Displaying 1-10 letters out of 580 published
Herpes virus must be considered as one of the causes for late onset sepsis
Dear Editor, Archives of Disease of childhood: Foetal and Neonatal edition
We read the review article by Dong et al(1) with interest. We wanted to congratulate the authors on a very balanced and clinically relevant review; highlighting the epidemiological, therapeutic and preventative aspects of late onset sepsis caused by bacteria and fungi. We believe that the review would have been even more clinically relevant, if it had included viral sepsis e.g. herpes simplex virus (HSV) infection. In a recent UK based study(2) we demonstrated a high neonatal herpes sepsis incidence (17.5 per 100,000 live births) highlighting the non- specific clinical presentation and high mortality of this disease. The majority of cases in our study presented between days 3 and 14 of life; with non-specific symptoms, with or without a herpetic rash. The differentiation from bacterial late onset sepsis at presentation is extremely difficult. Extrapolation of our data implies UK mortality due to herpes of over 1.5 times that of group B streptococcal sepsis(3).
Unless attending clinicians are vigilant and expand the differential diagnoses of suspected late onset sepsis, there will be increased morbidity and mortality from neonatal herpes infections. Raised Alanine transaminase (ALT) can be an early marker for HSV infection and should be part of the bloods for evaluation of sepsis. Intravenous acyclovir should routinely be included in the protocols of late onset sepsis.
Dushyant Batra Patrick Davies Craig Smith Nottingham University Hospitals NHS Trust, Nottingham UK
References: 1. Dong Y, Speer CP. Late onset sepsis: recent developments. Arch Dis Child Fetal Neonatal Ed 2015;100:F257-F263 doi;10.1136/archdischild-2014- 306213 2. Batra D, Davies P, Manktelow BN, Smith C. The incidence and presentation of neonatal herpes in a single UK tertiary centre, 2006-2013. Arch Dis Child 2014;99:916-921. 3. Edmond KM, Kortsalioudaki C, Scott S, et al. Group B streptococcal disease in infants aged younger than 3 months: systematic review and meta- analysis. Lancet 2012;379:547-556.
Conflict of Interest:
Re: Impact of the NICE early onset neonatal sepsis guideline in our neonatal unit: Length of stay and number of lumbar punctures performed are not increased.
Mukherjee et al. were interested by the response to their paper indicating that not all units may have seen an increase in antibiotic use and length of stay following introduction of NICE guidance CG149. The important difference for our unit was the introduction of a second CRP at 18-24 hours to inform further investigations (lumbar puncture) and length of antibiotic course. It is not surprising that units that already used a second CRP did not see this effect. In our unit the second CRP was frequently raised in asymptomatic infants. The NICE guidance places emphasis on the clinical evaluation of baby, but also includes in this the second CRP result. The second CRP may well lead to differences in interpretation about possible sepsis between units, particularly in infants, that have always been well and asymptomatic.
The guidance reads: 126.96.36.199 Consider performing a lumbar puncture to obtain a cerebrospinal fluid sample in a baby, who did not have a lumbar puncture at presentation, who is receiving antibiotics, if it is thought safe to do so and if the baby: *has a C-reactive protein concentration of 10 mg/litre or greater, or *has a positive blood culture, or *does not respond satisfactorily to antibiotic treatment.
In our unit the raised CRP has led to increased lumbar puncture and greater length of antibiotic courses in asymptomatic infants. We have a clear policy of careful clinical observation of 'at risk' infants, but inclusion of CRP in the assessment of asymptomatic infants may be problematic. We feel that a clearer distinction between the infants that have been always asymptomatic needs to be made, and the justification for a second CRP in this patient group is poorly studied. We believe that a more explicit statement about avoiding LP in babies that have always been asymptomatic may be helpful, or at least should be studied further in this patient group.
