Abstract: OBJECTIVE: Early neonatal mortality within the first 24 hours contributes substantially to overall neonatal mortality rates. The definition of birth asphyxia (BA) is imprecise, and reliable cause-specific mortality data are limited; thus the estimated proportion of BA-related deaths globally remains questionable. The objective was to determine the presumed causes of neonatal death within the first 24 hours in a rural hospital in Northern Tanzania. METHODS: This is a prospective descriptive observational study conducted in the delivery room and adjacent neonatal area. Research assistants were trained to observe and record events related to labor, neonatal resuscitation, and 24-hour postnatal course. BA was defined as failure to initiate spontaneous respirations and/or 5-minute Apgar score <7, prematurity as gestational age <36 weeks, and low birth weight (LBW) as birth weight <3rd centile for gestational age. Data were analyzed with χ2 and Student’s t tests. RESULTS: Over 1 year, 4720 infants were born and evaluated. Of these, 256 were admitted to the neonatal area. Forty-nine infants died secondary to BA (61%), prematurity (18%), LBW (8%), infection (2%), congenital abnormalities (8%), and unclear reason (2%). The 5-minute Apgar score was ≥7 in 50% of the infants who died secondary to BA. CONCLUSIONS: Most cases of early neonatal mortality were related to BA, and prematurity and LBW are additional important considerations. Reducing perinatal mortality requires a multifaceted approach with attention to issues related to BA, potential complications of prematurity, and LBW. The 5-minute Apgar score is a poor surrogate of BA. * Abbreviations: BA — : birth asphyxia BMV — : bag mask ventilation BW — : birth weight FHR — : fetal heart rate GA — : gestational age LBW — : low birth weight

Abstract: The current decline in under-five mortality shows an increase in share of neonatal deaths. In order to address neonatal mortality and possibly identify areas of prevention and intervention, we studied causes of admission and cause-specific neonatal mortality in a neonatal care unit at Kilimanjaro Christian Medical Centre (KCMC) in Tanzania. A total of 5033 inborn neonates admitted to a neonatal care unit (NCU) from 2000 to 2010 registered at the KCMC Medical Birth Registry and neonatal registry were studied. Clinical diagnosis, gestational age, birth weight, Apgar score and date at admission and discharge were registered. Cause-specific of neonatal deaths were classified by modified Wigglesworth classification. Statistical analysis was performed in SPSS 18.0. Leading causes of admission were birth asphyxia (26.8%), prematurity (18.4%), risk of infection (16.9%), neonatal infection (15.4%), and birth weight above 4000 g (10.7%). Overall mortality was 10.7% (536 deaths). Leading single causes of death were birth asphyxia (n = 245, 45.7%), prematurity (n = 188, 35.1%), congenital malformations (n = 49, 9.1%), and infections (n = 46, 8.6%). Babies with birth weight below 2500 g constituted 29% of all admissions and 52.1% of all deaths. Except for congenital malformations, case fatality declined with increasing birth weight. Birth asphyxia was the most frequent cause of death in normal birth weight babies (n = 179/246, 73.1%) and prematurity in low birth weight babies (n = 178/188, 94.7%). The majority of deaths (n = 304, 56.7%) occurred within 24 hours, and 490 (91.4%) within the first week. Birth asphyxia in normal birth weight babies and prematurity in low birth weight babies each accounted for one third of all deaths in this population. The high number of deaths attributable to birth asphyxia in normal birth weight babies suggests further studies to identify causal mechanisms. Strategies directed towards making obstetric and newborn care timely available with proper antenatal, maternal and newborn care support with regular training on resuscitation skills would improve child survival.

