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Umbilical Artery Thrombus
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Umbilical artery thrombi


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            Several published papers seem to imply a grave prognosis for umbilical arterial thrombus with a high incidence of fetal death, growth retardation and fetal distress. However, these were usually from selected groups of patients including autopsy series. In the few prospective reports of umbilical artery thrombosis the prognosis appears good including those discovered by intrauterine ultrasound. The mechanism or cause of the thrombosis may determine the risk.

Umbilical artery thrombosis could result from an acute compression of the artery from torsion, spasm or other hypothetical local mechanism. If there is no other complication, the infant may not sustain harm. The remaining artery via the Hyrtl anastomosis can perfuse the entire placenta. There are special circumstances in which umbilical artery thrombus could cause growth retardation or fetal death. The most obvious is with single umbilical artery or thrombosis of both umbilical arteries. A few percent of placentas do not have a Hyrtl anastomosis, and in this event a portion of placenta would cease to have fetal perfusion.  A thrombus can extent into and occlude the Hyrtl anastomosis with similar results. If an infant is already compromised, the potential rise in blood pressure from a thrombus in one artery could be lethal. Attention needs to be paid to the individual circumstances of death, distress or growth retardation in cases of umbilical artery thrombus.

In other cases, even with out compromise of the Hyrtl anastomsis, there is downstream fetal thrombotic vasculopathy which may occlude sufficient fetal perfusion of the placenta to decrease function resulting in growth retardation and even death. Most umbilical artery thrombi do not have evidence of fetal thrombophilia. Infrequently, distal thrombotic placental vasculopathy is due to embolism from a more proximal thrombus in the aorta or iliac arteries which eventually results in umbilical artery occlusion. Such an infant may also have thrombi in other organs. Fetal thrombotic vasculopathy and umbilical vein thrombi will be discussed in a separate section.

While seldom commented on as part of umbilical artery thrombosis, the atrophy or loss of one umbilical artery may be accompanied by thrombosis. In this case, the thrombus is in an atrophic artery. The histological distinction between a normal sized artery during early gestation that developed a thrombus, and a hypoplastic artery that developed thrombus later in gestation may not be easy. The significance of thrombus in an atrophic artery may be different from that in a normal artery since the thrombus may be from loss of distal placental flow.

            The pathological diagnosis of umbilical artery thrombus is not always easy.

Even if a single point of the artery is occluded, stasis will occur along the entire artery initiating endothelial injury and stasis. (Blood is at systemic pressure on either side of the occlusion due to direct pressure on the fetal side, and indirect pressure via the anastomosis of Hyrtl on the placental side.) With complete occlusion there may not even be a true thrombosis, but simply clotting of blood in the lumen. The concept of a thrombus is clotting in flowing blood which results in lamination of fibrin and cellular layers including platelets, and with accumulation of more fibrin than available in the lumen at any one moment. The histological definition of thrombus in many studies may encompass such a clot, but this is not really a thrombus. If the arterial occlusion is initially partial, true thrombosis could occur.

            The cessation of the flow in the entire artery can be detected if sufficient time is elapsed (?hours). With stasis, both blood cells and the arterial wall become ischemic. There is no vaso vasorum or alternate blood supply for the artery. The red cells along the entire artery become ischemic and leak hemoglobin. Initially, this may produce a red barber pole discoloration of the cord. Eventually the cord stains completely red similar to stillbirth, but in a living infant. Microscopically, there is necrosis of the arterial wall. Blood cells will eventually become pale and amorphous. With prolonged postmortem intrauterine retention of the fetus, degenerated blood in vessels can be mistaken for old thrombus. Studies should have clear definitions of the pathology, and some form of control or concordance testing.

More needs to be known about the specific mechanisms leading to arterial thrombus, and of the prognosis of such thrombi when found incidentally in the uncomplicated pregnancy, or with complications such as intrauterine growth retardation. The ability to detect umbilical artery thrombosis in utero by ultrasound, and especially Doppler, should increase our understanding of the mechanism and consequences.


Literature Review


            Case reports:

A single case of an umbilical artery thrombus was reported in an infant with a short (30cm) umbilical cord at 38 weeks of gestation with cord compression pattern deep variables in the first stage of labor[1]. A Cesarean section was performed with delivery of a 3,030 g infant with Apgars of 5/8 at 1/5 minutes. The infant had no complications except mild hepatomegaly. A thrombus was removed from the right umbilical artery of the cord stump. It is unclear if this is the same as the thrombus in situ that was palpated and inspected 3cm from the fetal side of the umbilical cord. There is a gross photograph of an in situ thrombus which by report was confirmed to be a thrombus with laminated fibrin. The authors speculate that the short cord had caused stretch that had led to vascular injury, stasis and thrombosis.

