Although very rare, umbilical cord hematoma (UCH) is a real serious complication of pregnancy. It represents a rare cause of acute fetal distress that may be shown by the decrease of fetal movement or fetal death [
Lately, a case of UCH resulted in perinatal death at our department stimulating our interest in performing this review of the literature, emphasizing the research on pathogenesis, diagnosis, and management for UCH.
The study by Dipple et al., with 36 cases, is the largest series published on this topic so far. It estimates an incidence rate of 1 in 5505. Although umbilical cord complications may be the second most common cause of stillbirth [
Our review of the English literature resulted in 9 publications of 11 cases of UCH in the years 2008–2017 [
A review of the literature was conducted in order to identify the case reports reported in the English language. We searched PubMed MEDLINE electronic database published between 2008 and 2017 on
Case reports described in literature.
Authors | Age/parity | Gestational age (wk) | Antenatal course | Mode of delivery | Macroscopical lesion | Hystopathological examination | Fetal outcome |
---|---|---|---|---|---|---|---|
Towers et al. [ |
23/1 | 31 | Decreased fetal movements for 18 hours | Cesarean | Umbilical cord hematoma 3 × 2 cm | Hematoma associated with umbilical vein. Thrombotic material was seen within the vein, but the vein was not totally occluded; the umbilical arteries were compressed to the side but patent. | None/AS 7 at 1 min and 9 at 5 min |
22/0 | 40 | Decreased fetal movements for 30 hours | Cesarean | Umbilical cord hematoma 4 × 2 cm | Vein/arterial lumens were compressed but both patent. | None/discharged well at follow up at 18 months/AS 2 at 1 min, 6 at 5 min and 8 at 10 min | |
39/1 | 38 | Absent fetal movements for 14 hours | Cesarean | Umbilical cord hematoma 3 × 2 cm | Vein/umbilical arteries appeared patent. | None/AS 8 at 1 min and 9 at 5 min | |
|
|||||||
Barbati et al. [ |
44/1 | 40 | Reduction of fetal movements, FHR with severe reduced variability of <5 bpm and late decelerations | Cesarean | Large cord hematoma (5 × 3.7 × 2.6) at 3 cm from the fetal insertion | Two arteries and one vein with no other abnormalities in the form of knots and loops. Extravasation of blood into the surrounding Wharton’s jelly caused by the rupture of a dilated umbilical artery | Tachypnea, cyanosis, and anemia without any other physical or neurological damage/AS 6 at 1 min and 9 at 5 min |
|
|||||||
Kumar et al. [ |
31/1 | 36 | Two vessel-cord, right pelvic kidney, decreased fetal movement for 12 hours | Cesarean | Marginal umbilical cord insertion, avulsed umbilical artery rupture: single artery is shown to be ruptured at the site of cord insertion to the placenta. | Fetal branch artery ruptured with a vessel wall significant for mild acute inflammation and necrotic muscle cells. | Tachycardia, tachypnea, and polyuric acute kidney failure secondary to cortical-sparing acute tubular necrosis; discharged well at 14 day/AS 3 and 5 at 1 and 5 min |
|
|||||||
Jouannelle et al. [ |
Not given | At term | Decreased fetal movements, fetal heart decelerations | Cesarean | Massive umbilical cord hematoma at the skin junction, with cord compression | Not given | Baby was flat/AS 0 at 1 min, 3 at 5 min, 7 at 10 min. |
|
|||||||
Tonni et al. [ |
19/0 | At term | Loss of fetal heart lasting 90 seconds, at birth | Vaginal | Fresh hematoma in the cord | A rupture in the wall of the umbilical vein with discontinuity in the layers of the subintimal and internal elastic lamina. One umbilical artery presented peripheral dissection, subintimal myxoid degeneration, and widespread disruption of the elastic fibers; marked reduction in myofibroblasts in Wharton’s jelly. |
Sever mixed acidosis, fetal anemia, and severe HIE/AS 3 at 1, 5, and 10 min |
|
|||||||
Abraham et al. [ |
27/multipara | 35 | Decreased fetal movements (ultrasound scan confirmed fetal death) | Vaginal | Central cord insertion. Umbilical cord had 4-5 sausage shaped swellings suggestive of cord hematoma of varying sizes all along the length of the cord with the largest measuring 6 × 3 cm | Cord had multiple swellings suggestive of umbilical cord hematoma. |
Stillbirth |
|
|||||||
McAdams and Chabra [ |
32/1 | At term | Uneventful | Vaginal | Umbilical cord hematoma | Not given | None |
|
|||||||
Hooper and Sebire [ |
Not given | At term | Uneventful | Vaginal | Umbilical cord proximal to the baby has dark red discoloration and increased thickness, measuring 4.5 in diameter at the widest part. | Not given | None |
|
|||||||
Arora et al. [ |
Not given | 39 | Uneventful | Vaginal | A 4 cm and 2 cm wide reddish purple, nontender swelling in the cord proximal to the level of the skin | Not given | None |
The exact etiology of UCH still remains unexplained. Many theories have been proposed but without final results. Probably a combination of different factors leads to UCH.
