus via the umbilical arteries and travels through the cord into the branching chorionic plate vessels. These in turn lead to the stem villi, which course through the decidual septa, and then further subdivide into the terminal villi. Here, the vasculature ends in an arteriocapillary–venous network with vessels closely apposed to the villous surface. A thin vasculosyncytial membrane lines the villi and is focally in direct contact with the capillary endothelium, across which gases, nutrients, and wastes can be exchanged between the fetal and maternal circulation. (Usually, there is no direct mixing of fetal and maternal blood.)

Within the fetus, like in adults, arterial perfusion to organs and vascular beds is regulated by the autonomic nervous system. When there is a significant decrease in the oxygen level in blood returning from the placenta, blood is preferentially shunted away from the peripheral organs to the heart and brain. Decreased blood flow to the gastrointestinal tract can trigger meconium release (see preceding text), and decreased blood flow to the kidneys can result in decreased urine output and oligohydramnios (also see preceding text).

However, the placenta lacks autonomic regulation and does not directly respond to changes in oxygen tension. Like the lungs, the placenta has low vascular resistance, and thus blood flow to the placenta is maintained in the short term, even under the most extreme circumstances. Chronic hypoxia/ischemia, though, results in infarctions and pathological lesions that increase resistance to blood flow in the placenta, in turn decreasing arterial flow and potentially beginning a cyclical spiral of hypoperfusion.

Placental venous flow begins with the return of blood from the villous capillaries and works its way back to the umbilical vein. Cord compression can obstruct venous return, as can any increase in fetal central venous pressure (right-sided heart failure, hydrops, etc.). This leads to venous stasis in the cord and chorionic plate veins and stem venules, which are then at increased risk of thrombosis and villous damage from increased pressure.

Maternal decidual vessels, as previously discussed, are remodeled and lined by trophoblast to allow unrestricted blood flow. As pregnancy advances, the fetus grows and so does its oxygen requirements. Maternal cardiac output increases, uterine arteries widen, and terminal villi increase in number and exchange efficiency to provide adequate capacity. Maternal vasculopathy, such as seen in hypertension, preeclampsia/eclampsia, and diabetes, can involve incomplete remodeling of the decidual vessels; with retained mural smooth muscle and/or atherotic changes, blood flow is reduced and uteroplacental insufficiency may result. Maternal blood drains from the intervillous space primarily via marginal veins at the edges of the disk and also from veins in the decidua basalis. Decreased venous flow can result from abnormal placental or uterine anatomy, decreased maternal cardiac output, or obstructed maternal venous return (such as by compression of the inferior vena cava by the uterus).

Thus, multiple intrinsic properties of several different vascular beds, in conjunction with various external factors, combine to determine net uteroplacental function. Insufficient blood flow can lead to fetal growth restriction.

Umbilicus.

After rupture of the umbilical cord, the two umbilical arteries retract actively, and the urachus is pulled back passively by these vessels into the abdomen. Smooth muscle contraction brings about luminal closure. The umbilical arteries ultimately become the lateral ligaments of the urinary bladder.

The umbilical vein does not retract but rather collapses in association with some minor smooth muscle contraction. The umbilical sheath shrinks and dries within 3 days postpartum. The body wall closes completely around the umbilical structures within days to a few weeks after birth.305

During the physical examination the navel is assessed for diameter, discharge, and pain while the neonatal ruminant is standing and again while it is in lateral recumbency. Abdominal palpation, using both hands pressing together, is useful for evaluating the umbilicus of standing calves. Enlargement of the umbilical arteries can be palpated coursing caudally toward the bladder and enlargement of the umbilical vein coursing cranially to the liver. Application of pressure caudal to the xiphoid often elicits a soft grunt from calves with a septic umbilicus and associated peritonitis. Extensive adhesion of bowel to inflamed umbilical structures produces a large, easily palpable intraabdominal mass. The uterine vein and artery may also be traced within the abdomen with the calf in recumbency. Common abnormalities of the calf umbilicus include umbilical hernias, omphalophlebitis, external umbilical abscess, urachal abscess, and omphaloarteritis. Patent urachus is uncommon in calves. Disorders of the urachus or the umbilical arteries are often associated with pollakiuria and a prolonged stance of urination. Umbilical hernias in cattle do not tend to close spontaneously and are believed to be hereditary.306