Conflict of Interest:
Management of infantile haemangiomas of the eyelid
In this review (Eye disorders in newborn infants (excluding retinopathy of prematurity), Wan MJ, VanderVeen DK, Arch Dis Child Fetal Neonatal Ed. 2015 May;100(3):F264-9. doi: 10.1136/archdischild-2014- 306215. Epub 2014 Nov 13, PMID:25395469) the authors describe clinical presentation, natural history and treatment of infantile haemangiomas (IH). These vascular tumors are common and if left untreated will result in visual compromise and we agree that an urgent ophalmological opinion is warranted. According to the authors treatment options include beta blockers, corticosreroids, surgery for small lesions and laser therapy for superficial lesions. However in reality beta blockers would be used in the vast majority of patients and to not clarify this point is misleading. The first report of the successful use of propranolol in 2008 and subsequent randomised controlled trials totally revolutionised treatment of IHs and, since then, propranolol has become the first-line therapeutic agent in the management of IHs. (1,2) Propranolol has been shown to be more effective than corticosteroids and it is associated with fewer side effects. Therefore surgical treatment is rarely required. Pulse dye laser may occasionally be an appropriate treatment for residual skin changes at a later stage. We feel that this is an important message to the readers of this journal: along with the ophthalmologist these patients need an urgent referral to a paediatric dermatologist for the medical treatment of IH. References: 1. A randomized, controlled trial of oral propranolol in infantile hemangioma. Leaute-Labreze C,et al, N Engl J Med. 2015 Feb 19;372(8):735- 46. doi: 10.1056/NEJMoa1404710. 2. Propranolol for severe hemangiomas of infancy.Leaute-Labreze C, Dumas de la Roque E, Hubiche T, Boralevi F, Thambo JB, Taeeb A.N Engl J Med. 2008 Jun 12;358(24):2649-51. doi: 10.1056/NEJMc0708819
Conflict of Interest:
Re: I know you don't like our American brand of English, but......
We thank Dr Perlin for his response which specifically refers to the prevention of early onset Group B streptococcus (GBS) infection.
Similar declines in GBS EONS have been seen in many other countries that have introduced screening for GBS and IAP. In contrast, in the UK the RCOG recommendation for a risk based approach has not been associated with a fall in the incidence of GBS EONS. If the incidence fell by 75%, as would be predicted from the experience of other countries, this would reduce GBS infection in at least 300 babies per year in the UK.
The UK National Screening Committee do not recommend universal screening for GBS for a number of reasons including that it is not cost effective. However Colbourn et al (BMJ. 2007;335:655) concluded from a detailed analysis that "culture testing for low risk term women, while treating all preterm and high risk term women, would be the most cost effective option". Kaambwa et al (BJOG. 2010;117:1616) concluded that "The current strategy of risk-factor-based screening is not cost-effective compared with screening based on culture". The best test for GBS is enhanced culture medium (ECM) testing of low vaginal and rectal swabs at an estimated cost of ?11, but is not routinely available in the UK. Conventional tests may miss GBS even if it is present.
Concerns have been expressed about penicillin allergy but true anaphylaxis is rare. Law et al reported (J Med Screen 2005;12:60) that there were no recorded deaths in the first 1.8 million women given IAP in the USA, and other reports have stressed that giving IAP under direct supervision is very safe. Concern has been expressed about the practice of giving women (and therefore their fetuses) large doses of broad spectrum antibiotic before skin incision for caesarean section, as currently recommended by the RCOG, in terms of the effect it might have on the development of the newborn's immune system. Around 33% of pregnant women currently receive antibiotics at some stage during pregnancy, including erythromycin for which there is now evidence of harm, yet the RCOG continue to recommend its use for women with preterm, pre-labour rupture of membranes (Meeraus et al, PLOS ONE | DOI:10.1371/journal.pone.0122034 March 25, 2015.) In contrast, penicillin is narrow spectrum, GBS has never developed resistance to it, and there is no evidence that preventing GBS EONS encourages other organisms to invade. The widespread use of penicillin for over 60 years means that any organisms able to become resistant to it will likely already have done so.
Current RCOG guidelines recommend giving IAP if a woman is found by chance to be a GBS carrier, yet is managed as if negative for GBS if no swab has been obtained. Her baby Is also managed differently if she is known to be GBS positive. This is illogical and women who have knowledge of GBS have very clearly stated that they wish to be screened for GBS. On the grounds of equity and choice, pregnant women at 35-37 weeks should be offered an equal opportunity to determine their GBS status and protect their babies, which can only be done by screening.
