Love them or hate them, everyone* has one. The umbilical stump is all that remains of the physical bond the neonate has with their mother. We’ve looked at the importance of the umbilical vessels as a means of oxygenation, but the time must come to cut the cord.
The normal umbilical cord
For those of you familiar with your embryology, you might recall that the umbilical cord starts off life as the yolk stalk, containing the vitelline duct, fused to the body stalk containing a pair of umbilical arteries, a single umbilical vein and the allantois, all slathered in Wharton’s jelly and covered with amnion. The vitelline duct obliterates around week 8 of fetal life. The umbilical arteries and veins become the lateral umbilical ligaments and ligamentum teres and the urachus becomes the median umbilical ligament.
It is normally the colour of freshly cooked calamari (with a similar consistency to calamari that has been overcooked) but occasionally it may be stained green (due to the passage of meconium) or yellow (due to the presence of hyperbilirubinaemia).
Around one percent of all cords have a single umbilical artery making it one of the most common congenital abnormalities.
The cord should separate by about day 8 but delayed separation has been linked with an increased incidence of omphalitis as well as a number of immune disorders such as leucocyte adhesion deficiency.
Immediate versus delayed cord clamping
When the baby is delivered about a third of the fetal-placental blood remains in the placenta (around 30 mls/kg) so with delayed cord clamping the infant gains around 25-30mls/kg of blood via a placental transfusion. The majority of this transfusion occurs within a minute if the neonate is held at the level of the uterus and is almost complete by three minutes.
A recent Cochrane review suggested that delayed cord clamping (by 1 to 3 minutes) is “likely to be beneficial as long as access to treatment for jaundice requiring phototherapy is available“. This review suggested no difference in adverse events such as severe maternal post-partum haemorrhage, low Apgar scores or worsening neonatal mortality figures when compared to immediate clamping. There did appear to be a correlation with increased birth weight (by about 100g) and increased haemoglobin with a concomitant increased risk of needing phototherapy for jaundice.
WHO recommend delaying clamping for at least one minute unless the baby is not breathing spontaneously and requires positive pressure ventilation. This holds true in both the developed and developing setting. The benefits of delayed clamping outweigh the risk of maternal-fetal transmission of HIV.
Animal studies have also shown that immediate cord clamping might lead to reduction in cardiac output. Once the cord has been clamped right ventricular volume drops leading to decreased RV output by around 50%. There is also an increase in LV afterload due to the lack of the low-resistance placental circulation.
What about “milking” the cord?
Milking refers to the practice of actively expressing blood from the cord. Small volume studies have been performed on pre-term infants and suggest milking leads to a higher haemoglobin concentration (than delayed clamping alone) and reduced need for transfusion as well as a shorter duration of mechanical ventilator support.
Problems with the umbilical stump
Omphalitis is an infection around the umbilical stump that first manifests as redness and erythema and can progress to life threatening sepsis. The devitalized stump provides a fertile medium for bacterial growth. Common infective agents include Staph. aureus, Streptococcus spp. and E. coli spp. Infection is linked to handling and poor hygiene and a rash of cases in the 1950s lead to regular local anti-bacterial treatment of the stump.
Risk factors for omphalitis:
- Maternal – prolonged rupture of the membranes, maternal infection, amnionitis
- Delivery – non-sterile birth, inappropriate cord care
- Neonatal – low birth weight, delayed cord separation, leukocyte adhesion deficiency, neonatal alloimmune neutropaenia
In developed countries the incidence of infection is low, in the region of 0.7%, and so “dry cord care” is recommended. Allowing the stump to air dry speeds up the separation process. In low income countries the incidence is much higher, up to 6%, and so this standard does not apply. One study, in Nepal, found that the use of 4% aqueous chlorhexidine decreased incidence of omphalitis by 75% and mortality by 24% when compared to the Westernized ideal of “dry cord care”. Better hygiene also decreases the incidence of neonatal tetanus. When an education initiative stopped the Kenyan Maasai from routinely smearing the umbilical stump with cattle dung the death rate from tetanus dropped from 82 per 1000 to 0.75 per 1000 infants.
Whilst mild cases may respond to good hygiene it can progress to necrotizing fasciitis of the abdominal wall if left unchecked. Because of this most cases require admission, close monitoring and treatment with parenteral antibiotics.
An umbilical hernia is one of the more common umbilical disorders and is seen in around 10% of Caucasian babies. They are also more common in premature infants and those with trisomy 21. Like all true hernias they may contain peritoneal fluid, pre-peritoneal fat, intestine or omentum protruding through a fascial defect.
The hernia is normally painless but as it is more obvious when the child screams and cries parents might bring the child to a healthcare provider concerned that something serious is going on. The defect in the deep fascia of the abdominal wall usually heals up over time with the majority closing spontaneously over the first three years of life. The larger the defect the less likely that spontaneous closure is to occur. Those defects that are less than 1.5cm in diameter are often left until the age of four to six years to close on their own. Incarceration of peritoneal contents is exceedingly rare.
Risk factors for umbilical hernias:
- Premature or low birth-weight infants
- Children of African descent
- Trisomy 21
- Marfan’s syndrome
Why is there an increase in the incidence in African children? A Nigerian study found them in 91% of children under the age of 6 and 64% of 6 to 9 year olds. Nutrition may be a factor as only 1.3% of children in the higher socio-economic groups had them. This has also been seen to be true in adults.
Umbilical granulomata are small (less than 1cm) lumps of umbilical tissue that remain following separation of the cord and are one of the more common causes of a persistent “wet umbilicus“. Small ones are typically pedunculated masses of moist, raw looking tissue and can be treated with topical application of silver nitrate. Larger ones might require formal resection. Take a look at Sean Fox’s summary here.
Vitelline duct remnants join the terminal ileum to the umbilicus. This omphalo-mesenteric remnant may persist as the famous Meckel’s diverticulum affecting 2% of the population. See what Pediatric EM Morsels has to say on the matter.
Urachal remnants connect the dome of the bladder to the anterior abdominal wall. During fetal development this patent tube allows free drainage of urine but becomes obliterated by solid tissue to become the median umbilical ligament. Occasionally it fails to close creating a patent urachus, a urachal sinus or a cyst. A urachal cyst may only declare itself later in life with symptoms that mimic appendicitis. Ultrasound may help make the diagnosis.They should all be referred to a paediatric surgeon for further assessment.
‘Innies’ versus ‘Outies’
I had always thought that it was something to do with how the cord was cut or clamped but that cannot be true so I fired up Dr Google to find an answer – it’s not the sort of thing you can find in PubMed. Apparently outies are due to a little extra scar tissue that affect about 10% of the population.
We’ll talk about umbilical access another time.
*So who doesn’t have a belly button and why?