Abstract: Objective Free-radical-induced reperfusion injury has been recognised as an important cause of brain tissue damage after birth asphyxia. Allopurinol reduces the formation of free radicals, thereby potentially limiting the amount of hypoxia–reperfusion damage. In this study the long-term outcome of neonatal allopurinol treatment after birth asphyxia was examined. Design Follow-up of 4 to 8 years of two earlier performed randomised controlled trials. Setting Leiden University Medical Center, University Medical Center Groningen and University Medical Center Utrecht, The Netherlands. Patients Fifty-four term infants were included when suffering from moderate-to-severe birth asphyxia in two previously performed trials. Intervention Infants either received 40 mg/kg allopurinol (with an interval of 12 h) starting within 4 h after birth or served as controls. Main outcome measures Children, who survived, were assessed with the Wechsler Preschool and Primary Scales of Intelligence test or Wechsler Intelligence Scale for Children and underwent a neurological examination. The effect of allopurinol on severe adverse outcome (defined as mortality or severe disability at the age of 4–8 years) was examined in the total group of asphyxiated infants and in a predefined subgroup of moderately asphyxiated infants (based on the amplitude integrated electroencephalogram). Results The mean age during follow-up (n=23) was 5 years and 5 months (SD 1 year and 2 months). There were no differences in long-term outcome between the allopurinol-treated infants and controls. However, subgroup analysis of the moderately asphyxiated group showed significantly less severe adverse outcome in the allopurinol-treated infants compared with controls (25% vs 65%; RR 0.40, 95%CI 0.17 to 0.94). Conclusions The reported data may suggest a (neuro)protective effect of neonatal allopurinol treatment in moderately asphyxiated infants.

Abstract: It is not possible to identify all pregnancies at risk of neonatal hypoxic-ischemic encephalopathy (HIE). Many women use some form of analgesia during childbirth and some anesthetic agents have been shown to be neuroprotective when used as analgesics at subanesthetic concentrations. In this study we sought to understand the effects of two anesthetic agents with presumptive analgesic activity and known preconditioning-neuroprotective properties (sevoflurane or xenon), in reducing hypoxia-induced brain damage in a model of intrauterine perinatal asphyxia. The analgesic and neuroprotective effects at subanesthetic levels of sevoflurane (0.35%) or xenon (35%) were tested in a rat model of intrauterine perinatal asphyxia. Analgesic effects were measured by assessing maternal behavior and spinal cord dorsal horn neuronal activation using c-Fos. In separate experiments, intrauterine fetal asphyxia was induced four hours after gas exposure; on post-insult day 3 apoptotic cell death was measured by caspase-3 immunostaining in hippocampal neurons and correlated with the number of viable neurons on postnatal day (PND) 7. A separate cohort of pups was nurtured by a surrogate mother for 50 days when cognitive testing with Morris water maze was performed. Both anesthetic agents provided analgesia as reflected by a reduction in the number of stretching movements and decreased c-Fos expression in the dorsal horn of the spinal cord. Both agents also reduced the number of caspase-3 positive (apoptotic) neurons and increased cell viability in the hippocampus at PND7. These acute histological changes were mirrored by improved cognitive function measured remotely after birth on PND 50 compared to control group. Subanesthetic doses of sevoflurane or xenon provided both analgesia and neuroprotection in this model of intrauterine perinatal asphyxia. These data suggest that anesthetic agents with neuroprotective properties may be effective in preventing HIE and should be tested in clinical trials in the future.

Abstract: Objective: To determine the risk factors for birth asphyxia Materials and Methods: After obtaining the approval from the Institutional Review Board, a retrospective case-control study recruited 450 women who delivered at Phramongkutklao Hospital between January 1, and December 31, 2009 were recruited by consecutive selection. The study sample comprised 150 women who delivered newborns with an APGAR score at 1 minute of 7 or less, while the control comprised 300 women who delivered newborns with an APGAR score at 1 minute more than 7. The risk factors for birth asphyxia were determined. Result: The risk factors associated with birth asphyxia included moderate to thick meconium (OR 5.51, 95% CI 2.58-11.77), breech presentation (OR 4.53, 95% CI 1.72-11.92), birth weight < 2,500 grams (OR 2.46, 95% CI 1.4-4.29), sedation with morphine or pethidine (OR 2.29, 95% CI 1.37-3.84) and preterm delivery (OR 2.08, 95% CI 1.24-3.51). Conclusion: Most risk factors associated with birth asphyxia can be prevented. Therefore the correct, quick and accurate diagnosis and proper management can reduce severe birth asphyxia.