Ultrasound examination of the calf is performed with the calf standing; occasionally the umbilical vein is easier to identify with the patient in left lateral recumbency.307 The umbilical vein courses from the umbilicus to the liver, which in the calf is located on the right side. The lumen is generally larger near the body wall, with a diameter ranging from 10 to 25 mm. It appears as a round-to-oval anechoic to hypoechogenic structure. Within 3 weeks after birth, ultrasonographic identification of the intraabdominal umbilical vein becomes impossible in up to 50% of healthy calves. If still visible, the vein appears hypoechogenic to the surrounding tissue and indistinctly marginated.305 In cattle the umbilical arteries and urachus retract into the abdominal cavity when the cord ruptures and thus cannot be identified in the external umbilical stalk in normal calves.307 The umbilical vein of calves is scanned from the umbilical stalk to the liver along the right abdominal wall. The umbilical vein enters the liver caudoventral to the gallbladder. The umbilical arteries are most easily located adjacent to the urinary bladder and cannot normally be identified much beyond the apex of the urinary bladder, unless enlarged and abnormal. Identification of a urachal remnant in calves is abnormal.307 Umbilical ultrasound is useful for evaluating the need for umbilical surgery and identifying other organs involved that may influence the complexity of the procedure (Fig. 19.5).

Umbilical Problems

The umbilicus contains a single umbilical vein, two umbilical arteries, the urachus, and vitelline vein remnant.398 Guidelines for routine care of the umbilicus after birth are discussed in Chapter 16. The most common postnatal problem of the umbilicus is patency of the urachus. The urachus is the anatomic connection between the bladder and allantoic sac. During gestation the predominant flow of urine is through the urachus, but as gestation proceeds some urine will enter amniotic sac via the urethra. The urachus is closed at the time that the cord is broken. Excessive coiling of the umbilical cord during gestation may result in partial obstruction of the urachus with overdistention of the structure, thereby interfering with the normal process of involution when the cord is torn after birth. This is estimated to occur in around 6% of normal foals.399 The structure may fail to close or reopen for a number of reasons, including cutting of the cord rather than tearing, infection, excessive handling, or weakness of the supporting abdominal musculature. The condition is a common complication in sick neonatal foals, particularly those that are mostly recumbent. Affected foals will typically dribble or stream urine from the umbilicus during urination. There may be excessive straining observed. Physical examination may reveal a moist umbilical stump. In a small number of foals a rent in the urachus occurs as it moves through the subcutaneous tissues, resulting in local swelling, that may be marked. If the tear in the urachus occurs intraabdominally, there will be uroperitoneum and in rare cases omentum may herniate externally through the urachal tear. Ultrasound is recommended, and a fluid-filled urachus is consistent with patency. The umbilical arteries and vein should be assessed for infection as an open urachus is a common finding in foals with umbilical remnant infections.400

Therapy for an uncomplicated patent urachus typically consists of conservative management, involving monitoring and frequent disinfection. Cauterization of the urachus using silver nitrate sticks or injection with procaine penicillin was once popular but appears to be used infrequently in recent times. Resection of the structure may be indicated if patency persists beyond 3 weeks of age.

When the umbilicus is enlarged and draining purulent material, infection is easily diagnosed. Many neonates may have a completely normal-appearing external umbilicus but have internal infection of the urachus, umbilical arteries, or vein. Ultrasound is the key tool to diagnose internal abnormalities of the umbilical structures. The umbilical area of neonates younger than 20 days of age with fever of unknown origin should be scanned, as well as any foal with suspected bone or joint infection. A description of normal US findings is described in Chapter 16.

The traditional approach was to surgically remove abnormal umbilical remnants if there were abnormalities detected on US or if the external umbilicus was enlarged and/or draining purulent material. The basis for this was to remove the potential for bacteremia with seeding of other structures, such as bone or joints. There is morbidity and cost associated with simple surgical removal, and there is little evidence that surgical excision is superior to long-term therapy with antimicrobial drugs. More recently, many clinicians favor long-term antimicrobial treatment with oral therapy, such as trimethoprim-sulfa combinations or minocycline. In this approach it is important to monitor responses to therapy using frequent US examinations. Surgical removal would be indicated if the internal appearance worsens in the face of medical treatment.

Omphalitis

Omphalitis is inflammation of umbilical structures that may include the umbilical arteries (omphaloarteritis), umbilical vein (omphalophlebitis), urachus, or tissues immediately surrounding the umbilicus. Umbilical infection is one of the most common diseases in newborn calves, occurring in 1.3%763 to 29.9% of newborn calves.764

Umbilical abscess or infection of any of the three components of the umbilicus may produce local infection or be a source of septicemia. The source of infection is most commonly the external environment, coupled with FPT. Bacteria isolated from calf umbilical cord remnant infection include T. pyogenes, E. coli, and Proteus and Enterococcus spp. Herd management variables that influence the risk of umbilical infection include maternity pen hygiene, cleanliness of the newborn calf environment, effectiveness of passive transfer, and umbilical cord management.765