Conflict of Interest:
Symptoms of breastfeeding difficulties are the main indication for lingual frenotomy
To the Editors: We have read with interest the article by Ingram et al (1) entitled "The development of a tongue assessment tool to assist with tongue-tie identification". The authors should be commended for simplifying and validating the ATLAF assessment. However, using their tool to decide upon whether or not to carry out lingual frenotomy has neither been proven nor is it justified. Unfortunately, this study, similar to most of the current discourse about lingual frenotomy, involves only terms pertaining to the descriptive anatomy of the tongue. Even the erroneously labeled "function items" in Hazelbaker's ATLAF (2) as well as those in the current study are actually descriptions of tongue mobility and not of the function of the tongue during breastfeeding. As our group recently demonstrated by means of an indirect ultrasound analysis, tongue biomechanics during breastfeeding are highly complex (3). No published studies have thus far succeeded in establishing a significant correlation between the description of the tongue by physical examination and the clinical presentation of breastfeeding difficulties. Indeed, the studies by Griffiths (4) and by our group (5), which were specifically designed to correlate anatomy with breastfeeding difficulties, had failed to identify such a correlation. In a recently published prospective study, we described the anatomy of the tongue in a group of non-selected infants without our having prior knowledge of the presence or absence of breastfeeding difficulties (6). We found no correlation between the appearance of the tongue and breastfeeding difficulties as reported by the mother. We therefore suggested that the terminology currently used to describe situations in which the lingual frenulum affects breastfeeding be altered, since the interchangeable terms of ''tongue-tie" "ankyloglossia'', ''sublingual frenulum'', and ''short frenulum" are misleading to both lay people and professionals. Our proposed terminology uses not only descriptive anatomy but also the previously overlooked but indispensable part of every clinical diagnosis, that of the patient's story. We had further suggested that infant and mother dyads who have breastfeeding difficulties that had not been solved by a lactation consultation and that were judged as being due to the infant's lingual frenulum be clinically diagnosed and termed as having ''symptomatic tongue-tie'' (or ''symptomatic ankyloglossia"), while infants with no breastfeeding difficulties and, alternatively, those with breastfeeding difficulties that had been corrected after a lactation consultation should be considered as having an asymptomatic ''sublingual frenulum", which is universally present (6). We believe that the terms ''short frenulum'' and "non-symptomatic tongue-tie" should be abandoned. Using the Bristol Tongue Assessment Tool as a means to decide upon performing lingual frenotomy is, therefore, not appropriate. Not only may the posterior symptomatic frenulum be missed, but based upon current research, we suggest that the decision to perform lingual frenotomy should depend primarily on the clinical picture, e.g., pain and latching difficulties during breastfeeding, and not upon visual inspection of the tongue. These symptoms, together with failure of improvement of these breastfeeding difficulties after professional lactation consultation, should be the almost exclusive medical indication to perform lingual frenotomy in a breastfed infant during the neonatal period.
Shaul Dollberg, MD Beilinson Medical Center and Eyal Botzer DMD, Tel Aviv Medical Center
References: 1. Ingram J, Johnson D, Copeland M, et al, The development of a tongue assessment tool to assist with tongue-tie identification. Arch Dis Child Fetal Neonatal Ed. 2015 (Online first) 2. Hazelbaker AK. Tongue-tie morphogenesis, impact, assessment and treatment. Columbus Ohio: Aiden & Eva Press, 2010. 3. Elad D, Kozlovsky P, Blum O, et al. Biomechanics of milk extraction during breast-feeding. Proc Natl Acad Sci. 2014;111:5230-5. 4. Griffiths DM. Do tongue ties affect breastfeeding? J Hum Lact. 2004;20:409-14. 5. Dollberg S, Marom R, Botzer E. Lingual frenotomy for breastfeeding difficulties: A prospective follow-up study. Breastfeed Med. 2014;9:286-9. 6. Haham A, Marom R, Mangel L, et al. Prevalence of breastfeeding difficulties in newborns with a lingual frenulum: A prospective cohort series. Breastfeed Med 2014;9:438-44.