Abstract: Aim: Serum S100B and neuron-specific enolase (NSE) levels are elevated after perinatal asphyxia, but the influence of hypothermia on these proteins has not been previously reported. The aim of this study was to evaluate the effect of systemic hypothermia on these protein levels after perinatal asphyxia, time course, and association with perinatal factors and neurodevelopmental outcome at 2 years of age. Methods: Serum S100B and NSE levels were measured at fixed time points in asphyxiated infants treated with standard intensive care on hypothermia (HT: n = 13) or normothermia (NT: n = 11). Results: Serum S100B and NSE levels were grossly elevated in both HT and NT groups. Compared with the values at 6 h of age, S100B values decreased over time in both groups (NT: p = 0.002, HT: p = 0.04). Serum S100B values were lower in HT infants compared with those in NT infants (p = 0.047 at 48 h). Serum S100B and NSE values were significantly higher in infants who died or developed severe neurological impairment (S100B, p < 0.05 at all time points; NSE, p = 0.036 at 24 h of age). Conclusion: Both NSE and S100B levels are highly elevated following asphyxia. Serum S100B levels were lower in the HT group and strongly correlated with the neurodevelopmental outcome.

Abstract: Perinatal asphyxia can lead to multi-organ insult which includes cardiovascular dysfunction. The objective was to study the relationship between cardiac function, perfusion and troponin. Unit database was accessed to identify infants with perinatal asphyxia over the last 2 years. Information from medical records and archived echocardiographic images was retrieved. Comparisons for echocardiographic information were made with healthy term infants. Seventeen infants with perinatal asphyxia were identified, of which three were excluded (one—33 weeks gestation, two—coagulopathy and pulmonary hypertension); 14 infants received therapeutic hypothermia. Median (range) gestation and birthweight were 39 (37–42) weeks and 3,550 (2,380–3,992) g respectively. Mean (S.D.) rectal temperature and time of echocardiogram were 33.5 ± 0.5 °C and median (range) 7.7 h [3, 4, 5, 6, 7, 8, 9, 10] respectively. Majority of infants had low biventricular outputs. Median (range) SVC flow was 29.8 ml/kg/min (13–96.2). Median (range) troponin was 0.77 μg/L (0.17–2.6); normal ≤ 0.08 μg/L. Markedly low coronary flows (diastolic VTI median (range) 2.1 (1.3–2.9) cm were noted compared to controls. Coronary flow had a significantly positive correlation with left ventricular output. Higher troponin levels were associated with lower aortic stroke velocity. A close association between cardiac output, perfusion and troponin was noted. A dichotomy between blood pressure and flow parameters was noted, indicating the wide variation in vascular resistance in these infants. Biventricular output, coronary and SVC flows were significantly higher in the control population. In conclusion, inter-variable relationship between cardiac output, coronary flow and troponin is an important addition to the understanding of cardiovascular impact of perinatal asphyxia.

Abstract: Background: Initial aEEG background pattern has been used as a predictor of neurological outcome after asphyxia and has been used as inclusion criterion for trial

Abstract: Background: Initial aEEG background pattern has been used as a predictor of neurological outcome after asphyxia and has been used as inclusion criterion for trial

Abstract: Background Despite progresses in neonatal care, the mortality and the incidence of neuro-motor disability after perinatal asphyxia have failed to show substantial improvements. In countries with a high level of perinatal care, the incidence of asphyxia responsible for moderate or severe encephalopathy is still 2–3 per 1000 term newborns. Recent trials have demonstrated that moderate hypothermia, started within 6 hours after birth and protracted for 72 hours, can significantly improve survival and reduce neurologic impairment in neonates with hypoxic-ischemic encephalopathy. It is not currently known whether neuroprotective drugs can further improve the beneficial effects of hypothermia. Topiramate has been proven to reduce brain injury in animal models of neonatal hypoxic ischemic encephalopathy. However, the association of mild hypothermia and topiramate treatment has never been studied in human newborns. The objective of this research project is to evaluate, through a multicenter randomized controlled trial, whether the efficacy of moderate hypothermia can be increased by concomitant topiramate treatment.