Risk factors for spontaneous umbilical cord hematoma are various. They include morphologic anomalies of the umbilical cord (both in length and in thickness), true knots, cord prolapse, traction or torsion, velamentous insertion of the cord, vessel wall abnormalities, umbilical cord cysts, abdominal trauma in pregnancy, postterm pregnancy, infections (chorioamnionitis and funisitis), deficiency of Wharton’s jelly, congenital defects, and many more remain unexplained [
Spontaneous bleeding in the umbilical cord is due to a disruption of the vessel wall through which, in most cases, an extravasation of blood into Wharton’s jelly occurs. [
In our analysis of 11 cases, 2 cases showed evidence of chorioamnionitis [
The diagnosis is usually made postnatally, but in some cases it can be made by Doppler ultrasound scan prenatally, assessing the cord and the blood flow in the umbilical vessels [
Detailed physical examination of the placenta and cord confirmed the presence of the hematoma in all 11 cases described. During macroscopic examination, umbilical cord may have abnormal appearance with dark red discoloration and markedly increased thickness [
Autopsy plays an important role in investigating the cause of stillbirth that occurs in the antenatal period.
A 29-year-old multipara woman, with an uncomplicated pregnancy, presented at 41 weeks and 3 days of gestation for elective labour induction. The patient showed Grade 1 obesity (BMI of 30 kg/m2).
Labour was induced with a controlled-release hydrogel pessary containing 10 mg prostaglandin E2. The patient was placed on continuous fetal heart rate (FHR) monitoring. After 24 hours from the labour induction, the Bishop score was unchanged and the vaginal insert removed. 3 hours later, the induction continued with intravenous injection of oxytocin 10 UI. After approximately 1 hour, spontaneous rupture of membranes with amniotic clear fluid was observed.
8 hours after induction patient delivered a hypotonic, with no evidence of cardiac activity, male newborn. FHR corresponded to type 1 and 0 of Piquard criteria during the second stage of the labour.
Venous pH at birth was 7.11 (base excess, 16.2 mMol/L), and arterious pH was 6.96 (base excess, 14.2 mMol/L). Apgar score at 1 minute was 0. After 40 minutes of continuous resuscitation, the fetus was still asystolic, and it was therefore decided to stop the resuscitation efforts.
The gross examination of the placenta and of the umbilical cord revealed the presence of blackish-reddish material in the proximity of the placental insertion measuring approximately 3 cm. The umbilical cord presented vascular ectasia at 18 cm from the placental insertion. An hematoma of the cord was noted at 34 cm from the placental insertion; the hematoma was described as an infiltrate of 2 cm, in the tones of black and red, extended to the whole umbilical cord section.
The histological examination of the cord highlighted oedema of Wharton’s jelly, circumscribed hematic infiltrates, marked venous ectasia with delamination and hematic infiltration of the venous walls, extensive hemorrhage of Wharton’s jelly within the whole portion of the cord. The lumen of the vein was completely occluded by coagulated hematic material.
The histological examination of the placenta highlighted intense vascular congestion of villi and hematic infiltrates as for intervillous hematomas.
Measurements of crown heel, crown rump, head circumference, foot length and weight indicated a regular intrauterine development.
The internal gross examination and the hystopathological examination of lung tissue revealed elements indicating physiological respiration in presence of FHR. The above pattern confirmed that the fetus started the respiratory activity after being delivered before dying.
The umbilical cord is called the fetal life line, and it is the vital link between the fetus and placenta. Various abnormalities are observed in the morphology and pathology of the umbilical cord but knowledge of them is quite poor.
A considerable number of stillbirths that are thought to be unexplained may be attributable to placental or cord pathologies. UCH can compromise the maternal-fetal circulation by compressing the vessels or because of the blood loss within the cord itself, leading to perinatal asphyxia and stillbirth [
Stillbirth can occur either antenatally or perinatally, but sometimes UCH is uneventful. In our case, the stillbirth was peripartum; the results from external inspection, hystopathological examination, and autopsy suggest the manifestation, before death, of a hyperacute asphyctic mechanism. Furthermore, macro- and microscopic analyses of the umbilical cord revealed pathological alterations indicating an acute trauma with compression, vascular laceration, and hemorrhagic infiltration.
This must be due to the occurrence of mechanical compression of the umbilical cord during labour, with acute interruption of the fetoplacental circulation. The cause of death is therefore attributable to an intrauterine asphyxia caused by acute mechanical compression of the umbilical cord, difficult to detect antenatally.
Cord accident (compromised umbilical blood flow) as a cause of stillbirth is underreported, mainly due to a lack of diagnostic criteria.
A complete fetopathological examination can state causality between hematoma and stillbirth, exclude another fetal or placental cause of death and consequently reassure the parents for the prognosis of another pregnancy. The issue of hematoma-related complications is also important because of its medicolegal aspect since litigation may occur. Timing of delivery should be based on gestational week as long as the fetus shows well-being signs. Preterm or urgent delivery should be performed in case of fetal distress or reduced movements.
Because of the rarity of this condition, every new case of UCH should be reported in order to improve the knowledge of predisposing factors, prenatal diagnosis, and clinical management.
The authors declare that they have no conflicts of interest.