Conflict of Interest:
I know you don't like our American brand of English, but......
I have read the most excellent review of early onset neonatal sepsis (EONS) published recently in these Archives by Dr's Bedford Russell and Kumar. We, in America, have witnessed the gradual evolution from a risk factor approach initially advocated by the American College of Obstetricians and Gynecologists, (as opposed to universal screening during gestation, as recommended by the American Academy of Pediatrics), to universal screening proposed by both organizations. This concordance of governing opinions was reached after data collection by the Centers for Disease Control determined a lower attack rate of EONS via the universal screening method as opposed to the risk factor approach. Dr's Bedford Russell and Kumar have identified this welcome reduction in the USA as well as the controversial nature of a continued risk factor approach in the UK.
I hope the Royal College of Obstetricians and the UK National Screening Committee come to soon support the relevant change in practice.
Conflict of Interest:
Congenital Chylothorax in the UK: Findings from a BPSU epidemiological study
We read with interest the publication by Bialkowski et al (1). Their paper on infants with congenital chylothorax (CCT) in Germany focused in detail on this patient group, in comparison to our recently published paper reporting on all infants and children >24 weeks gestation to <16 years who developed a chylothorax in UK (2).
When reviewing data from infants with CCT from our epidemiological study, we have included those defined with either a neonatal 'congenital' primary diagnosis of chylothorax, i.e. development of a chylothorax that was thought to be associated with any congenital condition or malformation existing at or before birth, e.g. lymphangiectasis, hydrops fetalis, prematurity, Down syndrome or Noonan syndrome, and presenting early in life; or those with a neonatal 'other' (non-cardiac) primary diagnosis, i.e. development of a chylothorax that was thought to be associated with any disorder, or condition that developed or occurred during the first month of life, e.g. persistent pulmonary hypertension of the newborn (PPHN), birth trauma or asphyxia. The number of all of these infants equaled 20% (34 /173) of our total study population of children with chylothorax. Of note, neonates who were identified as having developed chylothorax following congenital cardiac surgery were excluded from our CCT figures.
Using Office for National Statistics (ONS) data for live births in the UK (3) during our 13-month study period in 2010-11(874,800 live births), the calculated UK incidence of CCT infants was 1 in 25,000:
* Incidence = 34 / 874,800 = 0.00004 x 100% = 0.004% (4 in 100,000) = 1 in 25,000
Therefore, the overall UK incidence of CCT was very similar to the incidence of 1 in 24,000 in Germany, as reported by Bialkowski, and as noted in their study, much lower than previous estimates (4,5).
The gestational age of the CCT infants differed somewhat between the two studies, with the majority of the German CCT population (89%; 24/27) being born at <37 weeks gestation (range 30.0-39.1 weeks) following a prenatal diagnosis, a higher percentage than our UK study, in which 65% (22/34) of the infants were born at <37 weeks gestation (range 27.5-41 weeks). This difference was reflected in the birth weight of the infants, the UK group having a median weight of 2880g (range 960-4290g), which was slightly higher than the median weight of 2500g (range 740-3940g) reported in Bialkowski's study.
Similar to the German study, the majority of CCT infants in the UK were treated with insertion of a pleural drain and a medium-chain triglyceride (MCT) diet, 76% (26/34), with 50% (17/34) also receiving TPN and 20% (7/34) also receiving Octreotide/Somatostatin. Our study identified 15% (5/34) of infants as having additional syndromal anomalies (Downs Syndrome 3/34; Noonan's Syndrome 2/34), which was half the rate reported in Germany (32%; 9/28).
Within our UK study, 71% of the CCT infants were male (24/34), in line with the reported male:female ratio of 2:1 in other studies (5,6), including that of Bialkowski. However the reasons for this gender difference remain unclear. There was an overall mortality rate for CCT in the UK of 20% (7/34), which is in line with previously published figures (5,7), but is substantially higher than the reported 11% in Germany. Further investigation of the mortality rate and its causes in CCT would seem beneficial.
Whilst reporting some differences, which may be explained by the small numbers of infants affected, these two distinct national epidemiological studies have identified similar overall incidences for CCT across their populations, and both provide greater evidence for clinicians caring for infants with CCT.