Abstract: Background: Asphyxia is a medical condition in which placental or pulmonary gas exchange is impaired or they cease all together, typically producing a combination of progressive hypoxemia and hypercapnea. Objective: In addition to regional differences in its etiology; it is important to know its risk factors. Materials and Methods: This is a case-control study, all neonates born from May 2002 to September 2005 in Vali-e-Asr Hospital were studied. 9488 newborns were born of which 6091 of the live patients were hospitalized in NICU. 546 newborns were studied as case and control group. 260 neonates (48%) were female and 286 neonates (52%) were male. Among the neonates who were admitted, 182 of them were diagnosed with asphyxia and twice of them (364 newborns) were selected as a control group. The variables consist of; gestational age, type of delivery, birth weight, prenatal care, pregnancy and peripartum complications and neonatal disorders. Results: Our studies showed that 35 (19.2%) patients had mild asphyxia, 107 (58.8%) had moderate asphyxia and 40 (22%) were diagnosed as severe asphyxia. Mean maternal age was 34.23±4.29yr; (range: 23-38 yr); and mean of parity was 2±1.2; (range: 1-8). Risk factors in our study included emergent Caesarian Section, preterm labor (<37w), low birth weight (<2500g), 5 minute Apgar (less than 6), need for resuscitation, nuchal cord, impaired Biophysical Profile, neonatal anemia, and maternal infertility. Conclusion: All risk factors listed above play a role in asphyxia. The majority of these factors are avoidable by means of good perinatal care.

Abstract: Birth asphyxia results in a significant percentage of neonatal morbidity and mortality. A key factor in the management of this complication is the early and accurate detection of brain damage following asphyxia. Currently, reliable tools for such diagnosis are absent. Extensive research has focused on biomarkers in an attempt to solve this matter. Recent data marked serum and urine elevation of the S100B protein as an established peripheral biomarker for detection of brain injury including traumatic head injuries and brain damage following cardiac arrest and stroke. In the past decade, a substantial number of studies illustrated the potential use of S100B testing in order to detect brain damage in asphyxiated newborns. This review summarizes the available data regarding the use of S100B as a biomarker of brain damage following birth asphyxia.

Abstract: Objective : To document the number, disease pattern and outcome of patients admitted to a neonatal intensive care unit (NICU) at a high altitude having catchment areas of patients at about the same level. Design : Descriptive study Method : The study was conducted at a level II Care NICU at Sikkim Manipal Institute of Medical Sciences at Gangtok from November 2004 to October 2005. The data of all the admitted neonates were analyzed for age, weight at the time of admission, sex, cause of admission and outcome. Results : 212 neonates (58% males) were admitted during the study period. 17.5% were admitted within 6 hours of birth and 51.4% within 72 hours of birth. Neonatal jaundice, prematurity, infections and birth asphyxia were the major causes of admission. NICU mortality was 8%. The most common cause of death was prematurity followed by birth asphyxia. Conclusions: Study showed relatively increased incidence of neonatal jaundice and decreased neonatal infections at high altitude. (Key words: neonatal jaundice; birth asphyxia; high altitude) DOI: http://dx.doi.org/10.4038/sljch.v41i2.4396

Abstract: Background: Birth asphyxia is one of the commonest causes of neonatal morbidity and mortality in developing countries. Together with prematurity and neonatal sepsis, they account for over 80% of neonatal deaths.Aim: To determine the incidence and mortality rate of birth asphyxia in Warri Niger Delta of Nigeria. Materials and Method: Recovery of case notes of all the newborn babies seen from January 2000 to December 2007 at Central Hospital Warri and GN children’s Clinic, Warri, was undertaken. They were analyzed and those with birth asphyxia were further analyzed, noting the causes, severity of asphyxia, sex of the babies, management given. Results: A total of 864 out of 26,000 neonates seen within this period had birth asphyxia. 525 (28/1000 live births) had mild asphyxia while 32% were severely asphyxiated. 61.5% of the asphyxiated were born at maternities, churches or delivered by traditional birth attendants or at home. Prolonged labour was the commonest cause of asphyxia and asphyxia was more in neonates from unbooked patients. Conclusion: The incidence of bith asphyxia in Warri is 28/1000. Majority of patients are from prolonged labour and delivery at unrecognized centres. Health education will dratically reduce the burden of asphyxia neanatorum as unsubtanciated religous beliefs have done a great havoc.