The urachus is the most commonly affected structure in calves, and the umbilical arteries are the least affected.766 Omphalophlebitis may extend the length of the umbilical vein into the liver and result in liver abscessation. When the umbilicus is enlarged and draining purulent material, infection is easily noted. When the urachus is fixed to the abdominal wall, calves are prone to cystitis and may show signs of pollakiuria and dysuria. In other cases the umbilicus may be dry and larger in diameter than expected. In addition, neonates may have a completely normal-appearing, dry external navel and be severely ill from infection of the urachus, umbilical arteries, or umbilical vein. In a septic neonate without external signs of infection, involvement of the umbilicus can be difficult to determine. Abdominal palpation of the umbilical vein and arteries is a useful, simple, and effective means of assessing their size and detecting pain associated with these structures. Inflamed structures may be identified by standing behind the neonate and pressing the hands together above the umbilicus. Ultrasound is also a useful ancillary diagnostic aid.767 Persistent dilation of the umbilical vein or arteries with a hypoechoic-to-echogenic fluid, intraluminal gas, and wall thickening are findings consistent with infection. In calves, the urachus normally retracts up into the abdomen at birth, and ultrasonographic identification of a urachal remnant is abnormal.768

Overt signs of infection are heat, swelling, purulent discharge, or pain. Concurrent signs of systemic infection such as joint infection, pneumonia, diarrhea, meningitis, or uveitis may be noted. Calves with urachal abscesses may show signs of dysuria or pollakiuria.769,770 Infection in more than one umbilical vessel in the neonate is common, and urachal involvement is frequent. Umbilical abscessation that is walled off and does not involve deeper structures is a less severe problem and may be treated with drainage without surgical removal of the entire umbilicus.

Early treatment with antibiotics and supportive care may allow resolution before development of abscessation and distention of the urachus or the umbilical arteries and vein. Established infection usually requires surgical removal of involved structures in addition to medical therapy.766 When omphalophlebitis extends into the liver, the umbilical vein may be marsupialized to facilitate drainage and flushing.771 Prognosis is improved when adequate passive transfer of colostral immunoglobulins has occurred and when joints or other structures are not involved. Sequelae such as renal abscessation, joint or bone infection, peritonitis, and other complications described for septicemia may develop if therapy is started too late or discontinued prematurely.

Abdominal Cavity

1.

Before moving anything, carefully check all organs for position and completeness. Carefully examine umbilicus, umbilical arteries, vein (all the way up to liver), and urachus.

Separate omentum with spleen from stomach and pancreas.

Find distal colon, transect, and separate guts from mesentery as close as possible to its intestinal insertion. This will permit laying out intestines in long straight lines, which facilitates rapid opening along entire length. Be careful at the transverse colon to not cut off cecum and pancreas.

Pull liver back from diaphragm, and transect esophagus, aorta, and caudal vena cava; lift out liver, stomach, pancreas, and guts by transecting remaining connections. Secure adrenal glands cranial to kidneys (if they are not there, check dorsal margin of liver).

To check patency of bile duct, open duodenum and squeeze gall bladder to extrude bile. Remove liver from other organs.

Open stomach along greater curvature from cardia to pylorus and intestines with scissors (as if cutting fabric) along mesenteric insertion to preserve Peyer's patches.

Take samples for histopathology and additional testing (see Figures 31-7 and 31-8).

ANATOMY

The umbilicus is a remnant of the fetal-maternal connection. At birth the structure consists of the paired umbilical arteries, a single umbilical vein, and the urachus. Before birth, the umbilical vein serves as the source of oxygenated blood to the fetus via the liver and ductus venosus/portal vein. The paired umbilical arteries are branches of the internal iliac artery and carry waste materials and unoxygenated blood to the placenta. The urachus is the connection from the fetal bladder to the allantoic sac. Following a normal delivery, the smooth muscle that surrounds the umbilicus contracts in response to the stretching of the cord at parturition. Separation of the umbilical cord allows the umbilical arteries and urachus to retract into the abdomen, where they close by smooth muscle contraction.15 The umbilical vein and remnants of the amniotic membrane remain outside the body wall but rapidly collapse in association with smooth muscle contraction; therefore the umbilicus shrinks and shrivels. The umbilical stalk normally dries and thins out by 3 to 4 days postdelivery. The scabbed over and desiccated umbilical stalk should be totally eliminated by 3 to 4 weeks of age.16

As the animal matures, the umbilical vein undergoes fibrosis and becomes the round ligament of the liver suspended in the falciform ligament. The umbilical arteries collapse and become the lateral ligaments of the urinary bladder. The body wall normally closes completely around the umbilical structures within a few days, but occasionally, small openings in the linea alba (<1.2 cm) are palpable for a few months. These most often close spontaneously.