References 1. Bialkowski A., Poets CF, Franz AR. Congenital chylothorax: a prospective nationwide epidemiological study in Germany. Arch Dis Child Fetal Neonatal Ed 2015; 100:F169-F172
2. Haines C., Walsh B., Fletcher M, Davis PJ. Chylothorax development in infants and children in the UK. Arch Dis Child 2014; 99:724-30.
3. Office of National Statistics 2015 (http://ons.gov.uk/ons/taxonomy/index.html?nscl=Live+Births+and+Stillbirths#tab -data-tables)
4. Ergaz Z, Bar-Oz B, Yatsiv I, et al. Congenital chylothorax: clinical course and prognostic significance. Pediatr Pulmonol 2009; 44: 806-11.
5. Rocha G, Fernandez P, Rocha P, et al. Pleural effusions in the neonate. Acta Paediatr 2006; 95: 791-8
6. Downie I, Sasi A, Malhotra A. Congenital chylothorax: associations and neonatal outcomes. J Paediatr Child Health 2014; 50: 234-8
Conflict of Interest:
Impact of the NICE early onset neonatal sepsis guideline in our neonatal unit: Length of stay and number of lumbar punctures performed are not increased.
We were interested to read the experiences of other units 1-4 sharing their findings of increased duration of antibiotics, length of stay in hospital and lumbar punctures (LP) performed following implementation of the NICE guideline on prevention of early onset neonatal infection (EONI)5. We recently changed our practice to follow these NICE recommendations advocating observation of low risk infants to reduce antibiotic exposure whilst commencing antibiotics in those deemed higher risk 5. We have not yet found that the change in practice has increased our infant's length of stay, antibiotic days or LPs performed.
In the two months (September/October) prior to our change of practice, 69 babies were treated with IV antibiotics, averaging 2.4 babies/day, with 33.3% requiring treatment for >24hrs. In the two months (November/December) following the new guideline implementation a total of 66 babies required antibiotics, averaging 1.7 babies/day with 21.1% requiring treatment for >24hrs. We have seen no increase in the frequency of LPs performed since the change (5 babies total September/October vs. 2 November/ December). We have seen additional testing in the form of repeat FBC, UEs, LFTs for the small number of babies continuing antibiotics >24 hours as recommended by NICE (5 in the first month following implementation). We recognise this is a small sample population but our findings do not suggest a trend towards an increase in antibiotics or invasive procedures as experienced by other centres 1-4.
We acknowledge that the wide variation in clinical practice prior to the publication of NICE EONI guidelines makes it challenging to compare findings between units and may account for the differences observed. For example, we have always investigated infants receiving antibiotics with an initial CRP/blood cultures and repeat CRP at 18-24 hours to inform the decision to cease antibiotics. Conversely, our colleagues' letters suggest the second CRP is a change in their practice and therefore may account for the increased antibiotic duration they observed 1-4.
Variation in the threshold to perform an LP may account for the differing trends in frequency between units. NICE suggests consideration of LP with a CRP >10 2. Locally we do not have a set CRP number that would prompt an LP but make this decision based upon the baby's clinical picture with acknowledgment of the CRP. In our babies that had an LP, their CRP's ranged from 24-160. In our first month post-implementation we saw 5 babies with a CRP rise (13-25) that necessitated a prolonged antibiotic course but did not have an LP as the baby was clinically well, with no signs of CNS involvement.
We have developed a monitoring chart, the Neonatal Early Warning Score (NEWs) in order to record observations for all babies at risk of EONI. In our first month we saw 51 babies on NEWs monitoring - 32 required antibiotics and 16 on NEWs monitoring only. Despite initial concerns of increased workload for postnatal staff these charts have embedded into practice with the majority of infants (78%) appropriately commenced on the chart for the required time period and we hope this will improve with further familiarity and education. We acknowledge that our experiences are early but we will continue to practice the new guideline following an audit that has identified no significant issues or clinical concerns. Further audit will be undertaken in due course, combined with other units in our MCN who are shortly integrating the new guideline into their practice.
1) Naydeva-Grigorova T, Manzoor A, Ahmed M. Arch Dis Child Fetal Neonatal Ed 2015; 100:F93-F94.