Abstract: Systemic effects of whole-body cooling to 35 °C, 33.5 °C, and 30 °C in a piglet model of perinatal asphyxia: implications for therapeutic hypothermia

Abstract: Birth asphyxia is often associated with a high seizure burden that is predictive of poor neurodevelopmental outcome. The mechanisms underlying birth asphyxia seizures are unknown. Using an animal model of birth asphyxia based on 6-day-old rat pups, we have recently shown that the seizure burden is linked to an increase in brain extracellular pH that consists of the recovery from the asphyxia-induced acidosis, and of a subsequent plateau level well above normal extracellular pH. In the present study, two-photon imaging of intracellular pH in neocortical neurons in vivo showed that pH changes also underwent a biphasic acid–alkaline response, resulting in an alkaline plateau level. The mean alkaline overshoot was strongly suppressed by a graded restoration of normocapnia after asphyxia. The parallel post-asphyxia increase in extra- and intracellular pH levels indicated a net loss of acid equivalents from brain tissue that was not attributable to a disruption of the blood–brain barrier, as demonstrated by a lack of increased sodium fluorescein extravasation into the brain, and by the electrophysiological characteristics of the blood–brain barrier. Indeed, electrode recordings of pH in the brain and trunk demonstrated a net efflux of acid equivalents from the brain across the blood–brain barrier, which was abolished by the Na/H exchange inhibitor, N-methyl-isobutyl amiloride. Pharmacological inhibition of Na/H exchange also suppressed the seizure activity associated with the brain-specific alkalosis. Our findings show that the post-asphyxia seizures are attributable to an enhanced Na/H exchange-dependent net extrusion of acid equivalents across the blood–brain barrier and to consequent brain alkalosis. These results suggest targeting of blood–brain barrier-mediated pH regulation as a novel approach in the prevention and therapy of neonatal seizures.

Abstract: Background: Intermittent fetal heart rate (FHR) monitoring during labor using an acoustic stethoscope is the most frequent method for fetal assessment of well-bei

Abstract: In paediatrics, sick preterm infants are at highest risk of developing thrombotic complications. Haemostasis is in a fine balance in the neonatal period, despite age-related differences in coagulation proteins. However, both inherited and acquired risk factors can disrupt this balance and can lead to thrombosis. Important risk factors are sepsis, asphyxia, dehydration, central venous lines and inherited and acquired thrombophilia. Among various treatment modalities, anticoagulation is primarily used in the management of thrombosis. Different agents, dosages and durations of treatment in this age group are extrapolated from adult data. The article reviews the epidemiology, pathophysiology, risk factors, diagnosis and treatment of thrombotic disorders in preterm infants.

Abstract: Introduction Ventricular fibrillation (VF) and asphyxia account for most cardiac arrests but differ in cardiac arrest course, neurologic deficit, and myocardial damage. In VF resuscitation, cardiac mitochondria were known to be damaged via excess generation of reactive oxygen species. This study evaluated the difference of cardiac mitochondrial damages between VF and asphyxial cardiac arrests. Methods In the VF + electrical shock (ES) group, VF was induced and untreated for 5 minutes, followed by 1 minute of cardiopulmonary resuscitation (CPR) and 1 ES of 5 J. Animals were killed immediately after ES. In the asphyxia group, cardiac arrest was induced by airway obstruction, and then pulselessness was maintained for 5 minutes, followed by 1 minute of CPR. The animals were killed immediately after CPR. The histology and ultrastructural changes of myocardium and complex activities and respiration of mitochondria were evaluated. The mitochondrial permeability transition pore opening was measured based on mitochondrial swelling rate. Results The histopathologic examinations showed myocardial necrosis and mitochondrial damage in both cardiac arrests. Instead of regional damages of myocardium in the VF + ES group, the myocardial injury in the asphyxia group distributed diffusely. The asphyxia group demonstrated more severe mitochondrial damage than the VF + ES group, which had a faster mitochondrial swelling rate, more decreased cytochrome c oxidase activity, and more impaired respiration. Conclusions Both VF and asphyxial cardiac arrests caused myocardial injuries and mitochondrial damages. Asphyxial cardiac arrest presented more diffuse myocardial injuries and more severe mitochondrial damages than VF cardiac arrest.

