How immediate cord clamping causes intraventicular haemorrhage
Intraventricular haemorrhage is a well recognised complication of preterm birth. Immediate cord clamping increases the risk of this haemorrhage (1,2) and has been implicated in other forms of brain damage.(3)
How can immediate cord clamping cause brain damage?
We have developed a computer model of fetal and adult pattern circulation. (4) The model shows what might happen when the functional umbilical circulation is suddenly occluded with early cord clamping. In fetal circulation the two sides of the heart work in parallel. 40% of the combined cardiac output (CCO) flows through the umbilical cord, while the pulmonary circulation is only about 18%. After birth, the neonate changes to an adult pattern circulation in which the two sides of the heart work in series. The output from each side is equal and is therefore 50% of the CCO of the fetus just before birth. All the output from the right ventricle passes through the pulmonary circulation.
The model clarifies what must happen when the cord is clamped before the pulmonary circulation is fully functional. When the cord is clamped 40% of the CCO must be proportionately redirected to the residual circulation. The systemic pressure almost doubles as does the cerebral circulation. The model shows that blood flow in the aortic isthmus must reverse as most of the flow through the ductus arteriosus is directed back up the aorta to the carotid arteries. Once the pulmonary circulation increases the abnormal cerebral and aortal flow returns to normal. However early cord clamping results in a loss of 40% of the cardiac return from the placenta and so shortly after the return to normal, the systemic blood pressure falls further as the cardiac output falls. If ventilation has started by this stage the pulmonary circulation greatly increases and flow through the ductus arteriosus virtually ceases, further reducing the systemic blood pressure. The filled capacity of the fully functional pulmonary circulation also reduces the circulating volume for the rest of the body.
Could the sudden sharp increase in the cerebral pressure and flow be responsible for the vascular damage which later shows as intra-ventricular haemorrhage? It is commonly observed that quickly after clamping the cord of the apnoeic neonate, respiratory efforts commence. Could this be due to the sudden cerebral insult described above? Could the subsequent hypotension lead to hypoxic ischaemic encephalopathy. Could the sudden increase in blood pressure cause myocardial strain which leaves the heart weakened?
The model confirms that the precise time of clamping is less important than the state of the circulation when the clamp is applied. Clamping a functional placental circulation will always result in a sudden redirection of blood flow. Physiological transformation consists of a slow closure of the cord arteries flowed by a controlled closure of the ductus venosus. This will normally have been completed by three minutes.
1. Rabe H, Reynolds G, Diaz-Rossello J. Early versus delayed umbilical cord clamping in preterm infants. The Cochrane Database of Systematic Reviews 2004, Issue 3. Art. No.: CD003248.pub2. DOI: 10.1002/14651858.
2. Mercer J S, Vohr B R, McGrath M M, Padbury J F, Wallach M, Oh W. Delayed cord clamping in very preterm infants reduces the incidence of intraventricular haemorrhage and late onset sepsis: A randomised controlled trial. Pediatrics 2006 117 1235 - 1242
3. Hutchon DJR Immediate cord clamping must stop - no excuses! http://bmj.com/cgi/eletters/334/7602/1027-f#166259, 20 May 2007
4. Hutchon D, Ononeze B. A model to explain intra-ventricular haemorrhage following immediate cord clamping at birth. The British International Congress of Obstetrics and Gynaecology. London July 2007 P02.37
Competing interests: No competing interests