New Nigerian Journal of Clinical Research

: 2018  |  Volume : 7  |  Issue : 11  |  Page : 32--34

Umbilical cord thrombosis, a cause of intra-uterine fetal demise: A case study

Ezinne Chimdi Iwunze1, Charles Ikenna Iwunze2,  
1 Department of Community Medicine, University of Port Harcourt Teaching Hospital, Port Harcourt, Nigeria
2 Department of Surgery, University of Port Harcourt Teaching Hospital, Port Harcourt, Nigeria

Correspondence Address:
Charles Ikenna Iwunze
C/o Prof Ihekwaba A.E, P.O. Box: 245 Uniport, Choba, Port Harcourt, Rivers State


Umbilical vein thrombosis accompanies umbilical cord abnormalities that cause blood vessel ectasia and lead to perinatal mortality. The precise diagnosis and management remains an unsolved puzzle to clinicians. This is to report a case of umbilical cord thrombosis in a patient with intrauterine fetal demise and propose an addendum to the current management. Early detection of umbilical cord abnormalities, intensive fetal monitoring, prompt intervention, and preemptive delivery may prevent perinatal mortality.

How to cite this article:
Iwunze EC, Iwunze CI. Umbilical cord thrombosis, a cause of intra-uterine fetal demise: A case study.N Niger J Clin Res 2018;7:32-34

How to cite this URL:
Iwunze EC, Iwunze CI. Umbilical cord thrombosis, a cause of intra-uterine fetal demise: A case study. N Niger J Clin Res [serial online] 2018 [cited 2023 Mar 23 ];7:32-34
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Full Text


Stillbirths have remained a public health concern over the years although the international response has been poor.[1] The indicators for stillbirth are yet to be captured in the sustainable development goal initiative.[1] This neglected problem has a tremendous psychological impact on mothers and their families. The World Health Organization (WHO) estimates that 2.6 million stillbirths take place yearly on a global scale.[1],[2] South Asia and Sub-Saharan Africa account for about 75% of all stillbirths.[2] Approximately 7000 women have a stillbirth daily with 60% taking place in rural families.[1],[2] About half of all stillbirths occur during labor, making the intrapartum period very critical.[2],[3] Most of the stillbirths can be prevented.[3] The WHO defined stillbirth as a baby born with no signs of life at ≥28 completed weeks of gestation.[2],[4] The main causes of stillbirth are as follows: child birth complications, postterm pregnancy, maternal infections (malaria, syphilis, and HIV), maternal disorders (especially hypertension, obesity, and diabetes), fetal growth restriction, and congenital abnormalities.[2] Umbilical cord thrombosis is an unusual cause of perinatal mortality[5] with an estimated incidence of 1/1300 pregnancies and a slight male preponderance.[6]

Most cases of vascular thrombosis are venous[5] as in the index patient. The predisposing factors include abnormalities such as excessive twisting, very long or very short cord, presence of a true knot, marginal or velamentous placental insertion, loops around the body or cervical region, and very thin cord with little Wharton's jelly.[6],[7] These conditions result in vascular ectasia of the blood vessels of the cord, blood stasis and subsequently thrombosis, reduced blood flow leading to fetal hypoxia, and intrauterine fetal death[6],[7] as in the index patient.

 Case Report

Mrs. W was a 34-year-old civil servant in her third pregnancy who registered for antenatal care at 20 weeks of gestation. Index pregnancy was diagnosed using serum beta-human chorionic gonadotropin 3 weeks after her last normal menstrual period. She presented at the clinic at 40 weeks + 3 days gestation with complaints of absent fetal kicks 10 h before the presentation.

At presentation, fetal heart sounds were absent on auscultation. The cervix was 3 cm dilated. An urgent ultrasound scan and fetal Doppler flow analysis revealed absent cardiac activity and a diagnosis of intrauterine fetal death was made. She was admitted, and labor was induced by membrane sweep. She had a normal vaginal delivery of a stillborn female weighing 2.8 kg. Amniotic fluid at delivery was clear, with reduced volume. The placenta appeared normal. The umbilical cord was thick, approximately 60 cm in length with 5-cm length of blood clot within, and extending 20 cm from the fetal end of the umbilical cord [Figure 1]. She was discharged from the hospital the following day on antibiotics, sedatives, and hematinics.{Figure 1}

The index pregnancy was complicated by hypertension which developed during the postpartum period of her last confinement. Her blood pressure was adequately controlled with low-dose nifedipine, from which she was weaned at 37 weeks to prevent prolonged pregnancy. Weekly monitoring following nifedipine withdrawal showed sustained blood pressure control. Oral glucose tolerance test done at 24 weeks was normal.

Previous pregnancies were uneventful with good fetal outcomes. However, her last intrapartum period had a prolonged second-stage secondary to fetal macrosomia. She has a family history of diabetes and hypertension. At the booking visit, she was neither pale nor anicteric. She weighed 86 kg, with a body mass index of 34 kg/m.[2] Her blood pressure was 110/70 mmHg, pulse rate was 80/min, and fundal height of 20 cm above her pubic symphysis. Urinalysis done showed no abnormalities. Packed cell volume was 35%. Ultrasonography confirmed a viable singleton fetus at 20 weeks of gestation with no gross congenital anomaly. She attended antenatal clinic as scheduled and received hematinics, malaria chemoprophylaxis, and tetanus immunoprophylaxis. The fetal presentation was cephalic from 26 weeks until term. The maternal full blood count was essentially normal but with mild relative lymphocytosis of 50.2%. Her clotting profile revealed no abnormality.