Abstract: Objective: To determine the frequency of birth asphyxia and short term (early) outcome in relation to age at admission and place of delivery. Methods: A descriptive cross-sectional study was conducted in the Paediatric Department, Neonatal Ward of Liaquat University Hospital (LUH) Hyderabad from January to December 2009. All babies were received at our nursery or delivered in LUH with birth asphyxia were included, while babies having major congenital abnormalities, with birth weight < 1800 gm or preterm were excluded. After consent and enrollment their detailed history including peri-natal history, Apgar score, resuscitation measures, problems and outcome were recorded on a pre-designed study proforma. Short term outcome was measured after 7 hours as clinically improved, developed neurological disability (Hypoxic Ischaemic Encephalopathy stage II or III) or death. Results: The frequency was (n=600; 25%) of LUMHS born and (n=310; 61.63%) were received within 6 hours, (n=272 45% were LUMHS born and n=7 7% were out born), (n=37; 38.95%) within 24 hours and (n=9; 10.3%) after 24 hours. On initial neurological evaluation (n=90; 15%) were normal while clinical signs of HIE were present in 85%, with (n=180; 30%) in stage I, (n=210; 35%) in Stage II and (n=120; 20%) in stage III of HIE. Outcome was measured after 72 hours, around 53.3% (320) were normal, 31.6% (190) developed neurological disability, while 15% (90) babies expired. Outcome was better in Liaquat University of Medical Health Sciences (LUMHS) born than out-born with statistically significant difference in terms of disability (Chi-square test P-value <0.0001) but no difference was noted in terms of disability to death. There was a statistically improved outcome for babies received within 6 hours than those after 6 hours of birth (Chi-square test P-value <0.0255). Conclusion: Early recognition of birth asphyxia and timely referral to tertiary center can reduce morbidity and mortality.

Abstract: Accidents constitute one of the greatest risks to children, yet there are few medical reports that discuss the subject of accidental asphyxia. However, a systematic analysis of all documented cases in Germany over the years 2000-2008 has now been conducted, aiming at identifying patterns of accidental asphyxia, deducing findings, defining avoidance measures and recommending ways of increasing product safety and taking possible precautions. The analysis is based on a detailed retrospective analysis of all 91 relevant autopsy reports from 24 different German forensic institutes. A variety of demographic and morphological data was systematically collected and analysed. In 84 of the 91 cases, the sex of the victim was reported, resulting in a total of 57 boys (68 %) and 27 girls (32 %). The age spread ranged between 1 day and 14 years, with an average of 5.9 years. Most accidents occurred in the first year of life (20 %) or between the ages of 1 and 2 years (13 %). In 46 % of cases, the cause of death was strangulation, with the majority occurring in the home environment. In 31 % of all cases, the cause of death was positional asphyxia, the majority resulting from chest compression. In 23 % of cases, the cause of death was aspiration, mainly of foreign bodies. Today, accidental asphyxiation is a rare cause of death in children in Germany. Nevertheless, the majority of cases could have been avoided. Future incidence can be reduced by implementing two major precautions: increasing product safety and educating parents of potentially fatal risks. Specific recommendations relate to children's beds, toys and food.

Abstract: Limited predictive value of early changes in EEG spectral power for neural injury after asphyxia in preterm fetal sheep

Abstract: Objective: To carry out a nationwide epidemiologic survey on the neonates in urban hospitals with an attempt to understand the disease spectrum and treatment outcomes of hospitalized neonates in China. Methods: The clinical data of 43,289 hospitalized neonates from 86 hospitals in 47 Chinese cities (22 provinces) between January 1, 2005 and December 31, 2005 were retrospectively analyzed. Results: The male:female ratio was 1.73:1. Premature infants accounted for 26.2% of the hospitalized neonates, which was higher than that reported in 2002 (19.7%). The top three diseases during the neonatal period were jaundice, pneumonia, and hypoxic-ischemic encephalopathy. The incidences of pneumonia, meconium aspiration syndrome, and bilirubin encephalopathy in term infants were higher than those in premature infants, while the incidences of asphyxia, respiratory distress syndrome, and pulmonary hemorrhage in term infants were lower than those in premature infants. The incidences of asphyxia, small for gestational age infant, and wet lung were higher in neonates whose mother had pregnancy induced hypertension. The outcomes of these hospitalized neonates included: recovered, 63.9%; improved, 27.3%; discharged due to the family’s own decisions, 7.6%, and died, 1.2%. Nearly half (46.4%) of the neonatal death occurred within 24 hrs after admission. Conclusion: The incidence of premature birth shows an increasing trend among hospitalized neonates. Since the neonatal deaths mainly occur within 24 hrs after admission, monitoring during this period should be enhanced.