2) Mukherjee A, Davidson L, Anguvaa L et al. NICE neonatal early onset sepsis guidance: greater consistency, but more investigations, and greater length of stay. Arch Dis Child Fetal and Neonatal Ed. Published online first: 25 Jul 2014 doi:10.1136/archdischild-2014-306349
3) Mukherjee A, Ramalingaiah B, Kennea N et al. Letter: Management of neonatal early onset sepsis (CG149): compliance of neonatal units in the UK with NICE recommendations. Arch Dis Child Fetal Neonatal Ed. Published Online First: 19 December 2014 doi:10.1136/archdischild-2014-307776
4) Mukherjee A, Davidson L, Anguvaa L et al. Short research report: NICE neonatal early onset sepsis guidance: greater consistency, but more investigations and greater length of stay. Arch Dis Child Fetal Neonatal Ed. Published Online First: 25 July 2014 doi:10.1136/archdischild-2014- 306349
5) http://www.nice.org.uk/guidance/CG149 (accessed 19 Jan 2015)
Conflict of Interest:
Oxygenation is not the only factor regulating heart rates at birth.
The alternative explanation for the cardiovascular differences between immediate and delayed cord clamping at birth suggested in this commentary is not new and has been acknowledged for over 50 years. The basic premise is that asphyxia is the underlying cause of birth-related bradycardias and that avoiding asphyxia will avoid the bradycardia and associated cardiac instability. However, neonatologists have known for almost as long that lung aeration is the primary consideration when resuscitating bradycardic infants at birth. While it was thought that the beneficial effects are due to increased oxygenation, the Bhatt (1) study showed that increasing pulmonary blood flow and restoring venous return lost due to cord clamping, was also a major contributing factor. This is supported by studies in asphyxic, bradycardic lambs (2). Although the association between severe asphyxia and bradycardia is well- established, most birth related bradycardias are unlikely to be caused by asphyxia. Indeed, the birth-related cardiovascular changes are often unrelated to changes in oxygenation, which is shown in the heart rate normograms published by Dawson (3) et al. In normal healthy term infants, over 50% had a heart rate below 100 bpm at 1 min after birth and in some infants, the heart rates increased while oxygenation remained unchanged or decreased. The Bhatt et al (1) study was designed to replicate a relatively common clinical scenario, whereby the elapsed time between delivery, cord clamping and effective ventilation onset is ~2min. As preterm infants are commonly given an opportunity to transition unassisted at birth, a 2 min time window between birth and the onset of effective respiratory support is not uncommon. To put this into context, lambs at this age do not initiate gasping until 4-5 min after cord clamping, can easily be resuscitated after 10 min and take 12-13 min before becoming asystolic (4). In the Bhatt (1) study, lambs did not gasp and heart rates did not decrease below 100 bpm and so they were only mildly asphyxic at worst. As the fetal heart rate (in utero) responses to cord clamping markedly differ from the heart response to cord clamping ex utero (4), making conclusions about neonatal cardiac responses based on fetal data is problematic. Similar problems arise if the newborn's face is surrounded by liquid (4). We note that in the study cited by the author, a saline-filled bag was placed over the lamb's head and the lambs were ventilated via a tracheostomy. Nevertheless, the alternative interpretation of their findings is that reducing the timing between cord clamping and ventilation onset leads to a more labile transition not because of oxygenation differences, but because it reduces the time that venous return and cardiac output are reduced. This is consistent with the conclusion of Bhatt et al (1). We disagree with the author's suggestion that avoiding asphyxia will by itself improve cardiovascular stability at birth. This is not only because of the reasons cited above, but because this simple view of the physiology surrounding transition will encourage clinicians to intervene and attempt to assist infants earlier than is perhaps necessary.
1. Bhatt S, Alison B, Wallace EM, et al. Delaying cord clamping until ventilation onset improves cardiovascular function at birth in preterm lambs. J Physiol. 2013;591:2113-26.
2. Klingenberg C, Sobotka KS, Ong T, et al. Effect of sustained inflation duration; resuscitation of near-term asphyxiated lambs. Arch Dis Child Fetal Neonatal Ed. 2013;98:F222-7.
