Systemic Effects of Perinatal Asphyxia

Abstract

Perinatal asphyxia is one of the three most important causes of neonatal mortality and morbidity [1]. It is a major contributor to long term neurodevelopmental sequele in the developing world. During fetal hypoxia-ischemia, ‘diving reflex’ shunts blood from ‘non-vital areas’ such as skin and splanchnic circulation to the ‘vital organs’ like heart, adrenals, and brain to protect them from injury. Thus theoretically, any newborn with neurological injury due to asphyxia should also have derangements of the ‘non-vital organs’ like kidney and gut. However, even in cases of severe intrapartum asphyxia, the involvement of various organs is not consistent and ranges from 70 to 100 % [2, 3]. There could be multiple reasons behind this variation: (a) all organs may not be equally involved due to variable activation of ‘diving reflex’ [4], (b) use of different criteria to define multi-organ dysfunction (MOD) and asphyxia, and (c) variable timing of clinical and laboratory evaluation. The American Congress of Obstetricians and Gynecologists (ACOG) uses MOD as one of the contributory rather than essential criteria to determine the intrapartum timing of insult [5]. Although renal, cardiac, pulmonary, hepatic and gastrointestinal systems could all be affected by perinatal asphyxia, heart and kidneys are the two most important extra-cerebral organs involved. The incidence of renal injury is 50–72 % while cardiac injury has been seen in 29–78 % in various studies. Damage to these organs can be persistent and may predict outcomes [6]. Renal injury in neonatal encephalopathy is associated with more severe brain injury and adverse longterm neurodevelopmental outcome [7]. Hence, it is important to be able to make an early and reliable diagnosis of hypoxicischemic injury to these organs. Cardiac injury has been diagnosed on the basis of clinical grounds, echocardiography, electrocardiography (ECG) and elevation of cardiac enzymes. Echocardiography is most commonly used to assess myocardial dysfunction though Ctroponin-T has emerged as a marker having good correlation with severity and outcome. ECG criteria for cardiac injury in perinatal asphyxia have been described but are cumbersome to apply [8]. Moreover, there are technical difficulties in recording and interpreting ECGs in sick newborns. Traditionally, ECG criteria have used T/QRS ratio and changes in ST segment to evaluate myocardial ischemia in asphyxiated newborns. P-wave dispersion has been used to evaluate the discontinuous propagation of sinus impulse and predict atrial fibrillation in adult patients with anterior wall myocardial infarction [9]. The incidence of atrial fibrillation secondary to intrapartum asphyxia in the newborn is, however, not known. In this issue of the journal, Amoozgar et al. have attempted to understand the changes in P-wave dispersion in asphyxiated neonates [10]. They have also attempted to relate P-wave dispersion with severity of asphyxia, arrhythmias, Apgar scores and C-Troponin I. The research idea is novel as the effects of perinatal asphyxia on cardiac conduction system are not well described. Unfortunately, because of several flaws in design, methodology and analysis, reliable conclusions cannot be drawn from this study. It is not clear if all 4 of the listed criteria had to be met or any one was good enough for a diagnosis of asphyxia. The inclusion criteria for controls mention the requirement of a normal neurological examination at birth and first week. The ECGs were however recorded on day 3. It is not clear if and how many of the ‘enrolled’ infants were subsequently excluded. The authors chose a snapshot window on day 3 of life to look at the ECGs. However, the changes in the ECG are dynamic and may be A. Bhatti Department of Pediatrics, Government Medical College, Jammu, India