Abstract: A nuchal cord (or Cord-Around-the Neck (CAN)) occurs when the umbilical cord becomes wrapped around the fetal neck 360 degrees. Nuchal cords are very common, the incidence of nuchal cord increases with advancing gestation from 12% at 24 to 26 weeks to 37% at term [1]. Most are not associated with perinatal morbidity and mortality. In some fetuses and newborns CAN may cause problems, especially when the cord is tightly wrapped around the neck. The cluster of cardiorespiratory and neurological signs and symptoms associated with unique physical features that occur secondary to tight cord-round-the-neck has been referred to as 'tCAN syndrome' (tight Cord Around the Neck Syndrome) [2]. A small number of studies have shown that nuchal cord and or tCAN can affect the outcome of delivery and may have long-term effects on the infant [3] and but as a causative factor for stillbirth it is debatable [4,5]. However, some case reports of postmortem findings on stillbirths show negative pathology reports and tight cord around the neck being the only cause of death [6]. It is the unique physical features of tCAN syndrome that distinguishes it from birth asphyxia even though there are many similarities between these two conditions. Umbilical cord abnormalities are considered as one of the causative factor for birth asphyxia. The manifestation of tCAN symptomatology seems to happen both in the presence of normal and depressed AGPAR scores [7]. Umbilical cord compression due to tCAN may cause obstruction of blood flow first in thin walled umbilical vein, while infant’s blood continues to be pumped out of baby through the thicker walled umbilical arteries thus causing hypovolemia and hypotension resulting in acidosis [8]. Anemia [9] and mild respiratory distress may occur. Some of these infants may also have facial and conjuctival petechiae [10] and rarely petechiae of the neck and upper part of the chest and skin abrasion of neck [11] where the cord was tightly wrapped and facial suffusion [12], all of which can also be seen in some postmortem findings of stillbirth infants who had tCAN [Archana Bargaje, personal communication]. If born alive, some of these infants may also be somewhat obtunded with a low tone and have transient feeding difficulties. These findings raise the possibility of transient encephalopathy, which may lead to long-term complications. A stillbirth attributed to a cord problem should have evidence of cord obstruction or circulatory compromise. Other potential causes of stillbirth need to be excluded prior to labelling cord abnormalities as the causative factor, since cord abnormalities seen in more than a third of all normal live births. The tCAN Syndrome may conceptually be similar to strangulation which may result in non lethal problems or death. The pathophysiological mechanisms of strangulation injuries (lethal and non lethal) involves venous, arterial obstruction (arterial spasm due to carotid pressure) in the neck and vagal collapse (increased parasympathetic tone) [13]. This can lead to cerebral stagnation, hypoxia, and unconsciousness, which, in turn, produces loss of muscle tone. The same pathophysiology of strangulation may possibly be applicable to tCAN syndrome in neonates. A study on potentially asphyxiating conditions and spastic cerebral palsy in infants of normal birth weight showed evidence of association of tCAN in children with quadriplegia [14]. Intermittent umbilical cord occlusion in preterm and near term sheep caused a decline in pO2 and pH, and higher PCO2 and altered brain protein synthesis/degradation [6]. Whether human fetal intermittent strangulation by tCAN have similar brain protein alterations and thus long-term effects remains to be seen. Using specific placental histologic criteria for umbilical blood flow restriction in unexplained stillbirth Parast et al [4] showed significant correlation of placental changes of “minimal histologic criteria” with cord accidents (as tCAN is part of cord accidents). Nuchal cords showed highest rates of thrombosis-related placental histopathology and fetal thrombotic vasculopathy and thrombosis seems to be highly specific for cord related stillbirths [4,5].