The postmortem examination reported areas of placental infarcts, 58-cm long umbilical cord with eccentric insertion, and containing three vessels: two arteries and one vein. Approximately 22 cm from the fetal end was a dark red segment measuring 5 cm in length with thrombi within the vein. The histological analysis of the umbilical cord showed sections of dilated vascular channels containing thrombi with surrounding hemorrhagic areas. The cause of death was placental insufficiency from umbilical vein thrombosis.


The umbilical cord is the link between the maternal placenta and the fetus. It develops from the “primitive ridge” of the embryo around 7–8 weeks of postmenstruation.[8] It is flexible, allowing for fetal mobility which is vital for the overall development of the fetus, especially the neuromotor development.[8] The cord's outer layer (amniotic epithelium), Wharton's jelly, and the connective tissue contribute to its stability.[8] Originally, containing four umbilical vessels: Two arteries and two veins, the right vein atrophies by the 6th week of gestation, forming the typical three-vessel umbilical cord.[8] The “vein” delivers oxygenated blood and nutrients to the fetus while the “arteries” convey deoxygenated blood in the reverse direction to the placenta.[8] Traction force from fetal movements in the first trimester stimulates growth of the cord. The cord appears coiled and rope-like, the lack of which has been linked to reduced fetal movement and poor pregnancy outcome.[8],[9] Normal umbilical cord length ranges from 35 to 70 cm at birth, with coils at intervals of 0.3–0.5 coils/cm.[8]

Umbilical cord pathologies differ from those of the placenta.[9] Umbilical cord accidents are responsible for 10% of stillbirths.[9] Solitary venous thrombosis, simultaneous venous and arterial thrombosis, and arterial thrombosis alone are found in about 70%, 20%, and 10% of the cord thrombosis, respectively.[6] Umbilical cord abnormalities such as a short cord (<35 cm) or an excessively long cord (>70 cm) or diameter <8.0 mm, hypercoiling (>0.5 coils/cm) or hypocoiling (<0.3 coils/cm), placental umbilical cord insertion <2 cm from the placental edge,[8] presence of true knots, and loops are known risk factors for mechanical compression or vascular stasis.[5],[6],[7] These conditions lead to decreased blood flow and fetal hypoxia in most cases, and are often associated with intrauterine growth retardation, slight reduction in amniotic fluid volume, fetal distress, and ultimately fetal demise if appropriate intervention is not instituted[6] as observed in our patient. Failure to recognize these at-risk fetuses is the major problem facing mothers and clinicians and prevent request for additional investigation.[10] In addition, melatonin secretion which peaks to 60 pg at 3 a.m. (circadian rhythm) increases uterine stimulation and may overwhelm a compromised fetus leading to umbilical cord-related stillbirths, usually during maternal sleep, between 2 a.m. and 4 a.m.[9] as also noted by our patient.

Majority of stillbirths occurred after the age of fetal viability when the outcome would have been good if the baby was delivered in good condition.[10] The fetus responds to umbilical cord compression with hyperactivity. This is thought to help reposition the fetus and relieve umbilical cord compression.[9]

The identification of at-risk patients, diagnosis, and continuous monitoring until delivery requires that routine obstetric sonography should assess the appearance, location, composition, and size of the cord in each trimester.[9],[10] Targeted ultrasound examination in early pregnancy furnishes superior details than in later pregnancy.[8] A 24-h ultrasound study of fetal body movements noting fetal behavior (bedtime and midnight to 6 a.m.) may be indicated.[9] Comparing earlier maternal ultrasound findings with those at the later stages of the pregnancy is pertinent.

On detection of umbilical cord accidents, the mother should be admitted and ultrasound evaluation with color Doppler[8] and fetal heart rate monitoring for at least 24 h done. Abnormal fetal behavior or heart rate warrants extended observation, including weekly ultrasound monitoring, with thorough umbilical cord evaluation, and fetal pulmonary maturation treatment with corticosteroids (depending on the gestational age).[9] Prompt cesarean delivery is indicated.[6],[9] Intensive fetal monitoring is required during delivery.[6]

Postnatally, histological analysis of the umbilical cord and maternal and neonatal hematologist consultation may assist in making a more conclusive diagnosis, as a tool for preventing a future recurrence.


The risk of development of intrauterine complications should be well considered. Regular biophysical monitoring of the fetus coupled with prompt delivery is necessary to avert possible adverse fetal outcomes that may arise from umbilical cord abnormalities.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


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2WHO. Still Births; 2017. Available from: [Last accessed on 2017 Jun 25].
3WHO. True Magnitude of Stillbirths and Maternal and Neonatal Deaths Underreported; 2016. Available from: http://www.Who.Int/mediacentre/news/releases/2016/stillbirths-neonatal-deaths/en/. [Last accessed on 2017 Jun 25].
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