3. Dawson JA, Kamlin CO, Wong C, et al. Changes in heart rate in the first minutes after birth. Arch Dis Child Fetal Neonatal Ed. 2010;95:F177- 81.
4. Sobotka KS, Morley C, Ong T, et al. Circulatory Responses to Asphyxia Differ if the Asphyxia Occurs In Utero or Ex Utero in Near-Term Lambs. PLoS One. 2014;9:e112264.
Conflict of Interest:
Early cord clamping and stability of the circulatory transition during preterm birth
The review by Hooper et al1 is timely and mounts a compelling case for a stable circulatory transition during preterm birth. However, advocacy of early ventilation with delayed cord clamping as the primary way forward to ensure such a transition is open to question, as the main supportive evidence for this paradigm comes from an experimental study by the same group,2 for which an alternative interpretation of observed findings has recently come to light. Thus, in preterm lambs, Bhatt et al2 reported relatively minor perinatal changes in heart rate, blood pressure and right ventricular output with early ventilation and delayed cord clamping. By contrast, early cord clamping followed by ventilation 2 minutes later was associated with 1) bradycardia, arterial blood pressure swings and large reductions in right ventricular output before ventilation, and 2) substantial rises in heart rate, blood pressure and right ventricular output after ventilation. The 2 minute interval employed by Bhatt et al2 between early cord clamping and the onset of ventilation is potentially problematic, however, as prior studies in fetal lambs have shown that asphyxia can develop within 2 minutes after complete occlusion of uterine arteries or the umbilical cord.3 4 Indeed, a preterm lamb birth study employing a lesser cord clamp- to-ventilation interval (1.5 minutes) has now shown that an asphyxial state rapidly develops by 45 seconds after cord clamping on aortic blood gas analysis, with a haemoglobin O2 saturation of <10% and O2 tension of <10 mmHg, associated with a fall in pH and rise in CO2 tension.5 Furthermore, similar to the onset and offset phases of brief in utero asphyxia,3 4 this asphyxial state was accompanied by 1) bradycardia, marked falls in ventricular outputs/central blood flows and redistribution of systemic flow towards the brain before ventilation, and 2) tachycardia with blood pressure and flow surges after ventilation.5 These data therefore suggest that the findings of Bhatt et al2 primarily reflected the haemodynamic effects of asphyxia occurring with an extended cord clamping-to-ventilation interval, rather than beneficial effects per se of early ventilation with delayed cord clamping. Consistent with the foregoing proposition, reducing the cord clamping-to- ventilation interval from 1.5 to 0.5 minutes (to avoid development of an established asphyxial state) markedly blunted perinatal haemodynamic fluctuations.5 This finding thus implies that circulatory stability during the preterm birth transition hinges on avoidance of asphyxia. Such avoidance can be achieved not only with the advocated paradigm of early ventilation and delayed cord clamping,1 but also with early cord clamping, if this is followed by a short interval before the onset of ventilation.5 References 1. Hooper SB, Polglase GR, te Pas AB. A physiological approach to the timing of umbilical cord clamping at birth. Arch Dis Child Fetal Neonatal Ed 2014; DOI: 10.1136/archdischild-2013-305703. 2. Bhatt S, Alison BJ, Wallace EM, et al. Delaying cord clamping until ventilation onset improves cardiovascular function at birth in preterm lambs. J Physiol 2013;591:2113-26. 3. Jensen A, Garnier Y, Berger R. Dynamics of fetal circulatory responses to hypoxia and asphyxia. Eur J Obstet Gynecol Reprod Biol 1999;84:155-72. 4. Hunter CJ, Blood AB, Power GG. Cerebral metabolism during cord occlusion and hypoxia in the fetal sheep: a novel method of continuous measurement based on heat production. J Physiol 2003;552:241-51. 5. Smolich JJ, Kenna KR, Cheung MM. Onset of asphyxial state in non- respiring interval between cord clamping and ventilation increases hemodynamic lability of birth transition in preterm lambs. J Appl Physiol 2015; DOI: 10.1152/japplphysiol.01147.2014.
Conflict of Interest:
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