            Another case reports decreased fetal movement at 35 weeks gestation in a mother with a history of cigarette smoking, but ceased during the pregnancy [2]. She had a non-reactive fetal heart tracing. The ultrasound demonstrated an area echogenicity in one umbilical artery An Doppler ultrasound showed absent flow in one umbilical artery. A cesarean section delivered a 2,505 g infant with Apgars of 8/9 at 1/5 minutes. The infant had transient tachypnea and received antibiotics for neonatal sepsis and was discharged after seven days without further complications. The umbilical cord was 70 cm long with prominent left handed twists. The pathology report found many recent fibrin thrombi in the chorionic and stem vessels. The villous changes depicted appear to be normally found syncytial necrosis with fibrinoid, but there is a note that there was also karyorhexsis.

            Another report documents two infants with intrauterine ultrasound diagnosis of umbilical artery thrombus[3]. One mother had mild hypertension, a lichenoid pruritic skin rash, and elevated transaminases. An ultrasound examination of the fetus demonstrated a thrombus in an umbilical artery. As a result, a cesarean section was performed with delivery of a 37 week gestation, 2,360 g infant, with Apgar 10 at one minute. After delivery the maternal liver enzymes returned to normal, a livre biopsy was normal and the skin lesions resolved into hyperpigmented scars. The infant examination was normal. The gross examination of the umbilical cord revealed an arterial thrombus. The second mother was seen for intrauterine growth retardation and with during the fetal ultrasound an hyperechogenic area in one umbilical artery was discovered. At 37 week of gestation a 2.080 g infant with Apgar of 10 at one minute was delivered by Cesarean section. Examination of the placenta demonstrated umbilical arterial thrombosis with fibrinous thrombi at the insertion area. There was neither illustration of the pathology, nor comment on the microscopic findings.

            The case of aortic embolism from this institution demonstrated emboli to the distal vessels from an aortic thrombus with complete occlusion of one umbilical artery with a duration sufficient to produce hemoglobin diffusion with a red barber pole helix of the cord[4]. The infant had no complications and thrombophila studies were negative.

            A case report embedded in a series describes a stillborn infant with an aortic thrombus that extended into one umbilical artery[5]. The fetus was 28-30 weeks of gestation with a birth weight of 577 grams and a clinical history of 1 month of polyhydramnios. A section through the anastomosis of Hyrtl demonstrated thrombus there, and one half of the placenta was pale with avascular villi consistent with loss of fetal blood flow. Thus even with a Hyrtl anastomosis, umbilical artery thrombus can cause sudden loss of half the placental function, and presumably was the cause of fetal death. Pathologically the more proximal thrombus demonstrated organization, and the more distal was more acute. The wall of the umbilical artery with the thrombus demonstrated necrosis not present in the other artery.

In one case a Cesarean section done for a sinusoidal fetal heart rate pattern, a Doppler loss of end diastolic flow resulted in a severely asphyxiated (eventually tetraplegic), term, 3635 g infant[6]. The placenta showed deep green meconium staining. Light microscopy showed meconium macrophages in the cord, acute inflammation, and thrombi in both the artery and vein. The illustration shows a marked increase in nucleated red cells. I can not see a thrombus. The authors speculate that there was meconium injury to the vessels leading to thrombosis, but the argument is indirect.

Another case of intrauterine growth retardation at 32 weeks gestation in the infant of an insulin dependent diabetic mother had a prenatal diagnosis of thrombus of an umbilical artery[7]. Conservative observation was interrupted by Cesarean section for non-reassuring fetal heart rate. There was a thrombus of an umbilical artery and a contiguous 40% of the placenta demonstrated advanced lesions of absent fetal perfusion. The authors speculate that this was due to a lack of Hyrtl anastomosis or thrombosis of it. The umbilical cord was 70 cm long and twisted.

Thrombosis in the umbilical arteries and vein in a fetus with prolonged postmortem retention was found in a monoamniotic monochorionic twin placenta with an artery to artery anastomosis with the live twin[8]. There was umbilical cord torsion, but as the authors point out, the thrombus could have occurred post mortem.

In an infant with severe protein C deficiency although heterozygous an umbilical thrombus was noted in the cord near the insertion in the abdominal wall. No further description of the thrombus was provided[9].


Series: A single report combines 6 cases of umbilical thrombus found prospectively in an unselected population with all placentas examined, 14 cases found in a series of placentas examined for an obstetrical indication, and 32 cases found in 31 years of autopsies[5]. The majority of cases were of umbilical vein thrombus, with a pathologic definition of a coral-like framework of agglutinated platelets covered by leukocyte-containing layers of condensed fibrin. This is a highly subjective definition, and condensed fibrin compared to loose fibrin in a clot in an area of settling leukocytes (buffy coat) can be a difficult distinction. All six prospective cases had only vein thrombosis, and no untoward outcome. Of the 14 other placental cases, 6 had arterial thrombus, three were intrauterine fetal deaths, and one was an intrapartum stillbirth associated with a true knot and a nuchal cord with 5 wrappings. One of the stillborn infants was the case report described above. One of the two liveborn infants had a five minute Apgar of 3. All of the autopsy cases with arterial thrombosis had been dead in utero for more than a week or were described as macerated. I would be very suspect of the diagnosis of thrombosis with prolonged post mortem retention unless it was associated with clear organization or fibrin lamellae.

Another series was culled from 40,000 placental examinations from one institution which yielded 11 cases excluding any with umbilical vein and artery thrombosis[10]. The definition of thrombus was “agglutinated platelets covered by a leukocyte-containing layer of condensed fibrin”. The clinical history was not available in 3 cases, two were stillborn, and three had intrauterine growth retardation. One had fetal distress with Apgars of 6/9 and another infant had Apgars of 8/8. The only information listed on the last infant was proteinemia which could imply renal vein thrombus, but there was no further information. This paper draws conclusions as if there was no selective factor in submission of the placentas for pathology e.g. i.e. that umbilical artery thrombosis is associated with stillbirth and growth retardation. If the cases were selected and averaging approximately 1,100/year, then the inferences may be true, but there is likely an increased incidence of stillbirths, growth retardation, and fetal distress in the placentas that were sent for examination. The authors did note necrosis of the umbilical artery in the thrombosed vessel although often of only the very inner layer. Interestingly, the microphotograph demonstrates thrombus in a hypoplastic artery, and I do not think it is a thrombus, but is stasis of blood likely due to thrombus somewhere along the artery.

In the sheep with multiple separate cotyledons, ligation of a single umbilical artery does lead to growth retardation or death[11]. In the sheep, there is acute loss of half of the placental mass, similar to infants without a Hyrtl anastomosis.


Literature review


1.         Devlieger, H., et al., Thrombosis of the right umbilical artery, presumably related to the shortness of the umbilical cord: an unusual cause of fetal distress. Eur J Obstet Gynecol Reprod Biol, 1983. 16(2): p. 123-7.

2.         Solano Sanchez, S.R., et al., [Umbilical artery thrombosis. A report of a case and review of the literature]. Ginecol Obstet Mex, 2005. 73(6): p. 332-5.

3.         Afriat, R., et al., [Prenatal diagnosis of spontaneous thrombosis of the umbilical artery during the third trimester of pregnancy. Two cases with surviving infants]. J Gynecol Obstet Biol Reprod (Paris), 1995. 24(4): p. 411-4.

4.         Cook, V., et al., Umbilical artery occlusion and fetoplacental thromboembolism. Obstet Gynecol, 1995. 85(5 Pt 2): p. 870-2.

5.         Heifetz, S.A., Thrombosis of the umbilical cord: analysis of 52 cases and literature review. Pediatr Pathol, 1988. 8(1): p. 37-54.

6.         Larciprete, G., et al., Absent end diastolic flow in umbilical artery and umbilical cord thrombosis at term of pregnancy. Med Sci Monit, 2003. 9(5): p. CS29-33.

7.         Klaritsch, P., et al., Spontaneous intrauterine umbilical artery thrombosis leading to severe fetal growth restriction. Placenta, 2008. 29(4): p. 374-7.

8.         Colgan, T.J. and S.C. Luk, Umbilical-cord torsion, thrombosis, and intrauterine death of a twin fetus. Arch Pathol Lab Med, 1982. 106(2): p. 101.

9.         Goodwin, T., G. Gazit, and E. Gordon, Heterozygotes protein C deficiency presenting as severe protein C deficiency and peripartum thrombosis: Successful treatment with protein C concentrate. Obstet Gynecol, 1995. 86: p. 662-4.

10.       Sato, Y. and K. Benirschke, Umbilical arterial thrombosis with vascular wall necrosis: clinicopathologic findings of 11 cases. Placenta, 2006. 27(6-7): p. 715-8.

11.       Hobel, C.J., et al., Ligation of one umbilical artery in the fetal lamb; experimental production of fetal malnutrition. Obstet Gynecol, 1970. 36(4): p. 582-8.



Umbilical artery thrombosis
Candy stripe appearance from hemoglobin diffusion

Umbilical artery thrombosis
This cord had a true knot, ? role in etiology

Umbilical artery thrombus
Longer duration hemoglobin diffusion

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